Home >> Research Area >>Others>>Others>> Metformin HCl

Metformin HCl

Anti-diabetic drug CAS# 1115-70-4

Metformin HCl

Catalog No. BCC4799----Order now to get a substantial discount!

Product Name & Size Price Stock
Metformin HCl: 5mg $6 In Stock
Metformin HCl: 10mg Please Inquire In Stock
Metformin HCl: 20mg Please Inquire Please Inquire
Metformin HCl: 50mg Please Inquire Please Inquire
Metformin HCl: 100mg Please Inquire Please Inquire
Metformin HCl: 200mg Please Inquire Please Inquire
Metformin HCl: 500mg Please Inquire Please Inquire
Metformin HCl: 1000mg Please Inquire Please Inquire
Related Products

Quality Control of Metformin HCl

Number of papers citing our products

Chemical structure

Metformin HCl

3D structure

Chemical Properties of Metformin HCl

Cas No. 1115-70-4 SDF Download SDF
PubChem ID 14219 Appearance Powder
Formula C4H12ClN5 M.Wt 165.62
Type of Compound N/A Storage Desiccate at -20°C
Synonyms 1,1-Dimethylbiguanide hydrochloride
Solubility H2O : ≥ 32 mg/mL (193.21 mM)
DMSO : ≥ 1.7 mg/mL (10.26 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name N,N-Dimethylimidodicarbonimidic diamide hydrochloride
SMILES [H+].[Cl-].CN(C)C(=N)N=C(N)N
Standard InChIKey OETHQSJEHLVLGH-UHFFFAOYSA-N
Standard InChI InChI=1S/C4H11N5.ClH/c1-9(2)4(7)8-3(5)6;/h1-2H3,(H5,5,6,7,8);1H
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Metformin HCl

DescriptionAntidiabetic agent; lowers plasma glucose levels and improves insulin sensitivity. Inhibits hepatic gluconeogenesis via activation of the LKB1/AMPK pathway. Displays antiproliferative effects in cancer cell lines. Activates the aPKC-CBP pathway in neural precursors to promote neurogenesis. Activates autophagy.

Metformin HCl Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

Metformin HCl Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of Metformin HCl

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 6.0379 mL 30.1896 mL 60.3792 mL 120.7584 mL 150.948 mL
5 mM 1.2076 mL 6.0379 mL 12.0758 mL 24.1517 mL 30.1896 mL
10 mM 0.6038 mL 3.019 mL 6.0379 mL 12.0758 mL 15.0948 mL
50 mM 0.1208 mL 0.6038 mL 1.2076 mL 2.4152 mL 3.019 mL
100 mM 0.0604 mL 0.3019 mL 0.6038 mL 1.2076 mL 1.5095 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University

Background on Metformin HCl

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]

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.

Featured Products
New Products
 

References on Metformin HCl

Analytical Enantio-Separation of Linagliptin in Linagliptin and Metformin HCl Dosage Forms by Applying Two-Level Factorial Design.[Pubmed:27763526]

Sci Pharm. 2016 Oct 17;84(4):671-684.

A novel, stability indicating, reverse phase high-performance liquid chromatography (RP-HPLC) method was developed to determine the S-isomer of linagliptin (LGP) in linagliptin and metformin hydrochloride (MET HCl) tablets (LGP-MET HCl) by implementing design of experiment (DoE), i.e., two-level, full factorial design (2(3) + 3 centre points = 11 experiments) to understand the critical method parameters (CMP) and its relation with the critical method attribute (CMA), and to ensure robustness of the method. The separation of the S-isomer, LGP and MET HCl in the presence of their impurities was achieved on Chiralpak((R)) IA-3 (Amylose tris (3, 5-dimethylphenylcarbamate), immobilized on 3 microm silica gel) stationary phase (250 x 4.6 mm, 3 microm) using isocratic elution and detector wavelength at 225 nm with a flow rate of 0.5 mL.min(-1), an injection volume of 10 microL with a sample cooler (5 degrees C) and column oven temperature of 25 degrees C. Ethanol:Methanol:Monoethanolamine (EtOH:MeOH:MEA) in the ratio of 60:40:0.2 v/v/v was used as a mobile phase. The developed method was validated in accordance with international council for harmonisation (ICH) guidelines and was applied for the estimation of the S-isomer of LGP in LGP-MET HCl tablets. The same method also can be extended for the estimation of the S-isomer in LGP dosage forms.

Development and Validation of Stability-Indicating RP-HPLC Method for Simultaneous Determination of Metformin HCl and Glimepiride in Fixed-Dose Combination.[Pubmed:26997866]

Anal Chem Insights. 2016 Mar 13;11:13-20.

A simple reversed-phase high-performance liquid chromatography method was developed and validated for simultaneous determination of Metformin hydrochloride (MET) and Glimepiride (GLM) in combination and estimation of their principal degradation products. The separation was achieved using JASCO Finepak SIL (250 mm x 4.6 mm i.d. 5 mum) at ambient temperature. The optimized mobile phase composed of an aqueous phase (20 mM phosphate buffer, adjusted to pH 3.0) and an organic phase (methanol:acetonitrile; 62.5:37.5) in the ratio of 80:20. The flow rate was 1 mL/minute, and the analytes were detected at 230 nm. The developed method was validated for accuracy, precision, specificity, linearity, and sensitivity. The chromatographic analysis time was approximately six minutes with the complete resolution of MET (Rt = 2.75 minutes) and GLM (Rt = 5.87 minutes). The method exhibited good linearity over the range of 5-30 mug/mL for MET and 1-10 mug/mL for GLM. The drugs in combination were subjected to various stress degradation studies as per the International Conference Harmonization (ICH) guidelines. Results obtained from the stress degradation studies revealed that the developed method is applicable for stability studies.

Enhanced anti-tumor activity and cytotoxic effect on cancer stem cell population of metformin-butyrate compared with metformin HCl in breast cancer.[Pubmed:27223262]

Oncotarget. 2016 Jun 21;7(25):38500-38512.

Metformin, which is a drug commonly used to treat type 2 diabetes, has shown anti-tumor effects in numerous experimental, epidemiologic, observational, and clinical studies. Here, we report a new metformin derivative, metformin-butyrate (MFB). Compared to metformin-HCl, it more potently activates AMPK, inhibits mTOR, and impairs cell cycle progression at S and G2/M phases. Moreover, MFB inhibits the mammosphere formation of breast cancer cells and shows cytotoxic effects against CD44+CD24-/low populations in vitro and in vivo, indicating that it might have preferential effects on the cancer stem cell population. MFB showed synergistic cytotoxicity with docetaxel and cisplatin, and MFB pretreatment of breast cancer cells prior to their injection into the mammary fat pads of mice significantly decreased the obtained xenograft tumor volumes, compared with untreated or metformin-pretreated cells. Overall, MFB showed greater anti-neoplastic activity and greater efficacies in targeting the G2/M phase and breast cancer stem cell population, compared to metformin-HCl. This suggests that MFB may be a promising therapeutic agent against aggressive and resistant breast cancers.

Design and In-vitro Evaluation of Sustained Release Floating Tablets of Metformin HCl Based on Effervescence and Swelling.[Pubmed:27610147]

Iran J Pharm Res. 2016 Winter;15(1):53-70.

An oral sustained-release floating tablet formulation of Metformin HCl was designed and developed. Effervescence and swelling properties were attributed on the developed tablets by sodium bicarbonate and HPMC-PEO polymer combination, respectively. Tablet composition was optimized by response surface methodology (RSM). Seventeen (17) trial formulations were analyzed according to Box-Behnken design of experiment where polymer content of HPMC and PEO at 1: 4 ratio (A), amount of sodium bi-carbonate (B), and amount of SSG (C) were adopted as independent variables. Floating lag time in sec (Y1), cumulative percent drug released at 1 h (Y2) and 12 h (Y3) were chosen as response variables. Tablets from the optimized formulation were also stored at accelerated stability condition (40 degrees C and 75% RH) for 3 months to assess their stability profile. RSM could efficiently optimize the tablet composition with excellent prediction ability. In-vitro drug release until 12 h, floating lag time, and duration of floating were dependent on the amount of three selected independent variables. Optimized tablets remained floating for more than 24 h with a floating lag time of less than 4 min. Based on best fitting method, optimized formulation was found to follow Korsmeyer-Peppas release kinetic. Accelerated stability study revealed that optimized formulation was stable for three months without any major changes in assay, dissolution profile, floating lag time and other physical properties.

Metformin inhibits the inflammatory response associated with cellular transformation and cancer stem cell growth.[Pubmed:23277563]

Proc Natl Acad Sci U S A. 2013 Jan 15;110(3):972-7.

Metformin, the first-line drug for treating diabetes, inhibits cellular transformation and selectively kills cancer stem cells in breast cancer cell lines. In a Src-inducible model of cellular transformation, metformin inhibits the earliest known step in the process, activation of the inflammatory transcription factor NF-kappaB. Metformin strongly delays cellular transformation in a manner similar to that occurring upon a weaker inflammatory stimulus. Conversely, inhibition of transformation does not occur if metformin is added after the initial inflammatory stimulus. The antitransformation effect of metformin can be bypassed by overexpression of Lin28B or IL1beta, downstream targets of NF-kappaB. Metformin preferentially inhibits nuclear translocation of NF-kappaB and phosphorylation of STAT3 in cancer stem cells compared with non-stem cancer cells in the same population. The ability of metformin to block tumor growth and prolong remission in xenografts in combination with doxorubicin is associated with decreased function of the inflammatory feedback loop. Lastly, metformin-based combinatorial therapy is effective in xenografts involving inflammatory prostate and melanoma cell lines, whereas it is ineffective in noninflammatory cell lines from these lineages. Taken together, our observations suggest that metformin inhibits a signal transduction pathway that results in an inflammatory response. As metformin alters energy metabolism in diabetics, we speculate that metformin may block a metabolic stress response that stimulates the inflammatory pathway associated with a wide variety of cancers.

Metformin activates an atypical PKC-CBP pathway to promote neurogenesis and enhance spatial memory formation.[Pubmed:22770240]

Cell Stem Cell. 2012 Jul 6;11(1):23-35.

VIDEO ABSTRACT: Although endogenous recruitment of adult neural stem cells has been proposed as a therapeutic strategy, clinical approaches for achieving this are lacking. Here, we show that metformin, a widely used drug, promotes neurogenesis and enhances spatial memory formation. Specifically, we show that an atypical PKC-CBP pathway is essential for the normal genesis of neurons from neural precursors and that metformin activates this pathway to promote rodent and human neurogenesis in culture. Metformin also enhances neurogenesis in the adult mouse brain in a CBP-dependent fashion, and in so doing enhances spatial reversal learning in the water maze. Thus, metformin, by activating an aPKC-CBP pathway, recruits neural stem cells and enhances neural function, thereby providing a candidate pharmacological approach for nervous system therapy.

AMP-activated protein kinase in metabolic control and insulin signaling.[Pubmed:17307971]

Circ Res. 2007 Feb 16;100(3):328-41.

The AMP-activated protein kinase (AMPK) system acts as a sensor of cellular energy status that is conserved in all eukaryotic cells. It is activated by increases in the cellular AMP:ATP ratio caused by metabolic stresses that either interfere with ATP production (eg, deprivation for glucose or oxygen) or that accelerate ATP consumption (eg, muscle contraction). Activation in response to increases in AMP involves phosphorylation by an upstream kinase, the tumor suppressor LKB1. In certain cells (eg, neurones, endothelial cells, and lymphocytes), AMPK can also be activated by a Ca(2+)-dependent and AMP-independent process involving phosphorylation by an alternate upstream kinase, CaMKKbeta. Once activated, AMPK switches on catabolic pathways that generate ATP, while switching off ATP-consuming processes such as biosynthesis and cell growth and proliferation. The AMPK complex contains 3 subunits, with the alpha subunit being catalytic, the beta subunit containing a glycogen-sensing domain, and the gamma subunits containing 2 regulatory sites that bind the activating and inhibitory nucleotides AMP and ATP. Although it may have evolved to respond to metabolic stress at the cellular level, hormones and cytokines such as insulin, leptin, and adiponectin can interact with the system, and it now appears to play a key role in maintaining energy balance at the whole body level. The AMPK system may be partly responsible for the health benefits of exercise and is the target for the antidiabetic drug metformin. It is a key player in the development of new treatments for obesity, type 2 diabetes, and the metabolic syndrome.

The kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin.[Pubmed:16308421]

Science. 2005 Dec 9;310(5754):1642-6.

The Peutz-Jegher syndrome tumor-suppressor gene encodes a protein-threonine kinase, LKB1, which phosphorylates and activates AMPK [adenosine monophosphate (AMP)-activated protein kinase]. The deletion of LKB1 in the liver of adult mice resulted in a nearly complete loss of AMPK activity. Loss of LKB1 function resulted in hyperglycemia with increased gluconeogenic and lipogenic gene expression. In LKB1-deficient livers, TORC2, a transcriptional coactivator of CREB (cAMP response element-binding protein), was dephosphorylated and entered the nucleus, driving the expression of peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha), which in turn drives gluconeogenesis. Adenoviral small hairpin RNA (shRNA) for TORC2 reduced PGC-1alpha expression and normalized blood glucose levels in mice with deleted liver LKB1, indicating that TORC2 is a critical target of LKB1/AMPK signals in the regulation of gluconeogenesis. Finally, we show that metformin, one of the most widely prescribed type 2 diabetes therapeutics, requires LKB1 in the liver to lower blood glucose levels.

Description

Metformin hydrochloride (1,1-Dimethylbiguanide hydrochloride) inhibits the mitochondrial respiratory chain in the liver, leading to activation of AMPK, enhancing insulin sensitivity for type 2 diabetes research. Metformin hydrochloride triggers autophagy.

Keywords:

Metformin HCl,1115-70-4,1,1-Dimethylbiguanide hydrochloride,Natural Products,Others, buy Metformin HCl , Metformin HCl supplier , purchase Metformin HCl , Metformin HCl cost , Metformin HCl manufacturer , order Metformin HCl , high purity Metformin HCl

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: