Integrating functional genomics and phenotypic profiling to deconstruct RAS inhibitor mechanisms of action and resistance

Resistance to RAS inhibitors can arise through genetic alterations and changes in cellular signalling. Combining functional genomic screening with phenotypic and transcriptomic profiling helps researchers investigate these mechanisms and understand how mutation context influences drug response.

Read this scientific poster from our preclinical services team to see how their approach helps:

• Identify candidate resistance drivers: Use 3D CRISPR knockout screening to uncover genetic perturbations associated with resistance, including hits that may be missed in 2D models.
• Compare inhibitor selectivity: Characterize responses across RAS-mutant cell lines to distinguish mutation-specific activity from broader pan-RAS inhibition.
• Interpret pathway-level responses: Combine MERCURIUS™ DRUG-seq with PROGENy analysis to assess MAPK suppression, signalling changes and potential cross-reactivity.
• Investigate acquired resistance: Generate drug-resistant cell models through dose escalation to study how resistance emerges over time.
• Integrate complementary evidence to strengthen mechanism-of-action understanding and support more informed therapeutic development decisions.

Read the poster now.

For research use only. Not for use in diagnostic procedures.