TD52 dihydrochloride 是 Erlotinib 衍生物，一种具有口服活性的强效癌性蛋白磷酸酶 2A (CIP2A) 抑制剂。TD52 dihydrochloride 通过调节 CIP2A/PP2A/p-Akt 信号通路介导三阴性乳腺癌 (TNBC) 细胞的凋亡作用。TD52 dihydrochloride 通过干扰 Elk1 与 CIP2A 启动子的结合间接减少 CIP2A。TD52 dihydrochloride 具有小的 p-EGFR 抑制作用并具有抗癌活性。
货号:ajcx38590
CAS:N/A
分子式:C24H18Cl2N4
分子量：433.33
溶解度:DMSO : 25 mg/mL (57.69 mM; ultrasonic and warming and heat to 60°C)
纯度：98%
存储：Store at -20°C
库存：现货

Background:

TD52 dihydrochloride, an Erlotinib derivative, is an orally active, potent cancerous inhibitor of protein phosphatase 2A (CIP2A) inhibitor. TD52 dihydrochloride mediates the apoptotic effect in triple-negative breast cancer (TNBC) cells via regulating the CIP2A/PP2A/p-Akt signalling pathway. TD52 dihydrochloride indirectly reduced CIP2A by disturbing Elk1 binding to the CIP2A promoter. TD52 dihydrochloride has less p-EGFR inhibition and has potent anti-cancer activity[1].

TD52 dihydrochloride (2-10 μM; 48 hours) shows anti-proliferative ability and induces differential apoptotic effects in these cell lines[1]. TD52 dihydrochloride (5 μM; 48 hours) has minimal effects on p-EGFR or EGFR expression but downregulated CIP2A expression[1]. TD52 dihydrochloride (2.5, 5, 7.5 μM; 48 hours) time-dependently induces apoptosis accompanied with downregulating CIP2A and p-Akt[1]. TD52 dihydrochloride (5 μM; 24 hours) significantly increases the phosphatase activity of PP2A in TNBC cells[1]. TD52 dihydrochloride (5 μM; 48 hours) has no obvious effects on other common RTKs, such as IGFR, PDGFR and VEGFR2[1].

TD52 dihydrochloride (10 mg/kg/day; oral gavage; for 52 days) significantly inhibits MDA-MB-468 xenograft tumour size and tumour weight[1].

[1]. Chun-Yu Liu, et al. EGFR-independent Elk1/CIP2A signalling mediates apoptotic effect of an erlotinib derivative TD52 in triple-negative breast cancer cells. Eur J Cancer. 2017 Feb;72:112-123.