About ODYSSEYODYSSEY is the global Phase 3 trial program for investigational compound alirocumab. ODYSSEY currently comprises at least 12 clinical trials enrolling more than 23,000 patients with hypercholesterolemia in 2,000 study centers across North and South America, Europe, Australia, South Africa and Asia. The trials will evaluate alirocumab in combination with other lipid-lowering agents or as monotherapy across a broad patient population, including high cardiovascular risk patients with primary hypercholesterolemia, patients with primary hypercholesterolemia unable to tolerate statins, and patients with heterozygous familial hypercholesterolemia (HeFH) who are inadequately controlled by current lipid-modifying therapy. The primary study endpoint in the ODYSSEY trials (except ODYSSEY OUTCOMES) is mean percentage LDL-C reduction at 24 weeks. Several other lipid markers will be evaluated, and trials will continue up to 24 months. In ODYSSEY OUTCOMES, the primary endpoint is a composite of coronary heart disease (CHD) death, non-fatal MI, fatal and non-fatal ischemic stroke, and unstable angina requiring hospitalization. The ODYSSEY Phase 3 trials are designed to create options to help meet the needs of individual patients. Patients in the majority of ODYSSEY trials will receive a 75mg Q2w (once every two weeks) dose of alirocumab, and will only be up-titrated to 150mg Q2w if they do not show sufficient low-density lipoprotein cholesterol (LDL-C) lowering (to their target level based on risk) after 8 weeks. In addition, ODYSSEY CHOICE I is evaluating alirocumab dosed once every four weeks. All of the ODYSSEY trials, with the exception of ODYSSEY CHOICE I and ODYSSEY CHOICE II and ODYSSEY OUTCOMES, are fully enrolled. For more information on the ODYSSEY clinical trials, please visit http://www.odysseytrials.com or http://www.clinicaltrials.gov. About PCSK9 PCSK9 is known to be a determinant of circulating LDL levels, as it binds to LDL receptors resulting in their degradation so that fewer are available on liver cells to remove excess LDL-cholesterol from the blood. Moreover, traditional LDL-lowering therapies such as statins actually stimulate the production of PCSK9, which limits their own ability to lower LDL-cholesterol. Blocking the PCSK9 pathway is therefore a potentially novel mechanism for lowering LDL-cholesterol.