NGM Bio Announces Upcoming Oral Presentation of Phase 1 Study of NGM621 in Patients with Geographic Atrophy at Angiogenesis, Exudation, and Degeneration 2021 - Virtual Edition
--Humanized IgG1 monoclonal antibody engineered to potently inhibit complement C3, with the potential for extended every eight-week dosing--
--CATALINA Phase 2 study of NGM621 in patients with geographic atrophy (GA) currently underway--
SOUTH SAN FRANCISCO, Calif., Feb. 09, 2021 (GLOBE NEWSWIRE) -- NGM Biopharmaceuticals, Inc. (Nasdaq: NGM), a biotechnology company focused on discovering and developing transformative therapeutics for patients, today announced that additional data from its Phase 1 study of NGM621, an anti-complement C3 antibody, will be featured in an oral presentation at the Angiogenesis, Exudation, and Degeneration 2021 – Virtual Edition.
Details of the presentation are as follows:
Abstract Title: Inhibition of Complement C3 in Geographic Atrophy with NGM621: Phase 1 Study Results
Presenter Author: Charles C. Wykoff, M.D., Ph.D., Director of Research at Retina Consultants Houston and the Greater Houston Retina Research Foundation
Date and Time: Feb. 12, 2021 at 11:15 AM ET
The presentation will be available on the NGM Bio website at
About NGM621 and Complement C3 Inhibition
NGM621 is a humanized IgG1 monoclonal antibody engineered to potently inhibit complement C3, with the potential for extended every eight-week dosing without pegylation. In preclinical models, NGM621’s high affinity binding to C3 has demonstrated the potential for potent C3 inhibition. Preclinical data also suggest that NGM621 may not exacerbate choroidal neovascularization (CNV); the human translation of this observation is being investigated in the ongoing CATALINA Phase 2 clinical trial. C3 is a key component of the complement system, which helps orchestrate the body’s response to infection and maintains tissue homeostasis. The complement cascade can be activated through its three distinct pathways – classical, lectin and alternative – all of which converge to activate C3. When this cascade is dysregulated, the immune response may lead to the development and progression of GA. Inhibition of C3 represents a promising therapeutic approach that broadly inhibits downstream effector functions triggered by the excessive activation of C3, including inflammation, activation of the adaptive immune system, opsonization (the marking of a pathogen to be destroyed by phagocytes, a type of immune cell), phagocytosis and cell lysis (cell death).