Metformin (hydrochloride)

Metformin (1,1-Dimethylbiguanide) hydrochloride 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 hydrochloride exerts central glucose-lowering effects by inhibiting Ras-related protein 1 (Rap1) in SF1 hypothalamic neurons. Metformin hydrochloride also inhibits liver oxidative stress, nitrosative stress, inflammation, and apoptosis caused by liver ischemia/reperfusion injury. In addition, Metformin hydrochloride 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]}. In Vitro:Metformin (1,1-Dimethylbiguanide) hydrochloride 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 hydrochloride 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) hydrochloride decreases glycogen synthesis in a dose-dependent manner with an IC₅₀ value of 196.5 μM in cultured rat hepatocytes^[4].
Metformin hydrochloride shows cell viability and cytotoxic effects on PC-3 cells with IC₅₀ of 5 mM^[5].
Metformin (1-50 mM; 0-120 h) hydrochloride 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) glycinate stimulates AMPK and inhibited the mTOR signaling pathway in 786-O cells^[7].
In Vivo:Metformin (1,1-Dimethylbiguanide; 100 mg/kg, p.o.) hydrochloride alone, and Metformin (25, 50, 100 mg/kg) hydrochloride with isoproterenol groups attenuates myocyte necrosis through histopathological analysis^[1].
Metformin (> 900 mg/kg/day, p.o.) hydrochloride 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) hydrochloride 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) hydrochloride significantly reduces the growth of 786-O cell xenograft tumors in nude mice^[7].
When dissolved in PBS, the solution is strongly alkaline. Before animal administration, the pH needs to be adjusted to neutral (pH=7) with hydrochloric acid (e.g., 1M HCl).