NCT-58是一种有效的C端HSP90抑制剂。NCT-58不会引起热休克反应（HSR）。NCT-58通过同时下调HER家族成员以及抑制Akt磷酸化来激发抗肿瘤活性。NCT-58杀死对曲妥珠单抗耐药的乳腺癌干细胞样细胞。NCT-58诱导HER2阳性乳腺癌细胞凋亡。

NCT-58 is a potent C-terminal HSP90 inhibitor. NCT-58 does not induce the heat shock response (HSR). NCT-58 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.

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. NCT-58 treatment (0.1-20 μM; 72 hours) dose-dependently reduces cell viability in HER2-positive BT474 and SKBR3 cells. 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) causes a significant impediment of tumor growth and a marked decrease in tumor weight. NCT-58 (30 mg/kg; i.p.; every other day for 47 days) suppresses Trastuzumab-resistant tumor growth[1].

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NCT58

DMSO:40 mg/mL (85. mM),Need ultrasonic
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In solvent: -80°C for 2 years