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Metformin

(Synonyms: 1,1-Dimethylbiguanide)
199 Cited Publications
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Based on 199 publication(s) in Google Scholar

Metformin (1,1-Dimethylbiguanide) inhibits the mitochondrial respiratory chain in the liver, leading to AMPK activation and enhancing insulin sensitivity, and can be used in the study of type 2 diabetes. Metformin exerts central glucose-lowering effects by inhibiting Ras-related protein 1 (Rap1) in SF1 hypothalamic neurons. Metformin also inhibits liver oxidative stress, nitrosative stress, inflammation, and apoptosis caused by liver ischemia/reperfusion injury. In addition, Metformin regulates the expression of autophagy-related proteins by activating AMPK and inhibiting the mTOR signaling pathway, thereby inducing tumor cell autophagy and inhibiting the growth of renal cell carcinoma in vitro and in vivo.

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  • Reinheit: 99.96%
  • CAS. Nr.: 657-24-9
  • Formel: C4H11N5
  • Molecular Weight:129.17
  • Speicherung:

    -20°C, protect from light, stored under nitrogen

    * In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)

  • Metformin Chemical Structure
    Metformin Chemical Structure
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
  • Experimental Validation Results for Metformin
CAS. Nr.: 657-24-9
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  • Metformin Chemical Structure
    Metformin Chemical Structure
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  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Nature. 2025 Feb;638(8052):1112-1121. [Abstract]

    Customer Validation
     Metformin (2 mM; 16 h) significantly inhibits the mRNA expression of FOXM1 downstream genes (CDC25B, CCNA2) in HEK293T cells.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: J Adv Res. 2025 Mar 10:S2090-1232(25)00174-2. [Abstract]

    Customer Validation
     STAT3 levels in hBMSCs treated with metformin and the miR-140-3p inhibitor.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Cell Res. 2023 Dec;33(12):904-922. [Abstract]

    Customer Validation
     Cells were treated with mannose, MK-8722 (1 μM) or Metformin (1 mM) for 6 h. GSDME was immunoprecipitated using anti-GSDME antibody, and then the phosphorylation levels of GSDME T6 were detected.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Redox Biol. 2023 Aug:64:102786. [Abstract]

    Customer Validation
     Metformin hydrochloride (Metformin; 2, 6, 20 mM; 30 min) attenuates MGO-induced cell death in a concentration-dependent manner in ARPE-19 cells.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Redox Biol. 2023 Aug:64:102786. [Abstract]

    Customer Validation
     Metformin hydrochloride (Met; 3, 6 mM; 30 min) inhibits MGO-induced the increased expression of Bax and caspase-3 cleavage and decreased expression of Bcl-2 in ARPE-19 cells.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Circulation. 2023 Jan 10;147(2):158-174. [Abstract]

    Customer Validation
     Metformin. Western blot analysis of CB2R in the heart from db/db diabetic (DM) mice at different ages.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Endocrinology. 2018 May 1;159(5):2008-2021. [Abstract]

    Customer Validation
     Male C57BL/6 mice are intragastrically treated with Metformin or placebo at 3 mg/kg/day for 10 weeks in the presence of HFD after 10-week-HFD feeding and then sacrificed for sample collection. Western blot analysis of AMPKα1, AMPK, p-AMPK, SREBP1 and FAS.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Biochem Pharmacol. 2017 Aug 15:138:49-60. [Abstract]

    Customer Validation
     PP5 overexpression suppresses AMPK-Thr172 phosphorylation induced by AMPK activators, AICAR and metformin. Hep3B cells are transfected with indicated plasmids and treated with AICAR (2 mM; 3 h) or Metformin (3 mM; 16 h) to simulate AMPK phosphorylation.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Mol Cell Proteomics. 2017 Jul;16(7):1324-1334. [Abstract]

    Customer Validation
     To further validate the MS quantification results, Western blot analysis is carried out using an anti-H3K36 dimethylation antibody. Consistent with the mass spectrometric data, H3K36 dimethylation was elevated in DIO mouse livers, whereas Metformin treatment can significantly decrease histone H3K36 dimethylation in DIO mice to a level close to that of the chow-fed control mice.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Mol Oncol. 2017 Aug;11(8):1035-1049. [Abstract]

    Customer Validation
     Co-treatment of Metformin and Ribociclib induces cell death in Hep3B cells. Cells are exposed to Ribociclib at 25 μM and/or Metformin at 10 mM for 72 h.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Mol Oncol. 2017 Oct;11(10):1475-1492. [Abstract]

    Customer Validation
     MiaPaCa-2 cells are treated with a gradient concentration of Metformin for 24 h, and then, western blotting is performed to show the activation of p-AMPK and the suppression of HSF1 and HSP70.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Mol Oncol. 2017 Oct;11(10):1475-1492. [Abstract]

    Customer Validation
     (A) IHC staining of N-cadherin and E-cadherin in the pancreas from KPC mice treated with vehicle, Metformin, or KRIBB11. (B) Masson's trichrome staining and IHC staining of α-SMA in pancreatic tissues from mice treated with vehicle, Metformin, or KRIBB11.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Mol Neurobiol. 2017 Jul;54(5):3327-3341. [Abstract]

    Customer Validation
     Met attenuates apoptosis caused by traumatic spinal cord injury in rat. a, b Representative western blots and quantification data of cleaved caspase 3 and β-actin in each group rats. c, d Representative western blots and quantification data of Bax, Bcl-2, and β-actin in each group rats.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: J Cell Mol Med. 2017 Dec;21(12):3322-3336. [Abstract]

    Customer Validation
     Metformin prevents the loss of tight junction (TJ) proteins after SCI. Representative Western blots and quantification data of Occludin, Claudin-5, ZO-1 and β-actin at 3 day after injury.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Cell Physiol Biochem. 2017;44(4):1381-1395. [Abstract]

    Customer Validation
     U87 cells are treated with Met alone or in the presence of isogambogenic acid for 24 h. The expression levels of phosphorylated AMPK, mTOR and 4E-BP1 are assessed by western blotting, with total AMPK, mTOR and 4E-BP1 used as the internal controls.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Front Immunol. 2016 Dec 12:7:597. [Abstract]

    Customer Validation
     Metformin increases adenosine triphosphate-induced inflammasome activation in bone marrow-derived macrophages. (A) Cells are treated. Indicated protein levels in both cell lysates and supernatants are evaluated by western blotting. β-Tubulin is used as a loading control for cell lysates. (B–D) The quantitative analyses of the active caspase-1p10 (B), mature interleukin-1β (C), and HMGB1 (D) levels in the supernatants (A) are shown.

  • 1/16

    Metformin purchased from MedChemExpress. Usage Cited in: Front Pharmacol. 2016 Oct 20:7:390. [Abstract]

    Customer Validation
     Metformin, an AMPK agonist, counteracts the effect of Piperine on suppressing ATP-induced AMPK activation and inflammatory mediator release. J774A.1 cells are pre-treated with 80 μM Piperine and BMDMs are pre-treated with 160 μM Piperine for 4 h. Without being washed out of Piperine, these cells are primed with LPS (500 ng/mL) for 4 h. Next, the cells are treated with Metformin (1 mM) for 1 h (in the absence of Piperine and LPS). Finally, in the presence of Metformin, the BMDMs are stimulated wi

  • Metformin