by Dr. C.H. Weaver M.D. 8/2019

The U.S. Food and Drug Administration (FDA) has granted Breakthrough Therapy Designation for the investigational agent bempegaldesleukin (NKTR-214) in combination with Opdivo® (nivolumab) for the treatment of patients with previously untreated unresectable or metastatic melanoma.

The Breakthrough Therapy Designation is based on updated clinical data demonstrating that 53% of previously untreated advanced melanoma patients responded to treatment with the combination and 24% had a complete disappearance of their cancer.

The study results were reported at the 2019 American Society of Clinical Oncology (ASCO) Annual Meeting from patients with metastatic melanoma that were treated in the ongoing PIVOT-02 Phase 1/2 clinical study. (1)

About Bempegaldesleukin (NKTR-214)

Bempegaldesleukin is a novel precision cancer medicine designed to stimulate cancer-killing immune cells in the body by targeting CD122 receptors found on the surface of these immune cells. CD122, which is also known as the Interleukin-2 receptor beta subunit, is a key signaling receptor that is known to increase proliferation of these effector T cells. (2) In clinical and preclinical studies, treatment with bempegaldesleukin resulted in expansion of these cells and mobilization into the tumor micro-environment. (3,4)

About Opdivo

Opdivo is a programmed death-1 (PD-1) immune checkpoint inhibitor that is designed to harness the body’s own immune system to help restore anti-tumor immune response.

FDA Breakthrough Therapy Designation is intended to expedite the development and review of medicines aimed at treating a serious or life-threatening disease where there is preliminary clinical evidence that the investigational therapy may offer substantial improvement over existing therapies on at least one clinically significant endpoint.


  2. Boyman, J., et al., Nature Reviews Immunology, 2012, 12, 180-190.
  3. Charych, D., et al., Clin Can Res; 22(3) February 1, 2016
  4. Diab, A., et al., Journal for ImmunoTherapy of Cancer 2016, 4(Suppl 1): P369