OTS193320 是一种咪唑并 [1,2-a] 吡啶化合物，一种SUV39H2甲基转移酶活性抑制剂。OTS193320 降低乳腺癌细胞中的全局组蛋白 H3 赖氨酸 9 三甲基化水平并引发凋亡细胞死亡。与单一药剂 OTS193320 或 DOX 相比，OTS193320 与 Doxorubicin (DOX; HY-15142A) 的组合可以导致 γ-H2AX 水平以及癌细胞活力的降低。
| 生物活性 | OTS193320, a imidazo[1,2-a]pyridine compound, is aSUV39H2 methyltransferaseactivity inhibitor. OTS193320 decreases global histone H3 lysine 9 tri-methylation levels in breastcancercells and triggersapoptoticcell death. Combination of OTS193320 withDoxorubicin(DOX; HY-15142A) results in reduction of γ-H2AX levels as well ascancercell viability compared to a single agent OTS193320 or DOX[1]. |
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体外研究
(In Vitro) | OTS193320 (0.125-0.5 μM; 24 小时) 可以抑制乳腺癌细胞系的增殖。OTS193320 对 SUV39H2 阳性 A549 肺癌细胞具有生长抑制作用 (IC50=0.38 μM)[1]。
OTS193320 (0.5 μM; 48 小时) 诱导乳腺癌细胞凋亡[1]。
OTS193320 (0.125-0.5 μM; 24 小时) 以剂量依赖性方式降低 H3K9me3 水平[1]。
OTS193320 通过减弱 γ-H2AX 使乳腺癌细胞对多柔比星 (Doxorubicin) 敏感。与任一药物的单一药物治疗相比，OTS193320 和多柔比星的组合在体外显着降低癌细胞活力[1]。
Cell Viability Assay[1] | Cell Line: | MCF-7, SK-BR-3, ZR-75-1, T-47D, MDA-MB-231, BT-20 breast cancer cell lines | | Concentration: | 0-1 μM | | Incubation Time: | 72 hours | | Result: | Had Growth inhibitory effect on MCF-7, SK-BR-3, ZR-75-1, T-47D, MDA-MB-231, and BT-20 breast cancer cell lines with IC50values from 0.41 to 0.56 μM, respectively. |
Apoptosis Analysis[1] | Cell Line: | MDA-MB-231 and BT-20 cells | | Concentration: | 0.5 μM | | Incubation Time: | 48 hours | | Result: | Showed an increase in the number of cells at early- and late-stage apoptosis. |
Western Blot Analysis[1] | Cell Line: | MDA-MB-231 and BT-20 cells | | Concentration: | 0.125, 0.25, 0.5 μM | | Incubation Time: | 24 hours | | Result: | Caused attenuation of H3K9me3 levels in a dose-dependent manner. |
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| 运输条件 | Room temperature in continental US; may vary elsewhere. |
| 储存方式 | Please store the product under the recommended conditions in the Certificate of Analysis. |
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