- Innate Pharma and MedImmune will evaluate the combination of Innate Pharma’s first-in-class IPH5401 antibody and Imfinzi® (durvalumab) in a Phase I/II study for patients with selected solid tumors
- IPH5401 blocks C5aR, a receptor often overexpressed on myeloid-derived suppressor cells (MDSC) in the tumor microenvironment - preclinical findings suggest that C5aR blockade increases immune-mediated tumor killing and efficacy of checkpoint inhibitors
- Innate will sponsor the study with costs equally shared by both parties
Innate Pharma SA (the “Company” - Euronext Paris: FR0010331421 – IPH) today announces that it has entered into a clinical trial collaboration with MedImmune, the global biologics research and development arm of AstraZeneca. The Phase I/II study (STELLAR-001) will evaluate the safety and efficacy of durvalumab, an anti-PD-L1 immune checkpoint inhibitor, in combination with Innate’s investigational anti-C5aR monoclonal antibody, IPH5401, as a treatment for patients with selected solid tumors.
“Our collaboration with MedImmune provides further evidence of Innate’s commitment to exploring the full combination potential of IPH5401 as we progress our immuno-oncology portfolio,” said Mondher Mahjoubi, Chief Executive Officer of Innate Pharma. “We believe IPH5401 could become an important partner in PD-1/PD-L1 combination strategies.”
The Phase I part of the trial is expected to establish a recommended dose regimen of IPH5401 in combination with durvalumab in selected solid tumors, and the Phase II part will assess the safety and efficacy of the combination in these patients. The study will be conducted by Innate and the costs will be equally shared by both parties. The agreement between Innate Pharma and MedImmune is non-exclusive.
Both durvalumab and IPH5401 are cancer immunotherapies, a potent class of treatments that use the body's own immune system to help fight cancer. Durvalumab blocks PD-L1 interactions with PD-1 and CD80, countering the tumor’s immune-evading tactics and inducing an immune response. Preclinical findings suggest that C5aR blockade increases immune-mediated tumor killing and efficacy of checkpoint inhibitors. Complement cascade factor 5a (C5a), secreted by tumor cells, attracts and stimulates C5aR-overexpressing myeloid-derived suppressor cells (MDSC) and neutrophils in the tumor microenvironment. Part of the innate immune system, these types of cells promote tumor growth by secreting inflammatory mediators, immunosuppressive cytokines and angiogenic factors. They potently suppress T and NK cells and hamper the activities of PD-1/PD-L1 checkpoint blockers.
Innate Pharma and AstraZeneca have an existing co-development and commercialization agreement for monalizumab, a first-in-class humanized IgG4 targeting NKG2A receptors expressed on tumor infiltrating cytotoxic NK and CD8 T lymphocytes.