On June 29, 2023 Corvus Pharmaceuticals, Inc. (Nasdaq: CRVS), a clinical-stage biopharmaceutical company, reported new preclinical data for ciforadenant, the Company’s adenosine 2A receptor inhibitor, highlighting its mechanism of action and synergy with immune checkpoint inhibitors via combination with anti-CTLA-4 and anti-PD-1 therapies (Press release, Corvus Pharmaceuticals, JUN 29, 2023, View Source [SID1234632959]). The data is being presented in a poster at the 2nd Japanese Cancer Association and American Association for Cancer Research (AACR) (Free AACR Whitepaper) (JCA-AACR) Precision Cancer Medicine International Conference, which is taking place June 28-30, 2023 in Kyoto, Japan.

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"Our presentation at the JCA-AACR conference further supports the rationale for the synergistic combination of ciforadenant with checkpoint inhibitors to leverage multiple components of the immune response to cancer," said Richard A. Miller, M.D., co-founder, president and chief executive officer of Corvus. "We are exploring this combination in a Phase 1b/2 clinical trial that is being led by the Kidney Cancer Research Consortium. The clinical trial is exploring the potential of ciforadenant as a first line therapy for metastatic renal cell cancer in combination with anti-CTLA-4 and anti-PD-1 therapies, and is based on preclinical research published in 2018 demonstrating synergy when ciforadenant was combined with anti-CTLA-4 and anti-PD-1 therapies1. Enrollment in the clinical trial is ongoing and we plan to share initial data before the end of 2023."

Ciforadenant Data Presented at JCA-AACR Conference
The new ciforadenant preclinical data was presented by Dan Li, Ph.D., Senior Scientist at Corvus, in a poster session (abstract #12-1) today at the JCA-AACR conference. The poster is available to JCA-AACR attendees in the poster session and is also available on the Publications and Presentations page of the Corvus website. The poster presentation highlights preclinical data supporting the synergy between ciforadenant and immune checkpoint blockade (ICB), leading to a proinflammatory response:

Depletion of myeloid cells abolished the synergy of ciforadenant and ICB in a murine melanoma model.
The combination of ciforadenant with ICB upregulated the genes involved in the IL-12/STAT4 signaling axis, which leads to the development of CXCR3+ IFNγ-producing Th1 helper cells.
Ciforadenant treatment increased production of chemokine CXCL10, a ligand for recruitment of CXCR3+ Th1 helper cells into the tumor.
Ciforadenant modulated antitumor responses by turning the tumor microenvironment into the proinflammatory state.
The combination of ciforadenant with ICB promoted the production of several proinflammatory cytokines such as IL-6, TNFa, and IFNg.