A wide number of cancers exhibit misregulated genome packaging at the chromatin level. If chromatin that should be tightly condensed, becomes loosely packed (or vice-versa), the normal brakes on cell growth aren’t operant, leading to uncontrolled cell growth. Being able to regulate and control the chromatin state has been a high-value target for oncology. 

Coming from Geeta Narlikar’s lab at UCSF, TippingPoint has a proprietary platform that makes genome packaging states druggable. Specifically perturbing a disease causing chromatin state is difficult with targeted drug discovery platforms because they don’t provide enough biological context and the alternative of phenotypic screening can be incredibly resource intensive. TippingPoint’s platform addresses these limitations by recreating the biological context of cancer driving chromatin states in a controlled, cell-free environment. Instead of targeting a single factor, TippingPoint’s platform focuses on disrupting or restoring the unique protein-protein networks that package cell genomes, using phase-separated condensates as a readout. Unlike individual factors that may have similar functions in both healthy and diseased cells, the DNA packaging networks in cancer cells are significantly different, and can be exploited to enhance drug specificity and limit drug resistance.