Proposed Mechanism of Action in BRAF+ Melanoma

Dual inhibition of the MAPK and PD-1/PD-L1 pathways can improve tumor 
immunogenicity and suppress tumor growth compared to targeted therapy alone, based on mouse models 1,3

  • Increased antigen presentation 
  • Increased T cell infiltration and activation
TECENTRIQ targets and blocks the ligand PD-L1 to augment the antitumor immune response 1
  • PD-L1 can contribute to immune deactivation in the tumor microenvironment
  • Restoring T cell activity could affect both tumor and normal cells

PD-1=programmed death-1; PD-L1=programmed death-ligand 1.

Distinct features of TECENTRIQ
  • DIRECT: TECENTRIQ binds to the ligand PD-L1 on tumor cells and immune cells
  • COMPLETE: dual blockade of PD-L1 binding to its inhibitory receptors PD-1 and B7.1
BRAF/MEK inhibition with COTELLIC® (cobimetinib) + ZELBORAF® (vemurafenib) in the MAPK pathway activates the immune response, as demonstrated by:

Mutated BRAF leads to overactive downstream signaling, resulting in excessive cell proliferation and survival. Dual targeting of mutated BRAF with ZELBORAF and MEK with COTELLIC could lead to the inhibition of intracellular signaling and decreased tumor cell proliferation. 6,7


TECENTRIQ is the first FDA-approved, Fc-engineered, humanized anti-PDL1 antibody