目录号 | 产品详情 | 靶点 | |
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TQ0232 | Histone Methyltransferase | ||
UNC0646 是一种有效的、选择性的同源蛋白赖氨酸甲基转移酶 G9a 和 GLP 抑制剂,IC50分别为 6 和 15 nM,对 G9a/GLP 的选择性比 SETD7、SUV39H2、SETD8 和 PRMT3 高。它降低 MDA-MB-231 细胞中H3K9me2的水平,IC50为 26 nM。 | |||
T77657 | transporter | ||
MSNBA 是一种通过 GLUT5 转运的选择性且有效的果糖转运抑制剂,也可作为 GLUT5 转运蛋白的探针。MSNBA 对 MCF7 细胞中 GLUT5 果糖摄取有抑制作用,KI 为 3.2±0.4 μM。 | |||
TN1018 | PPAR | ||
Angeloylgomisin H 是从五味子中提取的一种木脂素类天然产物。它通过激活PPAR-γ来改善胰岛素刺激的葡萄糖摄取潜力。 | |||
TN1222 | NOS CDK NO Synthase | ||
23-epi-26-Deoxyactein (27-Deoxyactein) 是一种黑升麻中的主要成分,能够阻止 TCDD 诱导的成骨细胞的损伤。它对 AhR,CYP1A1 和 ERK 的水平升高具有抑制作用。 | |||
T16923 | c-RET | ||
SPP-86 是有效的、选择性的RET 酪氨酸激酶抑制剂,其IC50=8 nM。它能够抑制 MCF7 细胞中 RET 诱导激活的 PI3K/Akt 和 MAPK 信号通路,也能抑制 RET 诱导的 ERα 磷酸化。 | |||
T81054 | VEGFR | ||
T-1-MCPAB为一种高效VEGFR-2抑制剂(IC50=0.135 µM),其显著抑制MCF7细胞迁移,适用于癌症相关研究。 | |||
TN6569 | |||
cis-Moschamine exerts antitumour effects on HeLa, MCF7 and A431 cells. | |||
T63045 | |||
(1S,3R)-GNE-502 (compound 179) 是一种 Erα 的有效降解剂,能够在 MCF7 HCS 细胞中降解 ERα (EC50: 13 nM)。(1S,3R)-GNE-502 可以用于与雌激素受体相关癌症的研究。 | |||
T61280 | |||
Colletotrichalactones A is a polyketide with moderate-to-potent cytotoxic activity against MCF7 cells, exhibiting an IC50 value of 35.06 μM [1]. | |||
TN4321 | Others | ||
Isopteleine shows weak cytotoxic activities against human breast cancer cells (MCF7). |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPK-00785 | ANXA2 Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
ANXA2, highly expressed in invasive breast cancer cells, is closely related with poor prognosis, and acts as a molecular switch to EGFR activation. ANXA2 expression is inversely correlated with cell sensitivity to gefitinib. Knockdown of ANXA2 expression in MDA-MB-231 cells increased the gefitinib induced cell death. When ANXA2 was overexpressed in MCF7 cells, the gefitinib induced cell death was decreased. Furthermore, the phosphorylation of ANXA2 at Tyr23 is negatively correlated with the sensitivity of TNBC to gefitinib.
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TMPK-00784 | ANXA2 Protein, Human, Recombinant (His) | Human | E. coli | ||
ANXA2, highly expressed in invasive breast cancer cells, is closely related with poor prognosis, and acts as a molecular switch to EGFR activation. ANXA2 expression is inversely correlated with cell sensitivity to gefitinib. Knockdown of ANXA2 expression in MDA-MB-231 cells increased the gefitinib induced cell death. When ANXA2 was overexpressed in MCF7 cells, the gefitinib induced cell death was decreased. Furthermore, the phosphorylation of ANXA2 at Tyr23 is negatively correlated with the sensitivity of TNBC to gefitinib.
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