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Metformin hydrochloride

产品编号 T0740 CAS 1115-70-4

别名: Metformin HCl, 盐酸二甲双胍, 1, 1-Dimethylbiguanide hydrochloride, 1,1-Dimethylbiguanide hydrochloride

Metformin hydrochloride (1,1-Dimethylbiguanide hydrochloride) 是一种抗糖尿病药物，抑制结肠、前列腺等多种 Y 细胞的增殖，具有作为抗 Y 药物的潜在功能。它可以透过血脑屏障，诱导自噬。

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Metformin hydrochloride Chemical Structure

Metformin hydrochloride, CAS 1115-70-4

规格	价格/CNY	货期
50 mg	￥ 168	现货
100 mg	￥ 233	现货
500 mg	￥ 536	现货
1 g	￥ 728	现货
5 g	￥ 2,160	现货

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其他形式的 Metformin hydrochloride:

选择批次

纯度: 99.81%

纯度: 97.53%

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生物活性

化学信息

存储 & 溶解度

参考文献

相关产品

产品描述	Metformin hydrochloride (1,1-Dimethylbiguanide hydrochloride) , a widely used anti-diabetic drug, has a potential function as an anti-Y medicine. It inhibits the proliferation of a variety of Y cells including colon, prostate, and etc.
体外活性	In primary cultured hepatocytes from both rats and humans, metformin activated AMPK in a concentration- and time-dependent manner. rat hepatocytes were incubated with 10 μM or 20 μM metformin for 39 hours. Both 10 μM and 20 μM metformin produced significant AMPK activation [1]. Metformin inhibited proliferation of ESCs in a concentration-dependent manner. The IC50 was 2.45?mmol/l for adenomyotic endometrial stroma cells (A-ESCs) and 7.87?mmol/l for normal endometrial stromal cells (N-ESCs) [2]. Metformin selectively kills cancer stem cells (CSCs) and, as such, acts together with chemotherapy to inhibit tumor growth and prolong remission in mouse xenografts. In CSCs, metformin significantly inhibits expression of a variety of inflammatory genes, Lin28B gene expression, and VEGF protein expression [3].
体内活性	Hepatic fatty acid oxidation was induced in metformin-treated rats. Furthermore, metformin treatment produced significant decreases in hepatic expression of mRNAs for SREBP-1, FAS, and S14 [1]. Crl:CD(SD) rats were administered metformin at 0, 200, 600, 900 or 1200 mg/kg/day by oral gavage for 13 weeks. Administration of > or =900 mg/kg/day resulted in moribundity/mortality and clinical signs of toxicity. Other adverse findings included increased incidence of minimal necrosis with minimal to slight inflammation of the parotid salivary gland for males given 1200 mg/kg/day, body weight loss and clinical signs in rats given > or =600 mg/kg/day [4].
细胞实验	Hepatocytes were isolated from male Sprague Dawley (SD) rats by collagenase digestion. For the AMPK assay, cells were seeded in six-well plates at 1.5 × 10^6 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-aminoimidazole 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). For ACC assay, the 35% ammonium sulfate precipitate from digitonin-lysed hepatocytes (4 μg each) was used for determination of ACC activity via 14CO2 fixation in the presence of 20 mM citrate as done previously. For fatty acid oxidation, the oxidation of 14C-oleate to acid-soluble products was performed as done previously, but in medium M199 in the absence of albumin [1].
动物实验	Oral gavage was used to administer 1 ml of metformin (100 mg/ml) or water alone to male SD rats (300–350 g, n = 7–8). Rats were treated once or twice a day for 5 days. Rats were starved for 20 hours and then re-fed for 2 hours before the final dose; 4 hours after the final dose, the animals were anesthetized and livers rapidly removed by freeze clamping followed by blood withdrawal. RNA was prepared from the freeze-clamped liver by RNA isolation reagent. Nuclear extracts were prepared from a pool of seven rat livers. Glucose levels were determined using the standard glucose oxidase assay kit; β-hydroxybutyrate concentrations were assayed by measuring the reduction of NAD to NADH with a standard assay kit. FFA levels were measured with the assay kit [1]. MCF10A-ER-Src cells (5 × 10^6) were injected into the right flank of 18 female nu/nu mice, all of which developed tumors in 10 d with a size of ～100 mm^3. The mice were randomly distributed into six groups (three mice/group) that were untreated or treated by intratumoral injections every 5 d (four cycles) with 1 mg/kg or 4 mg/kg doxorubicin, 200 μg/mL metformin (diluted in the drinking water), or the combination. In another experiment, LNCaP and DU145 prostate cancer cells (5 × 10^6) were injected into the right flank of 12 female nu/nu mice, all of which developed tumors in 10 d with a size of ～75 mm^3. The mice were randomly distributed into four groups that were untreated or treated by intratumoral injections every 5 d (four cycles) with 4 mg/kg doxorubicin and/or 200 μg/mL metformin. In another experiment, A375 and MDA-MB-435 melanoma cells (7 × 10^6) were injected into the right flank of 12 female nu/nu mice, all of which developed tumors in 10 d with a size of ～50 mm3. The mice were randomly distributed into four groups that were untreated or treated by intratumoral injections every 5 d (four cycles) with 10 mg/kg cisplatin and/or 200 μg/mL metformin.Finally, SNU-449 liver cancer cells (10^7) were injected into the right flank of 12 female nu/nu mice, all of which developed tumors in 10 d with a size of ～50 mm^3. The mice were randomly distributed into four groups that were untreated or treated by intratumoral injections every 5 d (four cycles) with 10 mg/kg cisplatin and/or 200 μg/mL metformin. Tumor volume (mean ± SD) was measured at various times after the initial injection [3].

别名	Metformin HCl, 盐酸二甲双胍, 1, 1-Dimethylbiguanide hydrochloride, 1,1-Dimethylbiguanide hydrochloride
分子量	165.63
分子式	C4H12ClN5
CAS No.	1115-70-4

存储

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度

H2O: 193.21mM

DMSO: 100 mM

溶液配制表

可选溶剂	浓度体积质量	1 mg	5 mg	10 mg	25 mg
H2O / DMSO	1 mM	6.0376 mL	30.1878 mL	60.3755 mL	150.9388 mL
	5 mM	1.2075 mL	6.0376 mL	12.0751 mL	30.1878 mL
	10 mM	0.6038 mL	3.0188 mL	6.0376 mL	15.0939 mL
	20 mM	0.3019 mL	1.5094 mL	3.0188 mL	7.5469 mL
	50 mM	0.1208 mL	0.6038 mL	1.2075 mL	3.0188 mL
	100 mM	0.0604 mL	0.3019 mL	0.6038 mL	1.5094 mL

计算器

摩尔浓度计算器

稀释计算器

配液计算器

分子量计算器

质量

浓度

容积

分子量

浓度 (起始)

容积 (起始)

浓度 (终)

容积 (终)

溶液体积

质量

配液浓度

参考文献

1. Zhou G, et al. Role of AMP-activated protein kinase in mechanism of metformin action. J Clin Invest. 2001 Oct;108(8):1167-74. 2. Xue J, et al. Metformin inhibits growth of eutopic stromal cells from adenomyotic endometrium via AMPK activation and subsequent inhibition of AKT phosphorylation: a possible role in the treatment of adenomyosis. Reproduction. 2013 Aug 21;146(4):397-406. 3. Hirsch HA, et al. Metformin inhibits the inflammatory response associated with cellular transformation and cancer stem cell growth. Proc Natl Acad Sci U S A. 2013 Jan 15;110(3):972-7. 4. Quaile MP, et al. Toxicity and toxicokinetics of metformin in rats. Toxicol Appl Pharmacol. 2010 Mar 15;243(3):340-7. 5. Liang C, Sun R, Xu Y, et al. Effect of the Abnormal Expression of BMP-4 in the Blood of Diabetic Patients on the Osteogenic Differentiation Potential of Alveolar BMSCs and the Rescue Effect of Metformin: A Bioinformatics-Based Study[J]. BioMed Research International. 2020, 2020. 6. He Y, Xu K, Wang Y, et al. AMPK as a potential pharmacological target for alleviating LPS-induced acute lung injury partly via NLRC4 inflammasome pathway inhibition[J]. Experimental Gerontology. 2019: 110661. 7. Zhu X, Shen W, Liu Z, et al. Effect of metformin on cardiac metabolism and longevity in aged female mice[J]. Frontiers in Cell and Developmental Biology. 2020, 8. 8. Jia Y, Cui R, Wang C, et al. Metformin protects against intestinal ischemia-reperfusion injury and cell pyroptosis via TXNIP-NLRP3-GSDMD pathway[J]. Redox Biology. 2020: 101534. 9. Zhao H, Li T, Wang K, et al. AMPK-mediated activation of MCU stimulates mitochondrial Ca 2+ entry to promote mitotic progression[J]. Nature cell biology. 2019, 21(4): 476-486. 10. Tang Y, Fang G, Guo F, et al. Selective Inhibition of STRN3-Containing PP2A Phosphatase Restores Hippo Tumor-Suppressor Activity in Gastric Cancer[J]. Cancer Cell. 2020, 38(1): 115-128. e9.

文献引用

1. Tang Y, Fang G, Guo F, et al. Selective Inhibition of STRN3-Containing PP2A Phosphatase Restores Hippo Tumor-Suppressor Activity in Gastric Cancer. Cancer Cell. 2020, 38(1): 115-128. e9. 2. Zhao H, Li T, Wang K, et al. AMPK-mediated activation of MCU stimulates mitochondrial Ca 2+ entry to promote mitotic progression. Nature cell biology. 2019, 21(4): 476-486. 3. Jia Y, Cui R, Wang C, et al. Metformin protects against intestinal ischemia-reperfusion injury and cell pyroptosis via TXNIP-NLRP3-GSDMD pathway. Redox Biology. 2020: 101534. 4. Zhu X, Shen W, Liu Z, et al. Effect of metformin on cardiac metabolism and longevity in aged female mice. Frontiers in Cell and Developmental Biology. 2021 Jan 26;8:626011. doi: 10.3389/fcell.2020.626011. eCollection 2020. 5. He Y, Xu K, Wang Y, et al. AMPK as a potential pharmacological target for alleviating LPS-induced acute lung injury partly via NLRC4 inflammasome pathway inhibition. Experimental Gerontology. 2019: 110661. 6. Liang C, Sun R, Xu Y, et al. Effect of the Abnormal Expression of BMP-4 in the Blood of Diabetic Patients on the Osteogenic Differentiation Potential of Alveolar BMSCs and the Rescue Effect of Metformin: A Bioinformatics-Based Study. BioMed Research International. 2020, 2020 7. Cai Z, Wu X, Song Z, et al.Metformin potentiates nephrotoxicity by promoting NETosis in response to renal ferroptosis.Cell Discovery.2023, 9(1): 104.

剂量换算

对于不同动物的给药剂量换算，您也可以参考 更多...

体内实验配液计算器

请在以下方框中输入您的动物实验信息后点击计算，可以得到母液配置方法和体内配方的制备方法：比如您的给药剂量是10 mg/kg，每只动物体重20 g，给药体积100 μL，一共给药动物10 只，您使用的配方为5% DMSO+30% PEG300+5% Tween 80+60% ddH2O。那么您的工作液浓度为2 mg/mL。

母液配置方法：2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 50 μL DMSO 主液，加入 300 μL PEG300，混匀澄清，再加 50 μL Tween 80，混匀澄清，再加 600 μL ddH2O, 混匀澄清。

第一步：请输入动物实验的基本信息

剂量

mg/kg

每只动物体重

给药体积

μL

动物数量

第二步：请输入动物体内配方组成，不同的产品配方组成不同，如有配方需求，可先联系我们提供正确的体内配方。

% DMSO+

% +

% Tween 80+

% ddH₂O

%DMSO+

计算重置

计算结果如下:

工作液浓度: mg/ml;

母液配置方法: mg 药物溶于 μL DMSO (母液浓度为 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 μL DMSO 主液，加入 μL PEG300，混匀澄清，再加 μL Tween 80，混匀澄清，再加 μL ddH₂O, 混匀澄清。

备注:

要按顺序从左向右依次添加助溶剂。可配合物理方法，如涡流、超声波或热水浴使之帮助溶解。

技术支持

您可能有的问题的答案可以在抑制剂处理说明中找到，包括如何准备库存溶液，如何存储产品，以及基于细胞的分析和动物实验需要特别注意的问题。

Keywords

Metformin hydrochloride 1115-70-4 Autophagy Chromatin/Epigenetic PI3K/Akt/mTOR signaling Mitophagy AMPK insulin 1,1-Dimethylbiguanide Metformin HCl Inhibitor 1, 1-Dimethylbiguanide Hydrochloride respiratory AMP-activated protein kinase blood-brain inhibit 盐酸二甲双胍 chain Mitochondrial Autophagy sensitivity liver Metformin Metformin Hydrochloride barrier 1, 1-Dimethylbiguanide hydrochloride type 1,1-Dimethylbiguanide Hydrochloride diabetes mitochondrial 1,1-Dimethylbiguanide hydrochloride inhibitor

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Metformin hydrochloride

存储

溶解度

溶液配制表

计算器

输入分子式，点击计算，可计算出产品的分子量。

参考文献

文献引用

相关产品

相关化合物库

剂量换算

体内实验配液计算器

技术支持

Keywords