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September 10, 2018

Compugen doses first patient in Phase l trial of COM701

Compugen has dosed the first patient in a Phase l clinical trial of COM701 for the treatment of patients with advanced solid tumours.

Compugen has dosed the first patient in a Phase l clinical trial of COM701 for the treatment of patients with advanced solid tumours.

The open-label trial aims to evaluate the safety and tolerability of ascending doses of COM701 as a single agent and in combination with a PD-1 inhibitor in the enrolled patients.

It also intends to analyse the indication of preliminary anti-tumour activity of COM701 both as a monotherapy and in combination with a PD-1 inhibitor in patients with selected tumour types, such as non-small cell lung cancer, ovarian cancer, breast cancer and endometrial cancer.

The trial will enrol around 140 patients and will be carried out at several oncology clinical centres across the US.

The trial’s principal investigator Drew Rasco said: “Immunotherapy has revolutionised the landscape for oncology treatments by providing a new treatment option leading to lasting benefits for patients.

“Immunotherapy has revolutionised the landscape for oncology treatments by providing a new treatment option leading to lasting benefits for patients.”

“Yet, response rates vary greatly across different cancer indications, leaving a significant unmet medical need for many patients and a continuing challenge to discover new biological pathways that can result in the development of new cancer immunotherapies for non-responsive and refractory patients.

“COM701 preclinical data suggest that the newly discovered PVRIG pathway may be a dominant pathway in certain cancer subpopulations, including those that are unresponsive to PD-1 or PDL-1 inhibitors. As such, it is important to evaluate COM701 in clinical trials with these patient populations who have exhausted available standard therapy.”

COM701 is a humanised hybridoma antibody that binds with PVRIG, a new B7/CD28-like immune checkpoint target candidate identified by Compugen, by hindering its interaction with its ligand, PVRL2.

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