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    GNF351
    GNF351

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V4534
    CAS #: 1227634-69-6Purity ≥98%

    Description: GNF351 (GNF-351) is a novel and potent full aryl hydrocarbon receptor (AHR) antagonist with the potential to be used as new drugs in dermatology. GNF351 competes with a photoaffinity AHR ligand for binding to the AHR with an IC50 of 62 nM. GNF351 is minimal toxicity in mouse or human keratinocytes.  

    References: J Invest Dermatol. 2015 May;135(5):1320-1328.


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    GNF351

    Name: GNF351
    CAS#: 1227634-69-6
    Chemical Formula: C24H25N7
    Exact Mass: 411.2171
    Molecular Weight: 411.513 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Technical InformationSynonym: GNF-351; GNF351 GNF 351.
    Chemical Name: 8-(2-(1H-indol-3-yl)ethyl)-9-isopropyl-2-(5-methylpyridin-3-yl)-9H-purin-6-amine
    InChi Key: WWERDIHAUJLVQP-UHFFFAOYSA-N
    InChi Code: InChI=1S/C24H25N7/c1-14(2)31-20(9-8-16-13-27-19-7-5-4-6-18(16)19)28-21-22(25)29-23(30-24(21)31)17-10-15(3)11-26-12-17/h4-7,10-14,27H,8-9H2,1-3H3,(H2,25,29,30)
    SMILES Code: NC1=C2N=C(CCC3=CNC4=C3C=CC=C4)N(C(C)C)C2=NC(C5=CC(C)=CN=C5)=N1


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    GNF351 (GNF-351) is a novel and potent full aryl hydrocarbon receptor (AHR) antagonist. GNF351 competes with a photoaffinity AHR ligand for binding to the AHR with an IC50 of 62 nM. GNF351 is minimal toxicity in mouse or human keratinocytes.  Stimulation of the aryl hydrocarbon receptor (AHR) by xenobiotics is known to affect epidermal differentiation and skin barrier formation. The physiological role of endogenous AHR signaling in keratinocyte differentiation is not known. We used murine and human skin models to address the hypothesis that AHR activation is required for normal keratinocyte differentiation. Using transcriptome analysis of Ahr(-/-) and Ahr(+/+) murine keratinocytes, we found significant enrichment of differentially expressed genes linked to epidermal differentiation. Primary Ahr(-/-) keratinocytes showed a significant reduction in terminal differentiation gene and protein expression, similar to Ahr(+/+) keratinocytes treated with AHR antagonists GNF351 and CH223191, or the selective AHR modulator (SAhRM) SGA360. In vitro keratinocyte differentiation led to increased AHR levels and subsequent nuclear translocation, followed by induced CYP1A1 gene expression. Monolayer cultured primary human keratinocytes treated with AHR antagonists also showed an impaired terminal differentiation program. Inactivation of AHR activity during human skin equivalent development severely impaired epidermal stratification, terminal differentiation protein expression, and stratum corneum formation. As disturbed epidermal differentiation is a main feature of many skin diseases, pharmacological agents targeting AHR signaling or future identification of endogenous keratinocyte-derived AHR ligands should be considered as potential new drugs in dermatology.

    References: J Invest Dermatol. 2015 May;135(5):1320-1328.


    These protocols are for reference only. InvivoChem does not independently validate these methods.

    GNF351 (GNF-351) is a novel and potent full aryl hydrocarbon receptor (AHR) antagonist with the potential to be used as new drugs in dermatology. GNF351 competes with a photoaffinity AHR ligand for binding to the AHR with an IC50 of 62 nM. GNF351 is minimal toxicity in mouse or human keratinocytes.  

    References: J Invest Dermatol. 2015 May;135(5):1320-1328.


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