FT011, a new anti-fibrotic and an anti-inflammatory agent, prevents glycogen accumulation by reducing glycogenin mRNA translation.In vitro: FT011 do not change glycogen synthase or glycogen phosphorylase enzyme activities but prevent both glycogenin mRNA synthesis and accumulation of Armanni-Ebstein lesions in the diabetic kidney. [1] FT011 inhibit both TGF-β1 and PDGF-BB induced collagen production as well as PDGF-BB-mediated mesangial proliferation. FT011 reduced albuminuria, glomerulosclerosis and tubulointerstitial fibrosis. [3]In vivo: The reference for FT011 is 200 mg/kg/day [1]. rats are studied for 8 and 32 weeks and receiving intravitreal injections of FT011 (50 μM). FT011 reduces etinal leukostasis, microglial density and mRNA levels of intercellular adhesion molecule-1 (ICAM-1). Late intervention with FT011 reducesacellular capillaries and the elevated mRNA levels of collagen IV and fibronectin in diabetic rats. [2]
[1]. Lau X Attenuation of Armanni-Ebstein lesions in a rat model of diabetes by a new anti-fibrotic, anti-inflammatory agent, FT011. Diabetologia. 2013 Mar;56(3):675-9. [2]. Deliyanti D et al. FT011, a Novel Cardiorenal Protective Drug, Reduces Inflammation, Gliosis and Vascular Injury in Rats with Diabetic Retinopathy. PLoS One. 2015 Jul 29;10(7):e0134392. [3]. Gilbert RE et al. A purpose-synthesised anti-fibrotic agent attenuates experimental kidney diseases in the rat. PLoS One. 2012;7(10)