OSE Immunotherapeutics Presents New Data Supporting Bispecific Antibody Checkpoint Inhibitor Platform (BiCKI) and Bifunctional Therapy Targeting PD-1 and IL-7 (BiCKI-IL-7) For Cancer Immunotherapy

Data being presented in two poster presentations at AACR Virtual Meeting II 2020 – June 22-24

NANTES, France, June 10, 2020 (GLOBE NEWSWIRE) -- OSE Immunotherapeutics (ISIN: FR0012127173; Mnémo: OSE) will present the latest progress on its bispecific antibody platform, called BiCKI, based on an anti-PD1 backbone fused with cytokines or costimulatory molecules, and a preclinical update on its developmental BiCKI therapy, a bifunctional anti-PD-1 / interleukin-7 (IL-7) fusion protein, called BiCKI-IL-7⁽¹⁾, at the American Association of Cancer Research (AACR) Virtual Annual Meeting II, to be held on June 22-24, 2020.

Nicolas Poirier, Chief Scientific Officer of OSE Immunotherapeutics, commented: “The AACR update presentations show that our BiCKI bispecific anti-PD1 checkpoint inhibitor antibodies platform and novel bispecific therapy combining anti-PD-1 and the cytokine IL-7, called BiCKI-IL-7, will help overcome resistance mechanisms to anti-PD(L)-1 therapies and could potentially address the needs of a patient population in immune escape from checkpoint inhibitor treatment.”

Immune checkpoint inhibitors are now considered a new standard of care against a wide range of cancers. However, these therapies are ineffective in a significant percentage of patients, and some initial responders eventually develop resistance to these therapies with relapsed disease ⁽²⁾. Sustained tumor antigen stimulation may result in a state of functional impairment referred to as exhaustion of tumor T lymphocytes. Disarming T regulatory cells (Tregs) is also important as Tregs contribute to dampening anti-tumor response.

The poster entitled: “Bispecific anti-PD1 ChecKpoint Inhibitors antibodies (BiCKI), an optimized platform designed to tackle anti-PD-(L)1 primary and secondary resistance mechanisms” shows improvement of the BiCKI platform manufacturability and drug exposure by selectively designing the structure of bispecific antibodies. By fusing costimulatory molecules, either cytokines or a dominant negative receptor to the anti PD-1 blocking antibody, it is possible to generate and select a variety of efficient bispecific molecules that act synergistically to counteract primary and secondary resistance mechanisms of anti-PD(L)1 therapies.