The oral bioavailability in mouse, rat, and monkey is 78%, 86%, and 60%, respectively ^[1].

Batoprotafib (20 mg/kg; oral administration; twice daily for 40 days) suppresses tumor growth and exhibits enhanced efficacy when administered in combination with Dabrafenib plus Trametinib in nude mice harboring HT-29 xenografts ^[2].

Batoprotafib (7.5 mg/kg; pO.; b.iD. or qD. for 36 days) in combination with JDQ-443 (100 mg/kg; pO.; qD.) enhances the efficacy of JDQ443 alone in KRASG12C-mutated cell-derived (CDX) models in nude mice ^[3].

Batoprotafib exhibits an IC50 of 0.008 μM in the KYSE520 pERK assay and a 0.100 μM IC50 in the KYSE520 5-day cell proliferation assay. Off-target IC50 values are 18 μM, 6.9 μM, and 11 μM for Cav1.2, VMAT, and SST3, respectively ^[1].

Batoprotafib (0-1000 nM; 6 days) demonstrates inhibition of NCI-H3255, HCC827, and PC9 cell viability with IC50 values below 1.5 μM. It exhibits efficacy in EGFR-mutant NSCLC cell lines ^[2].

Batoprotafib is effective in acquired resistance models of EGFR inhibitors and shows synergistic effects when combined with EGFR inhibitors ^[2].

Batoprotafib improves the effectiveness of KRASG12C inhibitors in treating KRASG12C lung and colorectal cancers ^[2].

Batoprotafib suppresses immune-suppressive macrophages and enhances the effects of PD1 blockade ^[2].