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。

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.

TD52 dihydrochloride (2-10 μM; 48 hours) shows anti-proliferative ability and induces differential apoptotic effects in these cell lines. TD52 dihydrochloride (5 μM; 48 hours) has minimal effects on p-EGFR or EGFR expression but downregulated CIP2A expression. TD52 dihydrochloride (2.5, 5, 7.5 μM; 48 hours) time-dependently induces apoptosis accompanied with downregulating CIP2A and p-Akt. TD52 dihydrochloride (5 μM; 24 hours) significantly increases the phosphatase activity of PP2A in TNBC cells. 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].

C24H18Cl2N4

433.33

TD52 2HCl;TD52 dihydrochloride(1798328-24-1 Free base);TD52 dihydrochloride

DMSO:22.5mg/mL (51.9mM),ultrasonic and warming and heat to 60°C
Powder: -20°C for 3 years
In solvent: -80°C for 2 years