MK591 is selective and specific inhibitor of 5-Lipoxygenase-activating protein (FLAP).

>98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

Quiflapon sodium, MK-591, MK 591

10 mM in DMSO

FLAP

MK591 and SB203580 are able to block SEB-induced human PBMC cell proliferation. MK591 down regulates three genes that are up regulated by SEB. MK591 undergoes apoptosis within hours of treatment. MK591 also induces rapid activation of the stress kinase, c-Jun N-terminal kinase (JNK), which plays an important role in the apoptosis process. MK591 triggers apoptosis in prostate cancer cells without inhibition of PI3K-Akt, or ERK. Moreover, MK591 and LY294002 (an inhibitor of PI3K) exert synergistic effect in inducing apoptosis in prostate cancer cells. MK-591 influences cAMP response element-binding protein but not Sp1.

Hyperoxia groups of mice treated with MK-0591 (20, 40 mg/kg) show alveolarization that resembles that of room air controls while untreated hyperoxia groups show definite evidence of aberrant alveolarization but no inflammation. Comparison of the Aβ-immunopositive areas between the placebo and MK-591 (320 mg/kg)-treated group reveals a statistically significant reduction of the amyloid burden in the treated mice. MK-591 also has a significant reduction in brain levels of IL-1β. Mice treated with MK-591 show a statistically significant decrease in the steady-state levels of total CREB and its phosphorylated form at Ser133.