1-Aminobenzotriazole (ABT) alone considerably raised the CYP2B6 expression levels in two distinct hepatocytes (by 7.3 and 10.8 fold, respectively). The induction of CYP2B6 expression by CITCO or rifampicin was improved 12.6-fold and 4.0-fold for CITCO and 3.9-fold and 2.5-fold for rifampicin following co-treatment with 1-aminobenzotriazole. 1-Aminobenzotriazole has a more stimulating impact on CITCO than rifampicin does. 1. In two distinct hepatocytes, aminobenzotriazole alone elevated the expression levels of CYP3A4 by 2.0 and 3.8 times, respectively. The effect of CITCO on CYP3A4 expression levels was increased by 3.8 and 6.0 times after co-treatment with 1-aminobenzotriazole, respectively, in comparison to cells treated with CITCO alone [1]. When compared to a clear 1-aminobenzotriazole control, 1-aminobenzotriazole (ABT) (1 mM) demonstrated a significant (~95%) improvement in the production of N-CPU-based procainamide[2].

1-Aminobenzotriazole (ABT) alone considerably raised the CYP2B6 expression levels in two distinct hepatocytes (by 7.3 and 10.8 fold, respectively). The induction of CYP2B6 expression by CITCO or rifampicin was improved 12.6-fold and 4.0-fold for CITCO and 3.9-fold and 2.5-fold for rifampicin following co-treatment with 1-aminobenzotriazole. 1-Aminobenzotriazole has a more stimulating impact on CITCO than rifampicin does. 1. In two distinct hepatocytes, aminobenzotriazole alone elevated the expression levels of CYP3A4 by 2.0 and 3.8 times, respectively. The effect of CITCO on CYP3A4 expression levels was increased by 3.8 and 6.0 times after co-treatment with 1-aminobenzotriazole, respectively, in comparison to cells treated with CITCO alone [1]. When compared to a clear 1-aminobenzotriazole control, 1-aminobenzotriazole (ABT) (1 mM) demonstrated a significant (~95%) improvement in the production of N-CPU-based procainamide[2].

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ABT concentration-dependently increased the mRNA expression levels of CYP2B6 and CYP3A4 in freshly isolated primary human hepatocytes. At 1 mM, ABT alone increased CYP2B6 expression by 7.3-fold and 10.8-fold in hepatocytes from two donors, and increased CYP3A4 expression by 2.0-fold and 3.8-fold.
When co-treated with known inducers, ABT modulated their effects. It potentiated the CYP2B6-inducing effect of the CAR activator CITCO (from 7.3-fold to 12.6-fold and from 10.8-fold to 4.0-fold in two donors) and had an additive effect with the PXR activator rifampin. For CYP3A4, ABT potentiated the minimal effect of CITCO but did not show an additive effect with rifampin; it even decreased rifampin's effect in one donor.
In luciferase reporter assays using HepG2 cells, ABT (1 mM) significantly increased CYP2B6 promoter activity (2.4-fold) in cells transfected with human CAR, indicating direct or indirect CAR activation. ABT also increased the activity of a UGT1A1 enhancer (containing a PXR response element) in both control and PXR-transfected HepG2 cells (2.4-fold and 2.5-fold, respectively), suggesting a potential PXR-independent mechanism, possibly involving the aryl hydrocarbon receptor (AhR).
ABT (1 mM) also increased mRNA expression of CYP1A2, an AhR target gene, in human hepatocytes by 15-fold and 22.8-fold.

Wall 1-aminobenzotriazole (ABT) (100 mg/kg, 2 hours before laboratory) decreases the rate of intravenous procainamide clearance (45%), but N-aminobenzotriazole waste Reduced area under the curve ratio of 0.59 compared to 0.11 and decreased ratio of inamide to procainamide (0.74 vs. 0.21). The recovery of N-benzoprocainamide in stealing dropped from 13.3% to 6.5%, whereas the residual recovery of procainamide increased from 18% to 30% when 1-aminobenzotriazole was used [2]. Gastric emptying was markedly delayed by a pretreatment of 100 mg/kg oral 1-aminobenzotriazole (ABT), given two hours prior to a semi-solid caloric test meal. 1-Aminobenzotriazole also doubles the amount of space in the stomach [3].

Primary Human Hepatocyte Culture and Treatment: Freshly isolated human hepatocytes were recovered for 10 hours in serum-free Williams' E medium supplemented with dexamethasone, gentamicin, HEPES, L-glutamine, and insulin-transferrin-selenium. After recovery, cells were treated with test compounds (e.g., CITCO at 100 nM, rifampin at 10 μM, ABT at concentrations ranging from 1 μM to 1 mM) or vehicle (ethanol) for 72 hours. Media containing compounds were replaced daily.
Quantitative Real-Time PCR (qRT-PCR): Total RNA was isolated from treated hepatocytes. cDNA was synthesized and used as template for qRT-PCR using gene-specific assays for CYP2B6, CYP3A4, CYP1A2, and GAPDH (reference gene). Fold changes in mRNA levels were calculated using the 2^(-ΔΔCt) method.
HepG2 Cell Culture and Transfection: HepG2 cells were maintained in DMEM supplemented with fetal bovine serum, L-glutamine, penicillin/streptomycin, and non-essential amino acids. For reporter assays, cells were seeded in 12-well plates and co-transfected with a luciferase reporter plasmid (pGL3-CYP2B6-U2.2k containing PBREM or pGL3-UGT1A1 U2K containing PXRE), an expression plasmid for a nuclear receptor (pcDNA3-CAR, pcDNA3-PXR, or empty pcDNA3 vector), and a β-galactosidase expression plasmid (for normalization) using a transfection reagent.
Luciferase Reporter Assay: Twenty-four hours after transfection, cells were treated with ABT (1 mM), CITCO (100 nM), rifampin (10 μM), or vehicle (ethanol, 0.1%) for 24 hours. Cells were then harvested, and lysates were assayed for both luciferase and β-galactosidase activities. Luciferase activity was normalized to β-galactosidase activity to determine fold induction.

[1]. Induction of CYP2B6 and CYP3A4 expression by 1-aminobenzotriazole (ABT) in human hepatocytes. Drug Metab Lett. 2010 Aug;4(3):129-33.

[2]. 1-Aminobenzotriazole, a known cytochrome P450 inhibitor, is a substrate and inhibitor of N-acetyltransferase. Drug Metab Dispos. 2011 Sep;39(9):1674-9.

[3]. 1-Aminobenzotriazole modulates oral drug pharmacokinetics through cytochrome P450 inhibition and delay of gastric emptying in rats. Drug Metab Dispos. 2014 Jul;42(7):1117-24.

Abiraterone (ABT), a non-selective, mechanistic (irreversible) CYP enzyme inhibitor, is widely used in drug metabolism research to identify CYP-mediated metabolic pathways or inhibit metabolic activity in in vitro systems. This study reveals a previously undiscovered role of ABT: it induces the transcriptional expression of major drug-metabolizing enzymes CYP2B6 and CYP3A4 in human hepatocytes, primarily through activation of the nuclear receptor CAR. ABT can also modulate the effects of known CYP inducers such as cetirizine and rifampin. These findings suggest that using ABT as a tool to enhance the pharmacological effects of rapidly metabolizing compounds (e.g., by inhibiting their degradation to maintain higher concentrations) is limited and requires caution. ABT's own induction of CYP expression may interfere with research results, especially in experiments studying the regulation of CYP enzyme transcription levels.

C6H6N4

134.1386

134.059

1614-12-6

1367

White to light yellow solid powder

1.5±0.1 g/cm3

319.3±25.0 °C at 760 mmHg

81-84 °C(lit.)

146.9±23.2 °C

0.0±0.7 mmHg at 25°C

1.774

0.75

1

3

0

10

127

0

JCXKHYLLVKZPKE-UHFFFAOYSA-N

InChI=1S/C6H6N4/c7-10-6-4-2-1-3-5(6)8-9-10/h1-4H,7H2

benzotriazol-1-amine

1-Aminobenzotriazole; ABT; 3-Aminobenzotriazole

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~745.49 mM)
H2O : ~50 mg/mL (~372.74 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (15.51 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (15.51 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (15.51 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 25 mg/mL (186.37 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication (<60°C).

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 (Please use freshly prepared in vivo formulations for optimal results.)