Stop the start of disease
Our platform technology addresses two disease processes involving C1q.
C1q is the initiating molecule of the classical complement pathway, a powerful inflammatory cascade. When functioning normally, C1q works within the immune system to clear pathogens, damaged cells, and unwanted cellular components. Functioning within the brain, C1q helps to sculpt neuronal pathways during development by “pruning” weaker synapses away from neurons, reinforcing stronger synapses to make appropriate neuronal connections.
In contrast to its normal function, aberrant activation of C1q can trigger tissue destruction and disease. Annexon is focused on two distinct disease processes involving C1q, that underlie pathology in autoimmune and neurodegenerative disorders. In antibody-mediated autoimmune disease, C1q amplifies the activity of self-reactive antibodies to cause tissue damage. In neurodegenerative disorders, C1q drives the loss of synapses in the central nervous system causing progressive neuronal damage. Human genetics link classical complement components to neurodegeneration in both the brain and eye.
C1q inhibition blocked tissue-damaging components of the classical complement cascade and was protective in diverse models of autoimmune and neurodegenerative disease. While blocking the entire classical pathway, C1q inhibition is believed to leave the other complement pathways (lectin and alternative) intact for normal immune function.
First on the Path
As the initiating molecule of the classical complement pathway, C1q is believed to act as an “on/off switch” to stop the start of a disease process. Our C1q inhibitors are designed to block the initial step of the classical complement pathway and inhibit downstream inflammatory components and activities that lead to disease.
Annexon’s founding science described the role of C1q in brain development and neurodegenerative disease and we have established unique expertise in complement biology that enables us to target both autoimmune and neurodegenerative disorders. By blocking the initiation of the classical complement pathway and its downstream inflammatory components, our approach is distinct from targeting C3 or C5 downstream in the pathway. Inhibiting these downstream components blocks the activity of all three complement pathways (lectin, alternative and classical), while not affecting early components of the classical pathway involved in autoimmune and neurodegenerative disease.