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Metformin

MCE China：Metformin

Brand：MedChemExpress (MCE)

Cat. No.HY-B0627

CAS：657-24-9

Synonyms：1,1-Dimethylbiguanide

Purity：99.96%

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

Shipping：Room temperature in continental US; may vary elsewhere.

Description：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.

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]. Metformin (1–50 mM; 0-120 h) significantly inhibites the proliferation of both 786-O and OS-RC-2 RCC cell lines in a dose- and time-dependent manner[7]. Metformin (5 mM; 0-48 h) stimulates AMPK and inhibited the mTOR signaling pathway in 786-O cells[7].

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]. Metformin (200 mg/kg; i.p.; once a day for 6 consecutive days before induction of ischemia and at the beginning of reperfusion) significantly reduces the serum alanine aminotransferase (ALT) level in rats with ischemia-reperfusion model[6]. Metformin (250 mg/kg; i.p.; once daily for 22 days) significantly reduces the growth of 786-O cell xenograft tumors in nude mice[7].

IC50 & Target：AMPK

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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]