MJ33 (lithium salt)
In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
Tyramide Signal Amplification (TSA)
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Phos Binding Reagent Acrylamide
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
Cell Counting Kit-8 (CCK-8)
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
SYBR Safe DNA Gel Stain
Safe and sensitive stain for visualization of DNA or RNA in agarose or acrylamide gels.
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
MJ33 is an inhibitor of the acidic, calcium-independent (ai)PLA2 activity of Prdx6.
Peroxiredoxin-6 (Prdx6), a bifunctional enzyme, has both non-selenium glutathione peroxidase and phospholipase A2 (PLA2) activities. The PLA2 activity of Prdx6 is calcium-independent, functions optimally in acidic conditions, and facilitates the intracellular processing of surfactant lipids, such as dipalmitoylphosphatidylcholine.
In vitro: MJ33 was found to be 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 .
In vivo: 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 .
Clinical trial: So far, no clinical study has been conducted.
 Wu, Y. ,Feinstein, S.I.,Manevich, Y., et al. Mitogen-activated protein kinase-mediated phosphorylation of peroxiredoxin 6 regulates its phospholipase A2 activity. Biochem. 419(3), 669-679 (2009).
 Lee I, Dodia C, Chatterjee S, Feinstein SI, Fisher AB. Protection against LPS-induced acute lung injury by a mechanism-based inhibitor of NADPH oxidase (type 2). Am J Physiol Lung Cell Mol Physiol. 2014 Apr 1;306(7):L635-44.
|Physical Appearance||A crystalline solid|
|Storage||Store at -20°C|
|Solubility||≤2mg/ml in ethanol;0.25mg/ml in DMSO;0.5mg/ml in dimethyl formamide|
|Chemical Name||mono[1-[(hexadecyloxy)methyl]-2-(2,2,2-trifluoroethoxy)ethyl] monomethyl ester phosphoric acid, monolithium salt|
|Shipping Condition||Evaluation sample solution: ship with blue ice. All other available sizes: ship with RT, or blue ice upon request.|
|General tips||For obtaining a higher solubility, please warm the tube at 37°C and shake it in the ultrasonic bath for a while. Stock solution can be stored below -20°C for several months.|