TD52 dihydrochloride |
| Katalog-Nr.GC64936 |
TD52-Dihydrochlorid, ein Erlotinib-Derivat, ist ein oral aktiver, potenter Krebshemmer des Proteinphosphatase-2A-(CIP2A-)Hemmers. TD52-Dihydrochlorid vermittelt die apoptotische Wirkung in dreifach negativen Brustkrebszellen (TNBC) Über die Regulierung des CIP2A/PP2A/p-Akt-Signalwegs. TD52-Dihydrochlorid reduzierte indirekt CIP2A, indem es die Elk1-Bindung an den CIP2A-Promotor stÖrte. TD52-Dihydrochlorid hat eine geringere p-EGFR-Hemmung und eine starke Anti-Krebs-AktivitÄt.
Products are for research use only. Not for human use. We do not sell to patients.
Sample solution is provided at 25 µL, 10mM.
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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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