SAN DIEGO, Dec. 1, 2016 /PRNewswire/ -- TNK Therapeutics, Inc. ("TNK"), a subsidiary of Sorrento Therapeutics, Inc. (NASDAQ: SRNE; "Sorrento"), has provided an update on its lead chimeric antigen receptor (CAR) expressing T cells (CAR-T) programs for the treatment of hematological malignancies. Adoptive immunotherapy utilizing CAR-T cells represents a promising new paradigm in the treatment of cancer. Sorrento intends to present these findings at upcoming clinical conferences and in scientific publications.
The anti-CD38 CAR-T program is in development for the treatment of multiple myeloma. The membrane glycoprotein CD38 is highly expressed on multiple myeloma cells, and thus, represents a valuable therapeutic target against myeloma. TNK has developed a proprietary second generation anti-CD38 CAR based on a fully human anti-CD38 monoclonal antibody derived from Sorrento's G-MAB antibody library. To date, the anti-CD38 CAR-T cells have demonstrated specific activation through the CAR resulting in the production of cytokines and CAR-T proliferation. CD38-expressing multiple myeloma tumor cells were killed efficiently in vitro, and the CD38 CAR-T cells completely eradicated tumors in a xenograft mouse model of human multiple myeloma. Importantly, TNK's anti-CD38 CAR-T cells selectively lysed target cells expressing high levels of CD38 while not killing cells with normal or low levels of CD38. This unique characteristic might allow for a better safety and efficacy profile in humans as well as enable a more effective manufacturing process of the anti-CD38 CAR-T cells. The anti-CD123 CAR-T program is in development for the treatment of acute myeloid leukemia (AML). A proprietary anti-CD123 CAR was constructed based on a human fully anti-CD123 monoclonal antibody selected from Sorrento's G-MAB library. The anti-CD123 CAR-T cells were specifically activated through the CAR to produce cytokines and proliferate. To date, they have selectively lysed CD123-expressing AML tumor cells in vitro, and strongly suppressed the growth of established tumors in a xenograft mouse model of human AML.