JMKX1899 selectively inhibited cell viability across multiple KRAS G12C-mutant cell lines, exhibiting slightly greater potency than AMG510 and MRTX849. Early clinical data from KRAS G12C-mutant NSCLC patients with BM treated by JMXK1899 further confirm its blood-brain barrier penetration and antitumor activity. These findings strongly support the continued clinical development of JMKX1899 as a promising therapeutic candidate for NSCLC patients with KRAS G12C mutations and BM.