Simulating chalcogen bonding using molecular mechanics: a pseudoatom approach to model ebselen.

J Mol Model

Bio21 Institute and School of Chemistry, University of Melbourne, Parkville, Australia.

Published: February 2022

The organoselenium compound ebselen has recently been investigated as a treatment for COVID-19; however, efforts to model ebselen in silico have been hampered by the lack of an efficient and accurate method to assess its binding to biological macromolecules. We present here a Generalized Amber Force Field modification which incorporates classical parameters for the selenium atom in ebselen, as well as a positively charged pseudoatom to simulate the σ-hole, a quantum mechanical phenomenon that dominates the chemistry of ebselen. Our approach is justified using an energy decomposition analysis of a number of density functional theory-optimized structures, which shows that the σ-hole interaction is primarily electrostatic in origin. Finally, our model is verified by conducting molecular dynamics simulations on a number of simple complexes, as well as the clinically relevant enzyme SOD1 (superoxide dismutase), which is known to bind to ebselen. Graphical Abstract Ebselen is an organoselenium drug that has shown promise for the treatment of a number of conditions. Computational modelling of drug-target complexes is commonly performed to determine the likely mechanism of action, however this is difficult in the case of ebselen, as an important mode of interaction is not simulated using current techniques. We present here an extension to common methods, which accurately captures this interaction.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8867462PMC
http://dx.doi.org/10.1007/s00894-021-05023-5DOI Listing

Publication Analysis

Top Keywords

ebselen
8
model ebselen
8
ebselen organoselenium
8
simulating chalcogen
4
chalcogen bonding
4
bonding molecular
4
molecular mechanics
4
mechanics pseudoatom
4
pseudoatom approach
4
approach model
4

Similar Publications

Development of molecular Trojan horses targeting New Delhi metallo-β-lactamase-1 for the restoration of meropenem susceptibility in drug-resistant bacteria.

Eur J Med Chem

January 2025

Laboratory for Marine Drugs and Bioproducts, Qingdao Marine Science and Technology Center, School of Medicine and Pharmacy, Ocean University of China, Qingdao, 266071, China. Electronic address:

The emergence of New Delhi metallo-β-lactamase-1 (NDM-1) poses a significant threat to the clinical application of antibiotics, as it possesses the ability to hydrolyze nearly all β-lactam antibiotics. Regrettably, there are currently no clinical drugs targeting NDM-1, making it imperative to develop highly potent and minimally toxic NDM-1 inhibitors. Herein, a series of molecular Trojan horses targeting NDM-1 were synthesized by introducing ebselen into 7-aminocephalosporanic acid derivatives via a C-Se bond.

View Article and Find Full Text PDF

A practical and efficient reaction for C-selenylation of 1,4-naphthoquinones has been explored. This coupling reaction of two redox structural motifs, such as 2-bromo-1,4-naphthoquinone with diaryldiselenide/ebselen has been achieved by using sodium borohydride reducing agent at room temperature. Using this approach, several 2-selenylated-1,4-naphthoquinones were obtained in moderate to good yields and thoroughly characterized by multinuclear (H, C, and Se) NMR, cyclic voltammetry, and mass spectrometry.

View Article and Find Full Text PDF

Comparative efficacy and acceptability of pharmacological, psychological, and neurostimulatory interventions for ADHD in adults: a systematic review and component network meta-analysis.

Lancet Psychiatry

January 2025

Hampshire and Isle of Wight NHS Foundation Trust, Southampton, UK; Clinical and Experimental Sciences (CNS and Psychiatry), Faculty of Medicine, University of Southampton, Southampton, UK; Developmental EPI Evidence Synthesis, Prediction, Implementation Lab, Centre for Innovation in Mental Health-School of Psychology, Faculty of Environmental and Life Sciences, University of Southampton, Southampton, UK; New York University Child Study Center, Hassenfeld Children's Hospital at NYU Langone, New York, NY, USA; Department of Precision and Regenerative Medicine and Ionian Area, University of Studies of Bari Aldo Moro, Bari, Italy.

Background: The comparative benefits and harms of available interventions for ADHD in adults remain unclear. We aimed to address these important knowledge gaps.

Methods: In this systematic review and component network meta-analysis (NMA), we searched multiple databases for published and unpublished randomised controlled trials (RCTs) investigating pharmacological and non-pharmacological interventions for ADHD in adults from database inception to Sept 6, 2023.

View Article and Find Full Text PDF

Investigating the impact of SOD1 mutations on amyotrophic lateral sclerosis progression and potential drug repurposing through analysis.

J Biomol Struct Dyn

December 2024

Department of Medical Laboratory Technology, Faculty of Medical Applied Science, Northern Border University, Arar, Saudi Arabia.

Superoxide dismutase 1 (SOD1) is a vital enzyme responsible for attenuating oxidative stress through its ability to facilitate the dismutation of the superoxide radical into oxygen and hydrogen peroxide. The progressive loss of motor neurons characterize amyotrophic lateral sclerosis (ALS), a crippling neurodegenerative disease that is caused by mutations in the SOD1 gene. In this study, mutational analysis was performed to study the various mutations, the pathogenicity and stability ΔΔG (binding free energy) of the variant of SOD1.

View Article and Find Full Text PDF

METTL3/YTHDF1-mediated mA modification stabilizes USP12 to deubiquitinate FOXO3 and promote apoptosis in sepsis-induced myocardial dysfunction.

Mol Immunol

January 2025

Department of Critical Care Medicine, Affiliated Hospital of Nantong University, Nantong, China, Medical school of Nantong University, Nantong 226001, China. Electronic address:

Sepsis-induced myocardial dysfunction (SIMD) is a life-threatening complication primarily driven by inflammation, yet its molecular mechanisms remain unclear. In this study, we identified significant upregulation of the mA methyltransferase METTL3 (methyltransferase-like 3), the mA reader protein YTHDF1 (YTH N6-methyladenosine RNA binding protein 1), as well as increased expression levels of USP12 (ubiquitin-specific peptidase 12), FOXO3 (forkhead box O3), and key molecules in the intrinsic apoptotic pathway, PUMA (p53 upregulated modulator of apoptosis) and BAX (Bcl-2-associated X), through proteomic profiling in an LPS (Lipopolysaccharide)-induced SIMD mouse model. In vitro and in vivo experiments demonstrated that METTL3 and YTHDF1 regulated USP12 mRNA expression and stability through mA modification.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!