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NSCLC — SCE Medical Oncology MCQ

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HardLung CancerNSCLCSCE Medical Oncology

A patient with previously treated KRAS G12C-mutated NSCLC receives sotorasib. Which molecular interaction produces pathway inhibition?

Educational content. Not a substitute for clinical judgement or local policy.

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Correct answer: A — Covalent binding to mutant cysteine in the P2 pocket, stabilising inactive KRAS G12C

Explanation lettering: E = shown as A · A = shown as B · B = shown as C · C = shown as D · D = shown as E

E is correct. Sotorasib selectively and irreversibly binds the substituted cysteine of KRAS G12C in a pocket accessible in the inactive state, preventing downstream RAS-RAF-MEK-ERK signalling while largely sparing wild-type KRAS. A describes an EGFR inhibitor. B describes a different upstream strategy and is not selective for G12C. C places binding in the active GTP-loaded state and predicts continued RAF signalling. D invents wild-type KRAS degradation. The requirement for cycling into the inactive state helps explain adaptive resistance through upstream signalling that increases the GTP-bound fraction.

Reference: Lumykras UK Summary of Product Characteristics: https://www.medicines.org.uk/emc/product/12871/smpc