It disrupts Ras activation and effector binding to SII-P in vitro and inhibits proliferation in G12D mutant cancer cell models and KRASG12D-driven tumor growth in animal models.294–296 In another study, a bicyclic peptidyl pan-Ras inhibitor, cyclorasin B4-27, binds to GTP-bound form of WT KRAS and G12V mutant with ~20 nm affinity (KD). The gene discussed is KRAS; the disease is cancer.