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Annexon Announces Presentations Highlighting ANX007 Functional and Structural Differentiation in Geographic Atrophy at the Macula Society 48th Annual Meeting
Data Reinforce Neuroprotective Effect of C1q Blockade with ANX007 Against Inflammation and Neuronal Damage BRISBANE, Calif., Feb. 13, 2025 (GLOBE NEWSWIRE) --

About this update from Annexon, Inc.
[{"type":"text","content":"Data Reinforce Neuroprotective Effect of C1q Blockade with ANX007 Against Inflammation and Neuronal Damage\nBRISBANE, Calif., Feb. 13, 2025 (GLOBE NEWSWIRE) -- Annexon, Inc. (Nasdaq: ANNX), a biopharmaceutical company advancing a late-stage clinical platform of novel therapies for people living with devastating classical complement-mediated neuroinflammatory diseases of the body, brain, and eye, today announced presentations on ANX007 in geographic atrophy (GA) at the Macula Society 48th Annual Meeting being held February 12-15 in Charlotte Harbor, Florida. ANX007 is a first-in-kind, non-pegylated antigen-binding fragment (Fab) designed to block C1q locally in the eye with an intravitreal formulation. ANX007 is the only investigational therapy in GA to show significant vision preservation on the endpoints of best corrected visual acuity (BCVA) and low luminance visual acuity (LLVA), as well as significant preservation of central retinal photoreceptors necessary for visual acuity. Details of the presentations, which are available on the publications page of the company’s website, are as follows: “Impact of C1q Inhibition on Visual Acuity Protection and Central Subdomain Anatomical Preservation with ANX007 in the Phase 2 ARCHER Trial” Presenter: Dr. Rahul Khurana, Northern California Retina Vitreous Associates and UCSFDate/Time: Thursday, February 13, 2025, 8:05 am Eastern Time (ET) “C1q Inhibition Attenuates Microglia-Induced Neuronal Injury: Implications for GA and Neurodegenerative Diseases” Presenter: Dr. Eleonora Lad, MD, PhD, Duke Eye Center, North Carolina Date/Time: Thursday, February 13, 2025, 8:10 am ET About ANX007 and Phase 2 ARCHER TrialANX007 is an antigen-binding fragment (Fab) antibody designed as a first-in-kind therapeutic to selectively inhibit C1q, the initiating molecule of the classical complement pathway and a key driver of neurodegeneration. In advanced dry age-related macular degeneration (AMD) or geographic atrophy (GA), C1q binds to photoreceptor synapses, causing aberrant activation of the classical pathway with synapse loss, inflammation and neuronal damage that results in vision loss. Intravitreal administration of ANX007 fully stopped C1q and classical pathway activation. In animal models, the murine analog of ANX007 protected against loss of photoreceptor synapses and cells to preserve function. ANX...