LOX-1
Lectin-like oxidized low-density lipoprotein receptor-1
Unlike native low-density lipoprotein (LDL), modified LDL such
as oxidized, carbamylated, or acetylated LDL are not recognized by the native LDL receptor (LDL-R).1 Rather, modified
LDL binds to the lectin-like oxidized LDL receptor-1 (LOX-1).Upon activation by modified LDL, LOX-1 induces endothelial
dysfunction and uptake of the modified lipids.2 Endothelial dysfunction is the first stage in atherogenesis.3 Thus, the identification of LOX-1 through expression cloning as a major receptor
for oxLDL in endothelial cells (ECs) supports a putative role
for modified LDL in atherogenesis and has taken centre stage
in cardiovascular research.
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LOX-1 Produits associés (9)
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Anticorps (8)
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Golocdacimab
0 ImagesSynonyms: MEDI6570Gocdacimab (MEDI6570) is a fully human IgG1 monoclonal antibody inhibitor targeting the lectin-like oxidized low-density lipoprotein receptor LOX-1. By binding to LOX-1 and blocking its function, gocdacimab effectively reduces the level of free soluble LOX-1, thereby inhibiting key pathological processes such as lipid accumulation, foam cell formation, and vascular wall inflammation. Gocdacimab can interfere with atherosclerosis-related mechanisms, and it is used for research on atherosclerosis, and type 2 diabetes mellitus.
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Kansuinine A
0 ImagesKansuinine A is a diterpenoid compound. Kansuinine A is isolated from the roots of Euphorbia kansui. Kansuinine A inhibits H2O2-mediated upregulation of phosphorylated IKKβ, NF-κB and IκBα. Kansuinine A inhibits ROS production, reduces the Bax/Bcl-2 ratio and the expression of cleaved Caspase-3. Kansuinine A upregulates the expression of SOCS-3 and blocks IL-6-induced signal transduction. Kansuinine A decreases the expression of LOX-1 and inhibits Apoptosis. Kansuinine A reduces the atherosclerotic lesion area of the aortic arch, improves glucose/insulin tolerance, and enhances antioxidant capacity. Kansuinine A exhibits antiviral and antitumor activities. Kansuinine A can be used in research related to atherosclerosis, liver cancer and type 2 diabetes.
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COX-2-IN-30
0 ImagesCat. No.: HY-149269CAS No.: 1160498-08-7COX-2-IN-30 is a benzenesulfonamide derivative, as well as an orally active and dual inhibitor of COX (IC50=49 nM for COX-2, 10.4 μM for COX-1) and 5-LOX (IC50=2.4 μM). COX-2-IN-30 also inhibits transmembrane hCA IX and hCA XII isoform with nanomolar calss Ki values. COX-2-IN-30 exhibits analgesic, anti-inflammatory, and ulcerogenic activities, and does not show acute gastric effect.
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COX-2/5-LOX-IN-4
0 ImagesCat. No.: HY-116763CAS No.: 443919-96-8COX-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.
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15-LOX-1 inhibitor 2
0 ImagesCat. No.: HY-173332CAS No.: 3110518-96-915-LOX-1 inhibitor 2 (Compound 5i) is an inhibitor of 15-lipoxygenase-1 (15-LOX-1) with an IC50 of 1.7 μM. 15-LOX-1 inhibitor 2 inhibits the activity of 15-LOX-1 enzyme, reduces the production of lipid peroxides, thereby inhibiting lipid peroxidation and protecting cells from cell death induced by RSL3 (HY-100218A). 15-LOX-1 inhibitor 2 can be used in research on cell death mechanisms, oxidative stress-related diseases and other fields.
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AChE-IN-82
0 ImagesCat. No.: HY-170938AChE-IN-82 (compound 49) is an acetylcholinesterase (AChE) inhibitor. AChE-IN-82 inhibits eeAChE, eqBChE, hMAO-A, hMAO-B, and BACE-1 with IC50s of 0.072, 9.81, 14.52, 0.024, 2.42 μM, respectively. AChE-IN-82 inhibits COX-1, COX-2 and 5-LOX with IC50s of 60.41, 0.187, 0.18 μM, respectively. AChE-IN-82 shows an excellent neuroprotective effect by significantly reducing oxidative stress induced by H2 O2.
