“We are pleased to present these data at ASH, which further support our approach of targeting C1q in order to fully block the downstream components of the complement pathway,” said
Poster Title: Safety, Tolerability, and Clinical Pharmacology of ANX009, an Inhibitory Antibody Fab Fragment Against C1q, Administered Subcutaneously to
Data Summary: ANX009 is an antigen-binding fragment (Fab) that disrupts autoantibody complement activation through the inhibition of C1q. It is being developed as subcutaneously administered treatment for antibody-mediated autoimmune diseases of blood and vascular tissues. Data reported in the poster are from a single and multiple ascending dose Phase 1 trial of ANX009 in 48 healthy volunteers. Findings demonstrated that ANX009 was well-tolerated across all doses with no drug-related safety, dose-limiting toxicities, serious adverse events, or adverse events leading to discontinuations. Further, a dose-response was observed across dose cohorts with notable reductions in C1q in serum. Taken together, the findings support the clinical advancement of ANX009 in patients with complement-mediated autoimmune disorders.
Poster Title: Evidence of Classical Complement Pathway Involvement in a Subset of Patients with Warm Autoimmune Hemolytic Anemia (2001)
Data Summary: Autoimmune hemolytic anemia (AIHA) is a constellation of diseases caused by autoantibodies targeting red blood cells (RBCs) with or without complement activation, with the two main types being cold agglutinin disease (CAD) and wAIHA. To understand additional methods to suggest evidence of complement activation in AIHA patients,
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Source: Annexon Biosciences
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