Heterocyclic compounds that contain 4H,5H,6H,7H-thieno[2,3-c]pyridine as part of their structure.
Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system.
An effective inhibitor of platelet aggregation commonly used in the placement of STENTS in CORONARY ARTERIES.
Chemicals with two conjoined aromatic rings incorporating two nitrogen atoms and one of the carbons oxidized with a keto oxygen.
A subclass of purinergic P2Y receptors that have a preference for ADP binding and are coupled to GTP-BINDING PROTEIN ALPHA SUBUNIT, GI. The P2Y12 purinergic receptors are found in PLATELETS where they play an important role regulating PLATELET ACTIVATION.
Thiophenes are aromatic heterocyclic organic compounds containing a five-membered ring with four carbon atoms and one sulfur atom, which are found in various natural substances and synthesized for use in pharmaceuticals and agrochemicals.
Bleeding or escape of blood from a vessel.
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)
Platelet membrane glycoprotein complex important for platelet adhesion and aggregation. It is an integrin complex containing INTEGRIN ALPHAIIB and INTEGRIN BETA3 which recognizes the arginine-glycine-aspartic acid (RGD) sequence present on several adhesive proteins. As such, it is a receptor for FIBRINOGEN; VON WILLEBRAND FACTOR; FIBRONECTIN; VITRONECTIN; and THROMBOSPONDINS. A deficiency of GPIIb-IIIa results in GLANZMANN THROMBASTHENIA.
Works about clinical trials that involve at least one test treatment and one control treatment, concurrent enrollment and follow-up of the test- and control-treated groups, and in which the treatments to be administered are selected by a random process, such as the use of a random-numbers table.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.

Glutamate receptor signaling interplay modulates stress-sensitive mitogen-activated protein kinases and neuronal cell death. (1/32)

Glutamate receptors modulate multiple signaling pathways, several of which involve mitogen-activated protein (MAP) kinases, with subsequent physiological or pathological consequences. Here we report that stimulation of the N-methyl-D-aspartate (NMDA) receptor, using platelet-activating factor (PAF) as a messenger, activates MAP kinases, including c-Jun NH2-terminal kinase, p38, and extracellular signal-regulated kinase, in primary cultures of hippocampal neurons. Activation of the metabotropic glutamate receptor (mGluR) blocks this NMDA-signaling through PAF and MAP kinases, and the resultant cell death. Recombinant PAF-acetylhydrolase degrades PAF generated by NMDA-receptor activation; the hetrazepine BN50730 (an intracellular PAF receptor antagonist) also inhibits both NMDA-stimulated MAP kinases and neuronal cell death. The finding that the NMDA receptor-PAF-MAP kinase signaling pathway is attenuated by mGluR activation highlights the exquisite interplay between glutamate receptors in the decision making process between neuronal survival and death.  (+info)

Omega-3 fatty acids suppress monocyte adhesion to human endothelial cells: role of endothelial PAF generation. (2/32)

Monocyte-endothelium interaction is a fundamental process in many acute and chronic inflammatory diseases. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are fish oil-derived alternative (omega-3) precursor fatty acids implicated in the suppression of inflammatory events. We investigated their influence on rolling and adhesion of monocytes to human umbilical vein endothelial cells (HUVEC) under laminar flow conditions in vitro. Exposure of HUVEC to tumor necrosis factor (TNF-alpha) strongly increased 1) surface expression of intercellular adhesion molecule (ICAM-1), vascular cell adhesion molecule (VCAM-1), and E-selectin, 2) platelet-activating factor (PAF) synthesis as assessed by thrombin challenge, and 3) rate of rolling and adhesion of monocytes. Preincubation of HUVEC with EPA or DHA markedly suppressed PAF synthesis, monocyte rolling, and adherence, whereas expression of endothelial adhesion molecules was unchanged. Also, PAF receptor antagonists markedly suppressed the adhesion rate of monocytes, and EPA or DHA revealed no additional inhibitory capacity. In contrast, arachidonic acid partially reversed the effect of the antagonist. We conclude that omega-3 fatty acids suppress rolling and adherence of monocytes on activated endothelial cells in vitro by affecting endothelial PAF generation.  (+info)

Involvement of platelet-activating factor and tumour necrosis factor in the pathogenesis of joint inflammation in rabbits. (3/32)

We have studied the participation of platelet-activating factor (PAF) in antigen-induced arthritis in rabbits, as well as the possible co-operation between PAF and tumour necrosis factor (TNF) in their ability to induce joint inflammation when injected into the knees of healthy rabbits. The administration of two structurally different PAF receptor antagonists, BN52021 and Alprazolam, from 4 h before the intra-articular injection of ovalbumin in preimmunized rabbits, induced an important reduction in the synovial fluid volume, in the amount of cells infiltrating the articular cavity and the synovial membrane, as well as in the prostaglandin E2 (PGE2) concentration. Furthermore, proteoglycans of the articular cartilage, which were found diminished in animals with non-treated arthritis, were well preserved in rabbits treated with PAF antagonists. All the synovial fluids from joints with arthritis had detectable amounts of PAF. The injection of either TNF or PAF into the joints of normal rabbits induced a mild inflammation. When TNF was administered 1 h before PAF, a synergistic response was noted in the synovial fluid volume, in the accumulation of leucocytes, and in the amount of PGE2. The administration of BN50726, a hetrazepine with a potent PAF-receptor antagonist effect, induced a diminution in those parameters. Our results suggest that PAF may be an early and important mediator of joint damage, and that TNF can amplify the inflammatory response induced by PAF. PAF receptor antagonists could play some role in the treatment of inflammatory joint diseases.  (+info)

Dexamethasone-induced gastric mucosal damage in the rat: possible role of platelet-activating factor. (4/32)

1. The aim of the present experiments was to study the possible role of platelet-activating factor (PAF) in mediating gastric mucosal damage induced by dexamethasone in the rat by measuring gastric tissue levels of PAF during dexamethasone-treatment and by investigating the effects of specific PAF receptor antagonists on dexamethasone-induced gastric lesions. PAF-like bioactivity extracted from the rat glandular stomach was determined by a platelet aggregation assay. 2. Dexamethasone treatment (0.4-4 mg kg-1, daily for 1-6 days) produced time- and dose-dependent damage to the glandular mucosa of the stomach as characterized by extensive, uniform hyperaemia with multiple, focal petechiae and erosions. 3. These changes were accompanied by a time-, and dose-dependent increase in PAF content of the glandular stomach. Control rat stomach contained small amounts of PAF (0.14 +/- 0.04 ng per g wet weight), which increased over 40 fold in response to dexamethasone treatment (4 mg kg-1, daily for 6 consecutive days). The presence of PAF-like material in the stomach extract was ascertained by thin-layer chromatography, high performance liquid chromatography and by alkaline hydrolysis. 4. Pretreatment of the animals with one or other of the structurally unrelated PAF receptor antagonists, BN 52021 (10 mg kg-1, i.p.) or BN 50727 (1 mg kg-1, i.p.) significantly reduced dexamethasone-induced gastric damage. In these animals neither petechiae nor erosions were observed. 5. These observations suggest that PAF is a likely endogenous mediator of glucocorticoid-induced gastric mucosal damage in the rat.  (+info)

Effects of the PAF antagonists BN50726 and BN50739 on arrhythmogenesis and extent of necrosis during myocardial ischaemia/reperfusion in rabbits. (5/32)

1. The effects of two novel platelet activating factor (PAF) antagonists BN50726 and BN50739 on arrhythmias, haemodynamics and extent of necrosis during myocardial ischaemia and reperfusion were investigated in anaesthetized rabbits subjected to coronary artery ligation. 2. BN50739 reduced heart rate prior to coronary artery occlusion (P < 0.005) but had no other significant haemodynamic effects at this time. BN50739 and BN50726 did not significantly alter heart rate or blood pressure during 30 min of ischaemia or 30 min of reperfusion, compared to control hearts. 3. BN50739 and BN50726 had no effect on the incidence of arrhythmias during ischaemia. BN50726 significantly reduced the incidence of reperfusion ventricular fibrillation compared to controls (0% v 40%, P < 0.05), and improved survival (80% v 39%, P < 0.05). Similar trends were observed with BN50739. 4. BN50726 reduced the extent of necrosis compared to control hearts (18 +/- 2% v 30 +/- 3%, P < 0.01). A similar trend was observed with BN50739. 5. These results demonstrate that PAF antagonism with BN50726 attenuates reperfusion-induced arrhythmias and preserves myocardium in the early phase of ischaemia, independently of haemodynamic effects.  (+info)

Platelet-activating factor (PAF) induces corneal neovascularization and upregulates VEGF expression in endothelial cells. (6/32)

PURPOSE: Platelet-activating factor (PAF) is a potent proinflammatory mediator that accumulates in the cornea after injury and induces the expression of genes related to inflammation and wound healing. The current study was conducted to investigate the direct effect of PAF on corneal neovascularization and on the expression of angiogenic growth factors in vascular endothelial cells. METHODS: Pellets containing carbamyl-PAF (cPAF) were implanted in corneas of wild-type or PAF-receptor (PAF-R)-knockout mice, and the progression of angiogenesis was monitored by microscope. In some experiments, mice were treated with a daily intraperitoneal injection of the PAF-R antagonist LAU8080. Migration assays of human umbilical cord vein endothelial cells (HUVECs) and human dermal microvascular endothelial cells (HMVECs) were performed in a Boyden chamber after addition of various concentrations of cPAF or bovine fibroblast growth factor (FGF-2). Cell proliferation was assessed by fluorescence-binding assay in the presence of cPAF or FGF-2 for 8 days. Vascular endothelial growth factor (VEGF) and FGF-2 expression was studied by RT-PCR and Northern- and Western-blot analyses in cells stimulated with cPAF at different concentrations and for different times. RESULTS: Six days after cPAF pellet implantation, there were new vessels growing from the limbus to the center of the cornea. The PAF-induced neovascularization was significantly reduced in PAF-R-knockout mice and in mice treated with the PAF antagonist. cPAF added to the lower well of the Boyden chamber produced a dose-dependent migration of HUVECs and HMVECs that was inhibited in cells preincubated with LAU8080 or with a VEGF-blocking antibody. In contrast, cPAF did not stimulate proliferation of endothelial cells. cPAF induced VEGF mRNA and protein expression but not FGF-2 expression in HUVECs and HMVECs. CONCLUSIONS: PAF stimulates corneal neovascularization by a receptor-mediated mechanism. Induction of VEGF expression and stimulation of vascular endothelial cell migration are initial events in PAF-promoted corneal angiogenesis.  (+info)

In vitro activities of CG400549, a novel FabI inhibitor, against recently isolated clinical staphylococcal strains in Korea. (7/32)

The in vitro activities of CG400549, a novel FabI inhibitor, were compared to those of linezolid and commonly used antimicrobials against recent bacterial isolates. CG400549 had an MIC(90) of 0.5 microg/ml for Staphylococcus aureus strains and was more potent than either linezolid or vancomycin.  (+info)

Antistaphylococcal activity of CG400549, a new experimental FabI inhibitor, compared with that of other agents. (8/32)

Among 203 strains of Staphylococcus aureus, the MICs of CG400549 were 0.06 to 1.0 microg/ml, with MIC(50) and MIC(90) values of 0.25 microg/ml each. All strains were susceptible to linezolid and quinupristin-dalfopristin (MICs, 0.25 to 2.0 microg/ml). The daptomycin MICs were 0.25 to 2.0 microg/ml for methicillin-susceptible and 0.25 to 4.0 microg/ml against methicillin-resistant strains (including vancomycin-intermediate strains). Single-passage selection testing showed low resistance frequencies with CG400549, but multistep analysis showed that CG400549 yielded resistant mutants after 14 to 17 days in all strains tested.  (+info)

Thienopyridines are a class of antiplatelet medications that work by irreversibly inhibiting the ADP (adenosine diphosphate) receptor on platelets, thereby preventing platelet activation and aggregation. This class includes drugs such as clopidogrel (Plavix), prasugrel (Effient), and ticlopidine (Ticlid). They are commonly used in the prevention of arterial thrombosis, including the treatment of acute coronary syndrome and peripheral artery disease.

Platelet aggregation inhibitors are a class of medications that prevent platelets (small blood cells involved in clotting) from sticking together and forming a clot. These drugs work by interfering with the ability of platelets to adhere to each other and to the damaged vessel wall, thereby reducing the risk of thrombosis (blood clot formation).

Platelet aggregation inhibitors are often prescribed for people who have an increased risk of developing blood clots due to various medical conditions such as atrial fibrillation, coronary artery disease, peripheral artery disease, stroke, or a history of heart attack. They may also be used in patients undergoing certain medical procedures, such as angioplasty and stenting, to prevent blood clot formation in the stents.

Examples of platelet aggregation inhibitors include:

1. Aspirin: A nonsteroidal anti-inflammatory drug (NSAID) that irreversibly inhibits the enzyme cyclooxygenase, which is involved in platelet activation and aggregation.
2. Clopidogrel (Plavix): A P2Y12 receptor antagonist that selectively blocks ADP-induced platelet activation and aggregation.
3. Prasugrel (Effient): A third-generation thienopyridine P2Y12 receptor antagonist, similar to clopidogrel but with faster onset and greater potency.
4. Ticagrelor (Brilinta): A direct-acting P2Y12 receptor antagonist that does not require metabolic activation and has a reversible binding profile.
5. Dipyridamole (Persantine): An antiplatelet agent that inhibits platelet aggregation by increasing cyclic adenosine monophosphate (cAMP) levels in platelets, which leads to decreased platelet reactivity.
6. Iloprost (Ventavis): A prostacyclin analogue that inhibits platelet aggregation and causes vasodilation, often used in the treatment of pulmonary arterial hypertension.
7. Cilostazol (Pletal): A phosphodiesterase III inhibitor that increases cAMP levels in platelets, leading to decreased platelet activation and aggregation, as well as vasodilation.
8. Ticlopidine (Ticlid): An older P2Y12 receptor antagonist with a slower onset of action and more frequent side effects compared to clopidogrel or prasugrel.

Ticlopidine is defined as a platelet aggregation inhibitor drug, which works by preventing certain types of blood cells (platelets) from sticking together to form clots. It is used to reduce the risk of stroke and heart attack in patients who have already had a stroke or have peripheral arterial disease.

Ticlopidine is a thienopyridine derivative that selectively inhibits platelet activation and aggregation by blocking the ADP (adenosine diphosphate) receptor on the platelet surface. This action prevents the formation of platelet plugs, which can lead to the development of blood clots in the arteries.

Ticlopidine is available in oral form as tablets and is typically taken twice daily. Common side effects include diarrhea, skin rash, and itching. More serious side effects, such as neutropenia (low white blood cell count), thrombotic thrombocytopenic purpura (TTP), and aplastic anemia, are rare but can be life-threatening.

Due to the risk of serious side effects, ticlopidine is usually reserved for use in patients who cannot tolerate or have failed other antiplatelet therapies, such as aspirin or clopidogrel. It is important to monitor patients taking ticlopidine closely for signs of adverse reactions and to follow the prescribing instructions carefully.

Quinazolinones are a class of organic compounds that contain a quinazolinone core structure. Quinazolinone is a heterocyclic compound made up of a quinazoline ring fused to a ketone group. This structure contains nitrogen atoms at positions 1, 3, and 9 of the fused benzene and pyridine rings.

Quinazolinones have various biological activities, including anti-cancer, anti-malarial, anti-inflammatory, and kinase inhibitor properties. They are used as building blocks in the synthesis of pharmaceuticals and other organic compounds. Some drugs containing quinazolinone moieties include the chemotherapy agent gefitinib (Iressa) and the antimalarial drug chloroquine.

It is important to note that Quinazolinones are not a medication themselves, but rather a class of organic compounds with various potential medical applications.

Purinergic P2Y12 receptors are a type of G protein-coupled receptor that bind to and are activated by adenosine diphosphate (ADP). These receptors play an important role in regulating platelet activation and aggregation, which is crucial for the normal hemostatic response to vascular injury.

The P2Y12 receptor is a key component of the platelet signaling pathway that leads to the activation of integrin αIIbβ3, which mediates platelet aggregation. Inhibition of the P2Y12 receptor with drugs such as clopidogrel or ticagrelor is a standard treatment for preventing thrombosis in patients at risk of arterial occlusion, such as those with acute coronary syndrome or following percutaneous coronary intervention.

P2Y12 receptors are also expressed on other cell types, including immune cells and neurons, where they play roles in inflammation, neurotransmission, and other physiological processes.

Thiophenes are organic compounds that contain a heterocyclic ring made up of four carbon atoms and one sulfur atom. The structure of thiophene is similar to benzene, with the benzene ring being replaced by a thiophene ring. Thiophenes are aromatic compounds, which means they have a stable, planar ring structure and delocalized electrons.

Thiophenes can be found in various natural sources such as coal tar, crude oil, and some foods like onions and garlic. They also occur in certain medications, dyes, and pesticides. Some thiophene derivatives have been synthesized and studied for their potential therapeutic uses, including anti-inflammatory, antiviral, and antitumor activities.

In the medical field, thiophenes are used in some pharmaceuticals as building blocks to create drugs with various therapeutic effects. For example, tipepidine, a cough suppressant, contains a thiophene ring. Additionally, some anesthetics and antipsychotic medications also contain thiophene moieties.

It is important to note that while thiophenes themselves are not typically considered medical terms, they play a role in the chemistry of various pharmaceuticals and other medical-related compounds.

Hemorrhage is defined in the medical context as an excessive loss of blood from the circulatory system, which can occur due to various reasons such as injury, surgery, or underlying health conditions that affect blood clotting or the integrity of blood vessels. The bleeding may be internal, external, visible, or concealed, and it can vary in severity from minor to life-threatening, depending on the location and extent of the bleeding. Hemorrhage is a serious medical emergency that requires immediate attention and treatment to prevent further blood loss, organ damage, and potential death.

Aspirin is the common name for acetylsalicylic acid, which is a medication used to relieve pain, reduce inflammation, and lower fever. It works by inhibiting the activity of an enzyme called cyclooxygenase (COX), which is involved in the production of prostaglandins, hormone-like substances that cause inflammation and pain. Aspirin also has an antiplatelet effect, which means it can help prevent blood clots from forming. This makes it useful for preventing heart attacks and strokes.

Aspirin is available over-the-counter in various forms, including tablets, capsules, and chewable tablets. It is also available in prescription strengths for certain medical conditions. As with any medication, aspirin should be taken as directed by a healthcare provider, and its use should be avoided in children and teenagers with viral infections due to the risk of Reye's syndrome, a rare but serious condition that can affect the liver and brain.

The platelet glycoprotein GPIIb-IIIa complex, also known as integrin αIIbβ3 or CD41/CD61, is a heterodimeric transmembrane receptor found on the surface of platelets and megakaryocytes. It plays a crucial role in platelet aggregation and thrombus formation during hemostasis and pathological conditions such as arterial thrombosis.

The GPIIb-IIIa complex is composed of two non-covalently associated subunits, GPIIb (αIIb or CD41) and IIIa (β3 or CD61). Upon platelet activation by various agonists like ADP, thrombin, or collagen, the GPIIb-IIIa complex undergoes a conformational change that allows it to bind fibrinogen, von Willebrand factor, and other adhesive proteins. This binding event leads to platelet aggregation and the formation of a hemostatic plug or pathological thrombus.

Inhibition of the GPIIb-IIIa complex has been a target for antiplatelet therapy in the prevention and treatment of arterial thrombosis, such as myocardial infarction and stroke. Several pharmacological agents, including monoclonal antibodies and small molecule antagonists, have been developed to block this complex and reduce platelet aggregation.

A randomized controlled trial (RCT) is a type of clinical study in which participants are randomly assigned to receive either the experimental intervention or the control condition, which may be a standard of care, placebo, or no treatment. The goal of an RCT is to minimize bias and ensure that the results are due to the intervention being tested rather than other factors. This design allows for a comparison between the two groups to determine if there is a significant difference in outcomes. RCTs are often considered the gold standard for evaluating the safety and efficacy of medical interventions, as they provide a high level of evidence for causal relationships between the intervention and health outcomes.

Treatment outcome is a term used to describe the result or effect of medical treatment on a patient's health status. It can be measured in various ways, such as through symptoms improvement, disease remission, reduced disability, improved quality of life, or survival rates. The treatment outcome helps healthcare providers evaluate the effectiveness of a particular treatment plan and make informed decisions about future care. It is also used in clinical research to compare the efficacy of different treatments and improve patient care.

... is often listed with thienopyridine inhibitors and has similar indications for use but is not a thienopyridine. It is a cyclo- ... Thienopyridines are a class of selective, irreversible ADP receptor/P2Y12 inhibitors used for their anti-platelet activity. ... Angiolillo DJ, Bates ER, Bass TA (August 2008). "Clinical profile of prasugrel, a novel thienopyridine". Am. Heart J. 156 (2 ... v t e (Articles with short description, Short description matches Wikidata, Thienopyridines, All stub articles, Blood and blood ...
Thienopyridine therapy is recommended by the American Heart Association (AHA) and the American College of Cardiology (ACC) for ... Thienopyridines also are recommended by the American Heart Association (AHA) and the American College of Cardiology (ACC) for ... However, patients should restart thienopyridine therapy as soon as possible after the procedure because of the risk of late- ... For patients treated with a drug-eluting stent who are undergoing procedures for which thienopyridine therapy must be ...
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ACCF/ACG/AHA 2010 Expert Consensus Document on the concomitant use of proton pump inhibitors and thienopyridines: a focused ... design and baseline characteristics including a meta-analysis of the effects of thienopyridines in vascular disease. Eur Heart ...
Thienopyridines inhibit platelet aggregation for the lifetime of the platelet (7-10 days), so withholding a dose will not be ... Thienopyridines, including prasugrel, increase the risk of bleeding. With the dosing regimens used in TRITON-TIMI 38, TIMI ( ... For patients who received their last dose of thienopyridine within 4 to 7 days prior to CABG, the frequencies decreased to 11.3 ... For patients receiving a thienopyridine within 3 days prior to CABG, the frequencies of TIMI Major or Minor bleeding were 26.7 ...
... while thienopyridines were prescribed in almost all PCI patients and in very few CABG patients. Fewer patients with ...
Thienopyridines *Ticlopidine *Clopidogrel 80. (No Transcript) 81. Clopidogrel *Slightly more effective than aspirin ...
Clopidogrel, a thienopyridine, is a prodrug, which is converted to active thiol metabolites by hepatic cytochrome P450 after ... Thienopyridines in cardiovascular disease: focus on clopidogrel resistance. Thromb Haemost 2007;97:385-93. ... consisting of aspirin and a thienopyridine, has been used for more than a decade because aspirin monotherapy turned out to be ...
P2Y12 inhibitors (thienopyridines), including Plavix, increase the risk of bleeding.. P2Y12 inhibitors (thienopyridines), ... Plavix (clopidogrel tablets) is a thienopyridine class inhibitor of P2Y12 ADP platelet receptors. Chemically it is methyl (+)-( ... 5.5 Cross-Reactivity among Thienopyridines. Hypersensitivity including rash, angioedema or hematologic reaction has been ... including patients with a history of hypersensitivity or hematologic reaction to other thienopyridines [see Contraindications ( ...
Along with aspirin, many new antiplatelet agents including thienopyridines have been used clinically. All thienopyridines ... Ticlopidine, the first thienopyridine to be introduced, stepped out of the limelight largely because of its unacceptable side ... Thienopyridines are converted to active metabolites (Figure 1) that bind irreversibly to P2Y12 receptors on platelets and ... Prasugrel: a novel thienopyridine antiplatelet agent. A review of preclinical and clinical studies and the mechanistic basis ...
Dual antiplatelet therapy with aspirin plus thienopyridines has become the standard treatment of patients undergoing coronary ... I. Porto, S. Giubilato, G. L. De Maria, L. M. Biasucci, and F. Crea, "Platelet P2Y12 receptor inhibition by thienopyridines: ... Severe neutropenia has been reported as a rare adverse effect of thienopyridines, usually occurring from four weeks to three ... Dual antiplatelet therapy with aspirin plus thienopyridines has become the standard treatment of patients undergoing coronary ...
In the TRITON TIMI-38 trial, prasugrel, a more potent thienopyridine P2Y12 inhibitor, proved more effective than clopidogrel in ... ACCF/ACG/AHA 2010 Expert Consensus Document on the concomitant use of proton pump inhibitors and thienopyridines: a focused ... design and baseline characteristics including a meta-analysis of the effects of thienopyridines in vascular disease. Eur Heart ...
Thienopyridines inhibit platelet aggregation for the lifetime of the platelet (7-10 days), so withholding a dose will not be ... Thienopyridines, including Effient, increase the risk of bleeding. With the dosing regimens used in TRITON-TIMI 38, TIMI ( ... Discontinue thienopyridines, including Effient, for active bleeding, elective surgery, stroke, or TIA. The optimal duration of ... For patients who received their last dose of thienopyridine within 4 to 7 days prior to CABG, the frequencies decreased to 11.3 ...
Subject has known hypersensitivity or contraindication to thienopyridines. *Subject is currently taking a P2Y12 inhibitor (See ...
An inactive thienopyridine prodrug, is metabolized in the liver by CYP3A to an active metabolite. A potential interaction ...
Discontinue thienopyridines: 7 days for clopidogrel; 14 days for ticlopidine. Avoid neuraxial techniques after GP IIb IIIa ... Discontinue thienopyridines: 7 days for clopidogrel; 14 days for ticlopidine. Avoid neuraxial techniques after GP IIb IIIa ...
Thienopyridines such as clopidogrel, ticagrelor, and prasugrel are currently used in clinical practice for secondary prevention ...
Scientists at Sanofi Pharmaceuticals l synthesize thienopyridines, leading to the development of clopidogrel. ...
Background: Prasugrel is a potent thienopyridine that may be preferentially used in younger patients with lower bleeding risk. ... were adjusted using multivariable Cox regression for age-related risks and propensity score stratification for thienopyridine ...
Antiplatelet therapies: aspirin / thienopyridines/ glycoprotein Iib/IIIa receptor inhibitors.. Antithrombin drugs: LMWH, ...
P2Y12 inhibitors (thienopyridines), including clopidogrel, inhibit platelet aggregation for lifetime of platelet (7-10 days); ... Use caution or avoid in patients with hypersensitivity or hematologic reactions to previous thienopyridine use, including ... Allergic cross-reactivity including rash, angioedema, or hematologic reaction among thienopyridines (eg, ticlopidine, prasugrel ... thienopyridines such as prasugrel); or if you have any other allergies. This product may contain inactive ingredients, which ...
Synthesis and Reactions of New Thienopyridines, Pyridothienopyrimidines and Pyridothienotriazines. E. A. Bakhite, A. E. Abdel- ... Keywords: Thienopyridines, Pyrimidines, Triazines DOI: https://doi.org/10.5012/bkcs.2002.23.12.1709 ...
It is part of a class of medications known as thienopyridines. It works by preventing platelets from clumping together and ...
For example, there are variations in the durations of dual antiplatelet therapy tested, as well as different thienopyridine ... noting that the strongest predictor of stent thrombosis is stopping thienopyridine therapy within six months of stent ...
TAXUS DES Trials Results: How Long Should Thienopyridine Be Used After Drug Eluting Stent?. November 6, 2007 ... AudioMedica News TAXUS DES Trials Results: How Long Should Thienopyridine Be Used After Drug Eluting Stent? Play Episode Pause ...
Biotransformation of Prasugrel, a Novel Thienopyridine Antiplatelet Agent, to the Pharmacologically Active Metabolite Katsunobu ... Biotransformation of Prasugrel, a Novel Thienopyridine Antiplatelet Agent, to the Pharmacologically Active Metabolite Katsunobu ... Biotransformation of Prasugrel, a Novel Thienopyridine Antiplatelet Agent, to the Pharmacologically Active Metabolite Katsunobu ... Biotransformation of Prasugrel, a Novel Thienopyridine Antiplatelet Agent, to the Pharmacologically Active Metabolite Katsunobu ...
Ticagrelor, Cangrelor and Enilogrel represent the last generation of thienopyridines. This review is focused on the effects of ... The first family of adenosine diphosphate P2Y12 receptors inhibiting drug is represented by thienopyridines and among these ... The second generation of thienopyridines is represented by clopidogrel that has replaced ticlopidine in the clinical practice; ...
The oral thienopyridines, clopidogrel and prasugrel, are nondirect agents that irreversibly block the platelet ADP P2Y12 ... Therefore, the switch from ticagrelor to a thienopyridine theoretically would be best done with a loading dose followed by a ...
3. About 90% of the thienopyridine-treated patients received clopidogrel. Do you think the results (i.e., no significant ...

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