产品
编 号：F018065
分子式：C30H50O5
分子量：490.72
分子式：C30H50O5
分子量：490.72
产品类型
规格
价格
是否有货
1mg
询价
询价
5mg
询价
询价
结构图
CAS No: 104121-92-8
产品详情
生物活性：
Eldecalcitol (ED-71) is an orally active vitamin D3 analogue, inhibits bone resorption and increases bone mineral density. Eldecalcitol (ED-71) displays anti-tumor effect and inhibits cell proliferation, migration and induces apoptosis by suppressing GPx-1.
体内研究：
Eldecalcitol (0.5 μg/kg；口服；每周两次，持续 4 周) 通过抑制 GPx-1 (谷胱甘肽过氧化物酶) 显示出抗癌作用。 Eldecalcitol (10，30，或 90 ng/kg；口服；每周 5 次，持续 12 周)，作为一种更有效的维生素 D3 类似物，可刺激局灶性骨形成 (微型模型) 并比骨化三醇更强烈地抑制骨吸收。Animal Model:Xenograft tumor model in mice (male athymic nude BALB/c mice)
Dosage:0.5 μg/kg
Administration:Oral gavage; twice a week for 4 weeks
Result:Reduced the growth rate of tumors, and downregulated the expression levels of PCNA and MMP- 2 and upregulated the expression of Bax in the tumors.Resulted in decrease of proliferation, the inhibition of migration, and the promotion of apoptosis.
Animal Model:Ovariectomized (OVX) rat model
Dosage:10, 30, or 90 ng/kg
Administration:Oral gavage; 5-times per week for 12 weeks
Result:Increased the lumbar and femoral BMD in a dose dependent manner. Stimulated focal bone formation that started without prior bone resorption, a process known as bone minimodeling.
体外研究：
Eldecalcitol (0-50 nM；24 小时) 没有细胞毒性，可 (0.5-50 nM；24 小时) 减少 LPS (5 μg/mL) 诱导的细胞死亡。 Eldecalcitol (5 nM；24 h) 通过激活 Nrf2 及其效应分子 HO-1抑制 LPS 诱导的细胞焦亡。 Eldecalcitol (0.5-50 nM；24 h) 具有抗细胞焦亡能力，并以剂量依赖性方式降低 NLRP3、caspase-1 和 IL-1β 的表达。 Eldecalcitol (0.04-40 nM；0-48 h) 抑制SCC-15 和 CAL-27 细胞的增殖和迁移。 Eldecalcitol (0.4 nM；48 h) 使细胞周期停滞在 G0/G1 期，并通过抑制GPx-1 (谷胱甘肽过氧化物酶) 在胃癌细胞中的表达。
Eldecalcitol (ED-71) is an orally active vitamin D3 analogue, inhibits bone resorption and increases bone mineral density. Eldecalcitol (ED-71) displays anti-tumor effect and inhibits cell proliferation, migration and induces apoptosis by suppressing GPx-1.
体内研究：
Eldecalcitol (0.5 μg/kg；口服；每周两次，持续 4 周) 通过抑制 GPx-1 (谷胱甘肽过氧化物酶) 显示出抗癌作用。 Eldecalcitol (10，30，或 90 ng/kg；口服；每周 5 次，持续 12 周)，作为一种更有效的维生素 D3 类似物，可刺激局灶性骨形成 (微型模型) 并比骨化三醇更强烈地抑制骨吸收。Animal Model:Xenograft tumor model in mice (male athymic nude BALB/c mice)
Dosage:0.5 μg/kg
Administration:Oral gavage; twice a week for 4 weeks
Result:Reduced the growth rate of tumors, and downregulated the expression levels of PCNA and MMP- 2 and upregulated the expression of Bax in the tumors.Resulted in decrease of proliferation, the inhibition of migration, and the promotion of apoptosis.
Animal Model:Ovariectomized (OVX) rat model
Dosage:10, 30, or 90 ng/kg
Administration:Oral gavage; 5-times per week for 12 weeks
Result:Increased the lumbar and femoral BMD in a dose dependent manner. Stimulated focal bone formation that started without prior bone resorption, a process known as bone minimodeling.
体外研究：
Eldecalcitol (0-50 nM；24 小时) 没有细胞毒性，可 (0.5-50 nM；24 小时) 减少 LPS (5 μg/mL) 诱导的细胞死亡。 Eldecalcitol (5 nM；24 h) 通过激活 Nrf2 及其效应分子 HO-1抑制 LPS 诱导的细胞焦亡。 Eldecalcitol (0.5-50 nM；24 h) 具有抗细胞焦亡能力，并以剂量依赖性方式降低 NLRP3、caspase-1 和 IL-1β 的表达。 Eldecalcitol (0.04-40 nM；0-48 h) 抑制SCC-15 和 CAL-27 细胞的增殖和迁移。 Eldecalcitol (0.4 nM；48 h) 使细胞周期停滞在 G0/G1 期，并通过抑制GPx-1 (谷胱甘肽过氧化物酶) 在胃癌细胞中的表达。
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