QL-X-138 是一种有效和选择性的 BTK/MNK 双激酶抑制剂,表现出与 BTK 的共价结合和与 MNK 的非共价结合。QL-X-138 对 BTK、MNK1 和 MNK2 激酶的 IC50 值分别为 9.4 nM、107.4 nM 和 26 nM。QL-X-138 还显示出抗登革热病毒 2 活性,IC50 值为 3.5 μM。QL-X-138 可用于 B 细胞恶性肿瘤的研究。


QL-X-138 Chemical Structure

CAS No. : 1469988-63-3

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QL-X-138 is a potent and selective BTK/MNK dual kinase inhibitor, exhibits covalent binding to BTK and non-covalent binding to MNK. QL-X-138 shows IC50s of 9.4 nM, 107.4 nM and 26 nM for BTK, MNK1 and MNK2 kinases respectively. QL-X-138 also shows anti-dengue virus 2 activity, with an IC50 of 3.5 μM. QL-X-138 can be used for the research of B-cell malignancies[1][2].

(In Vitro)

QL-X-138 (72 h) exhibits anti-proliferation activity against lymphoma and leukemia cell lines, with an GI50s of 0.31, 1.2, 0.49,1.4, 0.4, 0.23, 0.95, 1.2, 1.4, 0.23, 1.3, 0.93, 1, and 2.4 μM for TMD8, U2932, Ramos, OCI-AML3, SKM-1, NOMO-1, NB4, HEL, U937, NALM6, MEC-1, MEC-2, Hs 505.T and REC-1 cells, respectively[1].
QL-X-138 (0.5-5 μM; 24-72 h) arrests the progression of Ramos, OCI-AML-3, U937 and U2932 cells cycle in a dose dependent manner[1].
QL-X-138 (0.5-5 μM; 8-72 h) induces apoptosis of Ramos, OCI-AML-3, U937 and U2932 cells in a time- and dose-dependent manner[1].
QL-X-138 (3-10000 nM; 4 h) blocks BTK- and MNK-mediated signaling in lymphoma and leukemia cell[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis[1]

Cell Line: Ramos, OCI-AML3, U2932, TMD8 and U937 cells
Concentration: 3, 10, 30, 100, 300, 1000, 3000, 10000 nM
Incubation Time: 4 hours
Result: Significantly suppressed BTK auto-phosphorylation of Y223 (EC50=11 nM).
Strongly blocked phosphorylation of the BTK downstream target PLCγ2 Y1217 (EC50=57 nM).
Suppressed the phosphorylation of the MNK downstream target eIF4E S209 at a concentration of 1 μM.








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  • [1]. Wu H, et, al. Discovery of a BTK/MNK dual inhibitor for lymphoma and leukemia. Leukemia. 2016 Jan;30(1):173-81.

    [2]. Wispelaere M, et, al. Discovery of host-targeted covalent inhibitors of dengue virus. Antiviral Res. 2017 Mar;139:171-179.