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- 详细信息
- 技术资料
- 保存条件：
Powder:-20℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year
- 保质期：
Powder:-20℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year
- 英文名：
Carvedilol Phosphate
- 库存：
现询
- 供应商：
北京索莱宝科技有限公司
- CAS号：
610309-89-2
- 规格：
100mg/50mg/25mg
| 规格： | 100mg | 产品价格： | ￥410.0 |
|---|---|---|---|
| 规格： | 50mg | 产品价格： | ￥250.0 |
| 规格： | 25mg | 产品价格： | ￥150.0 |
| 基本信息 | |
| CAS | No.610309-89-2 |
| 中文名称 | 卡维地洛磷酸盐 |
| 英文名称 | Carvedilol Phosphate |
| 别名 | BM 14190 phosphate hemihydrate |
| 分子式 | C24H26N2O4·H3PO4·1/2H2O |
| 分子量 | 513.48 |
| 溶解性 | Soluble in DMSO(Need ultrasonic) |
| 纯度 | ≥98% |
| 外观(性状) | Solid |
| 储存条件 | Powder:-20℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year |
| SMILES | COC1=CC=CC=C1OCCNCC(COC2=CC=CC3=C2C4=CC=CC=C4N3)O.COC1=CC=CC=C1OCCNCC(COC2=CC=CC3=C2C4=CC=CC=C4N3)O.O.OP(=O)(O)O.OP(=O)(O)O |
| InChIKey | LHNYXTULDSJZRB-UHFFFAOYSA-N |
| InChI | InChI=1S/2C24H26N2O4.2H3O4P.H2O/c2*1-28-21-10-4-5-11-22(21)29-14-13-25-15-17(27)16-30-23-12-6-9-20-24(23)18-7-2-3-8-19(18)26-20;2*1-5(2，3)4;/h2*2-12，17，25-27H，13-16H2，1H3;2*(H3，1，2，3，4);1H2 |
| PubChem CID | 11954344 |
| 靶点 | Adrenergic Receptor |
| 通路 | Endocrinology & Hormones;GPCR & G Protein；Neuronal Signaling |
| 背景说明 | 是一种非选择性 β/α-1 受体阻断剂。也是一种自噬 (autophagy) 诱导剂，可抑制 NLRP3 炎性体。 |
| 生物活性 | Carvedilol Phosphate 是一种非选择性β/α-1 阻滞剂。可抑制脂质过氧化反应，IC50 为 5 μM。是一种多效降压药，可用于治疗心绞痛和充血性心力衰竭。是一种自噬诱导剂，可抑制 NLRP3 炎性体。[1-3] |
| IC50 | lipid peroxidation: 5μM(IC50)[1] |
| In Vitro | Carvedilol inhibited lipid peroxidation in a dose-dependent manner with a 50% inhibitory concentration(IC50)of 5 mumol/l. Moreover，superoxide generation by activated human neutrophils in vitro was also inhibited by carvedilol with an IC50 of 28 mumol/l. Finally，carvedilol was shown to scavenge oxygen free radicals in a cell-free system with an IC50 of 25 mumol/l.[1] Carvedilol(CVL)attenuated NLRP3 inflammasome activation and pyroptosis in mouse macrophages，without affecting activation of the AIM2，NLRC4 and non-canonical inflammasomes. CVL caused autophagic induction through a Sirt1-dependent pathway，which inhibited the NLRP3 inflammasome.[2] In the in vivo mouse model of NLRP3-associated peritonitis，oral administration of CVL reduced peritoneal recruitment of neutrophils; the levels of IL-1β，IL-18，active caspase-1，ASC，IL-6，TNF-α，MCP-1，and CXCL1 in the lavage fluids; and the levels of NLRP3 and HO-1 in the peritoneal cells.[3] |
| 细胞实验 | After oral administration of one capsule of 25 mg or 50 mg carvedilol，significant reductions in the systolic and diastolic blood pressures(p less than 0.05-0.001)were observed in patients all had essential hypertension. Cardiac output showed a small，non-significant decrease from 5.81/min to 5.1 l/min.[1] In the rats of acute myocardial infarction，carvedilol(1 mg/kg，intravenously)reduced the infarct size by 47%(P < 0.01). In the minipigs the infarct size was reduced by 46 and 89%(P < 0.01)with carvedilol(0.3 or 1 mg/kg intravenously). In dogs with permanent coronary occlusion，carvedilol produced dose-dependent reductions in the infarct size of 46 and 63% for 0.3 and 1 mg/kg，respectively(P < 0.05).[2] |
| 数据来源文献 | [1]. Eggertsen R，et al. Acute haemodynamic effects of carvedilol (BM 14190)，a new combined beta-adrenoceptor blocker and precapillary vasodilating agent，in hypertensive patients. Eur J Clin Pharmacol. 1984;27(1):19-22. [2]. Feuerstein GZ，et al. Myocardial protection by the novel vasodilating beta-blocker，carvedilol: potential relevance of anti-oxidant activity. J Hypertens Suppl. 1993 Jun;11(4):S41-8. [3]. Wong WT，et al. Repositioning of the β-Blocker Carvedilol as a Novel Autophagy Inducer That Inhibits the NLRP3 Inflammasome. Front Immunol. 2018 Aug 22;9:1920. |
| 单位 | 瓶 |
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IC4360 卡维地洛磷酸盐 内分泌学/激素 索莱宝
￥150 - 410
