ArticleMolecular diversity2026
Deciphering the inhibitory mechanisms of Interleukin-17A through dynamic molecular insights: a path toward novel anti-inflammatory therapies.
Article in Molecular diversity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Olive (Olea europaea) phenolics for the control of psoriasis via targeting SMYD2 and IL-17A protein-protein interaction networks.Journal of natural medicines · 2026Article
- Interleukin-17 in disease pathogenesis and therapy: recent advances in targeted drug design and medicinal chemistry.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IL-17A is a pivotal pro-inflammatory cytokine implicated in a wide spectrum of immunological responses. However, its dysregulation is linked to the progression of various pathological conditions, from mild inflammation to malignant cancers. When IL-17A binds to its cognate receptor, IL-17RA, it forms a complex that initiates a series of molecular signaling cascades within the cell, contributing to various inflammatory processes. Currently, there are no specific oral drugs targeting this pathway, underscoring the urgent need for novel non-inflammatory drugs to address autoimmune and inflammatory diseases. Targeting IL-17A presents a unique opportunity to develop innovative therapies for autoimmune conditions. This research employs ligand-based pharmacophore modeling, followed by screening and docking simulations found six potential drugs that effectively disrupt the IL-17A-IL-17RA combination. Molecular dynamics simulations further demonstrated the stability and inhibitory potential of these compounds, highlighting their interactions within the IL-17A binding site. These interactions involve key residues such as Arg39, Trp51, Trp67, Gln94, Glu95, Leu97, Leu99, Lys114, and Ser118, which are crucial for locking the associated signaling cascade. Mechanistic studies, including dynamic simulations and calculation of free energy, support the efficacy of the identified compounds. Notably, Compounds 1 and 4 exhibit higher binding affinities compared to the native reference inhibitor of target. Our results revealed that both the peptide (Compound 1) and macrocyclic compounds (Compound 3) significantly disrupt the IL-17A/IL-17RA complex, confirming the validity of our approach and reinforcing its potential therapeutic relevance, as highlighted in prior studies. These IL-17A inhibitors show enormous promise as prospective therapeutic candidates for the treatment of inflammatory disorders.
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Registered trials
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