Dr. RAGHU PRASADA M SMBBS,MDASSISTANT PROFESSORDEPT. OF PHARMACOLOGYSSIMS & RC.

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ADP receptor blockerCLOPIDOGRELTICLOPIDINE

COXinhibitor(Aspirin)

Phosphodiesteraseinhibitor-

DIPYRIDAMOLE,CILOSTAZOLE

Gb IIb/IIIareceptorblockers

ABCIXIMABEPTIFIBATIDE

TIROFIBAN

TXA2 receptorTERUTROBAN

Aspirin

N.B. Aspirin inhibits Thromboxane A2 & prostacyclin too, but the former is moreaffected because platelets don’t have nuclei can’t synthesize new enzymes for

next 7 daysplatelets life span

Most authorities recommend initial therapy with adose of 160 mg (one half-tablet) to 325 mg (oneadult tablet)

Aspirin should be crushed/chewed (to facilitatefaster absorption by breaking the enteric-coateddelayed release tablet

Prophylaxis against unstable angina Post MI Post stroke

Adverse effectsGI –ulcerationProlonged bleeding time↑ risk of hemorrhage

It is an inhibitor of phosphodiesterase III (PDEIII) enzyme

Vasodilator and inhibitor of platelet aggregation Initially approved for Intermittent claudication Indicated for the reduction of events

(myocardial infarction, stroke, and vasculardeath) in patients with atherosclerosisdocumented by recent stroke, recent MI orestablished peripheral arterial disease.

ABCIXIMAB is composed of 7E3 Fab fragments.derived from murine (mouse)Humanized monoclonal antibody.directed against glycoprotein receptor type GPIIb/IIIa.Mechanism: The m7E3 Fab binds selectively to theglycoprotein GPIIb/IIIa receptors inhibiting plateletaggregationPlasma T1/2- 30min Bolus –followed by slow IVAngioplasty, recurrent MIMajor side effect- bleeding, thrombocytopenia,bleeding

TIROFIBAN -non-peptic Synthetic arginine-glycine-aspartic acid (R-G-D) sequence mimetics. Hence, itblocks the binding of fibrinogen to glycoproteinGPIIb/IIIa receptorsThey are given intravenously for the reduction ofthrombotic complications during coronary angioplasty (ifthey are given orally they are toxic)Clinical trials showed reductions in the incidence ofdeath and non-fatal MI in response to the use oftirofiban.

Synthetic cyclic Peptide inhibitor of fibrinogenbinding site on Gp IIb/ 3a receptors on plateletsIt does not bind to receptors for vWFDuration of action : 30 – 45 minsShould be continued for 18-24 hoursSuperior to Abciximab for upstream useS/E-bleeding

TICLOPIDINE & CLOPIDOGRELThey inhibit irreversibly ADP binding to receptors

inhibit platelet aggregationNo effect on PG synthesisUsed in aspirin intolerant patients

Acts by in inhibiting phoshodiesterase enzyme

Incompletely absorbed from the gastrointestinaltract with peak plasma concentration occurringabout 75 minutes after oral administration

More than 90% bound to plasma proteins

A terminal half-life of 10 to 12 hours

Metabolised in the liver

Mainly excreted as glucuronides in the bile;a small amount is excreted in the urine

It is an inhibitor of phosphodiesterase III (PDE III)enzymeVasodilator and inhibitor of platelet aggregationIntermittent claudicationIndicated for the reduction of events (myocardialinfarction, stroke, and vascular death) in patients withatherosclerosis documented by recent stroke, recentMI or established peripheral arterial diseaseC/I- CHF patients

PrasugrelThienopyridineMore rapid onset of action than clopidogrelIrreversible inhibitor of the P2Y12 receptorBeneficial in the treatment and prevention of ACS

and the prevention of thromboembolic events

Adenosine Diphosphate-Receptor Antagonists

TicagrelorCyclo-pentyl-triazo-pyrimidine (CPTP)More rapid onset of action than clopidogrelReversible inhibitor of the P2Y12 receptor

Myocardial infarction Unstable angina Coronary bypass implants Prosthetic heart valves and arteriovenous shunts Venous thromboembolism and PVD Cerebrovascular transient ischemic attacks