Tecentriq Approval in NSCLC 'Stops the Brakes' on PD-L1 Expression

The Food and Drug Administration recently approved the immunotherapy Tecentriq (atezolizumab) for adults with metastatic non-small cell lung cancer (NSCLC) who have no alterations to their EGFR or ALK genes but whose tumors have a high PD-L1 expression, a protein that acts as the “brakes” on a patient’s immune response to cancerous cells, according to Dr. Jorge Gomez.

Tecentriq itself is not a new drug, nor is it new to the treatment of patients with NSCLC. This is the fourth approval of this drug in the metastatic NSCLC space based off the phase 3 IMpower110 study that showed Tecentriq lengthened life in the target population compared to chemotherapy.

Gomez, medical director of the Thoracic Oncology Program and the World Trade Center oncology clinic at Mount Sinai Hospital in New York City, New York, and speaker for the American Lung Association, spoke with CURE® to discuss why this approval is different and the importance of its expansion into patients with a high PD-L1 expression.

Transcription:

PD-L1 is a marker that is present on many different cells, including cancer cells and some of the immune cells that actually carry out the attack on cancer. PD-L1 is what we call a checkpoint, it is a molecule that can turn off in response to what we call the activation of T-cells, T-cells are the cells that actually carry out the cell kill against cancer.

The PD-L1 actually turns off that activation and protects cancer cells and runaway cancer cells in the body from that immune response. So, it actually modulates the immune response depending on how much PD-L1 there is. Now that's very good for regular cells because it protects them against an overwhelming immune response but it's bad for cancer cells because it protects them from the body's immune system.

These drugs, the PD and PD-L1 inhibitors will turn off that inhibition, so it will stop the "brakes" on the immune system. The PD-L1 is one of the multiple brakes on the immune system and these drugs stop those brakes and allow the immune response to happen. And so, that immune response is not targeted specifically toward the cancer cells, but it does, in many patients, attack cancer cells.

Read CURE’s original coverage of the FDA approval here.