This segment focuses on developing therapies for neurodegenerative diseases such as Huntington's disease and amyotrophic lateral sclerosis (ALS). Annexon's approach involves targeting C1q, a key initiating molecule in the classical complement pathway, to prevent complement-mediated neurodegeneration. Research and development efforts are directed towards ANX005, a monoclonal antibody currently in Phase II clinical trials for Huntington's disease and ALS. The goal is to reduce synapse loss and neuronal damage by inhibiting C1q activity. This segment aims to provide innovative treatments that can slow disease progression and improve the quality of life for patients with these devastating conditions. Future opportunities include expanding the application of C1q inhibition to other neurodegenerative disorders and exploring combination therapies.

This segment is dedicated to the development of therapies for autoimmune diseases, including Guillain-Barré syndrome (GBS) and warm autoimmune hemolytic anemia (WAIHA). Annexon's lead product candidate, ANX005, is in Phase II/III clinical trials for GBS and Phase II trials for WAIHA. The therapeutic strategy involves blocking C1q to prevent the initiation of the classical complement pathway, which is implicated in the pathogenesis of these autoimmune disorders. Research and development activities include evaluating the safety and efficacy of ANX005 in reducing disease severity and improving patient outcomes. Additionally, ANX1502, an investigational oral small molecule, is being developed for the treatment of certain autoimmune indications. The segment aims to provide targeted therapies that can modulate the immune response and alleviate the symptoms of autoimmune diseases, offering new hope for patients with these chronic conditions.

This segment is focused on developing therapies for ophthalmic disorders, particularly geographic atrophy (GA). Annexon's product candidate, ANX007, is in Phase II clinical trials for the treatment of GA. The therapeutic approach involves inhibiting C1q to prevent complement-mediated damage to retinal cells, which is a key factor in the progression of GA. Research and development efforts are directed towards evaluating the safety and efficacy of ANX007 in slowing the progression of GA and preserving visual function. The segment aims to provide innovative treatments that can prevent vision loss and improve the quality of life for patients with GA. Future opportunities include exploring the application of C1q inhibition to other ophthalmic disorders and developing novel drug delivery methods to enhance therapeutic efficacy.