NCT-58 |
| Catalog No.GC64714 |
Le NCT-58 est un puissant inhibiteur de la HSP90 C-terminale. NCT-58 n'induit pas la réponse au choc thermique (HSR) en raison de son ciblage de la région C-terminale et provoque une activité anti-tumorale via la régulation négative simultanée des membres de la famille HER ainsi que l'inhibition de la phosphorylation d'Akt. Le NCT-58 tue les cellules souches du cancer du sein résistantes au trastuzumab. NCT-58 induit l'apoptose des cellules cancéreuses du sein HER2-positives.
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Cas No.: 2411429-33-7
Sample solution is provided at 25 µL, 10mM.
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NCT-58 is a potent inhibitor of C-terminal HSP90. NCT-58 does not induce the heat shock response (HSR) due to its targeting of the C-terminal region and elicits anti-tumor activity via the simultaneous downregulation of HER family members as well as inhibition of Akt phosphorylation. NCT-58 kills Trastuzumab-resistant breast cancer stem-like cells. NCT-58 induces apoptosis in HER2-positive breast cancer cells[1].
NCT-58 treatment (0.1-20 μM; 72 hours) dose-dependently reduces cell viability in HER2-positive BT474 and SKBR3 cells[1]. NCT-58 treatment (0.1-10 μM; 72 hours) increases the number of early and late apoptotic cells in HER2-positive BT474 and SKBR3 cells[1].NCT-58 treatment (2-10 μM; 72 hours) effectively reduced the levels of truncated p95HER2 and its phosphorylated form, as well as downregulation of Akt and phospho-Akt (Ser473) protein contents in JIMT-1 and MDA-MB-453 cells[1].
NCT-58 (30 mg/kg; i.p.; every other day for 47 days) suppresses Trastuzumab-resistant tumor growth[1].NCT-58 (30 mg/kg; i.p.; every other day for 47 days) causes a significant impediment of tumor growth and a marked decrease in tumor weight[1].
[1]. Park S, et al. The C-terminal HSP90 inhibitor NCT-58 kills trastuzumab-resistant breast cancer stem-like cells. Cell Death Discov. 2021;7(1):354.
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