CJ-2360 是一种有效的口服ALK抑制剂，对野生型 ALK 和 F1197M、G1269A、L1196M 和 S1206Y ALK 突变体的IC50分别为 2.2、4.0、8.8、6.3 和 8.9 nM。CJ-2360 对临床报道的两种 ALK 突变体 (C1156Y 和 L1196M) 以及 468 种激酶 (LTK、MERTK、CLK1、DAPK1 和 DAPK2) 具有较强的抑制活性。

CJ-2360 is a potent and orally active ALK inhibitor with IC 50 s of 2.2, 4.0, 8.8, 6.3, and 8.9 nM against wild-type ALK and F1197M, G1269A, L1196M, and S1206Y ALK mutants, respectively. CJ-2360 displays potent inhibitory activity against two clinically reported ALK mutants (C1156Y and L1196M) and a few other kinases (LTK, MERTK, CLK1, DAPK1, and DAPK2) among the 468 kinases evaluated [1].

CJ-2360 achieves an IC 50 value of 1.8 nM in inhibition of cell growth in the KARPAS-299 cell line. Further tested CJ-2360 for its potency in cell growth inhibition in the H3122 non-small-cell lung cell line carrying EML4-ALK and obtained an IC 50 value of 3 nM. CJ-2360 inhibits Mer tyrosine-protein kinase (MERTK), CLK1, DAPK1, DAPK2, and DAPK3 with IC 50 s of 6.3, 11, 31, 23, 22, and 260 nM, respectively. CJ-2360 displays >100-fold selectivity for ALK over the insulin receptor kinase (INSR) and shows no significant activity against IGF1R [1].

CJ-2360 (100 mg/kg; p.o.; twice daily for 22 days) is capable of achieving complete and long-lasting tumor regression in the KARPAS-299 xenograft tumor model [1]. CJ-2360 (100 mg/kg; p.o.) is very effective in inhibition of ALK phosphorylation, as well as ERK and STAT3 phosphorylation in KARPAS-299 tumor tissue, with the effect persisting for at least 24 h [1]. Animal Model: KARPAS-299 xenograft model (female SCID mice) [1] Dosage: 100 mg/kg Administration: P.o.; twice daily for 22 days Result: Very efficacious in the KARPAS-299 xenograft model. It achieves complete tumor regression in 100% of tumors and all tumors did not return until day 53, 23 days after the last dose.

2226742-61-4

C27H30FN5O2

475.56

(< 1 mg/ml refers to the product slightly soluble or insoluble )
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