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编 号：F749735
分子式：C23H24N2O7
分子量：440.45
分子式：C23H24N2O7
分子量：440.45
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CAS No: 2195411-63-1
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生物活性：
DSO-5a is a potent, selective, orally active BB3 agonist. DSO-5a is a representative DMAKO-00 derivative compound. DSO-5a upregulates ppar-γ activity through BB3 and activates ERK1/2 phosphorylation. DSO-5a can be used in diabetes-related research.
体内研究：
DSO-5a (3-30 mg/kg; P.O.; 30 分钟) 在 C57BL/6 小鼠中以剂量依赖性方式降低血糖波动。DSO-5a (10 mg/kg/day; P.O.; 2-4 周) 可以降低糖尿病 db/db 小鼠血糖浓度。Animal Model:C57BL/6 mice
Dosage:3 mg/kg; 10 mg/kg; 30 mg/kg
Administration:Oral administration;30 min before glucose challenge (3 g/kg)
Result:Showed that the change rates of AUC at 3, 10 and 30 mg/kg were 5.03, 16.42 and 28.30%, respectively.In BB3 knockout mice, DSO-5a failed to inhibit blood glucose drift.
Animal Model:Diabetic db/db mice
Dosage:10 mg/kg/day
Administration:Oral administration; 2-4 weeks
Result:After two weeks of treatment, the blood glucose excursion of db/db mice was significantly reduced.After four weeks, fasting blood glucose levels, glycosylated serum protein (GSP), and HOMA-IR were significantly decreased in the DSO-5a treatment group. Increased the protein expression of PPAR-gamma in white adipose tissue of db/db mice.
体外研究：
DSO-5a (50 nM; 60min) 在 hBB3-HEK 细胞中诱导 IP-1 积累，pEC50 值为 8.485，引起强烈的钙反应的 pEC50 值为 7.964。DSO-5a (500 nM; 60min) 在 mBB3-HEK 细胞中诱导 IP-1 积累，pEC50 值为 7.262，引起强烈的钙反应的 pEC50 值为 7.174。DSO-5a (0-100 nM； 8min) 在 hBB3-H1299 和 mBB3-HEK 细胞中引起 ERK1/2 的剂量依赖性激活。
DSO-5a is a potent, selective, orally active BB3 agonist. DSO-5a is a representative DMAKO-00 derivative compound. DSO-5a upregulates ppar-γ activity through BB3 and activates ERK1/2 phosphorylation. DSO-5a can be used in diabetes-related research.
体内研究：
DSO-5a (3-30 mg/kg; P.O.; 30 分钟) 在 C57BL/6 小鼠中以剂量依赖性方式降低血糖波动。DSO-5a (10 mg/kg/day; P.O.; 2-4 周) 可以降低糖尿病 db/db 小鼠血糖浓度。Animal Model:C57BL/6 mice
Dosage:3 mg/kg; 10 mg/kg; 30 mg/kg
Administration:Oral administration;30 min before glucose challenge (3 g/kg)
Result:Showed that the change rates of AUC at 3, 10 and 30 mg/kg were 5.03, 16.42 and 28.30%, respectively.In BB3 knockout mice, DSO-5a failed to inhibit blood glucose drift.
Animal Model:Diabetic db/db mice
Dosage:10 mg/kg/day
Administration:Oral administration; 2-4 weeks
Result:After two weeks of treatment, the blood glucose excursion of db/db mice was significantly reduced.After four weeks, fasting blood glucose levels, glycosylated serum protein (GSP), and HOMA-IR were significantly decreased in the DSO-5a treatment group. Increased the protein expression of PPAR-gamma in white adipose tissue of db/db mice.
体外研究：
DSO-5a (50 nM; 60min) 在 hBB3-HEK 细胞中诱导 IP-1 积累，pEC50 值为 8.485，引起强烈的钙反应的 pEC50 值为 7.964。DSO-5a (500 nM; 60min) 在 mBB3-HEK 细胞中诱导 IP-1 积累，pEC50 值为 7.262，引起强烈的钙反应的 pEC50 值为 7.174。DSO-5a (0-100 nM； 8min) 在 hBB3-H1299 和 mBB3-HEK 细胞中引起 ERK1/2 的剂量依赖性激活。
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