In vitro activity: 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.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

Kinase Assay: 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. 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.

Cell Assay: In Müller cells, FT011 reduced diabetes-induced gliosis and vascular endothelial growth factor (VEGF) immunolabeling and the hyperglycaemic-induced increase in ICAM-1, monocyte chemoattractant protein-1, CCL20, cytokine-induced neutrophil chemoattractant-1, VEGF and IL-6. Late intervention with FT011 reduced acellular capillaries and the elevated mRNA levels of collagen IV and fibronectin in diabetic rats. In conclusion, the protective effects of FT011 in cardiorenal disease extend to key elements of diabetic retinopathy and highlight its potential as a treatment approach.