Metformin HCl
Anti-diabetic agent / Clinically useful antidiabetic agent. Lowers plasma glucose levels and improves insulin sensitivity. Inhibits hepatic gluconeogenesis by activation of the AMP-activated protein kinase (AMPK) pathway.1,2 Displays antiproliferative and pro-apoptotic actions in a variety of cancer cell lines.3,4 Induces autophagy via inhibition of the mTOR pathway. Activates PGC1α and improves mitochondrial dynamics in renal tubular cells.5 Upregulates SIRT1 activity in endothelial cells.6 Neuroprotective and lowers α-synuclein phosphorylation in the Parkinson’s disease MPTP mouse model.7
Biochemicals & reagents
1115-70-4
1) Zhou et al. (2001), Role of AMP-activated protein kinase in mechanism of metformin action; J. Clin. Invest., 108 1167 2) Shaw et al. (2005), The kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin; Science, 310 1642 3) Shi et al. (2012), Therapeutic metformin/AMPK activation blocked lymphoma cell growth via inhibition of mTOR pathway and induction of autophagy; Cell Death Dis., 3 e275 4) Rego et al. (2017) Anti-tumor effects of metgormin on head and neck carcinoma cell lines: A systemic review; Oncol. Lett., 13 554 5) Lee et al. (2017) PGC1? Activators Mitigate Diabetic Tubulopathy by Improving Mitochondrial Dynamics and Quality Control; J. Diabetes Res., 2017 6483572 6) Zheng et al. (2012) Sirtuin 1-mediated cellular metabolic memory of high glucose via the LKB1/AMPK/ROS pathway and therapeutic effects of metformin; Diabetes, 61 217 7) Katila et al. (2017) Metformin lowers ?-synuclein phosphorylation and upregulates neurotrophic factor in the MPTP mouse model of Parkinson's disease; Neuropharmacology, 125 396
RT
TARGET: ATPase -- PATHWAY: Glycation; Autophagy; Carbohydrate metabolism; Mitochondrial function; Apoptosis inducer; AMPK pathway -- RESEARCH AREA: Cancer Stem Cells; Neuroscience; Cell death; Immunology -- DISEASE AREA: Diabetes; NeurodegenerationCancer; Inflammation