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Annexon is pioneering a class of new complement medicines for patients with classical complement-mediated disorders of the body, brain and eye. We are conducting ongoing clinical trials in multiple serious autoimmune, neurodegenerative and ophthalmic diseases.

INNOVATIVE PORTFOLIO OF DRUG candidates advancing for diseases of high unmet need

Franchise

Candidate

Preclinical

Phase 1

Phase 2

Phase 2/3

Autoimmune

ANX005 (IV)

ANX009 (SC)

ANX1502 (oral)

Guillain-Barré Syndrome (GBS)

Warm Autoimmune Hemolytic Anemia (wAIHA)

Lupus Nephritis (LN)*

Autoimmune

Guillain-Barré Syndrome (GBS) is a severe disease resulting from an autoantibody attack on the peripheral nerves, triggering the complement cascade (C1q) and causing neurodegenerative and cognitive impairment. Annexon’s clinical-stage investigational monoclonal antibody, ANX005, is intended to treat patients with GBS. This novel therapy is formulated for intravenous (IV) administration and is designed to inhibit C1q and the entire classical complement pathway. ANX005 has received both Fast Track and Orphan Drug designations from the U.S. Food and Drug Administration for the treatment of GBS.

Warm autoimmune hemolytic anemia (wAIHA) develops due to an attack of autoantibodies and destruction of red blood cells (RBCs), resulting in anemia. In certain patients, the activation of the complement pathway (C1q) amplifies the destruction of RBCs. Annexon’s clinical-stage investigational monoclonal antibody, ANX005, is intended to treat patients with wAIHA – a mechanistically related disorder of GBS. This novel therapy is formulated for intravenous (IV) administration and is designed to inhibit C1q and the entire classical complement pathway.

Multifocal motor neuropathy (MMN) is a devastating IgM autoantibody complement-mediated disease, resulting in muscle weakness that is chronic and progressive without any remission. There is a notable overlap in disease pathology to GBS, providing Annexon with the opportunity to translate our operational experience and biomarker research from GBS to MMN. Annexon’s clinical-stage investigational monoclonal antibody, ANX005, builds on this research to treat people with MMN. This novel therapy is formulated for intravenous (IV) administration and is designed to inhibit C1q and the entire classical complement pathway.

Lupus nephritis (LN) is a severe and life-threatening nephritic disease characterized by autoantibody-driven activation of C1q and the classical complement pathway. Endogenous pathogenic anti-C1q antibodies (PACAs) occur in the majority of patients with LN and have been shown to correlate with classical complement activation and disease activity. Annexon’s clinical-stage investigational drug candidate, ANX009, is a subcutaneously administered antigen-binding fragment (Fab) that disrupts autoantibody complement activation. It is being developed for the treatment of antibody-mediated autoimmune diseases of blood and vascular tissues.

ANX1502 is one of Annexon’s next generation, preclinical drug candidates. ANX1502 is an oral small molecule for autoimmune disorders.

Neuro
degeneration

ANX005 (IV)

ANX105 (IV)

Huntington’s Disease (HD)

Amyotrophic Lateral Sclerosis (ALS)

Neuro

Huntington’s disease (HD) is a progressive movement disorder, resulting in dementia and psychosis driven by the activation of the classical complement pathway. C1q is recognized as a major driver of synaptic loss and neurodegeneration. Annexon’s clinical-stage investigational monoclonal antibody, ANX005, targets aberrant C1q activity in complement-mediated neurodegenerative disorders like HD. This novel therapy is formulated for intravenous (IV) administration and is designed to inhibit C1q and the entire classical complement pathway.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the progressive weakness of the limb and respiratory muscles. Aberrant C1q activity potentially drives synaptic loss, resulting in this disability. Annexon’s clinical-stage investigational monoclonal antibody, ANX005, targets both central and peripheral nervous system aspects of ALS. This novel therapy is formulated for intravenous (IV) administration and is designed to inhibit C1q and the entire classical complement pathway.

ANX105 is one of Annexon’s next generation, preclinical drug candidates. ANX105 is a monoclonal antibody formulated for IV administration in neurodegenerative disorders.

Ophthalmology

ANX007 (IVT)

Geographic Atrophy (GA)

Geographic atrophy (GA) is an advanced form of dry, age-related macular degeneration (AMD) of the retina and is a chronic, progressive disease of the macula that results in loss of central vision. Excess classical complement activity in the retina is a key driver of GA. Annexon’s ANX007 is a clinical-stage investigational monoclonal antibody antigen-binding fragment (Fab) formulated for intravitreal (IVT) administration. ANX007 involves a differentiated neuroprotective approach designed to protect photoreceptor cells and retinal function by blocking C1q and the entire classical pathway, while allowing for normal immune activity of the lectin and alternative complement pathways.

IV, intravenous; IVT, intravitreal; SC, subcutaneous.
*Newly announced indications

STOP COMPLEMENT-MEDIATEDDISEASES AT THE START

INNOVATIVE PORTFOLIO OF DRUG candidates advancing for diseases of high unmet need

STOP COMPLEMENT-MEDIATED
DISEASES AT THE START