A synthetic prostaglandin E analog that protects the gastric mucosa, prevents ulceration, and promotes healing of peptic ulcers. The protective effect is independent of acid inhibition. It is also a potent inhibitor of pancreatic function and can inhibit the growth of experimental tumors.
Analogs or derivatives of prostaglandins E that do not occur naturally in the body. They do not include the product of the chemical synthesis of hormonal PGE.
Hydrochloric acid present in GASTRIC JUICE.
Alkyl compounds containing a hydroxyl group. They are classified according to relation of the carbon atom: primary alcohols, R-CH2OH; secondary alcohols, R2-CHOH; tertiary alcohols, R3-COH. (From Grant & Hackh's Chemical Dictionary, 5th ed)
Behaviors associated with the ingesting of alcoholic beverages, including social drinking.
A zinc-containing enzyme which oxidizes primary and secondary alcohols or hemiacetals in the presence of NAD. In alcoholic fermentation, it catalyzes the final step of reducing an aldehyde to an alcohol in the presence of NADH and hydrogen.
A subclass of enzymes which includes all dehydrogenases acting on primary and secondary alcohols as well as hemiacetals. They are further classified according to the acceptor which can be NAD+ or NADP+ (subclass 1.1.1), cytochrome (1.1.2), oxygen (1.1.3), quinone (1.1.5), or another acceptor (1.1.99).
Isomeric forms and derivatives of butanol (C4H9OH).
Compounds that bind to and stimulate PURINERGIC P2Y RECEPTORS. Included under this heading are agonists for specific P2Y receptor subtypes.
That portion of the electromagnetic spectrum immediately below the visible range and extending into the x-ray frequencies. The longer wavelengths (near-UV or biotic or vital rays) are necessary for the endogenous synthesis of vitamin D and are also called antirachitic rays; the shorter, ionizing wavelengths (far-UV or abiotic or extravital rays) are viricidal, bactericidal, mutagenic, and carcinogenic and are used as disinfectants.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
Substances produced from the reaction between acids and bases; compounds consisting of a metal (positive) and nonmetal (negative) radical. (Grant & Hackh's Chemical Dictionary, 5th ed)
Oligosaccharides containing two monosaccharide units linked by a glycosidic bond.
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.
Compounds with a core of fused benzo-pyran rings.
A potassium-channel opening vasodilator that has been investigated in the management of hypertension. It has also been tried in patients with asthma. (Martindale, The Extra Pharmacopoeia, 30th ed, p352)
A group of organic sulfur-containing nitrites, alkyl thionitrites. S-Nitrosothiols include compounds such as S-NITROSO-N-ACETYLPENICILLAMINE and S-NITROSOGLUTATHIONE.
Conversion into nitroso compounds. An example is the reaction of nitrites with amino compounds to form carcinogenic N-nitrosamines.
Exclusive legal rights or privileges applied to inventions, plants, etc.
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.
Compounds obtained by chemical synthesis that are analogs or derivatives of naturally occurring prostaglandins and that have similar activity.
The location of the atoms, groups or ions relative to one another in a molecule, as well as the number, type and location of covalent bonds.
The phenomenon whereby compounds whose molecules have the same number and kind of atoms and the same atomic arrangement, but differ in their spatial relationships. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)
Unsaturated hydrocarbons of the type Cn-H2n, indicated by the suffix -ene. (Grant & Hackh's Chemical Dictionary, 5th ed, p408)
(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.
Analogs or derivatives of prostaglandins F that do not occur naturally in the body. They do not include the product of the chemical synthesis of hormonal PGF.
Inorganic compounds that contain zinc as an integral part of the molecule.
Inorganic compounds that contain magnesium as an integral part of the molecule.
Organic and inorganic compounds that contain iron as an integral part of the molecule.
Inorganic compounds that contain calcium as an integral part of the molecule.
A trace element that constitutes about 27.6% of the earth's crust in the form of SILICON DIOXIDE. It does not occur free in nature. Silicon has the atomic symbol Si, atomic number 14, and atomic weight [28.084; 28.086].
Organic compounds that contain silicon as an integral part of the molecule.
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.
The portion of the GASTROINTESTINAL TRACT between the PYLORUS of the STOMACH and the ILEOCECAL VALVE of the LARGE INTESTINE. It is divisible into three portions: the DUODENUM, the JEJUNUM, and the ILEUM.
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.
A plant genus of the family TILIACEAE. Some species in this genus are called Limetree which is nearly the same as the common name for lime (CITRUS AURANTIIFOLIA). Some people are allergic to the POLLEN.
One or more layers of EPITHELIAL CELLS, supported by the basal lamina, which covers the inner or outer surfaces of the body.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
A sodium-glucose transporter that is expressed in the luminal membrane of the PROXIMAL KIDNEY TUBULES.
Monosaccharide transport proteins that function as active symporters. They utilize SODIUM or HYDROGEN IONS to transport GLUCOSE across CELL MEMBRANES.
Persons with no known significant health problems who are recruited to participate in research to test a new drug, device, or intervention as controls for a patient group. (from http://clinicalcenter.nih.gov/recruit/volunteers.html, accessed 2/14/2013)
Drugs which have received FDA approval for human testing but have yet to be approved for commercial marketing. This includes drugs used for treatment while they still are undergoing clinical trials (Treatment IND). The main heading includes drugs under investigation in foreign countries.
An oral hypoglycemic agent which is rapidly absorbed and completely metabolized.
Substances which lower blood glucose levels.
The disodium salt of selenious acid. It is used therapeutically to supply the trace element selenium and is prepared by the reaction of SELENIUM DIOXIDE with SODIUM HYDROXIDE.
An element with the atomic symbol Se, atomic number 34, and atomic weight 78.96. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of GLUTATHIONE PEROXIDASE.
A strong dibasic acid with the molecular formula H2SeO4. Included under this heading is the acid form, and inorganic salts of dihydrogen selenium tetraoxide.
Inorganic compounds that contain selenium as an integral part of the molecule.
The dry cells of any suitable strain of SACCHAROMYCES CEREVISIAE or CANDIDA. It can be obtained as a by-product from the brewing of beer or by growing on media not suitable for beer production. Dried yeast serves as a source of protein and VITAMIN B COMPLEX.
Diagnostic aid in pancreas function determination.
A selenium compound with the molecular formula H2SO3. It used as a source of SELENIUM, especially for patients that develop selenium deficiency following prolonged PARENTERAL NUTRITION.

Protective effects of arbaprostil against indomethacin-induced gastric lesions in rats: significance of maintained gastric blood flow. (1/6)

The purpose of the present study was to investigate the relationship between the effects of 15(R)-15-methylprostaglandin E2 (arbaprostil) on gastric blood flow (GBF) and its protective effects on gastric lesions in rats. The GBF of anesthetized rats was measured by two different methods: Total blood flow into the stomach (total GBF) was determined by means of an ultrasonic pulsed Doppler flow meter; and gastric mucosal blood flow (mucosal GBF) was measured by nonradioactive microspheres. Systemic blood pressure (SBP), heart rate (HR) and gastric vascular resistance (GVR) were recorded simultaneously. Arbaprostil (10-100 micrograms/kg) given i.v. did not affect resting total or mucosal GBF even though it decreased SBP and GVR. Significant improvement of the total and mucosal GBF decreased by indomethacin pretreatment (10 mg/kg, i.v.) was observed by administration of arbaprostil (10-100 micrograms/kg, i.v.) in a dose-dependent manner. Furthermore, i.v.-administration of this agent, in the same dose-range, prevented the formation of gastric lesions induced by indomethacin. The present result suggests that mitigation for the ischemic state of the gastric mucosa may be one of the important mechanisms for the prophylactic and curative effect of arbaprostil on gastric lesions induced by indomethacin.  (+info)

Acid-promoted epimerization of arbaprostil, 15(R)-15-methylprostaglandin E2, elicits gastric antisecretory activities in rats. (2/6)

Gastric acid antisecretory activities of 15(R)-15-methylprostaglandin E2 (arbaprostil) preincubated or not preincubated with 0.9% physiological saline, the pH of which was precisely adjusted to less than 4.30, were examined in pylorus-ligated rats, and compared with those of 15(S)-15-methylprostaglandin E2 (15(S), epimer of arbaprostil). 15(S), unlike arbaprostil without preincubation, when s.c.-administered to rats significantly inhibited gastric acid secretion in a dose-dependent manner (30-300 micrograms/kg). However, arbaprostil preincubated at 37 degrees C for 30 min with 0.9% saline, at pHs of 4.30, 2.75 and 1.20, respectively, showed the following order of pH-dependent antisecretory activities: 1.20 greater than 2.75 greater than 4.30. An increase in 15(S) formation from arbaprostil in a pH-dependent manner was also observed by radioisotopic experiments under the same incubation conditions using [3H]-labeled arbaprostil. The present result suggests that the gastric antisecretory effect of arbaprostil can be mainly explained in terms of the formation of 15(S) after oral administration.  (+info)

Gastric antisecretory activity of 15(R)-15-methylprostaglandin E2, arbaprostil, in dogs. (3/6)

The gastric antisecretory activity of 15(R)-15-methylprostaglandin E2 (arbaprostil) was compared with that of natural prostaglandin (PG) E2 in Pavlov pouch dogs. Arbaprostil significantly inhibited pentagastrin- and food-stimulated gastric secretion when it was administered directly into the pouch at a dose of 10-30 micrograms/pouch and 30-300 micrograms/pouch, respectively. Natural PGE2, however, was inactive up to 1000 micrograms/pouch. The data indicate that arbaprostil is a potent, long-acting orally active antisecretory drug that may be useful for the treatment of peptic ulcer disease.  (+info)

Effects of 15(R)-15-methyl prostaglandin E2 (arbaprostil) on gastric secretion and various gastric lesions induced in rats. (4/6)

We studied the effects of 15(R)-15-methyl prostaglandin E2 (arbaprostil) on gastric secretion and various acute and chronic gastric lesions produced in rats. Arbaprostil significantly inhibited gastric secretion in 4 hr-pylorus-ligated preparations when given intraduodenally in a dose of 30 or 100 micrograms/kg. The agent, however, significantly stimulated gastric secretion of rats with either a ligated or intact pylorus when given orally in doses of 3-100 micrograms/kg. Orally administered arbaprostil dose-dependently prevented the development of HCI-ethanol-, histamine-, water-immersion stress-, or indomethacin-induced gastric erosions. Intraduodenally administered arbaprostil also dose-dependently prevented the development of aspirin-induced gastric erosions in pylorus-ligated rats. Arbaprostil, given orally in doses of 1-100 micrograms/kg twice daily for 2 weeks, had little or no effect on the healing of acetic acid-induced gastric ulcers. However, oral administration of the agent in a dose of 3 or 10 micrograms/kg twice daily for 4 weeks significantly accelerated the healing of acetic acid-induced gastric ulcers. The increase in doses up to 100 micrograms/kg twice daily for 4 weeks had no effect on ulcer healing. These results indicate that arbaprostil, at either antisecretory or even acid stimulating doses, is effective in preventing the development of acute gastric erosions and in accelerating the healing of chronic gastric ulcers.  (+info)

Femtomole analysis of prostaglandin pharmaceuticals. (5/6)

An analytical method is described whereby the major classes of prostaglandins are fully resolved by microcolumn liquid chromatography and detected at the subfemtomole level by laser-induced fluorescence. The prostaglandins are labeled with the fluorescent reagent 4-bromo-methyl-7-methoxycoumarin and are subsequently separated on a high-efficiency fused-silica microcolumn (0.2 mm i.d., 1.06 m length, 150,000 theoretical plates). The optimal chromatographic conditions consist of a 3-micron octadecylsilica packing material and an isocratic mobile phase of 47.6% methanol, 23.8% acetonitrile, and 28.6% water. The prostaglandin derivatives are detected directly on the microcolumn by laser fluorimetry, using a helium/cadmium laser (325 nm, 15 mW) as the excitation source together with a simple filter/photo-multiplier optical detection system. In real sample matrices, the prostaglandin PGF2 alpha is readily quantifiable from the detection limit (0.3 fmol) to the formulation strength of the therapeutic agent Lutalyse (Upjohn), spanning more than six orders of magnitude in concentration. The simplicity and general applicability of the present analytical methodology and instrumentation suggest that this technique can be used to attack a wide variety of biomedically important problems with exceptional sensitivity and selectivity.  (+info)

Dose response inhibition in man of meal-stimulated gastric acid secretion by 15(R)-15-methyl prostaglandin E2, given orally. (6/6)

15(R)-15-methyl prostaglandin E2 was given orally to healthy male volunteers. Thirty minutes later a 10% peptone meal was introduced into the stomach, and the acid response was measured by continuous intragastric titration with 0.5 N NaOH for the next two hours. The prostaglandin inhibited acid output in a dose dependent manner; the ED50 (dose inhibiting acid output by 50%) was as little as 10 micrograms per subject (or approximately 140 ng/kg). This compound is the most potent orally active inhibitor of gastric acid secretion in man that is known. It is likely that the antisecretory and cytoprotective properties shared by 15(R)-15-methyl prostaglandin E2 would be beneficial in the treatment of peptic ulcer and in preventing recurrences.  (+info)

BioAssay record AID 177813 submitted by ChEMBL: Compound was evaluated in vivo for the gastric antisecretory activity in the lumen perfused stomach of the anesthetized rat after iv administration.
WebMD explains some common complications of diabetes -- such as erectile dysfunction, vision problems, and infections -- so you can recognize the early warning signs.
The stem bark of M. oleifera was used traditionally for the treatment of ulcer sores. The high antioxidant/radical scavenging effects observed for different parts appear to provide justification for their widespread use in traditional medicine. The effect of Moringa oleifera (Lam.) aqueous extract was evaluated in albino wistar rats against ethanol induced gastric ulcer model. It was found effective at dose of 200 mg/kg. The percentage inhibition of ulcer in ethanol induced ulcer was found to be 64.30%. All treatment groups showed a marked increase in the amount of PH. The decreased ulcer lesions, gastric volume, free acidity and total acidity confirmed a significant increase in ulcer reduction. Moringa oleifera was shown to exert mucoprotective and gastric antisecretory activity and the mechanism involved may be due to the presence of flavonoids and terpenoids. ...
Prostaglandins of the E series have been shown, both in animals and humans to produce gastrointestinal antisecretory and antiulcer effects. Enprostil, a modified allenic prostaglandin E was found to be a highly potent inhibitor of gastric HCl secretion in a variety of species. In rats, in which both the pylorus and esophagus were ligated, p.o. ED50 values and 95% CL for inhibiting acid secretion evoked by histamine, pentagastrin and carbachol were 9.9 (6.7-15), 40 (11-145) and 0.83 (0.78-0.89) micrograms/kg, respectively. In inhibiting histamine-evoked acid secretion, enprostil was more potent when administered p.o. than when injected into the duodenum or s.c. When enprostil was injected directly into the pouch of Heidenhein dogs, intense antisecretory activity occurred, ED50 = 0.9 (0.7-1.1) micrograms/kg, whereas, when given p.o. to the main stomach the ED50 was 6.6 (3.2-13.6) micrograms/kg. Administration of cimetidine either p.o. or to the pouch resulted in virtually identical ED50 values, ...
Arbaprostil Bai J, Sun Q, Zhai H (January 2014). "A comparison of oxytocin and carboprost tromethamine in the prevention of ...
arbaclofen placarbil (USAN, INN) arbaprostil (INN) arbekacin (INN) arbutamine (INN) Arcalyst Arcet arcitumomab (INN) arclofenin ...
... arbaprostil MeSH D10.251.355.255.550.700.450.300 - 16,16-dimethylprostaglandin e2 MeSH D10.251.355.255.550.700.450.350 - ...
... arbaprostil MeSH D23.469.700.660.200 - 16,16-dimethylprostaglandin e2 MeSH D23.469.700.660.250 - enprostil MeSH D23.469.700.660 ...
InChI=1S/C26H32N4O4S/c1-20(2)30(16-10-11-17-34-19-24(31)29-35(3,32)33)23-18-27-25(21-12-6-4-7-13-21)26(28-23)22-14-8-5-9-15-22/h4-9,12-15,18,20H,10-11,16-17,19H2,1-3H3,(H,29,31) ...
In the US, ketorolac is the only widely available intravenous NSAID. An IV form of paracetamol, which is not an NSAID, became available in Europe in 2009 and then in the US.[13] The Syntex company, of Palo Alto, California developed the ophthalmic solution Acular[25] around 2006, which is currently licensed by Allergan, Inc.[26][27] In 2007, there were concerns about the high incidence of reported side effects. This led to restriction in its dosage and maximum duration of use. In the UK, treatment was initiated only in a hospital, although this was not designed to exclude its use in prehospital care and mountain rescue settings.[1] Dosing guidelines were published at that time.[28] Concerns over the high incidence of reported side effects with ketorolac trometamol led to its withdrawal (apart from the ophthalmic formulation) in several countries, while in others its permitted dosage and maximum duration of treatment have been reduced. From 1990 to 1993, 97 reactions with a fatal outcome were ...
... , also known as mesalamine or 5-aminosalicylic acid (5-ASA), is a medication used to treat inflammatory bowel disease, including ulcerative colitis and Crohn's disease.[2] It is generally used for mildly to moderately severe disease.[2] It is taken by mouth or rectally.[2] The formulations which are taken by mouth appear to be similarly effective.[3] Common side effects include headache, nausea, abdominal pain, and fever.[2] Serious side effects may include pericarditis, liver problems, and kidney problems.[2][3] Use in pregnancy and breastfeeding appears safe.[3] In people with a sulfa allergy certain formulations may result in problems.[2] Mesalazine is an aminosalicylate and anti-inflammatory.[2][3] It works by direct contact with the intestines.[2] Mesalazine was approved for medical use in the United States in 1987.[2][4] It is available as a generic medication and sold under many brand names worldwide.[5][2] A month supply in the United Kingdom costs the NHS about £43 as of ...
... is an organic compound, which, especially in its ester form, is called fenamate.[1]:458 serves as a parent structure for several nonsteroidal anti-inflammatory drugs (NSAIDs), including mefenamic acid, tolfenamic acid, flufenamic acid, and meclofenamic acid. These drugs are commonly referred to as "anthranilic acid derivatives" or "fenamates" because fenamic acid is a derivative of anthranilic acid.[2]:235[3]:17[2] ...
... (INN), or benorylate, is an ester-linked codrug of aspirin with paracetamol. It is used as an anti-inflammatory and antipyretic medication. In the treatment of childhood fever, it has been shown to be inferior to paracetamol and aspirin taken separately. In addition, because it is converted to aspirin, benorylate is not recommended in children due to concerns about Reye syndrome.[1] ...
The VIGOR (Vioxx GI Outcomes Research) study, conducted by Bombardier, et al., which compared the efficacy and adverse effect profiles of rofecoxib and naproxen, had indicated a significant 4-fold increased risk of acute myocardial infarction (heart attack) in rofecoxib patients when compared with naproxen patients (0.4% vs 0.1%, RR 0.25) over the 12-month span of the study. The elevated risk began during the second month on rofecoxib. There was no significant difference in the mortality from cardiovascular events between the two groups, nor was there any significant difference in the rate of myocardial infarction between the rofecoxib and naproxen treatment groups in patients without high cardiovascular risk. The difference in overall risk was by the patients at higher risk of heart attack, i.e. those meeting the criteria for low-dose aspirin prophylaxis of secondary cardiovascular events (previous myocardial infarction, angina, cerebrovascular accident, transient ischemic attack, or coronary ...
Acetylsalicylic acid is a weak acid, and very little of it is ionized in the stomach after oral administration. Acetylsalicylic acid is quickly absorbed through the cell membrane in the acidic conditions of the stomach. The increased pH and larger surface area of the small intestine causes aspirin to be absorbed more slowly there, as more of it is ionised. Owing to the formation of concretions, aspirin is absorbed much more slowly during overdose, and plasma concentrations can continue to rise for up to 24 hours after ingestion.[152][153][154] About 50-80% of salicylate in the blood is bound to albumin protein, while the rest remains in the active, ionized state; protein binding is concentration-dependent. Saturation of binding sites leads to more free salicylate and increased toxicity. The volume of distribution is 0.1-0.2 L/kg. Acidosis increases the volume of distribution because of enhancement of tissue penetration of salicylates.[154] As much as 80% of therapeutic doses of salicylic acid is ...
Synthesis of diacylglycerol begins with glycerol-3-phosphate, which is derived primarily from dihydroxyacetone phosphate, a product of glycolysis (usually in the cytoplasm of liver or adipose tissue cells). Glycerol-3-phosphate is first acylated with acyl-coenzyme A (acyl-CoA) to form lysophosphatidic acid, which is then acylated with another molecule of acyl-CoA to yield phosphatidic acid. Phosphatidic acid is then de-phosphorylated to form diacylglycerol. Dietary fat is mainly composed of triglycerides. Because triglycerides cannot be absorbed by the digestive system, triglycerides must first be enzymatically digested into monoacylglycerol, diacylglycerol, or free fatty acids.(See Dietary sources of fatty acids, their digestion, absorption, transport in the blood and storage for more detail.) Diacylglycerol is a precursor to triacylglycerol (triglyceride), which is formed in the addition of a third fatty acid to the diacylglycerol under the catalysis of diglyceride acyltransferase. Since ...
CySLTR2 mRNA is co-expressed along with CysLRR1 in human blood eosinophils and platelets, and tissue mast cells, macrophages, airway epithelial cells, and vascular endothelial cells. It is also expressed without CysLTR1 throughout the heart, including Purkinje cells, adrenal gland, and brain as well as some vascular endothelial, airway epithelial, and smooth muscle cells.[10][11][12][13] CysLTR2, similar to CysLTR1, is a G protein-coupled receptor that links to and when bound to its CysLT ligands activates the Gq alpha subunit and/or Ga subunit of its coupled G protein, depending or the cell type. Acting through these G proteins and their subunits, ligand-bound CysLTR1 activates a series of pathways that lead to cell function (see Gq alpha subunit#function and Ga subunit#function for details); the order of potency of the cysLTs in stimulating CysLTR2 is LTD4=LTC4,LTE4 with LTE4 probably lacking sufficient potency to have much activity that operates through CysLTR1 in vivo. By comparison, the ...
GLA is obtained from vegetable oils such as evening primrose (Oenothera biennis) oil (EPO), blackcurrant seed oil, borage seed oil, and hemp seed oil. GLA is also found in varying amounts in edible hemp seeds, oats, barley,[3] and spirulina. Normal safflower (Carthamus tinctorius) oil does not contain GLA, but a genetically modified GLA safflower oil available in commercial quantities since 2011 contains 40% GLA.[4] Borage oil contains 20% GLA, evening primrose oil ranges from 8% to 10% GLA, and black-currant oil contains 15-20%.[5] It also constitutes 12.23% of the fats from the fruit of the durian species Durio graveolens.[6] The human body produces GLA from linoleic acid (LA). This reaction is catalyzed by Δ6-desaturase (D6D), an enzyme that allows the creation of a double bond on the sixth carbon counting from the carboxyl terminus. LA is consumed sufficiently in most diets, from such abundant sources as cooking oils and meats. However, a lack of GLA can occur when there is a reduction of ...
... s or prostanoid receptors represent a sub-class of cell surface membrane receptors that are regarded as the primary receptors for one or more of the classical, naturally occurring prostanoids viz., prostaglandin D2, (i.e. PGD2), PGE2, PGF2alpha, prostacyclin (PGI2), thromboxane A2 (TXA2), and PGH2.[1] They are named based on the prostanoid to which they preferentially bind and respond, e.g. the receptor responsive to PGI2 at lower concentrations than any other prostanoid is named the Prostacyclin receptor (IP). One exception to this rule is the receptor for thromboxane A2 (TP) which binds and responds to PGH2 and TXA2 equally well. All of the prostanoid receptors are G protein-coupled receptors belonging to the Subfamily A14 of the rhodopsin-like receptor family except for the Prostaglandin DP2 receptor which is more closely related in amino acid sequence and functionality to chemotactic factor receptors such as the receptors for C5a and leukotriene B4.[2] Prostanoid ...
The COX-2 enzyme was discovered in 1988 by Daniel Simmons, a Brigham Young University researcher.[23] The mouse COX-2 gene was cloned by UCLA scientist Dr. Harvey Herschman, a finding published in 1991.[24]. The basic research leading to the discovery of COX-2 inhibitors has been the subject of at least two lawsuits. Brigham Young University has sued Pfizer, alleging breach of contract from relations BYU had with the company at the time of Dr. Simmons's work.[25][26] A settlement was reached in April 2012 in which Pfizer agreed to pay $450 million.[27][28] The other litigation is based on United States Pat. No. 6,048,850[29] owned by University of Rochester, which claimed a method to treat pain without causing gastro-intestinal distress by selectively inhibiting COX-2. When the patent issued, the university sued Searle (later Pfizer) in a case called, University of Rochester v. G.D. Searle & Co., 358 F.3d 916 (Fed. Cir. 2004). The court ruled in favor of Searle in 2004, holding in essence that ...
G protein-coupled receptors (GPCRs) such as DP2 are integral membrane proteins that, when bound by their cognate ligands (or, in some cases, even when not ligand-bound and thereby acting continuously in a constitutive manner {see Receptor (biochemistry)#Constitutive activity}), mobilize one or more types of Heterotrimeric G proteins. DP2 is classified as a "contractile" prostanoid receptor in that it can cause the contraction of smooth muscle. As evidenced by its initial discovery as a receptor for PGD2 in T-helper type 2 cells, activated DP2 triggers Gi alpha subunit-linked heterotrimeric G proteins to dissociate into their component a) Gi alpha subunits (also termed Giα subunits) inhibit adenylyl cyclase b) G beta-gamma complex of subunits (Gβγ) have many potential functions, including simulation of phospholipase C to cleave phosphatidylinositol triphosphate into inositol triphosphate (IP3) and diacylglycerol (DAG), inhibition or stimulation of adenylyl cyclase depending on the isoform, ...
Prostaglandin F2α (PGF2α in prostanoid nomenclature), pharmaceutically termed carboprost, is a naturally occurring prostaglandin used in medicine to induce labor and as an abortifacient.[1] In domestic mammals, it is produced by the uterus when stimulated by oxytocin, in the event that there has been no implantation during the luteal phase. It acts on the corpus luteum to cause luteolysis, forming a corpus albicans and stopping the production of progesterone. Action of PGF2α is dependent on the number of receptors on the corpus luteum membrane. The PGF2α isoform 8-iso-PGF2α was found in significantly increased amounts in patients with endometriosis, thus being a potential causative link in endometriosis-associated oxidative stress.[2] ...
... , as a lipophilic ester, easily penetrates the cornea and is then activated to the carboxylic acid, tafluprost acid. Onset of action is 2 to 4 hours after application, the maximal effect is reached after 12 hours, and ocular pressure remains lowered for at least 24 hours.[2][3] Tafluprost acid is inactivated by beta oxidation to 1,2-dinortafluprost acid, 1,2,3,4-tetranortafluprost acid, and its lactone, which are subsequently glucuronidated or hydroxylated. The cytochrome P450 liver enzymes play no role in the metabolism.[3] An analogous pathway (at least up to the tetranor-metabolites) has been found for latanoprost and travoprost. ...
It is believed that the vasoconstriction caused by thromboxanes plays a role in Prinzmetal's angina. Omega-3 fatty acids are metabolized to produce higher levels of TxA,3 which is relatively less potent than TxA2 and PGI3; therefore, there is a balance shift toward inhibition of vasoconstriction and platelet aggregation. It is believed that this shift in balance lowers the incidence of myocardial infarction (heart attack) and stroke. Vasoconstriction and, perhaps, various proinflammatory effects exerted by TxA on tissue microvasculature, is probable reason why the TxA is pathogenic in various diseases, such as ischemia-reperfusion injury.,[2] hepatic inflammatory processes,[3] acute hepatotoxicity [4] etc. TxB2, a stable degradation product of TxA2, plays a role in acute hepatoxicity induced by acetaminophen.[5][6] ...
... is a nonsteroidal anti-inflammatory drug (NSAID). Fenoprofen calcium is used for symptomatic relief for rheumatoid arthritis, osteoarthritis, and mild to moderate pain. Fenoprofen is marketed in the US as Nalfon. As of 2015 the cost for a typical month of medication in the United States is 50 to US$100.[1] ...
The drug is clear with a pH of 10.[7] Its production is inhibited indirectly by NSAIDs, which inhibit the cyclooxygenase enzymes COX1 and COX2. These convert arachidonic acid to prostaglandin H2 (PGH2), the immediate precursor of prostacyclin. Since thromboxane (an eicosanoid stimulator of platelet aggregation) is also downstream of COX enzymes, one might think that the effect of NSAIDs would act to balance. However, prostacyclin concentrations recover much faster than thromboxane levels, so aspirin administration initially has little to no effect but eventually prevents platelet aggregation (the effect of prostaglandins predominates as they are regenerated). This is explained by understanding the cells that produce each molecule, TXA2 and PGI2. Since PGI2 is primarily produced in a nucleated endothelial cell, the COX inhibition by NSAID can be overcome with time by increased COX gene activation and subsequent production of more COX enzymes to catalyze the formation of PGI2. In contrast, TXA2 is ...
... , also known as selenium sulfide, is a medication used to treat pityriasis versicolor, seborrhoeic dermatitis, and dandruff.[1] It is applied to the affected area as a lotion or shampoo.[2] Dandruff frequently returns if treatment is stopped.[3] Side effects include hair loss, irritation of the skin, weakness, and feeling tired.[1] Use is not recommended in children less than 2-5 years old.[3][1] Use in pregnancy or breastfeeding has not been studied.[4] Selenium disulfide is an inorganic compound with the chemical formula SeS2.[5] Selenium disulfide was approved for medical use in the United States at least as early as 1951.[3] It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system.[6] Selenium disulfide is available as a generic medication and over the counter.[2] In the United States a month of treatment costs less than 25 USD.[2] In the United Kingdom 100 ml of 2.5% shampoo costs the NHS about ...
... was available over-the-counter in the United States in the form of 12.5 mg coated tablets (Orudis KT and Actron), but this form has been discontinued. It is available by prescription capsules. Ketoprofen is also available as a 2.5% gel for topical application, and it is also available as a patch for topical analgesia and anti-inflammatory action. However, the gel is not sold in the United States. Brand names in Australia are Orudis and Oruvail. It is available in Japan in a transdermal patch Mohrus Tape, made by Hisamitsu Pharmaceutical. It is available in the UK as Ketoflam and Oruvail, in Ireland as Fastum Gel, in Estonia as Keto, Ketonal, and Fastum Gel, in Finland as Ketorin, Keto, Ketomex, and Orudis; in France as Profénid, Bi-Profénid and Ketum; in Italy as Ketodol, Fastum Gel, Lasonil, Orudis and Oki; in Poland, Serbia, Slovenia and Croatia as Knavon and Ketonal; in Romania as Ketonal and Fastum Gel; in Mexico as Arthril; in Norway as Zon and Orudis; in Russia as ОКИ ...
... supplementation in daily doses of 1,000-1,500 mg for 50 days has been well tolerated during several clinical studies, with no significant side effects reported. All common markers of health, including kidney and liver function,[35] serum lipids,[39] immunity,[40] and platelet aggregation[34] appear to be unaffected with this level and duration of use. Furthermore, higher concentrations of ARA in muscle tissue may be correlated with improved insulin sensitivity.[41] Arachidonic acid supplementation of the diets of healthy adults appears to offer no toxicity or significant safety risk. While studies looking at arachidonic acid supplementation in sedentary subjects have failed to find changes in resting inflammatory markers in doses up to 1,500 mg daily, strength-trained subjects may respond differently. One study reported a significant reduction in resting inflammation (via marker IL-6) in young men supplementing 1,000 mg/day of arachidonic acid for 50 days in combination with ...
Alprostadil is sold in the United States as urethral suppositories and in injectable form. The suppositories are sold under the brand name Muse.[6] The injectable forms are Edex[7] and Caverject.[8] Muse delivers alprostadil as a penile suppository, inserted into the urethra, at least ten minutes before the erection is needed. Caverject and Edex are similarly fast-acting, but instead are injected by syringe directly into the corpus cavernosum of the penis. Alprostadil is also available as a generic. The major cost is that it must be mixed by a compounding pharmacy and supplies may be difficult to obtain. The different formulations, including Bimix and Trimix, may include papaverine and/or phentolamine. A typical mix might be 30 mg of papaverine, 2 mg of phentolamine, and 20 μg alprostadil. As a generic, it is much less expensive than the packaged injectables. It is premixed and must be kept refrigerated and the user must load a syringe with the quantity needed. Most recently, the compound has ...
... , also known as mesalamine or 5-aminosalicylic acid (5-ASA), is an aminosalicylate anti-inflammatory drug[2] used to treat inflammatory bowel disease, including ulcerative colitis,[3][4][5] or inflamed anus or rectum,[6] and to maintain remission in Crohn's disease.[3][7] It is sold in an oral form to maintain remission in ulcerative colitis and Crohn's disease,[3] and as a rectal suppository[4][6] and an enema for the lower bowel conditions.[5] It is generic and sold under many brand names worldwide,[1] and there are many formulations.[8] There are no data on use in pregnant women, but the drug does cross the placenta and is excreted in breast milk. The drug should not be used in children under two, people with kidney disease, or people who are allergic to aspirin.[4] Side effects are primarily gastrointestinal but may also include headache; GI effects include nausea, diarrhea and abdominal pain. There have been scattered reports of various problems when the oral form is used, ...
PTGS2 (COX-2) is unexpressed under normal conditions in most cells, but elevated levels are found during inflammation. PTGS1 (COX-1) is constitutively expressed in many tissues and is the predominant form in gastric mucosa and in the kidneys. Inhibition of PTGS1 (COX-1) reduces the basal production of cytoprotective PGE2 and PGI2 in the stomach, which may contribute to gastric ulceration. Since PTGS2 (COX-2) is generally expressed only in cells where prostaglandins are upregulated (e.g., during inflammation), drug-candidates that selectively inhibit PTGS2 (COX-2) were suspected to show fewer side-effects[25] but proved to substantially increase risk for cardiovascular events such as heart attack and stroke. Two different mechanisms may explain contradictory effects. Low-dose aspirin protects against heart attacks and strokes by blocking PTGS1 (COX-1) from forming a prostaglandin called thromboxane A2. It sticks platelets together and promotes clotting; inhibiting this helps prevent heart ...
Kotani M, Tanaka I, Ogawa Y, Usui T, Mori K, Ichikawa A, Narumiya S, Yoshimi T, Nakao K (November 1995). "Molecular cloning and expression of multiple isoforms of human prostaglandin E receptor EP3 subtype generated by alternative messenger RNA splicing: multiple second messenger systems and tissue-specific distributions". Molecular Pharmacology. 48 (5): 869-79. PMID 7476918 ...
Ang Mefenamic acid o Asidong mefenamiko ay isang miyembro ng klaseng deribatibong asidong anthraniliko (o fenamate) ng mga gamot NSAID. Kadalasan itong ginagamit na panlunas sa kaunti hanggang katamtamang kirot, kasama na ang kirot dulot ng sapanahon o pagreregla, at ginagamit rin para malunasan ang mga sakit ng ulo na kaugnay ng pagreregla.[1][2] Hindi ito malawakang ginagamit dahil sa mga naitatalang kasamang epekto.[3][4]:334 Natuklasan at naibenta ito sa pamilihan ng Parke-Davis noong dekada ng 1960 sa ilalim ng pangalang Ponstan, Ponalar, Ponstyl, at Ponstel. Naging heneriko ito noong dekada ng 1980 at nagagamit na sa buong mundo sa ilalim ng ibat-ibang pangalan..[5] Noong 2015, mahigit 200 USD ang halaga ng medikasyon ng mefenamic acid sa Estados Unidos.[6] ...
alcohol secundario (es); 第2級アルコール (ja); Alcool secondaire (fr); alkohol drugorzędowy (pl); вторичный спирт (ru); 仲醇 (lzh); 이차 알코올 (ko); secondary alcohol (en); sekundara alkoholo (eo); sekundární alkohol (cs); 仲醇 (zh) każdy alkohol, w którym grupa hydroksylowa przyłączona jest do drugorzędowego atomu węgla (pl) вторичные спирты (ru); Alcool Secondaire (fr); 2차 알코올 (ko); secondary alcohols (en); alkohole drugorzędowe (pl ...
ácido carboxílico (es); Карбон қышқылдары (kk-kz); Asid karboksilik (ms); كاربون قىشقىلدارى (kk-cn); Карбоксилна киселина (bg); کاربوکسلک تیزاب (pnb); 羧酸 (zh-hk); Karboxylová kyselina (sk); карбонові кислоти (uk); 羧酸 (zh-hant); 羧酸 (zh-cn); 카복실산 (ko); Carboxylsýra (fo); karboksilata acido (eo); Карбоксилна киселина (mk); Karboksilne kiseline (bs); কার্বক্সিলিক অ্যাসিড (bn); acide carboxylique (fr); Karboksilne kiseline (hr); axit cacboxylic (vi); كاربون قىشقىلدارى (kk-arab); Karbon qışqıldarı (kk-latn); Karboksielsuur (af); карбоксилна киселина (sr); 羧酸 (zh-sg); Карбон қышқылдары (kk-cyrl); karboksylsyre (nn); karboksylsyre (nb); Asam karboksilat (su); 羧酸 (lzh); ترشی کاربۆکسیلی (ckb); carboxylic acid (en); حمض كربوكسيلي (ar); 羧酸 (yue); ...
Arbaprostil. A synthetic prostaglandin E analog that protects the gastric mucosa, prevents ulceration, and promotes healing of ...
Arbaprostil Bai J, Sun Q, Zhai H (January 2014). "A comparison of oxytocin and carboprost tromethamine in the prevention of ...
3914178 - Lack of effect of arbaprostil on the human non-pregnant uterus.. 9763058 - Pregnancy and homozygous beta thalassaemia ...
... arbaprostil, unoprostone, trimoprostil, carboprost, limaprost, gemeprost, lantanoprost, ornoprostil, beraprost, sulpostrone, ...
An Evaluation of Arbaprostil at Multiple Doses for the Treatment of Acute Duodenal Ulcer: A Randomized Double Blind Placebo- ... Six hundred and thirty patients were enrolled in a randomized double-blind placebo-controlled trial evaluating two arbaprostil ...
arbaclofen placarbil (USAN, INN) arbaprostil (INN) arbekacin (INN) arbutamine (INN) Arcalyst Arcet arcitumomab (INN) arclofenin ...
... arbaprostil, arbekacin, arbutamine, arcitumomab, arclofenin, ardacin, ardeparin sodium, arfalasin, arfendazam, argatroban, ... arbaprostil, arbekacin, arbutamine, arcitumomab, arclofenin, ardacin, ardenermin, ardeparin sodium, arfalasin, arfendazam, ... arbaprostil, arbékacine, arbutamine, arcitumomab, arclofénine, ardacine, ardéparine sodique, arfalasine, arfendazam, argatroban ... arbaprostil, arbékacine, arbutamine, arcitumomab, arclofénine, ardacine, ardénermine, ardéparine sodique, arfalasine, ...
... arbaprostil, arbekacin, arclofenin, arfendazam, arginine, arginine glutamat, arildone, arnolol, aronixil, arotinolol, arpinocid ...
... arbaprostil, enisoprost, mexiprostil, dimoxaprost, tiprostanide, and remiprostol as well as other prostaglandin analogues in ...
... arbaprostil, rotraxate, triimoprostil, omeprazole, beperidium iodide, lansoprazole, nizatidine, rioprostil, polaprezinc, ...
InChI=1S/C26H32N4O4S/c1-20(2)30(16-10-11-17-34-19-24(31)29-35(3,32)33)23-18-27-25(21-12-6-4-7-13-21)26(28-23)22-14-8-5-9-15-22/h4-9,12-15,18,20H,10-11,16-17,19H2,1-3H3,(H,29,31) ...
In the US, ketorolac is the only widely available intravenous NSAID. An IV form of paracetamol, which is not an NSAID, became available in Europe in 2009 and then in the US.[13] The Syntex company, of Palo Alto, California developed the ophthalmic solution Acular[25] around 2006, which is currently licensed by Allergan, Inc.[26][27] In 2007, there were concerns about the high incidence of reported side effects. This led to restriction in its dosage and maximum duration of use. In the UK, treatment was initiated only in a hospital, although this was not designed to exclude its use in prehospital care and mountain rescue settings.[1] Dosing guidelines were published at that time.[28] Concerns over the high incidence of reported side effects with ketorolac trometamol led to its withdrawal (apart from the ophthalmic formulation) in several countries, while in others its permitted dosage and maximum duration of treatment have been reduced. From 1990 to 1993, 97 reactions with a fatal outcome were ...
... is a nonsteroidal anti-inflammatory drug (NSAID) analog of diclofenac. It is used for the relief of pain and inflammation in rheumatoid arthritis, osteoarthritis and ankylosing spondylitis. Aceclofenac (C16H13Cl2NO4), chemically [(2-{2, 6-dichlorophenyl) amino} phenylacetooxyacetic acid], is a crystalline powder with a molecular weight of 354.19. It is practically insoluble in water with good permeability. It is metabolized in human hepatocytes and human microsomes to form [2-(2,6-dichloro-4-hydroxy- phenylamino) phenyl] acetoxyacetic acid as the major metabolite, which is then further conjugated. According to the Biopharmaceutical Classification System (BCS) drug substances are classified to four classes upon their solubility and permeability. Aceclofenac falls under the BCS Class II, poorly soluble and highly permeable drug.[1] Aceclofenac works by inhibiting the action of cyclooxygenase (COX) that is involved in the production of prostaglandins (PG) which is accountable for ...
arbaprostil 55028-70-1 C21H34O5 366.50 7.10 rioprostil 77287-05-9 C21H38O4 354.53 7.09 lafutidine 118288-08-7 C22H29N3O4S ...
Arbaprostil / pharmacology * Bacitracin / pharmacology * Cell Division / drug effects * Cell Division / physiology * ...
In pure form, methyl salicylate is harmful, when taken orally. A single teaspoon (5 ml) of methyl salicylate contains approximately 6 g of salicylate,[19] which is equivalent to almost twenty 300 mg aspirin tablets (5 mL * 1.174 g/mL = 5.87 g). The lowest published lethal dose is 101 mg/kg body weight in adult humans,[20] (or 7.07 grams for a 70-kg adult). It has proven fatal to small children in doses as small as 4 ml.[10] A seventeen-year-old cross-country runner at Notre Dame Academy on Staten Island died in April 2007 after her body absorbed methyl salicylate through excessive use of topical muscle-pain relief products.[21]. Most instances of human toxicity due to methyl salicylate are a result of over-application of topical analgesics, especially involving children. Some people have intentionally ingested large amounts of oil of wintergreen. Salicylate, the major metabolite of methyl salicylate, may be quantitated in blood, plasma or serum to confirm a diagnosis of poisoning in hospitalized ...
The major source of retinoids from the diet are plant pigments such as carotenes and retinyl esters derived from animal sources. Retinyl esters are hydrolyzed in the intestinal lumen to yield free retinol and the corresponding fatty acid (i.e. palmitate or stearate). After hydrolysis, retinol is taken up by the enterocytes. Retinyl ester hydrolysis requires the presence of bile salts that serve to solubilize the retinyl esters in mixed micelles and to activate the hydrolyzing enzymes [3]. Several enzymes that are present in the intestinal lumen may be involved in the hydrolysis of dietary retinyl esters. Cholesterol esterase is secreted into the intestinal lumen from the pancreas and has been shown, in vitro, to display retinyl ester hydrolase activity. In addition, a retinyl ester hydrolase that is intrinsic to the brush-border membrane of the small intestine has been characterized in the rat as well as in the human. The different hydrolyzing enzymes are activated by different types of bile ...
EP4 is classified as a relaxant type of prostaglandin receptor based on its ability, upon activation, to relax the contraction of certain smooth muscle preparations and smooth muscle-containing tissues that have been pre-contracted by stimulation.[6] When bound to PGE2 or other of its agonists, it mobilizes G proteins containing the Gs alpha subunit (i.e. Gαs)-G beta-gammaes (i.e. Gβγ) complex. The complex then dissociate into its Gαs and Gβγ components which act to regulate cell signaling pathways. In particular, Gαs stimulates adenyl cyclase to raise cellular levels of cAMP; cAMP activates PKA, a kinase which in turn activates signaling molecules, in particular, the transcription factor, CREB. Activated CREB stimulates the expression of genes such as c-fos, somatostatin, and corticotropin-releasing hormone that regulate cellular proliferation, cellular differentiation, cellular survival, and angiogenesis. EP4 activation of G proteins also activate PI3K/AKT/mTOR, ERK, and p38 MARK ...
Lewis JH and Stine JG. Nonsteroidal Antiinflammatory Drugs and Leukotriene Receptor Antagonists, Ch 22 in Drug-induced Liver Disease (Third Edition). Eds Neil Kaplowitz and Laurie D. DeLeve. Elsevier Inc, 2013. ISBN 9780123878175 ...
... arbaprostil when Law cheap dapagliflozin dapagliflozin cleansed ethologically buy farxiga from canada regarding whoever ... arbaprostil when Law cleansed ethologically regarding whoever unelliptical demurest. 2019:380:347-357. Apr 30, 2021 · ...
Together with the related barium and zinc selenites, sodium selenite is mainly used in the manufacture of colorless glass. The pink color imparted by these selenites cancels out the green color imparted by iron impurities.[3] Because selenium is an essential element, sodium selenite is an ingredient in dietary supplements such as multi-vitamin/mineral products, but supplements that provide only selenium use L-selenomethionine or a selenium-enriched yeast. The US Food and Drug Administration approved a selenium supplement to animal diets; the most common form is sodium selenite for pet foods. According to one article, "not much was known about which selenium compounds to approve for use in animal feeds when the decisions were made back in the 1970s .. At the time the regulatory action was taken, only the inorganic selenium salts (sodium selenite and sodium selenate) were available at a cost permitting their use in animal feed." [4] ...
Mikashima, H.; Goto, K. (Jan 1982). "[Inhibitory effect of 2-(4-(2-imidazo(1,2-a)pyridyl)phenyl) propionic acid (miroprofen) on platelet aggregation and prostaglandin I2 generation (authors transl)]". Yakugaku Zasshi. 102 (1): 99-103. PMID 7045328 ...
Synthesis of Arbaprostil (共著) 1991 126. 論文 Highly Efficient Synthesis of 13-Dehydroprostaglandins by 1,4-Addition Reaction of ...
Arbaprostil ‎ (← links). *Allatostatin ‎ (← links). *Carbonic acid inhibitor ‎ (← links). *Tissue-inhibitor of ...
In primary agent (atropine sulphate), used as the ribs are pge2 (enprostil, arbaprostil, rioprostil), given alone. Those ...
Kotani M, Tanaka I, Ogawa Y, Usui T, Mori K, Ichikawa A, Narumiya S, Yoshimi T, Nakao K (November 1995). "Molecular cloning and expression of multiple isoforms of human prostaglandin E receptor EP3 subtype generated by alternative messenger RNA splicing: multiple second messenger systems and tissue-specific distributions". Molecular Pharmacology. 48 (5): 869-79. PMID 7476918 ...
Ang Mefenamic acid o Asidong mefenamiko ay isang miyembro ng klaseng deribatibong asidong anthraniliko (o fenamate) ng mga gamot NSAID. Kadalasan itong ginagamit na panlunas sa kaunti hanggang katamtamang kirot, kasama na ang kirot dulot ng sapanahon o pagreregla, at ginagamit rin para malunasan ang mga sakit ng ulo na kaugnay ng pagreregla.[1][2] Hindi ito malawakang ginagamit dahil sa mga naitatalang kasamang epekto.[3][4]:334 Natuklasan at naibenta ito sa pamilihan ng Parke-Davis noong dekada ng 1960 sa ilalim ng pangalang Ponstan, Ponalar, Ponstyl, at Ponstel. Naging heneriko ito noong dekada ng 1980 at nagagamit na sa buong mundo sa ilalim ng ibat-ibang pangalan..[5] Noong 2015, mahigit 200 USD ang halaga ng medikasyon ng mefenamic acid sa Estados Unidos.[6] ...
upang ipakita ang padron/suleras na ito sa its nakatagong katayuan nito yun ay kung mayroon pang ibang padron/suleras ng parehong uri pahina. (Ito ay kadalasang naka-default ...

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