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Corbus Presents Latest Preclinical Data for CRB-601 at the New York Academy of Sciences Frontiers in Cancer Immunotherapy Conference

  • CRB-601 is a highly potent and selective anti-αvβ8 integrin monoclonal antibody designed to block the activation of TGFb in the local tumor microenvironment
  • Additional non-clinical data demonstrates combination benefit across a diverse range of syngeneic models with differential sensitivity to checkpoint inhibition
  • Anti-tumor activity correlates with increases in proliferating CD4+ and CD8+ T-cells as well as the NK cell population and a shift towards M1 macrophage polarization, supporting the hypothesis the CRB-601 may overcome immune cell exclusion

Excerpt from the Press Release:

NORWOOD, Mass., May 11, 2022 /PRNewswire/ — Corbus Pharmaceuticals Holdings, Inc. (NASDAQ: CRBP) (“Corbus” or the “Company”), an immunology company, announced that new preclinical data for CRB-601 are being presented today in an oral presentation at the New York Academy of Sciences (NYAS) Frontiers in Cancer Immunotherapy Conference in New York, NY.  

The latest preclinical data for CRB-601 demonstrate its significant effects on inhibiting tumor growth as a single agent and in combination with anti-PD-1 treatment in the MC38 and EMT6 syngeneic tumor models. In addition, CRB-601 restores an anti-PD-1 effect in the 4T1 syngeneic tumor model, a “cold” immune cell-depleted tumor model, when added in combination. This data marks the first time such an effect has been documented in this model with an anti-αvβ8 agent.

The anti-tumor effects in the immune excluded EMT6 model correlated with changes in the immune cell populations in the tumor micro-environment. There were increases in proliferating CD4+ and CD8+ T-cells, NK cells, and a shift in macrophage polarization to the inflammatory M1 phenotype. Collectively these data suggest that treatment with CRB-601 could overcome the immune excluded phenotype established in this model and enhance the efficacy of treatment with anti-PD-1 therapy.   

Additionally, in a rechallenge model, tumor-bearing mice initially rendered tumor-free by treatment with CRB-601 + anti-PD-1 were subsequently reinoculated with the same tumor cells (MC38) and monitored for tumor regrowth. After 30 days no tumors had formed in this cohort of animals, whereas all the treatment naïve control mice succumbed to the burden of tumor growth. These data illustrate that the combination treatment of CRB-601 + anti-PD-1 led to durable T-cell memory protection.

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