Scientific Co-Founder Dr. Ben Barres
C1q is the initiating molecule of the classical complement pathway that activates a powerful inflammatory cascade. Our upstream complement approach targeting C1q acts as an “on/off switch” designed to block all downstream components of the classical complement pathway that lead to excess inflammation, tissue damage and patient disability in a host of complement-mediated autoimmune, neurodegenerative and ophthalmic diseases.
Prevents downstream activation of all tissue-damaging components
C1q directly binds to and accumulates on tissues in complement-mediated diseases. It anchors complement activation on the tissue surface and drives disease processes. Inhibiting C1q at the start of the classical pathway stops downstream inflammation and tissue damage.
Guillain-Barre syndrome C1q
C1q Targeting the
HUNTINGTON’S Disease C1q
GEOGRAPHIC ATROPHY C1q
Aberrant activation of C1q can lead to damage of healthy tissue and destruction of functioning synapses in multiple antibody-mediated autoimmune and complement-mediated neurodegenerative disorders. Our platform holds tremendous promise across a broad range of diseases in three therapeutic franchises:
In antibody-mediated autoimmune disease, aberrant activation of C1q on cells and tissues can lead to damaging inflammatory responses.
In complement-mediated neurodegeneration, aberrant activation of C1q at synapses in aging and disease can lead to excessive synapse loss and neuronal damage.
Aberrant activation of C1q in the eye can lead to the loss of photoreceptor neurons and drive disease progression.