icam 3

Anti-ICAM3/CD50 Antibody is a highly specialized monoclonal antibody target the human intercellular adhesion molecule 3, which is also known as CD50, inhibition of ligand-receptor interactions between leukocytes and endothelial cells across various preclinical experimental models to modulate immune cell adhesion and inflammatory responses.

(±)14(15)-EET is a metabolite of arachidonic acid that is formed via epoxidation of arachidonic acid by cytochrome P450.[1],[2] It prevents increases in leukotriene B4, ICAM-1, and chemokine (C-C motif) ligand 1 (CCL2) induced by oxidized LDL in primary rat pulmonary artery endothelial cells (RPAECs) when used at a concentration of 1 μM.[3] (±)14(15)-EET induces dilation of preconstricted isolated canine coronary arterioles (EC50 = 0.2 pM).[4] It reduces myocardial infarct size as a percentage of the area at risk in a canine model of ischemia-reperfusion injury induced by left anterior descending coronary artery (LAD) occlusion when administered at a dose of 0.128 mg/kg prior to occlusion or reperfusion.[5] Reference:[1]. Chacos, N., Falck, J.R., Wixtrom, C., et al. Novel epoxides formed during the liver cytochrome P-450 oxidation of arachidonic acid. Biochem. Biophys. Res. Commun. 104(3), 916-922 (1982).[2]. Oliw, E.H., Guengerich, F.P., and Oates, J.A. Oxygenation of arachidonic acid by hepatic monooxygenases. Isolation and metabolism of four epoxide intermediates. J. Biol. Chem. 257(7), 3771-3781 (1982).[3]. Jiang, J.-X., Zhang, S.-J., Xiong, Y.-K., et al. EETs attenuate ox-LDL-induced LTB4 production and activity by inhibiting p38 MAPK phosphorylation and 5-LO/BLT1 receptor expression in rat pulmonary arterial endothelial cells. PLoS One 10(6), e0128278 (2015).[4]. Oltman, C.L., Weintraub, N.L., VanRollins, M., et al. Epoxyeicosatrienoic acids and dihydroxyeicosatrienoic acids are potent vasodilators in the canine coronary microcirculation. Circ. Res. 83(9), 932-939 (1998).[5]. Nithipatikom, K., Moore, J.M., Isbell, M.A., et al. Epoxyeicosatrienoic acids in cardioprotection: Ischemic versus reperfusion injury. Am. J. Physiol. Heart Circ. Physiol. 291(2), H537-H542 (2006).

(±)11(12)-EET is a fully racemic version of the R/S enantiomeric forms biosynthesized from arachidonic acid by cytochrome P450 enzymes.[1][2][3] A higher proportion of 11(R),12(S)-EET is produced by the CYP450 isoforms CYP2C23 and CYP2C24, while CYP2B2 produces a higher proportion of 11(S),12(R)-EET.[3] 11(12)-EET has been shown, along with 8(9)-EET, to play a role in the recovery of depleted calcium pools in cultured smooth muscle cells.[4] It also inhibits basolateral 18-pS potassium channels in the renal cortical collecting duct at a concentration of 100 nM.[5] 11(12)-EET (50 μg/kg per day) increases adhesion of isolated peripheral blood leukocytes in a chamber coated with P-selectin and ICAM-1 but does not affect choroidal neovascularization size following laser photocoagulation.[6] It also has anti-inflammatory, angiogenic, and cardioprotective properties.[7]

3-Hydroxyxanthone (3-Hydroxy-xanthen-9-one), a xanthone derivative, inhibits NADPH-catalyzed lipid peroxidation in human umbilical vein endothelial cells (HUVECs) and suppresses TNF-alpha-induced ICAM-1 expression [1].

2'-Hydroxychalcone is a drug synthesis intermediate for the synthesis of flavonoids. 2'-Hydroxychalcone loaded in nanoemulsion showed fungicidal activity against Coccidioides parapsilosis in Danio rerio model.2'-Hydroxychalcone induced cytotoxicity through oxidative stress in lipid-loaded Hepg2 cells.2'-Hydroxychalcone inhibited the induction of ICAM-1, VCAM-α, tumor necrosis factor-α, and tumor necrosis factor-alpha as determined by reverse transcription-polymerase chain reaction determined by tumor necrosis factor-alpha induces steady-state transcript levels of ICAM-1, VCAM-1, and E-selectin, and therefore may interfere with the transcription of their genes.