D-myo-Inositol 1,4,5-trisphosphate (sodium salt) [108340-81-4]

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Description

D-myo-inositol 1,4,5-trisphosphate sodium salt is a widely distributed intracellular second messenger. D-myo-inositol 1,4,5-trisphosphate sodium salt acts as a potent agonist of the Ins (1,4,5) P3 receptor with an EC50 of 0.12 μM and inhibits bovine PLC-δ1, with an IC50 of 5.4 μM for binding and an IC50 of 12.4 μM for hydrolysis. D-myo-inositol 1,4,5-trisphosphate sodium saltis metabolized into Ins (1,4) P2 and Ins (1,3,4,5) P4. D-myo-inositol 1,4,5-trisphosphate sodium salt mediates various cellular processes, including growth, development, fertilization, secretion, contraction and neuromodulation. D-myo-inositol 1,4,5-trisphosphate sodium salt inhibits PIP2 hydrolysis and Ca2+-ATPase activity. D-myo-inositol 1,4,5-trisphosphate sodium salt is used for cardiac preconditioning, exerts cardioprotective effects and mimics ischemic preconditioning. D-myo-inositol 1,4,5-trisphosphate sodium salt is applied in studies related to intracellular calcium and phosphoinositol signaling pathways[1][2][3][4].

In Vitro

D-myo-inositol 1,4,5-trisphosphate sodium salt acts as the natural substrate for human erythrocyte membrane Ins(1,4,5)P3 5-phosphatase with a Km of 40 μM, and potently mobilizes intracellular Ca2+ in electrically permeabilized human neuroblastoma cells with an EC50 of 0.12 μM[1].
D-myo-inositol 1,4,5-trisphosphate sodium salt acts as the natural substrate for crude rat brain Ins(1,4,5)P3 3-kinase with a Km of 0.6 μM[1].
D-myo-inositol 1,4,5-trisphosphate (15-60 μM; room temperature) sodium salt competitively inhibits the binding of PLC-δ1 to PC/PIP2 (98:2) LUVs with an IC50 of 5.4 μM[2].
D-myo-Inositol 1,4,5-trisphosphate (60 μM; 2-5 min preincubation for some experiments) sodium salt inhibits PLC-δ1-catalyzed PIP2 hydrolysis in PC/PIP2 (95:5) LUVs with an IC50 of 12.4 μM[2].
D-myo-Inositol 1,4,5-trisphosphate (2 mM MgCl2; 2 min) sodium salt is broken down by a Mg2+-dependent phosphatase in partially purified rat hepatocyte plasma membranes[3].
D-myo-Inositol 1,4,5-trisphosphate (1.5 mM free Mg2+; 10 min at 37 °C) sodium salt phosphatase activity is almost exclusively localized to the plasma membrane fraction of rat liver[3].
D-myo-Inositol 1,4,5-trisphosphate (1.0-5.0 mM calcium, manganese, putrescine, spermidine, spermine; 0.5-1.5 mM free Mg2+) sodium salt phosphatase activity in purified rat hepatocyte plasma membranes is Mg2+-dependent, with maximal activity at 0.5-1.5 mM free Mg2+[3].
D-myo-Inositol 1,4,5-trisphosphate (1.5 mM free Mg2+; 1-60 min at 37 °C) sodium salt is degraded linearly for the first 20 min by purified rat hepatocyte plasma membranes, with approximately 65% of the substrate broken down after 60 min[3].
D-myo-Inositol 1,4,5-trisphosphate sodium salt potently induces dose-dependent Ca2+ release from rat brain microsomes with an EC50 of 0.13 μM, fully mobilizing the Ins(1,4,5)P3-sensitive Ca2+ store[4].
D-myo-Inositol 1,4,5-trisphosphate sodium salt potently displaces specific [3H]Ins(1,4,5)P3 binding to rat cerebellar microsomes with an IC50 of 0.031 μM, indicating strong affinity for the Ins(1,4,5)P3 receptor[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

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