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 |
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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). |
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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 |
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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 |
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