Imeglimin hydrochloride (EMD 387008 hydrochloride） is an oral hypoglycemic agent. Imeglimin improves insulin sensitivity, inhibits the production of reactive oxygen species, increases mitochondrial DNA, and improves mitochondrial function.

METHODS: HMEC-1 cells were cultured in complete MCDB medium with indicated concentrations of glucose for 48 h in the absence or presence of 1 μM CsA, 250 μM N-acetylcysteine ​​(NAC), or 100 μM Imeglimin hydrochloride (EMD 387008 hydrochloride). Cytotoxicity was assessed by staining cells with Alexa Fluor-conjugated Annexin V and PI.
RESULTS Imeglimin hydrochloride prevented hyperglycemia-induced endothelial cell death. [1]
METHODS: HepG2 cells were treated with 1, 3, or 10 mM Imeglimin hydrochloride for 3 h and the resulting changes in basal oxygen consumption rate (OCR) and ATP production were observed.
RESULTS Imeglimin hydrochloride inhibited basal OCR and ATP production as well as maximal mitochondrial respiration in a concentration-dependent manner. [2]

METHODS: Male C57BL/6J OlaHsd mice received imeglimin hydrochloride (EMD 387008 hydrochloride) (200 mg/kg b.i.d) by oral gavage during the last 6 weeks of HFHSD feeding to observe the antidiabetic effects of imeglimin.
RESULTS Imeglimin hydrochloride significantly reduced blood glucose and restored normal glucose tolerance. [3]
METHODS: C57BL/6J mice were maintained on a normal diet and a 12-h light/12-h dark cycle. At 8 weeks of age, male mice were deprived of food overnight, allowed to refeed for 5 h, and then injected intravenously with 250 mg/kg of imeglimin hydrochloride. Blood samples were collected from the tail vein 1 h after injection and blood glucose levels were measured using a glucometer.
RESULTS Imeglimin hydrochloride significantly reduced blood glucose, while plasma insulin levels were not affected by imeglimin. [3]