Avila Therapeutics™, Inc., a biotechnology company developing targeted covalent drugs that treat diseases through protein silencing, today announced results of preclinical studies demonstrating that its clinical candidate, AVL-292, potently inhibits B cell receptor signaling, and demonstrates efficacy in a rodent model of rheumatoid arthritis. These new data were presented Saturday, June 26, 2010 at the Federation of Clinical Immunology Societies (FOCIS) 2010 annual meeting in Boston, MA.
“These results show very profound disease-modifying effects of AVL-292 in both prophylactic and therapeutic models of rheumatoid arthritis. In conjunction with the safety testing Avila Therapeutics has completed, the efficacy data provide exciting validation for this program as we advance AVL-292 into clinical studies this year.”
AVL-292 is a novel, orally available, covalent drug that targets Bruton's tyrosine kinase (Btk). Inhibition of Btk is a promising new approach to treatment of diseases that are driven by B cells, which are part of the immune system. AVL-292 bonds selectively and covalently with Btk to shut down and silence its activity. This unique mechanism of action confers greater target selectivity and a longer duration of action than is typical of conventional small molecule drugs.
Btk plays a crucial role in the activation of normal B lymphocytes and contributes to the proliferation and survival of B cell lymphomas. AVL-292, with its ability to irreversibly inhibit and silence Btk, may represent a new best-in-class therapeutic option for the treatment of autoimmune diseases such as rheumatoid arthritis, as well as B cell-related hematological cancers, including non-Hodgkin lymphoma (NHL) and B cell chronic lymphocytic leukemia (B-CLL).
In an oral presentation at FOCIS entitled "A Novel Covalent Inhibitor of Btk Inhibits B Cell Receptor Signaling and Demonstrates Efficacy in CIA Rheumatoid Arthritis Model", Erica Evans, Ph.D., Senior Scientist, Avila Therapeutics, presented data from preclinical studies that evaluated the efficacy of AVL-292 in the mouse collagen-induced arthritis model. Highlights of the data demonstrate: