1. Epigenetics
    PI3K/Akt/mTOR
    Autophagy
  2. AMPK
    Autophagy
    Mitophagy
  3. Metformin

Metformin (Synonyms: 1,1-Dimethylbiguanide)

Cat. No.: HY-B0627 Purity: >95.0%
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Metformin (1,1-Dimethylbiguanide) inhibits the mitochondrial respiratory chain in the liver, leading to activation of AMPK, enhancing insulin sensitivity for type 2 diabetes research. Metformin can cross the blood-brain barrier and triggers autophagy.

For research use only. We do not sell to patients.

Metformin Chemical Structure

Metformin Chemical Structure

CAS No. : 657-24-9

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Top Publications Citing Use of Products

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

    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.

    Metformin purchased from MCE. Usage Cited in: Front Pharmacol. 2016 Oct 20;7:390.

    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 purchased from MCE. Usage Cited in: Mol Cell Proteomics. 2017 Jul;16(7):1324-1334.

    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.

    Metformin purchased from MCE. Usage Cited in: Biochem Pharmacol. 2017 Aug 15;138:49-60.

    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.

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

    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.

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

    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.

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

    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.

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

    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.

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

    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.

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

    (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.
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    Description

    Metformin (1,1-Dimethylbiguanide) inhibits the mitochondrial respiratory chain in the liver, leading to activation of AMPK, enhancing insulin sensitivity for type 2 diabetes research. Metformin can cross the blood-brain barrier and triggers autophagy[1].

    IC50 & Target[1]

    AMPK

     

    In Vitro

    Metformin (1,1-Dimethylbiguanide) inhibits proliferation of ESCs in a concentration-dependent manner. The IC50 is 2.45 mM for A-ESCs and 7.87 mM for N-ESCs. Metformin shows pronounced effects on activation of AMPK signaling in A-ESCs from secretory phase than in cells from proliferative phase[3].
    Metformin (0-500 μM) decreases glycogen synthesis in a dose-dependent manner with an IC50 value of 196.5 μM in cultured rat hepatocytes[4].
    Metformin shows cell viability and cytotoxic effects on PC-3 cells with IC50 of 5 mM[5].

    In Vivo

    Metformin (1,1-Dimethylbiguanide; 100 mg/kg, p.o.) alone, and metformin (25, 50, 100 mg/kg) with isoproterenol groups attenuates myocyte necrosis through histopathological analysis[1].
    Metformin (> 900 mg/kg/day, p.o.) results in moribundity/mortality and clinical signs of toxicity in Crl:CD(SD) rats[2].

    Molecular Weight

    129.16

    Formula

    C₄H₁₁N₅

    CAS No.

    657-24-9

    SMILES

    NC(NC(N(C)C)=N)=N

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage

    4°C, protect from light

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

    Solvent & Solubility
    In Vivo:
    • 1.

      Metformin is dissolved in PBS at 300 mM and stored at -20°C. The working solution of metformin is freshly prepared[1].

    References

    Purity: >95.0%

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    Keywords:

    Metformin1,1-DimethylbiguanideAMPKAutophagyMitophagyAMP-activated protein kinaseMitochondrial Autophagymitochondrialrespiratorychainliverinsulinsensitivitytype2diabetesblood-brainbarrierInhibitorinhibitorinhibit

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