CAS: 657-24-9; N,N-Dimethylimidodicarbonimidic Diamide

该化合物是一种主要用于管理2型糖尿病的口服抗合血糖剂,它属于大抗原类药物和功能,通过减少肝糖生产,增强胰岛素敏感性,提高外阴素的敏感度以及改善外围葡萄糖的吸收和利用.Metformin的特点是水溶性相对较低,可影响其吸收和生物利用率.Metformin的化学配方是C4H11N5, 其分子重量约为129.16克/摩尔.它通常以盐盐的形式进行施用,增强其稳定性和溶性.Metformin一般都具有良好的耐受性,胃肠胃侧效应最为常见.重要的是,它不会造成重量增加,而且单独使用时也与低的低缺血糖风险有关.此外,Metformin已经研究潜在的心血管效益,并且可能在体重管理和多细胞综合症(PCOS)中发挥作用.其安全性特征和功效使其成为第2型糖尿病的治疗.

⚠️《化妆品禁用原料目录》
英文名称N,N-Dimethylimidodicarbonimidic Diamide
中文名称二甲双胍
IUPAC名称3-(diaminomethylidene)-1,1-dimethylguanidine
其它别名N,N-Dimethylimidodicarbonimidic diamide; 1-Carbamimidamido-N,N-dimethylmethanimidamide
CAS编号657-24-9
MFCD编号:MFCD00242652
EINECS号:211-517-8
分子式:C4H11N5
分子量:129.16
产品CID: 1638748
同类组份化合物CAS1115-70-4 (HCl)657-24-9 (free base)121369-64-0 (glycinate)34461-22-8 ( embonate)58840-24-7 (orotate)1384526-74-2 (icosapent)
产品分类原料药 → 激素及调节内分泌功能类药 → 胰腺激素及其它调节血糖药

相似结构搜索
InChIKey: XZWYZXLIPXDOLR-UHFFFAOYSA-N
InChI=1S/C4H11N5/c1-9(2)4(7)8-3(5)6/h1-2H3,(H5,5,6,7,8)…
计算化学: 氢键受体数1.0氢键供体数3.0可旋转键数2.0

物理性质

熔点199-200 °C
沸点229.23 °C
闪点58.1±22.6 °C
密度1.0743
pKa:pKa 2.8(H2O,t =32) (Uncertain)
PSA:88.99
LogP:-2.31
折射率1.576
蒸汽压1.3±0.3 mmHg at 25°C
溶解性Acetonitrile (Slightly), Aqueous Acid (Slightly), Dichloromethane (Slightly)
外观形态白色至浅棕色固体
储存条件请置于阴暗处, 惰性气氛中,室温
产品应用该化合物用作降低节食和春后高血糖,提高外围组织(如肌肉和脂肪组织)对胰岛素的敏感性,增加食用葡萄糖,促进厌食性凝解,抑制肝血管凝胶的产生,减少肝糖素产出,抑制肠溶胶的吸收,对非依赖性糖尿病的成年人进行抑制,并有利于某些依赖胰岛分泌的病人.在患者中,可以使用甲基素作为单体不适应饮食的单体疗法,或与磺酰胺或胰岛结合,以加强控制.由于体重中和体重下降作用,乙型糖尿病特别适合超重或肥胖的病人,在控制范围以外,甲型血压通过整体的胆碱和胆碱水平降低三基胆碱.

MSDS等安全信息

GHS象形图
GHS符号GHS07;
注释: Exclamation mark
危险类别急性毒性类别4(经口)
警示词Warning(警告)
危险描述H302 |吞咽有害.
防范说明P264-P270-P301+P312-P330-P501
安全声明IDENTIFICATION AND USE: Metformin is antihyperglycemic, not hypoglycemic agent. It does not cause insulin release from the pancreas and does not cause hypoglycemia, even in large doses. HUMAN EXPOSURE AND TOXICITY: Metformin is believed to work by inhibiting hepatic glucose production and increasing the sensitivity of peripheral tissue to insulin. It does not stimulate insulin secretion, which explains the absence of hypoglycemia. Metformin also has beneficial effects on the plasma lipid concentrations and promotes weight loss. Accumulation of metformin may occur in patients with renal impairment, and such accumulation rarely can result in lactic acidosis, a serious, potentially fatal metabolic disease. Lactic acidosis constitutes a medical emergency requiring immediate hospitalization and treatment; lactic acidosis is characterized by elevated blood lactate concentrations, decreased blood pH, electrolyte disturbances with an increased anion gap, and an increased lactate/pyruvate ratio. Lactic acidosis also may occur in association with a variety of pathophysiologic conditions, including diabetes mellitus, and whenever substantial tissue hypoperfusion and hypoxemia exist. Approximately 50% of cases of metformin-associated lactic acidosis have been reported to be fatal. No evidence of mutagenicity or chromosomal damage was observed in in vitro test systems, including human lymphocytes assay. ANIMAL STUDIES: No evidence of carcinogenic potential was seen in a 104-week study in male and female rats receiving metformin hydrochloride dosages up to and including 900 mg/kg daily or in a 91-week study in male and female mice receiving metformin hydrochloride at dosages up to and including 1500 mg/kg daily. Cancer preventive effect of metformin (MF) has been studied in mice, rats and hamsters. In the majority of cases metformin treatment leads to inhibition of carcinogenesis. No evidence of impaired fertility was observed in rats following administration of metformin hydrochloride dosages of 600 mg/kg daily. Reproduction studies in rats and rabbits given metformin hydrochloride dosages of 600 mg/kg daily have not revealed teratogenicity. No evidence of mutagenicity or chromosomal damage was observed in vivo in a micronucleus test in mice or in in vitro test systems, including microbial (Ames test) and mammalian (mouse lymphoma) assays. Pretreatment of rat cerebellar granule neurons with metformin greatly enhanced cell viability against glutamate-induced neurotoxicity. In aged male mice fed high-fat diet supplemented with metformin for 6 months, metformin decreased body fat composition and attenuated declines in motor function induced by a high fat diet. Performance in the Morris water maze test of hippocampal based memory function, showed that metformin prevented impairment of spatial reference memory associated with the high fat diet. ECOTOXICITY STUDIES: Adult fathead minnows (Pimephales promelas) were chronically exposed to metformin for 4 wk, at 40 ug/L. Metformin treatment induced significant up-regulation of messenger ribonucleic acid (mRNA) encoding the egg-protein vitellogenin in male fish, an indication of endocrine disruption. | Metformin overdose is associated with hypoglycemia and lactic acidosis. If the clinicians suspect lactic acidosis due to toxic metformin levels, they immediately recommend discontinuing the medication and initiating hemodialysis. Metformin is easily dialyzable owing to its small molecular weight and minimal protein binding. In cases of metformin toxicity, treatment primarily involves supportive care, as no specific antidote is available yet. | Metformin's mechanisms of action differ from other classes of oral antihyperglycemic agents. Metformin decreases blood glucose levels by decreasing hepatic glucose production, decreasing intestinal absorption of glucose, and improving insulin sensitivity by increasing peripheral glucose uptake and utilization. These effects are mediated by the initial activation by metformin of AMP-activated protein kinase (AMPK), a liver enzyme that plays an important role in insulin signaling, whole body energy balance, and the metabolism of glucose and fats. Activation of AMPK is required for metformin's inhibitory effect on the production of glucose by liver cells. Increased peripheral utilization of glucose may be due to improved insulin binding to insulin receptors. Metformin administration also increases AMPK activity in skeletal muscle. AMPK is known to cause GLUT4 deployment to the plasma membrane, resulting in insulin-independent glucose uptake. The rare side effect, lactic acidosis, is thought to be caused by decreased liver uptake of serum lactate, one of the substrates of gluconeogenesis. In those with healthy renal function, the slight excess is simply cleared. However, those with severe renal impairment may accumulate clinically significant serum lactic acid levels. Other conditions that may precipitate lactic acidosis include severe hepatic disease and acute/decompensated heart failure.

欧盟法规

ECHA物质ECHA物质化妆品禁用物质清单C&L通报REACH预注册

上下游产品

合成工艺路线路线简述

合成目标产物 Metformin 主要起始原料 Metformin Hydrochloride
(文献来源)合成步骤主要原料 Metformin Hydrochloride

N1,N1-Dimethyl-S-Phenyl-N4-Thiohydroxybiguanidine置于human Serum体系中,化学反应生成二甲双胍
参考文献: Novel Prodrugs Of Metformin[fr] Nouveaux Promédicaments De La Metformine
标题: Novel Prodrugs Of Metformin[fr] Nouveaux Promédicaments De La Metformine
摘要:本发明涉及新型二甲双胍前药,其药用盐,含有前药的药物组合物,以及使用前药的方法.具体而言,本发明涉及将含硫的前体连接到二甲双胍上,形成新型可逆生物硫酰基胍(n-S)二甲双胍前药,其具有改善的口服吸收性能,从而提高生物利用度.

海关参考信息

2921199090-其他无环单胺
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主要参考文献

1: Sutter A, Landis D, Nugent K. Metformin has immunomodulatory effects which support its potential use as adjunctive therapy in tuberculosis. Indian J Tuberc. 2024 Jan;71(1):89-95. doi: 10.1016/j.ijtb.2023.05.011. Epub 2023 May 16.
182:15-23. doi: 10.1016/j.ygyno.2024.01.007. Epub ahead of print. 25(1):323. doi: 10.3390/ijms25010323.
9: Alatawi AM. Metformin versus sodium glucose co-transporters inhibitors as first-line for atherosclerotic cardiovascular disease: A meta-analysis. Pak J Med Sci. 2024 Jan-Feb;40(1Part-I):209-213. doi: 10.12669/pjms.40.1.6982.