Vivreon Biosciences ? NIAID SBIR # PA-16-302 Project Summary Vivreon Biosciences is pleased to apply for NIAID SBIR Solicitation #PA-16-302. Vivreon Biosciences is an innovative life sciences company that is developing a novel small molecule, Ca2+ channel inhibitor for the treatment of ulcerative colitis (UC). Our lead compound, VV2003, achieves immunosuppression by an entirely new mechanism ? colon-restricted inhibition of Ca2+ release-activated Ca2+ (CRAC) channels to block colitis. Vivreon seeks NIAID funding to bridge the gap between discovery and development. We will perform formulation chemistry and in vivo colitis efficacy studies. Upon successful completion of the program, our preclinical candidate will be the first to specifically target the CRAC pathway for immunosuppression in UC, thus comprising an entirely new tool in the battle against inflammatory bowel diseases (IBD). Vivreon has discovered a lead compound VV2003, which inhibits inflammation by blocking CRAC channel activity with nM potency; suppressing M1-like NF-?B activity, while preserving M2-like phagocytosis. Importantly, VV2003 has extremely low epithelial permeability, a key feature of many topical oral IBD therapeutics that remain in the gut lumen. This permits VV2003 to achieve colon-restricted immunosuppression, avoiding unwanted systemic side effects. We have developed several strategies for a novel oral colon-targeted delivery, and these routes will be pursued to identify a formulation suitable for future Investigational New Drug (IND)-enabling studies. The candidate will be confirmed using an animal model suitable for UC (adoptive transfer colitis, Dr. Cahalan, University of California, Irvine).
The final aim for this proposal is characterization and testing of the first CRAC channel inhibitor for UC therapy.
Vivreon Biosciences ? NIAID SBIR # PA-16-302 Project Narrative Vivreon Biosciences is conducting predevelopment studies for VV2003, a novel therapeutic to block pathogenic inflammation in persons with ulcerative colitis (UC). VV2003 does not penetrate epithelial layers, allowing for colon-targeted immunosuppression, without systemic side effects. Numerous UC patients are unresponsive to current therapies, and VV2003 provides a new therapeutic mechanism for targeted inhibition of gut-resident inflammatory Ca2+ release-activated Ca2+ (CRAC) channels.
