| Indication |
Used for the treatment of pulmonary arterial hypertension. |
| Pharmacodynamics |
Iloprost is a synthetic analogue of prostacyclin PGI2. Iloprost
dilates systemic and pulmonary arterial vascular beds. It also affects
platelet aggregation but the relevance of this effect to the treatment
of pulmonary hypertension is unknown. The two diastereoisomers of
iloprost differ in their potency in dilating blood vessels, with the 4S
isomer substantially more potent than the 4R isomer. |
| Mechanism of action |
Iloprost is a second generation structural analog of prostacyclin
(PGI) with about ten-fold greater potency than the first generation
stable analogs, such as carbaprostacyclin. Iloprost binds with equal
affinity to human prostacyclin (Prostanoid IP) and prostaglandin EP1
receptors. Iloprost constricts the ilium and fundus circular smooth
muscle as strongly as prostaglandin E2 (PGE2) itself. Iloprost inhibits
the ADP, thrombin, and collagen-induced aggregation of human platelets.
In whole animals, iloprost acts as a vasodilator, hypotensive,
antidiuretic, and prolongs bleeding time. All of these properties help
to antagonize the pathological changes that take place in the small
pulmonary arteries of patients with pulmonary hypertension. |
| Absorption |
Rapidly absorbed with bioavailability of 63% |
| Volume of distribution |
|
| Protein binding |
60% |
| Metabolism |
Primarily hepatic. Iloprost is metabolized principally via beta-oxidation of the carboxyl side chain. |
| Route of elimination |
Not Available |
| Half life |
20-30 minutes |
| Clearance |
- 20 mL/min/kg [Normal subjects]
|
| Toxicity |
Overdoses can lead to hypotension, headache, flushing, nausea, vomiting, and diarrhea. |
