160341-65-1

Upstream product

• 35949-53-2 (-)-4,5-cyclohexylidenequinic acid lactone 
• 108-94-1 cyclohexanone 
• 77-95-2 D-(-)-quinic acid 

Downstream Products

• 219547-37-2 C₂₀H₂₇NO₅ 
• 219547-38-3 (3R,5R)-1-Benzyloxy-3,4,5-trihydroxy-cyclohexanecarboxylic acid amide 

Relevant academic research and scientific papers

Synthesis of α-trinositol analogues derived from D-(-)-quinic acid as affinity probe precursors

D-(-)-Quinic acid was appropriately protected to permit the phosphorylation of the three vicinal hydroxyl groups. Final deprotection lead to tris(phosphates) possessing the same configuration as the parent α-trinositol and an arm suitable for the attachement of a photoactivable group.

Chlorogenic acid and synthetic chlorogenic acid derivatives: Novel inhibitors of hepatic glucose-6-phosphate translocase

The enzyme system glucose-6-phosphatase (EC 3.1.3.9) plays a major role in the homeostatic regulation of blood glucose. It is responsible for the formation of endogenous glucose originating from gluconeogenesis and glycogenolysis. Recently, chlorogenic acid was identified as a specific inhibitor of the glucose-6-phosphate translocase component (Gl-6-P translocase) of this enzyme system in microsomes of rat liver. Glucose 6- phosphate hydrolysis was determined in the presence of chlorogenic acid or of new synthesized derivatives in intact rat liver microsomes in order to assess the inhibitory potency of the compounds on the translocase component. Variation in the 3-position of chlorogenic acid had only poor effects on inhibitory potency. Introduction of lipohilic side chain in the 1-position led to 100-fold more potent inhibitors. Functional assays on isolated perfused rat liver with compound 29i, a representative of the more potent derivatives, showed a dose-dependent inhibition of gluconeogenesis and glycogenolyosis, suggesting glucose-6-phosphatase as the locus of interference of the compound for inhibition of hepatic glucose production also in the isolated organ model. Gl-6-P translocase inhibitors may be useful for the reduction of inappropriately high rates of hepatic glucose output often found in non-insulin-dependent diabetes.