Nektar Announces First Patient Dosed in Phase 1/2 Clinical Study of NKTR-214, a CD122-Biased Immuno-Stimulatory Cytokine

Nektar Therapeutics (NASDAQ: NKTR) today announced that dosing has commenced in the Phase 1/2 clinical study evaluating the efficacy and safety of NKTR-214 in the treatment of solid tumors. NKTR-214 is a novel CD122-biased cytokine designed to preferentially activate the beta and gamma sub-units of the IL-2 receptor in order to proliferate tumor-killing T cells within the body (CD8-positive effector T cells and natural killer T cells) without stimulating regulatory T cells (CD4-positive T cells). "NKTR-214 is a unique immuno-oncology candidate that is specifically designed to activate and multiply the patient's own tumor-killing T cells in order to fight cancer more effectively," said Ivan Gergel, M.D., Senior Vice President and Chief Medical Officer of Nektar. "With NKTR-214 in preclinical models, we observed a preferential increase of CD8-positive effector T cells of more than 400-fold compared to regulatory T cells within the tumor itself. We are excited about the start of the clinical study and the potential of NKTR-214 to provide a positive benefit for patients with cancer."The Phase 1/2 study of NKTR-214 is designed to evaluate patients with advanced solid tumors, including melanoma, renal cell carcinoma and non-small cell lung cancer. The study is being conducted initially at two primary investigator sites: MD Anderson Cancer Center under Drs. Patrick Hwu and Adi Diab; and Yale Cancer Center, under Drs. Mario Sznol and Michael Hurwitz. NKTR-214 is designed to be administered similarly to the dosing schedules for approved PD-1 and CTLA-4 agents, and will be evaluated on a once every three week dosing schedule in the Phase 1/2 clinical trial. In preclinical studies, NKTR-214 demonstrated a mean ratio of 450:1 within the tumor micro-environment of CD8-positive effector T-cells, which promote tumor killing, compared with CD4-positive regulatory T cells, which are a type of cell that can suppress tumor killing.2