ArticleChemMedChem2017
Functional N-Formyl Peptide Receptor 2 (FPR2) Antagonists Based on the Ureidopropanamide Scaffold Have Potential To Protect Against Inflammation-Associated Oxidative Stress.
Article in ChemMedChem, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Article
- Article
- Pyridazinones and Structurally Related Derivatives with Anti-Inflammatory Activity.Molecules (Basel, Switzerland) · 2022Article
- Design, Synthesis, Biological Evaluation, and Computational Studies of Novel Ureidopropanamides as Formyl Peptide Receptor 2 (FPR2) Agonists to Target the Resolution of Inflammation in Central Nervous System Disorders.Journal of medicinal chemistry · 2022Article
- Identification and validation of a prognostic signature and combination drug therapy for immunotherapy of head and neck squamous cell carcinoma.Computational and structural biotechnology journal · 2021Article
- Allicin Attenuated Advanced Oxidation Protein Product-Induced Oxidative Stress and Mitochondrial Apoptosis in Human Nucleus Pulposus Cells.Oxidative medicine and cellular longevity · 2020Article
- Formyl Peptide Receptor 2 Activation Ameliorates Dermal Fibrosis and Inflammation in Bleomycin-Induced Scleroderma.Frontiers in immunology · 2019Article
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Authors and funding
8 authors.
Funding
Abstract
Formyl peptide receptor 2 (FPR2) is a G protein coupled receptor belonging to the N-formyl peptide receptor (FPR) family that plays critical roles in peripheral and brain inflammatory responses. FPR2 has been proposed as a target for the development of drugs that could facilitate the resolution of chronic inflammatory reactions by enhancing endogenous anti-inflammation systems. Starting from lead compounds previously identified in our laboratories, we designed a new series of ureidopropanamide derivatives with the goal of converting functional activity from agonism into antagonism and to develop new FPR2 antagonists. Although none of the compounds behaved as antagonists, some of the compounds were able to induce receptor desensitization and, thus, functionally behaved as antagonists. Evaluation of these compounds in an in vitro model of neuroinflammation showed that they decreased the production of reactive oxygen species in mouse microglial N9 cells after stimulation with lipopolysaccharide. These FPR2 ligands may protect cells from damage due to inflammation-associated oxidative stress.
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