ANI-7 是一种AhR途径的激活剂。ANI-7 抑制多种癌细胞的生长，并有选择地抑制 MCF-7 乳腺癌细胞的生长，GI50为 0.56 μM。ANI-7 通过激活AhR途径诱导 CYP1 代谢单加氧酶，并在敏感的乳腺癌细胞系中诱导 DNA 损伤，检查点激酶 (Chk2) 激活，S 期细胞周期停滞和细胞死亡。
| 生物活性 | ANI-7 is an activator ofaryl hydrocarbon receptor(AhR)pathway. ANI-7 inhibits the growth of multiplecancercells, and potently and selectively inhibits the growth of MCF-7 breastcancercells with a GI50of 0.56 μM. ANI-7 induces CYP1-metabolizing mono-oxygenases by activatingAhRpathway, and also induces DNA damage,checkpoint Kinase 2 (Chk2)activation, S-phase cell cycle arrest, and cell death in sensitive breastcancercell lines[1][2][3]. |
| IC50& Target[1] | Aryl Hydrocarbon Receptor | Chk2 |
|
体外研究
(In Vitro) | ANI-7 (2.5 μM; 24 hours; MCF10A and MDA-MB-468 cells) treatment induces significant S-phase and G2 + M-phase cell cycle arrest within 24 hours of treatment in MDA-MB-468 cells, and negligible effect in normal breast MCF10A cells[1].
ANI-7 (2 μM; 12-24 hours; MDA-MB-468 cells) treatment results in a significant increase in the content and phosphorylation of CHK2, and induces a significant increase in H2AX? in MDA-MB-468 cells, indicative of DNA double-strand damage[1].
Inhibition of the AhR pathway ameliorates the effects of ANI-7. ANI-7 activates XRE activity and expression of the AhR and CYP1 members[1].
Comparisons of the GI50values show that ANI-7 produces a GI50value of 0.38 μM in MCF-7 cells, whereas values of 3.0-42 μM are observed in cell lines from lung, colon, ovary, neuronal, glial, prostate, and pancreas. The only other tumor type that shows appreciable growth inhibition by ANI-7 is the A431 vulva cell line (GI50of 0.51μM)[1][1].
ANI-7 potently inhibits the growth of T47D, ZR-75-1, MCF-7, SKBR3, and MDA-MB-468 breast cancer cells (GI50range of 0.16-0.38 μM), moderately inhibits the growth of BT20 and BT474 cells (GI50 range of 1-2 μM), and essentially fails to inhibit the growth of MDA-MB-231 and MCF10A cells (GI50range of 17-26 μM). Moreover, ANI-7 maintained its ability to inhibit the growth of drug-resistant cells (MCF-7/VP16: GI50of 0.21 μM)[1].
Cell Cycle Analysis[1] | Cell Line: | MCF10A and MDA-MB-468 cells | | Concentration: | 2.5 μM | | Incubation Time: | 24 hours | | Result: | Induced significant S-phase and G2 + M-phase cell cycle arrest in MDA-MB-468 cells, and negligible effect in normal breast MCF10A cells. |
Western Blot Analysis[1] | Cell Line: | MDA-MB-468 cells | | Concentration: | 2 μM | | Incubation Time: | 12 hours, 24 hours | | Result: | Resulted in a significant increase in the content and phosphorylation of CHK2 (25-fold increase),and induced a significant increase in H2AX? (3.5-fold increase). |
|
| 分子量 | |
| 性状 | |
| Formula | |
| CAS 号 | |
| 运输条件 | Room temperature in continental US; may vary elsewhere. |
| 储存方式 | | Powder | -20°C | 3 years | | 4°C | 2 years | | In solvent | -80°C | 6 months | | -20°C | 1 month |
|
| 溶解性数据 | In Vitro: DMSO : 20.83 mg/mL(79.17 mM;Need ultrasonic) 配制储备液 | 1 mM | 3.8005 mL | 19.0027 mL | 38.0055 mL | | 5 mM | 0.7601 mL | 3.8005 mL | 7.6011 mL | | 10 mM | 0.3801 mL | 1.9003 mL | 3.8005 mL |
*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℃, 6 months; -20℃, 1 month。-80℃ 储存时，请在 6 个月内使用，-20℃ 储存时，请在 1 个月内使用。 In Vivo: 请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照In Vitro方式配制澄清的储备液，再依次添加助溶剂： ——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用；
以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶 1. 请依序添加每种溶剂： 10% DMSO 40%PEG300 5%Tween-80 45% saline Solubility: ≥ 2.08 mg/mL (7.91 mM); Clear solution
此方案可获得 ≥ 2.08 mg/mL (7.91 mM，饱和度未知) 的澄清溶液。 以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。 2. 请依序添加每种溶剂： 10% DMSO 90%corn oil Solubility: ≥ 2.08 mg/mL (7.91 mM); Clear solution
此方案可获得 ≥ 2.08 mg/mL (7.91 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。 以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。 *以上所有助溶剂都可在本网站选购。
|
