TD52 dihydrochloride, an Erlotinib (HY-50896) derivative, is an orally active, potent cancerous inhibitor ofproteinphosphatase2A (CIP2A)inhibitor. TD52 dihydrochloride mediates theapoptoticeffect in triple-negative breastcancer(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].

433.33

Solid

C₂₄H₁₈Cl₂N₄

Room temperature in continental US; may vary elsewhere.

DMSO : 25 mg/mL(57.69 mM;ultrasonic and warming and heat to 60℃)

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