This proposal is built on the premise that newly recognized similarities between SSc and the pathways driving cellular aging, including increased CD38 expression and activity in disease that caused NAD+ depletion and SIRT activity decline, which results in unresolving myofibroblast activation and tissue fibrosis. Employing anti-CD38 antibody, by selectively blocking CD38 NADase activity, will restore NAD+ homeostasis, and prevents and reverses fibrosis in inflammation-dependent (BLM) fibrosis model. Inhibition of CD38 NADase by anti-CD38 antibody might be a novel therapy for systemic scleroderma.
|Effective start/end date||3/13/19 → 8/31/20|
- TeneoBio, Inc. (Agmt 3/13/19)