ITE

ITE is an endogenous aryl hydrocarbon receptor (AhR) agonist.¹ It binds to AhR (K_d = 65 nM) and induces AhR-dependent transcription in luciferase reporter assays when used at a concentration of 0.01 µM. ITE (1 µM) inhibits anti-CD40- and IL-4-induced differentiation of isolated mouse splenic B cells, as well as proliferation and migration of SKOV3 ovarian cancer cells.^2,3 In vivo, ITE (200 µg/animal, i.p.) reduces retinal detachment and ocular inflammatory cell infiltration in a mouse model of experimental autoimmune uveitis induced by complete Freund's adjuvant (CFA) and M. tuberculosis.⁴ ITE (80 mg/kg, i.p.) reduces tumor growth by 39% in an OVCAR-3 mouse xenograft model.³

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1. Henry, E.C., Bemis, J.C., Henry, O., et al. A potential endogenous ligand for the aryl hydrocarbon receptor has potent agonist activity in vitro and in vivo. Arch. Biochem. Biophys. 450(1), 67-77 (2006).

2. Yoshida, T., Katsuya, K., Oka, T., et al. Effects of AhR ligands on the production of immunoglobulins in purified mouse B cells. Biomed. Res. 33(2), 67-74 (2012).

3. Wang, K., Li, Y., Jiang, Y.-Z., et al. An endogenous aryl hydrocarbon receptor ligand inhibits proliferation and migration of human ovarian cancer cells. Cancer Lett. 340(1), 63-71 (2013).

4. Nugent, J.F., Shi, G.S., Vistica, B.P., et al. ITE, a novel endogenous nontoxic aryl hydrocarbon receptor ligand, efficiently suppresses EAU and T-cell–mediated immunity. Invest. Ophthalmol. Vis. Sci. 54(12), 7463-7469 (2013).