2,7-Dibromocarbazole

2,7-Dibromocarbazole (2,7-DBCZ) is an orally active AhR agonist and MAOB inhibitor that can cross the blood-brain barrier. 2,7-Dibromocarbazole induces CYP1A/CYP1B1, developmental toxicity and oxidative toxicity, Akt phosphorylation, apoptosis, mitochondrial depolarization, and calcium elevation. 2,7-Dibromocarbazole disrupts dopamine homeostasis, promotes α-synuclein aggregation and transcriptomic dysregulation, leading to hepatic lipid accumulation, liver lesions, brain injury, and angiogenesis/energy metabolism disorders, while activating ERα and inhibiting GRα. 2,7-Dibromocarbazole can be used in research on cardiotoxicity and Parkinson's disease^{[1][2][3][4][5][6][7][8]}. In Vitro:2,7-Dibromocarbazole (10 μM-1 nM; 48 h) showed no cytotoxicity against recombinant HepG2 cells^[1].
2,7-Dibromocarbazole (10 μM-0.1 μM; 48 h) showed weak AhR agonist activity in a recombinant HepG2 luciferase reporter gene assay^[1].
2,7-Dibromocarbazole (2,7-DBCZ) (10 nM-100 μM; 48 h) reduces H9c2 cell viability, with 100 μM being cytotoxic^[2].
2,7-Dibromocarbazole (10 μM; 48 h) demethylates the Ang2 promoter in HUVECs, reducing region 2 by approximately 11%^[7].
2,7-Dibromocarbazole (0.1-2 μM; 96 h) induced developmental toxicity and pericardial edema in wild-type zebrafish embryos, with a 96-h LC₅₀ of 581.8 μg/L and an EC₅₀ for pericardial edema of 201.5 μg/L^[8].
2,7-Dibromocarbazole upregulates the expression of AhR1 and CYP1A in zebrafish embryos, consistent with AhR activation^[8].
2,7-Dibromocarbazole (2,7-DBCZ) (10 μM) inhibits the viability of normal HepG2 cells^[1].
2,7-Dibromocarbazole (1 μM; 48 h) does not induce CYP1A1 and inhibits the expression of AHR, PAI-2, and HSP90 in normal HepG2 cells^[1].
2,7-Dibromocarbazole (10 μM; 48 h) induces early and late apoptosis in H9c2 cells and inhibits mitochondrial membrane potential^[2].
2,7-Dibromocarbazole (10 μM; 48 h) dysregulated apoptosis-related genes in H9c2 cells, including upregulation of CD40LG and ANXA5^[2].
2,7-Dibromocarbazole (10 μM; 48 h) co-modulates apoptosis, Akt phosphorylation, and Ca²⁺ elevation in H9c2 cells together with SC79/BAPTA-AM/Ppp2ca RNAi (10-100 μM; 1-3 h pre-exposure)^[2].
2,7-Dibromocarbazole (10 μM; 48 h) increases the p-Akt/Akt ratio, Akt signaling gene expression, and intracellular Ca²⁺ in H9c2 cells^[2].
2,7-Dibromocarbazole (100 nM-10 μM; 24 h) inhibits HUVEC tube formation, with 1 μM reducing tube size and length by 1.69-fold and 1.52-fold, respectively, and 10 μM eliminating tube structures^[7].
2,7-Dibromocarbazole (100 nM-10 μM; 48 h) alters angiogenesis-related gene expression in HUVECs, most strongly upregulating Ang2 while decreasing VEGFB^[7].
2,7-Dibromocarbazole (10 μM; 48 h post-transfection) inhibited HUVEC tube formation, whereas Ang2 silencing restored it^[7]. In Vivo:2,7-Dibromocarbazole (100 nM-10 μM; water exposure; every 24 h; 96 h) induced EGFP expression in Tg (cyp1a-12DRE:EGFP) transgenic zebrafish embryos in a concentration-dependent manner, with the strongest response among the tested PHCZs at 100 nM^[1].
2,7-Dibromocarbazole (2,7-DBCZ) (0.1-100 mg/kg/d; oral gavage; once daily; 14 days) induces cardiac tissue apoptosis and increases cardiac CYP1B1, CYP1A1, CD40LG, and ANXA5 expression in male Sprague-Dawley rats^[2].