Metformin HCl
Catalog No.S1950
Molecular Weight(MW): 165.62
Metformin HCl decreases hyperglycemia in hepatocytes primarily by suppressing glucose production by the liver (hepatic gluconeogenesis).
Cited by 6 Publications
2 Customer Reviews
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Cropped immunoblot analyses for downstream effector proteins of the MAPK and PI3K/AKT/mTOR signaling pathways for NRASQ61 mutant lung carcinoma and neuroblastoma cell lines. Dual pathway inhibition can be achieved by combining metformin and trametinib, as evidenced by the abolishment of p-ERK and p-S6.
Oncotarget, 2015, 6(2): 969-78 . Metformin HCl purchased from Selleck.
Metformin added to atorvastatin therapy has no additional lipid-lowering effect. At the beginning of the experiment, rabbits were fed a high-cholesterol diet. After 2 weeks, rabbits were randomly stratified into the normal sodium (Ctrl group), atorvastatin (AT group), metformin (MT group), or atorvastatin/metformin combination therapy (AT + MT group) for a period of 10 weeks. Lipid levels were measured at −2, 0, 2, 6, 10 weeks after drug administration. Time-dependent changes and their AUC values of serum TC levels (A,B) are presented. Data are mean ± SD, n = 7 for each group. *P < 0.05, compared with Ctrl group. AUC, area under the curve; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; TC, total cholesterol.
Sci Rep, 2017, 7(1):2169. Metformin HCl purchased from Selleck.
Purity & Quality Control
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Biological Activity
| Description | Metformin HCl decreases hyperglycemia in hepatocytes primarily by suppressing glucose production by the liver (hepatic gluconeogenesis). | ||||||||||||||||||||||||||||||||||||||||||||
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| Targets |
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| 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] |
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| Cell Data |
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| 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] |
Protocol
Solubility (25°C)
| In vitro | Water | 33 mg/mL warmed (199.25 mM) |
|---|---|---|
| DMSO | Insoluble warmed | |
| 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 |
|---|---|
| Formula | C4H11N5.HCl |
| CAS No. | 1115-70-4 |
| Storage | powder |
| in solvent | |
| Synonyms | N/A |
Bio Calculators
Molarity Calculator
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This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )
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Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
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Molarity Calculator
Clinical Trial Information
| NCT Number | Recruitment | Conditions | Sponsor/Collaborators | Start Date | Phases |
|---|---|---|---|---|---|
| NCT03467763 | Recruiting | Metformin Adverse Reaction|Tolerance | Weill Medical College of Cornell University|Agency for Healthcare Research and Quality (AHRQ) | February 9 2018 | Phase 4 |
| NCT03686722 | Completed | Diabetes Mellitus Type 2|Hepatitis C|Drug Interactions | Mohamed Raslan|Ain Shams University|Drug Research Centre Cairo Egypt | September 9 2017 | Phase 1 |
| NCT03202563 | Active not recruiting | Type 2 Diabetes Mellitus | LG Chem | August 9 2017 | Phase 4 |
| NCT02284893 | Completed | Type 2 Diabetes | AstraZeneca | September 9 2014 | Phase 3 |
| NCT01917656 | Completed | Diabetes|Diabetes Mellitus Type 2 | Novo Nordisk A/S | January 9 2014 | Phase 4 |
| NCT01819129 | Completed | Diabetes|Diabetes Mellitus Type 2 | Novo Nordisk A/S | September 9 2013 | Phase 3 |
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