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Pathways Recommended: MAPK/ERK Pathway
Results for "

arachidonic acid pathway

" in MedChemExpress (MCE) Product Catalog:

28

Inhibitors & Agonists

4

Natural
Products

1

Isotope-Labeled Compounds

1

Oligonucleotides

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-141570

    Phospholipase Others
    Lyso-PAF C-16 is a precursor and metabolite of 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine (PAF C-16). Lyso-PAF C-16 is a substrate for either PAF C-16 formation by the remodeling pathway or selective acylation with arachidonic acid by a CoA-independent transacylase .
    Lyso-PAF C-16
  • HY-B1153
    Glafenine
    4 Publications Verification

    Glafenin

    COX CFTR Apoptosis Endoplasmic Reticulum Oxidoreductase 1 (ERO1) Metabolic Disease Inflammation/Immunology
    Glafenine (Glafenin) is a non-selective, non-steroidal anti-inflammatory drug-based COX-1/COX-2 inhibitor. Glafenine exerts anti-inflammatory, anti-proliferative and anti-cell migration effects by inhibiting the arachidonic acid metabolic pathway and reducing prostaglandin synthesis. Glafenine can induce cell cycle arrest in vascular smooth muscle cells and endothelial cells and reduce the synthesis of the extracellular matrix protein Tenascin. Glafenine can be used in the research of inflammatory-related diseases, vascular restenosis and cystic fibrosis (CF) .
    Glafenine
  • HY-124108

    ETYA

    COX Lipoxygenase Orthopoxvirus Potassium Channel DNA/RNA Synthesis Drug Derivative Infection Neurological Disease Inflammation/Immunology Cancer
    Eicosatetraynoic acid (ETYA) is a non-metabolizable analog of Arachidonic acid (HY-109590) and also an inhibitor of the lipoxygenase (LOX)/cyclooxygenase (COX) pathway (ID50 = 8 μM and 4 μM). Eicosatetraynoic acid acts as a suicide substrate to inhibit the production of inflammatory mediators such as leukotrienes and prostaglandins. Eicosatetraynoic acid acts directly on cell membranes and membrane proteins to exert a wide range of effects, including blocking potassium channels, increasing cell membrane fluidity, elevating intracellular calcium levels, inhibiting DNA synthesis in tumor cells, inducing differentiation of certain cells, and specifically inhibiting the assembly and replication of orthopoxviruses. Eicosatetraynoic acid alleviates acute lung injury induced by chemicals such as phosgene .
    Eicosatetraynoic acid
  • HY-113439
    12-HETE
    2 Publications Verification

    Apoptosis Cardiovascular Disease Inflammation/Immunology
    12-HETE, a major metabolic product of arachidonic acid using 12-LOX catalysis, inhibits cell apoptosis in a dose-dependent manner. 12-HETE promotes the activation and nuclear translocation of NF-κB through the integrin-linked kinase (ILK) pathway .12-HETE has both anti-thrombotic and pro-thrombotic effects . 12-HETE is a neuromodulator .
    12-HETE
  • HY-113439S
    12-HETE-d8
    2 Publications Verification

    Apoptosis Cardiovascular Disease Inflammation/Immunology
    12-HETE-d8 is the deuterium labeled 12-HETE. 12-HETE, a major metabolic product of arachidonic acid using 12-LOX catalysis, inhibits cell apoptosis in a dose-dependent manner. 12-HETE promotes the activation and nuclear translocation of NF-κB through the integrin-linked kinase (ILK) pathway .12-HETE has both anti-thrombotic and pro-thrombotic effects . 12-HETE is a neuromodulator .
    12-HETE-d8
  • HY-113438

    Drug Metabolite Bcl-2 Family Akt Apoptosis Cardiovascular Disease Inflammation/Immunology Cancer
    15(S)-HPETE is a precursor of 15(S)-HETE (HY-113336). 15(S)-HPETE is a product of Arachidonic acid (HY-109590) in the 15-lipoxygenase pathway. 15(S)-HPETE reduces Bcl-2, Akt, and phosphorylated Akt protein levels. 15(S)-HPETE induces Apoptosis. 15(S)-HPETE antagonizes the angiogenic effects of 15(S)-HETE. 15(S)-HPETE exhibits antitumor effects against chronic myeloid leukemia. 15(S)-HPETE can be used in adipose tissue explant studies .
    15(S)-HPETE
  • HY-E70127

    Brasan; Dasen

    Ser/Thr Protease COX Bacterial Prostaglandin Receptor Interleukin Related Cardiovascular Disease Infection Neurological Disease Inflammation/Immunology Cancer
    Serratiopeptidase (Brasan; Dasen) is an orally active zinc-containing metalloprotease belonging to the serralysin family. Serratiopeptidase reduces the release of inflammatory mediators such as prostaglandins, thromboxanes and interleukins by inhibiting COX, thereby relieving pain, swelling and redness. Serratiopeptidase exhibits antibiofilm, mucolytic and wound-healing activities. As a serine protease, Serratiopeptidase has the ability to dissolve blood clots, fibrin and atherosclerotic plaques. Serratiopeptidase degrades amyloid fibrils and has potential anti-Alzheimer's effects. Serratiopeptidase shows cytotoxicity against colon cancer cells .
    Serratiopeptidase
  • HY-150084

    (±)14(15)-EET

    Cytochrome P450 Mitosis Cancer
    (±)14,15-Epoxyeicosatrienoic acid ((±)14(15)-EET) is the Cytochrome P450 metabolite of arachidonic acid. While CYP3A4 may be involved in breast cancer cell growth, (±)14,15-Epoxyeicosatrienoic acid may promote mitosis and anchorage-dependent cloning through STAT3 affected by CYP3A4. (±)14,15-Epoxyeicosatrienoic acid exhibits STAT3-dependent cell growth promotion and may also participate in the autocrine/paracrine pathway that drives cell growth .
    (±)14,15-Epoxyeicosatrienoic acid
  • HY-B1153A
    Glafenine hydrochloride
    4 Publications Verification

    Glafenin hydrochloride

    COX CFTR Apoptosis Endoplasmic Reticulum Oxidoreductase 1 (ERO1) Metabolic Disease Inflammation/Immunology
    Glafenine (Glafenin) hydrochloride is a non-selective, non-steroidal anti-inflammatory drug-based COX-1/COX-2 inhibitor. Glafenine hydrochloride exerts anti-inflammatory, anti-proliferative and anti-cell migration effects by inhibiting the arachidonic acid metabolic pathway and reducing prostaglandin synthesis. Glafenine hydrochloride can induce cell cycle arrest in vascular smooth muscle cells and endothelial cells and reduce the synthesis of the extracellular matrix protein Tenascin. Glafenine hydrochloride can be used in the research of inflammatory-related diseases, vascular restenosis and cystic fibrosis (CF) .
    Glafenine hydrochloride
  • HY-W011297

    arachidonic acid methyl ester

    PKC Metabolic Disease
    Methyl arachidonate is a protein kinase C activator and also an orally active substrate that undergoes esterase-mediated hydrolysis. Methyl arachidonate indirectly activates protein kinase C via eicosanoid metabolites generated through the arachidonic acid metabolic pathway, exerting effects via cyclooxygenase products at low concentrations and via lipoxygenase products at high concentrations. Methyl arachidonate can be used in studies related to lipodystrophy .
    Methyl arachidonate
  • HY-B1153R

    Glafenin (Standard)

    COX CFTR Apoptosis Endoplasmic Reticulum Oxidoreductase 1 (ERO1) Reference Standards Metabolic Disease Inflammation/Immunology
    Glafenine (Standard) is the analytical standard of Glafenine. This product is intended for research and analytical applications. Glafenine (Glafenin) is a non-selective, non-steroidal anti-inflammatory drug-based COX-1/COX-2 inhibitor. Glafenine exerts anti-inflammatory, anti-proliferative and anti-cell migration effects by inhibiting the arachidonic acid metabolic pathway and reducing prostaglandin synthesis. Glafenine can induce cell cycle arrest in vascular smooth muscle cells and endothelial cells and reduce the synthesis of the extracellular matrix protein Tenascin. Glafenine can be used in the research of inflammatory-related diseases, vascular restenosis and cystic fibrosis (CF) .
    Glafenine (Standard)
  • HY-113445

    COX Endogenous Metabolite Endocrinology
    Thromboxane B3 is a prostaglandin analog derived from arachidonic acid (AA) in the cyclooxygenase (COX) metabolic pathway. Thromboxane B3 is generated from arachidonic acid (AA) in platelets and vascular endothelial cells through the catalysis of cyclooxygenase (COX) and thromboxane synthase (TXS). Thromboxane B3 has been reported to be formed by human platelets upon ingestion of eicosapentaenoic acid (C20: 5ω3) .
    Thromboxane B3
  • HY-116196

    Na+/K+ ATPase Cytochrome P450 Cardiovascular Disease Inflammation/Immunology
    17-HETE is arachidonic acid metabolite through cytochrome P-450 pathways, which consists of 17R-HETE and 17S-HETE enantiomers. 17-HETE serves as allosteric activator of the cytochrome P450 1B1 and inhibitor of ATPase, induces cardic hypertrophy .
    17-HETE
  • HY-116763

    COX LOX-1
    COX-2/5-LOX-IN-4 (Compound 1) is a dual inhibitor that acts on both COX-2 and 5-LOX, with IC50 values of 0.05 μM for COX-2 and 0.003 μM for 5-LOX. By inhibiting the arachidonic acid metabolism pathway, COX-2/5-LOX-IN-4 reduces the production of prostaglandins and leukotrienes, alleviating inflammatory responses. In a rat ear edema model, intravenous administration (0.01 and 0.1 mg/kg) reduced edema by 41% and 44%, respectively, demonstrating significant anti-inflammatory effects. COX-2/5-LOX-IN-4 shows promise for studying the mechanisms of inflammatory diseases .
    COX-2/5-LOX-IN-4
  • HY-124404

    Aryl Hydrocarbon Receptor Na+/K+ ATPase Prostaglandin Receptor Inflammation/Immunology
    12(R)-HETE is a CYP-dependent arachidonic acid metabolite that acts as a proinflammatory lipid mediator. 12 (R)-HETE widely exists in various tissues including the eye, skin and liver. In the cornea, 12(R)-HETE is metabolized via pathways such as β-oxidation into the precursor of 12(R)-HETrE. Without direct receptor binding, 12(R)-HETE indirectly activates AHR-mediated target gene transcription, while inhibiting the enzymatic activity of Na+,K+-ATPase and the intracellular calcium elevation induced by TP agonists. 12(R)-HETE also possesses multiple physiological effects such as chemotaxis, proangiogenesis, vasodilation, natriuresis, diuresis and intraocular pressure reduction, and can be widely used in studies related to psoriasis, inflammatory skin diseases and ocular inflammation .
    12(R)-HETE
  • HY-158843

    15(S)-Hydroxyeicosatetraenoic acid-biotin

    Endogenous Metabolite Others
    15(S)-Hete-biotin (15(S)-Hydroxyeicosatetraenoic acid-biotin) can be used to detect 15(S)-HETE binding proteins and/or receptors. 15(S)-HETE is an arachidonic acid metabolite produced by the 15-lipoxygenase pathway .
    15(S)-Hete-biotin
  • HY-W747548

    Lipoxygenase Leukotriene Receptor Inflammation/Immunology
    12(S)-HEPE is a monohydroxy fatty acid synthesized from EPA by the action of 12-LO. Unstimulated neutrophils metabolize 12(S)-HEPE to 12(S),20-diHEPE, whereas stimulated neutrophils produce 5(S),12(S)-HEPE via the 5-lipoxygenase pathway. The competitive action of 12(S)-HEPE with arachidonic acid as a substrate for 5-LO in the formation of leukotrienes may provide a basis for the anti-inflammatory potential of ω-3 fatty acids.
    12(S)-HEPE
  • HY-160431

    PPAR NF-κB COX Drug Metabolite Metabolic Disease
    8(9)-EET is one of the main metabolites produced by the metabolism of arachidonic acid (HY-109590) through the cytochrome P450 epoxide pathway. 8(9)-EET is an effective substrate for COX-1 and COX-2. 8(9)-EET activates PPARα in HEK293 cells and inhibits the activity of NF-κB induced by IL-1β in a PPARα-dependent and -independent manner. The (8S,9R)-isomer of 8(9)-EET ([(8S,9R)-EET]) causes vasoconstriction, thereby reducing renal plasma flow and glomerular filtration rate .
    8(9)-EET
  • HY-169430

    PGE synthase
    AGU654 (Compound 44) is a selective mPGES-1 inhibitor with an IC50 of 2.9 nM against mPGES-1. AGU654 inhibits mPGES-1 to block the pathway converting arachidonic acid into prostaglandin E2 (PGE2) by COX-1/2, thereby alleviating inflammatory responses, pain, and fever. In activated human monocyte-derived macrophages and human whole blood models, AGU654 selectively suppresses bacterial exotoxin-induced PGE2 production while preserving the production of other prostaglandins. In guinea pig models, AGU654 significantly alleviates fever, inflammation, and inflammatory pain, exhibiting excellent anti-inflammatory, analgesic, and antipyretic effects. AGU654 holds promise as a strategy for studying inflammatory diseases and pain .
    AGU654
  • HY-137493

    14,15-LTD4; Eoxin D4

    Endogenous Metabolite Inflammation/Immunology
    14,15-Leukotriene D4 (14,15-LTD4) is a leukotriene that producted by eosinophils with Arachidonic acid (HY-109590), and through the 15-lipoxygenase-1 pathway .
    14,15-Leukotriene D4
  • HY-116050A

    Cytochrome P450 Others
    17R-HETE is an arachidonic acid metabolite through cytochrome P-450 pathways. 17R-HETE exhibits efficacy in inducing cardic hypertrophy with less efficiency with compared to 17S-HETE .
    17(R)-HETE
  • HY-116050

    Cytochrome P450 Na+/K+ ATPase Cardiovascular Disease Inflammation/Immunology
    17S-HETE is arachidonic acid metabolite through cytochrome P-450 pathways. 17S-HETE serves as allosteric activator of the cytochrome P450 1B1 and inhibitor of ATPase, induces cardic hypertrophy .
    17(S)-HETE
  • HY-B1153AR

    Glafenin hydrochloride (Standard)

    COX CFTR Apoptosis Endoplasmic Reticulum Oxidoreductase 1 (ERO1) Reference Standards Metabolic Disease Inflammation/Immunology
    Glafenine (hydrochloride) (Standard) is the analytical standard of Glafenine (hydrochloride). This product is intended for research and analytical applications. Glafenine (Glafenin) hydrochloride is a non-selective, non-steroidal anti-inflammatory drug-based COX-1/COX-2 inhibitor. Glafenine hydrochloride exerts anti-inflammatory, anti-proliferative and anti-cell migration effects by inhibiting the arachidonic acid metabolic pathway and reducing prostaglandin synthesis. Glafenine hydrochloride can induce cell cycle arrest in vascular smooth muscle cells and endothelial cells and reduce the synthesis of the extracellular matrix protein Tenascin. Glafenine hydrochloride can be used in the research of inflammatory-related diseases, vascular restenosis and cystic fibrosis (CF) .
    Glafenine hydrochloride (Standard)
  • HY-176074

    Prostaglandin Receptor Others
    U-46619 Glycine methyl ester has a modification at the C-1 position of U-46619, which uniquely alter its binding properties to the TP receptor or any of the PGH2-metabolizing enzymes. U-46619 is a stable analog of the endoperoxide PGH2. U-46619 is also an agonist of TP receptor. U-46619 can change the shape of platelet, aggregation and contraction of vascular smooth muscle. U-46619 Glycine methyl ester can be studied in research to explore the inhibition of various enzymes in the arachidonic acid metabolic pathway. U-46619 Glycine methyl ester can also act as a lipophilic prodrug form of U-46619 that alters its distribution and pharmacokinetic properties .
    U-46619 Glycine methyl ester
  • HY-157874

    14,15-Leukotriene A4

    Endogenous Metabolite Cardiovascular Disease Inflammation/Immunology
    Eoxin A4 (14,15-Leukotriene A4) is an Arachidonic acid (HY-109590) metabolite. Eoxin A4 forms via the 15-lipoxygenase pathway .
    Eoxin A4
  • HY-N18311

    Others Cardiovascular Disease
    Caragiside B is an isoflavone glucoside that can be isolated from the whole plant of Caragana densa. Caragiside B inhibits arachidonic acid (HY-109590)-induced platelet aggregation by interfering with platelet aggregation pathways .
    Caragiside B
  • HY-N19724

    Fungal Lipoxygenase COX Infection
    Buddledin A is a 5-LOX inhibitor (IC50 = 50.4 μM) and a COX inhibitor (IC50 = 13.7 μM). Buddedin A inhibits arachidonic acid metabolism via the 5-LOX and COX pathways, suppresses fungal growth, and exerts toxic effects on fish. Buddedin A may play an ecological role in protecting plant roots and stem barks from fungal infection. Buddedin A can be used in studies related to fungal infections .
    Buddledin A
  • HY-179488

    PPAR NF-κB COX Drug Metabolite Metabolic Disease
    (±)8(9)-EET is one of the main metabolites produced by the metabolism of arachidonic acid (HY-109590) through the cytochrome P450 epoxide pathway. (±)8(9)-EET is an effective substrate for COX-1 and COX-2. (±)8(9)-EET activates PPARα in HEK293 cells and inhibits the activity of NF-κB induced by IL-1β in a PPARα-dependent and -independent manner. The (8S,9R)-isomer of (±)8(9)-EET ([(8S,9R)-EET]) causes vasoconstriction, thereby reducing renal plasma flow and glomerular filtration rate .
    (±)8(9)-EET

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