Metformin HCl

For research use only.

Catalog No.S1950

36 publications

Metformin HCl  Chemical Structure

CAS No. 1115-70-4

Metformin HCl decreases hyperglycemia in hepatocytes primarily by suppressing glucose production by the liver (hepatic gluconeogenesis). Metformin promotes mitophagy in mononuclear cells. Metformin induces apoptosis of lung cancer cells through activating JNK/p38 MAPK pathway and GADD153.

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Selleck's Metformin HCl has been cited by 36 publications

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Description Metformin HCl decreases hyperglycemia in hepatocytes primarily by suppressing glucose production by the liver (hepatic gluconeogenesis). Metformin promotes mitophagy in mononuclear cells. Metformin induces apoptosis of lung cancer cells through activating JNK/p38 MAPK pathway and GADD153.
AMPK [1]
In vitro

Metformin (500 μM) activates AMPK in hepatocytes, as a result, acetyl-CoA carboxylase (ACC) activity is reduced, fatty acid oxidation is induced, and expression of lipogenic enzymes is suppressed. Metformin (2 mM) activates muscle AMPK and promotes glucose uptake. Metformin (500 μM) or AICAR strongly suppresses SREBP-1 mRNA expression in rat hepatocytes. Metformin ameliorates hyperglycemia without stimulating insulin secretion, promoting weight gain, or causing hypoglycemia. Metformin has beneficial effects on circulating lipids linked to increased cardiovascular risk. Metformin decreases hepatic glucose production and increases skeletal myocyte glucose uptake. [1] Metformin requires LKB1 in the liver to lower blood glucose levels. [2] Metformin (2 mM) leads to a significant increase in the activity of both α1- and α2-containing complexes in muscle cells. Metformin (2 mM) also increases threonine 172 phosphorylation in muscle cells. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human HepG2 cells MlfjSpVv[3Srb36gZZN{[Xl? MlXpNlQhcA>? Mle1TY5kemWjc3WgbY4h\2y3Y3;z[UBkd26|dX3weIlwdiCrbjDpcpN2dGmwLYLld4l{fGGwdDDoeY1idiCKZYDHNkBk\WyuczDh[pRmeiB{NDDodpMtKEWFNUC9NE4zPyEQvF2u MkXYNlE5PTZyNEi=
human MDA-MB-231 cells MYfGeY5kfGmxbjDhd5NigQ>? Mn3iNUB1dyB{MDDtUS=> NVLKOmhMOjRiaB?= MXnBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE2GQT3NRk0zOzFiY3XscJMh[XRiMTD0c{AzOCCvTTDh[pRmeiB{NDDodpMh[nliTWTUJIF{e2G7Lh?= M4T4clIzPDV7MkC4
human HepG2 cells M3;6UmZ2dmO2aX;uJIF{e2G7 MmjzNUBuVQ>? Mm\LNlQhcA>? M1fhWnJm\HWldHnvckBw\iCpbIXjc5NmKGOxboP1cZB1cW:wIHnuJIlve3WuaX6tdoV{cXO2YX70JIh2dWGwIFjldGczKGOnbHzzJIF1KDFibV2gZYZ1\XJiMkSgbJJ{KGK7IHfseYNwe2Vib4jp[IF{\SCvZYToc4QhcW5icILld4Vv[2Vib3[gNlIvOiCvTTDv[kBodHWlb4Pl MVeyN|AzPTJ2NB?=
mouse 3T3L1 cells MVnGeY5kfGmxbjDhd5NigQ>? M{TaeVEhdU1? NEjZO5BKdmS3Y4Tpc44hd2ZiQV3QT{BxcG:|cHjvdplt[XSrb36gbY4hdW:3c3WgN3Q{VDFiY3XscJMh[XRiMTDtUUBjgSCZZYP0[ZJvKGKub4SgZY5idHm|aYO= MUmyOVIyPjN5OR?=
human HepG2 cells NGCxRXJHfW6ldHnvckBie3OjeR?= NU\KSmxGOSCvTR?= M1yydVI1KGh? NGTQRpNC[3SrdnH0bY9vKG:oIFHNVGshcW5iaIXtZY4hUGWyR{KgZ4VtdHNiYYPz[ZN{\WRiYYOgdoVlfWO2aX;uJI9nKGeudXPvcoVw\2WwZYPpd{BifCBzIH3NJIFnfGW{IEK0JIhzeyCkeTDlcpp6dWG2aXOgZ49td3KrbXX0dolkKGG|c3H5 M{fjV|I3PDdzMEmw

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot
p-AMPK / AMPK / p-mTOR / mTOR / p-S6K / S6K; 

PubMed: 24505341     

The combined effects of metformin and heating were studied by heating the cells at 39.5–41°C for 1 h with 5 mM metformin and then incubating at 37°C for 47 h.

TTP / p-STAT3 / STAT3 / c-Myc ; 

PubMed: 26956973     

Metformin treatment increases phospho-AMPK (pAMPK) but decreases c-Myc and phospho-STAT3 (pSTAT3) in MCF7 and MDA-MB-231 cells. MCF7 and MDA-MB-231 cells were treated with 6 mM metformin for the indicated length of time, and the levels of TTP, STAT3, pSTAT3, AMPK, pAMPK, and c-Myc were measured by Western blotting.

pACC / ACC / pS6 / S6; 

PubMed: 26172303     

Western blot of pACC Ser79 (280 kDa), ACC (265 kDa), pS6 Ser240/244 (32 kDa), S6 (32 kDa), and β-actin (42 kDa) in HeyA8 cells treated with 0-5 mM metformin in normoglycemic or hyperglycemic conditions for 24 h.

pSTAT3 (Ser727) / STAT3 / Jak2 / Cdk5 / pNFκB / Bcl-2 / Bcl-XL / c-Myc; 

PubMed: 28114390     

Western blot of STAT3 and its regulatory proteins in Ishikawa cells after treatment with control, 10 mM, or 20 mM metformin for 48h in high-glucose conditions.

24505341 26956973 26172303 28114390

PubMed: 29601127     

LKB1 location with or without 10 lmol/L metformin treatment in Capan-2 wtLKB1 cell line. Scale bar, 50 μm.

PAR ; 

PubMed: 21422199     

A. MCF7 (left panel) or MDA-MB-231 (right panel) cells were treated with (Met) or without (Con) metformin for 2.5 days and then PAR (red) was detected by immunofluorescence using confocal microscopy. Nuclei (blue) were stained with DAPI.

CD86 / CD206; 

PubMed: 30899369     

Representative images of immunofluorescence analysis of macrophage phenotype in vitro, CD86 (M1 green) or CD206 (M2 red) were analysis. Scale bar 50 μm.

beta-catenin / AMPK; 

PubMed: 30854043     

Cells were treated with metformin for 24 h and subjected to immunofluorescence staining for β-catenin and AMPK. Magnification, ×400.

29601127 21422199 30899369 30854043
Growth inhibition assay
Cell viability ; 

PubMed: 26956973     

MCF7 and MDA-MB-231 cells were treated with the indicated concentrations of metformin for 24 h. Cell viability was assessed by measuring absorbance at 490 nm using an MTS cell proliferation assay. The values obtained with mock-treated cells were set to 100. Values are the mean ± SD (n = 3). *p < 0.05, **p < 0.01, ***p < 0.001.

In vivo Metformin (100 mg/ml, po) treatment produces significant decreases in hepatic expression of mRNAs for SREBP-1, FAS, and S14 in SD rats that are consistent with effects documented in cells. Metformin also decreases hepatic lipids in obese mice. [1] Metformin (250 mg/kg, i.p.) increases AMPK phosphorylation in livers of wild-type mice. Metformin (250 mg/kg, i.p.) treatment reduces blood glucose by more than 50% in the wild-type mice on a high-fat diet. Metformin (250 mg/kg, i.p.) treatment also loweres blood glucose in the ob/ob mice by 40%. [2]


Solubility (25°C)

In vitro Water 33 mg/mL warmed (199.25 mM)
DMSO Insoluble
Ethanol Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 165.62


CAS No. 1115-70-4
Storage powder
in solvent
Synonyms N/A
Smiles CN(C)C(=N)N=C(N)N.Cl

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT02394652 Recruiting Drug: Metformin|Drug: Cisplatin|Drug: FAZA Uterine Cervical Neoplasms|Squamous Cell Carcinoma|Adenocarcinoma|Carcinoma Adenosquamous University Health Network Toronto May 2022 Phase 2
NCT04477590 Not yet recruiting Drug: EXERCISE TRAINING WITH OR WITHOUT MEDICATION Metabolic Syndrome Protection Against|Exercise Training|Metformin|Statins|Angiotensin-Converting-Enzyme Inhibitor|Fasting Intermittent|Angiotensin Hypertension University of Castilla-La Mancha|Spanish Ministry of Economy and Comptetitiveness|Servicio de Salud de Castilla-La Mancha (SESCAM) September 7 2020 Not Applicable
NCT04267809 Not yet recruiting Drug: Metformin Hydrochloride Endoplasmic Reticulum Stress|Viral Infection|Yellow Fever Singapore General Hospital|Duke-NUS Graduate Medical School August 2020 Phase 2
NCT04530383 Active not recruiting Drug: Metformin Hydrochloride Cystic Fibrosis-related Diabetes|Cystic Fibrosis University of Kansas Medical Center August 22 2020 Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID