Kite and Pfizer to assess combination therapy for lymphoma

22nd January 2018 (Last Updated January 22nd, 2018 00:00)

Gilead Sciences' subsidiary Kite has signed a clinical trial collaboration to evaluate its Yescarta (axicabtagene ciloleucel) in combination with Pfizer’s utomilumab for the treatment of refractory large B-cell lymphoma. 

Gilead Sciences' subsidiary Kite has signed a clinical trial collaboration to evaluate its Yescarta (axicabtagene ciloleucel) in combination with Pfizer’s utomilumab for the treatment of refractory large B-cell lymphoma.

Over the coming months, the firms will conduct a multi-centre Phase I/II trial to investigate safety and efficacy of the combination.

Results from the trial will be used to explore options for further development of this combined therapy or similar combinations of Kite’s engineered T-cell products and utomilumab.

Kite research and development worldwide head and chief medical officer David Chang said: “Kite is committed to realising the full potential of Yescarta and other cell therapy technologies across a range of cancers.

"This study with utomilumab adds to the growing number of combination approaches we are exploring with Yescarta for patients living with lymphoma."

“We are pleased to collaborate with Pfizer on this study with utomilumab, which adds to the growing number of combination approaches we are exploring with Yescarta for patients living with lymphoma.”

Yescarta is a first chimeric antigen receptor T (CAR-T) cell therapy indicated to treat adults suffering from relapsed or refractory large B-cell lymphoma, following two or more lines of systemic therapy.

Utomilumab is an investigational, fully humanised 4-1BB agonist monoclonal antibody being studied as a monotherapy and combination agent in various hematologic cancers and solid tumours.

In pre-clinical studies, utomilumab is reported to have improved T-cell-mediated immune responses. It is expected to enhance T-cell proliferation and activity by boosting Yescarta’s CD28 costimulatory domain through exogenous 4-1BB signalling.