MJ33 is an inhibitor of Prdx6. Which has the acidic, calcium-independent PLA2 activity

MJ33 was found to specifically inhibit the aiPLA2 activity of the protein. Moreover, the Ca2+-independent PLA2 activity of phosphorylated rat Prdx6 could be abolished by the treatment of either MJ33 or surfactant protein A (SP-A), known inhibitors of aiPLA2 activity. Further supporting the results with intact cells, recombinant Prdx6 was phosphorylated in vitro by ERK and p38, but not by JNK. Phosphorylation in vitro led to a great increase in PLA2 activity that was Ca2+-independent and ould be inhibited by both MJ33 and by SP-A, which was similar to native lung enzyme [1].

A previous study evaluated the effect of MJ33 on manifestations of acute lung injury. Results showed that MJ33 could inhibit reactive oxygen species generation by lungs when measured LPS treatment. LPS at either a low or high dose significantly increased lung infiltration with inflammatory cells, secretion of proinflammatory cytokines, expression of lung vascular cell adhesion molecule, lung permeability, tissue lipid peroxidation, tissue protein oxidation, and activation of NF-κB. MJ33, given either concurrently or 2 h subsequent to LPS, was able to significantly reduce all of these measured parameters [2].

T22985

C22H43F3O6P·Li

498.5

MJ33 (lithium salt)

DMSO:0.25mg/ml
Ethanol:≤2mg/mL
Powder: -20°C for 3 years
In solvent: -80°C for 2 years