Date: 2014-11-18
Type of information: Presentation of results at a congress
phase:
Announcement: presentation of results at the American Heart Association Scientific Sessions in Chicago
Company: CSL (Australia)
Product: CSL112
Action
mechanism: CSL112 is a novel formulation of apolipoprotein A-I (apoA-I), the primary functional component of high-density lipoprotein (HDL). It is purified from human plasma and reconstituted to form HDL particles suitable for intravenous infusion. Studies have shown that the infusion of CSL112 rapidly elevates markers of reverse cholesterol transport, a process by which cholesterol is removed from arteries and transported to the liver for clearance. CSL112 may offer a novel option for rapidly stabilizing atherosclerotic lesions and is being studied for reduction in the risk of early atherothrombotic events in acute myocardial infarction patients.
Disease: early recurrent cardiovascular events in post myocardial infarction patients
Therapeutic area: Cardiovascular diseases
Country:
Trial details:
Latest
news: * On November 18, 2014, CSL announced that two research studies have been presented at the American Heart Association Scientific Sessions in Chicago. These data provide further understanding of the mechanisms by which CSL112, a novel formulation of apolipoprotein A-1 (apoA-1), may reduce the high incidence of early recurrent cardiovascular events seen in post myocardial infarction patients. Early recurrent cardiovascular events are associated with high morbidity and mortality, and reducing early events is an important target for new therapies. Andreas Gille, M.D., Ph.D., CSL Head of Clinical and Translational Science Strategy, presented a poster session titled, CSL112 enhances cholesterol efflux equally in patients with high and low HDL functionality. Data pooled from studies in 93 healthy subjects and 44 patients with stable atherosclerotic disease showed that CSL112 caused strong and quantitatively similar elevation in cholesterol efflux, independent of baseline efflux activity. Patients with cardiovascular disease are known to have lower cholesterol efflux capacity, and these data suggest that CSL112 may effectively elevate efflux in patients with impaired HDL function.
The mechanism by which CSL112 rapidly increases cholesterol efflux capacity was the topic of a poster presentation by Svetlana Didichenko, Ph.D., CSL Senior Scientist, titled, Mechanism of HDL remodeling induced by CSL112. In vitro studies showed that infused CSL112 is rapidly remodeled to form pre-beta1 HDL, a type of HDL with superior cholesterol efflux capacity, and that this remodeling accounts for the immediate and robust increase in cholesterol efflux capacity observed upon infusion of CSL112.
