FICZ (6-Formylindolo[3,2-b]carbazole) is a potent aryl agonist for the hydrocarbon receptor (AhR, Kd: 70 pM).

AhR:70 pM (Kd)

FICZ（0.01 nM-1 μM）单独或与50 nM MNF联用，可持续激活CYP1A1活性，通过线粒体依赖的路径引起氧化应激和细胞凋亡的激活。在HepG2细胞中，FICZ在低浓度时刺激细胞生长，而在高浓度时抑制细胞生长[1]。FICZ (10-30 μM) 显著减少CEH活力，估计的LC50（95%置信区间）为14 μM。FICZ对CEH培养中EROD活性显示出浓度依赖性效应，分别在3、8、24小时的平均EC50值为0.016 nM、0.80 nM和11 nM[2]。FICZ存在时，CYP1的抑制导致AHR激活增强，表明当其代谢受阻时，FICZ在细胞内积累。CYP1酶在调控FICZ的生物效应中起作用[3]。FICZ处理以剂量依赖的方式增加了原代iPSC系和CYP1A1靶向克隆中CYP1A1转录表达[4]。

The cell viability of CEH treated with FICZ or TCDD is studied with the untreated cells (used as a live cell control) and sodium hypochlorite (5%)-treated cells (used as a dead cell control). This assay is based upon the bioluminescent measurement of adenosine triphosphate (ATP) that is present in all metabolically active cells. Luciferase is utilized in this method to catalyze the formation of light from ATP and luciferin. CEH is lysed 24 h after dosing and the luminescence emitted from the ATP-dependent oxidation of luciferin is measured with a LuminoSkan Ascent luminometer [2].