产品
编 号：F198292
分子式：C27H30F6N2O2
分子量：528.53
分子式：C27H30F6N2O2
分子量：528.53
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
5mg
442
In-stock
10mg
708
In-stock
50mg
2232
In-stock
100mg
3348
In-stock
结构图
CAS No: 164656-23-9
产品详情
生物活性：
Dutasteride (GG745) is a potent inhibitor of both 5α-reductase isozymes. Dutasteride may possess off-target effects on the androgen receptor (AR) due to its structural similarity to DHT.
体内研究：
GG745 has a terminal half-life of approximately 240 hr, and single doses of >10 mg decreased DHT levels significantly more than did single 5-mg doses of finasteride.In placebo treated men without prostate cancer there was an 8.3% median increase in PSA at month 24 compared with -59.5% in those who received dutasteride, using doubled values to correct for dutasteride treatment.Toxicity: Dutasteride may affect male fertility and steroid hormone dynamics. Therefore, a 21-day reproduction study was conducted to determine the effects of dutasteride (10, 32 and 100 μg/L) on fish reproduction. Exposure to dutasteride significantly reduced fecundity of fish and affected several aspects of reproductive endocrine functions in both males and females.
体外研究：
Dutasteride inhibits 3H-T conversion to3H-DHT and, as anticipated, inhibits T-induced secretion of PSA and proliferation. However the drug also inhibited DHT-induced PSA secretion and cell proliferation (IC50 approximately 1 μM). Dutasteride competes for binding the LNCaP cell AR with an IC50 approximately 1.5 μM. High concentrations of dutasteride (10-50 μM), but not finasteride, in steroid-free medium, resulted in enhanced cell death, possibly by apoptosis. Dutasteride reduces cell viability and cell proliferation in both cell lines tested (androgen-responsive (LNCaP) and androgen-unresponsive (DU145) human prostate cancer (PCa)) .
Dutasteride (GG745) is a potent inhibitor of both 5α-reductase isozymes. Dutasteride may possess off-target effects on the androgen receptor (AR) due to its structural similarity to DHT.
体内研究：
GG745 has a terminal half-life of approximately 240 hr, and single doses of >10 mg decreased DHT levels significantly more than did single 5-mg doses of finasteride.In placebo treated men without prostate cancer there was an 8.3% median increase in PSA at month 24 compared with -59.5% in those who received dutasteride, using doubled values to correct for dutasteride treatment.Toxicity: Dutasteride may affect male fertility and steroid hormone dynamics. Therefore, a 21-day reproduction study was conducted to determine the effects of dutasteride (10, 32 and 100 μg/L) on fish reproduction. Exposure to dutasteride significantly reduced fecundity of fish and affected several aspects of reproductive endocrine functions in both males and females.
体外研究：
Dutasteride inhibits 3H-T conversion to3H-DHT and, as anticipated, inhibits T-induced secretion of PSA and proliferation. However the drug also inhibited DHT-induced PSA secretion and cell proliferation (IC50 approximately 1 μM). Dutasteride competes for binding the LNCaP cell AR with an IC50 approximately 1.5 μM. High concentrations of dutasteride (10-50 μM), but not finasteride, in steroid-free medium, resulted in enhanced cell death, possibly by apoptosis. Dutasteride reduces cell viability and cell proliferation in both cell lines tested (androgen-responsive (LNCaP) and androgen-unresponsive (DU145) human prostate cancer (PCa)) .
产品资料
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