TD52, an Erlotinib derivative, is an orally active, potent cancerous inhibitor of protein phosphatase 2A (CIP2A) inhibitor. TD52 mediates the apoptotic effect in triple-negative breast cancer (TNBC) cells via regulating the CIP2A/PP2A/p-Akt signalling pathway. TD52 indirectly reduced CIP2A by disturbing Elk1 binding to the CIP2A promoter. TD52 has less p-EGFR inhibition and has potent anti-cancer activity. In Vitro TD52 (2-10 μM; 48 hours) shows anti-proliferative ability and induces differential apoptotic effects in these cell lines. TD52 (5 μM; 48 hours) has minimal effects on p-EGFR or EGFR expression but downregulated CIP2A expression. TD52 (2.5, 5, 7.5 μM; 48 hours) time-dependently induces apoptosis accompanied with downregulating CIP2A and p-Akt. TD52 (5 μM; 24 hours) significantly increases the phosphatase activity of PP2A in TNBC cells. TD52 (5 μM; 48 hours) has no obvious effects on other common RTKs, such as IGFR, PDGFR and VEGFR2. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Apoptosis AnalysisCell Line: Three TNBC cell lines including HCC-1937, MDA-MB-231 and MDA-MB-468 cells Concentration: 2, 4, 6, 8, 10 μM Incubation Time: 48 hours Result: Showed anti-proliferative ability and induced differential apoptotic effects in these cell lines. Western Blot AnalysisCell Line: MDA-MB-231 cell Concentration: 5 μM Incubation Time: 48 hours Result: Had minimal effects on p-EGFR or EGFR expression but downregulated CIP2A expression. In Vivo TD52 (10 mg/kg/day; oral gavage; for 52 days) significantly inhibits MDA-MB-468 xenograft tumour size and tumour weight . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Female NCr athymic nude mice (5-7 weeks of age) Dosage: 10 mg/kg Administration: Oral gavage; daily; for 52 days Result: Significantly inhibits MDA-MB-468 xenograft tumour size and tumour weight. Decreased the protein expressions of CIP2A and p-Akt in the three MDA-MB-468 xenograft tumours. Form:Solid