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Incyte, Genentech to assess combination of two new cancer immunotherapies

US-based biopharmaceutical firm Incyte has entered into a clinical trial agreement with Genentech to assess the combination of two new cancer immunotherapies for patients with non-small cell lung cancer (NSCLC).

The clinical trial is designed to evaluate the safety, tolerability and preliminary efficacy of Incyte’s oral indoleamine dioxygenase-1 (IDO1) inhibitor, INCB24360, in combination with Genentech’s PD-L1 immune checkpoint inhibitor, MPDL3280A.

Both the immunotherapies are part of a new class of cancer treatments that are designed to improve the body’s own defenses in fighting cancer; both agents target distinct regulatory components of the immune system.

Incyte president and chief executive officer Hervé Hoppenot said the collaboration with Genentech is a further illustration of the company’s desire to investigate the therapeutic value of its IDO1 inhibitor in multiple tumor types as rapidly as possible.

"We believe the combination of INCB24360 with other novel immunotherapies represents a promising new approach to treating cancer, and research collaborations such as this have the potential to accelerate our understanding and support our goal of addressing the needs of patients with a wide range of cancers," Hoppenot said.

As part of the deal, the two firms will collaborate on a non-exclusive basis to assess the combination.

The deal will see Incyte responsible for carrying out the study and the results will be used to determine whether further clinical development of this combination is warranted.

INCB24360 is an orally bioavailable small molecule inhibitor of IDO1 that has nanomolar potency in both biochemical and cellular assays, potent activity in enhancing T lymphocyte, dendritic cell and natural killer cell responses in vitro, with a high degree of selectivity.

MPDL3280A, an investigational monoclonal antibody designed to interfere with a protein called Programmed Death-Ligand 1(PD-L1), is designed to make cancer cells more vulnerable to the body’s own immune system by interfering with PD-L1.