Ensartinib (X-396) is a potent and dualALK/METinhibitor withIC₅₀s of<0.4 nM and 0.74 nM, respectively.

IC50:<0.4 nM (ALK), 0.74 nM (MET)^[1]

The ability of Ensartinib (X-396) to inhibit the growth of different cancer cell lines harboring ALK fusions or point mutations is tested. Ensartinib is potent in H3122 lung cancer cells harboringEML4-ALKE13;A20 (IC₅₀: 15nM). Ensartinib is also potent in H2228 lung cancer cells harboringEML4-ALKE6a/b; A20 (IC₅₀: 45 nM). Furthermore, X-376 is potent in SUDHL-1 lymphoma cells harboringNPM-ALK(IC₅₀: 9 nM). X-376 also inhibits SY5Y neuroblastoma cells harboringALKF1174L, MKN-45 gastric carcinoma cells harboring MET dependent, HepG2 cells and PC-9 lung cancer cell lines harboringEGFRexon 19 del with IC₅₀s of 68 nM, 156 nM, 9.644 μM and 2.989 μM, respectively^[1].

The effects of Ensartinib (X-396) in vivo against H3122 xenografts are examined. A pharmacokinetic study reveals that Ensartinib shows substantial bioavailability and moderate half-lives in vivo. Nude mice harboring H3122 xenografts are treated with Ensartinib at 25mg/kg bid. Ensartinib significantly delays the growth of tumors compared to vehicle alone. In the xenograft experiments, Ensartinib appears well-tolerated in vivo. Mouse weight is unaffected by Ensartinib treatment. Drug-treated mice appear healthy and do not display any signs of compound related toxicity. To further assess potential side effects of Ensartinib, additional systemic toxicity and toxico-kinetic studies are performed in Sprague Dawley (SD) rats. Following 10 days of repeated oral administration of Ensartinib at 20, 40, 80 mg/kg in SD rats, all animals survive to study termination. The no significant toxicity (NST) levels are determined to be 80mg/kg for Ensartinib. At NST levels, Ensartinib achieves an AUC of 66 μM×hr and a C_maxof 7.19 μM^[1].

561.44

C₂₆H₂₇Cl₂FN₆O₃

1370651-20-9

爱沙替尼

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