June 28, 2011 09:02 AM Eastern Daylight Time
- Phase 3 Studies HighlightInvestigational Drug’s Potential in Lowering Lp(a) and Reducing Necessity for Lipid-Apheresis -
PARIS & CARLSBAD, Calif.--(BUSINESS WIRE)--Genzyme, a Sanofi company (EURONEXT: SAN and NYSE: SNY), and Isis Pharmaceuticals Inc. (NASDAQ: ISIS) announced today that two additional analyses from phase 3 studies of mipomersen were presented at the 79th European Atherosclerosis Society (EAS) Congress.
“The findings presented at EAS highlight mipomersen’s potential to treat the unique needs of patients with severe forms of FH”
In a presentation entitled “Mipomersen, A First-in-Class ApoB Synthesis Inhibitor, Lowers Lp(a) in Patients with Heterozygous Familial Hypercholesterolemia (HeFH) and High Baseline Lp(a): Results from two Phase 3 studies,” Elisabeth Steinhagen-Thiessen, M.D., of the Lipid Ambulatory Clinic, University of Berlin, Germany, focused on the effects of mipomersen on elevated Lp(a) levels.
Lp(a) is an independent risk factor for heart disease and cardiovascular events. Elevated Lp(a) levels are recognized to have a strong genetic component and are particularly common in people with familial hypercholesterolemia (FH). The EAS consensus panel recommended screening and treatment for elevated Lp(a) in 2010, and the U.S.-based National Lipid Association’s expert panel on FH published guidance this year noting that having elevated Lp(a) levels places FH patients at very high cardiovascular risk.
Data from two randomized, placebo-controlled phase 3 trials in patients with HeFH showed that mipomersen reduced Lp(a), LDL-C, and other measures of atherogenic lipoproteins when added to existing lipid-lowering therapy. One study included 124 HeFH patients with CAD, and the other included 58 severe HeFH patients. All of the patients were already taking a maximally tolerated dose of a statin, as well as additional lipid-lowering drugs in most cases. Both trials met all of their primary, secondary and tertiary endpoints. In these trials, mipomersen decreased LDL-C by 28 and 36 percent compared with increases of 5 and 13 percent for placebo, respectively (both p<0.001), meeting primary endpoints in both studies.
In addition to evaluating percent reduction in LDL-C as their primary endpoints, both trials also evaluated percent reduction in Lp(a) as tertiary endpoints. Most patients in the two trials (71 and 62 percent) had elevated Lp(a) levels >20 mg/dl at baseline. Mipomersen decreased Lp(a) by a median 21 and 39 percent, compared with zero and five percent for the placebo groups (both p<0.001). Mipomersen lowered Lp(a) by