2. Epigenetics PI3K/Akt/mTOR Autophagy Apoptosis
  3. AMPK Autophagy Mitophagy Apoptosis mTOR
  4. Metformin (glycinate)

Metformin (glycinate)  (Synonyms: 1,1-Dimethylbiguanide (glycinate))

Cat. No.: HY-B0627A
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Metformin (1,1-Dimethylbiguanide) glycinate 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 glycinate also inhibits liver oxidative stress, nitrosative stress, inflammation, and apoptosis caused by liver ischemia/reperfusion injury. In addition, metformin glycinate 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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Metformin (glycinate) Chemical Structure

Metformin (glycinate) Chemical Structure

CAS No. : 121369-64-0

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Metformin (glycinate) Related Antibodies

Top Publications Citing Use of Products

132 Publications Citing Use of MCE Metformin (glycinate)

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    Metformin (glycinate) purchased from MedChemExpress. Usage Cited in: Redox Biol. 2023 Jun 15, 102786.

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

    Metformin (glycinate) purchased from MedChemExpress. Usage Cited in: Redox Biol. 2023 Jun 15, 102786.

    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.

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

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

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

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

    (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.

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

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

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

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

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

    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 (glycinate) purchased from MedChemExpress. Usage Cited in: Front Immunol. 2016 Dec 12;7:597.  [Abstract]

    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.

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

    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

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    Description

    Metformin (1,1-Dimethylbiguanide) glycinate 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 glycinate also inhibits liver oxidative stress, nitrosative stress, inflammation, and apoptosis caused by liver ischemia/reperfusion injury. In addition, metformin glycinate 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[1][2][3][4][5][6][7].

    Molecular Weight

    204.23

    Formula

    C6H16N6O2
    CAS No.
    SMILES

    O=C(CN)O.N=C(NC(N(C)C)=N)N
    Shipping

    Room temperature in continental US; may vary elsewhere.
    Storage

    Please store the product under the recommended conditions in the Certificate of Analysis.
    Purity & Documentation
    References
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    Metformin (glycinate) Related Classifications

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    • Do most proteins show cross-species activity?

      Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

    Keywords:

    Metformin (glycinate)121369-64-01,1-Dimethylbiguanide (glycinate)AMPKAutophagyMitophagyApoptosismTORAMP-activated protein kinaseMitochondrial AutophagyMammalian target of Rapamycinmitochondrialrespiratorychainliverinsulinsensitivitytype2diabetesblood-brainbarrierInhibitorinhibitorinhibit

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