Non-specific Irreversible platelet cyclooxygenase inhibitor
(COX-1 and 2) via acetylation of serine residues → ↓formation PG precursors.
- Inhibits formation of thromboxane (TXA) → inhibit aggregation
- At higher doses prostacyclin (PFI2) synthesis also inhibited → vasoconstriction (but endothelium can regenerate COX)

Allosteric, reversible antagonist at P2Y12-R (an ADP receptor), preventing activation of glycoprotein IIb/IIIa→ prevents platelet crosslinking

Similar mechanism as tirofiban but monoclonal
antibody

Antagonises the GpIIb/IIIa
receptor, preventing the
binding of fibrinogen and
platelet crosslinking and
aggregation.

- PO. BA. 50%.
- 300mg Loading. 100mg maint.

BA=40%

85% protein binding, pKa 3

Vd 10L

- Converted to salicylic acid in GI mucosa and liver
- Hepatic conjugation (saturable)

Metabolized by CYP3A4

Platelet function
typically returns to
normal 24-48 hours after
infusion ceases

Limited metabolism in humans.

- Renal as salicylate

Platelet function
typically returns to
normal 24-48 hours after
infusion ceases

Excreted in urine and faeces, mostly
unchanged

- T1/2b 15~20 mins when first order
- Dur: 4-6 hrs. (Effect on platelet aggregation will last life of current cohort of platelets (7-10 days)

HL 1.9-2.2 hrs

Bleeding
Bronchospasm, Renal toxicity
Reye’s Syndrome, GI ulceration
Caution with other anticoagulants

Haemorrhage, thrombocytopenia, human antichimeric antibody development, allergic reaction

Haemorrhage
Difficulty reversing agent
Dose adjustment in renal impairment

Antiplatelet

Antiplatelet

Antiplatelet

Antiplatelet

COX inhibitor

ADP Receptor Antagonist - Thienopyridine

GP IIb/IIIA Inhibitor

GP IIb/IIIA Inhibitor

Level 1

Level 3

Level 3

Level 3

Platelet inhibition

Platelet inhibition

Platelet inhibition

Platelet inhibition