Quiflapon (MK-591) causes cell apoptosis. Quiflapon is a selective and specific 5-lipoxygenase-activating protein (FLAP) inhibitor (IC50: 1.6 nM in a FLAP binding assay) and is also an effective and orally active Leukotriene biosynthesis (LT) inhibitor (IC50: 3.1 and 6.1 nM in intact human and elicited rat PMNLs, respectively).

Fiboflapon (GSK2190915) is an orally available and effective 5-lipoxygenase-activating protein (FLAP) inhibitor that binds FLAP with a titer of 2.9 nM and inhibition of LTB4 in human blood with an IC50 of 76 nM.

Quiflapon sodium (MK591) is a selective inhibitor of 5-Lipoxygenase-activating protein (FLAP).

sEH/FLAP-IN-1 (Compound 46A) serves as a dual inhibitor targeting both sEH and FLAP, effectively suppressing 5-LOX product formation with an EC50 of 11 nM in SACM-stimulated PBMCs, inhibiting sEH activity (EC50: 18 nM), and reducing thromboxane production. This compound is utilized in the study of inflammatory diseases [1].

FEN1-IN-7 (compound 16), a selective Flap endonuclease-1 (FEN1) inhibitor with an IC50 of 18 nM, plays a role in DNA damage repair in mammalian cells. Additionally, it targets the related endonuclease, xeroderma pigmentosum G (XPG), with an IC50 of 3.04 μM. FEN1-IN-7 enhances the sensitivity of cancer cells to potent DNA alkylating or methylating agents [1].

FEN1-IN-6 (compound 9) is a potent Flap endonuclease-1 (FEN1, IC50 = 10 nM) inhibitor, crucial for DNA damage repair in mammalian cells, and also targets the related endonuclease xeroderma pigmentosum G (XPG) with an IC50 of 23 nM [1].

FEN1-IN-5 (compound 12A) is a potent inhibitor of Flap endonuclease-1 (FEN1) with an IC50 of 12 nM, contributing to DNA repair mechanisms [1].