产品
编 号：F196890
分子式：C14H20O
分子量：204.31
分子式：C14H20O
分子量：204.31
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
1mg
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5mg
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10mg
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25mg
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询价
结构图
CAS No: 1637741-58-2
产品详情
生物活性：
Cipepofol (Ciprofol), a novel 2,6-disubstituted phenol derivative, is a positive allosteric modulator and direct agonist of the GABAA receptor. Cipepofol can cause the central nerve inhibition and promote sleep based on the structural modification of Propofol (HY-B0649). Cipepofol can activate the sirtuin1 (Sirt1)/Nrf2 pathway. Cipepofol protects the heart against Isoproterenol (ISO; HY-B0468)-induced myocardial infarction by reducing cardiac oxidative stress, inflammatory response and cardiomyocyte apoptosis.
体内研究：
Cipepofol (Ciprofol；100 μL；ISO 前 1 小时植入小鼠腹部) 可抑制 ISO 诱导的心肌损伤、心功能障碍、炎症和心肌细胞凋亡。 Animal Model:Eighty male C57BL/6 mice (20-24 g, 8-10 weeks)
Dosage:100 μl
Administration:Implanted into the abdomen of mice 1 h before ISO
Result:Attenuated increased the content of serum CK-MB, LDH, and cTnT by ISO insults (100 mg/kg; sc; for 2 consecutive days to induce experimental myocardial infarction). Significantly improved ISO-induced LV systolic and diastolic dysfunction.Largely suppressed the increases in IL-6 IL-17 and TNF-α expression.
体外研究：
Cipepofol (Ciprofol) 可通过与 GABAA 受体氯离子通道中的丁基双环硫代磷酸酯和叔丁基双环原苯甲酸酯靶标竞争性结合来引发氯离子流入。氯离子的流入可引起神经细胞膜超极化，通过增加细胞内氯离子浓度，进一步激活 GABA 能神经元，实现中枢神经抑制。Cipepofol (5 μM；ISO 损伤前；持续 6 小时) 可减弱 ISO 处理的 H9c2 细胞中 CK-MB、LDH 和 cTnT 含量的增加。Cipepofol 减弱 ISO 诱导的体外心肌细胞凋亡。
Cipepofol (Ciprofol), a novel 2,6-disubstituted phenol derivative, is a positive allosteric modulator and direct agonist of the GABAA receptor. Cipepofol can cause the central nerve inhibition and promote sleep based on the structural modification of Propofol (HY-B0649). Cipepofol can activate the sirtuin1 (Sirt1)/Nrf2 pathway. Cipepofol protects the heart against Isoproterenol (ISO; HY-B0468)-induced myocardial infarction by reducing cardiac oxidative stress, inflammatory response and cardiomyocyte apoptosis.
体内研究：
Cipepofol (Ciprofol；100 μL；ISO 前 1 小时植入小鼠腹部) 可抑制 ISO 诱导的心肌损伤、心功能障碍、炎症和心肌细胞凋亡。 Animal Model:Eighty male C57BL/6 mice (20-24 g, 8-10 weeks)
Dosage:100 μl
Administration:Implanted into the abdomen of mice 1 h before ISO
Result:Attenuated increased the content of serum CK-MB, LDH, and cTnT by ISO insults (100 mg/kg; sc; for 2 consecutive days to induce experimental myocardial infarction). Significantly improved ISO-induced LV systolic and diastolic dysfunction.Largely suppressed the increases in IL-6 IL-17 and TNF-α expression.
体外研究：
Cipepofol (Ciprofol) 可通过与 GABAA 受体氯离子通道中的丁基双环硫代磷酸酯和叔丁基双环原苯甲酸酯靶标竞争性结合来引发氯离子流入。氯离子的流入可引起神经细胞膜超极化，通过增加细胞内氯离子浓度，进一步激活 GABA 能神经元，实现中枢神经抑制。Cipepofol (5 μM；ISO 损伤前；持续 6 小时) 可减弱 ISO 处理的 H9c2 细胞中 CK-MB、LDH 和 cTnT 含量的增加。Cipepofol 减弱 ISO 诱导的体外心肌细胞凋亡。
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