How Do I Choose the Right Model Panel for my Agent?
Choice of panel depends upon the scientific question you are looking to answer.
The syngeneic model panel is used when you need to interrogate heterogenous immune phenotypes, which takes advantage of the diversity seen within syngeneic models. This panel can potentially help to provide insight into the lack of immunotherapy response in certain patient subsets.
The syngeneic MuScreen panel is also useful for:
- Evaluating efficacy through proof of concept studies
- Assessing an agent’s PD effect on tumor immune profiles, to potentially uncover predictive biomarkers and understand mechanisms of action
The tumor homograft model panel features models with clinically relevant, disease-specific oncogenic driver mutations in genes such as KRAS and p53, and the tumor architecture relevant to the original TME is preserved. Therefore, the tumor homograft MuScreen panel is ideal for evaluating immunotherapies or looking at combinations of targeted agents and I/O within specific disease relevant oncogenic pathways and TME.
Why Have the Particular Models been Selected?
For the syngeneic panels, models with various sensitivities to checkpoint inhibitors and various tumor growth kinetics are included. A range of sensitivities to ICI reflect the diversity in immune profiles across models that may lead to different responses to your I/O regimen.
The tumor homograft panel is comprised of robust models that harbor the most commonly sought after mutations such as KRAS and p53. In addition, they span various sensitivities to ICI and SoC.
What are Tumor Homograft Models?
Tumor homograft models (MuPrime™) are transplants of spontaneous or carcinogen-induced GEMM tumors into immunocompetent syngeneic hosts. The original GEMM tumors have never been passaged in vitro, so the artificial selection pressure is minimized and the tumor architecture relevant to the original TME is preserved. MuPrime tumor homografts feature disease-specific oncogenic driver mutations in genes such as KRAS and p53, which makes them more clinically relevant than standard syngeneic models.
Read our blog post on how tumor homografts supported the currently tested clinical strategy of a targeted therapy with ICI.