ArticleCell biochemistry and biophysics2025
Computational Development of Allosteric Peptide Inhibitors Targeting LIM Kinases as a Novel Therapeutic Intervention.
Article in Cell biochemistry and biophysics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Probing Allosteric Kinase Modulators as Next Game-Changers in Fighting Neurodegeneration.Journal of medicinal chemistry · 2026Review
- Repurposing Cofilin-Targeting Compounds for Ischemic Stroke Through Cheminformatics and Network Pharmacology.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Advancements in Protein Kinase Inhibitors: From Discovery to Clinical Applications.Research (Washington, D.C.) · 2025Review
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Authors and funding
4 authors.
Funding
Abstract
LIM Kinases (LIMKs) have emerged as critical therapeutic targets in cancer research due to their central role in regulating cytoskeletal dynamics and cell motility via cofilin phosphorylation. Allosteric inhibitors, which bind outside the ATP-binding pocket, offer distinct advantages over ATP-competitive inhibitors, such as increased specificity, reduced off-target effects, and the ability to overcome resistance. This study investigates a series of novel tetrapeptides mimicking the binding mode of TH470, an allosteric LIMK inhibitor, using in silico docking and molecular dynamics simulations to identify potential lead compounds with high specificity, binding affinity, and favorable pharmacokinetic properties. Structural analyses revealed critical interactions between TH470 and LIMKs, particularly with conserved residues such as Thr405 (gatekeeper residue), Ile408 (hinge region), and Asp469 (XDFG motif), which are essential for stabilizing inhibitor binding. Molecular dynamics simulations confirmed the stability of TH470-LIMK1 and TH470-LIMK2 complexes, with lower RMS deviations and robust interaction patterns enhancing binding affinity. From the set of tetrapeptides mimicking TH470 binding mode, only YFYW, WPHW, and YWFP for LIMK1, and PYWG, FYWV, and WFVW for LIMK2 demonstrated high binding affinities, non-toxic profiles, and promising anti-cancer, anti-angiogenic, and anti-inflammatory properties. Among the studied peptides, LIMK1-YFYW and LIMK2-WFVW exhibited the most substantial binding affinities, supported by high hydrogen bond occupancy with key residues such as Ile416 and Thr405. The findings highlight the therapeutic potential of allosteric peptide inhibitors targeting LIMK-mediated pathways in cancer progression. The study underscores the importance of specific interactions with conserved LIMK residues, providing a foundation for further developing selective inhibitors to modulate actin dynamics and combat cancer-related processes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.