Cicaprost (ZK 96480) is a potent prostacyclin receptor (IP) agonist, inducing artery relaxation through concentration-dependent mechanisms with an EC50 value of 5.8 nM [1].

Cicaprost significantly inhibits the proliferation of human pulmonary artery smooth muscle cells (HPASMC) that is induced by fetal bovine serum (FBS), exhibiting considerable antiproliferative effects at a concentration of 30 nM [2]. Additionally, it promotes the production of [3H]cyclic AMP and [3H]inositol phosphate, with half-maximal effective concentration (EC50) values ranging from 1.5 to 22 nM for the former and 49 to 457 nM for the latter, excluding effects on SK-N-SH cells [3]. In a Cell Proliferation Assay [2] using HPASMC, across a range of concentrations from 10 pM to 10 μM, Cicaprost displayed a dose-dependent reduction in cell proliferation, achieving an EC50 of 24.1 nM.

Cicaprost modifies pain perception and inflammatory responses by targeting the prostacyclin receptor; its absence in mice does not alter these effects. Specifically, intravenous administration of Cicaprost at a dosage of 1 μg/kg induces a significant decrease in blood pressure (approximately 30 mm Hg) in anesthetized wild-type mice. However, this hypotensive response is absent in IP-deficient mice, even when the dosage is increased to 10 μg/kg. This differential effect underscores the role of the prostacyclin receptor in mediating Cicaprost's cardiovascular activity.