KRAS G12C: Covalent Inhibitor Switch (2D)
Interactive 2D model of KRAS G12C-mutant signalling: watch a projected population of KRAS molecules cycle between GDP-off and GTP-on states, then apply a sotorasib-like covalent inhibitor that irreversibly traps the mutant in its inactive pocket, and see downstream ERK signal and tumour growth rate respond live.
KRAS is the most commonly mutated oncogene in human cancer, and for decades its smooth, pocket-free surface made it "undruggable." This simulator renders a live population of KRAS molecules as a rotatable 2D-projected cloud, each one independently cycling between an inactive GDP-bound state and a signalling-active GTP-bound state under a real stochastic two-state switch. Dialling in a sotorasib-like covalent inhibitor exploits a cryptic pocket that only the G12C mutant exposes while GDP-bound, irreversibly locking molecules off one at a time — while the wild-type control stays completely unaffected, and an optional resistance mutation shows exactly how tumours escape the drug in the clinic. A live line chart and a state-transition network panel track the active GTP fraction, the drug-locked fraction, downstream ERK signal, and the resulting net tumour growth rate as the population responds in real time.
Watch a rotatable 2D-projected population of KRAS molecules cycle between GDP-off and GTP-on states, then dose a sotorasib-like covalent inhibitor that irreversibly locks the G12C mutant into its inactive pocket while wild-type KRAS stays unaffected, and see downstream ERK signal and tumour growth rate respond live on a linked time-series chart and state-transition network.
2D · HTML5 Canvas 2D · 60 FPS target · runs fully client-side, no install