ITE MedChemExpress (MCE)

Product Name	methyl 2-(1H-indole-3-carbonyl)thiazole-4-carboxylate
Synonyms	ITE ARYL HYDROCARBON RECEPTOR LIGAND methyl 2-(1H-indole-3-carbonyl)thiazole-4-carboxylate Methyl 2-(1H-indole-3-carbonyl)thiazole-4-carboxylate 2-(1'H-INDOLE-3'-CARBONYL)-THIAZOLE-4-CARBOXYLIC ACID Synonyms ITE ARYL HYDROCARBON RECEPTOR LIGAND methyl 2-(1H-indole-3-carbonyl)thiazole-4-carboxylate Methyl 2-(1H-indole-3-carbonyl)thiazole-4-carboxylate 2-(1'H-INDOLE-3'-CARBONYL)-THIAZOLE-4-CARBOXYLIC ACID methyl 2-(1H-indole-3-carbonyl)-1,3-thiazole-4-carboxylate 2-(1H-INDOL-3-YLCARBONYL)-4-THIAZOLECARBOXYLIC ACID METHYL ESTER 2-(1'H-indole-37-carbonyl)-thiasole-4-carboxylic acid methyl ester 4-Thiazolecarboxylic acid, 2-(1H-indol-3-ylcarbonyl)-, methyl ester
CAS	448906-42-1
EINECS
Chemical Formula	C14H10N2O3S
Molecular Weight	286.31
inchi
Package	10 mM * 1 mL;1 mg;5 mg;10 mg;50 mg;100 mg
Price	Email to quote
Descriptions	ITE ITE MedChemExpress (MCE) HY-19317 448906-42-1 99.27% Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year Room temperature in continental US Descriptions ITE ITE MedChemExpress (MCE) HY-19317 448906-42-1 99.27% Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year Room temperature in continental US may vary elsewhere. ITE is a potent endogenous agonist of aryl hydrocarbon receptor (AhR), binding directly to AHR, with a Ki of 3 nM. ITE also has immunosuppressive activity. ITE is an endogenous agonist of AhR, binding directly to AHR, with a Ki of 3 nM[1]. ITE (0.03-30 mg/mL) decreases the antigen-specific T-cell proliferative responses[2]. ITE potently inhibits human pulmonary artery endothelial (HPAECs) growth at 10 and 20 μM, but shows no effect at 0.01-5 μM. ITE does not affect cell cycle progress of HPAECs at 10 and 20 μM, or induce expression of cleaved caspase-3 protein in HPAECs at 20 μM. In addition, ITE (20 μM) elevates CYP1A1 and CYP1B1 mRNA levels and decreases the levels of AhR protein in HPAECs[3]. ITE (200 μg, i.p.) significantly suppresses the development of experimental autoimmune uveitis (EAU) in mice. ITE reduces the proportions of cells expressing IFN-γ, IL-17, or IL-10 in mice. ITE also suppresses the secretion of inflammatory cytokines by LN cells in mice[2]. Mice[2] Eight- to 12-week-old female B10.A mice is used in the assay. Daily treatment starts on day 0 and consists of 200 μg of ITE suspended in 0.2 mL PBS, given intraperitoneally. Control mice are similarly treated with 0.2 mL of the vehicle, PBS containing 3.6% DMSO[2]. Subconfluent cells (25, 000 cells/well) are seeded in 96-well plates. Cells are treated with ITE at 5, 10 and 20 µM or DMSO (0.1% v/v) in ECM for 2, 4 or 6 days with a change of ECM containing DMSO or ITE every other day (5 wells/treatment). At the end of treatment, cells are incubated with MTT reagent for 4 hr, and solubilized in crystal dissolving solution (100 µL/well) for 20 min. The absorbance is determined at 570 nm using the microplate reader[3]. Ki: 3 nM (AhR)[1] In Vitro ITE is an endogenous agonist of AhR, binding directly to AHR, with a Ki of 3 nM[1]. ITE (0.03-30 mg/mL) decreases the antigen-specific T-cell proliferative responses[2]. ITE potently inhibits human pulmonary artery endothelial (HPAECs) growth at 10 and 20 μM, but shows no effect at 0.01-5 μM. ITE does not affect cell cycle progress of HPAECs at 10 and 20 μM, or induce expression of cleaved caspase-3 protein in HPAECs at 20 μM. In addition, ITE (20 μM) elevates CYP1A1 and CYP1B1 mRNA levels and decreases the levels of AhR protein in HPAECs[3]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> ITE Related Antibodies \| \| \| \| \| \| \| \| \| \| [1]. Song J, et al. A ligand for the aryl hydrocarbon receptor isolated from lung. Proc Natl Acad Sci U S A. 2002 Nov 12 99(23):14694-9. [Content Brief] [2]. Nugent LF, et al. ITE, a novel endogenous nontoxic aryl hydrocarbon receptor ligand, efficiently suppresses EAU and T-cell-mediated immunity. Invest Ophthalmol Vis Sci. 2013 Nov 13 54(12):7463-9. [Content Brief] [3]. Pang LP, et al. ITE inhibits growth of human pulmonary artery endothelial cells. Exp Lung Res. 2017 Oct 43(8):283-292. [Content Brief]
Last Update	2025-04-01 14:45:47

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