CH-223191 Unit size Cat. code Docs Qty Price
2-methyl-2H-pyrazole-3-carboxylic acid; AhR Antagonist
10 mg

Inhibition of AhR signaling by CH-223191
Inhibition of AhR signaling by CH-223191

AhR Antagonist

CH-223191 is a synthetic antagonist for the cytosolic aryl hydrocarborn receptor (AhR) transcription factor [1]. AhR is a ligand-dependent transcriptional factor able to sense a wide range of structurally different exogenous and endogenous molecules.

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Mode of action:

CH-223191 exerts a ligand-selective antagonism and appears to be more effective on halogenated aromatic hydrocarbons such as the xenobiotic 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), than on polycyclic aromatic hydrocarbons and non-halogenated aromatic hydrocarbons such as FICZ and ITE, respectively [2]. 

Notably, CH-223191 is a pure AhR antagonist that does not stimulate AhR-dependent transcription even at concentrations up to 100 μM [1], unlike other AhR antagonists which display agonist activity at high concentrations. Moreover, CH-223191 is specific for AhR, displaying no affinity for the estrogen receptor, in contrast to other AhR antagonists [1].

InvivoGen's CH-223191 is of high quality, guaranteed free of bacterial contamination, and has been functionally tested on HepG2-Lucia™ AhR and HT29-Lucia™ AhR reporter cells.

Key features of CH-223191:

  • A potent and specific AhR antagonist
  • Ligand-selective antagonist activity
  • Each lot is highly pure (≥95%) and functionally tested


Read our review on AhR's key role in the intestinal microbiota and immunity.



1. Kim, S.H. et al., 2006. Novel compound 2-methyl-2H-pyrazole-3-carboxylic acid (2-methyl-4-o-tolylazo-phenyl)-amide (CH-223191) prevents 2,3,7,8-TCDD-Induced toxicity by antagonizing the aryl hydrocarbon receptor. Mol. Pharmacol. 69:1871-78.
2. Zhao B. et al., 2010. CH223191 is a ligand-selective antagonist of the Ah (Dioxin) receptor. Toxicol. Sci. 117:393-403.


Evaluation of cellular AhR inhibition by CH-223191
Evaluation of cellular AhR inhibition by CH-223191

Inhibition of AhR activity by CH-223191 in HepG2-Lucia™ Ahr cells.
The cells were stimulated with 30 nM TCDD or 30 μM ITE in the presence of 10 μM CH-223191. After overnight incubation, the AhR response was assessed by  determining Lucia  luciferase activity in the supernatant using.QUANTI-Luc™.
Percentages of the maximal response for the ligand with no inhibitor are shown.

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CAS number: 301326-22-7

Synonym: 2-methyl-2H-pyrazole-3-carboxylic acid

Solubility: 90 mM (30 mg/ml) in DMSO

Working concentration: 1 µM (333 ng/ml) to 30 µM (10.1 μg/ml) for cell culture assays

Formula: C19H19N5O

Molecular weight: 333.4 g/mol

Quality control:

  • Purity ≥ 95% (UHPLC).
  • The absence of bacterial contamination (e.g. lipoproteins and endotoxins) has been confirmed using HEK-Blue™ TLR2 and HEK‑Blue™ TLR4 cells.
  • The inhibitory activity has been validated using cellular assays.
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  • 10 mg CH-223191

CH-223191 is shipped at room temperature.

Store at -20°C. 

Alert Protect this product from light.

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The aryl hydrocarbon receptor:

The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcriptional factor widely expressed among immune, epithelial, endothelial and stromal cells in barrier tissues [1]. While historically studied in the context of chemical pollutants such as dioxin, AhR was more recently revealed as a central sensor of a wider range of environmental cues, ensuring intestinal homeostasis between the host and gut microbiota [1].
AhR canonical signaling has been extensively reviewed [1]. Briefly, in the absence of ligands crossing the cell membrane, AhR resides in the cytoplasm within a Hsp90:XAP2:p23:Src chaperone protein complex. Upon ligand binding, the complex undergoes conformational changes and translocates into the nucleus. The chaperones are released and AhR heterodimerizes with AhR nuclear translocator (ARNT). The AhR:ligand:ARNT trimer binds to dioxin response elements (DREs) in the upstream regulatory regions of AhR target genes, which include the cytochrome P450-dependent monooxygenase Cyp1a1, the AhR repressor (AhRR), and the IL-22 interleukin.
Of note, non-canonical AhR signaling pathways have also been reported, either at the genomic level through association with other transcription factors (e.g. NF-κB), or at the non-genomic level (e.g. through the release of the Src kinase) [2,3].
Besides xenobiotics, including the prototypic AhR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a variety of dietary-derived AhR ligands have been identified, many of which are byproducts of tryptophan (Trp) amino acid metabolism [4]. AhR has emerged as a regulator of host-microbiome symbiosis. On the one hand, AhR activation by dietary ligands shapes the intestinal bacterial composition [5]. On the other hand, AhR sensing regulates the homeostasis and functionality of the gut immune cells [6].


1. Stockinger B. et al., 2014. The aryl hydrocarbon receptor: multitasking in the immune system. Annu. Rev. Immunol. 32:403-32.
2. Lamas B. et al., 2018. Aryl hydrocarbon receptor and intestinal immunity. Mucosal Immunol. 11(4):1024-38.
3. Gutiérrez-Vasquez C. et al., 2018. Regulation of the immune response by the aryl hydrocarbon receptor. Immunity. 48:19-33.
4. Hubbard T.D. et al., 2015. Indole and tryptophan metabolism: endogenous and dietary routes to Ah receptor activation. Drug Metab. Dispos. 43:1522-35.
5. Murray I.A. et al., 2016. Expression of the aryl hydrocarbon receptor contributes to the establishment of intestinal microbial community structure in mice. Sci. Rep. 6:33969.
6. Cervantes-Barragan L. & Colonna M., 2018. AHR signaling in the development and function of intestinal immune cells and beyond. Semin. Immunopathol. 40(4):371-77.


Chemical structure of CH-223191:

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