4-异丙氧基-N-(2-甲基喹啉-8-基)苯甲酰胺

生物活性靶点体外研究体内研究 4-异丙氧基-N-(2-甲基喹啉-8-基)苯甲酰胺试剂级价格

CAS号:892711-75-0
英文名:CDN 1163
中文名:4-异丙氧基-N-(2-甲基喹啉-8-基)苯甲酰胺
CBNumber:CB92722925
分子式:C20H20N2O2
分子量:320.39
MOL File:892711-75-0.mol

4-异丙氧基-N-(2-甲基喹啉-8-基)苯甲酰胺化学性质

熔点 :87 - 89°C
储存条件 :2-8°C
溶解度 :Soluble in DMSO (>25 mg/ml)
形态 :powder
颜色 :white to beige
稳定性 :Stable for 1 year as supplied. Solutions in DMSO may be stored at -20°C for up to 3 months.

4-异丙氧基-N-(2-甲基喹啉-8-基)苯甲酰胺性质、用途与生产工艺

生物活性 CDN1163是一种 sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) 的小分子变构激活剂，可改善 Ca2+ 稳态。
靶点
Target Value
SERCA
()

体外研究

CDN1163 (5.5-25 mM; 0-8 hours; rat cardiac myocyte cells) treatment reduces high glucose-induced resistin and nuclear NFATc expression and increases the phosphorylation of AMPKα in a time-dependent manner.

Western Blot Analysis

Cell Line:	Rat cardiac myocyte cells (H9c2)
Concentration:	5.5 mM, 25 mM
Incubation Time:	0 hour, 4 hours, 8 hours
Result:	High glucose-induced resistin and nuclear NFATc expression were significantly reduced. The phosphorylation of AMPKα is increased in a time-dependent manner.

体内研究

CDN1163 (50 mg/kg; intraperitoneal injection; for 5 days; male ob/ob mice and lean ob/+ mice) increases SERCA2 Ca ²⁺ -ATPase activity, decreases endoplasmic reticulum (ER) stress-induced cell death in vitro and improves liver Ca ²⁺ transport activity. CDN1163 reduces blood glucose levels and improves metabolic parameters and gluconeogenic gene expression, reverses hepatic steatosis, inhibits ER stress and ER stress-induced apoptosis, and improves mitochondrial efficiency in ob/ob mice in vivo.

Animal Model:	Male 8-10-week old ob/ob mice and lean ob/+ mice
Dosage:	50 mg/kg
Administration:	Intraperitoneal injection; for 5 days
Result:	Markedly lowered fasting blood glucose, improved glucose tolerance, and ameliorated hepatosteatosis but did not alter glucose levels or body weight. Increased expression of uncoupling protein 1 (UCP1) and UCP3 in brown adipose tissue and reduced the hepatic expression of genes involved in gluconeogenesis and lipogenesis, attenuated ER stress response and ER stress-induced apoptosis, and improved mitochondrial biogenesis, possibly through SERCA2-mediated activation of AMP-activated protein kinase pathway.