Cell permeable, potent and selective NADPH oxidase 1 (NOX1) inhibitor (IC50 = 20 nM), which exhibits selectivity for NOX1 over NOX2, NOX4, NOX5 and xanthine oxidase. It inhibits NOX1-derived O2- production in HT-29 human colon cancer cells, and attenuates VEGF-induced human pulmonary artery endothelial cell migration under hypoxic conditions in vitro.
CAT No: R1050
CAS No:1435893-78-9
Synonyms/Alias:NoxA1ds;1435893-78-9;AKOS027470303;PD079935;G15861;
NoxA1ds is a synthetic peptide inhibitor specifically designed to disrupt the activation of NADPH oxidase 1 (NOX1) by targeting its essential activator, NoxA1. As a cell-permeable peptide, NoxA1ds mimics the docking sequence of NoxA1, competitively inhibiting its interaction with NOX1 and thereby modulating the production of reactive oxygen species (ROS) in various cellular systems. This compound has become an important tool in the study of redox biology, oxidative stress signaling, and the mechanistic dissection of NOX1-dependent pathways due to its selectivity and functional relevance in both basic and applied research contexts.
Target validation: Researchers utilize NoxA1ds to specifically interrogate the role of NOX1-derived ROS in diverse cellular models. By providing a means to selectively inhibit NOX1 activity without affecting other NOX isoforms, this peptide enables precise delineation of NOX1's contribution to oxidative signaling cascades, cell proliferation, and inflammatory processes. Such targeted inhibition is instrumental in validating NOX1 as a molecular driver in various physiological and pathological settings, facilitating the identification of downstream effectors and pathway-specific responses.
Redox signaling studies: The peptide is widely employed in studies aimed at elucidating the molecular mechanisms of redox regulation. By modulating NOX1-generated superoxide and hydrogen peroxide levels, NoxA1ds allows scientists to dissect the effects of controlled ROS production on transcriptional regulation, post-translational modifications, and signal transduction networks. Its use supports investigations into redox-sensitive proteins, gene expression changes, and cellular adaptation to oxidative environments, thereby advancing understanding of oxidative stress biology.
Inflammation and immune response research: NoxA1ds serves as a valuable reagent in exploring the influence of NOX1 activity on inflammatory signaling and immune cell function. By attenuating NOX1-dependent ROS generation, the peptide aids in clarifying the interplay between oxidative bursts, cytokine production, and leukocyte activation. Such studies are critical for mapping the molecular underpinnings of inflammation, immune modulation, and host-pathogen interactions, especially within the context of redox-dependent immune regulation.
Cellular model development: The compound is frequently incorporated into experimental systems to generate NOX1-deficient phenotypes in vitro. Through transient inhibition of NOX1, researchers can model oxidative stress conditions or simulate genetic knockdown effects without the need for permanent genetic modifications. This approach is particularly advantageous for high-throughput screening, mechanistic studies, and the development of disease-relevant cell models where temporal control of NOX1 activity is required.
Oxidative damage assessment: NoxA1ds is instrumental in experiments designed to quantify the impact of NOX1-derived ROS on biomolecular integrity. By selectively suppressing NOX1 activity, the peptide enables controlled investigation of oxidative modifications to lipids, proteins, and nucleic acids. These studies provide insights into the mechanisms of oxidative injury, cellular defense responses, and the role of NOX1 in redox imbalance, supporting broader research into cellular homeostasis and stress adaptation.
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