| Indication |
For treatment, in combination with heparin, of acute coronary
syndrome, including patients who are to be managed medically and those
undergoing PTCA or atherectomy. |
| Pharmacodynamics |
Tirofiban prevents the blood from clotting during episodes of
chest pain or a heart attack, or while the patient is undergoing a
procedure to treat a blocked coronary artery. It is a non-peptide
antagonist of the platelet glycoprotein (GP) IIb/IIIa receptor, and
inhibits platelet aggregation. When administered intravenously,
tirofiban inhibits ex vivo platelet aggregation in a dose- and
concentration-dependent manner. When given according to the recommended
regimen, >90% inhibition is attained by the end of the 30-minute
infusion. Tirofiban has been recently shown in patients with unstable
angina to reduce ischemic events at 48 hours following infusion when
compared to standard heparin therapy. |
| Mechanism of action |
Tirofiban is a reversible antagonist of fibrinogen binding to the
GP IIb/IIIa receptor, the major platelet surface receptor involved in
platelet aggregation. Platelet aggregation inhibition is reversible
following cessation of the infusion of tirofiban. |
| Absorption |
Not Available |
| Volume of distribution |
|
| Protein binding |
65% |
| Metabolism |
Metabolism appears to be limited. |
| Route of elimination |
It is cleared from the plasma largely by renal excretion, with
about 65% of an administered dose appearing in urine and about 25% in
feces, both largely as unchanged tirofiban. |
| Half life |
2 hours |
| Clearance |
- 213 – 314 mL/min [Healthy subjects]
- 152 – 267 mL/min [patients with coronary artery disease]
|
| Toxicity |
Not Available |
