Newly-Created Company, LipimetiX, Focused on Peptide Therapeutics for High Risk Cardiovascular Patients
Company Led by Experienced Biotech Executives and Scientists Through Partnership of Two Companies
BOSTON, MA--(Marketwire - April 26, 2010) - Exponential Pharma Ventures LLC and Benu Biopharma, Inc. announced today that they have created a new company, LipimetiX LLC, to develop a series of peptides therapeutics that mimic the function of Apolipoprotein E (Apo E), focused on lipid-lowering treatments for high-risk cardiovascular patients. LipimetiX has initiated discussions with prospective venture capital investors and commercial pharmaceutical companies regarding its clinical development program.
The newly-created virtual company was formed under the leadership of experienced scientists and biotech business executives through a partnership between Benu BioPharma and Exponential Pharma Ventures. LipimetiX will focus on Acute Coronary Syndrome (ACS) and the treatment of patients with refractory hyperlipidemia due to genetic conditions. Benu's team of executives, experienced in cardiovascular drug development, are responsible for managing R&D, while Exponential is contributing corporate development and fundraising expertise.
The company's two lead product candidates, referred to as AEM-28 and AEM-18, are currently in late-stage preclinical development and have demonstrated, in animal models, selective non-HDL cholesterol clearance, excretion of excess cholesterol, and rapid restoration of vasorelaxation(1). These products may also qualify for orphan drug status, which would enable the proof-of-concept clinical studies for refractory hyperlipidemia to have a rapid development and regulatory path with minimal investment.
Dennis Goldberg, Ph.D., President and CEO of LipimetiX commented, "LipimetiX is managed by a team of seasoned and successful executives with specific experience in lipid metabolism and peptide-based drugs, and who are dedicated to the development of this technology with a well-defined path through manufacturing, pre-clinical and into early clinical development."
Dr. Goldberg continued, "Our approach is unlike any other therapy for high cholesterol. Rather than inhibiting liver functions to reduce cholesterol, AEM-28 corrects the receptor binding defects found in many patients and directly enhances the body's natural process of cholesterol elimination."
LipimetiX's peptide mimetics reconstitute reverse cholesterol transport, the process by which normal healthy individuals carry cholesterol-rich molecules back to the liver for processing. In several genetic conditions, defects in apolipoproteins or in liver receptors cripple this important process. The novel mechanism for the lead peptide, AEM-28, has been well characterized in animal models of type II and type III hyperlipidemia, where it caused selective removal of VLDL, ß-VLDL, and LDL from circulation while increasing the excretion of excess cholesterol. Due to its rapid effects on cholesterol and restoration of vasorelaxation, AEM-28 also holds promise for addressing ACS, which is responsible for almost 2 million hospitalizations yearly in the US.
Current treatment modalities for ACS focus on prevention of blood clots and interventions to reopen major arteries. There is, however, no treatment that rapidly reduces the unstable fatty lesions found in the distal vascular tree, and rapidly restores endothelial dependent vasorelaxation to allow expansion of the coronary arteries during increased oxygen demand.
"LipimetiX has an elegant approach to serious diseases that have proved intractable despite much research," said Mike Webb, Managing Director at Exponential. "We believe this novel technology provides a significant opportunity to better manage genetic hyperlipidemias and ACS."
LipimetiX has in-licensed these assets from The University of Alabama at Birmingham, including AEM-28, AEM-18, additional Apo E mimetics, and the related Ligand Replacement Therapy (LRT) technology. For more information, please visit www.lipimetix.com.
About Genetic Hyperlipidemias
Several conditions result in high blood concentrations of cholesterol due to a genetic disorder that prevents proper cholesterol metabolism. Patients with one of these conditions experience a markedly increased risk of premature cardiovascular diseases (CVD) and CVD-related death.
Type II hyperlipidemia, or familial hypercholesterolemia (FH), affects up to 1.5 million Americans and leads to life-threatening levels of LDL-cholesterol in more than 30,000. FH has two forms: homozygous (hoFH), where the same defective gene is inherited from both parents, or heterozygous (heFH), where the defective gene is inherited from only one parent, so that some function is preserved. The homozygous form is a very rare condition estimated to affect approximately one in a million people. Children with hoFH are at high risk for early coronary events and sudden death as young as age one. HeFH is more common, with a prevalence of approximately one in 500. Patients with heFH also experience elevated LDL-cholesterol and are at high risk for early coronary events. For undiagnosed or untreated heFH, the cumulative risk of a coronary heart disease (CHD) by age 60 years is 60-85% among men and 30-50% among women, with a mean age of onset of approximately 47 years.
Type III hyperlipidemia (broad beta disease, or familial dysbetalipoprotienemia) is due to homozygous ApoE2 alleles. The E2 variant of apolipoprotein E is defective in binding to receptors that normally clear harmful lipid particles called beta-VLDL from the circulation. One percent of the general population has the E2/E2 genotype, and development of the serious lipid disorder occurs in 1-5% of these predisposed individuals, triggered by secondary genetic, hormonal or environmental factors. This population is growing because of the increased incidence of known triggers such as obesity and diabetes.
About Acute Coronary Syndrome
ACS is an umbrella term used to cover any group of clinical symptoms compatible with acute myocardial ischemia. Acute myocardial ischemia is chest pain due to insufficient blood supply to the heart muscle that results from coronary artery disease (also called coronary heart disease). It includes unstable angina and heart attack. About 10-25% of patients with ACS experience a major cardiovascular event within the next 12 months. Approximately 2 million people are hospitalized with ACS in the US each year, with an annual cost of about $165 billion.
About Exponential Pharma Ventures
Exponential Pharma Ventures creates virtual new business enterprises to efficiently and quickly translate novel therapeutics into the clinic and then to clinical proof-of-concept. The firm leverages operating experience to match entrepreneurs, technologists, researchers, contract research organizations, and investors. For more information, visit www.exrxventures.com.
About Benu Biopharma, Inc.
Benu Biopharma, Inc. is a biopharmaceutical development management and consulting company. Benu contracts and manages service providers for virtual development efforts. With experienced executives as principals, Benu coordinates and controls the development of technology to achieve maximum value and efficiency. For more information, visit www.benubio.com.
ExponentialTM is a trademark of Exponential Pharma Ventures LLC. All rights reserved.
(1)Anti-inflammatory and recycling properties of an apolipoprotein mimetic peptide, Ac-hE18A-NH2. Geeta Dattaa, C. Roger Whiteb, Nassrin Dashtia, Manjula Chaddhaa, Mayakonda N. Palgunacharia, Himanshu Gupta b, Shaila P. Handattua, David W. Garbera, G.M. Anantharamaiaha, c. Atherosclerosis 208 (2010) 134-141
Apolipoprotein E Mimetic Peptide Dramatically Lowers Plasma Cholesterol and Restores Endothelial Function in Watanabe Heritable Hyperlipidemic Rabbits. Manjula Chaddha, Lijun Dai, Sandra H. Gianturco, William A. Bradley and G.M. Himanshu Gupta, C. Roger White, Shaila Handattu, David W. Garber, Geeta Datta, Manjula Chaddha, Lijun Dai, Sandra H. Gianturco, William A. Bradley and G.M. Circulation (2005);111;3112-3118
Effect of an arginine-rich amphipathic helical peptide on plasma cholesterol in dyslipidemic mice. David W. Garber, Shaila Handattu, Ibrahim Aslan, Geeta Datta, Manjula Chaddha, G.M. Anantharamaiah. Atherosclerosis 168 (2003) 229-237