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Atuliflapon (AZD5718) is an orally active inhibitor of FLAP (5‑Lipoxygenase activating protein), with an IC50 of 2 nM. Atuliflapon is used in the study for coronary artery disease .
FLAP-IN-1 (Intermediate 14) is a 5-lipoxygenase-activating protein (FLAP) inhibitor with an IC50 value of 654 nM. FLAP-IN-1 can be used in cardiovascular disease research .
sEH/FLAP-IN-1 (Compound 46A) is a sEH/FLAP inhibitor. sEH/FLAP-IN-1 inhibits 5-LOX product formation in SACM-stimulated PBMCs (EC50: 11 nM). sEH/FLAP-IN-1 inhibit sEH (EC50: 18 nM) and thromboxane production. sEH/FLAP-IN-1 can be used for research of inflammatory diseases .
BI 665915 is an orally active and potent 5-lipoxygenase-activating protein (FLAP) inhibitor. BI 665915 inhibits FLAP production that blocks LTB4 biosynthesis in mice. BI 665915 is promising for research of various inflammatory diseases, including respiratory and cardiovascular diseases .
(S)-BI 665915 is an orally active oxadiazole-containing 5-lipoxygenase-activating protein (FLAP) inhibitor with an IC50 of 1.7 nM for FLAP binding. (S)-BI 665915 inhibits FLAP functional in human whole blood with an IC50 of 45 nM. (S)-BI 665915 demonstrates an excellent cross-species agent metabolism and pharmacokinetics (DMPK) profile and a dose-dependent inhibition of LTB4 production .
LTB4-IN-2 (Comopund 6x) is a Leukotriene B4 (LTB4) inhibitor. LTB4-IN-2 inhibits Leukotriene B4 formation (IC50: 1.15 μM) by selectively targeting 5-Lipoxygenase-activating protein (FLAP). LTB4-IN-2 can be used for anti-inflammatory research .
sEH inhibitor-12 (compound 34) is a sEH inhibitor with an IC50 value of 0.7 μM. sEH inhibitor-12 inhibits the 5-lipoxygenase-activating protein (FLAP)-mediated leukotriene (LT) biosynthesis with an IC50 value of 2.9 μM. sEH inhibitor-12 can be used for the research of inflammation .
AM103 (free acid) is a selective FLAP inhibitor that can block the first step of the LT pathway, which is 5-LO activation. AM103 (free acid) can inhibit the production of LTB4 and cysteinyl leukotrienes (CysLT). AM103 (free acid) has anti-inflammatory activity in a mouse model of chronic lung inflammation and can extend the survival time of mice injected with platelet-activating factor. AM103 (free acid) can be used for research on respiratory diseases such as asthma .
Fiboflapon (GSK2190915; AM-803) is a potent and orally bioavailable 5-lipoxygenase-activating protein (FLAP) inhibitor with a potency of 2.9 nM in FLAP binding, an IC50 of 76 nM for inhibition of LTB4 in human blood .
Fiboflapon sodium (GSK2190915; AM-803) is a potent and orally bioavailable 5-lipoxygenase-activating protein (FLAP) inhibitor with a potency of 2.9 nM in FLAP binding, an IC50 of 76 nM for inhibition of LTB4 in human blood .
L-691678 can bind to FLAP by recognizing the amino acid residues of 5-lipoxygenase-activating protein (FLAP), thereby inhibiting leukotriene biosynthesis. L-691678 can be used in the study of leukotriene-related diseases such as allergies, asthma, and inflammation .
AM679 is a potent, selective 5-lipoxygenase-activating protein (FLAP) inhibitor with an IC50 of 2 nM in a human FLAP membrane binding assay. AM679 markedly reduces the respiratory syncytial virus-driven ocular pathology as well as the synthesis of cysteinyl leukotrienes (CysLTs) in the eye .
Quiflapon (MK-591) is a selective and specific 5-lipoxygenase-activating protein (FLAP) inhibitor with an IC50?of 1.6 nM in a FLAP binding assay. Quiflapon is also a potent and orally active?Leukotriene biosynthesis (LT)?inhibitor, shows IC50?values of 3.1 and 6.1 nM in intact human and elicited rat PMNLs, respectively. Quiflapon induces cell apoptosis .
Quiflapon sodium (MK-591 sodium) is a selective and specific 5-Lipoxygenase-activating protein (FLAP) inhibitor. Quiflapon sodium is an orally active Leukotriene biosynthesis inhibitor. Induces apoptosis.
Veliflapon (BAY X 1005; DG-031) is an orally active and selective 5-lipoxygenase activating protein (FLAP) inhibitor . Veliflapon inhibits the synthesis of the leukotrienes B4 and C4 .
FEN1-IN-1 (compound 1) is a flap endonuclease 1 (FEN1) inhibitor. FEN1-IN-1 binds to the active site of FEN1 and partly achieves inhibition by the co-ordination of Mg 2+ ions .
FEN1-IN-6 (compound 9) is a potent inhibitor of Flapendonuclease-1 (FEN1, IC50=10 nM), involving in mammalian cells to repair DNA damage. FEN1-IN-6 also targets to related endonuclease, xeroderma pigmentosum G (XPG) with an IC50 value of 23 nM .
MK-886 (L 663536) sodium salt is a potent, cell-permeable and orally active FLAP (IC50 of 30 nM) and leukotriene biosynthesis (IC50s of 3 nM and 1.1 μM in intact leukocytes and human whole blood, respectively) inhibitor. MK-886 sodium salt is also a non-competitive PPARα antagonist and can induce apoptosis .
MK-886 (L 663536) is a potent, cell-permeable and orally active FLAP (IC50 of 30 nM) and leukotriene biosynthesis (IC50s of 3 nM and 1.1 μM in intact leukocytes and human whole blood, respectively) inhibitor. MK-886 is also a non-competitive PPARα antagonist and can induce apoptosis .
ALR-6 is an antagonist of the 5-lipoxygenase (5-LOX) activating protein FLAP and has anti-inflammatory activity. ALR-6 potently inhibits 5-LOX product formation (>80%) in pro-inflammatory M1-MDM and has no significant effect on direct inhibition of 5-LOX .
Diflapolin is a highly active dual 5-lipoxygenase-activating protein (FLAP)/soluble epoxide hydrolase (sEH) inhibitor with marked anti-inflammatory efficacy and high target selectivity. Diflapolin inhibits 5-LOX product formation in intact human monocytes and neutrophils with IC50s?of? 30 and 170?nM, respectively, and suppressed the activity of isolated sEH (IC50=20?nM) .
(S)-Veliflapon ((S)-BAY X 1005) is an orally active inhibitor of leukotriene biosynthesis and 5-lipoxygenase activating protein (FLAP). (S)-Veliflapon inhibits the formation of leukotriene B4 (LTB4) in rat, mouse and human leukocytes with IC50 values of 0.026 µM, 0.039 µM and 0.22 µM respectively. (S)-Veliflapon showes enantioselectivity in human whole blood .
FEN1-IN-7 (compound 16) is a selective inhibitor of Flapendonuclease-1 (FEN1, IC50=18 nM), involving in mammalian cells to repair DNA damage. FEN1-IN-7 also targets to related endonuclease, xeroderma pigmentosum G (XPG) with an IC50 value of 3.04 μM. FEN1-IN-7 increases the cellular sensitivity of cancer cells to potent DNA alkylating agents or methylating agents .
ALR-27 is an antagonist of the 5-lipoxygenase (5-LOX) activating protein FLAP and has anti-inflammatory activity. ALR-27 potently inhibits 5-LOX product formation (>80%) in pro-inflammatory M1-MDM, with no significant direct inhibition of 5-LOX. ALR-27 not only reduces prostaglandin and leukotriene (LT) production in neutrophils but also increases the production of specialized prolytic mediators in specific human macrophage phenotypes .
L-699333 is a 5-lipoxygenase (5-LO) inhibitor belonging to the thieno[2,3,4-cd]indole class. This compound has a 2-ethoxybutyric acid side chain and is a potent inhibitor of the biosynthesis of 5-HPETE and LTB4 produced from human 5-LO, with ICm values of 22 nM, 7 nM, and 3.8 pM for human neutrophils and whole blood, respectively. L-699333 has shown anti-inflammatory and antiasthmatic effects in a variety of animal models, including rat pleurisy models, antigen-induced wheezing models, and awake macaque and sheep asthma models. Its inhibition of 5-LO is highly selective, with higher ICm values or stronger competitive inhibition in FLAP binding assays compared to inhibition of human 15-LO, porcine 12-LO, and ram epididymal cyclooxygenase. The racemic enantiomer 14g of L-699333 is the most potent enantiomer to date, with inhibitory effects similar to those of the known MK-0591, which has been shown in clinical trials to inhibit the biochemical effects of LTB4 biosynthesis in vitro and LTE4 excretion in urine.
Flap endonuclease 1 (FEN-1) is a structure-specific nuclease crucial for DNA replication and repair. In replication, it cleaves 5'-overhanging flaps, guiding DNA polymerase and creating a nick for ligation. FEN-1 is integral to the long patch base excision repair pathway, preventing genomic instability. It exhibits 5'-3' exonuclease and RNase H activities, playing roles in rDNA and mitochondrial DNA replication and repair. Flap endonuclease 1/FEN-1 Protein, Human is the recombinant human-derived Flap endonuclease 1/FEN-1 protein, expressed by E. coli , with tag free.
Flap endonuclease 1 (FEN-1) is a structure-specific nuclease crucial for DNA replication and repair. In replication, it cleaves 5'-overhanging flaps, guiding DNA polymerase and creating a nick for ligation. FEN-1 is integral to the long patch base excision repair pathway, preventing genomic instability. It exhibits 5'-3' exonuclease and RNase H activities, playing roles in rDNA and mitochondrial DNA replication and repair. Flap endonuclease 1/FEN-1 Protein, Human (His, Myc) is the recombinant human-derived Flap endonuclease 1/FEN-1 protein, expressed by E. coli , with N-10*His, C-Myc labeled tag.
FLAP Antibody (YA2703) is a biotin-conjugated non-conjugated IgG antibody, targeting FLAP, with a predicted molecular weight of 18 kDa (observed band size: 18 kDa). FLAP Antibody (YA2703) can be used for WB experiment in human background.
FEN1 Antibody (YA765) is a non-conjugated and Mouse origined monoclonal antibody about 43 kDa, targeting to FEN1 (1E7). It can be used for WB,IP assays with tag free, in the background of Human, Mouse, Rat.
L-691678 can bind to FLAP by recognizing the amino acid residues of 5-lipoxygenase-activating protein (FLAP), thereby inhibiting leukotriene biosynthesis. L-691678 can be used in the study of leukotriene-related diseases such as allergies, asthma, and inflammation .
L-669083 is a leukotriene biosynthesis inhibitor whose structure is based on a mixture of indole and quinoline. In this study, a potent radioiodinated photoaffinity analog of L-689,037, [125I] L-691,678, was developed and characterized for immunoprecipitation studies showing that the quindole series of leukotriene biosynthesis inhibitors directly interact with FLAP. In addition, the results showed that MK-886, L-674,573, and L-689,037 competed with [125I] L-691,678 and [125I] L-669083 for binding to FLAP in a concentration-dependent manner, indicating that these three leukotriene biosynthesis inhibitors share a binding site on FLAP, further demonstrating that FLAP is a suitable target for structurally diverse leukotriene biosynthesis inhibitors.
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