TD52 dihydrochloride |
Catalog No.GC64936 |
Erlotinib 유도체인 TD52 dihydrochloride는 경구 활성, 단백질 포스파타제 2A(CIP2A) 억제제의 강력한 암 억제제입니다. TD52 이염산염은 CIP2A/PP2A/p-Akt 신호 전달 경로를 조절하여 삼중 음성 유방암(TNBC) 세포에서 세포자멸사 효과를 매개합니다. TD52 이염산염은 CIP2A 프로모터에 대한 Elk1의 결합을 방해하여 CIP2A를 간접적으로 감소시켰습니다. TD52 dihydrochloride는 p-EGFR 억제가 적고 강력한 항암 활성을 가지고 있습니다.
Products are for research use only. Not for human use. We do not sell to patients.
Sample solution is provided at 25 µL, 10mM.
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.
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