DTHIB

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

DTHIB 强烈抑制 HSF1 癌症基因特征和前列腺癌细胞增殖。

DTHIB robustly inhibits the HSF1 cancer gene signature and prostate cancer cell proliferation.

DTHIB (5 μM; 48 hours) treatment of C4-2 cells induces cell cycle arrest, with accumulation in the G1 phase. DTHIB stimulates C4-2 PCa cell entry into senescence. DTHIB (0.5-5 μM; 48 hours; C4-2 prostate cancer) treatment reduces steady-state protein abundance of the molecular chaperones P23, HSP27, HSP70, and HSP90-all bona fide HSF1 targets in C4-2 cells. DTHIB dose-dependently reduces the clonal expansion of both C4-2 and PC-3 PCa cells with EC50 values of 1.2 μM and 3.0 μM, respectively. In mouse embryonic fibroblasts (MEFs), DTHIB (0.5-10 μM) attenuates the robust acute heat shock induction of the HSP70 and HSP25 molecular chaperones in a dose-dependent manner. DTHIB attenuates the heat shock response by reducing the steady-state transcript abundance of multiple molecular chaperones. Cell Cycle Analysis Cell Line:C4-2 cells Concentration:5 μM Incubation Time:48 hours Result:Induced cell cycle arrest.Western Blot Analysis Cell Line:C4-2 prostate cancer (PCa) cells Concentration:0.5 μM, 1 μM, 2.5 μM, 5 μM Incubation Time:48 hours Result:Dose-dependently inhibited expression of molecular chaperones in C4-2 PCa cells.

DTHIB (5 mg/kg; intraperitoneal injection; daily; for 3 weeks) treatment potently attenuates tumor progression in a C4-2 xenograft mouse model. Animal Model:Nude mice (6 weeks of age) injected with C4-2 cells Dosage:5 mg/kg Administration:Intraperitoneal injection; daily; for 3 weeks Result:Showed no visible tumor growth over a 3-week period and a 40% reduction in median tumor volume.

——

Cytoskeleton/Cell Adhesion Molecules

HSP

HSF1

——

——

897326-30-6

309.68

C13H9ClFN3O3

>98% (HPLC)

DMSO:10 mM

O=C(NC1=CC=C(F)C=C1)NC2=CC=C(Cl)C([N+]([O-])=O)=C2

——

(-20℃)

With Ice Pack

≥ 2 years