ATC Group: B01AC Platelet aggregation inhibitors excl. heparin

Anatomical Therapeutic Chemical Classification System

Translations

Language
Translation
  English
Platelet aggregation inhibitors excl. heparin

Hierarchical Position

Level
Code
Title
4
B01AC
Platelet aggregation inhibitors excl. heparin

Contents

Code
Title
B01AC01
B01AC02
B01AC03
B01AC04
B01AC05
B01AC07
B01AC09
B01AC10
B01AC11
B01AC13
B01AC15
B01AC16
B01AC17
B01AC18
B01AC19
B01AC21
B01AC22
B01AC23
B01AC24
B01AC25
B01AC26
B01AC27
B01AC30

Active Ingredients

Chemical substance
Description

Abciximab is the Fab fragment of the chimeric monoclonal antibody 7E3. It is directed against the glycoprotein (GP) IIb/IIIa (╬▒IIb╬▓3) receptor located on the surface of human platelets. Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets.

Acetylsalicylic acid combines significant advantages such as strong anti-pyretic, analgesic and anti-inflammatory action, that is the measure of comparison with all the newer NSAIDs.

Cangrelor is a direct P2Y12 platelet receptor antagonist that blocks adenosine diphosphate (ADP)-induced platelet activation and aggregation in vitro and ex vivo. Cangrelor binds selectively and reversibly to the P2Y12 receptor to prevent further signalling and platelet activation.

Cilostazol and several of its metabolites are phosphodiesterase III inhibitors which suppress cyclic AMP degradation, resulting in increased cAMP in a variety of tissues including platelets and blood vessels. Studies in animals and in man (in vivo and ex vivo) have shown that cilostazol causes reversible inhibition of platelet aggregation.

Clopidogrel is a prodrug, one of whose metabolites is an inhibitor of platelet aggregation. Clopidogrel must be metabolised by CYP450 enzymes to produce the active metabolite that inhibits platelet aggregation.

Dipyridamole is an antithrombotic agent with antiplatelet activity. Dipyridamole has an antithrombotic action based on its ability to modify various aspects of platelet function, such as platelet aggregation, adhesion and survival, which are factors associated with the initiation of thrombus formation.

Epoprostenol sodium, the monosodium salt of epoprostenol, a naturally occurring prostaglandin produced by the intima of blood vessels. Epoprostenol is the most potent inhibitor of platelet aggregation known. It is also a potent vasodilator.

Eptifibatide is an inhibitor of platelet aggregation and belongs to the class of RGD (arginine-glycine-aspartate)-mimetics. Eptifibatide reversibly inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor and other adhesive ligands to the glycoprotein (GP) IIb/IIIa receptors.

Iloprost is a synthetic prostacyclin analogue. After inhalation of iloprost direct vasodilatation of the pulmonary arterial bed occur with consecutive significant improvement of pulmonary artery pressure, pulmonary vascular resistance and cardiac output as well as mixed venous oxygen saturation.

Prasugrel is an inhibitor of platelet activation and aggregation through the irreversible binding of its active metabolite to the P2Y12 class of ADP receptors on platelets. Since platelets participate in the initiation and/or evolution of thrombotic complications of atherosclerotic disease, inhibition of platelet function can result in the reduction of the rate of cardiovascular events such as death, myocardial infarction, or stroke.

Selexipag is a selective IP receptor agonist distinct from prostacyclin and its analogues. Selexipag is hydrolysed by carboxylesterases to yield its active metabolite, which is approximately 37-fold more potent than selexipag. Stimulation of the IP receptor by selexipag and the active metabolite leads to vasodilatory as well as anti-proliferative and anti-fibrotic effects.

Ticagrelor is an oral, direct acting, selective and reversibly binding P2Y12 receptor antagonist that prevents ADP-mediated P2Y12 dependent platelet activation and aggregation. Since platelets participate in the initiation and/or evolution of thrombotic complications of atherosclerotic disease, inhibition of platelet function has been shown to reduce the risk of CV events such as death, MI or stroke.

Tirofiban is a non-peptidal antagonist of the GP IIb/IIIa receptor, an important platelet surface receptor involved in platelet aggregation. Tirofiban prevents fibrinogen from binding to the GP IIb/IIIa receptor, thus blocking platelet aggregation.

Treprostinil is a vasodilator that is used for the treatment of pulmonary arterial hypertension. Treprostinil is a potent oral antiplatelet agent. The major pharmacologic actions of treprostinil are direct vasodilation of pulmonary and systemic arterial vascular beds and inhibition of platelet aggregation. Other studies have shown that treprostinil causes a dose-related negative inotropic and lusitropic effect. Treprostinil had high affinity for the Prostaglandin D2 receptor (DP1), Prostaglandin E2 receptor EP2 subtype (EP2) and Prostaglandin D2 receptor (IP) receptors (Ki 4.4, 3.6 and 32 nM, respectively), low affinity for EP1 and EP4 receptors and even lower affinity for EP3, Prostaglandin F (FP) and thromboxane (TP) receptors. Treprostinil has demonstrated a unique effect on PPAR gamma, a transcription factor important in vascular pathogenesis as a mediator of proliferation, inflammation and apoptosis.

Triflusal reduces thromboxan biosynthesis through irreversible inhibition of platelet cyclooxygenase, sparing prostacyclin biosynthesis because its effect on vascular cyclooxygenase at therapeutic doses is negligible.

Vorapaxar is a selective and reversible inhibitor of the PAR-1 receptors on platelets that are activated by thrombin.