ITE

Research use only, not for human use.

A endogenous ligand, potent aryl hydrocarbon receptor (AhR) agonist in vitro; activates the murine AhR in vivo.

A endogenous ligand, potent aryl hydrocarbon receptor (AhR) agonist in vitro; activates the murine AhR in vivo, but does not induce toxicity; induces the differentiation of stem-like cancer cells and reduces their tumorigenic potential in both subcutaneous and orthotopic xenograft tumour models.(In Vitro):ITE is an endogenous agonist of AhR, binding directly to AHR, with a Ki of 3 nM. ITE (0.03-30 mg/mL) decreases the antigen-specific T-cell proliferative responses. 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.(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.

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Endocrinology/Hormones

AhR

AhR

Cancer

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448906-42-1

286.3058

C14H10N2O3S

>98% (HPLC)

DMSO: ≥ 41 mg/mL

COC(=O)C1=CSC(=N1)C(=O)C2=CNC3=CC=CC=C32

4-Thiazolecarboxylic acid, 2-(1H-indol-3-ylcarbonyl)-, methyl ester

(-20℃)

With Ice Pack

≥ 2 years