Incode BioPharmaceutics, Inc., has developed a product candidate, HC3-1496, that specifically targets the complement pathway. The unique mechanism-of-action of HC3-1496 results in enzymatic depletion of the complement protein C3, the key component for all three pathways of complement activation (alternative, classical, and mannose-lectin). Our preclinical results show rapid depletion of C3 without any observed significant adverse events, including in primates. Importantly, HC3-1496 depletes C3 without the downstream activation of C5, thus preventing the formation of the C5a anaphylatoxin.
A recent exciting result is the demonstration that HC3-1496 enhances the efficacy of an anti-CD20 mAb in a murine cancer model. These data will be presented at the upcoming American Society of Hematology (ASH) meeting in December. This clinical avenue is a high priority for InCode, and also underscores the increased appreciation for the role of complement in certain oncologic settings.
We have also demonstrated efficacy in several other animal models of human disease, including collagen-induced arthritis (RA), myocardial ischemia/reperfusion, and age related macular degeneration (AMD). We have also demonstrated that HC3-1496 prevents the lysis of erythrocytes in patients with paroxysmal nocturnal hemoglobinuria (PNH).
Given the emerging role of complement activation in the pathogenesis of grievous human disease, Incode intends to exploit the unique and potent activity of HC3-1496. We intend to initiate human clinical trials in selected indications within 18 months.
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