产品
编 号：F506790
分子式：C13H9ClFN3O3
分子量：309.68
分子式：C13H9ClFN3O3
分子量：309.68
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
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1mg
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5mg
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10mg
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25mg
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50mg
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100mg
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结构图
CAS No: 897326-30-6
产品详情
生物活性：
DTHIB is a direct and selective heat shock factor 1 (HSF1) inhibitor with a Kd of 160 nM for DTHIB binding to the HSF1 DNA binding domain (DBD). DTHIB inhibits HSF1 cancer gene signature (HSF1 CaSig) and selectively stimulates degradation of nuclear HSF1. DTHIB has potently anticancer activities and can be used for prostate cancer research.
体内研究：
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.
体外研究：
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.
DTHIB is a direct and selective heat shock factor 1 (HSF1) inhibitor with a Kd of 160 nM for DTHIB binding to the HSF1 DNA binding domain (DBD). DTHIB inhibits HSF1 cancer gene signature (HSF1 CaSig) and selectively stimulates degradation of nuclear HSF1. DTHIB has potently anticancer activities and can be used for prostate cancer research.
体内研究：
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.
体外研究：
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.
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