Background:

AMP-activated protein kinase (AMPK) acts as an integrator of regulatory signals to monitor systemic and cellular energy status. Imeglimin targets on three main organs involved in glucose homeostasis: liver, muscle and the pancreas and thus has a distinct mode of action in comparison to existing Type 2 diabetes treatments.
In vitro: In liver mitochondria, imeglimin redirects substrate flows in favor of complex II. Moreover, imeglimin inhibits complex I and restores complex III activities, advicing an increase of fatty acid oxidation, further supported by an increase in hepatic 3-hydroxyacetyl-CoA dehydrogenase activity and acylcarnitine profile. Imeglimin was also found to reduce the production of reactive oxygen species and increases the DNA of mitochondrial [1].
In vivo: A previous study used a model of 16-week high-fat, high-sucrose diet (HFHSD) mice to characterize imeglimin’s antidiabetic effects. Six-week imeglimin treatment could decrease glycemia, restore normal glucose tolerance, and improve insulin sensitivity, body weights and food intake significantly. This was associated with an increase of insulin-stimulated protein kinase B phosphorylation in the liver and muscle. In conclusion, imeglimin could normalize glucose tolerance and insulin sensitivity via preserving mitochondrial function from oxidative stress and favoring lipid oxidation in liver of HFHSD mice [1].
Clinical trial: Imeglimin is an experimental drug being developed as an oral anti-diabetic. Imeglimin is in development (completed phase IIb clinical trials) for use both as monotherapy and in combination with other type-2 diabetes treatments. Various research protocols are being known through various scientists. Early studies showed that imeglimin is as effective as metformin in regulating glycaemic control.
Reference:
[1] Vial G, Chauvin MA, Bendridi N, Durand A, Meugnier E, Madec AM, Bernoud-Hubac N, Pais de Barros JP, Fontaine É, Acquaviva C, Hallakou-Bozec S, Bolze S, Vidal H, Rieusset J.Imeglimin Normalizes Glucose Tolerance and Insulin Sensitivity and Improves Mitochondrial Function in Liver of a High-Fat High-Sucrose Diet Mice Model. Diabetes. 2014. pii: db141220