For research use only.
Molecular Weight(MW): 165.62
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.
Selleck's Metformin HCl has been cited by 35 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.|
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.  Metformin requires LKB1 in the liver to lower blood glucose levels.  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. 
|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.  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%. |
|In vitro||Water||33 mg/mL warmed (199.25 mM)|
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|Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)|
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Method for preparing DMSO master liquid: ： mg drug pre-dissolved in μL DMSO (Master liquid concentration mg/mL，)
Method for preparing in vivo formulation：Take DMSO master liquid, next addμL PEG300， mix and clarify, next addμL Tween 80，mix and clarify, next add μL ddH2O，mix and clarify.
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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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