OUR PATH TO DEVELOP CLINICAL-STAGE
Our pipeline is designed to block C1q and the entire classical complement pathway in a broad set of complement-mediated diseases. Our approach is based on our platform technology addressing well-researched classical complement-mediated autoimmune and neurodegenerative disease processes, both of which involve aberrant activation of C1q. Evidence suggests that potent and selective inhibition of C1q can prevent tissue damage in antibody-mediated autoimmune disease and protect against the loss of functioning synapses that drives cognitive and functional decline in complement-mediated neurodegeneration.
Our first product candidate, ANX005, is a full-length monoclonal antibody formulated for intravenous (IV) administration in autoimmune and neurodegenerative disorders. Our second product candidate, ANX007, is an antigen-binding fragment, or Fab, formulated for intravitreal (IVT) administration for the treatment of neurodegenerative ophthalmic disorders. We are also developing ANX009, an investigational, subcutaneous formulation designed for the treatment of systemic autoimmune diseases.
We have completed Phase 1b clinical trials for ANX005 and ANX007 in patients with Guillain-Barré Syndrome (GBS) and glaucoma, respectively. While the trials were not statistically powered for significance on the efficacy measures, both molecules were well-tolerated and showed full inhibition of C1q and the classical complement pathway.
We are utilizing a stepwise development strategy and a biomarker-led approach designed to increase the probability of technical success over shorter development timelines. Based on learnings from our initial trials, we are advancing our current programs while evaluating additional orphan and large market indications. We are also developing additional product candidates designed to inhibit C1q and other components of the early classical complement cascade with the goal of further broadening our portfolio. We have maintained worldwide rights to all of our novel C1q inhibitors.More About ANX005 More About ANX007