On April 17, 2023 Corbus Pharmaceuticals Holdings, Inc. (NASDAQ: CRBP) ("Corbus" or the "Company"), a precision oncology company, reported details of new pre-clinical data on CRB-601, its avβ8 blocking antibody, presented as a poster at the 2023 American Association for Cancer Research (AACR) (Free AACR Whitepaper) annual meeting, held April 14-19, 2023 in Orlando, FL (Press release, Corbus Pharmaceuticals, APR 17, 2023, View Source [SID1234630193]).
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The poster titled "CRB-601, an avβ8 blocking antibody, prevents activation of TGFβ and exhibits anti-tumor activity associated with immune cell remodeling of the tumor microenvironment" explores the relationship between CRB-601 antitumor activity, PK and its binding to the αvβ8 receptor in the tumor. In addition, the impact on TGFβ pathway signaling and tumor immune cell population are also presented. Tumor growth was evaluated in mice bearing orthotopically implanted murine breast cancer EMT6 or colon cancer MC38 and treated with CRB-601.
CRB-601 exhibited dose dependent tumor growth inhibition (TGI) in the EMT6 tumor model which was significantly augmented in combination with anti-PD1 therapy. These effects were associated with changes in tumor micro-environment (TME) immune cell populations with marked increases in infiltrating T cells, NK cells and M1 polarized macrophages. Efficacy correlated with cell surface αvβ8 occupancy by CRB-601. CRB-601 treatment downregulated phosphorylation of SMAD proteins pSMAD2 and pSMAD3, consistent with blockade of the canonical TGFβ signaling pathway.
Rachael Brake, PhD, Chief Scientific Officer of Corbus stated: "We are building on our early efficacy. We can now demonstrate that CRB-601 has robust anti-tumor activity alone and as a combination partner with anti-PD-1 and that these effects are associated with documented receptor engagement, a reduction of TGFb1 levels in the tumor micro-environment (TME), and inhibition of downstream canonical TGFb signaling. Together this data reinforces the potential of this new approach in blocking activation of TGFb locally in the TME."