NAARDEN, Netherlands--(BUSINESS WIRE)--Dezima Pharma (‘Dezima’), the biotechnology company developing innovative drugs in the field of dyslipidemia, announced today the initiation of a double blind, placebo controlled, Phase 2b dose ranging study of DEZ-001 (previously TA-8995), alone and in combination with statins, in order to study the effects on a wide range of lipids and other biomarkers of cardiovascular disease (CVD) in patients with mild dyslipidemia.
“The start of the TULIP study is an exciting milestone for Dezima Pharma”
The TULIP (“TA-8995: its Use in patients with mild dysLIPidemia”) study will take place in specialized centres across Denmark and the Netherlands and will investigate the effects of different doses of DEZ-001 on established CVD biomarkers over a 3 month dosing period. DEZ-001 is a CETP inhibitor that has already demonstrated clinically relevant improvements on low-density lipoprotein (LDL) and high-density lipoprotein (HDL) levels as well as other lipid parameters in healthy volunteers.
Professor John Kastelein, Chief Scientific Officer and founder of Dezima, commented, “I am very pleased that the TULIP study has kicked off with this very promising new compound for patients with dyslipidemia. If successful, this trial will pave the way for larger scale Phase 3 pivotal clinical trials.”
“The start of the TULIP study is an exciting milestone for Dezima Pharma,” Rob de Ree, CEO of Dezima added. “Being the most potent CETP inhibitor in clinical development with excellent safety, pharmacokinetic and pharmacodynamic properties we firmly believe that our compound can further improve the outcome for patients suffering from cardiovascular disease due to dyslipidemia.”
Dezima Pharma was founded in 2012 by John J.P. Kastelein, Professor of Medicine at the Department of Vascular Medicine at the Academic Medical Centre, University of Amsterdam. The Company recently raised €14.2m from a Series A financing with participation of Forbion Capital Partners, BioGeneration Ventures and New Science Ventures, and a loan from the AgentschapNL, an agency of the Dutch Ministry of Economic Affairs. Dezima Pharma focuses on the development of novel products to treat dyslipidemic patients suffering from cardiovascular disease. Its lead program DEZ-001 involves the development of the CETP inhibitor TA-8995, which was in-licensed from Mitsubishi Tanabe Pharma Corporation.
About Dezima Pharma B.V.
Dezima Pharma was founded in 2012 by Prof. John Kastelein, Professor of Medicine at the Department of Vascular Medicine at the Academic Medical Center of the University of Amsterdam, The Netherlands, and financed by Forbion Capital Partners, BioGeneration Ventures and New Science Ventures, to develop novel products to treat dyslipidemic patients suffering from cardiovascular disease (CVD). The company’s lead product DEZ-001 (previously TA-8995) has been in-licenced from Mitsubishi Tanabe Pharma Corporation and is a potentially best-in-class CETP inhibitor. The company has an outstanding Scientific Advisory Board including world-leading experts in the dyslipidemia space such as Dr Philip Barter, Professor at The Heart Research Institute, Sydney, Australia, and Dr Bryan Brewer, Senior Research Consultant of Lipoprotein and Atherosclerosis Research at the Medstar Research Institute, Washington DC, USA.
About dyslipidemia and CETP inhibitors
Dyslipidemia is a generally asymptomatic disease in which serum lipid levels deviate from the normal level. It is considered to be a modifiable risk factor for cardiovascular disease due the direct relation with atherosclerosis. The market for dyslipidemic drugs, including statins, fish oils and fibrates, topped $25Bn in 2010. Though current treatment is relatively effective a high unmet need remains: about 60% of treated patients have a considerable chance of experiencing a cardiovascular event, which comes with significant morbidity and mortality.
The Cholesteryl Ester Transfer Protein (CETP) facilitates the transfer of cholesterol from HDL to other lipoproteins including LDL, in exchange for triglycerides. The CETP mediated transfer of cholesterol into LDL particles results into maturation of those LDL particles to more atherogenic LDL particles, which contribute to macrophage foam cell, and eventually plaque formation. Large Mendelian Randomization studies, epidemiological as well as preclinical studies have provided evidence for the notion that CETP activity is inversely related to cardiovascular mortality and reduced activity of CETP by pharmaceutical means or by naturally occurring mutations in the CETP gene results in increased HDL and decreased LDL levels. This provides a rationale for inhibition of CETP activity as a therapeutic intervention in dyslipidemic conditions characterized by either low HDL or high LDL cholesterol.