DTHIB

Research use only, not for human use.

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

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