CRESTWOOD, KY November 20, 2014 – Apellis Pharmaceuticals Inc.
Complement inhibition is the only mechanism thus far to show reductions in the growth of dry AMD. Potentia was the first company to develop a complement inhibitor for the treatment of AMD. APL-2 has the same mechanism of action as Potentia’s original drug compound but has a significantly improved half-life in the eye. APL-2 is in late preclinical development in ophthalmology and is expected to enter Phase II clinical testing in patients with AMD by the middle of 2015.
Cedric Francois, MD, PhD and CEO of Apellis commented, “We are delighted to be back in retinal drug development. Ophthalmology is a unique therapeutic area that is very dear to us. We have learned much about complement since our first venture in this area a decade ago, and have great hopes that complement inhibition will be the first effective treatment for patients with dry AMD.” Phil Rosenfeld, MD, a retinal specialist at Bascom Palmer and advisor to Apellis, added: “There’s overwhelming scientific and clinical evidence to suggest that complement inhibition should slow the progression of dry AMD. I’m optimistic that based on its mechanism of action and its target within the complement cascade, APL-2 offers us the best chance to help our AMD patients. “
Apellis is a clinical stage immunotherapy company and targets the complement pathways to correct auto-immune conditions. Apellis was spun out of Potentia Pharmaceuticals, the first company to test complement-inhibiting therapies in AMD. Apellis will seek to further explore the interface between complement and adaptive immunity in a range of indications, including paroxysmal nocturnal hemoglobinuria (PNH), AMD, chronic obstructive pulmonary disease (COPD), as well as graft-versus-host disease (GvHD), ABO-incompatible transplantation, periodontitis and ischemia reperfusion injury. www.apellis.com
APL-2 is a next-generation inhibitor of the class of compstatin derivatives with improved physicochemical properties. APL-2 is currently being tested in a number of Phase I clinical trials and has received Orphan Drug Designation from the FDA to treat PNH. APL-2 inhibits complement at the levels of complement factor C3, thus blocking all downstream effector pathways of the complement cascade.
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