ITE
目录号 : GC12628
ITE是一种有效的免疫抑制性内源性芳香烃受体（AhR）激动剂，与AhR结合的Ki值为3nM。
Cas No.:448906-42-1
Sample solution is provided at 25 µL, 10mM.
_1-3.$$$39978408@51.jpg');)
_1-9.$$$38538795@65.jpg');)
_1-9.$$$39112701@51.jpg');)
_1-7.$$$37316672@70.jpg');)
_366-372.$$$36198801@70.jpg');)
.$$$38565142@65.jpg');)
_1867-1883.$$$33248023@67.jpg');)
_eads6055.$$$39977546@45.jpg');)
_eadm9805.$$$40080571@45.jpg');)
_eadj3020.$$$39666821@45.jpg');)
_1-20.$$$39757301@28.jpg');)
_1-24.$$$38898113@28.jpg');)
_273-287.$$$36806353@46.jpg');)
_1-16.$$$37156877@44.jpg');)
_1-19.$$$37460805@44.jpg');)
_1291-1307.$$$34518654@46.jpg');)
ITE is an effective immunosuppressive endogenous aromatic hydrocarbon receptor (AhR) agonist, with a Ki value of 3nM for binding to AhR [1]. AhR is a ligand-dependent transcription factor that mediates the toxicity of several xenobiotics and plays important physiological roles in differentiation, reproduction, and immunity [2]. ITE has immunomodulatory and anti-cancer effects [3-4].
In vitro, ITE (0.1–5000nM; 1-6 days) treatment inhibited the proliferation and migration of ovarian cancer cells (SKOV-3, OVCAR-3, and IOSE-385) in a dose- and time-dependent manner, reduced AhR, and increased CYP1A1 levels [5]. ITE (0.01, 0.1, 1, 5, 10, and 20μM; 2, 4, or 6 days) could inhibit the proliferation of human pulmonary artery endothelial cells (HPAEC) in a dose- and time-dependent manner, reduced AhR protein levels, and simultaneously increased the mRNA levels of cytochrome P450 (CYP), CYP1A1, and CYP1B1 [6].
In vivo, ITE (200μg/0.2mL/day; 14 days; i.p.) treatment could significantly inhibit retinal detachment and ocular inflammatory cell infiltration in mice with experimental autoimmune uveitis (EAU) induced by Freund's adjuvant and Mycobacterium tuberculosis, reduced the proportion of IFN-γ, IL-17, or IL-10 cells in mice, and inhibited the secretion of inflammatory cytokines by mouse lymphocytes [7]. ITE (80mg/kg/day; 28 days; i.p.) treatment could reduce tumor growth by 39% in OVCAR-3 xenograft model mice [5].
References:
[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] Henry E C, Welle S L, Gasiewicz T A. TCDD and a putative endogenous AhR ligand, ITE, elicit the same immediate changes in gene expression in mouse lung fibroblasts[J]. Toxicological Sciences, 2010, 114(1): 90-100.
[3] Dolciami D, Gargaro M, Cerra B, et al. Binding mode and structure–activity relationships of ITE as an aryl hydrocarbon receptor (AhR) agonist[J]. ChemMedChem, 2018, 13(3): 270-279.
[4] Simpson S R, Middleton D D, Lukesh N R, et al. Microparticles incorporating dual apoptotic factors to inhibit inflammatory effects in macrophages[J]. Journal of Pharmaceutical Sciences, 2024, 113(11): 3196-3205.
[5] Wang K, Li Y, Jiang YZ, et al. An endogenous aryl hydrocarbon receptor ligand inhibits proliferation and migration of human ovarian cancer cells. Cancer Lett. 2013;340(1):63-71.
[6] Pang L, Li Y, Zou Q, et al. ITE inhibits growth of human pulmonary artery endothelial cells[J]. Experimental lung research, 2017, 43(8): 283-292.
[7] Nugent LF, Shi G, Vistica BP, Ogbeifun O, Hinshaw SJ, Gery I. 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.
ITE是一种有效的免疫抑制性内源性芳香烃受体（AhR）激动剂，与AhR结合的Ki值为3nM [1]。AhR是一种配体依赖性转录因子，介导几类异生素的毒性，并且在分化、繁殖和免疫中具有重要的生理作用 [2]。ITE具有免疫调节和抗癌作用 [3-4]。
在体外，ITE（0.1–5000Nm; 1-6 days）处理以剂量和时间依赖性抑制卵巢癌细胞（SKOV-3，OVCAR-3和IOSE-385）的增殖和迁移，降低AhR水平并增加CYP1A1水平 [5]。ITE（0.01, 0.1, 1, 5, 10 and 20μM; 2, 4, or 6 days）能够以剂量和时间依赖性抑制人肺动脉内皮细胞（HPAEC）的增殖，降低了AhR蛋白水平，同时增加了细胞色素P450（CYP）、CYP1A1和CYP1B1的mRNA水平 [6]。
在体内，ITE（200μg/0.2mL/day; 14 days; i.p.）治疗能够显著抑制弗氏佐剂（CFA）和结核分枝杆菌诱导的实验性自身免疫性葡萄膜炎（EAU）小鼠的视网膜脱离以及眼部炎症细胞浸润现象，降低小鼠IFN-γ、IL-17或IL-10的细胞比例，还抑制小鼠淋巴细胞分泌炎性细胞因子 [7]。ITE（80mg/kg/day; 28 days; i.p.）治疗能够使OVCAR-3异种移植模型小鼠中的肿瘤生长减少39% [5]。
| Cell experiment [1]: | |
Cell lines | SKOV-3, OVCAR-3, and IOSE-385 cells |
Preparation Method | After 16h (Day 0) of seeding in 96-well plates (1000, 5000, and 5000 cells/well for SKOV-3, OVCAR-3, and IOSE-385, respectively; 6 wells/dose), cells were treated with different concentration of ITE (0.1–5000nM) or DMSO (0.1% v/v) in the complete growth media up to 6 days with daily change of media containing dimethyl sulfoxide (DMSO, the vehicle control) or ITE. At the end of treatment, the number of cells per well was determined using a crystal violet method as described. After treatment, cells were rinsed with PBS (5mM phosphate, 145mM NaCl, 5mM KCl, pH 7.5), fixed in methanol for 15min, air-dried for 5min and stained with 0.1% (w/v) crystal violet for 5min. After staining, wells were rinsed with distilled water, and air dried again. Once dry, cells were solubilized with 2% (w/v) sodium deoxycholate solution for 30min with gentle agitation. Absorbance was measured at 570nm on a microplate reader. |
Reaction Conditions | 0.1–5000nM; 1-6 days |
Applications | The ITE treatment exhibited dose- and time-dependent inhibition of the proliferation and migration of ovarian cancer cells. |
| Animal experiment [1]: | |
Animal models | BALB/c nude mice |
Preparation Method | Each mouse was inoculated subcutaneously at the right flank with 5 × 106 of OVCAR-3 cells. When the tumor volume reached approximately 110mm3, the mice were divided into homogeneous blocks based on their tumor volumes followed by randomly assigning each block into the vehicle control and ITE treatment groups (n = 8/group). The vehicle (DMSO) or ITE (80mg/mL in DMSO) was administered to the mice by i.p. injection once daily for 28 days at a volume of 1mL/kg body weight. After the final injection, mice were given an additional 5 days to further monitor tumor volume, body weight, and other clinical signs. |
Dosage form | 80mg/kg/day; 28 days; i.p. |
Applications | The treatment with ITE was able to reduce tumor growth by 39% in the OVCAR-3 xenograft model mice. |
References: | |
| Cas No. | 448906-42-1 | SDF | |
| 化学名 | methyl 2-(1H-indole-3-carbonyl)-1,3-thiazole-4-carboxylate | ||
| Canonical SMILES | COC(=O)C1=CSC(=N1)C(=O)C2=CNC3=CC=CC=C32 | ||
| 分子式 | C14H10N2O3S | 分子量 | 286.3 |
| 溶解度 | ≥ 28.6mg/mL in DMSO | 储存条件 | Store at RT |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 3.4928 mL | 17.4642 mL | 34.9284 mL |
| 5 mM | 698.6 μL | 3.4928 mL | 6.9857 mL |
| 10 mM | 349.3 μL | 1.7464 mL | 3.4928 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet