2. Epigenetics PI3K/Akt/mTOR Autophagy Apoptosis
  3. AMPK Autophagy Mitophagy Apoptosis mTOR
  4. 657-24-9

657-24-9

Metformin Chemical Structure

657-24-9

Chemical Structure

  • Metformin
  • Synonym(s): 1,1-Dimethylbiguanide
  • CAS No: 657-24-9
    Formula: C4H11N5
    Molecular Weight: 129.17
  • InChIKey: XZWYZXLIPXDOLR-UHFFFAOYSA-N
  • SMILES: NC(NC(N(C)C)=N)=N

Biological Activity: 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 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[1][2][3][4][5][6][7].

Cat. No. Product Name Purity Description
HY-B0627 Metformin 99.96% 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 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.
HY-B0627S Metformin-d6 Metformin-d6 (1,1-Dimethylbiguanide-d6) is a deuterated labeled Metformin (HY-B0627). Metformin 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 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.

References

[1]. Soraya H, et al. Acute treatment with metformin improves cardiac function following isoproterenol induced myocardial infarction in rats. Pharmacol Rep. 2012;64(6):1476-84. [Content Brief]
[2]. Quaile MP, et al. Toxicity and toxicokinetics of metformin in rats. Toxicol Appl Pharmacol. 2010 Mar 15;243(3):340-7. [Content Brief]
[3]. Xue J, et al. Metformin inhibits growth of eutopic stromal cells from adenomyotic endometrium via AMPK activation and subsequent inhibition of AKT phosphorylation: a possible role in the treatment of adenomyosis. Reproduction. 2013 Aug 21;146(4):397-406. [Content Brief]
[4]. Otto M, et al. Metformin inhibits glycogen synthesis and gluconeogenesis in cultured rat hepatocytes. Diabetes Obes Metab. 2003 May;5(3):189-94. [Content Brief]
[5]. Avci CB, et al. Therapeutic potential of an anti-diabetic drug, metformin: alteration of miRNA expression in prostate cancer cells. Asian Pac J Cancer Prev. 2013;14(2):765-8. [Content Brief]
[6]. Abdel-Zaher AO, et al. Novel mechanistic insights of the potential role of gasotransmitters and autophagy in the protective effect of metformin against hepatic ischemia/reperfusion injury in rats. Naunyn Schmiedebergs Arch Pharmacol. 2025 Feb 6. [Content Brief]
[7]. Liu J, et al. Metformin inhibits renal cell carcinoma in vitro and in vivo xenograft. Urol Oncol. 2013 Feb;31(2):264-70. [Content Brief]

Keywords:

MetforminMetformin-d6