Immunotherapeutic Discovery & Development

Validated with standard-of-care chemotherapeutics and small molecule inhibitors known to modulate immune responses, our predictive translational platform for immuno-oncology produces rich data to inform better decision making. Watch this video to learn more, and then see our step-wise approach for success.

  • Video Transcript

    The promise of immunotherapies is reflected in its record number of clinical trials, yet these trials have produced the highest failure rates. Progress often comes to a grinding halt during syngeneic mouse in vivo studies. Why? The problem isn't with the therapeutic, but with the approach. Presuming knowledge of their lead compound, researchers often forge ahead without first fully characterizing their compound in more complex, disease-relevant environments. Given the complexity of the tumor microenvironment, it is imperative to create models that include all major immune cell types a compound may interact with.

    What if there was a way to improve the chance that therapies translate more effectively across the discovery continuum? Investigating with a multicellular phenotypic assay enables us to take a different look at a compound's responses in a platform specifically designed to mimic the disease state. Optimized cellular assays provide critical information to validate the efficacy of a compound in simple and increasingly complex multicellular assays, delivering insights that serve as better predictors for the transition to in vivo studies.

    Failed assays don't have to derail your development. Arming yourself with more information about your compound in a combination of assays improves predictability of its performance in in vivo, syngeneic models, humanized models, and ultimately, the clinic. Charles River's translational platform for immuno-oncology supports the collection of rich data to inform better decision-making, moving you effectively from target discovery and validation through to humanized mouse models and on to the clinic.