目录号 | 产品详情 | 靶点 | |
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T9122 | DUB | ||
XL177A 是一种选择性不可逆的 USP7 抑制剂,IC50为 0.34 nM。它通过 p53 依赖性机制引发癌杀伤细胞作用。 | |||
T9636 | CDK | ||
Dalpiciclib (SHR-6390) 是一种高选择性、口服生物利用度和相当效力的 CDK4 和 CKD6 抑制剂,IC50 分别为 12.4 nM 和 9.9 nM。它通过抑制磷酸化 Rb 蛋白和诱导 G1 细胞周期阻滞在食管鳞状细胞癌中发挥有效的抗肿瘤活性。 | |||
T5755 | Tyrosinase | ||
Aloesin 是芦荟的活性成分之一,能够通过 MAPK 信号通路发挥抗癌作用,并具有抗炎、紫外线保护和抗菌作用。 | |||
T16745 | Apoptosis Rho Ras | ||
Rhosin hydrochloride 是一种特异性 RhoA 亚家族Rho GTPases 抑制剂,抑制 RhoA-GEF 相互作用。它通过增强 D1 中棘神经元的可塑性和降低过度兴奋性来促进应激恢复,可诱导细胞凋亡。 | |||
T9629 | Epigenetic Reader Domain | ||
BRD4 Inhibitor-24 是一种具有抗肿瘤活性的 BRD4 小分子抑制剂。 | |||
T9205 | Phosphatase Others | ||
NCGC00378430 是一种 SIX1/EYA2 相互作用抑制剂。它部分逆转 SIX1 过表达介导的转录和代谢谱,并逆转 SIX1 诱导的 TGF-β 信号传导和上皮-间质转化。在小鼠模型中,它能够抑制 SIX1 介导的乳腺癌转移。 | |||
T12134 | Apoptosis c-Myc | ||
MYCMI-6 (NSC-354961) 是一种内源性MYC:MAX 蛋白相互作用抑制剂,选择性结合 MYC bHLHZip 域,Kd 值为 1.6 μM。它阻断 MYC 驱动的转录,以 MYC 依赖性的方式抑制肿瘤细胞的生长 ,诱导细胞凋亡。 | |||
T2679 | CDK | ||
BMS-265246 是一种有效的选择性 CDK1/2 抑制剂,对 CDK1/cyclin B 和 CDK2/cyclin E 的 IC50分别为6 nM 和9 nM。 | |||
T60002 | Histone Methyltransferase | ||
DC-S239 (DC-S239) 是一种选择性的组蛋白甲基转移酶 SETD7 抑制剂 (IC50 = 4.59 μM),具有抗癌活性。 | |||
T4459 | DNA Alkylator/Crosslinker | ||
PK11000 是一种烷化剂,可通过共价半胱氨酸修饰来稳定野生型和突变型p53的 DNA 结合结构域。 |
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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