Carbaprostacyclin is a stable analog of PGI2. When infused in rabbits or dogs, it inhibits ex vivo platelet aggregation, but the effect persists only 10 minutes after termination of the infusion. This implies rapid metabolic inactivation of carbaprostacyclin. Carbaprostacyclin inhibits platelet aggregation with 10% of the molar potency exhibited by PGI2. The ED50 of carbaprostacyclin for the in vitro inhibition of ADP-induced platelet aggregation in human PRP is 47 nM. It was also shown to effect terminal differentiation of preadipose into adipose cells and enhance the expression of angiotensinogen and adipose fatty acid binding protein with an EC50 of about 0.5 µM.