| Bioactivity | 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. | ||||||||||||
| Target | Ki: 3 nM (AhR) | ||||||||||||
| Invitro | 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]. | ||||||||||||
| In Vivo | 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]. | ||||||||||||
| Name | ITE | ||||||||||||
| CAS | 448906-42-1 | ||||||||||||
| Formula | C14H10N2O3S | ||||||||||||
| Molar Mass | 286.31 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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| Reference | [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. [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. [3]. Pang LP, et al. ITE inhibits growth of human pulmonary artery endothelial cells. Exp Lung Res. 2017 Oct;43(8):283-292. |