HomeMolecular BiologyKRAS G12C: Covalent Inhibitor Switch (2D)

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.

Molecular Biology2DAdvanced60 FPS📱 Mobile-adapted⇄ 3D version
2d-biology-ext-topic-45 ↗ Open standalone

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.

⚙ Under the hood

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.

KRASoncogenecancer biologycovalent inhibitormolecular biologysignal transduction

2D · HTML5 Canvas 2D · 60 FPS target · runs fully client-side, no install

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