Cited by 166Redox biology and oxidative stressNeutrophil, Myeloperoxidase and Oxidative MechanismsNitric Oxide and Endothelin Effects

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Therapeutic potential of NADPH oxidase 1/4 inhibitors

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Teixeira, G, Szyndralewiez, C, Molango, S, Carnesecchi, S, Heitz, F, Wiesel, P, Wood, J M·2017·British Journal of Pharmacology

DOI 10.1111/bph.13532PMC PMC5446584

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Abstract

The NADPH oxidase (NOX) family of enzymes produces ROS as their sole function and is becoming recognized as key modulators of signal transduction pathways with a physiological role under acute stress and a pathological role after excessive activation under chronic stress. The seven isoforms differ in their regulation, tissue and subcellular localization and ROS products. The most studied are NOX1, 2 and 4. Genetic deletion of NOX1 and 4, in contrast to NOX2, has revealed no significant spontaneous pathologies and a pathogenic relevance of both NOX1 and 4 across multiple organs in a wide range of diseases and in particular inflammatory and fibrotic diseases. This has stimulated interest in NOX inhibitors for therapeutic application. GKT136901 and GKT137831 are two structurally related compounds demonstrating a preferential inhibition of NOX1 and 4 that have suitable properties for in vivo studies and have consequently been evaluated across a range of disease models and compared with gene deletion. In contrast to gene deletion, these inhibitors do not completely suppress ROS production, maintaining some basal level of ROS. Despite this and consistent with most gene deletion studies, these inhibitors are well tolerated and slow or prevent disease progression in a range of models of chronic inflammatory and fibrotic diseases by modulating common signal transduction pathways. Clinical trials in patients with GKT137831 have demonstrated excellent tolerability and reduction of various markers of chronic inflammation. NOX1/4 inhibition may provide a safe and effective therapeutic strategy for a range of inflammatory and fibrotic diseases. Linked Articles: This article is part of a themed section on Redox Biology and Oxidative Stress in Health and Disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.12/issuetoc

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Authors: Teixeira, G., Szyndralewiez, C., Molango, S., Carnesecchi, S., Heitz, F., Wiesel, P., & Wood, J. M.
Affiliations: Evotec (Germany) (DE)
Genkyotex (Switzerland) (CH)
Genkyotex SA Plan les Ouates Switzerland
Inovaid Biel‐Benken Switzerland
Corresponding author: Wood, J M
ORCID: Wiesel, P
Venue: British Journal of Pharmacology
Publisher: Wiley
Published: 2016-07-14
Volume: 174
Issue: 12
Pages: 1647-1669
ISSN: 0007-1188 (ISSN-L)
1476-5381
DOI: 10.1111/bph.13532
PMC: PMC5446584
OpenAlex: W2414686680
Semantic Scholar: 3495831cf5de9bc9c88751dc4734fc06fde77667
Cited by: 163
References: 224
Citations by year: 2026: 10 · 2025: 13 · 2024: 9 · 2023: 12 · 2022: 15 · 2021: 15 · 2020: 28 · 2019: 17 · 2018: 22 · 2017: 16 · 2016: 5
FWCI: 1.81
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: British Journal of Pharmacology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Keywords: NADPH oxidase, NOX1, NOX4, NOX2, reactive oxygen species, NADPH oxidase inhibitors, GKT137831, chronic inflammation, fibrotic diseases, redox signaling, signal transduction, oxidative stress
MeSH terms: NADPH Oxidase 1, NADPH Oxidase 2, Animals, Anti-Inflammatory Agents, Enzyme Inhibitors, Fibrosis, Humans, Inflammation, Pyrazoles, Pyridines, Pyridones, Pyrazolones

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Therapeutic potential of NADPH oxidase 1/4 inhibitors

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