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 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 hydrochloride (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 shows pronounced effects on activation of AMPK signaling in A-ESCs from secretory phase than in cells from proliferative phase^[2].
Metformin hydrochloride (0-500 μM) decreases glycogen synthesis in a dose-dependent manner with an IC₅₀ value of 196.5 μM in cultured rat hepatocytes^[3].
Metformin hydrochloride shows cell viability and cytotoxic effects on PC-3 cells with IC₅₀ of 5 mM^[4]. In Vivo: Metformin hydrochloride (1,1-Dimethylbiguanide hydrochloride; 100 mg/kg, p.o.) alone, and metformin (25, 50, 100 mg/kg) with NSC 37745 groups attenuates myocyte necrosis through histopathological analysis^[1].