NCT-58是 HSP90 C末端的有效抑制剂。NCT-58 不诱导热休克反应 (HSR)，因为它靶向 C 末端区域，并通过同时下调 HER 家族成员以及抑制 Akt 磷酸化来引发抗肿瘤活性。NCT-58 可杀死曲妥珠单抗耐药 (Trastuzumab-resistant) 的乳腺癌干细胞样细胞。NCT-58 诱导 HER2 阳性乳腺癌细胞凋亡。在抗曲妥珠单抗异种移植模型中，NCT-58 可抑制生长和血管生成。

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.

Solid

HSP90 Apoptosis

NCT-58 treatment (0.1-20?μM;?72 hours) dose-dependently reduces cell viability in HER2-positive BT474 and SKBR3 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 (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. has not independently confirmed the accuracy of these methods. They are for reference only.

NCT-58 (30?mg/kg; i.p.; every other day for 47 days) suppresses Trastuzumab-resistant tumor growth.
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. has not independently confirmed the accuracy of these methods. They are for reference only.

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[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.

In Vitro: DMSO : 50 mg/mL (107.17 mM; Need ultrasonic)配制储备液