Impax Laboratories, Inc. (NASDAQ:IPXL) confirms that it has initiated a challenge of patents listed by Daiichi Sankyo, Inc. in connection with its WELCHOL ® (Colesevelam HCl) tablets, 625 mg. Impax filed its Abbreviated New Drug Application ("ANDA") containing a paragraph IV certification for a generic version of WELCHOL® with the U.S. Food & Drug Administration ("FDA"). Following receipt of the notice from the FDA that Impax's ANDA had been accepted for filing, Impax notified the New Drug Application holder and patent owners of its paragraph IV certification. On January 14, 2010, Daiichi Sankyo, Inc. and Genzyme Corporation filed suit for patent infringement against Impax in the United States District Court for the District of Delaware. This action formally initiates the patent challenge process under the Hatch-Waxman Act. Based on the filing date of the ANDA, the Company believes that it is the first to file an ANDA with a paragraph IV certification and expects to be entitled to 180 days of market exclusivity.
Tekmira Pharmaceuticals Corporation (TSX:TKM) announced that it has concluded its ApoB SNALP Phase 1 human clinical trial. ApoB SNALP is designed to reduce the production of apolipoprotein B (ApoB), a protein produced in the liver that plays a central role in cholesterol metabolism. Tekmira enrolled a total of 23 subjects in its Phase 1 clinical trial. Of the 23 subjects enrolled, 17 subjects received a single dose of ApoB SNALP at one of seven different dosing levels and six subjects received a placebo. The primary endpoints of the ApoB SNALP Phase 1 clinical trial were measures of safety and tolerability. ApoB SNALP was well tolerated overall in this study with no evidence of liver toxicity, which was the anticipated dose-limiting toxicity observed in preclinical studies. Of the two subjects treated at the highest dose level, one subject experienced flu-like symptoms consistent with stimulation of the immune system caused by the ApoB siRNA payload. The other subject treated at the highest dose level experienced no side effects.
High-density lipoprotein (HDL), known as "good" cholesterol, isn't as protective for people with type 2 diabetes, according to research reported in Circulation: Journal of the American Heart Association. HDL carries cholesterol out of the arteries, and high levels are associated with a lower risk of heart disease. HDL also helps protect blood vessels by reducing the production of damaging chemicals, increasing the vessels' ability to expand, and repairing damage to the vessel lining. Researchers at the University Hospital Zurich and the Medical School of Hannover in Germany and Switzerland compared the vessel-protecting action of HDL taken from 10 healthy adults with that of 33 patients who had type 2 diabetes and metabolic syndrome, a condition that includes having low HDL levels (under 40 mg/dL in men and 50mg/dL in women). The diabetes patients were taking cholesterol-lowering medication. In laboratory testing, investigators found that the protective benefits on blood vessels were "substantially impaired" in HDL from the diabetic patients.
Although seen as a potential heart disease therapy, raising high-density lipoprotein (HDL) cholesterol levels by inhibiting activity of a transfer protein may not be effective, a new study suggests. Scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging (USDA HNRCA) at Tufts University and Boston University School of Medicine found an association between low plasma cholesterol ester transfer protein (CETP) activity and increased risk of heart disease in the Framingham Heart Study population. CETP is a protein that shuttles cholesterol throughout the body, thus controlling the levels of HDL, low-density lipoprotein (LDL), and very-low-density lipoprotein (VLDL) in the blood. "Our findings differ from studies suggesting that inhibiting CETP activity would bring a cardiovascular benefit by raising HDL, the so-called good cholesterol credited with lowering the risk of heart disease, " says senior author Jose Ordovas, PhD, director of the Nutritional Genomics Laboratory at the USDA HNRCA.
Special issue focuses on cardiovascular disease prevention and outcomes Emerging research on cardiovascular risk factors and treatment effects are helping clinicians gain a better understanding of which patients are most likely to benefit from close monitoring, lifestyle changes and/or additional therapeutic interventions. New findings published in the December 15/22, 2009, Prevention and Outcomes Focus Issue of the Journal of the American College of Cardiology aim to disentangle the influence of menopause versus chronological aging in upping women's post-menopausal risk for heart disease, evaluate the role of smoking status, physical activity and diet-induced weight loss in certain patient populations, and more fully describe the effects of intensive lipid-lowering therapy on subsequent cardiovascular events. Highlights from select studies published in the current issue of JACC find: Menopause Linked to Harmful Changes in Blood Cholesterol, But Not Other Cardiovascular Risk Factors Whether the jump in heart disease risk among post-menopausal women is a function of aging or a consequence of the menopausal transition and the associated loss of endogenous estrogen, or both, has been hotly debated.
New research shows a long-term benefit in screening people for CRP, a marker for inflammation, even if they have normal levels of bad cholesterol, because of increased long-term risk for heart attack, stroke and death. These findings, which will be published online today in the Journal of the American College of Cardiology (JACC), demonstrate that a very simple screening, age plus CRP, can identify individuals who may benefit from statin therapy. "This study builds on results from the landmark JUPITER trial, which showed that statins can prevent heart disease in people with normal LDL-c, or bad cholesterol, and an increased level of CRP, " said Dr. Christie Ballantyne, director of the Center for Cardiovascular Disease Prevention at the Methodist DeBakey Heart & Vascular Center and last author on the study. "We have demonstrated that the cardiovascular disease event rates persist over time, validating that the risks identified in the JUPITER trial persist for nearly seven years.
The first genetic historical map of the Han Chinese, the largest ethnic population in the world, as they migrated from south to north over evolutionary time was published online by the American Journal of Human Genetics by scientists at the Genome Institute of Singapore (GIS). Based on genome-wide DNA variation information in over 6, 000 Han Chinese samples from 10 provinces in China, this new map provides information about the population structure and evolutionary history of this group of people that can help scientists to identify subtle differences in the genetic diversity of Asian populations. Understanding these differences may aid in the design and interpretation of studies to identify genes that confer susceptibility to such common diseases as diabetes in ethnic Chinese individuals. Understanding these differences also is crucial in exploring how genes and environment interact to cause diseases. With the genetic map, the GIS scientists were able to show that the northern inhabitants of China were genetically distinguishable from those in the south, a finding that seems very consistent with the Han Chinese's historical migration pattern.
How do fruit flies get high cholesterol and become obese? The same way as people do - by eating a diet that's too rich in fats. More importantly, according to two new studies led by a University of Utah human geneticist, fruit flies use the same molecular mechanisms as humans to help maintain proper balances of cholesterol and a key form of stored fat that contributes to obesity. The findings mean that as researchers try to learn more about the genetic and biological processes through which people regulate cholesterol and fat metabolism, the humble fruit fly, also called Drosophila, can teach humans much about themselves. "Not a lot is known about these regulatory mechanisms in people, " says Carl S. Thummel, Ph.D., professor of human genetics at the U of U School of Medicine and senior author on the two studies. "But we can learn a lot by studying metabolic control in fruit flies and apply what we learn to humans." High cholesterol and obesity, which affects an estimated 25 percent to 30 percent of the U.
Abbott Seeks FDA Approval Of New Dosage Strengths Of SIMCOR reg; niacin Extended-release simvastatin
Abbott has submitted a supplemental new drug application (sNDA) to the U.S. Food and Drug Administration (FDA) for two new dosage strengths of SIMCOR® , a cholesterol medication. SIMCOR is a fixed-dose combination of niacin extended-release and simvastatin. Abbott is seeking FDA approval for the following new dosage strengths of SIMCOR: 500/40 mg and 1000/40 mg (niacin extended-release/simvastatin). SIMCOR was approved by the FDA in February 2008 in the following strengths: 500/20 mg, 750/20 mg and 1000/20 mg. The original FDA approval was supported by results from the SEACOAST trial, which demonstrated efficacy and safety of SIMCOR up to doses of 2000/40 mg daily in patients with mixed dyslipidemia and type II hyperlipidemia. SIMCOR is a prescription medicine used along with diet in people who cannot control their cholesterol levels by diet and exercise alone. SIMCOR is approved to lower levels of elevated total cholesterol, LDL "bad" cholesterol and triglycerides, and to raise HDL "good" cholesterol.
The 2010 Avanti Award in Lipids, which recognizes outstanding research contributions in the area of lipid research, has been awarded to David W. Russell, the Eugene McDermott distinguished chair of molecular genetics at the University of Texas Southwestern Medical Center at Dallas. Russell will present an award lecture, titled "Oxysterols: Cholesterol Metabolites of Diverse Function in Mice and Men, " at 2:15 p.m. Sunday, April 25, at the 2010 annual meeting in Anaheim, Calif. Russell received his bachelor's degree in biology from the University of Texas at Austin in 1975 and a doctorate in chemistry from the University of North Carolina in 1980. He then moved on to the University of British Columbia as a Damon Runyon Cancer Research Foundation postdoctoral fellow, working with Nobel laureate Michael Smith before joining the faculty at UT-Southwestern in 1982. During his time at UT-Southwestern, Russell has emerged as a scientific leader in elucidating the enzymatic pathways responsible for the metabolic breakdown of cholesterol into other components such as sterol hormones, vitamins and bile acids.