Vitae Pharmaceuticals Announces Promising Data for VTP-4, Drug Candidate Advancing toward Clinical Testing for the Treatment of Atherosclerosis

Data Presentation at the Frontiers in Lipid Biology conference in Banff, Canada

FORT WASHINGTON, Pa.--(BUSINESS WIRE)--Sep 6, 2012 -Vitae Pharmaceuticals, a clinical?stage biopharmaceutical company discovering and developing novel, small molecule, best?in?class compounds, today announced the presentation of promising preclinical in vivo data for the Company’s Liver X Receptor (LXR) modulator, VTP-4, being studied for the treatment of atherosclerosis. VTP-4 is a potent and selective modulator of LXRβ, activation of which has been shown to stimulate reverse cholesterol transport (RCT), to decrease vascular inflammation and to provide protection in several in vivo models of atherosclerosis.

As presented today during the Frontiers in Lipid Biology conference in Banff, Canada, results from multiple studies and in multiple animal species demonstrate that oral administration of VTP-4 leads to significant, dose dependent increases in key biomarkers of reverse cholesterol transport (RCT). In mice, administration of VTP-4 resulted in significant increases of the ABCA1 biomarker with all doses tested. In another mouse study, VTP-4 showed significant increases in reverse cholesterol transport and cholesterol excretion compared to vehicle. In primates, VTP-4 demonstrated strong induction of RCT biomarkers at all doses tested.

RCT biomarker activity has been previously reported by other companies, however, those non-selective compounds have routinely experienced significant increases in plasma and liver triglycerides. Uniquely with VTP-4, the RCT biomarker effects in the primate study were observed at doses much lower (≥30X) than the doses that cause triglyceride elevations in the plasma or liver.

Vitae Chief Scientific Officer, Richard Gregg, M.D., commented, “Vitae has discovered a novel, potent LXRβ selective modulator that has demonstrated positive effects on biomarkers of reverse cholesterol transport in multiple preclinical models. VTP-4 has been shown to have positive biomarker effects at doses providing significant separation from doses that increase liver triglycerides, a historical challenge for this target.”

Dr. Gregg continued, “Based on these findings, we believe VTP-4 has great promise in activating RCT pathways for the chronic treatment of atherosclerotic disease. The preclinical data are highly encouraging, and our plan is to enter the clinic with VTP-4 in the first half of 2013.”

About Vitae Pharmaceuticals

Vitae Pharmaceuticals is a clinical?stage biopharmaceutical company discovering and developing a portfolio of novel, small molecule, best?in?class compounds that address important disease areas, including: chronic kidney disease, diabetes, Alzheimer’s disease and atherosclerosis. Vitae’s lead compound, VTP?27999, is a wholly owned, novel, potent and selective renin inhibitor offering the potential for superior renal protection in patients suffering from chronic kidney disease. Vitae is expert in structure?based drug discovery and combines a proprietary technical platform with the experience and insight of world class scientists to advance best?in?class compounds for high value, hard?to?drug targets. Vitae’s proprietary, discovery platform has clear advantages in creating and analyzing novel drug candidates that meet pre?defined physicochemical and biochemical characteristics. The accuracy and speed of this system has enabled Vitae to solve challenging targets in multiple therapeutic areas – discovering and advancing attractive compounds in a rapid and highly capital efficient manner. Vitae Pharmaceuticals is financed by leading corporate and venture capital investors; its last venture round was in 2004. Vitae’s 45 scientists are located in Fort Washington, Pennsylvania. For additional information, please visit the company’s website at www.vitaepharma.com.


Contacts
Media:
Burns McClellan on behalf of Vitae
Justin Jackson, 212-213-0006
jjackson@burnsmc.com

 


 

Posted: September 2012

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