Biological Activity
5-Iodotubercidin (Itu) has been shown to inhibit mitogen-activated protein kinase (ERK2) (Ki = 525 nM), adenosine kinase (ADK) (Ki = 30 nM), casein kinases 1 & 2 (CSNK1A1 & CSNK2A1), protein kinase A (PKA) and insulin receptor kinase (IC50 ranging from 0.
In Vitro
5-Iodotubercidin (40 μM) enhances the rate of phosphorylase inactivation and shortens the lag before the activation of glycogen synthase. 5-Iodotubercidin (50 μM) antagonizes the effects of glucagon and vasopressin, but does not affect the basal concentration of free calcium in single hepatocytes[1]. 5-Iodotubercidin (20 μM) causes an important decrease in ATP concentration, and a concomitant smaller increase in AMP concentration. 5-Iodotubercidin decreases the activity of ACC and the rates of synthesis of fatty acids and cholesterol. In line with the iodotubercidin-mediated inhibition of ACC, 5-iodotubercidin induces a marked decrease in the intracellular concentration of malonyl-CoA[3]. 5-Iodotubercidin causes a strong decrease in the immunofluorescence levels of P-T3-H3, and depletion of P-T3-H3 is complete at 10 µM 5-5-iodotubercidin[4].
In Vivo
5-Iodotubercidin (1 mL/kg, i.p.) is in agreement with activity observed against bicuculline-induced seizures following local administration of the AKI into the prepiriform cortex[2].
References & source
Published experimental findings depend on the model and assay conditions. They do not guarantee equivalent performance in every application. For laboratory research use only.
