Metformin HCl
(Synonyms: 盐酸二甲双胍; 1,1-Dimethylbiguanide hydrochloride) 目录号 : GC17443A biguanide with diverse biological activities
Cas No.:1115-70-4
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Kinase experiment [1]: | |
AMPK assay |
For the AMPK assay, cells were seeded in six-well plates at 1.5 × 106 cells/well in DMEM containing 100 U/ml penicillin, 100 μg/ml streptomycin, 10% FBS, 100 nM insulin, 100 nM dexamethasone, and 5 μg/ml transferrin for 4 hours. Cells were then cultured in serum-free DMEM for 16 hours followed by treatment for 1 hour or 7 hours with control medium, 5-amino-imidazole carboxamide riboside (AICAR), or metformin at concentrations indicated. For a 39-hour treatment, cells for both control and metformin (10 or 20 μM) groups were cultured in DMEM plus 5% FBS and 100 nM insulin, and the fresh control and metformin-containing medium were replaced every 12 hours (last medium change was 3 hours before harvest). After treatment, the cells were directly lysed in digitonin-containing and phosphatase inhibitor–containing buffer A , followed by precipitation with ammonium sulfate at 35% saturation. AMPK activity was determined by measurement of phosphorylation of a synthetic peptide substrate, SAMS (HMRSAMSGLHLVKRR). |
Cell experiment [1]: | |
Cell lines |
Rat primary hepatocytes |
Preparation method |
The solubility of this compound in DMSO is limited. General tips for obtaining a higher concentration: Please warm the tube at 37℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months. |
Reacting condition |
10, 20, 500 μM, 2 mM; 39h; |
Applications |
Metformin activated AMPK in primary hepatocytes. Moreover, Metformin (2 mM, 3 hours) stimulated AMPK activity in skeletal muscle in association with induction of glucose uptake. Metformin (500 μM) reduced hepatic SREBP-1 expression in rat hepatocytes. |
Animal experiment: | |
Animal models |
Male C57BL/6 mice model; |
Dosage form |
200 mg/kg, oral gavage, twice daily for 5 days; or 250 mg/kg, intraperitoneal injection, for 3 days |
Applications |
Acetyl-CoA carboxylase (ACC) activity were reduced in metformin-treated rats [1]. Moreover, metformin required LKB1 in the liver to lower blood glucose levels [2]. |
Other notes |
Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
References: 1. Zhou, G., Myers, R., Li, Y., Chen, Y., Shen, X., Fenyk-Melody, J., Wu, M., Ventre, J., Doebber, T., Fujii, N., Musi, N., Hirshman, M. F., Goodyear, L. J. and Moller, D. E. (2001) Role of AMP-activated protein kinase in mechanism of metformin action. J Clin Invest. 108, 1167-1174 2. Shaw, R. J., Lamia, K. A., Vasquez, D., Koo, S. H., Bardeesy, N., Depinho, R. A., Montminy, M. and Cantley, L. C. (2005) The kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin. Science. 310, 1642-1646 |
Metformin HCl is one of the most effective and widely used therapeutics for treatment of type 2 diabetes. It selectively lowers the hepatic gluconeogenesis without rising insulin production, causing weight gain or hypoglycemia. [1]
AMPK (5'AMP-activated protein kinase) acts as a metabolic master switch regulating several intracellular systems including the cellular uptake of glucose, the β-oxidation of fatty acids and the biogenesis of GLUT4 (glucose transporter 4) and mitochondria.
In hepatocytes, AMPK was activated by metformin, followed by decreased ACC (acetyl-CoA carboxylase) activity, induction of fatty acid oxidization and suppression of lipogenic enzyme expression.[2] Metformin also inhibited mGPD (mitochondrial lycerophosphate dehydrogenase),a redox shuttle enzyme, leading to an altered hepatocellular redox state, decreased conversion of lactate and reduced hepatic gluconeogenesis. [1]
In rats treated with metformin, hepatic expression of SEREP-1 mRNAs/protein and activity of ACC were reduced. [2] In metformin treated mice, LKB1 in liver was essential for the ability of metformin to reduce blood glucose [3]. In ASO (Antisense oligonucleotide) knockdown of hepatic mGOD in rats, the phenotype was similar to chronic metformin treatment. It abolished mefromin-induced cytosolic redox state, reduction in plasma glucose concentration and EGP inhibition. [1]
盐酸二甲双胍是治疗2型糖尿病最有效、应用最广泛的药物之一。它选择性地降低肝脏糖异生,而不会增加胰岛素产量,导致体重增加或低血糖。[1]
AMPK(5’AMP活化的蛋白激酶)作为代谢主开关,调节几个细胞内系统,包括葡萄糖的细胞摄取、脂肪酸的β-氧化以及GLUT4(葡萄糖转运蛋白4)和线粒体的生物发生。
在肝细胞中,AMPK被二甲双胍激活,随后ACC(乙酰辅酶A羧化酶)活性降低,诱导脂肪酸氧化并抑制脂肪生成酶的表达。[2] 二甲双胍还抑制mGPD(线粒体甘油磷酸脱氢酶),这是一种氧化还原穿梭酶,导致肝细胞氧化还原状态改变,乳酸转化率降低,肝糖异生减少。[1]
在用二甲双胍治疗的大鼠中,肝脏SEREP-1 mRNA/蛋白的表达和ACC的活性降低。[2] 在二甲双胍治疗的小鼠中,肝脏中的LKB1对二甲双胍降低血糖的能力至关重要[3]。在大鼠肝mGOD的ASO(反义寡核苷酸)敲除中,表型与慢性二甲双胍治疗相似。它消除了mefromin诱导的胞质氧化还原状态、血浆葡萄糖浓度降低和EGP抑制。[1]
References:
1. Madiraju AK, Erion DM, Rahimi Y et al. Metformin suppresses gluconeogenesis by inhibiting mitochondrial glycerophosphate dehydrogenase. Nature. 2014 Jun 26;510(7506):542-6.
2. Zhou G, Myers R, Li Y et al. Role of AMP-activated protein kinase in mechanism of metformin action. J Clin Invest. 2001 Oct;108(8):1167-74.
3. Shaw RJ, Lamia KA, Vasquez D et al. The kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin. Science. 2005 Dec 9;310(5754):1642-6.
Cas No. | 1115-70-4 | SDF | |
别名 | 盐酸二甲双胍; 1,1-Dimethylbiguanide hydrochloride | ||
化学名 | 3-(diaminomethylidene)-1,1-dimethylguanidine;hydrochloride | ||
Canonical SMILES | CN(C)C(=N)N=C(N)N.Cl | ||
分子式 | C4H12ClN5 | 分子量 | 165.62 |
溶解度 | ≥ 8.3mg/mL in DMSO, ≥ 30.7mg/mL in Water | 储存条件 | Store at -20°C |
General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效。 储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。 为了提高溶解度,请将管子加热至37℃,然后在超声波浴中震荡一段时间。 |
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Shipping Condition | 评估样品解决方案:配备蓝冰进行发货。所有其他可用尺寸:配备RT,或根据请求配备蓝冰。 |
制备储备液 | |||
1 mg | 5 mg | 10 mg | |
1 mM | 6.0379 mL | 30.1896 mL | 60.3792 mL |
5 mM | 1.2076 mL | 6.0379 mL | 12.0758 mL |
10 mM | 0.6038 mL | 3.019 mL | 6.0379 mL |
第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量) | ||||||||||
给药剂量 | mg/kg | 动物平均体重 | g | 每只动物给药体积 | ul | 动物数量 | 只 | |||
第二步:请输入动物体内配方组成(配方适用于不溶于水的药物;不同批次药物配方比例不同,请联系GLPBIO为您提供正确的澄清溶液配方) | ||||||||||
% DMSO % % Tween 80 % saline | ||||||||||
计算重置 |
计算结果:
工作液浓度: mg/ml;
DMSO母液配制方法: mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL,
体内配方配制方法:取 μL DMSO母液,加入 μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入 μL saline,混匀澄清。
1. 首先保证母液是澄清的;
2.
一定要按照顺序依次将溶剂加入,进行下一步操作之前必须保证上一步操作得到的是澄清的溶液,可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。