5-Iodotubercidin increases fatty acid oxidation activity and glycogen synthesis in hepatocytes. 5-Iodotubercidin is also a potent inhibitor of adenosine uptake into brain. Potent inhibitor of adenosine uptake into brain, and of adenosine kinase and subsequent metabolism of adenine nucleotides. In cultured rat hepatocytes, 5-iodotubercidin inhibits both acetyl-CoA carboxylase and de novo synthesis of fatty acids and cholesterol.1
Diadenosine polyphosphate functions as a second messenger in pancreatic cells, stimulates phospholipase D, changes intracellular calcium levels, induces nitric oxide release, activates 5′-nucleotidase, and inhibits adenosine kinase activity in vitro. Diadenosine polyphosphate is stored in secretory granules of thrombocytes, chromaffin, and neuronal cells. After release into the extracellular space, it affects a variety of biological activities in a wide range of target tissues. It appears to function as a second messenger in pancreatic cells. In rat liver cells. it stimulates phospholipase D and changes intracellular calcium levels. It has been shown to induce nitric oxide release from endothelial cells. In the nervous system it acts through various purinoceptors. It also activates 5′-nucleotidase and inhibits adenosine kinase activity in vitro. Ap4A is metabolized by soluble enzymes in the blood plasma and by membrane-bound ectoenzymes of a number of cell types including endothelial cells, smooth muscle cell.
Allosteric enhancer of A1 adenosine receptor. Studies in carrageenin-inflamed rats have reported that T62 can reverse thermal hypersensitivity1. T62 has also been reported to reduce mechanical allodynia and induce drug tolerance over time in rat models of neuropathic pain2.