Evidence map›Paper›PMID 40287570›Full record

ArticleCell biochemistry and biophysics2025

A Computational Approach for Designing a Peptide-Based Acetyl-CoA Synthetase 2 Inhibitor: A New Horizon for Anticancer Development.

Musab Ali, Ernest Oduro-Kwateng, Ibrahim Oluwatobi Kehinde, Narasimham L Parinandi, Mahmoud E S Soliman

Abstract read
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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 1 paper.

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0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Musab AliMolecular Bio-Computation and Drug Design Research Group, School of Health Sciences, University of KwaZulu Natal, Westville Campus, Durban, South Africa.
Ernest Oduro-KwatengMolecular Bio-Computation and Drug Design Research Group, School of Health Sciences, University of KwaZulu Natal, Westville Campus, Durban, South Africa.
Ibrahim Oluwatobi KehindeMolecular Bio-Computation and Drug Design Research Group, School of Health Sciences, University of KwaZulu Natal, Westville Campus, Durban, South Africa.
Narasimham L ParinandiDivision of Pulmonary, Critical Care and Sleep Medicine Department of Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Weber Medical Center, Columbus, OH, USA.
Mahmoud E S SolimanMolecular Bio-Computation and Drug Design Research Group, School of Health Sciences, University of KwaZulu Natal, Westville Campus, Durban, South Africa. soliman@ukzn.ac.za.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetyl-CoA Synthetase 2 (ACSS2) has emerged as a new target for anticancer development owing to its high expression in various tumours and its enhancement of malignancy. Stressing the growing interest in peptide-derived drugs featuring better selectivity and efficacy, a computational protocol was applied to design a peptide inhibitor for ACSS2. Herein, 3600 peptide sequences derived from ACSS2 nucleotide motif were generated by classifying the 20 amino acids into six physiochemical groups. De novo modeling maintained essential binding interactions, and a refined library of 16 peptides was derived using Support Vector Machine filters to ensure proper bioavailability, toxicity, and therapeutic relevance. Structural and folding predictions, along with molecular docking, identified the top candidate, Pep16, which demonstrated significantly higher binding affinity (91.1 ± 1.6 kcal/mol) compared to a known inhibitor (53.7 ± 0.7 kcal/mol). Further molecular dynamics simulations and binding free energy calculations revealed that Pep16 enhances ACSS2 conformational variability, occupies a larger binding interface, and achieved firm binding. MM/GBSA analysis highlighted key electrostatic interactions with specific ACSS2 residues, including ARG 373, ARG 526, ARG 628, ARG 631, and LYS 632. Overall, Pep16 appears to lock the ACSS2 nucleotide pocket into a compact, rigid conformation, potentially blocking ATP binding and catalytic activity, and may serve as a novel specific ACSS2 inhibitor. Though, we urge further research to confirm and compare its therapeutic potential to existing inhibitors. We also believe that this systematic methodology would represent an indispensable tool for prospective peptide-based drug discovery.

Indexed as

Acetate-CoA LigaseAntineoplastic AgentsDrug DesignEnzyme InhibitorsPeptidesAmino Acid SequenceHumansMolecular Docking SimulationMolecular Dynamics SimulationThermodynamicsAcetate-CoA LigaseAntineoplastic AgentsEnzyme InhibitorsPeptidesACSS2Anticancer agentsMolecular dockingMolecular dynamics simulationsPeptide inhibitor

Identifiers

PMID40287570
PMCPMC12414092

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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.