Description
MK591(Quiflapon sodium) is selective and specific inhibitor of 5-Lipoxygenase-activating protein (FLAP).
Product Overview
IC50: 1.6 nM in a FLAP binding assay for MK-0591, which is the acid form of MK591. Arachidonate 5-lipoxygenase-activating protein is necessary for the activation of 5-lipoxygenase and therefore for the production of leukotrienes. MK-591 (MK-0591 sodium) is a selective and specific 5-Lipoxygenase-activating protein (FLAP) inhibitor. Clinical trial: In an open-label and pilot study, short-term therapy with MK-591 reduces proteinuria by restoring glomerular size selectivity and thus reduces transglomerular protein trafficking. These benefits may result from glomerular leukotriene biosynthesis inhibition, but other MK-591-specific actions cannot be excluded.
Synonyms
Quiflapon sodium; MK-591; MK 591
Molecular Formula
C34H34ClN2NaO3S
Chemical Name
sodium; 3-[3-tert-butylsulfanyl-1-[(4-chlorophenyl)methyl]-5-(quinolin-2-ylmethoxy)indol-2-yl]-2,2-dimethylpropanoate
Solubility
Soluble in DMSO
Shipping Conditions
Evaluation sample solution: ship with blue ice. All other available size: ship with RT, or blue ice upon request
In vitro
A series of performed inhibitor studies identified a specific inhibitor of 5-LO (MK-591), which has the ability to block JNK, MAPK and 5-LO signaling-cascades and drastically reducing the activity of pro-inflammatory cytokine TNF-a. Further evaluation of MK-591 utilizing cell proliferation assays in PBMCs, human proximal tubule cells showed a decrease in cell proliferation.
In vivo
Amyloid β peptide (Aβ) deposition in the brains of mice receiving MK-591 was significantly reduced when compared with controls. MK-591 treatment did not cause any change in the steady-state levels ofβ-site amyloid precursor protein cleaving enzyme 1, amyloid-β precursor protein or disintegrin and metalloproteinase domain-containing protein 10.By contrast, MK-591 caused a significant reduction of the γ-secretase complex, at the protein and message level.
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