CSL112 Found to Elevate Cholesterol Efflux in Patients with Coronary Artery Disease and Mechanism for Rapid Cholesterol Efflux Capacity Demonstrated

Two research studies presented today at the American Heart Association Scientific Sessions in Chicago 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 MI patients. Early recurrent cardiovascular events are associated with high morbidity and mortality, and reducing early events is an important target for new therapies.

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Two research studies presented today at the American Heart Association Scientific Sessions in Chicago 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 MI 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, M.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-β1 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.

“Both studies advance our understanding of the role of CSL112 in rapidly inducing cholesterol efflux, the first step in reverse cholesterol transport, and its potential to rapidly reduce early recurrent cardiovascular events in the post MI setting,” said Samuel Wright, Global Strategic Director of Cardiovascular Therapeutics, CSL Behring.


About CSL112 
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.

About CSL 
Headquartered in Melbourne, Australia, CSL Limited is a global biopharmaceutical company that develops, manufactures and markets biotherapies to prevent and treat rare and serious human diseases. CSL owns major facilities in Australia, Germany, Switzerland and the United States, and employs over 13,000 people in more than 27 countries. Visit www.csl.com.au for more information.

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Contacts:


Natalie de Vane
Senior Director, Communications
CSL Behring
O: 610-878-4468
 
Amanda Merced
Senior Account Supervisor
MCS Healthcare Public Relations
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Email:  amandam@mcspr.com