The promise of immuno-therapies 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.
Charles River has established a powerful translational immuno-oncology platform with the capability of progressing biologics or small-molecule modulators of immune response from in vitro to in vivo assays using human and mouse variants of current checkpoint inhibitors and small molecules.
Failed assays don’t have to derail immunotherapies. Arming researchers with a more information about potential therapies in a combination of disease-relevant assays improves predictability of its performance in in vivo, syngeneic models, humanized models, and ultimately the clinic.