TD52, a derivative of Erlotinib, is an orally active and potent inhibitor of protein phosphatase 2A (CIP2A). It induces apoptosis in triple-negative breast cancer (TNBC) cells by modulating the CIP2A/PP2A/p-Akt signaling pathway. TD52 indirectly decreases CIP2A levels by disrupting Elk1 binding to the CIP2A promoter. Despite exhibiting lower inhibition of p-EGFR, TD52 demonstrates significant anti-cancer activity [1]. TD52 functions as a click chemistry reagent, featuring an alkyne group enabling it to undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing azide groups.
体内研究
TD52 (10 mg/kg/day; oral gavage; for 52 days) markedly reduces both the size and weight of MDA-MB-468 xenograft tumors [1].
体外研究
TD52 (2-10 μM; 48 hours) exhibits anti-proliferative effects and induces varying apoptotic responses in these cell lines [1].
TD52 (5 μM; 48 hours) has negligible impact on p-EGFR or EGFR expression but reduces the expression of CIP2A [1].
TD52 (2.5, 5, 7.5 μM; 48 hours) induces apoptosis in a time-dependent manner, concomitant with the downregulation of CIP2A and p-Akt [1].
TD52 (5 μM; 24 hours) markedly enhances the phosphatase activity of PP2A in TNBC cells [1].
TD52 (5 μM; 48 hours) does not exert noticeable effects on other common RTKs, including IGFR, PDGFR, and VEGFR2 [1].
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