An inducibly-expressed subtype of prostaglandin-endoperoxide synthase. It plays an important role in many cellular processes and INFLAMMATION. It is the target of COX2 INHIBITORS.
A constitutively-expressed subtype of prostaglandin-endoperoxide synthase. It plays an important role in many cellular processes.
Compounds or agents that combine with cyclooxygenase (PROSTAGLANDIN-ENDOPEROXIDE SYNTHASES) and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of eicosanoids, prostaglandins, and thromboxanes.
A subclass of cyclooxygenase inhibitors with specificity for CYCLOOXYGENASE-2.
Enzyme complexes that catalyze the formation of PROSTAGLANDINS from the appropriate unsaturated FATTY ACIDS, molecular OXYGEN, and a reduced acceptor.
The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.
A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes.
A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes.
Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics.
An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes.
Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.
Compounds that bind to and inhibit that enzymatic activity of LIPOXYGENASES. Included under this category are inhibitors that are specific for lipoxygenase subtypes and act to reduce the production of LEUKOTRIENES.
A nonsteroidal anti-inflammatory agent with analgesic properties used in the therapy of rheumatism and arthritis.
A group of compounds that contain the structure SO2NH2.
Azoles of two nitrogens at the 1,2 positions, next to each other, in contrast with IMIDAZOLES in which they are at the 1,3 positions.
A stable, physiologically active compound formed in vivo from the prostaglandin endoperoxides. It is important in the platelet-release reaction (release of ADP and serotonin).
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
An anti-inflammatory analgesic and antipyretic of the phenylalkynoic acid series. It has been shown to reduce bone resorption in periodontal disease by inhibiting CARBONIC ANHYDRASE.
An enzyme of the oxidoreductase class primarily found in PLANTS. It catalyzes reactions between linoleate and other fatty acids and oxygen to form hydroperoxy-fatty acid derivatives.
The physiologically active and stable hydrolysis product of EPOPROSTENOL. Found in nearly all mammalian tissue.
A class of compounds named after and generally derived from C20 fatty acids (EICOSANOIC ACIDS) that includes PROSTAGLANDINS; LEUKOTRIENES; THROMBOXANES, and HYDROXYEICOSATETRAENOIC ACIDS. They have hormone-like effects mediated by specialized receptors (RECEPTORS, EICOSANOID).
A prostaglandin that is a powerful vasodilator and inhibits platelet aggregation. It is biosynthesized enzymatically from PROSTAGLANDIN ENDOPEROXIDES in human vascular tissue. The sodium salt has been also used to treat primary pulmonary hypertension (HYPERTENSION, PULMONARY).
A potent lipoxygenase inhibitor that interferes with arachidonic acid metabolism. The compound also inhibits formyltetrahydrofolate synthetase, carboxylesterase, and cyclooxygenase to a lesser extent. It also serves as an antioxidant in fats and oils.
The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5)
A cyclooxygenase inhibiting, non-steroidal anti-inflammatory agent (NSAID) that is well established in treating rheumatoid arthritis and osteoarthritis and used for musculoskeletal disorders, dysmenorrhea, and postoperative pain. Its long half-life enables it to be administered once daily.
An unstable intermediate between the prostaglandin endoperoxides and thromboxane B2. The compound has a bicyclic oxaneoxetane structure. It is a potent inducer of platelet aggregation and causes vasoconstriction. It is the principal component of rabbit aorta contracting substance (RCS).
A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt.
Enzymes of the isomerase class that catalyze the oxidation of one part of a molecule with a corresponding reduction of another part of the same molecule. They include enzymes converting aldoses to ketoses (ALDOSE-KETOSE ISOMERASES), enzymes shifting a carbon-carbon double bond (CARBON-CARBON DOUBLE BOND ISOMERASES), and enzymes transposing S-S bonds (SULFUR-SULFUR BOND ISOMERASES). (From Enzyme Nomenclature, 1992) EC 5.3.
Cell surface receptors which bind prostaglandins with a high affinity and trigger intracellular changes which influence the behavior of cells. Prostaglandin E receptors prefer prostaglandin E2 to other endogenous prostaglandins. They are subdivided into EP1, EP2, and EP3 types based on their effects and their pharmacology.
An enzyme found predominantly in platelet microsomes. It catalyzes the conversion of PGG(2) and PGH(2) (prostaglandin endoperoxides) to thromboxane A2. EC
An anti-inflammatory agent with analgesic and antipyretic properties. Both the acid and its sodium salt are used in the treatment of rheumatoid arthritis and other rheumatic or musculoskeletal disorders, dysmenorrhea, and acute gout.
An enzyme that catalyzes the oxidation of arachidonic acid to yield 5-hydroperoxyarachidonate (5-HPETE) which is rapidly converted by a peroxidase to 5-hydroxy-6,8,11,14-eicosatetraenoate (5-HETE). The 5-hydroperoxides are preferentially formed in leukocytes.
Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase.
A non-steroidal anti-inflammatory agent with antipyretic and antigranulation activities. It also inhibits prostaglandin biosynthesis.
Eicosatetraenoic acids substituted in any position by one or more hydroxy groups. They are important intermediates in a series of biosynthetic processes leading from arachidonic acid to a number of biologically active compounds such as prostaglandins, thromboxanes, and leukotrienes.
A group of physiologically active prostaglandin endoperoxides. They are precursors in the biosynthesis of prostaglandins and thromboxanes. Most frequently encountered member of this group is the prostaglandin G2.
A saclike, glandular diverticulum on each ductus deferens in male vertebrates. It is united with the excretory duct and serves for temporary storage of semen. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
A 20-carbon unsaturated fatty acid containing 4 alkyne bonds. It inhibits the enzymatic conversion of arachidonic acid to prostaglandins E(2) and F(2a).
A naturally occurring prostaglandin that has oxytocic, luteolytic, and abortifacient activities. Due to its vasocontractile properties, the compound has a variety of other biological actions.
A dual inhibitor of both cyclooxygenase and lipoxygenase pathways. It exerts an anti-inflammatory effect by inhibiting the formation of prostaglandins and leukotrienes. The drug also enhances pulmonary hypoxic vasoconstriction and has a protective effect after myocardial ischemia.
(11 alpha,13E,15S)-11,15-Dihydroxy-9-oxoprost-13-en-1-oic acid (PGE(1)); (5Z,11 alpha,13E,15S)-11,15-dihydroxy-9-oxoprosta-5,13-dien-1-oic acid (PGE(2)); and (5Z,11 alpha,13E,15S,17Z)-11,15-dihydroxy-9-oxoprosta-5,13,17-trien-1-oic acid (PGE(3)). Three of the six naturally occurring prostaglandins. They are considered primary in that no one is derived from another in living organisms. Originally isolated from sheep seminal fluid and vesicles, they are found in many organs and tissues and play a major role in mediating various physiological activities.
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
Cyclic esters of hydroxy carboxylic acids, containing a 1-oxacycloalkan-2-one structure. Large cyclic lactones of over a dozen atoms are MACROLIDES.
The relationship between the dose of an administered drug and the response of the organism to the drug.
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
Phospholipases that hydrolyze one of the acyl groups of phosphoglycerides or glycerophosphatidates.
A cyclic endoperoxide intermediate produced by the action of CYCLOOXYGENASE on ARACHIDONIC ACID. It is further converted by a series of specific enzymes to the series 2 prostaglandins.
Phospholipases that hydrolyze the acyl group attached to the 2-position of PHOSPHOGLYCERIDES.
An increase in the rate of synthesis of an enzyme due to the presence of an inducer which acts to derepress the gene responsible for enzyme synthesis.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in enzyme synthesis.
A sulfinylindene derivative prodrug whose sulfinyl moiety is converted in vivo to an active NSAID analgesic. Specifically, the prodrug is converted by liver enzymes to a sulfide which is excreted in the bile and then reabsorbed from the intestine. This helps to maintain constant blood levels with reduced gastrointestinal side effects.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system.
A 20-carbon-chain fatty acid, unsaturated at positions 8, 11, and 14. It differs from arachidonic acid, 5,8,11,14-eicosatetraenoic acid, only at position 5.
A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is an NSAID and is used principally for its analgesic activity. (From Martindale The Extra Pharmacopoeia, 31st ed)
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Enzymes catalyzing the oxidation of arachidonic acid to hydroperoxyarachidonates. These products are then rapidly converted by a peroxidase to hydroxyeicosatetraenoic acids. The positional specificity of the enzyme reaction varies from tissue to tissue. The final lipoxygenase pathway leads to the leukotrienes. EC 1.13.11.- .
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Cell surface proteins that bind THROMBOXANES with high affinity and trigger intracellular changes influencing the behavior of cells. Some thromboxane receptors act via the inositol phosphate and diacylglycerol second messenger systems.
The principal cyclooxygenase metabolite of arachidonic acid. It is released upon activation of mast cells and is also synthesized by alveolar macrophages. Among its many biological actions, the most important are its bronchoconstrictor, platelet-activating-factor-inhibitory, and cytotoxic effects.
A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.
A subtype of prostaglandin E receptors that specifically couples to GS ALPHA GTP-BINDING PROTEIN SUBUNITS and subsequently activates ADENYLYL CYCLASES. The receptor may also signal through the activation of PHOSPHATIDYLINOSITOL 3-KINASE.
A subtype of prostaglandin E receptors that specifically couples to GTP-BINDING PROTEIN ALPHA SUBUNIT, GQ and the subsequently activates TYPE C PHOSPHOLIPASES. Additional evidence has shown that the receptor can act through a calcium-dependent signaling pathway.
Compounds that inhibit the action of prostaglandins.
The major metabolite in neutrophil polymorphonuclear leukocytes. It stimulates polymorphonuclear cell function (degranulation, formation of oxygen-centered free radicals, arachidonic acid release, and metabolism). (From Dictionary of Prostaglandins and Related Compounds, 1990)
An ionophorous, polyether antibiotic from Streptomyces chartreusensis. It binds and transports CALCIUM and other divalent cations across membranes and uncouples oxidative phosphorylation while inhibiting ATPase of rat liver mitochondria. The substance is used mostly as a biochemical tool to study the role of divalent cations in various biological systems.
A group of physiologically active prostaglandin endoperoxides. They are precursors in the biosynthesis of prostaglandins and thromboxanes. The most frequently encountered member of this group is the prostaglandin H2.
The salts or esters of salicylic acids, or salicylate esters of an organic acid. Some of these have analgesic, antipyretic, and anti-inflammatory activities by inhibiting prostaglandin synthesis.
A non-steroidal anti-inflammatory agent (ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL) similar in mode of action to INDOMETHACIN.
Any of the ruminant mammals with curved horns in the genus Ovis, family Bovidae. They possess lachrymal grooves and interdigital glands, which are absent in GOATS.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
A subtype of prostaglandin E receptors that specifically couples to GS ALPHA GTP-BINDING PROTEIN SUBUNITS and subsequently activates ADENYLYL CYCLASES.
A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation.
Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed)
A CALCIUM-independent subtype of nitric oxide synthase that may play a role in immune function. It is an inducible enzyme whose expression is transcriptionally regulated by a variety of CYTOKINES.
Cell surface receptors that bind prostaglandins with high affinity and trigger intracellular changes which influence the behavior of cells. Prostaglandin receptor subtypes have been tentatively named according to their relative affinities for the endogenous prostaglandins. They include those which prefer prostaglandin D2 (DP receptors), prostaglandin E2 (EP1, EP2, and EP3 receptors), prostaglandin F2-alpha (FP receptors), and prostacyclin (IP receptors).
A lipoxygenase metabolite of ARACHIDONIC ACID. It is a highly selective ligand used to label mu-opioid receptors in both membranes and tissue sections. The 12-S-HETE analog has been reported to augment tumor cell metastatic potential through activation of protein kinase C. (J Pharmacol Exp Ther 1995; 274(3):1545-51; J Natl Cancer Inst 1994; 86(15):1145-51)
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
The attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.
An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It is used in the treatment of rheumatoid arthritis and osteoarthritis.
A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is a non-steroidal anti-inflammatory agent used for analgesia for postoperative pain and inhibits cyclooxygenase activity.
An inhibitor of nitric oxide synthetase which has been shown to prevent glutamate toxicity. Nitroarginine has been experimentally tested for its ability to prevent ammonia toxicity and ammonia-induced alterations in brain energy and ammonia metabolites. (Neurochem Res 1995:200(4):451-6)
Drugs used to cause dilation of the blood vessels.
A stable prostaglandin endoperoxide analog which serves as a thromboxane mimetic. Its actions include mimicking the hydro-osmotic effect of VASOPRESSIN and activation of TYPE C PHOSPHOLIPASES. (From J Pharmacol Exp Ther 1983;224(1): 108-117; Biochem J 1984;222(1):103-110)
Endogenously-synthesized compounds that influence biological processes not otherwise classified under ENZYMES; HORMONES or HORMONE ANTAGONISTS.
A group of LEUKOTRIENES; (LTC4; LTD4; and LTE4) that is the major mediator of BRONCHOCONSTRICTION; HYPERSENSITIVITY; and other allergic reactions. Earlier studies described a "slow-reacting substance of ANAPHYLAXIS" released from lung by cobra venom or after anaphylactic shock. The relationship between SRS-A leukotrienes was established by UV which showed the presence of the conjugated triene. (From Merck Index, 11th ed)
A subtype of prostaglandin E receptors that specifically couples to GTP-BINDING PROTEIN ALPHA SUBUNIT, GI and subsequently inhibits ADENYLYL CYCLASES.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
Drugs used to cause constriction of the blood vessels.
A subclass of eicosanoid receptors that have specificity for THROMBOXANE A2 and PROSTAGLANDIN H2.
Artifactual vesicles formed from the endoplasmic reticulum when cells are disrupted. They are isolated by differential centrifugation and are composed of three structural features: rough vesicles, smooth vesicles, and ribosomes. Numerous enzyme activities are associated with the microsomal fraction. (Glick, Glossary of Biochemistry and Molecular Biology, 1990; from Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)
Substances that reduce or suppress INFLAMMATION.
The smallest divisions of the arteries located between the muscular arteries and the capillaries.
An acridine derivative formerly widely used as an antimalarial but superseded by chloroquine in recent years. It has also been used as an anthelmintic and in the treatment of giardiasis and malignant effusions. It is used in cell biological experiments as an inhibitor of phospholipase A2.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
(9 alpha,11 alpha,13E,15S)-9,11,15-Trihydroxyprost-13-en-1-oic acid (PGF(1 alpha)); (5Z,9 alpha,11,alpha,13E,15S)-9,11,15-trihydroxyprosta-5,13-dien-1-oic acid (PGF(2 alpha)); (5Z,9 alpha,11 alpha,13E,15S,17Z)-9,11,15-trihydroxyprosta-5,13,17-trien-1-oic acid (PGF(3 alpha)). A family of prostaglandins that includes three of the six naturally occurring prostaglandins. All naturally occurring PGF have an alpha configuration at the 9-carbon position. They stimulate uterine and bronchial smooth muscle and are often used as oxytocics.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Lining of the STOMACH, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. The surface cells produce MUCUS that protects the stomach from attack by digestive acid and enzymes. When the epithelium invaginates into the LAMINA PROPRIA at various region of the stomach (CARDIA; GASTRIC FUNDUS; and PYLORUS), different tubular gastric glands are formed. These glands consist of cells that secrete mucus, enzymes, HYDROCHLORIC ACID, or hormones.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
A subcategory of phospholipases A2 that occur in the CYTOSOL.
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
Ulceration of the GASTRIC MUCOSA due to contact with GASTRIC JUICE. It is often associated with HELICOBACTER PYLORI infection or consumption of nonsteroidal anti-inflammatory drugs (NSAIDS).
The nonstriated involuntary muscle tissue of blood vessels.
Catalyzes reversibly the oxidation of hydroxyl groups of prostaglandins.
Arteries which arise from the abdominal aorta and distribute to most of the intestines.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
Trihydroxy derivatives of eicosanoic acids. They are primarily derived from arachidonic acid, however eicosapentaenoic acid derivatives also exist. Many of them are naturally occurring mediators of immune regulation.
FATTY ACIDS in which the carbon chain contains one or more double or triple carbon-carbon bonds.
The rate dynamics in chemical or physical systems.
An anti-inflammatory 9-fluoro-glucocorticoid.
Elements of limited time intervals, contributing to particular results or situations.
Established cell cultures that have the potential to propagate indefinitely.
A non-steroidal anti-inflammatory agent that is less effective than equal doses of ASPIRIN in relieving pain and reducing fever. However, individuals who are hypersensitive to ASPIRIN may tolerate sodium salicylate. In general, this salicylate produces the same adverse reactions as ASPIRIN, but there is less occult gastrointestinal bleeding. (From AMA Drug Evaluations Annual, 1992, p120)
Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated.
An enzyme that catalyzes the oxidation of arachidonic acid to yield 12-hydroperoxyarachidonate (12-HPETE) which is itself rapidly converted by a peroxidase to 12-hydroxy-5,8,10,14-eicosatetraenoate (12-HETE). The 12-hydroperoxides are preferentially formed in PLATELETS.
Ubiquitous, inducible, nuclear transcriptional activator that binds to enhancer elements in many different cell types and is activated by pathogenic stimuli. The NF-kappa B complex is a heterodimer composed of two DNA-binding subunits: NF-kappa B1 and relA.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
Azoles with an OXYGEN and a NITROGEN next to each other at the 1,2 positions, in contrast to OXAZOLES that have nitrogens at the 1,3 positions.
A competitive inhibitor of nitric oxide synthetase.
A group of compounds that contain a bivalent O-O group, i.e., the oxygen atoms are univalent. They can either be inorganic or organic in nature. Such compounds release atomic (nascent) oxygen readily. Thus they are strong oxidizing agents and fire hazards when in contact with combustible materials, especially under high-temperature conditions. The chief industrial uses of peroxides are as oxidizing agents, bleaching agents, and initiators of polymerization. (From Hawley's Condensed Chemical Dictionary, 11th ed)
A cytosolic phospholipase A2 group that plays an important role in the release of free ARACHIDONIC ACID, which in turn is metabolized to PROSTAGLANDINS by the CYCLOOXYGENASE pathway and to LEUKOTRIENES by the 5-LIPOXYGENASE pathway.
A superfamily of hundreds of closely related HEMEPROTEINS found throughout the phylogenetic spectrum, from animals, plants, fungi, to bacteria. They include numerous complex monooxygenases (MIXED FUNCTION OXYGENASES). In animals, these P-450 enzymes serve two major functions: (1) biosynthesis of steroids, fatty acids, and bile acids; (2) metabolism of endogenous and a wide variety of exogenous substrates, such as toxins and drugs (BIOTRANSFORMATION). They are classified, according to their sequence similarities rather than functions, into CYP gene families (>40% homology) and subfamilies (>59% homology). For example, enzymes from the CYP1, CYP2, and CYP3 gene families are responsible for most drug metabolism.
A potent vasodilator agent that increases peripheral blood flow.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
A chemically diverse group of substances produced by various tissues in the body that cause slow contraction of smooth muscle; they have other intense but varied pharmacologic activities.
A class of cyclic prostaglandins that contain the 6,9-epoxy bond. Endogenous members of this family are biosynthesized enzymatically from PROSTAGLANDIN ENDOPEROXIDES.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.
Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.
A doubly unsaturated fatty acid, occurring widely in plant glycosides. It is an essential fatty acid in mammalian nutrition and is used in the biosynthesis of prostaglandins and cell membranes. (From Stedman, 26th ed)
A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins.
Peroxides produced in the presence of a free radical by the oxidation of unsaturated fatty acids in the cell in the presence of molecular oxygen. The formation of lipid peroxides results in the destruction of the original lipid leading to the loss of integrity of the membranes. They therefore cause a variety of toxic effects in vivo and their formation is considered a pathological process in biological systems. Their formation can be inhibited by antioxidants, such as vitamin E, structural separation or low oxygen tension.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
A drug that has analgesic and anti-inflammatory properties. Following reports of adverse reactions including reports of carcinogenicity in animal studies it was withdrawn from the market worldwide. (From Martindale, The Extra Pharmacopoeia, 30th ed, p21)
A series of prostaglandin-like compounds that are produced by the attack of free-radical species on unsaturated fatty acids, especially ARACHIDONIC ACID, of cellular MEMBRANES. Once cleaved from the lipid membrane by the action of phospholipases they can circulate into various bodily fluids and eventually be excreted. Although these compounds resemble enzymatically synthesized prostaglandins their stereoisometric arrangement is usually different than the "naturally occurring" compounds.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
An inhibitor of drug metabolism and CYTOCHROME P-450 ENZYME SYSTEM activity.
Lining of the INTESTINES, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. In the SMALL INTESTINE, the mucosa is characterized by a series of folds and abundance of absorptive cells (ENTEROCYTES) with MICROVILLI.
Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
20-carbon saturated monocarboxylic acids.
Synthetic compounds that are analogs of the naturally occurring prostaglandin endoperoxides and that mimic their pharmacologic and physiologic activities. They are usually more stable than the naturally occurring compounds.
Paracrine substances produced by the VASCULAR ENDOTHELIUM with VASCULAR SMOOTH MUSCLE relaxation (VASODILATION) activities. Several factors have been identified, including NITRIC OXIDE and PROSTACYCLIN.
Cell surface receptors for EPOPROSTENOL. They are coupled to HETEROTRIMERIC G-PROTEINS.
Tumors or cancer of the COLON.
A salicylate derivative and anti-inflammatory analgesic with actions and side effects similar to those of ASPIRIN.
A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-.
Physiologically active prostaglandins found in many tissues and organs. They show pressor activity, are mediators of inflammation, and have potential antithrombotic effects.
The main trunk of the systemic arteries.
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
Precursors in the biosynthesis of prostaglandins and thromboxanes from arachidonic acid. They are physiologically active compounds, having effect on vascular and airway smooth muscles, platelet aggregation, etc.
A group of 1,2-benzenediols that contain the general formula R-C6H5O2.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
A water-soluble extractive mixture of sulfated polysaccharides from RED ALGAE. Chief sources are the Irish moss CHONDRUS CRISPUS (Carrageen), and Gigartina stellata. It is used as a stabilizer, for suspending COCOA in chocolate manufacture, and to clarify BEVERAGES.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
The circulation of the BLOOD through the MICROVASCULAR NETWORK.
A phospholipid derivative formed by PLATELETS; BASOPHILS; NEUTROPHILS; MONOCYTES; and MACROPHAGES. It is a potent platelet aggregating agent and inducer of systemic anaphylactic symptoms, including HYPOTENSION; THROMBOCYTOPENIA; NEUTROPENIA; and BRONCHOCONSTRICTION.
The flow of BLOOD through or around an organ or region of the body.
A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans.
The circulation of the BLOOD through the LUNGS.
The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT.
A diverse group of agents, with unique chemical structures and biochemical requirements, which generate NITRIC OXIDE. These compounds have been used in the treatment of cardiovascular diseases and the management of acute myocardial infarction, acute and chronic congestive heart failure, and surgical control of blood pressure. (Adv Pharmacol 1995;34:361-81)
An enzyme that catalyzes the oxidation of arachidonic acid to yield 15-hydroperoxyarachidonate (15-HPETE) which is rapidly converted to 15-hydroxy-5,8,11,13-eicosatetraenoate (15-HETE). The 15-hydroperoxides are preferentially formed in NEUTROPHILS and LYMPHOCYTES.
Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
The endogenous compounds that mediate inflammation (AUTACOIDS) and related exogenous compounds including the synthetic prostaglandins (PROSTAGLANDINS, SYNTHETIC).
A phorbol ester found in CROTON OIL with very effective tumor promoting activity. It stimulates the synthesis of both DNA and RNA.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.
A subclass of analgesic agents that typically do not bind to OPIOID RECEPTORS and are not addictive. Many non-narcotic analgesics are offered as NONPRESCRIPTION DRUGS.
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).
An essential amino acid that is physiologically active in the L-form.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
Agents that reduce the frequency or rate of spontaneous or induced tumors independently of the mechanism involved.
A hemeprotein from leukocytes. Deficiency of this enzyme leads to a hereditary disorder coupled with disseminated moniliasis. It catalyzes the conversion of a donor and peroxide to an oxidized donor and water. EC
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Fatty acid derivatives that have specificity for CANNABINOID RECEPTORS. They are structurally distinct from CANNABINOIDS and were originally discovered as a group of endogenous CANNABINOID RECEPTOR AGONISTS.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
An antiseptic and disinfectant aromatic alcohol.
Compounds with a 5-membered ring of four carbons and an oxygen. They are aromatic heterocycles. The reduced form is tetrahydrofuran.
The action of a drug in promoting or enhancing the effectiveness of another drug.
A compound composed of a two CYCLIC PEPTIDES attached to a phenoxazine that is derived from STREPTOMYCES parvullus. It binds to DNA and inhibits RNA synthesis (transcription), with chain elongation more sensitive than initiation, termination, or release. As a result of impaired mRNA production, protein synthesis also declines after dactinomycin therapy. (From AMA Drug Evaluations Annual, 1993, p2015)

Mechanisms of prostaglandin E2 release by intact cells expressing cyclooxygenase-2: evidence for a 'two-component' model. (1/1887)

Prostaglandin (PG) release in cells expressing constitutive cyclooxygenase-1 is known to be regulated by liberation of arachidonic acid by phospholipase A2 followed by metabolism by cyclooxygenase. However, the relative contribution of phospholipase A2 to the release of PGs in cells expressing cyclooxygenase-2 is not clear. We addressed this question by using radioimmunoassay to measure PGE2 release by human cells (A549) induced to express cyclooxygenase-2 (measured by Western blot analysis) by interleukin-1beta. Cells were either unstimulated or stimulated with agents known to activate phospholipase A2 (bradykinin, Des-Arg10-kallidin, or the calcium ionophore A23187) or treated with exogenous arachidonic acid. When cells were treated to express cyclooxygenase-2, the levels of PGE2 released over 15 min were undetectable; however, in the same cells stimulated with bradykinin, A23187, or arachidonic acid, large amounts of prostanoid were produced. Using selective inhibitors/antagonists, we found that the effects of bradykinin were mediated by B2 receptor activation and that prostanoid release was due to cyclooxygenase-2, and not cyclooxygenase-1, activity. In addition, we show that the release of PGE2 stimulated by either bradykinin, A23187, or arachidonic acid was inhibited by the phospholipase A2 inhibitor arachidonate trifluoromethyl ketone. Hence, we have demonstrated that PGE2 is released by two components: induction of cyclooxygenase-2 and supply of substrate, probably via activation of phospholipase A2. This is illustrated in A549 cells by a clear synergy between the cytokine interleukin-1beta and the kinin bradykinin.  (+info)

Inhibition of prostaglandin synthesis up-regulates cyclooxygenase-2 induced by lipopolysaccharide and peroxisomal proliferators. (2/1887)

Primary cultures of fetal hepatocytes expressed cyclooxygenase-2 (COX-2) upon stimulation with bacterial lipopolysaccharide (LPS) or peroxisomal proliferators. This enzyme was active and a good correlation between the mRNA levels, the amount of protein, and the synthesis of prostaglandin E2 was observed. However, when cells were incubated in the presence of indomethacin or the COX-2-specific inhibitor NS398, the amount of COX-2 protein increased 5-fold after activation with LPS and 2-fold after treatment with clofibrate. This up-regulation of COX-2 was not observed at the mRNA level. The mechanism of protein accumulation might involve either a direct stabilization of the enzyme by the inhibitors or the absence of prostaglandins involved in the regulation of its turnover. Among the prostaglandins assayed, only 15-deoxy-Prostaglandin J2 exerted a statistically significant decrease in the COX-2 levels in cells stimulated with LPS or LPS plus NS398. The accumulation of COX-2 in the presence of inhibitors was also observed in peritoneal macrophages treated under identical conditions. These results indicate that COX-2 protein accumulates after enzyme inhibition, and because removal of the inhibitors restored the enzyme activity, suppression of treatment with reversible COX-2 inhibitors may cause a transient overproduction of prostaglandins.  (+info)

Characterization of the analgesic and anti-inflammatory activities of ketorolac and its enantiomers in the rat. (3/1887)

The marked analgesic efficacy of ketorolac in humans, relative to other nonsteroidal anti-inflammatory drugs (NSAIDs), has lead to speculation as to whether additional non-NSAID mechanism(s) contribute to its analgesic actions. To evaluate this possibility, we characterized (R,S)-ketorolac's pharmacological properties in vivo and in vitro using the nonselective cyclooxygenase (COX) inhibitors [indomethacin (INDO) and diclofenac sodium (DS)] as well as the selective COX-2 inhibitor, celecoxib, as references. The potency of racemic (R,S)-ketorolac was similar in tests of acetic acid-induced writhing, carrageenan-induced paw hyperalgesia, and carrageenan-induced edema formation in rats; ID50 values = 0.24, 0. 29, and 0.08 mg/kg, respectively. (R,S)-ketorolac's actions were stereospecific, with (S)-ketorolac possessing the biological activity of the racemate in the above tests. The analgesic potencies for (R,S)-, (S)-, and (R)-ketorolac, INDO, and DS were highly correlated with their anti-inflammatory potencies, suggesting a common mechanism. (R,S)-ketorolac was significantly more potent than INDO or DS in vivo. Neither difference in relative potency of COX inhibition for (R,S)-ketorolac over INDO and DS nor activity of (S)-ketorolac at a number of other enzymes, channels, or receptors could account for the differences in observed potency. The distribution coefficient for (R,S)-ketorolac was approximately 30-fold less than for DS or INDO, indicating that (R,S)-ketorolac is much less lipophilic than these NSAIDs. Therefore, the physicochemical and pharmacokinetics properties of (R,S)-ketorolac may optimize the concentrations of (S)-ketorolac at its biological target(s), resulting in greater efficacy and potency in vivo.  (+info)

Oxidative bioactivation of the lactol prodrug of a lactone cyclooxygenase-2 inhibitor. (4/1887)

The lactol derivative of a lactone cyclooxygenase-2 inhibitor (DFU) was evaluated in vivo and in vitro for its potential suitability as a prodrug. DFU-lactol was found to be 10 to 20 times more soluble than DFU in a variety of aqueous vehicles. After administration of DFU-lactol at 20 mg kg-1 p.o. in rats, a Cmax of 7.5 microM DFU was reached in the plasma. After oral administration, the ED50s of DFU-lactol in the carrageenan-induced paw edema and lipopolysaccharide-induced pyresis assays in rats are comparable with the ED50s observed when dosing with DFU. Incubations of DFU-lactol with rat and human hepatocytes demonstrated that the oxidation of DFU-lactol can be mediated by liver enzymes and that a competing pathway is direct glucuronidation of the DFU-lactol hydroxyl group. Assays with subcellular fractions from rat liver indicated that most of the oxidation of DFU-lactol occurs in the cytosolic fraction and requires NAD(P)+. Human liver cytosol can also support the oxidation of DFU-lactol to DFU when NAD(P)+ is added to the incubations. Fractionation of human liver cytosolic proteins showed that at least three enzymes are capable of efficiently effecting the oxidation of DFU-lactol to DFU. Incubations with commercially available dehydrogenases suggest that alcohol and hydroxysteroid dehydrogenases are involved in this oxidative process. These data together suggest that lactols may represent useful prodrugs for lactone-containing drugs.  (+info)

Inhibition of cyclooxygenase-2 expression by 4-trifluoromethyl derivatives of salicylate, triflusal, and its deacetylated metabolite, 2-hydroxy-4-trifluoromethylbenzoic acid. (5/1887)

The therapeutic potential of drugs that block the induction of cyclooxygenase-2 has been emphasized. When two 4-trifluoromethyl salicylate derivatives [2-acetoxy-4-trifluoromethyl-benzoic acid (triflusal) and its deacetylated metabolite 2-hydroxy-4-trifluoromethylbenzoic acid (HTB)] were compared with aspirin and sodium salicylate as cyclooxygenase-2 (COX-2) inhibitors, we observed that in bacterial lipopolysaccharide-activated human blood, triflusal, aspirin, and HTB, but not sodium salicylate, inhibited COX-2-mediated prostaglandin E2 (PGE2) production (IC50 = 0.16, 0.18, 0.39, and >10 mM, respectively). However, only triflusal and aspirin inhibited purified COX-2 enzyme. To test this apparent discrepancy, we realized that HTB and triflusal (but neither aspirin nor salicylate) produced a concentration-dependent inhibition of COX-2 protein expression in peripheral human mononuclear cells. This observation was further confirmed in a rat air pouch model in vivo, in which both aspirin and triflusal inhibited PGE2 production (ID50 = 18.9 and 11.4 mg/kg p.o., respectively) but only triflusal-treated animals showed a decrease in COX-2 expression. This different behavior may be, at least in part, due to the ability of HTB and triflusal to block the activation of the transcription factor nuclear factor-kappaB to a higher extent than aspirin and sodium salicylate. Thus, in addition to inhibiting the COX-2 activity at therapeutic concentrations, triflusal is able to block through its metabolite HTB the expression of new enzyme, and hence the resumption of PGE2 synthesis. Triflusal and HTB may exert beneficial effects in processes in which de novo COX-2 expression is involved and, in a broader sense, in pathological situations in which genes under nuclear factor-kappaB control are up-regulated.  (+info)

Cyclo-oxygenase-2 mediates P2Y receptor-induced reactive astrogliosis. (6/1887)

Excessive cyclo-oxygenase-2 (COX-2) induction may play a role in chronic neurological diseases characterized by inflammation and astrogliosis. We have previously identified an astroglial receptor for extracellular nucleotides, a P2Y receptor, whose stimulation leads to arachidonic acid (AA) release, followed, 3 days later, by morphological changes resembling reactive astrogliosis. Since COX-2 may be upregulated by AA metabolites, we assessed a possible role for COX-2 in P2Y receptor-mediated astrogliosis. A brief challenge of rat astrocytes with the ATP analogue alpha,beta-methylene ATP (alpha,beta(me)ATP) resulted, 24 h later, in significantly increased COX-2 expression. The selective COX-2 inhibitor NS-398 completely abolished alpha,beta(me)ATP-induced astrocytic activation. Constitutive astroglial COX-1 or COX-2 did not play any role in purine-induced reactive astrogliosis. PGE2, a main metabolite of COX-2, also induced astrocytic activation. These data suggest that a P2Y receptor mediates reactive astrogliosis via induction of COX-2. Antagonists selective for this receptor may counteract excessive COX-2 activation in both acute and chronic neurological diseases.  (+info)

Curcumin inhibits cyclooxygenase-2 transcription in bile acid- and phorbol ester-treated human gastrointestinal epithelial cells. (7/1887)

We investigated whether curcumin, a chemopreventive agent, inhibited chenodeoxycholate (CD)- or phorbol ester (PMA)-mediated induction of cyclooxygenase-2 (COX-2) in several gastrointestinal cell lines (SK-GT-4, SCC450, IEC-18 and HCA-7). Treatment with curcumin suppressed CD- and PMA-mediated induction of COX-2 protein and synthesis of prostaglandin E2. Curcumin also suppressed the induction of COX-2 mRNA by CD and PMA. Nuclear run-offs revealed increased rates of COX-2 transcription after treatment with CD or PMA and these effects were inhibited by curcumin. Treatment with CD or PMA increased binding of AP-1 to DNA. This effect was also blocked by curcumin. In addition to the above effects on gene expression, we found that curcumin directly inhibited the activity of COX-2. These data provide new insights into the anticancer properties of curcumin.  (+info)

Angiotensin II attenuates renal cortical cyclooxygenase-2 expression. (8/1887)

We have previously shown that in rat renal cortex, cyclooxygenase-2 (COX-2) expression is localized to cTALH cells in the region of the macula densa, and that dietary salt restriction increases COX-2 expression. Administration of the angiotensin converting inhibitor, captopril, further increased COX-2 mRNA and renal cortical COX-2 immunoreactivity, with the most pronounced expression in the macula densa. Administration of an AT1 receptor antagonist, losartan, also significantly increased cortical COX-2 mRNA expression and COX-2 immunoreactivity. Mutant mice homozygous for both Agtr1a and Agtr1b null mutations (Agtr1a-/-,Agtr1b-/-) demonstrated large increases in immunoreactive COX-2 expression inthe cTALH/macula densa. To determine whether increased COX-2expression in response to ACE inhibition mediated increases in renin production, rats were treated with captopril for one week with or without the specific COX-2 inhibitor, SC58236. Plasma renin activity increased significantly in the captropril group, and this increase was significantly inhibited by simultaneous treatment with SC58236. Thus, these studies indicated that angiotensin II inhibitors augment upregulation of renal cortical COX-2 in states of volume depletion, suggesting that negative feedback by the renin-angiotensin system modulates renal cortical COX-2 expression and that COX-2 is a mediator of increased renin production in response to inhibition of angiotension II production.  (+info)

After the doctor knows what kind of arthritis youve, he or she will talk with you about the best way to treat it. The doctor may give you a prescription for medicine that will help with the pain, stiffness, and inflammation. The good news is that now there is a way to stop your pain with a medication . Celebrex is a nonsteroidal anti-inflammatory drug (NSAID), specifically a COX-2 inhibitor, which relieves pain and swelling inflammation). It represents a huge breakthrough in the treatment of soreness, inflammation, and stiffness of arthritis. Celebrex is thought to fight pain and swelling by inhibiting the effect of a natural enzyme called COX-2. Unlike the older medicines, however, it does not interfere with an identical substance, called COX-1, which puts a protective effect on the lining of the stomach. Celebrex wont make the stomach bleeding and also sores that traditional nonsteroidal anti-inflammatory drugs (NSAIDs) might ...
Several studies suggest that cyclooxygenase-2 contributes to the delayed progression of ischemic brain damage. In this study we examined whether the highly selective cyclooxygenase-2 inhibitor DFU reduces neuronal damage when administered several hours after 5 min of transient forebrain ischemia in gerbils. The extent of ischemic injury was assessed behaviorally by measuring the increases in locomotor activity and by histopathological evaluation of the extent of CA1 hippocampal pyramidal cell injury 7 days after ischemia. DFU treatment (10 mg/kg, p.o.) significantly reduced hippocampal neuronal damage even if the treatment is delayed until 12 h after ischemia. These results suggest that selective cyclooxygenase-2 inhibitors may be a valuable therapeutic strategy for ischemic brain injury. ...
An analysis of 20 years of data on the health of over 900 adults has found that long-term use of traditional nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen and naproxen, cuts the risk for oral cancer in smokers by half.
Patients with arthritis taking a COX-2 selective nonsteroidal anti-inflammatory drug (NSAID) appear to have a lower risk of adverse gastrointestinal events compared with those on a nonselective NSAID
This study demonstrated dose-related excess mortality associated with the use of NSAIDs in patients with prior MI. There was a trend for increased risk of rehospitalization for MI, although the dose-related response in risk was not as clear as for death.. The VIGOR study was the first to report increased cardiovascular risk associated with the selective COX-2 inhibitors.1 Since then, several studies,5,6,8,12,23 although not all,2,24-26 have confirmed the findings. Several recently published observational studies have also indicated an increased cardiovascular risk associated with the nonselective NSAIDs.7-9,13. The present study is the first to address the risk of all NSAIDs in a selected population of post-MI patients. These patients are elderly, are frequently treated with NSAIDs, and have a high risk of additional cardiovascular events. Many of the randomized trials have excluded these patients. The results of the present study indicate acute or subacute effects of both the selective COX-2 ...
Nonsteroidal anti-inflammatory drugs (NSAIDs) are used to reduce inflammatory pain and swelling in inflammatory bowel disease (IBD) patients with rheumatological manifestations (e.g. arthritis). While these drugs effectively reduce musculoskeletal pain and stiffness, long-term use is limited by gastrointestinal (GI) side effects and disease exacerbation (i.e. an increase in the severity of a disease or its signs and symptoms). As an alternative to NSAIDs, selective cyclooxygenase 2 (COX-2) inhibitors were developed to improve tolerability (i.e. the degree to which the side effects of a drug can be tolerated by a patient). COX-2 inhibitors include drugs such as celecoxib, rofecoxib, valdecoxib, etoricoxib, and lumiracoxib. Rofecoxib and valdecoxib have been withdrawn from the market worldwide due to safety concerns (most importantly an increased risk of heart attack or stroke) and lumiracoxib has been withdrawn in many countries due to liver toxicity. However, celecoxib and etoricoxib are ...
Celecoxib and rofecoxib belong to a new class of NSAIDs that specifically inhibits COX-2. They have a significant anti-inflammatory and analgesic properties but are far less toxic than traditional NSAIDs, which inhibit both COX-1 and COX-2 (20 , 21) . However, not all COX-2 inhibitors share the same anticancer effects. The predictive discrepancy between the in vitro growth inhibitions of celecoxib and rofecoxib may be indicative of the difference in their mechanism of action. The present study provides the first direct comparison of the in vitro anticancer effects of the two clinically available COX-2 inhibitors.. The antiproliferative effect of celecoxib was noted to particularly inhibit the growth of the transformed but not the growth of the normal cells. Exposure to 10 μm celecoxib, for 72 h, inhibited transformed cell growth by 50% but had very little effect on the growth of normal cells (Fig. 1)⇓ . The IC50s of celecoxib ranges between 5 and 20 μm across this entire panel of cell lines. ...
Unwanted side effects can be minimized by taking the least effective dose for the shortest period of administration required for symptoms control. In case of treatment ineffectiveness (reduction of disease symptoms), this preparation therapy should be discontinued. There were reports on cases of liver severe reactions, including fatal ones, during Nimesulide use. Patients with symptoms similar to symptoms of liver lesion during Nimid® treatment, such as anorexia, nausea, vomiting, abdominal pain, fatigue, dark urine, or patients, which laboratory parameters of liver function are abnormal, should stop this preparation usage. Re-administration of Nimesulide to such patients is contraindicated. It is necessary to avoid other analgesics use during Nimid® treatment. It is necessary to avoid concomitant use of other NSAIDs, including selective cyclooxygenase-2. Patients who used Nimesulide and who have symptoms similar to flu or colds should discontinue its use. There are increased incidences of ...
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Preclinical CRO PhysioStim is expected to complete its range of cardiovascular safety studies and create a new alliance to answer upcoming CiPA guidelines
COX-1抑制劑篩選K548 | COX活性測定試劑盒 | COX-2抑制劑篩選試劑盒 | 環氧合酶2(COX-2)ELISA試劑盒 | PTGS2 / COX-2(人類)ELISA試劑 COX-1抑制劑篩選試劑盒 | 貨號K548 Cyclooxygenase-1 (COX-1) Inhibitor
Synonyms for COX 2 inhibitor in Free Thesaurus. Antonyms for COX 2 inhibitor. 8 words related to Cox-2 inhibitor: anti-inflammatory, anti-inflammatory drug, Celebrex, celecoxib, rofecoxib, Vioxx, Bextra, valdecoxib. What are synonyms for COX 2 inhibitor?
The size of the PCR products from cyclooxygenase-1 and cyclooxygenase-2 are 524 and 583 base pairs, respectively. The specificity of the PCR reaction for cyclooxygenase-1 and cyclooxygenase-2 complementary deoxyribonucleic acid (cDNA) was confirmed by digestion of PCR products by sequence-specific restriction enzymes (cyclooxygenase-1: Sac I and Sma I; cyclooxygenase-2: Pst I and Nco I). For quantitation of cyclooxygenase-1 and cyclooxygenase-2 mRNA levels, the Escherichia coli plasmid pT2M containing specific internal standards for cyclooxygenase-1 and cyclooxygenase-2 was constructed by internal deletion of sequences: The truncated fragments (320 base pairs) from cyclooxygenase-1 and cyclooxygenase-2 PCR products were incorporated into the E. coli cloning plasmid pBSII SK(+)(Stratagene, La Jolla, CA) at the EcoR I and Kpn I restriction sites and multiplied as plasmids in an E. coli strain Dh5 alpha. Plasmid solutions were adjusted to 1 x 104molecules/micro liter after double digestion by ...
Meloxicam (under the brand name Mobicox) is a new arthritis drug. Unlike other COX-II selective nonsteroidal anti-inflammatory drugs (NSAID) known as coxibs, Meloxicam, an oxicam COX-2 selective NSAID, is a unique class of COX-II selective NSAIDs that appear to not carry the same risk of blood clots that other coxibs have.
TY - JOUR. T1 - Inhibition of human neuroblastoma cell growth by CAY10404, a highly selective Cox-2 inhibitor. AU - Parashar, Bhupesh. AU - Shankar, Sai Latha. AU - OGuin, Kathleen. AU - Butler, James. AU - Vikram, Bhadrasain. AU - Shafit-Zagardo, Bridget. PY - 2005/1/1. Y1 - 2005/1/1. N2 - Neuroblastomas constitute about 10% of childhood cancers and are responsible for 15% of pediatric cancer mortality. We evaluated the efficacy and the mechanism of cell death induced by CAY10404, a selective cyclooxygenase-2 (Cox-2) inhibitor in four human neuroblastoma cell lines (SH-EP, SH-SY5Y, SK-N-MC and MSN). Treatment with CAY10404 in the range of 15-115 μM revealed a dose-dependent decrease in cell number and an average IC50(inhibitory concentration 50%) of 60 μM. About 20-30% of the cells were terminal deoxynucleotidyltransferase-mediated UTP nick-end-labeling (TUNEL) positive 48 h after treatment. Western blot analysis of CAY10404-treated cells showed poly(ADP-ribose) polymerase (PARP) cleavage ...
Varas-Lorenzo, C., Castellsague, J., Stang, M. R., Perez-Gutthann, S., Aguado, J. and Rodriguez, L. A. G. (2009), The use of selective cyclooxygenase-2 inhibitors and the risk of acute myocardial infarction in Saskatchewan, Canada . Pharmacoepidem. Drug Safe., 18: 1016-1025. doi: 10.1002/pds.1815 ...
Objective:To identify factors that influence prescribers in their selection and use of cyclo-oxygenase-2 (COX-2) selective inhibitors as opposed to non-selective non-steroidal anti-inflammatory...
BACKGROUND: Adverse reactions to nonsteroidal antiinflammatory drugs (NSAIDs) are frequently reported, particularly among asthmatic patients. To date, there is no causal treatment available apart from tolerance induction. Therefore, the search for safe alternative drugs is of pivotal importance in clinical practice.. OBJECTIVE: The aim of our prospective study was to investigate the tolerance to celecoxib, a selective cyclooxygenase-2 inhibitor, in a large group of patients with positive case history of NSAID intolerance in comparison to paracetamol and nimesulide.. METHODS: 106 NSAID-sensitive patients, 46 (43.4%) of whom had experienced reactions only to one NSAID (single hypersensitivity), 60 (56.6%) to several NSAIDs (multiple hypersensitivity), were included in a single-blinded drug challenge protocol with cumulative doses of 175 mg of celecoxib, 875 mg of paracetamol and 175 mg of nimesulide. Objective and subjective symptoms during challenge were documented.. RESULTS: Of 261 challenges in ...
This is the first study to demonstrate that a selective COX-2 inhibitor on top of standard therapy improves endothelial function and reduces markers of inflammation and oxidative stress in patients with coronary artery disease. Recognition that COX-2 is an inducible enzyme particularly associated with inflammation led to the development of selective COX-2 inhibitors that offer comparable efficacy and fewer unwanted side effects attributable to COX-1 inhibition, gastric ulceration in particular.1,2 Gastrointestinal safety of selective COX-2 inhibitors, however, may come at the cost of increased cardiovascular events, as suggested by the results of the VIGOR trial.5 Cardiovascular safety of coxibs was additionally challenged by studies in mice deficient in the PGI2 or TXA2 receptor.10 PGI2 receptor-deficient animals showed enhanced injury-induced vascular proliferation and platelet activation that was abolished in mice deficient of both PGI2 and TXA2 receptor, suggesting that PGI2 inhibition with ...
Selective COX-2 inhibitors are a type of nonsteroidal anti-inflammatory drug (NSAID) that directly targets cyclooxygenase-2, COX-2, an enzyme responsible for inflammation and pain. Targeting selectivity for COX-2 reduces the risk of peptic ulceration, and is the main feature of celecoxib, rofecoxib and other members of this drug class. After several COX-2 inhibiting drugs were approved for marketing, data from clinical trials revealed that COX-2 inhibitors caused a significant increase in heart attacks and strokes, with some drugs in the class having worse risks than others. Rofecoxib (commonly known as Vioxx) was taken off the market in 2004 because of these concerns and celecoxib and traditional NSAIDs received boxed warnings on their labels. Many COX-2-specific inhibitors have been removed from the U.S. market. As of December 2011, only Celebrex (generic name is celecoxib) is still available for purchase in the United States. Some COX-2 inhibitors are used in a single dose to treat pain after ...
When we considered all the randomised trial data, selective COX 2 inhibitors were associated with a highly significant 1.4-fold increased risk of serious vascular events, largely due to a twofold increased risk of myocardial infarction. Although we found no significant excesses in the incidence of stroke or vascular death, the confidence intervals for each were wide, so we could not exclude a clinically important excess. If, as some people have suggested (on the basis of the delayed divergence of survival curves), the hazard emerges only after a year or 18 months,4 5 then combining short term and long term trials might underestimate the effects of long term exposure to a selective COX 2 inhibitor. We were not able to assess time dependent variation in the rate ratio because we sought numbers of events and person time only for the whole period of follow-up in each trial. However, as figure 2 clearly shows, when all the long term trials are considered, the summary rate ratio is similar to that ...
Introduction Cyclooxygenase-2 (COX-2) is frequently over-expressed in primary breast cancer. In transgenic breast cancer models, over-expression of COX-2 leads to tumour formation while COX-2...
TY - JOUR. T1 - What Did Safe Mean To Prescribes Of Selective Cox-2 Inhibitors?. AU - McGettigan, Patricia. AU - Peel, Roseanne. AU - Stokes, Barrie J.. AU - Henderson, Kim M.. AU - Whitaker, Diana. AU - Henry, David A. PY - 2009. Y1 - 2009. N2 - Introduction: Among vulnerable individuals, cyclo-oxygenase-2(COX-2) inhibition increases the risk of cardiovascular thromboticevents. Promotional safety messages led to channeling of selectiveCOX-2 inhibitors to individuals with gastrointestinal risks.Aims: We investigated whether this was associated with inappropriatechanneling of COX-2 inhibitors to patients at risk of cardiovascular events.Methods: Case-control study, August 2003-October 2006. Cases:patients admitted to hospital with acute coronary syndrome (ACS, myocardial infarction/unstable angina) (n = 814). Controls:Patients admitted for reasons other than acute vascular ischaemia, heartfailure, renal failure, or upper gastro-intestinal ulceration/bleeding(n = 1500). Structured interviews ...
COX-2 preferentially leads to synthesis of prostacyclin which have anti-platelet aggregation effects. COX-1 preferentially leads to synthesis of thromboxane which induces platelet aggregation. One would then expect COX-1 inhibition to cause more blood-thinning than COX-2 inhibition. This is the reason COX-2 inhibitors are associated with increased risk of cardiovascular events (by inhibiting prostacyclin synthesis without inhibiting thromboxane synthesis). However, Celebrex is not as selective a COX-2 inhibitor as other coxibs such as rofecoxib (which was removed from the market in 2004), and has minor activity against COX-1 ...
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Etodolac (Lodine) is a COX inhibitor with an IC50 of 53.5 nM. Find all the information about Etodolac (Lodine) for cell signaling research.
This trial assessed the safety and efficacy of a single dose of lumiracoxib 400 mg compared to placebo and to a single dose of celecoxib 200mg. It also assessed safety and efficacy of 400mg lumiracoxib administered once a day for 7 days compared to placebo and to 200 mg celecoxib twice daily ...
Experts discuss the use of firocoxib in horses, including benefits of selective COX-2 inhibition, FDA restrictions, and the importance of proper dosing.
The present meta--analysis attempted to assess whether an unfavourable cardiovascular risk profile could be identified in the case of two COX2 selective inhibitors (COXIBs), namely celecoxib and etoricoxib. Based on the data from the literature, our
COX-2 inhibitors, including celecoxib (brand name Celebrex). Two drugs in this class have already been withdrawn from the market because of cardiovascular toxicity: rofecoxib (brand name Vioxx), and valdecoxib (brand name Bextra). These drugs are a special class of NSAID and were developed to be safer for the stomach, but have the same risk as other NSAIDs do for kidney damage ...
3. COX-2 inhibitors, including celecoxib (brand name Celebrex). Two drugs in this class have been withdrawn from the market because of cardiovascular toxicity: rofecoxib (brand name Vioxx), and valdecoxib (brand name Bextra). These drugs are a special class of NSAID that were developed to be safer for the stomach, but have the same risk as other NSAIDs for kidney damage ...
Professor Mitchell added: This review shows us that despite the large scale use of NSAIDs and COX-2 inhibitors for a number of years, we still need more information on their benefits and potential risks and that more research needs to be done in this area. Looking at existing evidence, however, it would seem COX-2 inhibitors may be the best option for some patients. They are as effective as traditional NSAIDs, but with less gastric side effects than some older drugs ...
Riva-Celecoxib: Celecoxib belongs to the group of medications called selective COX-2 inhibitors, which is a kind of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by reducing a substance in the body that leads to inflammation (swelling) and pain.
Priva-Celecoxib: Celecoxib belongs to the group of medications called selective COX-2 inhibitors, which is a kind of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by reducing a substance in the body that leads to inflammation (swelling) and pain.
Celecoxib belongs to the group of medications called selective COX-2 inhibitors, which is a kind of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by reducing a substance in the body that leads to inflammation (swelling) and pain.
Celecoxib belongs to the group of medications called selective COX-2 inhibitors, which is a kind of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by reducing a substance in the body that leads to inflammation (swelling) and pain.
Get this from a library! Nimesulide--actions and uses. [K D Rainsford;] -- Nimesulide is a non-steroidal anti-inflammatory drug (NSAID) which acts as a cyclooxygenase- 2 inhibitor but also has other novel pharmacological features which account for its effect in the control ...
Modelled structure of COX-1 and COX-2.Comparison of modelled structures with their template structures revealed the active sites of located in the enzymes. (A)
ab120295 NS 398, COX-2 inhibitor (CAS番号: 123653-11-2) 分子量: 314.36 化学式: C13H18N2O5S COX-2 阻害剤 アブカムの高純度な生理活性物質(アゴニスト・アンタゴニスト・アクティベーター・阻害剤)
Интерлеукин 17A је протеин који је код људи кодиран IL17A геном.[1][2][3] Протеин кодиран овим геном је проинфламаторни цитокин произведен активираним Т ћелијама.[4] Овај цитокин регулише активности НФ-капаБ и митоген активираних протеин киназа. Овај цитокин може да стимулише изражавање ИЛ-6 и циклооксигеназе-2 (PTGS2/COX-2), као и да појача продукцију нитрик оксида (NO). Високи нивои овог цитокина су асоцирани са неколико хроничних инфламаторних обољења укључујући реуматоидни артритис, псоријазу и мултиплу склерозу.[2] ...
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Interaction with platelet function by non-steroidal anti-inflammatory drugs (NSAIDs) is related to the inhibition of cyclo-oxygenase-1 (COX-1). In pat
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The use of cyclo-oxygenase 2 selective nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with increased risk of acute myocardial infarction (AMI). The association between the risks of AMI with nonselective NSAIDs is less clear. We reviewed the published evidence and assessed the risk of AMI with nonselective NSAIDs. We performed a meta-analysis of all studies containing data from population databases that compared the risk of AMI in NSAID users with that in non-users or remote NSAID users. The primary outcome was objectively confirmed AMI. Fourteen studies met predefined criteria for inclusion in the meta-analysis. Nonselective NSAIDs as a class was associated with increased AMI risk (relative AMI risk 1.19, 95% confidence interval [CI] 1.08 to 1.31). Similar findings were found with diclofenac (relative AMI risk 1.38, 95% CI 1.22-1.57) and ibuprofen (relative AMI risk 1.11, 95% CI 1.06 to 1.17). However, this effect was not observed with naproxen (relative AMI risk 0.99, 95% CI 0.88-1.11). In
In a previous study, we reported that the short-term treatment with celecoxib, a non-steroidal anti-inflammatory drug (NSAID) attenuates the activation of brain structures related to nociception and does not interfere with orthodontic incisor separation in rats. The conclusion was that celecoxib could possibly be prescribed for pain in orthodontic patients. However, we did not analyze the effects of this drug in periodontium. The aim of this follow-up study was to analyze effects of celecoxib treatment on recruitment and activation of osteoclasts and alveolar bone resorption after inserting an activated orthodontic appliance between the incisors in our rat model. Twenty rats (400-420 g) were pretreated through oral gavage with celecoxib (50 mg/kg) or vehicle (carboxymethylcellulose 0.4%). After 30 min, they received an activated (30 g) orthodontic appliance, set not to cause any palate disjunction. In sham animals, the appliance was immediately removed after introduction. All animals received ...
Celecoxib is a COX-2 selective nonsteroidal anti-inflammatory drug (NSAID). It is used to treat the pain and inflammation of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, acute pain in adults, painful menstruation, and juvenile rheumatoid arthritis in people two years or older.. Celecoxib is a nonsteroidal anti-inflammatory drug (NSAID). It works by reducing hormones that cause inflammation and pain in the body.. Celecoxib is used to treat pain or inflammation caused by many conditions such as arthritis, ankylosing spondylitis, and menstrual pain.. Celecoxib is used to treat juvenile rheumatoid arthritis in children who are at least 2 years old. It is also used in the treatment of hereditary polyps in the colon.. Celebrex was one of Pfizers best-selling drugs, amounting to more than $2.5 billion in sales [by 2012], and was prescribed to 2.4 million people in 2011. By 2012, 33 million Americans had taken Celebrex. As of 2015, the cost for a typical month of medication in the ...
A dermally deliverable pharmaceutical composition comprises at least one selective cyclooxygenase-2 (COX-2) inhibitory drug or prodrug thereof solubilized in a pharmaceutically acceptable carrier that comprises a low molecular weight monohydric alcohol, and exhibits a skin permeation rate of the therapeutic agent at least equal to that exhibited by a reference solution of the therapeutic agent in 70% aqueous ethanol. A method of effecting targeted delivery of a selective COX-2 inhibitory drug to a site of pain and/or inflammation in a subject comprises topically administering such a composition to skin of the subject, preferably at a locus overlying or adjacent to the site of pain and/or inflammation. A method of effecting systemic treatment of a subject having a COX-2 mediated disorder comprises transdermally administering such a composition, preferably by contacting the composition with an area of skin of the subject not greater than about 400 cm2.
Third generation aromatase inhibitors (AIs) are more effective than tamoxifen in the treatment of estrogen receptor (ER) positive breast cancer. However, long-term use of AIs commonly results in resistance. We examined whether compound JCC76{Cyclohexanecarboxylic acid [3-(2,5-dimethyl-benzyloxy)-4-(methanesulfonyl-methyl-amino)-phenyl]-amide}, an analog of Cyclooxygenase-2 (COX-2) inhibitor nimesulide, can inhibit the growth of AI-insensitive breast cancer cells and the mechanisms by which the compound affects cell proliferation. LTEDaro (long term estrogen deprived MCF-7aro cell) cells, which are a model for AI resistance, were used in this study. JCC76 effectively inhibited LTEDaro cell proliferation with an IC(50) of 2.75 ± 0.31 μM. Further investigations reveal that the compound significantly induced apoptosis in LTEDaro cells by decreasing pAKT, BCL-2 and pBad protein levels, which were all up regulated in the cells after long term estrogen deprivation. LTEDaro tumor size and weight were
TY - JOUR. T1 - Cyclooxygenase-2 inhibitor celecoxib augments chemotherapeutic drug-induced apoptosis by enhancing activation of caspase-3 and -9 in prostate cancer cells. AU - Dandekar, Devendra S.. AU - Lopez, Monica. AU - Carey, Robert I.. AU - Lokeshwar, Bal L.. N1 - Copyright: Copyright 2008 Elsevier B.V., All rights reserved.. PY - 2005/6/20. Y1 - 2005/6/20. N2 - Many tumors constitutively express high levels of the inducible form of proinflammatory enzyme, cyclooxygenase-2 (COX-2). Increased COX-2 expression is associated with tumor cell resistance to many cytotoxic chemotherapy drugs. Furthermore, increased resistance to cytotoxic antitumor drugs is also known to be dependent on associated stromal cells in many tumors. We investigated whether prostate tumor-associated stromal cells, marrow-derived osteoblasts, affect cytotoxicity of 2 antitumor drugs, COL-3 and docetaxel (TXTR), and whether it is dependent on COX-2 activity. We further examined whether inhibiting the activity of COX-2 ...
Historical Perspectives -- Anti-Inflammatory Drugs in the 21st Century -- Inflammatory Mechanisms of Pathogenesis -- Nitric Oxide Synthase and Cyclooxygenase Interactions in Cartilage and Meniscus -- Obesity, Inflammation, and Vascular Disease -- Cyclooxygenase-2 (COX-2) and the Inflammogenesis of Cancer -- Role of COX-2 in Inflammatory and Degenerative Brain Diseases -- Inflammation and Cardiovascular Disease: The Coxib Controversy -- Cardiovascular Effects of the Selective Cyclooxygenase-2 Inhibitors -- COX-2 Inhibitors And Cardiovascular Risk -- A Biological Rationale for the Cardiotoxic Effects of Rofecoxib -- Cox-2 Blockade in Cancer Prevention and Therapy -- Cancer Chemoprevention by Cyclooxygenase 2 (COX-2) Blockade -- Strategies for Colon Cancer Prevention -- Inflammation and Neurodegenerative Disease -- NSAIDs for the Chemoprevention of Alzheimer?셲 Disease -- Inflammation in parkinson?셲 disease -- Nutrition, Inflammation and Chronic Disease -- Essential Polyunsaturated Fatty Acids, ...
TY - JOUR. T1 - COX-2 inhibitor celecoxib prevents chronic morphine-induced promotion of angiogenesis, tumour growth, metastasis and mortality, without compromising analgesia. AU - Farooqui, M.. AU - Li, Y.. AU - Rogers, T.. AU - Poonawala, T.. AU - Griffin, R. J.. AU - Song, C. W.. AU - Gupta, K.. N1 - Funding Information: We are thankful to Mihir Gupta, Pankaj Gupta, MD and Michael J Franklin for critical review of the paper, to Ms Carol Taubert for preparation of the document, and to Brent W Williams for technical assistance. This work is supported by NIH Grants HL68802, CA109582 and the Susan G Komen Breast Cancer Foundation (to KG) and CA109582 (to RJG).. PY - 2007/12/3. Y1 - 2007/12/3. N2 - Morphine and its congener opioids are the main therapy for severe pain in cancer. However, chronic morphine treatment stimulates angiogenesis and tumour growth in mice. We examined if celecoxib (a cyclooxygenase-2 (COX-2) inhibitor) prevents morphine-induced tumour growth without compromising analgesia. ...
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The Food and Drug Administration on Nov. 21 granted orphan drug designation to rofecoxib (TRM-201), a cyclooxygenase 2-selective nonsteroidal anti-inflammatory
Medications from several classes have been shown to have moderate, mostly short-term benefits for patients with low back pain. Acetaminophen (Tylenol®) is a slightly weaker pain medication than non-steroidal anti-inflammatories (NSAIDs). However, acetaminophen is generally safer and less costly. Acetaminophen can cause liver enzyme elevations at dosages of 4 g (4,000 mg)/day even in healthy adults. The clinical significance of the liver enzyme elevation is uncertain.. NSAIDs can be selective, or non-selective. Advil® and Motrin® (ibuprofen); and Aleve® (naproxen) are examples of over-the-counter non-selective NSAIDs. Celebrex® is the only selective NSAID available in the United States. Nonselective NSAIDs, while more effective than acetaminophen, are known to cause stomach and kidney problems. Selective NSAIDs such as Celebrex® and most non-selective NSAIDS also increase risk for heart attack. The lowest effective doses for the shortest periods necessary are recommended. If you ...
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Several studies suggest that cyclooxygenase (COX)-2 plays a pivotal role in the progression of ischemic brain damage. In the present study, we investigated the effects of selective inhibition of COX-2 with nimesulide (12 mg/kg) and selective inhibition of COX-1 with valeryl salicylate (VAS, 12-120 mg/kg) on prostaglandin E2 (PGE2) levels, myeloperoxidase (MPO) activity, Evans Blue (EB) extravasation and infarct volume in a standardized model of transient focal cerebral ischemia in the rat. Postischemic treatment with nimesulide markedly reduced the increase in PGE2 levels in the ischemic cerebral cortex 24 h after stroke and diminished infarct size by 48 % with respect to vehicle-treated animals after 3 days of reperfusion. Furthermore, nimesulide significantly attenuated the blood-brain barrier (BBB) damage and leukocyte infiltration (as measured by EB leakage and MPO activity, respectively) seen at 48 h after the initial ischemic episode. These studies provide the first experimental evidence ...
Indications: RA, juvenile idiopathic arthritis, osteoarthritis, ankylosing spondylitis, spondyloarthropathy, gout, pain. Mechanism of Action: Anti-inflammatory and antiplatelet properties are mediated by the inhibition of COX enzymes and decreased production of prostaglandins. Drugs that inhibit COX-2 are anti-inflammatory because they decrease the formation of prostaglandins by activated cells. Drugs that inhibit COX-1 decrease the production of thromboxane and thus decrease platelet activation. Because COX-1 contributes to the maintenance of gastric mucosa, blocking COX-1 increases the risk of peptic ulceration. NSAIDs are classified according to whether they inhibit both COX-1 and COX-2 (nonselective NSAIDs) or whether they are more selective for COX-2 and spare COX-1 (COX-2 selective NSAIDs or coxibs). Nonacetylated salicylates such as salsalate are weak inhibitors of COX, and their mechanism of action is poorly understood.. Contraindications: Hypersensitivity to NSAIDs, GI ulceration, ...
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In this study, we analyzed a nationwide health insurance claims database and found an increased risk for ischemic and hemorrhagic stroke was evident for all selective and nonselective NSAIDs, particularly when used parenterally. Risk was highest for ketorolac as compared with other NSAIDs.. Four population-based studies in Denmark, the United Kingdom, the United States, and The Netherlands investigated nonselective NSAIDs, selective COX-2 inhibitors, and the risk of ischemic stroke.6-9 They found the ORs for ischemic stroke ranged from 1.2 to 1.7 for a variety of nonselective NSAIDs, including ibuprofen, indomethacin, diclofenac, and naproxen. A nested case-control study observed an exposure period as short as 14 days was associated with a significantly increased risk of ischemic stroke.6 In a prospective population-based cohort study, Haag and colleagues found use of any NSAID was related to the risk of hemorrhagic stroke with a hazard ratio of 2.03, albeit nonsignificant.8 Conflicting results ...
William Penn College. I. Ressel, MD: Order Celecoxib on line amex.. Modulation of the MEP in biceps and triceps brachii by ulnar volleys in a long-suffering with a spinal lesion at the C6 C7 intersection purchase celecoxib 100 mg on line arthritis knee leg. The lesion (bristling level dotted graft) is presumed to horn in axons of PNs and on the whole to save the corticospinal projections to MNs and segmental INs order celecoxib 200mg on-line arthritis in neck and feet. Samples of averaged (20 sweeps) rectified in check (condensed lines) and conditioned (thin lines) MEPs (expressed as a interest of the backstage EMG) are illustrated inasmuch as the biceps at the 4 discount 200 mg celecoxib free shipping chinese medicine arthritis diet. Sway MEPs in triceps (here the lesion) had the same latency (в€ј13 ms) and alike resemble quarter on both sides purchase tadapox discount, consistent with the relative sparing of the corticospinal projections to low-cervical MNs and segmental INs order ...
Purpose Non-selective (NSAIDs) and selective (COX-2) nonsteroidal anti-inflammatory drugs are commonly used for their analgesic and anti-inflammatory effects. Their role after orthopaedic surgery has...
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There are no restrictions on food, beverages, or activity while taking celecoxib unless otherwise directed by your doctor. Concomitant use of celecoxib with aspirin or other NSAIDs (e.g., ibuprofen, naproxen, etc.) may increase the occurrence of stomach and intestinal ulcers. Fluconazole (Diflucan) increases the concentration of celecoxib in the body by inhibiting the breakdown of celecoxib in the liver. Therefore, treatment with celecoxib should be initiated at the lowest recommended doses in patients who are taking fluconazole. Celecoxib increases the concentration of lithium (Eskalith) in the blood by 17%. Therefore, lithium therapy should be closely monitored during and after therapy with celecoxib. Persons, taking the anticoagulant (blood thinner) warfarin (Coumadin), should have their blood tested when initiating or changing celecoxib treatment, particularly in the first few days, for any changes in the effects of the anticoagulant. Persons, who drink more than 3 alcoholic beverages per ...
There are no restrictions on food, beverages, or activity while taking celecoxib unless otherwise directed by your doctor. Concomitant use of celecoxib with aspirin or other NSAIDs (e.g., ibuprofen, naproxen, etc.) may increase the occurrence of stomach and intestinal ulcers. Fluconazole (Diflucan) increases the concentration of celecoxib in the body by inhibiting the breakdown of celecoxib in the liver. Therefore, treatment with celecoxib should be initiated at the lowest recommended doses in patients who are taking fluconazole. Celecoxib increases the concentration of lithium (Eskalith) in the blood by 17%. Therefore, lithium therapy should be closely monitored during and after therapy with celecoxib. Persons, taking the anticoagulant (blood thinner) warfarin (Coumadin), should have their blood tested when initiating or changing celecoxib treatment, particularly in the first few days, for any changes in the effects of the anticoagulant. Persons, who drink more than 3 alcoholic beverages per ...
Unfortunately its margin of safety (the difference between effective and toxic levels of a drug) was very narrow and the number of unacceptable side effects and toxicity problems kept it from being. . Celebrex comes in two strengths - 100 mg and 200 mg. It is perfectly fine to continue to take it every day while using the acetaminophen on a more as-needed basis. The medical literature includes studies showing an increased risk of serious cardiovascular problems with celecoxib, as well as other NSAIDs. Lynne Weixel answered. Depending on the severity of your condition, Celebrex should be taken once or twice daily. The lowest GoodRx price for the most common version of generic Celebrex is around $8.23, 95% off the average retail price of $190.24. It is used to treat the symptoms of osteoarthritis, ankylosing spondylitis, and …. Vioxx and Bextra have been withdrawn, whilst Arcoxia (Etoricoxib) and Prexige (Lumiracoxib have been refused approval. How to take celecoxib capsules (100mg and 200 mg ...
The simultaneous use of nonsteroidal anti-inflammatory drugs (NSAIDs), including selective cyclooxygenase-2 inhibitors and non-selective NSAIDs, such as acetylsalicylic acid in doses that provide anti-inflammatory action (more than 3 g per day) reduced antihypertensive effect of ramipril and indapamide; It increases the risk of renal impairment, until the development of acute renal failure; increases the content of potassium in the blood plasma of patients with pre-existing renal impairment. This combination is recommended to be used with caution, especially in elderly patients. Patients must be compensated BCC, and to carry out monitoring of renal function prior to and after the start of treatment KONSILAR-D24 ...
Epidemiological and clinical studies suggest that non-steroidal anti-inflammatory drugs (NSAIDs), including cyclooxygenase (COX)-2 selective inhibitors, reduce the risk of developing cancer. Experimental studies in human cancer cell lines and rodent models of carcinogenesis support these observations by providing strong evidence for the antineoplastic properties of NSAIDs. The involvement of COX-2 in tumorigenesis and its overexpression in various cancer tissues suggest that inhibition of COX-2 is responsible for the chemopreventive efficacy of these agents. However, the precise mechanisms by which NSAIDs exert their antiproliferative effects are still a matter of debate. Numerous other studies have shown that NSAIDs can act through COX-independent mechanisms. This review provides a detailed description of the major COX-independent molecular targets of NSAIDs and discusses how these targets may be involved in their anticancer effects. Toxicities resulting from COX inhibition and the suppression of
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1. Health Technol Assess. 2008 Apr12(11):1-278, iii. Cyclooxygenase-2 selective non-steroidal anti-inflammatory drugs (etodolac, meloxicam, celecoxib, rofecoxib
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The SOS project focused on the safety of non-steroidal anti-inflammatory drugs with a specific focus on the evaluation of the gastro-intestinal and cardiovascular effects of traditional NSAIDs and COX-II selective NSAIDs (coxibs). The project used various resources for the assessment of the gastrointestinal (GI) and cardiovascular (CV) effects of tNSAIDs and coxibs. The meta-analyses were published and showed that clinical trials were mostly not large enough to demonstrate NSAID GI and CV safety, especially not prior to the COXIB era, and not at all in children. The meta-analyses from observational studies yielded estimates for GI, acute myocardial infarction and stroke but none for heart failure. Information on dose and duration effects was missing and several methodological gaps were identified, as well as a lack of data in children.. The SOS healthcare database study allowed for the study of the association between 13 individual and all study outcomes through a nested case control study in a ...
The results of this study demonstrate that single doses of celecoxib, a highly selective COX-2 inhibitor in vitro, are well tolerated by healthy volunteers. All doses inhibited LPS-stimulated monocyte PGE2 formation ex vivo, an index of COX-2 activity, to a degree that approximated that attained after 800 mg ibuprofen, a therapeutic dose of a nonselective, conventional NSAID. Although interindividual differences in response were apparent and the biochemical selectivity of Celecoxib for COX-2 was relative, rather than absolute, in humans, it did not influence TxA2-dependant platelet aggregation ex vivo. Surprisingly, celecoxib and ibuprofen had comparable suppressive effects on the excretion of PGI-M. Celecoxib also suppressed urinary 6-keto PGF1α. This implies a major role for COX-2 in the biosynthesis of both systemic and renal PGI2 under physiological conditions in young volunteers.. The two COX isoforms are distinct gene products prone to differential patterns of regulation (5-9, 13-17). ...
Our in vitro results revealed that, in HNSCC cells, the selective Cox-2 inhibitors led to the suppression of the EMT by restoring the expression of E-cadherin through the downregulation of its transcriptional repressors. Moreover, the extent of the effect of Cox-2 inhibition was shown to depend on the baseline expression levels of both E-cadherin and Cox-2 in each cell; i.e., tumor cells expressing lower E-cadherin and higher Cox-2 are expected to be more sensitive to Cox-2 inhibition in terms of the restoration of E-cadherin expression. Such a finding is consistent with a previous study of bladder cancer cells using another Cox-2 inhibitor, etodolac. In that study, etodolac upregulated E-cadherin expression only in T24 cells, which express the highest level of Cox-2 and the lowest level of E-cadherin; it did not do so in 5637 cells or K47 cells, which express a lower level of Cox-2 and a higher level of E-cadherin [42]. Interestingly, using the same three bladder cancer cell lines and three ...
We were not asleep at the wheel, we were actually engaged in reviewing a lot of data, Dr. Lourdes Villalba told a joint meeting of the Food and Drug Administrations arthritis advisory committee and its drug safety and risk management advisory committee, which are looking into Vioxx, Celebrex and Bextra. Celebrex and Bextra, made by Pfizer Inc., remain on the market, though some studies have also indicated they, too, may carry an added heart risk. Villalba, medical officer responsible for Vioxx at the FDAs Center for Drug Evaluation and Research, pointed out that a study done in 2000 comparing Vioxx with the painkiller naproxen, showed a higher rate of heart problems with Vioxx, but other studies had conflicting results. In discussions with Merck officials, she said, the company suggested naproxen might have a heart protective effect. Nonetheless, in 2002 the agency required an added warning on the Vioxx label urging caution in prescribing it for people with heart conditions. We never bought ...
The results of a clinical trial (PRECISION)1 comparing the cardiovascular safety of the COX-2 selective NSAID celecoxib (Celebrex, and generics) with that of ibuprofen and naproxen, which are nonselective, have been described in the lay press in terms that may overestimate the safety of celecoxib.. NSAID PHARMACOLOGY - NSAIDs inhibit the enzyme cyclooxygenase (COX), which is required for synthesis of prostaglandins and thromboxane. COX-1 inhibition blocks the protective effect of prostaglandins on the gastric mucosa, which can cause gastrointestinal toxicity, and has an antiplatelet effect that can cause bleeding. COX-2 inhibition produces therapeutic anti-inflammatory and analgesic effects, but it has effects on vascular endothelium that can be prothrombotic.. Ibuprofen and naproxen inhibit COX-1 more than COX-2. The COX-2 selective NSAID rofecoxib (Vioxx), ... more ...
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15.3 deaths/100,000 NSAID/aspirin users, and hypothesis that anti-inflammatory effects are usu- that up to one third of all NSAID/aspirin deaths ally due to COX-2 inhibition and that adverse can be attributed to low-dose aspirin use.12 In an effects usually occur because of COX-1 inhibi- endoscopic evaluation of patients who had contin- tion, selective COX-2 inhibitors (celecoxib, rofe- uously used NSAIDs over the previous 6 months, coxib, valdecoxib, etc.) were developed to reduce gastroduodenal ulcers were detected in 24% of NSAID-associated GI toxicities.19 Several clinical patients, and approximately 1-2% of NSAID users trials showed a 41-57% reduction in the rate of developed ulcer-related complications (bleeding, GI toxicities with the use of selective COX-2 in- perforation, obstruction) annually.13,14 Notably, hibitors.20 However, the VIGOR trial raised the the majority of patients with NSAID-related GI issue of the cardiovascular safety of the coxibs complications did not have preceding ...
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Ive recently been experiencing a lot of joint pain. Its mostly my SI joints, fingers, and toes. Its feeling very much like it did years ago when the docs thought I had rheumatoid arthritis. Tylenol is doing nothing to touch the pain. So, I asked my gastro for something else. He said he normally gives IBD patients Tramadol, but he couldnt give it to me. Apparently, Tramadol and most SSRI antidepressants dont mix well. Its not to the point of needing narcotics yet. He prescribed Celebrex with the promise that I wouldnt take it every day. Celebrex is still an NSAID, but he says its better than the others. Does anyone else here take Celebrex for joint pain? If so, how often do you take it? Have you had any problems with GI bleeding, etc. with it ...
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Reversible COX-1/COX-2 inhibition.. Topical.. No data.. Skin disorders.. Skin conditions, such as contact dermatitis. ... Thus, the COX2 inhibitors were developed to inhibit only the COX2 enzyme (traditional NSAIDs block both versions in general). ... Reversible COX-1/COX-2 inhibition.. PO, IM, IV, rectal.. No data.. Pain.. As per diclofenac. ... Irreversibly inhibits COX-1 and COX-2; hence inhibiting prostaglandin synthesis.. PO, IM, IV, rectal. Bioavailability = 80-100 ...
FitzGerald, Garret (2001). "COX-2 inhibitors and the cardiovascular system". Clin Exp Rheumatol. 19 (6 Suppl 25): S31-6. PMID ... 164 (2): 317-31. doi:10.1111/j.1476-5381.2011.01269.x. PMC 3174413. PMID 21323900. Hughes, J (1975). "Identification of two ... Hothersall, J (2011). "The design, synthesis and pharmacological characterization of novel beta(2)-adrenoceptor antagonists". ...
Peres MF, Silberstein SD (2002). "Hemicrania continua responds to cyclooxygenase-2 inhibitors". Headache. 42 (6): 530-1. doi: ... 2, by G.S.Davis, and the incident has been cited in King's American Dispensatory (1898 and later editions) in the description ... Changing the 'cocktail' to include (for example) 10 mls of .5% Marcaine and changing to 2% Lignocaine, whilst in theory should ... Davis, G.S. (1881). The Therapeutic Gazette, Volume 2. p. 54. King; Felter; Lloyd, John; Harvey Wickes; John Uri (1898). King's ...
Likofelon beraksi dengan menghambat LOX (lipooksigenase) & COX dan karenanya dikenal sebagai 5-LOX/COX inhibitor ... COX-2 inhibitor selektif (koksib atau Coxibs)[sunting , sunting sumber]. *Selekoksib (Perhatian FDA[7]) ... COX-2) in vitro". Bioorg. Med. Chem. 19 (16): 4882-6. doi:10.1016/j.bmc.2011.06.069. PMID 21775152.. ... "Effects of β-glucosidase hydrolyzed products of harpagide and harpagoside on cyclooxygenase-2 ( ...
... an important difference with reversible inhibitors. Furthermore, aspirin, while inhibiting the ability of COX-2 to form pro- ... At least two different types of cyclooxygenases, COX-1 and COX-2, are acted on by aspirin. Aspirin irreversibly inhibits COX-1 ... Warner TD, Mitchell JA (October 2002). "Cyclooxygenase-3 (COX-3): filling in the gaps toward a COX continuum?". Proceedings of ... Blockade of COX-1 by aspirin apparently results in the upregulation of COX-2 as part of a gastric defense and that taking COX-2 ...
... as well as the IL-12/IL-23 inhibitor ustekinumab, and the IL-17a inhibitor secukinumab. Recently, the Jak inhibitor, ... "Nonsteroid drug selectivities for cyclo-oxygenase-1 rather than cyclo-oxygenase-2 are associated with human gastrointestinal ... Both COX-2 inhibitors and other non-selective NSAIDS have potential adverse effects that include damage to the kidneys. These ... Coxibs (COX-2 inhibitors) e.g. Celecoxib or Etoricoxib, are associated with a statistically significant 50 to 66% relative risk ...
Among them are serotonin, a neurotransmitter; indometacin, a non-steroidal anti-inflammatory agent; L-761,066, a COX-2 ... inhibitor; and LY311727, an inhibitor of secretory phospholipase. Currently, one of the most interesting applications of the ... Huang, Yun-Sheng; Zhang, W.; Zhang, X.; Wang, J. (2010). "Manufacturing synthesis of 5-hydroxy-2-methyl-1H-indole". Research on ... Nenitzescu, C.D. (1929). "Derivatives of 2-methyl-5-hydroxyindole". Bull. Soc. Chim. Romania. 11: 37-43. Allen, G.; Pidacks, C ...
It is also known for its release of the first bulk laxative, Metamucil, in 1934; Dramamine, for motion sickness; the COX-2 ... inhibitors Celebrex and Bextra; Ambien for insomnia; and NutraSweet (also known as aspartame), an artificial sweetener, in 1965 ... which Searle developed and which became the first selective COX-2 inhibitor to be approved by the FDA on December 31, 1998. ...
... , along with other COX-2 selective inhibitors, celecoxib, valdecoxib, and parecoxib, were discovered by a team at the ... October 2010). "The pharmacokinetics of mavacoxib, a long-acting COX-2 inhibitor, in young adult laboratory dogs". Journal of ... European Public Assessment Report (EPAR): Trocoxil, European Medicines Agency Cox SR, Lesman SP, Boucher JF, Krautmann MJ, ... 52 (5): 2. May 2001. Archived from the original (PDF) on 15 April 2018. v t e v t e. ...
It acts as a COX-2 inhibitor. Reaction of the imine with TosMIC in the presence of potassium carbonate leads to what may be ... Activity Relationship of a New Series of COX-2 Selective Inhibitors: 1,5-Diarylimidazoles". Journal of Medicinal Chemistry. 46 ... viewed as 2+3 cycloaddition of the nitrogen analogue of a ketene to form the imidazole ring. "European Public Assessment Report ...
FDA Alert on Bextra withdrawal Large systematic review of adverse renal and arrhythmia risk of valdcoxib and other COX-2 ... inhibitors, JAMA 2006. ... It is a selective cyclooxygenase-2 inhibitor. It was patented ... Zhang J, Ding EL, Song Y (October 2006). "Adverse effects of cyclooxygenase 2 inhibitors on renal and arrhythmia events: meta- ... Discovery and development of cyclooxygenase 2 inhibitors Parecoxib Apricoxib Fischer J, Ganellin CR (2006). Analogue-based Drug ...
It is a COX-2 inhibitor (coxib). Gaynor JS, Muir WM (2014). "Robenacoxib". Handbook of Veterinary Pain Management (3rd, revised ...
inhibitors). COX. (PTGS). *Salicylic acids: Aloxiprin. *Aspirin (acetylsalicylic acid). *Benorilate (benorylate). *Carbasalate ... Increasing DGLA intake may allow DGLA to act as a competitive inhibitor of 2-series PGs and 4-series LTs and, thus, suppress ... 1984). "Determination of the structure of cholesterol inhibitor II isolated from high-protein barley flour (HPBF)". Fed. Proc. ... InChI=1S/C18H30O2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18(19)20/h6-7,9-10,12-13H,2-5,8,11,14-17H2,1H3,(H,19,20)/b7-6-,10- ...
NSAIDs such as Ibuprofen/paracetamol work to reduce the immediate inflammation by inhibiting Cox-1 and Cox-2 enzymes, which are ... Day, Richard O.; Graham, Garry G. (1 December 2004). "The Vascular Effects of COX-2 selective inhibitors". Australian ... 21 (2): 317-331. doi:10.1016/j.berh.2006.12.004. PMID 17512485. Prentice, William E. (2014). "Tissue Response to Injury" (PDF ... 8 (2): 137-145. doi:10.1007/s11420-011-9239-7. ISSN 1556-3316. PMC 3715623. PMID 23874254. Neustaedter, Randy. "Natural ...
... is a COX-2 selective inhibitor nonsteroidal anti-inflammatory drug. Its structure is different from that of other ... Shi, S; Klotz, U (March 2008). "Clinical use and pharmacological properties of selective COX-2 inhibitors". European Journal of ... Tacconelli S, Capone ML, Patrignani P (2004). "Clinical pharmacology of novel selective COX-2 inhibitors". Curr Pharm Des. 10 ( ... it binds to a different site on the COX-2 enzyme than do other COX-2 inhibitors; it is the only acidic coxib and has the ...
COX). Ketorolac is a non-selective COX inhibitor.[24] It is considered a first-generation NSAID.[20] ... Lee IO, Seo Y (March 2008). "The effects of intrathecal cyclooxygenase-1, cyclooxygenase-2, or nonselective inhibitors on pain ... Retrieved 2 June 2018.. *^ a b c d e f g h i "Ketorolac Tromethamine Monograph for Professionals". American Society ... Ketorolac works by blocking cyclooxygenase 1 and 2 (COX1 and COX2), thereby decreasing production of prostaglandins.[2][4] ...
inhibitors). COX. (PTGS). *Salicylic acids: Aloxiprin. *Aspirin (acetylsalicylic acid). *Benorilate (benorylate). *Carbasalate ... InChI=1S/C17H15NO5/c1-11(19)18-13-7-9-14(10-8-13)23-17(21)15-5-3-4-6-16(15)22-12(2)20/h3-10H,1-2H3,(H,18,19) N ...
inhibitors). COX. (PTGS). *Salicylic acids: Aloxiprin. *Aspirin (acetylsalicylic acid). *Benorilate (benorylate). *Carbasalate ... COX-1 and COX-2) enzymes reversibly, which decreases production of proinflammatory prostaglandin precursors.[10][12] ... doi:10.1208/s12249-009-9367-2. PMC 2850498. PMID 20087696.. *^ Sarzi-Puttini, P; Atzeni, F; Lanata, L; Bagnasco, M (2013). " ... Ketoprofen, (RS)-2-(3-benzoylphenyl)-propionic acid (chemical formula C16H14O3) is one of the propionic acid class of ...
Traditional NSAIDs and COX-2 inhibitor NSAIDs are effective for treating axSpA. The potential harms may not differ when ... The expression was introduced in order to unify (1) less severe forms of spondylitis, (2) the early phase of ankylosing ...
No COX-2 selective inhibitor has been approved in the US since that time, regardless of the safety profile of parecoxib in ... Parecoxib is a COX2 selective inhibitor. It is injectable. It is approved through much of Europe for short term perioperative ... Gajraj NM (2007). "COX-2 inhibitors celecoxib and parecoxib: valuable options for postoperative pain management". Current ... Parecoxib is the first parenteral COX-2 selective inhibitor available for clinical use in pain management. It is well known ...
Cyclooxygenase (COX) has two well-studied isoforms, called COX-1 and COX-2. COX-1 mediates the synthesis of prostaglandins ... Rofecoxib was a COX-2 selective nonsteroidal anti-inflammatory drug (NSAID). It was marketed by Merck & Co. to treat ... In 2005, the FDA issued a memo concluding that along with the other approved COX-2 selective NSAIDs available at the time (i.e ... By creating "selective" NSAIDs that inhibit COX-2, but not COX-1, the same pain relief as traditional NSAIDs is offered, but ...
It is categorized as an inhibitor of cyclooxygenase-2. In experimental biology, it has been employed to inhibit chloride ... 41 (2): 217-22. PMID 1371581. Balderas E, Ateaga-Tlecuitl R, Rivera M, Gomora JC, Darszon A (June 2012). "Niflumic acid blocks ...
inhibitors). COX. (PTGS). *Salicylic acids: Aloxiprin. *Aspirin (acetylsalicylic acid). *Benorilate (benorylate). *Carbasalate ... At least two different types of cyclooxygenases, COX-1 and COX-2, are acted on by aspirin. Aspirin irreversibly inhibits COX-1 ... Blockade of COX-1 by aspirin apparently results in the upregulation of COX-2 as part of a gastric defense[96] and that taking ... "Cyclooxygenase-3 (COX-3): filling in the gaps toward a COX continuum?". Proceedings of the National Academy of Sciences of the ...
NSAIDs inhibit cyclooxygenase-1, or COX-1, an enzyme responsible for the biosynthesis of eicosanoids in the stomach, which ... Most use a combination of two antibiotics and a proton pump inhibitor. Sometimes bismuth is added to the regimen. In 1,000 A.D ... When antacids do not provide enough relief, medications such as H2 blockers and proton-pump inhibitors that help reduce the ... Boparai V, Rajagopalan J, Triadafilopoulos G (2008). "Guide to the use of proton pump inhibitors in adult patients". Drugs. 68 ...
Starting with linked COX-2 inhibitors, such as Vioxx (rofecoxib) in 2001, Nissen was one of the first physicians to link it to ... Mukherjee D, Nissen SE, Topol EJ (2001). "Risk of cardiovascular events associated with selective COX-2 inhibitors". JAMA. 286 ... Steven Nissen MD, physician profile [1], Cleveland Clinic, retrieved 2/2010 Nissen SE, Gurley JC, Grines CL, Booth DC, McClure ... an experimental type 2 diabetes drug. When an U.S. Food and Drug Administration (FDA) advisory panel charged with reviewing the ...
Proton pump inhibitors (PPI) may reduce mortality in those with severe disease as well as the risk of re-bleeding and the need ... NSAIDs or COX-2 inhibitors increase the risk about fourfold. SSRIs, corticosteroids, and anticoagulants may also increase the ... Proton pump inhibitors, if they have not been started earlier, are recommended in those in whom high risk signs for bleeding ... Wu, LC; Cao, YF; Huang, JH; Liao, C; Gao, F (2010-05-28). "High-dose vs low-dose proton pump inhibitors for upper ...
Mukherjee D, Nissen SE, Topol EJ (2001). "Risk of Cardiovascular Events Associated With Selective COX-2 Inhibitors". JAMA. 286 ... Topol, Eric (October 2, 2004). "Good Riddance to a Bad Drug". The New York Times. Retrieved July 9, 2010. Topol EJ (October ... In 2008 he forged a new educational program with Qualcomm and Scripps Health to train physicians in wireless medicine, a 2-year ... Archived from the original on 2 June 2013. Retrieved 2010-05-12. Stencel, Christine; Shamir, Judith (18 October 2004). " ...
Most NSAIDs act as nonselective inhibitors of the cyclooxygenase (COX) enzymes, inhibiting both the cyclooxygenase-1 (COX-1) ... Non-steroidal anti-inflammatory drugs (NSAIDs) are the competitive inhibitors of cyclooxygenase (COX), the enzyme which ... NSAIDs work by inhibiting the activity of cyclooxygenase enzymes (COX-1 or COX-2). In cells, these enzymes are involved in the ... and COX and hence known as 5-LOX/COX inhibitor H-harpagide in figwort or devil's claw Most NSAIDs are chiral molecules; ...
inhibitors). COX. (PTGS). *Salicylic acids: Aloxiprin. *Aspirin (acetylsalicylic acid). *Benorilate (benorylate). *Carbasalate ... InChI=1S/C13H11NO2/c15-13(16)11-8-4-5-9-12(11)14-10-6-2-1-3-7-10/h1-9,14H,(H,15,16) N ... 2] See also[edit]. *synthesis of Fenamic acid: C. F. H. Allen, G. H. W. McKee (1939). "Acridone". 2: 6. doi:10.15227/orgsyn. ... Jack DeRuiter, Principles of Drug Action 2, Fall 2002 1: Non-Steroidal Antiinflammatory Drugs (NSAIDS) ...
... endogenous angiogenesis inhibitors, fumagillin analogues, statins, cyclo-oxygenase-2 inhibitors, phytochemical compounds, ... Examples of aromatase inhibitors include anastrozole and letrozole. Evidence for aromatase inhibitors is limited due to the ... Ibuprofen and naproxen are combined COX-1 and COX-2 inhibitors. COX-2 selective agents such as celecoxib have a more limited ... Aromatase inhibitors are medications that block the formation of estrogen and have become of interest for researchers who are ...
Yi, John S.; Cox, Maureen A.; Zajac, Allan J. T-cell exhaustion: characteristics, causes and conversion. Immunology. 2010-04, ... U.S. FDA Approved Immune-Checkpoint Inhibitors and Immunotherapies. Medical Writer Agency , 香港醫學作家 , MediPR , MediPaper Hong ... T细胞耗竭的直接原因包括持续的抗原刺激、以及CD4细胞的缺失[42]。长时间的抗原暴露和高病毒负载可以加重T细胞耗竭的程度
... the high risk of birth defects with 5α-reductase inhibitors limits their use in women.[1][138] However, 5α-reductase inhibitors ... Simpson NB, Cunliffe WJ (2004). "Disorders of the sebaceous glands". In Burns, Tony, Breathnach, Stephen, Cox, Neil, Griffiths ... Azzouni F, Zeitouni N, Mohler J (February 2013). "Role of 5α-reductase inhibitors in androgen-stimulated skin disorders". ... and inhibitors of the stearoyl-CoA desaturase-1 enzyme are also a focus of research efforts.[10][91] Particles that release ...
March 2004). "The cyclooxygenase isozyme inhibitors parecoxib and paracetamol reduce central hyperalgesia in humans". Pain. 108 ... 98 (2): 246-54. doi:10.1093/bja/ael344. PMID 17251214.. *^ Warncke T, Stubhaug A, Jørum E (August 1997). "Ketamine, an NMDA ...
5α-Reductase inhibitorsEdit. 5α-Reductase inhibitors such as finasteride and dutasteride are inhibitors of 5α-reductase, an ... Boris, A.; Scott, J. W.; DeMartino, L.; Cox, D. C. (1973). "ENDOCRINE PROFILE OF A NONSTEROIDAL ANTIANDROGEN N-(3,5-DIMETHYL-4- ... Androgen synthesis inhibitorsEdit. Androgen synthesis inhibitors are enzyme inhibitors that prevent the biosynthesis of ... androgen synthesis inhibitors can be further divided mostly into CYP17A1 inhibitors and 5α-reductase inhibitors; and ...
c-Met inhibitors. *Cyclooxygenase 2 inhibitors. *Dipeptidyl peptidase-4 inhibitors. *Direct thrombin inhibitors ... 19 (2): 578-88. PMID 9880578.. *^ a b Majewska MD, Harrison NL, Schwartz RD, Barker JL, Paul SM (May 1986). "Steroid hormone ... 300 (1): 2-8. doi:10.1124/jpet.300.1.2. PMID 11752090.. *^ Perrais D, Ropert N (Jan 1999). "Effect of zolpidem on miniature ... Fig 2. Schematic diagram of a GABAA receptor protein ((α1)2(β2)2(γ2)) which illustrates the five combined subunits that form ...
is modified to include binding of the inhibitor to the free enzyme:. EI. +. S. ⇌. k. 3. k. −. 3. E. +. S. +. I. ⇌. k. −. 1. k. ... 2. [. ES. ]. =. k. 2. K. i. [. S. ]. [. E. ]. 0. K. m. K. i. +. K. i. [. S. ]. +. K. m. [. I. ]. {\displaystyle V_{0}=k_{2}[{\ ... is the inhibitor concentration.. V. max. {\displaystyle V_{\max }}. remains the same because the presence of the inhibitor can ... To compute the concentration of competitive inhibitor [. I. ]. {\displaystyle {\ce {[I]}}}. that yields a fraction f. V. 0. {\ ...
Cox, PA; Banack, SA; Murch, SJ; Rasmussen, U; Tien, G; Bidigare, RR; Metcalf, JS; Morrison, LF; Codd, GA; Bergman, B. (2005). " ... UV protectants and specific inhibitors of enzymes.[16][17] ... Cox PA, Davis DA, Mash DC, Metcalf JS, Banack SA (2015). " ... 25 (1-2): 425-432.. *^ Forc, N.S.W.B.G.A.T. (1992). "Final report of the NSW Blue-Green Algae Task Force". Parramatta: NSW ... 24 (2): 175-207. doi:10.1081/TXR-200057850.. *^ Francis G (1878). "Poisonous Australian Lake". Nature. 18 (444): 11-12. Bibcode ...
... zaviranje COX-1 pa povzroča neželene učinke.[6] Kasneje so odkrili še tretjo izoobliko encima, poimenovano COX-3, ki je v večji ... Thomas, Mc (februar 2000). "Diuretics, ACE inhibitors and NSAIDs-the triple whammy". The Medical journal of Australia. 172 (4 ... Sklepajo, da je COX-3 možno mesto delovanja paracetamola, vendar tudi drugi analgetiki in antipiretiki v in vitro poskusih ... Zaviranje COX 1 zato povzroča neželene učinke na prebavilih. Neželeni učinki na prebavila so močneje izraženi pri tistih NSAID ...
t-PA and urokinase are themselves inhibited by plasminogen activator inhibitor-1 and plasminogen activator inhibitor-2 (PAI-1 ... Factor Xa inhibitors. (with some II inhibition). Heparin group/. glycosaminoglycans/. (bind antithrombin). *Low molecular ... Coagulation inhibitors. *Antithrombin (inhibits II, IX, X, XI, XII). *Protein C (inhibits V, VIII)/Protein S (cofactor for ... Antifibrinolytics, such as aminocaproic acid (ε-aminocaproic acid) and tranexamic acid are used as inhibitors of fibrinolysis. ...
Inhibitors of squalene epoxidase have found application mainly as antifungal drugs: butenafine naftifine terbinafine Since ... Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (Jun 2011). "A conditional knockout ... "Transcriptional regulation of squalene epoxidase by sterols and inhibitors in HeLa cells". The Journal of Biological Chemistry ... 200 (1-2): 149-56. doi:10.1016/S0378-1119(97)00411-3. PMID 9373149. Lu Y, Dollé ME, Imholz S, van 't Slot R, Verschuren WM, ...
Simpson CR, Hippisley-Cox J, Sheikh A (July 2010). "Trends in the epidemiology of chronic obstructive pulmonary disease in ... and breakdown of the connective tissue of the lungs by proteases that are insufficiently inhibited by protease inhibitors. The ... 2: CD012066. doi:10.1002/14651858.CD012066.pub2. PMC 6464543. PMID 28185242.. *^ Zheng Y, Zhu J, Liu Y, Lai W, Lin C, Qiu K, et ... 25 (2): 139-148. doi:10.1111/resp.13530. PMID 30907495.. *^ Nici L (2011). Chronic Obstructive Pulmonary Disease: Co- ...
The influence of isotretinoin and 5-a reductase inhibitors in metaloproteases of connective tissue in patients with ance] (in ... Goodfield MJ, Cox NH, Bowser A, McMillan JC, Millard LG, Simpson NB, Ormerod AD (June 2010). "Advice on the safe introduction ... the tissue inhibitors of metalloproteases).[69] It is already known that metalloproteases play an important role in the ... 26 (2): 124-8. doi:10.1159/000267402. PMID 8196934.. *^ Griffin JN, Pinali D, Olds K, Lu N, Appleby L, Doan L, Lane MA ( ...
6 (2): 61-74. doi:10.1007/bf02081999. PMID 4615073.. *^ Clinical trial number NCT01324141 for "Topical MTS-01 for Dermatitis ... COX-inhibiting nitric oxide donator: Naproxcinod. N-Arylanthranilic acids. (fenamates). *Azapropazone. *Clonixin ... doi:10.1016/S1360-1385(01)01898-2. PMID 11286918.. *^ Corpas FJ, Fernández-Ocaña A, Carreras A, Valderrama R, Luque F, Esteban ... The superoxide anion radical (O2−) spontaneously dismutes to O2 and hydrogen peroxide (H2O2) quite rapidly (~105 M−1s−1 at pH 7 ...
Sanger, F; Nicklen, S; Coulson, AR (1977). "DNA sequencing with chain-terminating inhibitors". Proceedings of the National ... Cox DR, James MR, Bentley D, Deloukas P, Lander ES, Hudson TJ (October 1996). "A gene map of the human genome". Science 274 ( ... 2 (12): 919-29. doi:10.1038/35103511. PMID 11733745. *↑ Crick, Francis (1962). The genetic code. WH Freeman and Company. PMID ... SciTable (Nature Publishing Group) 4 (2): 1. *↑ ೬೩.೦ ೬೩.೧ Guerzoni, D; McLysaght, A (November 2011). "De novo origins of human ...
2 (6): 746-767. doi:10.1002/cmdc.200600207. PMID 17295372.. *^ Ji, Jianguo; Bunnelle, William H.; Anderson, David J.; Faltynek ... InChI=1S/C11H12N4/c12-2-8-1-10(5-13-3-8)15-7-9-4-14-6-11(9)15/h1,3,5,9,11,14H,4,6-7H2/t9-,11-/m1/s1 N ... 2] Its structure has a nicotinonitrile (3-cyanopyridine) core bound through C5 to the N6 of (1R,5S)-3,6-diazabicyclo[3.2.0] ...
가 나 다 라 마 David L. Nelson, Michael M. Cox. , 《Lehninger principles of biochemistry 4th》, New York : W. H. Freeman, 2005, 23~24 ... Wlodawer A, Vondrasek J (1998). "Inhibitors of HIV-1 protease: a major success of structure-assisted drug design". 》Annual ... 2. +. H. 2. O. →. 탄산무수화효소. H. 2. CO. 3. {\displaystyle {\ce {CO2{}+H2O-,[{\text{탄산무수화효소}}]H2CO3}}}. (조직에서 CO2 농도가 높을 때) ... 2. +. H. 2. O. ←. 탄산무수화효소. H. 2. CO. 3. {\displaystyle {\ce {CO2{}+H2O,-[{\text{탄산무수화효소}}]H2CO3}}}. (폐에서 CO2 농도가 낮을 때) ...
Cox M, Lehninger AL, Nelson DR (2000). Lehninger principles of biochemistry. New York: Worth Publishers. pp. 306-308. ISBN 1- ...
... is a weak inhibitor of dihydrofolate reductase,[69] but whether this effect is sufficient to contribute to a ... It is known that lamotrigine is a weak inhibitor of human dihydrofolate reductase (DHFR) and other, more powerful, human DHFR ... 2 (5): 199-205. doi:10.1177/2045125312451270. PMC 3736944. PMID 23983976.. *^ Erfurth A, Walden J, Grunze H (October 1998). " ... 24 (2): E38-9. doi:10.1176/appi.neuropsych.11040093. PMID 22772697.. *^ Ishioka M, Yasui-Furukori N, Hashimoto K, Sugawara N ( ...
HDAC inhibitor (small molecule) benzamide M344 MC 19 fatty acid Sodium butyrate M (y) 5, 6, 7 ; H (ny) D (y) 11 M (y) 14; R (y ... COX-2. At the individual gene level, hypomethylation and thus derepression of COX-2 occurs, inhibition of which reduces ... DNA methyltransferase inhibitors, and histone demethylase inhibitors.[6][7] The majority of epigenetic drugs tested for use ... DNA-methylation inhibitor chemical analogue of cytidine Azathioprine M (ny) M (ny) ...
Neuraminidase inhibitors. Overall the benefits of neuraminidase inhibitors in those who are otherwise healthy do not appear to ... Cox NJ, Subbarao K (October 1999). "Influenza". Lancet. 354 (9186): 1277-82. doi:10.1016/S0140-6736(99)01241-6. PMID 10520648. ... M2 inhibitors. The antiviral drugs amantadine and rimantadine inhibit a viral ion channel (M2 protein), thus inhibiting ... Bright RA, Medina MJ, Xu X, Perez-Oronoz G, Wallis TR, Davis XM, Povinelli L, Cox NJ, Klimov AI (October 2005). "Incidence of ...
Anti-allergy: mast cell inhibitors. *Anti-glaucoma: adrenergic agonists, beta-blockers, carbonic anhydrase inhibitors/ ... The main categories of drugs for musculoskeletal disorders are: NSAIDs (including COX-2 selective inhibitors), muscle relaxants ... HMG-CoA reductase inhibitors (statins) for lowering LDL cholesterol inhibitors: hypolipidaemic agents. ... cytotoxic drugs, therapeutic antibodies, sex hormones, aromatase inhibitors, somatostatin inhibitors, recombinant interleukins ...
"Matrix metalloproteinase inhibitors". Georgetown University Hospital, Vincent T. Lombardi Cancer Center, Division of Medical ... Selain itu, akan tampak ekspresi gen iNOS di sel vaskular maupun sel yang mengalami peradangan dan ekspresi gen COX-2 di sel ... "Reducing bleeding complications after thrombolytic therapy for stroke: clinical potential of metalloproteinase inhibitors and ... faktor jaringan dan tissue factor pathway inhibitor.[22] Disfungsi endotelial yang menyebabkan defisiensi sawar darah otak, ...
inhibitors). COX. (PTGS). *Salicylic acids: Aloxiprin. *Aspirin (acetylsalicylic acid). *Benorilate (benorylate). *Carbasalate ... In Europe, use of selexipag together with strong inhibitors of the liver enzyme [CYP2C8], such as gemfibrozil, is ... 2-{4-[(5,6-diphenylpyrazin-2-yl)(propan-2-yl)amino]butoxy}-N-(methanesulfonyl)acetamide ...
Nelson, D. L.; Cox M. M. (2004). Lehninger Principles of Biochemistry (4th ed.). W. H. Freeman. ISBN 0-7167-4339-6.. ... Vigabatrin is an irreversible inhibitor of GABA transaminases which leads to decreased levels of GHB and elevation of GABA. ... 63 (2): 399-408. doi:10.1086/301964. PMC 1377305 . PMID 9683595.. *^ a b c d e Pearl, P. L.; Novotny, E. J.; Acosta, M. T.; ... doi:10.1007/s10545-007-0574-2. PMID 17457693.. *^ Ren, X.; Mody, I. (2003). "Gamma-hydroxybutyrate reduces mitogen-activated ...
Cox BS (1965). "[PSI], a cytoplasmic suppressor of super-suppression in yeast". Heredity. 20 (4): 505-521. doi:10.1038/hdy. ... "The histone methyltransferase inhibitor BIX01294 enhances the cardiac potential of bone marrow cells.". Stem Cells Dev. 22: ... doi:10.1007/s12035-015-9526-2.. *^ a b Short, A K; Fennell, K A; Perreau, V M; Fox, A; O'Bryan, M K; Kim, J H; Bredy, T W; Pang ... 2: 117. PMC 3445916 . PMID 23050241. doi:10.3389/fonc.2012.00117.. *^ Cuozzo C, Porcellini A, Angrisano T, Morano A, Lee B, Di ...
... selective monoamine oxidase inhibitor,[5][6][9] and as a low affinity, non-competitive NMDA receptor antagonist.[1][2][10] A ... Mattia C, Coluzzi F (September 2007). "Indantadol, a novel NMDA antagonist and nonselective MAO inhibitor for the potential ... 306 (2): 804-14. doi:10.1124/jpet.103.050039. PMID 12750440.. *^ a b "CHF 3381". Drugs in R&D. 5 (1): 28-30. 2004. doi:10.2165/ ... a N-methyl-D-aspartate receptor antagonist and monoamine oxidase-A inhibitor, attenuates secondary hyperalgesia in a human pain ...
... shepherding the subunits of COX together into a functional protein complex. This results in a deficit of COX protein, reducing ... Murphy, Jerome V (1974). "Leigh Disease: Biochemical Characteristics of the Inhibitor". Archives of Neurology. 31 (4): 220-7. ... Mutations in mitochondrial DNA (mtDNA) and over 30 genes in nuclear DNA (gene SURF1[8] and some COX assembly factors) have been ... Kidney and heart tissues were found to not have a COX deficiency.[12] ...
Factor Xa inhibitors. (with some II inhibition). Heparin group/. glycosaminoglycans/. (bind antithrombin). *Low molecular ... Endogenous plasma protease inhibitors deactivate drotrecogin. Therefore, no dose adjustment is needed in elderly patients, or ... Recent administration (within 7 days) of ,650 mg/day of aspirin or other platelet inhibitors ... Recent administration (within 7 days) of oral anticoagulants or GP IIb/IIIa inhibitors ...
Nonsteroidal anti-inflammatory drug − cyclooxygenase inhibitor. *Proton-pump inhibitor. *Renin inhibitor. *Selective ... Enzyme target mechanisms include activator or inhibitor. Ion channel modulators include opener or blocker. The following are ...
COX inhibitors have been shown to reduce the occurrence of cancers and pre-cancerous growths. The National Cancer Institute has ... Lau L, Hansford LM, Cheng LS, Hang M, Baruchel S, Kaplan DR, Irwin MS (Mar 2007). "Cyclooxygenase inhibitors modulate the p53/ ... Prostaglandins whose synthesis involves the cyclooxygenase-I enzyme, or COX-1, are responsible for maintenance and protection ... 170-fold more potent in inhibiting COX-1 than COX-2.[32] Studies of meloxicam 7.5 mg per day for 23 days find a level of ...
... Laurel J. Mengle-Gaw and Benjamin D. Schwartz ... Laurel J. Mengle-Gaw and Benjamin D. Schwartz, "Cyclooxygenase-2 inhibitors: promise or peril?," Mediators of Inflammation, vol ...
However, the chief investigator is stressing that the study is not a reason for people to stop taking COX-2 inhibitors and that ... A new study in mice could help shed light on why COX-2 inhibitors might increase the risk of thrombotic events. ... COX-1, the form of cyclooxygenase found in platelets, makes TxA2, which causes blood vessels to constrict and platelets ... COX-2, by contrast, is expressed in blood vessels and is a major source of PGI2, which dilates blood vessels and prevents the ...
Non-steroidal anti-inflammatory drugs (NSAIDs) are the competitive inhibitors of cyclooxygenase (COX), the enzyme which ... cyclooxygenase. Prostaglandins whose synthesis involves the cyclooxygenase-I enzyme, or COX-1, are responsible for maintenance ... COX inhibitors have been shown to reduce the occurrence of cancers and pre-cancerous growths. The National Cancer Institute has ... Lau L, Hansford LM, Cheng LS, Hang M, Baruchel S, Kaplan DR, Irwin MS (Mar 2007). "Cyclooxygenase inhibitors modulate the p53/ ...
... inhibitors, both of which can irritate the digestive tract. At times additional drugs are co-prescribed with NSAIDs or COX-2 ... Cox 2 Inhibitor News and Research. RSS Cox-2 Inhibitors are nonsteroidal anti-inflammatory drugs used to relieve pain and ... The cyclooxygenase-2 enzyme is just such a protein, as the concentration of COX-2 is greater in cancer cells than in adjacent ... COX-2 inhibitor extends sunitinib activity in renal cell carcinoma The effectiveness of sunitinib for the treatment of renal ...
Cyclooxygenases have two main isoforms that are called COX-1 and COX-2 (as well as a COX-3). COX-1 is responsible for the ... COX enzyme proved to be difficult to purify and was not sequenced until 1988. In 1991 the existence of the COX-2 enzyme was ... Celecoxib was the first specific inhibitor of COX-2 approved to treat patients with rheumatism and osteoarthritis. A study ... The side-chain of Leu384, at the top of the receptor channel, is oriented into the active site of COX-1, but, in COX-2, it is ...
Another COX-2 inhibitor has been shot down by the FDA. Having spent the last two months reviewing the safety of the COX-2- ... THE COX-2s: Oh well, back to the drawing board. What Doctors Dont Tell You ... COX-2 AGAIN: Sorry, we havent finished with you yet. What Doctors Dont Tell You ... COX-2 drugs:A Pandoras box of adverse effects. What Doctors Dont Tell You ...
Two large pivotal trials have been published, in which the efficacy and safety of the COX 2 inhibitors celecoxib and rofecoxib ... Efficacy and safety of COX 2 inhibitors New data are encouraging but the risk:benefit ratio remains unclear ... with more specific inhibitory effects on cyclo-oxygenase 2 (COX 2) pathways, promised equivalent efficacy with greater safety ... Efficacy and safety of COX 2 inhibitors. BMJ 2002; 325 doi: (Published 21 September ...
We also touch on the COX-1/COX-2 selectivity of NSAIDs, the localization of COX enzymes in kidneys, and clinical studies ... Selective cyclooxygenase-2 (COX-2) inhibitors have provided relief for patients suffering from chronic pain and other ... NSAIDs and the kidney revisited: are selective cyclooxygenase-2 inhibitors safe?. Eras J1, Perazella MA. ... Therefore, this article reviews the role of cyclooxygenase enzyme activity and associated prostaglandins in the kidney and the ...
COX 2 inhibitors, traditional NSAIDs, and the heart BMJ 2005; 330 :1342 doi:10.1136/bmj.330.7504.1342 ... COX 2 inhibitors, traditional NSAIDs, and the heart. BMJ 2005; 330 doi: (Published 09 ...
Cox-2 inhibitor definition at, a free online dictionary with pronunciation, synonyms and translation. Look it up ... cox-2 inhibitor in Medicine Expand. COX-2 inhibitor n. Any of a class of nonsteroidal anti-inflammatory drugs thought to have ...
COX-2 inhibitors are associated with increased risk of heart attack, heart failure and death from stroke. ... COX-2 inhibitors linked to increased risk of stroke death. Written by David McNamee on November 6, 2014 ... Last year, Medical News Today also reported on a study that suggested a possible "fix" for the side effects associated with COX ... The study shows that people who were current users of COX-2 inhibitors were 19% more likely to die after a stroke than people ...
The effect of celecoxib, a cyclooxygenase-2 inhibitor, in familial adenomatous polyposis.. Steinbach G1, Lynch PM, Phillips RK ... In patients with familial adenomatous polyposis, six months of twice-daily treatment with 400 mg of celecoxib, a cyclooxygenase ... We studied the effect of celecoxib, a selective cyclooxygenase-2 inhibitor, on colorectal polyps in patients with familial ... the chemopreventive effects of nonsteroidal antiinflammatory drugs may be related to their inhibition of cyclooxygenase-2. ...
Two related isoforms of the cyclo-oxygenase (COX) enzyme have been described: COX-1 (PGHS-1) and COX-2 (PGHS-2). COX-1 is ... COX-2 inhibitors and gastroduodenal toxicity: Major clinical trials. Author. Mark Feldman, MD, MACP, AGAF, FACG. Mark Feldman, ... COX-2 inhibitors. Lancet 1999; 353:307.. *Simon LS, Weaver AL, Graham DY, et al. Anti-inflammatory and upper gastrointestinal ... Other COX-2 inhibitors are available in some countries. Parecoxib is a prodrug that is converted to valdecoxib. Etoricoxib and ...
Hypertension and Cyclooxygenase-2 Inhibitors. Target: The Renal Medulla. Chuan-Ming Hao, Matthew D. Breyer ...
... is one type of COX-2 inhibitor used to treat inflammation and back pain. This article includes information about potential side ... See Understanding COX-2 Inhibitor Side Effects. Celebrex is still available, but with strong warnings, as are required for all ... See Safe Use of COX-2 Inhibitors and Other NSAIDs. However, many reports of heart attacks and stroke prompted the FDA to re- ... As a COX-2 inhibitor, celecoxib blocks an inflammation-promoting enzyme called COX-2. Medications known as COX-2 inhibitors ...
Sponsors of other COX-2 inhibitors will also be asked for updated safety data, including details of any studies underway. ... The local pattern of use indicated that users of COX-2 inhibitors were older, had other co-morbidities and were often on ... Prescribers can assist in monitoring the safety of all COX-2 inhibitors by reporting adverse events to the Centre for Adverse ... The Australian Prescriber journal has made available an advance publication of their article on the vascular effects of COX-2 ...
If a COX-2 inhibitor is considered necessary for a patient taking warfarin, the INR should be checked a few days after ... The interaction between COX-2 inhibitors and warfarin has now been included in the list of adverse reactions of current concern ... Reports of COX-2 and warfarin interaction: INR increase, haemorrhage. The New Zealand Centre for Adverse Reactions Monitoring ( ... If the INR increases, it may be possible to continue the selective COX-2 inhibitor by reducing the dose of warfarin.2,3 ...
... a nonspecific COX inhibitor NSAID (piroxicam), or a COX-2 selective NSAID (celecoxib). Both prednisone and celecoxib decreased ... In contrast, nonspecific COX inhibitors showed a tendency towards a decreased rate of proteoglycan synthesis [18]. The in vitro ... There are two isoforms of the COX enzyme: COX-1, found in most tissues and constitutively expressed in normal cells, and COX-2 ... Nonspecific COX inhibitors did not demonstrate these findings but instead showed a tendency towards a lower synthesis rate of ...
Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus ... COX-2 inhibitors. Class Summary. Cyclooxygenase 2 (COX-2) inhibitors have a lower incidence of GI bleeding as compared with ... Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, induced by pain and inflammatory stimuli. ... Their mechanism of action is not known, but they may inhibit cyclo-oxygenase activity and prostaglandin synthesis. Other ...
The co-administration of acetylsalicylic acid might reduce the safety advantage of COX-2s over that of nonselective NSAIDs. ... COX-2s appear to offer greater upper GI safety and are better tolerated than nonselective NSAIDs. ... Conclusions: COX-2s appear to offer greater upper GI safety and are better tolerated than nonselective NSAIDs. The co- ... Gastrointestinal safety of cyclooxygenase-2 inhibitors: a Cochrane Collaboration systematic review Clin Gastroenterol Hepatol. ...
... inhibitors. Class Summary. These agents inhibit COX-2, thus suppress production of prostaglandin E2 at inflammation sites. ... NSAIDs suppress cyclooxygenase-2 (COX-2), which affects epithelial proliferation and apoptosis. ... but it thought that it is at least in part due to inhibition of cyclooxygenase 2 (COX2) and the resultant decrease in ... but it thought that it is at least in part due to inhibition of cyclooxygenase 2 (COX2) and the resultant decrease in ...
Make research projects and school reports about COX-2 inhibitor easy with credible articles from our FREE, online encyclopedia ... and pictures about COX-2 inhibitor at ... "COX-2 inhibitor." A Dictionary of Nursing. . ... COX-2 inhibitor n. an anti-inflammatory drug (see NSAID) that selectively blocks the action of the enzyme cyclo-oxygenase 2 ( ... COX-2 inhibitor A Dictionary of Nursing © A Dictionary of Nursing 2008, originally published by Oxford University Press 2008. ...
"By inhibiting COX-2 in human patients, we may have an option to delay the progression of lesions," said lead author Guido Eibl ... COX-2, an enzyme which causes inflammation, is no stranger to cancer researchers. Studies of breast, colon, and pancreatic ... COX-2 inhibitors delay pancreatic cancer precursors in mice. 03.08.2007. Nimesulide, a cyclooxygenase-2 (COX-2) inhibitor, ... To study the effects of COX-2 on PanIN progression, Dr. Eibl and colleagues focused on the KrasG12D mouse, an animal model that ...
... has a pretty funny take on the whole COX-2 inhibitor thing. Like this quote: A couple peoples hearts explode, and everyone ... The Onion, a satiric Web site, has a pretty funny take on the whole COX-2 inhibitor thing. Like this quote:. "A couple peoples ... The Onion on COX-2 inhibitors. Sue Pelletier 2 , Feb 22, 2005 ... Webinar] Meetings Master Classes 2019 Session 2: Getting to ...
... disorders comprising the administration to a subject of a potassium ion channel modulator in combination with a cyclooxygenase- ... PREPARATION OF RECOMBINANT COX BACULOVIRUSES. [0440] Recombinant COX-1 and COX-2 are prepared as described by Gierse et al, [J ... with a higher percentage indicating a greater degree of COX inhibition. In addition, the IC50 value for COX-1 and COX-2 can ... Inhibitors of the cyclooxygenase pathway in the metabolism of arachidonic acid used in the present method may inhibit enzyme ...
Two isoforms of the membrane protein COX are known: COX-1, which is constitutively expressed in most tissues, is responsible ... The pharmacological target of NSAIDs is cyclooxygenase (COX, also known as PGH synthase), which catalyses the first committed ... The pharmacological target of NSAIDs is cyclooxygenase (COX, also known as PGH synthase), which catalyses the first committed ... CYCLOOXYGENASE-2. A, B, C, D. 587. Mus musculus. Mutation(s): 0 Gene Names: Ptgs2, Cox-2, Cox2, Pghs-b, Tis10. EC: ...
Ibuprofen, COX-2 Inhibitors Increase Risk of Atrial Fibrillation. By Deborah Mitchell G+ Jul 5 2011 - 7:06am ... NSAIDs, COX-2 inhibitors increase heart attack risk Atrial fibrillation is the most common rhythm disorder seen in clinical ... Patients and controls were classified based on their use of NSAIDs and COX-2 inhibitors: no use, recent use, current use (those ... If you use painkillers such as ibuprofen and other nonsteroidal anti-inflammatory drugs (NSAIDs) or COX-2 inhibitors to treat ...
Risk of adverse gastrointestinal outcomes in patients taking cyclo-oxygenase-2 inhibitors or conventional non-steroidal anti- ... Of 88,867 controls, 33% had been prescribed an NSAID and 6% had been prescribed a COX-2 inhibitor. Increased risks of adverse ... There is no evidence to back up claims that the new generation of anti-inflammatory drugs (COX-2 inhibitors) are less harmful ... These results suggest that COX-2 inhibitors may not be as safe as originally thought, although a possible confounding effect ...
COX)-2 inhibitor celecoxib is an effective treatment for the signs and symptoms of osteoarthritis and rheumatoid arthritis. ... which are nonspecific inhibitors of COX-1 and COX-2. Numerous studies suggest that inhibition of renal prostaglandin synthesis ... The novel cyclooxygenase- (COX)-2 inhibitor celecoxib is an effective treatment for the signs and symptoms of osteoarthritis ... Renal safety and tolerability of celecoxib, a novel cyclooxygenase-2 inhibitor Am J Ther. 2000 May;7(3):159-75. doi: 10.1097/ ...
  • COX-2 inhibitors appear to work as well as nonselective NSAIDS. (
  • Having spent the last two months reviewing the safety of the COX-2-selective non-steroidal anti-inflammatory drugs (NSAIDs), the US regulatory agency. (
  • Rofecoxib is one of the new breed of anti-inflammatories known as COX-2 (cyclo-oxygenase-2) inhibitors that are supposed to be safer than NSAIDs such as aspirin. (
  • But NSAIDs quickly became COX-2 inhibitors associated with adverse gastrointestinal effects such as peptic. (
  • The impetus for development of selective COX-2 inhibitors was the adverse gastrointestinal side-effects of NSAIDs. (
  • Soon after the discovery of the mechanism of action of NSAIDs, strong indications emerged for alternative forms of COX, but little supporting evidence was found. (
  • Before the confirmation of COX-2 existence, the Dupont company had developed a compound, DuP-697, that was potent in many anti-inflammatory assays but did not have the ulcerogenic effects of NSAIDs. (
  • Enormous effort was spent on the development of NSAIDs between the 1960s and 1980 so there were numerous pharmacophores to test when COX-2 was discovered. (
  • Efforts have been made to convert NSAIDs into selective COX-2 inhibitors such as indometacin by lengthening of the alkylcarboxylic acid side-chain, but none have been marketed. (
  • Two large pivotal trials have been published, in which the efficacy and safety of the COX 2 inhibitors celecoxib and rofecoxib were compared with various traditional NSAIDs. (
  • NSAIDs and the kidney revisited: are selective cyclooxygenase-2 inhibitors safe? (
  • In addition, studies evaluating the renal effects of the selective nonsteroidal anti-inflammatory drugs (NSAIDs) are inconclusive, and available data on the renal effects of COX-2-selective inhibitors are conflicting. (
  • Therefore, this article reviews the role of cyclooxygenase enzyme activity and associated prostaglandins in the kidney and the adverse renal effects of nonselective NSAIDs. (
  • We also touch on the COX-1/COX-2 selectivity of NSAIDs, the localization of COX enzymes in kidneys, and clinical studies examining the renal effects of selective COX-2 inhibitors. (
  • This topic review will summarize the major clinical trials that have focused on the gastroduodenal protective effects of the COX-2 inhibitors as compared to nonselective NSAIDs. (
  • Medications known as COX-2 inhibitors were developed to work as well as traditional NSAIDs but with fewer stomach problems. (
  • This requires consideration of both the adverse event profile of possible substitutes (such as NSAIDs or other COX-2 inhibitors) and patients' individual risk factors for gastrointestinal and cardiovascular harm. (
  • Patients with osteoarthritis (OA), a condition characterized by cartilage degradation, are often treated with steroids, nonsteroidal anti-inflammatory drugs (NSAIDs), and cyclooxygenase-2 (COX-2) selective NSAIDs. (
  • The anti-inflammatory effects of NSAIDs are mainly due to their ability to inhibit cyclooxygenase (COX), impairing production of prostaglandins, which are important mediators of both pain and the inflammatory response. (
  • Beneficial effects of NSAIDs on inflammation are mediated by COX-2 inhibition, whereas unwanted gastrointestinal effects are caused by primarily inhibition of COX-1 [ 12 ]. (
  • Cyclooxygenase 2 (COX-2) inhibitors have a lower incidence of GI bleeding as compared with other NSAIDs, although there is still a risk involved. (
  • At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased when compared to nonselective NSAIDs. (
  • Nonselective non-steroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 inhibitors (COX-2s) are used to treat a variety of arthritic and inflammatory conditions. (
  • The aim of this study was to assess the upper gastrointestinal (GI) harms of the long-term use of COX-2s, compared with nonselective NSAIDs and placebo, in arthritis sufferers. (
  • RCTs of celecoxib, rofecoxib, etoricoxib, valdecoxib, and lumiracoxib were included if they reported on endoscopic ulcers, clinically important ulcer complications, or adverse gastrointestinal (GI) symptoms with the use of these COX-2s, compared with placebo or with nonselective NSAIDs. (
  • COX-2s appear to offer greater upper GI safety and are better tolerated than nonselective NSAIDs. (
  • The co-administration of acetylsalicylic acid might reduce the safety advantage of COX-2s over that of nonselective NSAIDs. (
  • NSAIDs suppress cyclooxygenase-2 (COX-2), which affects epithelial proliferation and apoptosis. (
  • The structure of ovine COX-1 complexed with several NSAIDs has been determined. (
  • If you use painkillers such as ibuprofen and other nonsteroidal anti-inflammatory drugs (NSAIDs) or COX-2 inhibitors to treat inflammation, you may be at increased risk of irregular heart rhythm, or atrial fibrillation. (
  • Before now, no study had explored whether NSAIDs and COX-2 inhibitors could increase the risk of this disorder. (
  • Investigators looked at their use of six commonly used painkillers: non-aspirin NSAIDS (ibuprofen, naproxen) and both older (diclofenac, etodolac) and newer (celecoxib, rofecoxib) COX-2 inhibitors. (
  • Patients and controls were classified based on their use of NSAIDs and COX-2 inhibitors: no use, recent use, current use (those who got their first prescription within 60 days of their diagnosis), long-term use, and new use. (
  • The increased risk differed depending on the drugs used: there was about a 40 percent increased risk for those who used non-selective NSAIDs and 70 percent among those who used COX-2 inhibitors. (
  • Both non-selective NSAIDS and COX-2 inhibitors have been associated with a number of side effects (e.g., gastrointestinal problems) and serious long-term risks, including an increased chance of a stroke and heart attack. (
  • Conventional treatment for these debilitating conditions routinely involves the use of conventional nonsteroidal anti-inflammatory drugs (NSAIDs), which are nonspecific inhibitors of COX-1 and COX-2. (
  • Recently developed non-steroidal anti-inflammatory drugs (NSAIDS) are targeted to inhibit COX-2 and treat inflammation and arthritic pain. (
  • It is thought that the therapeutic effects of these agents are related to the inhibition of COX-2 at sites of inflammation whereas the adverse gastrointestinal effects and bleeding associated with NSAIDs are attributed to inhibition of COX-1 in gastric epithelium and in platelets, respectively ( 27 ). (
  • COX-2 selective inhibitors are a new class of nonsteroidal anti-inflammatory drugs, or NSAIDs that directly targets the COX-2 enzyme. (
  • Because they selectively block the COX-2 enzymeâ€"the enzyme responsible for inflammation and painâ€"and not the COX-1 enzyme, these drugs are uniquely different from traditional NSAIDs. (
  • Dr. Blanke said that numerous studies have assessed the effects on the development of colorectal cancer of a wide variety of nonsteroidal anti-inflammatory drugs (NSAIDS), which inhibit COX-2, and acetaminophen. (
  • To determine whether race is a predictor of a patient's likelihood of being prescribed selective cyclooxygenase-2 inhibitors (COX-2s) versus other nonsteroidal anti-inflammatory agents (NSAIDs) in Medicaid managed care plans (MCO). (
  • Cox-2 inhibitors are non-steroidal anti-inflammatory drugs (NSAIDs) which selectively inhibit cyclooxygenase-2. (
  • The traditional NSAIDs inhibit both cyclooxygenase 1 and 2 (Cox-1 and Cox-2). (
  • The development of the Cox-2 selective inhibitors was intended to provide drugs that would offer the same pain relieving and anti-inflammatory effects as the traditional NSAIDs without causing the gastric ulcers that have been associated with the older drugs. (
  • Traditional NSAIDs inhibit the constitutional cyclooxygenase-1 (COX-1) enzyme responsible for eicosanoids biosynthesis not only in joints, a beneficial effect, but also in the stomach, a detrimental effect. (
  • Selective NSAIDs were specifically designed to preferentially inhibit the cyclooxygenase-2 (COX-2), an inducible enzyme mediating the production of inflammatory eicosanoids in the joints but sparing the endogenous protective eicosanoids in the stomach. (
  • Additional comprehensive, long-term, prospective investigations comparing the CV and GI safety profile of marketed NSAIDs against each other and against selective inhibitors are needed to address the controversy of COX inhibitors. (
  • The efficacy and toxicity of NSAIDs is a consequence of the inhibition of the COX enzymes [2]. (
  • Such important findings led to the development and subsequent introduction of the selective COX-2 inhibitors celecoxib, valdecoxib and rofecoxib, which have considerably reduced GI ulcerogenicity potential when compared with the older, non-selective NSAIDs [5]. (
  • The introduction of selective cyclooxygenase-2 (COX-2) inhibitors, a group of NSAIDs, has resulted in a rapid increase in the number of people exposed to NSAIDs. (
  • Many patients who would otherwise not have used an NSAID are now using COX-2 inhibitors without a corresponding decrease in the use of more traditional nonselective NSAIDs. (
  • 1 , 2 Although COX-2 inhibitors have been found to be associated with a lower risk of significant adverse gastrointestinal events than have traditional nonselective NSAIDs at the level of the individual patient, 3 , 4 recent evidence suggests that the market expansion created by COX-2 inhibitors may increase rates of hospital admissions because of upper gastrointestinal (GI) bleeding at the population level. (
  • For example, COX-2 inhibitors were listed in the Ontario Drug Benefit (ODB) formulary in April 2000 as limited-use drugs, which means that prescribers must indicate that the recipient has failed a trial of at least 3 nonselective NSAIDs or has clinically significant GI disease. (
  • The prevalence of NSAID use in each interval was determined by dividing the unique number of people dispensed any NSAID (either nonselective NSAIDs or COX-2 inhibitors) by the total number of people alive at the beginning of the interval. (
  • 45% of the patients had received traditional non-steroidal anti-inflammatory drugs (NSAIDs), and 10% had received COX-2 inhibitors. (
  • The report authors concluded that even though COX-2 drugs were designed to provide pain relief without the serious gastrointestinal side-effects associated with conventional NSAIDs, 'we found no consistent evidence of enhanced safety against gastrointestinal events with any of the new cyclo-oxygenase-2 inhibitors [cox-2 inhibitors], compared with non-selective, nonsteroidal, anti-inflammatory drugs. (
  • Background- The selective cyclooxygenase-2 (COX-2) inhibitors and other nonselective nonsteroidal antiinflammatory drugs (NSAIDs) have been associated with increased cardiovascular risk, but the risk in patients with established cardiovascular disease is unknown. (
  • We analyzed the risk of rehospitalization for acute myocardial infarction (MI) and death related to the use of NSAIDs including selective COX-2 inhibitors in patients with prior MI. (
  • The risk of death and rehospitalization for MI associated with the use of selective COX-2 inhibitors and nonselective NSAIDs was studied with the use of multivariable proportional hazards models and case-crossover analysis. (
  • There were trends for increased risk of rehospitalization for MI associated with the use of both the selective COX-2 inhibitors and the nonselective NSAIDs. (
  • Conclusions- Selective COX-2 inhibitors in all dosages and nonselective NSAIDs in high dosages increase mortality in patients with previous MI and should therefore be used with particular caution in these patients. (
  • Little is known about the extent to which the cardiovascular risk of selective COX-2 inhibitors relates to this population and whether other nonselective NSAIDs are also associated with increased risk. (
  • Therefore, we used nationwide administrative registers of hospitalization and drug dispensing from pharmacies in Denmark to study the risk of recurrent MI and death related to the use of selective COX-2 inhibitors and nonselective NSAIDs in patients discharged after first-time acute MI between 1995 and 2002. (
  • In recent studies, the cyclooxygenase-2 (COX-2) inhibitor rofecoxib demonstrated analgesic effects similar to those of NSAIDs in the treatment of acute pain and primary dysmenorrhea. (
  • Use of cyclo-oxygenase 2 inhibitors (COX-2) and prescription non-steroidal anti-inflammatory drugs (NSAIDS) in UK and USA populations. (
  • BACKGROUND: COX-2 and NSAIDS differ in their gastrointestinal (GI) and cardiovascular (CV) toxicity from pharmacological, clinical and epidemiologic point of views. (
  • OBJECTIVE: Describe the patterns of use of NSAIDS and COX-2 in The Health Improvement Network (THIN) database in UK and the PharMetrics database in USA. (
  • Diclofenac and ibuprofen (NSAIDS), and celecoxib and rofecoxib (COX-2) were the agents prescribed most frequently. (
  • More COX-2 users than NSAIDS users received concomitant gastroprotective agents (GPA), corticosteroids and anti-platelet therapy, and had a history of thromboembolic events and hypertension. (
  • PharMetrics patients were prescribed higher doses of NSAIDS and COX-2. (
  • However, one must ask why would we choose selective COX-2 inhibitors instead of conventional non-steroidal anti-inflammatory drugs (NSAIDs) for patients taking anti-platelet therapy? (
  • A most promising approach seemed to be the preparation of novel NSAIDs, specific for the inducible isoform of cyclooxygenase (COX-2): they appear to be devoid of gastrointestinal toxicity, in that they spare mucosal prostaglandin synthesis. (
  • Moreover, COX-2 selective NSAIDs have lost the cardiovascular protective effects of non-selective NSAIDs, effects which are mediated through COX-1 inhibition (in addition, COX-2 has a role in sustaining vascular prostacyclin production). (
  • Non-steroidal anti-inflammatory drugs (NSAIDs) have potentially dangerous side effects, which has led to intense interest in the development of the cyclo-oxygenase (COX) inhibitors. (
  • As an alternative to NSAIDs, selective cyclooxygenase 2 (COX-2) inhibitors were developed to improve tolerability (i.e. the degree to which the side effects of a drug can be tolerated by a patient). (
  • FARMINGTON, CONN. Careful monitoring and control of blood pressure are key when NSAIDS or COX-2 inhibitors are used for osteoarthritis management for patients with hypertension and type 2-diabetes, according to a study published in the January 24 issue of Archives of Internal Medicine . (
  • This is because both COX-1 and COX-2 enzymes are inhibited to varying degrees by all currently available (1st generation) NSAIDs. (
  • Studies published so far support the hypothesis that the undesirable side effects of NSAIDs such as gastric erosion and renal dysfunction are due to the inhibition of COX-1 enzymes, while the anti-inflammatory (therapeutic) effects are due to the inhibition of COX-2 enzymes. (
  • Here is the key: Inhibitory potency and selectivity of the conventional, 1st generation NSAIDs for COX-1 and COX-2 enzymes vary greatly. (
  • Some NSAIDs (e.g., ketoprofen) are relatively COX-1 selective, some (ibuprofen and naproxen) are essentially non-selective, while others (e.g., diclofenac) are relatively COX-2 selective. (
  • A new type of NSAID, called cyclooxygenase-2 (COX-2) inhibitors, affects some important body processes less than do earlier NSAIDs (COX-1/COX-2 inhibitors). (
  • To identify factors that influence prescribers in their selection and use of cyclo-oxygenase-2 (COX-2) selective inhibitors as opposed to non-selective non-steroidal anti-inflammatory drugs (NSAIDs) and report the tendency to co-prescribe gastro-protection with these agents. (
  • Local authoritative guidance and history of GI complications highly influenced the GPs in their use and choice of either COX-2 selective inhibitors or non-selective NSAIDs. (
  • As expected the use of gastro-protection was more frequently chosen with non-selective NSAIDs than COX-2 selective inhibitors. (
  • Teeling, M, Bennett, K, Feely, J. 2004 Have COX-2 inhibitors influenced the co-prescription of anti-ulcer drugs with NSAIDs? (
  • THU0182 Significant reduction in serious upper gastrointestinal (ugi) events with celecoxib, a cox-2 specific inhibitor, compared with conventional nsaids. (
  • In both osteoarthritis and rheumatoid arthritis, COX-2 inhibitors have been shown to be superior in pain relief to acetaminophen and placebo, and equivalent to nonselective nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen and naproxen. (
  • Because nonselective NSAIDs inhibit not only COX-2 but also inhibit COX-1, which plays a role in platelet aggregation and gastric mucosal protection, their use is associated with a higher risk of gastrointestinal bleeding than that of selective COX-2 inhibitors. (
  • For these reasons and because they are more expensive than NSAIDs, COX-2 inhibitors are indicated chiefly in patients who are at increased risk of gastrointestinal bleeding. (
  • Structural features characteristic of nonsteroidal antiinflammatory drugs (NSAIDs) selectively acting on each of the COX isoforms are established for the first time. (
  • Selective inhibitors of the inducible cyclooxygenase (COX)-2 enzyme are important new therapies which, by sparing COX-1, undoubtedly reduce the risk of upper gastrointestinal bleeding caused by NSAIDs, and may abolish it, leading to extremely low event rates in patients without other risk factors. (
  • The advent of effective protective therapies, such as co- prescription of misoprostol or PPIs or use of safer NSAIDs, including COX-2 inhibitors, makes this information of practical importance. (
  • The inhibition of COX-2 is paramount for the anti-inflammatory and analgesic function of the selective COX-2 inhibitor celecoxib. (
  • However, with regard to this drug's promise for the therapy of advanced cancers, it is unclear whether the inhibition of COX-2 plays a dominant role, and this has become a controversial and intensely researched issue. (
  • However, when the ability of all these compounds to kill tumor cells in cell culture was investigated, it turned out that the antitumor potency did not at all depend on whether or not the respective compound could inhibit COX-2, showing that inhibition of COX-2 was not required for the anticancer effects. (
  • As of 2012 results have been converging on the hypothesis that the adverse cardiovascular effects are most likely due to inhibition of COX-2 in blood vessels, which leads to a decrease in the production of prostacyclin in them. (
  • In this disease, the chemopreventive effects of nonsteroidal antiinflammatory drugs may be related to their inhibition of cyclooxygenase-2. (
  • These drugs have at least a 200- to 300-fold selectivity for inhibition of COX-2 over COX-1. (
  • Inhibition of COX-1 may contribute to NSAID GI toxicity. (
  • The mechanism of NSAID-induced polyp regression is not completely known, but it thought that it is at least in part due to inhibition of cyclooxygenase 2 (COX2) and the resultant decrease in prostaglandin synthesis although a non-COX mechanism may also contribute. (
  • These structures explain the structural basis for the selective inhibition of COX-2, and demonstrate some of the conformational changes associated with time-dependent inhibition. (
  • There was no significant difference between the doses of celecoxib on COX-2 inhibition. (
  • Given this background, attempts to combine COX-2 inhibition with chemotherapy constitute a logical next step. (
  • The effects of COX-2 inhibition and radiation are synergistic, and treatment increases the actual cure rate. (
  • COX-2 overexpression is independently associated with disease-free survival, and COX-2 inhibition might be useful in preventing hematogenous metastasis,' he said. (
  • Selective COX-2 inhibition enhances mitomycin-C-induced apoptosis,' Dr. Blanke said. (
  • Clinical trials should incorporate COX-2 inhibition into treatment regimens,' he concluded. (
  • Epidemiological and laboratory studies suggest that nonsteroidal anti-inflammatory drugs reduce the risk of colon cancer and that the inhibition of colon carcinogenesis is mediated through modulation of prostaglandin production by cyclooxygenase (COX) isozymes (COX-1 and -2). (
  • This effect was found to be due to inhibition of COX-2 enzyme activity by chamomile. (
  • The cyclooxygenase-2 inhibition by ester derivatives of indomethacin is highly correlated with the thermodynamic (MR) and sterimol (B5, L) parameters, which in turn describes the importance of steric effect, indicating that a lipophilic bulkier group width-wise is required for good biological activity. (
  • Salmachroman demonstrated significant duel inhibition potential against pro-inflammatory enzymes, cyclooxygense-2 (IC50 1.29 mM) and 5-lipoxygenase (IC50 1.39 mM). (
  • COX-2 inhibition with celecoxib is an effective approach for the treatment of osteoarthritis , as seen by clinical improvement in signs and symptoms comparable to treatment with naproxen . (
  • However, several lines of evidence suggest that mechanisms of COX-2 inhibitor beyond the inhibition of COX and PG biosynthesis might also play an important role in their antinociception. (
  • Rofecoxib is a time-dependent inhibitor of purified human recombinant COX-2 (IC 50 = 0.34 μM) but caused inhibition of purified human COX-1 in a non-time-dependent manner that could only be observed at a very low substrate concentration (IC 50 = 26 μM at 0.1 μM arachidonic acid concentration). (
  • In an in vitro human whole blood assay, rofecoxib selectively inhibited lipopolysaccharide-induced, COX-2-derived PGE 2 synthesis with an IC 50 value of 0.53 ± 0.02 μM compared with an IC 50 value of 18.8 ± 0.9 μM for the inhibition of COX-1-derived thromboxane B 2 synthesis after blood coagulation. (
  • COX inhibitors and β-blockers were recently suggested to reduce cancer progression through inhibition of tumor proliferation and growth factor secretion, induction of tumor apoptosis, and prevention of cellular immune suppression during the critical perioperative period. (
  • COX-2 inhibition, but not COX-1 inhibition, reduced postoperative LTR. (
  • Treatment combining perioperative COX-2 inhibition and β-blockade is practical in operated cancer patients, and our study suggests potential immunological and clinical benefits. (
  • Cyclooxygenase-2 inhibition induces apoptosis signaling via death receptors and mitochondria in hepatocellular carcinoma. (
  • The summary below is from the full report titled "Effect of Cyclooxygenase-2 Inhibition on Renal Function in Elderly Persons Receiving a Low-Salt Diet. (
  • The aim of the study was to determine the effect of aromatase and/or COX-2 inhibition on epithelial proliferation and apoptosis in a presurgical study of estrogen receptor (ER)-positive DCIS. (
  • Inhibition of DCIS epithelial proliferation by exemestane in a placebo-controlled trial provides proof of principle that aromatase inhibitors will do likewise in the current ongoing adjuvant trials in DCIS. (
  • It has become apparent that cyclooxygenase (COX)-2 plays an important role in cancer growth, invasion and metastasis and that there is potential for chemoprevention via inhibition of these processes. (
  • In the present study, we investigated the effects of selective inhibition of COX-2 with nimesulide (12 mg/kg) and selective inhibition of COX-1 with valeryl salicylate (VAS, 12-120 mg/kg) on prostaglandin E2 (PGE2) levels, myeloperoxidase (MPO) activity, Evans Blue (EB) extravasation and infarct volume in a standardized model of transient focal cerebral ischemia in the rat. (
  • These studies provide the first experimental evidence that COX-2 inhibition with nimesulide is able to limit BBB disruption and leukocyte infiltration following transient focal cerebral ischemia. (
  • On the other hand, selective inhibition of COX-1 with VAS had no significant effect on the evaluated parameters. (
  • These data suggest that COX-2 activity, but not COX-1 activity, contributes to the progression of focal ischemic brain injury, and that the beneficial effects observed with non-selective COX inhibitors are probably associated to COX-2 rather than to COX-1 inhibition. (
  • Zurück zum Zitat Bezerra MM, de Lima V, Alencar VB (2000) Selective cyclooxygenase-2 inhibition prevents alveolar bone loss in experimental periodontitis in rats. (
  • Targeting selectivity for COX-2 reduces the risk of peptic ulceration , and is the main feature of celecoxib , rofecoxib and other members of this drug class. (
  • Concerns about the potential prothrombotic effects of COX-2 inhibitors first arose with rofecoxib (Vioxx® - Merck) in the Vioxx Gastrointestinal Outcomes Research (VIGOR) trial, when the rate of MIs in patients taking rofecoxib was higher than in those taking the comparator NSAID naproxen . (
  • Celecoxib and rofecoxib, the first COX-2 inhibitors to reach market, were based on DuP-697. (
  • It took less than eight years to develop and market the first COX-2 inhibitor, with Celebrex (celecoxib) launched in December 1998 and Vioxx (rofecoxib) launched in May 1999. (
  • Examples of COX-2 inhibitors include older drugs such as diclofenac, etodolac, nabumeton and meloxicam, and newer drugs like celecoxib and rofecoxib. (
  • Rofecoxib is a COX-2 inhibitor that was removed due to an increased risk of stroke and myocardial infarction with long-term use. (
  • From the date of first marketing, Medsafe (and other regulatory agencies around the world) have collected and analysed adverse reaction reports for rofecoxib and the other COX-2 inhibitors as part of standard post-marketing monitoring practice. (
  • Medsafe will be asking the MARC to determine whether the risk of cardiovascular events is similar for the other COX-2 inhibitors, in comparison to rofecoxib. (
  • The selective COX-2 inhibitors, celecoxib ( Celebrex ™) and rofecoxib (Vioxx™), may interact with warfarin causing an increase in the international normalised ratio (INR) and putting the patient at risk of a haemorrhagic event. (
  • 1,2 Less is known about the interaction with rofecoxib. (
  • If celecoxib or rofecoxib are considered necessary for a patient taking warfarin, the INR should be checked a few days after introduction of the COX-2 inhibitor and monitored closely for the first two weeks. (
  • However, a French review warned that certain selective Cox-2 inhibitors (i.e. celecoxib, rofecoxib) have not been tested for safety on patients with ulcers or cardiovascular or renal disease. (
  • The availability of the COX-2-specific inhibitor (CSI) class of anti-inflammatory drugs, namely celecoxib and rofecoxib, has raised a number of questions. (
  • The risk was significantly higher for the COX-2 inhibitors naproxen, and rofecoxib (Vioxx), and diclofenac (Voltaren). (
  • 5-14 This caused the pharmaceutical company Merck to withdraw their COX-2 inhibitor rofecoxib (Vioxx) from the market, and health authorities in several countries have issued a warning about the cardiovascular risk associated with the use of COX-2 inhibitors. (
  • The present randomized, single-dose, double-blind, double-dummy, placebo- and active-comparator-controlled, parallel-group study was undertaken to compare the analgesic efficacy of the COX-2 inhibitors rofecoxib 50 mg and celecoxib 200 mg with that of ibuprofen 400 mg and placebo in patients with postoperative dental pain. (
  • or =2 third molars were randomized according to pain severity (moderate vs severe) to receive a single dose of placebo (n = 45), rofecoxib 50 mg (n = 90), celecoxib 200 mg (n = 91), or ibuprofen 400 mg (n = 46). (
  • In the present study, the preclinical pharmacological and biochemical profiles of rofecoxib [Vioxx, also known as MK-0966, 4-(4′-methylsulfonylphenyl)-3-phenyl-2-( 5H )-furanone], an orally active COX-2 inhibitor, are described. (
  • In several in vivo rodent models, rofecoxib is a potent inhibitor of carrageenan-induced paw edema (ID 50 = 1.5 mg/kg), carrageenan-induced paw hyperalgesia (ID 50 = 1.0 mg/kg), lipopolysaccharide-induced pyresis (ID 50 = 0.24 mg/kg), and adjuvant-induced arthritis (ID 50 = 0.74 mg/kg/day). (
  • Rofecoxib is a novel COX-2 inhibitor with a biochemical and pharmacological profile clearly distinct from that of current nonsteroidal anti-inflammatory drugs and represents a new therapeutic class of anti-inflammatory agents for the treatment of the symptoms of osteoarthritis and rheumatoid arthritis with improved gastrointestinal tolerability. (
  • This review does not include any studies that assessed the tolerability and safety of the withdrawn COX-2 inhibitors rofecoxib, valdecoxib, or lumiracoxib.This review identified two studies that included a total of 381 participants with IBD who were experiencing rheumatological manifestations. (
  • The Celecoxib Rofecoxib Efficacy and Safety in Comorbodities Evaluation Trial, or Crescent, evaluated the effects of the COX-2 inhibitors and naproxen on 24-hour blood pressure reading in patients with type-2 diabetes, hypertension, and osteoarthritis. (
  • This suggests that COX-2 inhibitors (for example, rofecoxib) may cause fewer side effects in patients than COX-1/COX-2 inhibitors (for example, ibuprofen and indomethacin). (
  • To see if the COX-2 inhibitor rofecoxib affects kidney function. (
  • Patients in both parts of the study had reversible decreases in kidney function with the COX-2 inhibitor (rofecoxib) that were similar to those with the COX-1 inhibitor (indomethacin). (
  • Guidance on the use of cyclo-oxygenase (COX) II selective inhibitors, celecoxib, rofecoxib, meloxicam and etodolac for osteoarthritis and rheumatoid arthritis. (
  • In view of the ongoing controversy of cardiorenal safety of selective COX-2 inhibitors (coxibs), the present study was designed to examine the effects of 2 different coxibs, celecoxib and rofecoxib, compared with a traditional NSAID, diclofenac, and placebo on renal morphology and function in salt-sensitive hypertension. (
  • Selective COX-2 inhibitors are a type of nonsteroidal anti-inflammatory drug (NSAID) that directly targets cyclooxygenase-2, COX-2 , an enzyme responsible for inflammation and pain . (
  • Scientists have succeeded in reducing levels of the bovine leukemia virus in cows with severe infections by combining an immune checkpoint inhibitor and an enzyme inhibitor. (
  • The cyclooxygenase-2 enzyme is just such a protein, as the concentration of COX-2 is greater in cancer cells than in adjacent normal tissues. (
  • The COX-2 enzyme was discovered in 1988 by Daniel Simmons, a Brigham Young University researcher. (
  • COX enzyme proved to be difficult to purify and was not sequenced until 1988. (
  • In 1991 the existence of the COX-2 enzyme was confirmed by being cloned by Dr. Dan Simmons at Brigham Young University. (
  • Once the COX-2 enzyme was identified, Dup-697 became the building-block for synthesis of COX-2 inhibitors. (
  • In 1991, during the investigation of the expression of early-response genes in fibroblasts transformed with Rous sarcoma virus, a novel mRNA transcript that was similar, but not identical, to the seminal COX enzyme was identified. (
  • The same laboratory showed that this gene truly expressed a novel COX enzyme. (
  • The two enzymes were renamed COX-1, referring to the original enzyme and COX-2. (
  • In vitro recombinant enzyme assays provided powerful means for assessing COX selectivity and potency and led to the discovery and clinical development of the first rationally designed COX-2 selective inhibitor, celecoxib. (
  • However, kidney tissue seems to possess "constitutive" or homeostatic COX-2 enzyme, suggesting a role for prostaglandins produced by this isoform. (
  • The study found that the COX-2 enzyme is mostly found just in the brain, gut, kidney and thymus gland. (
  • Two related isoforms of the cyclo-oxygenase (COX) enzyme have been described: COX-1 (PGHS-1) and COX-2 (PGHS-2). (
  • As a COX-2 inhibitor, celecoxib blocks an inflammation-promoting enzyme called COX-2. (
  • There are two isoforms of the COX enzyme: COX-1, found in most tissues and constitutively expressed in normal cells, and COX-2, which is not expressed in healthy tissue but is induced by various catabolic mediators, such as cytokines, growth factors, and mechanical stress [ 11 ]. (
  • COX-2, an enzyme which causes inflammation, is no stranger to cancer researchers. (
  • Furthermore, there was no evidence of drug-drug interactions between celecoxib and concomitant angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, calcium channel blockers, or diuretics. (
  • COX-2 specific inhibitors are thought to relieve pain and inflammation by targeting the COX-2 enzyme. (
  • Cyclo-oxygenase-2 (COX-2) is a key enzyme in the production of prostaglandins (PG), and evidence suggests that COX-2 plays an important role in the pathogenesis of acute lung injury (ALI). (
  • Previous research has linked the cyclooxygenase-2 enzyme, commonly known as COX-2, to many cancer types, including prostate cancer , said Mukhtar. (
  • More interestingly, this effect is independent of the COX-2 enzyme. (
  • COX-2 inhibitors are newly developed drugs for inflammation that selectively block the COX-2 enzyme. (
  • Blocking the COX-2 enzyme stops the production of the chemical messengersâ€"or prostaglandinsâ€"that cause the pain and swelling of arthritis inflammation. (
  • Recent research has disclosed at least two types of COX enzymes exits: COX-1 is a constitutive enzyme responsible for housekeeping functions in organs such as the stomach, kidney, intestine and platelets, while COX-2 is an inducible enzyme exerting its action at inflammatory sites of the joints and muscles [3,4]. (
  • Cyclooxygenase (COX) is an enzyme naturally present in our body. (
  • Scientists discovered there were two forms of this Cyclooxygenase COX enzyme -- COX-1 and COX-2 enzymes. (
  • Simply put, by continually having an unbalanced fatty acid intake we are giving the COX-2 enzyme the raw material to create fire, but not the raw material to put out the fire. (
  • No, as mentioned previously, COX-2 enzyme production occurs due to a myriad of factors and COX-2 production does not indicate that you are in a state of disease. (
  • Hence, the introduction of dietary modifications that inhibit the COX-2 enzyme. (
  • So, even though research is examining the role of excessive COX-2 enzyme production as a factor, healthy individuals can experience COX-2 enzyme production in amounts higher than normal, whether it is from diet, trauma or stress, or foreign invaders. (
  • Herbs that directly target COX-2, an enzyme responsible for inflammation and pain, are often used to treat long term pain and arthritis. (
  • Previous research has linked the cyclooxygenase-2 enzyme commonly. (
  • Prostanoids that mediate inflammation, pain, and fever are synthesized through the action of cyclooxygenase-2 (COX-2), an enzyme that is constitutively expressed in the brain but can be induced in other tissues by cytokines. (
  • The COX-2 inhibitor chosen is Etodlac (Etopan), which has the advantage of being a selective COX-2 inhibitor which is synthesized during injury and inflammation, with little effect on the COX-1 enzyme, which is associated with ongoing maintenance of tissues. (
  • Given the broad range of therapeutic effects attributed to noni (Morinda citrifolia), the authors tested their hypothesis that Tahitian Noni® Equine Essentials® would modulate endotoxin (microbial toxin that can cause inflammation) inflammatory responses in equine foal monocytes (young blood cells) by regulating COX-2 expression (an enzyme involved in inflammation). (
  • The drugs assessed in the study - COX-2 inhibitors - are a type of "selective" nonsteroidal anti-inflammatory drug ( NSAID ). (
  • It had been proposed that the ideal NSAID would inhibit the inducible COX-2 isoform (thereby decreasing inflammation) without having any effect on the constitutive COX-l isoform (thereby minimizing gastric toxicity) [ 1 ]. (
  • One NSAID that selectively inhibits COX-2, celecoxib, is currently approved by the US Food and Drug Administration (FDA). (
  • The chondrocytes were then treated with either a steroid (prednisone), a nonspecific COX inhibitor NSAID (piroxicam), or a COX-2 selective NSAID (celecoxib). (
  • Of 9407 cases, 45% had been prescribed a conventional non-steroidal anti-inflammatory drug (NSAID) in the previous three years and 10% had been prescribed a COX-2 inhibitor. (
  • Of 88,867 controls, 33% had been prescribed an NSAID and 6% had been prescribed a COX-2 inhibitor. (
  • As celecoxib inhibits COX-2 and spares COX-1 at therapeutic doses, we hypothesized that it may offer an improved renal safety profile in patients at risk for NSAID-induced renal toxicity. (
  • All medical and prescription claims for Medicaid MCO enrollees receiving at least one prescription for a COX-2 or NSAID between January 2000 and June 2002 were retrieved. (
  • Of the 16,868 enrollees meeting the selection criteria, 4,005 (24%) were prescribed a COX-2 and 12,863 another NSAID. (
  • These differences in the nature and timing of reimbursement for COX-2 inhibitors have contributed to vastly different rates of NSAID use at the population level. (
  • To explore this issue further, we conducted a population-based study to compare changes over time in the prevalence of NSAID use and rates of admission to hospital because of upper GI bleeding after the introduction of COX-2 inhibitors in the elderly populations of British Columbia and Ontario. (
  • Patients were evaluated with standard measures of efficacy 2 to 7 days after discontinuing previous NSAID or analgesic therapy and after 2, 6, and 12 weeks of treatment with the study drug. (
  • Recommendations to use COX-2 inhibitors in high risk patients unduly discounts this ability to minimise residual risk in low risk patients and may be misplaced if the potential of proton pump inhibitor (PPI) prophylaxis to reduce non-specific as well as NSAID specific risk is shown to lead to lower overall event rates in such individuals. (
  • The extent and nature of NSAID or COX-2 inhibitor interactions with aspirin in influencing both cardiovascular and gastrointestinal outcomes needs clarifying. (
  • [12] Moreover, a recent study with various malignant tumor cells showed that celecoxib could inhibit the growth of these cells, even though some of these cancer cells didn't even contain COX-2. (
  • These agents inhibit COX-2, thus suppress production of prostaglandin E2 at inflammation sites. (
  • This explains the efforts to obtain drugs able to inhibit both 5-lipoxygenase and cyclooxygenases: the so-called dual acting anti-inflammatory drugs. (
  • Our study shows that a cyclooxygenase (COX)-2 inhibitor, nimesulide, can inhibit proliferation of non-small cell lung cancer cell lines in vitro in a dose-dependent manner, in part by inducing apoptosis even at clinically achievable low concentrations. (
  • In this study, we examined whether nimesulide can inhibit the proliferation of NSCLC cells and whether sensitivity to nimesulide is related to COX-2 expression levels and the p53 gene status. (
  • Apparently, cox-2 inhibitor inhibit the activity of cox-2 causing prostacyclin levels to decrease which makes arteries more prone to clotting, high blood pressure, heart attack and stroke. (
  • COX-2 is considered an inducible isoenzyme, induced by pain and inflammatory stimuli. (
  • To examine selectivity of tolerated doses of an inhibitor of the inducible COX-2 in humans, we examined the effects of celecoxib on indices of COX-1-dependent platelet thromboxane (Tx) A 2 and on systemic biosynthesis of prostacyclin in vivo . (
  • Inducible cyclooxygenase (COX-2) has been implicated in the process of inflammation and carcinogenesis. (
  • The discoveries that cyclooxygenase (COX)-2 is an inducible form of COX involved in inflammation and that COX-1 is the major isoform responsible for the production of prostaglandins (PGs) in the gastrointestinal tract have provided a rationale for the development of specific COX-2 inhibitors as a new class of anti-inflammatory agents with improved gastrointestinal tolerability. (
  • Inducible prostaglandin synthase (cyclooxygenase-2, COX-2) is expressed in rheumatoid and osteoarthritic cartilage and produces high amounts of proinflammatory prostanoids in the joint. (
  • Volunteers received doses of 100, 400, or 800 mg of celecoxib or 800 mg of a nonselective inhibitor, ibuprofen. (
  • Selective COX-2 inhibitors (COXIBs) have been shown to possess much improved GI tolerability and reduced GI related adverse events when compared with nonselective COX-1inhibitors. (
  • This head-to-head comparison of selective and nonselective COX inhibitors demonstrates differential effects of coxibs on renal morphology and function in salt-dependent hypertension. (
  • Selective cyclooxygenase-2 (COX-2) inhibitors have provided relief for patients suffering from chronic pain and other inflammatory conditions and have reduced adverse gastrointestinal effects. (
  • Increased risks of adverse gastrointestinal events were associated with current use of COX-2 inhibitors and with conventional non-steroidal anti-inflammatory drugs. (
  • Evidence of enhanced gastrointestinal safety with any of the new cyclo-oxygenase-2 inhibitors compared with non-selective non-steroidal anti-inflammatory drugs is lacking, say the authors. (
  • The benefit of cyclo-oxygenase-2 (COX-2) inhibitors in preventing serious gastrointestinal adverse events is likely overstated. (
  • Population rates of upper gastrointestinal (GI) hemorrhage have been observed to increase with the introduction and rapid uptake of selective cyclooxygenase-2 (COX-2) inhibitors. (
  • Dr. A Mark Fendrick, professor of internal medicine and health management and policy at the University of Michigan, believes that this study illuminates the increased dangers of gastrointestinal (GI) bleeding when a COX-2 inhibitor and aspirin are used together. (
  • However, the use of the COX-2 inhibitors and the associated excess cardiovascular risk has caused increasing concern since the publication of the Vioxx Gastrointestinal Outcomes Research (VIGOR) study 1 in 2000. (
  • 2006) Risk of upper gastrointestinal ulcer bleeding associated with selective cyclo-oxygenase-2 inhibitors, traditional non-aspirin non-steroidal anti-inflammatory drugs, aspirin and combinations. (
  • 1 The literature suggests that the principal 'advantage' of upper gastrointestinal safety is lost when a COX-2 inhibitor is co-prescribed with aspirin. (
  • However, a number of recent studies raised serious questions about the two central tenets that support this approach, namely that the prostaglandins that mediate inflammation and pain are produced solely via COX-2 and that the prostaglandins that are important in gastrointestinal and renal function are produced solely via COX-1. (
  • Structure activity relationship (SAR) studies for diaryl heterocyclic compounds have indicated that a cis-stilbene moiety and changes in the para-position of one of the aryl rings play an important role in COX-2 selectivity. (
  • 2. The method of claim 1 wherein the cyclooxgenase-2 selective inhibitor has a selectivity ratio of COX-1 IC 50 to COX-2 IC 50 not less than about 50. (
  • Six compounds had potencies in the submicromolar range against COX-2 and higher selectivity for COX-2 vs. COX-1 compared to the currently used drug celecoxib. (
  • A model for predicting cyclooxygenase (COX-1 and COX-2) selectivity of chemical compounds is developed using a computer Structure-Activity Relationship & Design (SARD-21) system. (
  • Cox-2 Inhibitors are nonsteroidal anti-inflammatory drugs used to relieve pain and inflammation. (
  • COX-2 inhibitors have analgesic and anti-inflammatory activity by blocking the transformation of arachidonic acid into prostaglandin H2 selectively. (
  • 1 - 3 The introduction of new anti-inflammatory agents, with more specific inhibitory effects on cyclo-oxygenase 2 (COX 2) pathways, promised equivalent efficacy with greater safety and tolerability. (
  • While inflammation has been shown to be a factor in many forms of cancer, the researchers say this is the first study to demonstrate the effect of an anti-inflammatory COX-2 inhibitor on the development of pancreatic cancer. (
  • There is no evidence to back up claims that the new generation of anti-inflammatory drugs (COX-2 inhibitors) are less harmful to the stomach lining than many traditional anti-inflammatory drugs, concludes a study in this week s BMJ. (
  • COX-2 inhibitors are important drugs with analgesic and anti-inflammatory effects. (
  • Chamomile, a novel and selective COX-2 inhibitor with anti-inflammatory activity. (
  • The non-steroidal anti-inflammatory drug, sulindac and a specific COX-2 inhibitor, NS398, were shown to act similarly in LPS-activated RAW 264.7 cells. (
  • A new report in the December 3 issue of the British Medical Journal finds that COX-2 inhibitors are just as harmful to the stomach as traditional anti-inflammatory medications like aspirin. (
  • Serrapeptase is also a natural COX-2 inhibitor, a natural pain killer, parts of Asia and Europe have been using Serrapeptase instead of the traditional steroidal anti-inflammatory drugs prescribed now a days. (
  • The binding properties of the compound with the active site of cyclooxygense-2 and 5-lipoxygenase enzymes, combined with its higher electronic parameters as attributed by the structure-activity relationship accounted for its significant anti-inflammatory properties. (
  • Francis P, Chakraborty K. An anti-inflammatory salmachroman from the sea urchin Salmacis bicolor: a prospective duel inhibitor of cyclooxygenase-2 and 5-lipoxygenase. (
  • Significant pain relief occurred within 2 days of the initiation of treatment, and maximum anti-inflammatory and analgesic activity, evident within 2 weeks, was sustained throughout the 12-week study. (
  • Etoricoxib is a non steroidal anti-inflammatory agent, acting as a selective and orally active COX-2 inhibitor, with IC50s of 1.1 μM and 116 μM for COX-2 and COX-1 in human whole blood. (
  • The results of this study suggest the need for careful monitoring and control of blood pressure when COX-2-specific inhibitors and nonspecific nonsteroidal anti-inflammatory drugs are prescribed to patients with hypertension and type-2 diabetes, said Dr. White. (
  • Can Natriuretic Peptide Levels Predict the Cardiovascular Complications of COX-2 Inhibitors and Nonsteroidal Anti-inflammatory Drugs? (
  • Because natriuretic peptide levels reflect intravascular volume and pressure, it is hypothesized that when patients are prescribed medications that promote fluid retention-such as non-selective nonsteroidal anti-inflammatory drugs and cyclooxygenase-2 inhibitors-monitoring natriuretic peptide levels before and after initiating the medication may allow these medications to be used more safely. (
  • Purpose The purpose of this study is to evaluate the effect of two anti-inflammatory drugs, fish oil capsules and the COX-2 inhibitor celecoxib, on pregnancy associated breast cancer (PABC). (
  • F344 rats were treated with COX-1 inhibitors (SC560), COX-2 inhibitors (indomethacin, etodolac, or celecoxib), a β-blocker (propranolol), or a combination of a COX-2 inhibitor and a β-blocker (etodolac and propranolol). (
  • We injected colon 26, a colorectal cancer cell line, in CDF1 mouse spleen and, from the following day, two kinds of COX-2 inhibitor (etodolac and nimesulide) were administered orally. (
  • The expression of COX-2 mRNA was also significantly lower in the etodolac-treated group than in controls (p=0.04), but not in the nimesulide-treated group. (
  • These findings indicate that the selective COX-2 inhibitor, etodolac, suppresses liver metastasis by reducing MMP-9 activity. (
  • In rats undergoing a laparotomy, peri-operative administration of β- adrenergic blockers(propranolol or nadolol) together with COX-2 inhibitors (etodolac or indomethacin) significantly abrogated the NK cell suppression as well as the enhanced susceptibility to metastases after surgery (4,7). (
  • Nimesulide, a cyclooxygenase-2 (COX-2) inhibitor, delays the progression of precancerous pancreatic lesions in mice, according to researchers at David Geffen School of Medicine at UCLA. (
  • Their analyses revealed that the nimesulide diet greatly reduced the number of late-stage PanINs in KrasG12D (10 percent of pancreatic ducts had PanIN-2 or -3 in KrasG12D mice on nimesulide diet versus 40 percent of pancreatic ducts had PanIN-2 or -3 in KrasG12D mice on normal diet). (
  • In the future, Dr. Eibl and others plan to study the long-term effects of nimesulide and additional COX-2 inhibitors on the onset and progression of pancreatic cancer. (
  • In vitro studies of NSCLC cells treated with irinotecan (Camptosar), docetaxel (Taxotere), etoposide (VePesid), or cisplatin (Platinol), with or without the COX-2 inhibitor nimesulide showed that the COX-2 inhibitor alone induced apoptosis at low concentrations and was 'near-synergistic' for selected anticancer agents, according to Dr. Blanke. (
  • Neuroprotection afforded by nimesulide is observed even when the treatment is delayed until 6 h after the onset of ischemia, confirming a wide therapeutic window of COX-2 inhibitors in experimental stroke. (
  • Cyclooxygenases are enzymes that take part in a complex biosynthetic cascade that results in the conversion of polyunsaturated fatty acids to prostaglandins and thromboxane(s). (
  • and COX-2, which is induced by cytokines, mitogens and endotoxins in inflammatory cells, is responsible for the elevated production of prostaglandins during inflammation. (
  • Prostaglandins and thromboxane are formed by the enzymatic oxidation of arachidonic acid catalyzed by the cyclooxygenases, COX 1 and COX-2. (
  • This rate-limiting, committed step in the formation of prostaglandins results in the formation of an unstable endoperoxide intermediate, PGH 2 . (
  • In turn, PGH 2 serves as substrate for cell-specific isomerases and synthases to produce the prostaglandins PGE 2 , PGD 2 , prostacyclin (PGI 2 ), and thromboxane (Tx) A 2 ( 3 , 4 ). (
  • The cyclooxygenases are required for the creation of prostaglandins. (
  • COX-1 and COX-2 enzymes act upon arachadonic acid to form molecules called prostaglandins. (
  • From a clinical perspective, one of the enzymes that are involved in the production of the destructive prostaglandins, called cyclooxygenase-2 (COX-2), is the target of nutritional intervention in order to suppress these substances. (
  • Mitomycin-C (Mutamycin) induces COX-2 in MKN-74 gastric cancer cells, and this induction causes cellular resistance to apoptosis. (
  • Paired baseline and end point biopsies were analyzed for proliferation (Ki67), apoptosis, human epidermal growth factor receptor 2 (HER2), COX-2, and progesterone receptor (PR) expression by immunohistochemistry. (
  • Cycloxygenase-2 is expressed in DCIS but the cycloxygenase-2 inhibitor celecoxib had no effect on either proliferation or apoptosis and is unlikely to have therapeutic value in DCIS. (
  • Here we report the structures of unliganded murine COX-2 and complexes with flurbiprofen, indomethacin and SC-558, a selective COX-2 inhibitor, determined at 3.0 to 2.5 A resolution. (
  • Cyclooxygenase-2 inhibitors of indomethacin ester derivative series were subjected to quantitative structure activity relationship analysis with an attempt to derive and understand a correlation between the biological activity as dependent variable and various descriptors as independent variables. (
  • Plots of MetaSite predictions for sites of metabolism for indomethacin and 2-(1-(4-chlorobenzoyl)-5-methoxy-2-methyl-1 H -indol-3-yl)- N -phenethyl-acetamide ( 1 ). (
  • LC-MS/MS analysis of an incubation mixture containing indomethacin-4-fluorophenyl amide ( 2 ) (A), indomethacin-4-fluoropyridinyl amide ( 3 ) (B), and indomethacin-glycine amide ( 4 ) (C) (20 μM concentrations each) and NADPH-supplemented human liver microsomes. (
  • CID spectrum of indomethacin-4-fluorophenyl amide ( 2 ) (A) and its O -demethylated metabolite (B). amu, atomic mass units. (
  • ATLANTA-Parecoxib, the first injectable COX-2 inhibitor, demonstrated impressive analgesic efficacy in postsurgical patients, according to a study presented at the 19th Annual Scientific Meeting of the American Pain Society (APS). (
  • Dr. Blanke said that COX-2 inhibitors enhance the efficacy of radiotherapy in mouse sarcomas. (
  • Early studies have also found that COX-2 inhibitors can increase the efficacy of cytotoxic drugs. (
  • In conjunction with the recent development of next generation, highly selective COX-2 inhibitors, they can be expected to lead to even greater efficacy of their use as adjuncts to various anticancer agents for the treatment of high-risk patients without compromising their quality of life. (
  • Efficacy Assessment of Meloxicam, a Preferential Cyclooxygenase-2 Inhibitor, in Acute Coronary Syndromes Without ST-Segment Elevation. (
  • COX-1 is responsible for the synthesis of prostaglandin and thromboxane in many types of cells, including the gastro-intestinal tract and blood platelets. (
  • DuP-697 was a building-block for synthesis of COX-2 inhibitors and served as the basic chemical model for the coxibs that are the only selective COX-2 inhibitors on the market today. (
  • This study can help in rational drug design and synthesis of new selective cyclooxygenase-2 inhibitors with predetermined affinity. (
  • The comparative molecular field analysis model was found to be highly predictive and it can be used to design potent cyclooxygenase-2 inhibitors prior to their synthesis. (
  • We developed a convenient synthesis of the known imidazole-based selective COX-2 inhibitors bearing primary sulphonamide and methyl sulfone substituents, via Pd-catalyzed imidazoline N-arylation as a key step, followed by dehydrogenation. (
  • SB203580 (an inhibitor of p38 pathway) but not its negative control compound SB202474 inhibited COX-2 protein and mRNA expression and subsequent PGE2 synthesis at micromolar drug concentrations. (
  • Cyclooxygenases have two main isoforms that are called COX-1 and COX-2 (as well as a COX-3). (
  • volume of conference proceedings reviews the general pathophysiological significance of the isoforms of cyclooxygenase, and the likely value of selective COX-2 inhibitors in the treatment of rheumatoid conditions. (
  • Phloretin inhibits phorbol ester-induced tumor promotion and expression of cyclooxygenase-2 in mouse skin. (
  • Primarily inhibits COX-2. (
  • COX-2 inhibitors are used in the treatment of arthritis and acute gout. (
  • They included older people and patients with chronic kidney disease or rheumatoid arthritis who started treatment with COX-2 inhibitors. (
  • The novel cyclooxygenase- (COX)-2 inhibitor celecoxib is an effective treatment for the signs and symptoms of osteoarthritis and rheumatoid arthritis. (
  • The regulator's remarks come close on the heels of comments by a U.S. advisory panel on Friday that Merck & Co Inc.'s withdrawn COX-2 inhibitor arthritis drug, Vioxx, was safe enough to rejoin Pfizer's rival pain relievers, Celebrex and Bextra, on the U.S. market. (
  • As an example, at the time of writing, a perusal of the South Africa n MIM S (September 2010) indicated that there are three locally available specific cyclooxygenase-2 inhibitors (COXIBs) namely, celecoxib, etoricoxib (indicated for the treatment of rheumatoid arthritis and osteoarthritis) and parecoxib (indicated for the treatment postoperative pain) that all contain a sulfonamide substituent. (
  • The cox-2 class is generally aimed at treating chronic pain of arthritis and other conditions. (
  • In rheumatoid arthritis, COX-2 inhibitors are not disease-modifying drugs. (
  • Increased expression of COX-2, but not of COX-1, has been demonstrated in rheumatoid synovial tissues in vivo ( 17 ). (
  • We studied the effect of celecoxib, a selective cyclooxygenase-2 inhibitor, on colorectal polyps in patients with familial adenomatous polyposis. (
  • GW406381, a highly selective cyclooxygenase-2 (COX-2) inhibitor, attenuates spontaneous ectopic discharge in sural nerves of rats following chronic constriction injury. (
  • The selective cyclooxygenase-2 (COX-2) inhibitors have been used widely for the treatment of pain and rheumatic disease since they were introduced in the late 1990s. (
  • Comparative protection against liver inflammation and fibrosis by a selective cyclooxygenase-2 inhibitor and a nonredox-type 5-lipoxygenase inhibitor. (
  • This comparative study validates the effectiveness of perioperative administration of oral selective cyclooxygenase-2 (COX-2) inhibitors as a part of multimodal analgesia in an enhanced recovery after surgery protocol to significantly reduce opioid requirement (but not pain score) after open colorectal surgery. (
  • Mikhail Krasavin, "Pd-Catalyzed N-arylation of 2-imidazolines Provides Convenient Access to Selective Cyclooxygenase-2 Inhibitors", Letters in Organic Chemistry (2013) 10: 235. (
  • In this study we examined whether the highly selective cyclooxygenase-2 inhibitor DFU reduces neuronal damage when administered several hours after 5 min of transient forebrain ischemia in gerbils. (
  • These results suggest that selective cyclooxygenase-2 inhibitors may be a valuable therapeutic strategy for ischemic brain injury. (
  • Investigators from Rush Medical College at Rush-Presbyterian-St. Luke?s Medical Center in Chicago, Ill., found that perioperative use of a selective cyclooxygenase-2 (COX-2) inhibitor is an effective component of multimodal analgesia that improves outcomes following TKA. (
  • Pharmacokinetic/pharmacodynamic (PK/PD) models were developed and clinical trial simulations were conducted to recommend a study design to test the hypothesis that a dose of SC-75416, a selective cyclooxygenase-2 inhibitor, can be identified that achieves superior pain relief (PR) compared to 400mg ibuprofen in a post-oral surgery pain model. (
  • Celecoxib and other COX-2 selective inhibitors, valdecoxib, parecoxib, and mavacoxib, were discovered by a team at the Searle division of Monsanto led by John Talley. (
  • At this stage, there is insufficient information available to comment on the cardiovascular safety of the other COX-2 inhibitors (i.e. celecoxib, etoricoxib, meloxicam, parecoxib and valdecoxib). (
  • Similarly, COX-2 mRNA is increased in 86% of CRC and in over 40% of colorectal polyps. (
  • In addition, chamomile caused reduction in LPS-induced COX-2 mRNA and protein expression, without affecting COX-1 expression. (
  • In addition, COX-2 mRNA, matrix metalloproteinase (MMP)-9 mRNA, and tissue inhibitor of MMP (TIMP)-1 mRNA of cancer tissue were measured by means of real-time RT-PCR. (
  • Expression of COX-2 mRNA and MMP-9 mRNA correlated significantly (r=0.78, p=0.001), but there was no correlation between either COX-2 mRNA and TIMP-1 mRNA expression or between MMP-9 mRNA and TIMP-1 mRNA expression. (
  • 13] J. Koistinaho, S. Koponen, P.H. Chan, Expression of cyclooxygenase-2 mRNA after global ischemia is regulated by AMPA receptors and glucocorticoids, Stroke 30 (1999) 1900-1906. (
  • Renal cortex mRNA was isolated for determination of COX-2, eNOS, and CRP mRNA by real-time reverse-transcriptase polymerase chain reaction. (
  • SP600125 did not downregulate IL-1-induced COX-2 mRNA expression when measured 2 h after addition of IL-1β but suppressed mRNA levels in the later time points suggesting post-transcriptional regulation. (
  • The treated foals showed a dramatic fold reduction in COX-2, TNF-ά (tumor necrosis factor), ILs-1β, -8, and -6 (interleukins, protein mediators between white blood cells) mRNA (messenger RNA), compared to the untreated controls. (
  • The researchers were able to achieve similar heart-stopping results in rat cardiac cells, whereas aspirin, another potent COX-2 inhibitor, had no effect, confirming that another mechanism is at work. (
  • 4-(4′-Methylsulfonylphenyl)-3-phenyl-2-(5H)-furanone]: A Potent and Orally Active Cyclooxygenase-2 Inhibitor. (
  • 4-(4′-Methylsulfonylphenyl)-3-phenyl-2-(5 H )-furanone]: A Potent and Orally Active Cyclooxygenase-2 Inhibitor. (
  • The team looked at information on these patients' history of COX-2 inhibitor use, including when they were using these drugs and what type of COX-2 inhibitors they were taking. (
  • In patients with familial adenomatous polyposis, six months of twice-daily treatment with 400 mg of celecoxib, a cyclooxygenase-2 inhibitor, leads to a significant reduction in the number of colorectal polyps. (
  • The study, published in the August 1 issue of Cancer Research, a journal of the American Association for Cancer Research, suggests a potential role for COX-2 inhibitors in pancreatic cancer prevention among high-risk patients. (
  • Methods: After approval by the institutional ethics and a scientific committee, and obtaining informed consent , patients admitted to the emergency department (ED) due to blunt trauma with a diagnosis of lung contusion will be enrolled in the study.The effects of statins and COX 2 inhibitors on ALI will be assessed by recording clinical parameters and measuring inflammatory mediators levels in the serum and in the bronchoalveolar space. (
  • In patients with previous peptic ulcer, is celecoxib (Celebrex) safer than naproxen taken with an proton pump inhibitor? (
  • Patients receiving celecoxib were more likely to report dyspepsia symptoms during treatment, though other adverse events were similar between the 2 groups. (
  • PORTLAND, Oregon-Cyclooxygenase 2 (COX-2) inhibitors are attracting attention as potential anti-cancer drugs because of evidence of increased survival in patients with low levels of COX-2. (
  • Dr. Blanke said that COX-2 overexpression is significantly correlated with metastases, and particularly with hematogenous metastasis in patients with resected large bowel malignancies. (
  • Patients at risk of CV disease or with a history of CV disease were the most significant determinants of CV events after receiving COX inhibitors. (
  • Doctors must be on the lookout for potential kidney side effects when they prescribe COX-2 inhibitors, particularly in older patients. (
  • Most patients with DCIS are treated with breast conservation surgery with subsequent adjuvant therapy with radiation and/or tamoxifen ( 1 , 2 ). (
  • Patients with heart failure are more likely to die suddenly compared with persons with normal left ventricular ejection fractions, 2 ,3 and the lower the left ventricular ejection fraction, the higher the mortality rate. (
  • This is the first randomized outcomes trial to demonstrate that administration of a selective COX-2 inhibitor during the pre- and postoperative period in patients undergoing TKA improves surgical outcomes, said Asokumar Buvanendran, M.D., assistant professor in the department of anesthesiology at Rush Medical College, who was the lead author of the study. (
  • When pharmacists note that patients are on high doses of opioids, they should consult with the physician regarding the need for COX-2 inhibitor therapy. (
  • He added that pharmacists dispensing postoperative drugs should verify that those patients who are candidates for COX-2 inhibitor therapy are receiving it. (
  • sulfones and sulfonamides are selective for COX-2 but sulfoxides and sulfides are not. (
  • The professional information leaflets of three locally available specific cyclooxygenase-2 inhibitors indicate that these drugs are contraindicated in persons with a known allergy to sulfonamides. (
  • See 'COX-2 selective inhibitors: Adverse cardiovascular effects' . (
  • COX-2 inhibitors also have been shown to cause adverse cardiovascular effects when administered at high doses over long durations. (
  • Reviewing the clinical evidence, particularly the complex cardiovascular effects of the COX inhibitors, the article discusses the clinical relevance of their thrombogenic and anti-atherosclerotic potential. (
  • Since many of the studies are retrospective analyses, randomised clinical trials are needed to ascertain whether these cardiovascular effects constitute a problem or an unexpected benefit, and whether there are differences between the different COX-2 inhibitors. (
  • The Onion, a satiric Web site, has a pretty funny take on the whole COX-2 inhibitor thing . (
  • The FDA is planning to hold a public forum on the viability of the whole cox-2 inhibitor class of drugs. (
  • Our recent study indicated that celecoxib (SC-58635), a specific COX-2 inhibitor, suppressed colonic aberrant crypt foci formation induced by azoxymethane in rats and led us to investigate more specifically the chemopreventive potential of this compound using colon tumors as end points. (
  • The results of this study provide evidence, for the first time, that a specific COX-2 inhibitor, celecoxib, possesses strong chemopreventive activity against colon carcinogenesis. (
  • It is fine to take a cox-2 inhibitor for joint pain and an aspirin for your heart, but "when you combine these two, they really present GI problems. (
  • An even greater risk was noted in a study on mice where aspirin was used in conjunction with cox-2 inhibitors. (
  • At therapeutic doses, they do not affect COX-1, which helps regulate normal cell function in the stomach and blood. (
  • The re-emergence, in the recent years, of cyclooxygenase as a biological target in therapeutic areas other than inflammation is likely to require new optimized leads, particularly suited for the requirements of specific drug development programs. (
  • Cyclooxygenase-2 (COX-2) is overexpressed in DCIS, representing another potential therapeutic target. (
  • The study shows that people who were current users of COX-2 inhibitors were 19% more likely to die after a stroke than people who did not use COX-2 inhibitors. (
  • The local pattern of use indicated that users of COX-2 inhibitors were older, had other co-morbidities and were often on multiple medicines that could have increased their risk of this type of event. (
  • These results suggest that COX-2 inhibitors may not be as safe as originally thought, although a possible confounding effect cannot be ruled out, they conclude. (
  • However, some studies in animals suggest that COX-2 inhibitors also can cause kidney problems. (
  • A 2006 review of 138 randomized trials and almost 150,000 participants revealed selective COX-2 inhibitors were associated with a moderately increased risk of vascular events, mainly due to a twofold-increased risk of myocardial infarction. (
  • The COX inhibitors associated CV toxicity has multiple manifestations, which include the induction of myocardial infarction (MI), edema, thrombosis, blood pressure destabilization and death. (
  • Although some studies have reported mixed results with regard to the cardiovascular risk, 2-4 several recently published randomized trials and population-based studies have established an increased risk of acute myocardial infarction (MI) and thromboembolic events related to the use of most COX-2 inhibitors. (
  • The new injectable cyclooxygenase (COX)-2 inhibitor may provide a new postoperative pain management option. (
  • COX-2 inhibitors have been found to be effective in suppressing inflammatory neurodegenerative pathways in mental illness, with beneficial results in trials for major depressive disorder as well as schizophrenia . (
  • COX-2 plays a major role in prostaglandin biosynthesis in inflammatory cells and in the central nervous system. (
  • however, the upregulation of pro-inflammatory COX-2 and increased production of COX-2 derived metabolites have been implicated in diabetic nephropathy. (
  • These observations have led to the hypothesis that COX-2 expression mediates the enhanced prostanoid release, which characterizes the inflammatory response ( 21 ). (
  • Intrathecal DUP-697, a selective COX-2 inhibitor, effectively relieved inflammatory pain in rats. (
  • Thus, µ, δ and κ opioid receptor antagonists were intrathecally administered to investigate the ability of opioid receptor subtype antagonists to reverse the antinociception induced by COX-2 inhibitor in the formalin test which shows an early phase of acute nociceptive response followed by a late phase response being related to more complex inflammatory reactions. (
  • Lumiracoxib is a selective inhibitor of cyclooxygenase-2 (COX-2) approved for the relief of symptoms of chronic inflammatory conditions. (
  • Celecoxib and ibuprofen suppressed urinary excretion of the prostacyclin metabolite 2,3 dinor 6-keto PGF 1α . (
  • Ibuprofen [ 2 ] and ketorolac [ 3 ] raised blood levels of endogenous opioids in human and rats, respectively. (
  • However, while Cox-2 is associated with inflammation and pain , Cox-1 maintains the integrity of the gastric mucosa, mediates normal platelet function, and regulates renal blood flow. (
  • A drug class that relieves inflammation and pain by inhibiting the action of cyclooxygenase-2. (
  • Jones, P. and Lamdin, R. (2010) Oral Cyclo-Oxygenase 2 Inhibitors versus Other Oral Analgesics for Acute Soft Tissue Injury Systematic Review and Meta-Analysis. (
  • The δ and κ opioid receptors are involved in the activity of COX-2 inhibitor on the facilitated state as well as acute pain at the spinal level, whereas the µ opioid receptor is related only to facilitated pain. (
  • After several COX-2 inhibiting drugs were approved for marketing, data from clinical trials revealed that COX-2 inhibitors caused a significant increase in heart attacks and strokes, with some drugs in the class having worse risks than others. (
  • However, he stressed to heart wire , "a mouse study is not reason enough for people to stop taking COX-2 inhibitors," and that much more clinical work would be required to determine whether the murine data can be extrapolated into humans. (
  • In the March 1 issue of Clinical Cancer Research , researchers from University of Wisconsin-Madison demonstrate that low doses of the COX-2 inhibitor celecoxib, administered with a green tea polyphenol called pigallocatechin-3-gallate (EGCG), can slow the growth of human prostate cancer . (
  • Patient race is a significant predictor of COX-2 prescriptions in the Medicaid population, even after adjusting for other demographic and clinical variables. (
  • Another expert, Dr. Eric Matteson, a professor of medicine at the Mayo Clinic College of Medicine in Rochester, Minnesota, believes the study reveals COX-2 inhibitors increase the risk of GI bleeding and ulcers when used in clinical practice. (
  • The typical use of COX-2 agents in practice is for shorter duration, and at lower doses, than was employed in randomized clinical trials. (
  • Because our previous studies have indicated a significantly increased COX-2 expression in up to 70% of adenocarcinoma cases, the present findings are of great clinical interest. (
  • COX-1 protects the gastric mucosa, preventing ulcers, bleeding, and other digestive tract problems. (
  • Unlike ketorolac, which affects both COX-1 and COX-2, COX-2-specific inhibitors like parecoxib are less likely to cause GI ulceration or promote bleeding, while still effectively reducing pain and inflammation. (
  • Of course, if this is so, all of the hype and expense associated with the COX-2s was for naught and the only ones that benefited from the drugs were (and are) Merck and Pfizer, which have made tens of billions of dollars in profits from Vioxx, Celebrex, and Bextra. (
  • The German regulator said that COX-2 inhibitors-- the general category to which Arcoxia, Vioxx, Celebrex and Bextra belong -- should be taken only in the smallest possible effective dose and only as long as absolutely needed. (
  • In recent years, several additional intracellular components (besides COX-2) were discovered that appear to be important for mediating the anticancer effects of celecoxib in the absence of COX-2. (
  • Additional support for the idea that other targets besides COX-2 are important for celecoxib's anticancer effects has come from studies with chemically modified versions of celecoxib. (
  • Similarly, mice that overexpressed receptors for TxA 2 also produced these exaggerated effects. (
  • Last year, Medical News Today also reported on a study that suggested a possible "fix" for the side effects associated with COX-2 inhibitors. (
  • To study the effects of COX-2 on PanIN progression, Dr. Eibl and colleagues focused on the KrasG12D mouse, an animal model that mimics the early stages of pancreatic cancer. (
  • Aims: The current study aims at evaluating the beneficial effects of statins and COX-2 receptor inhibitors on ALI elicited by blunt trauma to the chest. (
  • Singh and colleagues point out that since these arrhythmia effects bypass COX-2, it is unclear if other COX-2 inhibitors would yield similar results. (
  • They also stress it is too early to speculate on human effects, although their results suggest Drosophilaâ€"one of the most valuable of organisms in biological research and has been used as a model research organism for almost a centuryâ€"are a valuable tool to investigate other COX-2 drugs. (
  • Pre-treatment with naltrexone diminished the analgesic effects of a COX-2 inhibitor, and its antinociception was abolished in rats made tolerant to the analgesic effects of morphine [ 4 ]. (
  • 28 - 33 Stimulation of the sympathetic nervous system, activation of the renin-angiotensin system, effects on endothelial nitric oxide, and, in the case of type 2 diabetes mellitus, atherogenic properties of insulin itself, have been invoked as possible explanations as to why these disease states are associated with endothelial dysfunction. (
  • In the present study we investigated the effects of the inhibitors of mitogen-activated protein kinase (MAPK) pathways Erk1/2, p38, and JNK on COX-2 expression and prostaglandin E2 (PGE2) production in human chondrocytes. (
  • The aim of this study was to evaluate the effects of this specific inhibitor of COX-2 as adjunctive treatment on induced periodontitis in rats. (
  • The other study (222 participants) compared 2 weeks of treatment with celecoxib (200 mg twice daily) to placebo in people with ulcerative colitis who were in remission. (
  • The results for disease exacerbation and AEs between the COX-2 inhibitors celecoxib and etoricoxib and placebo were uncertain. (
  • Postmenopausal women with ER-positive DCIS diagnosed by core biopsy were randomized to a 2 × 2 design of either 14 days of exemestane or placebo and celecoxib, or placebo immediately before surgery. (
  • Some COX-2 inhibitors are used in a single dose to treat pain after surgery. (
  • More particularly, the invention provides a combination therapy for the treatment of pain, inflammation or inflammation mediated disorders comprising the administration to a subject of a potassium ion channel modulator in combination with a cyclooxygenase-2 selective inhibitor. (
  • COX-2 inhibitors, as they are called, are selective non-steroidal anti-inflammatories which act by inhibiting an enzyme's action and therefore reduce pain producing substances. (
  • Selective inhibitors of cyclooxygenase (COX)-2 are commonly used analgesics in various pain conditions. (
  • COX-2 enzymes are necessary for inducing pain. (
  • When COX-2 is produced on a continual basis, constant pain ensues. (
  • Therefore, inhibiting COX-2 is an option for muscle pain management. (
  • FRANKFURT (Reuters) - Germany will issue guidelines in the next few days to significantly restrict the use of so-called COX-2 inhibitors to ease pain, the country's drug regulator said on Monday. (
  • In all types of OA, mechanical stress and overuse result in stimulation of proinflammatory cytokines like TNF- α (tumor necrosis factor) and matrix metalloproteinases (MMPs) [ 2 - 4 ]. (
  • COX-2 expression has also been implicated in tumor angiogenesis. (
  • Dr. Blanke said that COX-2 is expressed in human colorectal cancer neovasculature, including liver metastases, and that expression in the neovasculature is actually greater than in the tumor cells. (
  • COX-2 is also thought to play a role in survival of tumor cells after radiation therapy. (
  • Cyclooxygenase inhibitors retard murine mammary tumor progression by reducing tumor cell migration, invasiveness and angiogenesis. (
  • Norepinephrine up-regulates the expression of vascular endothelial growth factor, matrix metalloproteinase (MMP)-2, and MMP-9 in nasopharyngeal carcinoma tumor cells. (