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Molecular Biology in Drug Design and Precision Therapy

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 8250

Special Issue Editors

Dr. Cristina Manuela Dragoi

E-Mail Website
Guest Editor
Department of Biochemistry, Faculty of Pharmacy, Carol Davila University of Medicine and Pharmacy, 020956 Bucharest, Romania
Interests: biochemistry; chronobiology; drug interactions; mechanisms of action; pharmaceutical research; molecular pharmacology
Special Issues, Collections and Topics in MDPI journals
Dr. Ion-Bogdan Dumitrescu

E-Mail Website
Guest Editor
Faculty of Pharmacy, University of Medicine and Pharmacy “Carol Davila”, 020956 Bucharest, Romania
Interests: pharmaceutical 3D printing; computer-aided design; clinical pharmacy
Special Issues, Collections and Topics in MDPI journals
Dr. Alina Crenguța Nicolae

E-Mail Website
Guest Editor
Faculty of Pharmacy, University of Medicine and Pharmacy “Carol Davila”, 020956 Bucharest, Romania
Interests: biochemistry; nutrition; drug resistance; P-glycoprotein; neuroscience; clinical research; personalized medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The realm of drug design is currently at the core of a remarkable transformation, marked by the exploration of groundbreaking approaches that exceed conventional norms and expectations. Central to this evolution is a comprehensive grasp of the molecular underpinnings that drive various diseases, coupled with the continuous refinement and advancement of cutting-edge tools and technologies. Drawing upon insights from disciplines such as molecular biology, computational chemistry, and bioinformatics, researchers are equipped with sophisticated means to delve into the intricate mechanisms of biological systems in order to better understand the genesis and development of diseases and to foster tailored interventions that target specific molecular pathways. This integration of diverse scientific fields not only enhances our understanding of disease processes but also expands the horizons of drug design, paving the way for the creation of more effective and precisely targeted therapies. Thus, the current era of drug design represents a convergence of scientific ingenuity and technological innovation, meant to revolutionize the landscape of modern medicine.

The Special Issue "Molecular Biology in Drug Design and Precision Therapy" aims to explore the interplay between molecular biology and the development of novel therapeutic strategies, with a particular focus on precision medicine. In biomedical research, molecular biology has a tremendous role in elucidating the fundamental mechanisms implicated in disease pathogenesis, simplifying the road to targeted therapies tailored to individual patients.

This Special Issue invites contributions that explore the molecular intricacies of disease processes, encompassing a wide array of topics such as molecular signaling pathways, gene expression regulation, protein interactions, and cellular mechanisms implicated in disease progression. Emphasizing the molecular level of investigation, manuscripts are encouraged to elucidate the molecular targets of therapeutic interventions, as well as mechanisms of drug action and resistance, and explore the potential of precision medicine approaches to optimize treatment outcomes. Furthermore, this Special Issue seeks to showcase cutting-edge methodologies and technologies utilized in molecular biology research, including next-generation sequencing, transcriptomics, proteomics, metabolomics, and computational modeling. Through a comprehensive understanding of molecular mechanisms, this Special Issue aims to drive advancements in drug discovery, development, and personalized therapy, ultimately translating molecular insights into improved clinical outcomes for patients.

Contributions from researchers across diverse disciplines, including molecular biology, pharmacology, biochemistry, and biotechnology, are welcome, to foster interdisciplinary dialogue and innovation in the field of drug design and precision therapy, and we further invite scientists and drug specialists to publish their original research works, review articles, and communications on this wide health domain.

Dr. Cristina Manuela Dragoi
Dr. Ion-Bogdan Dumitrescu
Dr. Alina Crenguța Nicolae
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • molecular biology
  • drug design
  • molecular targets
  • disease mechanisms
  • structural biology
  • computational chemistry
  • pharmacology
  • precision medicine
  • molecular pathways
  • personalized therapy
  • drug research

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Published Papers (7 papers)

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Research

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24 pages, 10329 KiB  
Article
Exploring the Molecular Mechanism of 1,25(OH)2D3 Reversal of Sorafenib Resistance in Hepatocellular Carcinoma Based on Network Pharmacology and Experimental Validation
by Zhiyan Long, Xiangyi Wu, Tianxin Luo, Xiaomei Chen, Jian Huang and Shu Zhang
Curr. Issues Mol. Biol. 2025, 47(5), 319; https://doi.org/10.3390/cimb47050319 - 29 Apr 2025
Abstract
Sorafenib is currently the first-line therapeutic agent for advanced hepatocellular carcinoma (HCC). However, sorafenib resistance remains a major clinical challenge. Studies have reported that 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) can synergize with multiple chemotherapeutic drugs to enhance their antitumor efficacy, but [...] Read more.
Sorafenib is currently the first-line therapeutic agent for advanced hepatocellular carcinoma (HCC). However, sorafenib resistance remains a major clinical challenge. Studies have reported that 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) can synergize with multiple chemotherapeutic drugs to enhance their antitumor efficacy, but the combinatorial effect between 1,25(OH)2D3 and sorafenib has not yet been investigated. This study aimed to investigate the potential molecular mechanism by which 1,25(OH)2D3 reverses sorafenib resistance in hepatocellular carcinoma using network pharmacology, molecular docking, and experimental validation. We predicted a web-based pharmacological approach to predict potential targets of 1,25(OH)2D3 and its derivatives, as well as sorafenib resistance genes in hepatocellular carcinoma from public databases. We then constructed 1,25(OH)2D3 chemo-sensitizing expression profiles through intersection analysis. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were employed to predict the potential pathways involved in 1,25(OH)2D3 chemosensitization, followed by molecular docking analysis and analysis of molecular dynamics simulations. Finally, experimental validation were conducted to elucidate the potential mechanisms by which 1,25(OH)2D3 enhances the sensitivity of HCC to sorafenib. Compound and target screening identified 730 predicted targets of 1,25(OH)2D3 and its derivatives, 1144 genes associated with sorafenib resistance in hepatocellular carcinoma, and 56 potential chemosensitization targets from the intersection analysis. KEGG analysis suggested that the chemosensitization effect of 1,25(OH)2D3 might be mediated by the FoxO signaling pathway. Molecular docking showed that both 1,25(OH)2D3 and its derivatives could stably bind to FOXO3A, a key gene in the FoxO family, and molecular dynamics simulation analysis further indicated that the two bind well together. In vitro experiments demonstrated the synergistic effects of 1,25(OH)2D3 and sorafenib, significantly inhibiting the viability and colony formation rate of sorafenib-resistant hepatocellular carcinoma cells. Additionally, the combination treatment promoted apoptosis and inhibited autophagy. Furthermore, the combination modulated the FOXO3A/FOXM1 signaling axis. This study reveals that 1,25(OH)2D3 enhances the chemosensitivity of hepatocellular carcinoma (HCC) to sorafenib, with underlying mechanisms potentially involving the targeted modulation of the FOXO3A/FOXM1 signaling axis and the reversal of sorafenib-resistant phenotypes through the regulation of apoptotic and autophagic pathways. Full article
(This article belongs to the Special Issue Molecular Biology in Drug Design and Precision Therapy)
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21 pages, 18989 KiB  
Article
In Silico Identification of Potential Antagonists Targeting the HPV16 E2-E1 Interaction: A Step Toward Novel Therapeutics for Cervical Cancer
by Jesús Alonso Gandara-Mireles, Verónica Loera Castañeda, Julio Cesar Grijalva Ávila, Ignacio Villanueva Fierro, Cynthia Mora Muñoz, Hugo Payan Gándara, Guadalupe Antonio Loera Castañeda, Leslie Patrón Romero and Horacio Almanza Reyes
Curr. Issues Mol. Biol. 2025, 47(4), 288; https://doi.org/10.3390/cimb47040288 - 18 Apr 2025
Viewed by 186
Abstract
Human papillomavirus (HPV) infection is the most prevalent sexually transmitted disease, and a primary cause of persistent infection leading to cervical cancer (CC). CC remains one of the most common malignancies among women worldwide, with approximately 660,000 new cases and 350,000 deaths annually. [...] Read more.
Human papillomavirus (HPV) infection is the most prevalent sexually transmitted disease, and a primary cause of persistent infection leading to cervical cancer (CC). CC remains one of the most common malignancies among women worldwide, with approximately 660,000 new cases and 350,000 deaths annually. In Mexico, this cancer accounts for 13.9% of female deaths. Currently, no antiviral treatment exists for HPV infection. Available therapies for dysplasia and CC focus on the destruction or surgical removal of infected tissue using cytotoxic agents. While the prophylactic HPV vaccine effectively prevents new infections, it does not benefit the millions already infected, underscoring the urgent need for novel therapeutic strategies. This study aimed to identify potential antagonists for the interaction between the HPV16 E2 and E1 proteins through in silico screening. A virtual screening was performed targeting the TAD of the HPV16 E2 protein (PDB ID: 1DTO) using the Maybridge HitFinder™ small molecule library. Six molecules with the best binding energies were identified: 11419, 11829, 10756, 10708, 10632, and 10726. Among these, molecules 10756, 10708, 10632, and 10726 demonstrated promising potential as antagonists, interacting with Tyr19 and/or Glu39 residues. These findings highlight potent therapeutic candidates against HPV-related diseases. Full article
(This article belongs to the Special Issue Molecular Biology in Drug Design and Precision Therapy)
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14 pages, 1928 KiB  
Article
The Derivative Difluoroboranyl-Fluoroquinolone “7a” Generates Effective Inhibition Against the S. aureus Strain in a Murine Model of Acute Pneumonia
by L. Angel Veyna-Hurtado, Hiram Hernández-López, Fuensanta del Rocío Reyes-Escobedo, Denisse de Loera, Salvador García-Cruz, Lorena Troncoso-Vázquez, Marisol Galván-Valencia, Julio E. Castañeda-Delgado and Alberto Rafael Cervantes-Villagrana
Curr. Issues Mol. Biol. 2025, 47(2), 110; https://doi.org/10.3390/cimb47020110 - 10 Feb 2025
Viewed by 1818
Abstract
During the last decades, most bacterial strains have become increasingly resistant to antibiotics. This led the WHO to declare a global emergency in 2017 and urge the development of new active compounds. Some families of antibiotics still show high antibacterial efficacy, as is [...] Read more.
During the last decades, most bacterial strains have become increasingly resistant to antibiotics. This led the WHO to declare a global emergency in 2017 and urge the development of new active compounds. Some families of antibiotics still show high antibacterial efficacy, as is the case of fluoroquinolones, which have a broad spectrum of action. For this reason, our research group derived several compounds from fluoroquinolones, selecting a compound with good antibacterial activity for further evaluations, a difluoroboranil-fluoroquinolone complex labeled 7a. Antibacterial activity was evaluated using the Kirby–Bauer method against S. aureus (clinical isolate HGZ2201#ID). The MIC and MBC were obtained by macrodilutions and reseeding. In vivo antimicrobial activity was evaluated in a Balb/c mouse model infected intratracheally with S. aureus and subsequently treated with ciprofloxacin or 7a (80 mg/kg/day) for five days. A mean of 8.55 ± 0.395 cm2 inhibition area was observed using 7a, while ciprofloxacin generated a mean inhibition of 7.86 ± 0.231 cm2. Compound 7a showed a MIC and MBC of 0.25 μg/mL. This reduced the generation of pneumonic lung tissue to 5.83%, while the untreated infected group generated 60.51% of pneumonic tissue. Compound 7a proved to be an antimicrobial agent capable of inhibiting the in vitro development of S. aureus. Furthermore, 7a showed effectiveness in decreasing the progression of acute pneumonia induced by S. aureus in a murine model. Full article
(This article belongs to the Special Issue Molecular Biology in Drug Design and Precision Therapy)
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17 pages, 1113 KiB  
Article
Using Precision Medicine to Disentangle Genotype–Phenotype Relationships in Twins with Rett Syndrome: A Case Report
by Jatinder Singh, Georgina Wilkins, Ella Goodman-Vincent, Samiya Chishti, Ruben Bonilla Guerrero, Federico Fiori, Shashidhar Ameenpur, Leighton McFadden, Zvi Zahavi and Paramala Santosh
Curr. Issues Mol. Biol. 2024, 46(8), 8424-8440; https://doi.org/10.3390/cimb46080497 - 2 Aug 2024
Cited by 1 | Viewed by 1366
Abstract
Rett syndrome (RTT) is a paediatric neurodevelopmental disorder spanning four developmental stages. This multi-system disorder offers a unique window to explore genotype–phenotype relationships in a disease model. However, genetic prognosticators of RTT have limited clinical value due to the disorder’s heterogeneity on multiple [...] Read more.
Rett syndrome (RTT) is a paediatric neurodevelopmental disorder spanning four developmental stages. This multi-system disorder offers a unique window to explore genotype–phenotype relationships in a disease model. However, genetic prognosticators of RTT have limited clinical value due to the disorder’s heterogeneity on multiple levels. This case report used a precision medicine approach to better understand the clinical phenotype of RTT twins with an identical pathogenic MECP2 mutation and discordant neurodevelopmental profiles. Targeted genotyping, objective physiological monitoring of heart rate variability (HRV) parameters, and clinical severity were assessed in a RTT twin pair (5 years 7 months old) with an identical pathogenic MECP2 mutation. Longitudinal assessment of autonomic HRV parameters was conducted using the Empatica E4 wristband device, and clinical severity was assessed using the RTT-anchored Clinical Global Impression Scale (RTT-CGI) and the Multi-System Profile of Symptoms Scale (MPSS). Genotype data revealed impaired BDNF function for twin A when compared to twin B. Twin A also had poorer autonomic health than twin B, as indicated by lower autonomic metrics (autonomic inflexibility). Hospitalisation, RTT-CGI-S, and MPSS subscale scores were used as measures of clinical severity, and these were worse in twin A. Treatment using buspirone shifted twin A from an inflexible to a flexible autonomic profile. This was mirrored in the MPSS scores, which showed a reduction in autonomic and cardiac symptoms following buspirone treatment. Our findings showed that a combination of a co-occurring rs6265 BDNF polymorphism, and worse autonomic and clinical profiles led to a poorer prognosis for twin A compared to twin B. Buspirone was able to shift a rigid autonomic profile to a more flexible one for twin A and thereby prevent cardiac and autonomic symptoms from worsening. The clinical profile for twin A represents a departure from the disorder trajectory typically observed in RTT and underscores the importance of wider genotype profiling and longitudinal objective physiological monitoring alongside measures of clinical symptoms and severity when assessing genotype–phenotype relationships in RTT patients with identical pathogenic mutations. A precision medicine approach that assesses genetic and physiological risk factors can be extended to other neurodevelopmental disorders to monitor risk when genotype–phenotype relationships are not so obvious. Full article
(This article belongs to the Special Issue Molecular Biology in Drug Design and Precision Therapy)
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15 pages, 1425 KiB  
Article
The Promising Effect of Ascorbic Acid and Paracetamol as Anti-Biofilm and Anti-Virulence Agents against Resistant Escherichia coli
by Sara M. Eltabey, Ali H. Ibrahim, Mahmoud M. Zaky, Adel Ehab Ibrahim, Yahya Bin Abdullah Alrashdi, Sami El Deeb and Moustafa M. Saleh
Curr. Issues Mol. Biol. 2024, 46(7), 6805-6819; https://doi.org/10.3390/cimb46070406 - 2 Jul 2024
Cited by 4 | Viewed by 2030
Abstract
Escherichia coli is a major cause of serious infections, with antibiotic resistance rendering many treatments ineffective. Hence, novel strategies to combat this pathogen are needed. Anti-virulence therapy is a promising new approach for the subsequent era. Recent research has examined the impact of [...] Read more.
Escherichia coli is a major cause of serious infections, with antibiotic resistance rendering many treatments ineffective. Hence, novel strategies to combat this pathogen are needed. Anti-virulence therapy is a promising new approach for the subsequent era. Recent research has examined the impact of sub-inhibitory doses of ascorbic acid and paracetamol on Escherichia coli virulence factors. This study evaluated biofilm formation, protease production, motility behavior, serum resistance, expression of virulence-regulating genes (using RT-PCR), and survival rates in a mouse model. Ascorbic acid significantly reduced biofilm formation, protease production, motility, and serum resistance from 100% in untreated isolates to 22–89%, 10–89%, 2–57%, and 31–35% in treated isolates, respectively. Paracetamol also reduced these factors from 100% in untreated isolates to 16–76%, 1–43%, 16–38%, and 31–35%, respectively. Both drugs significantly down-regulated virulence-regulating genes papC, fimH, ompT_m, stcE, fliC, and kpsMTII. Mice treated with these drugs had a 100% survival rate compared with 60% in the positive control group control inoculated with untreated bacteria. This study highlights the potential of ascorbic acid and paracetamol as anti-virulence agents, suggesting their use as adjunct therapies alongside conventional antimicrobials or as alternative treatments for resistant Escherichia coli infections. Full article
(This article belongs to the Special Issue Molecular Biology in Drug Design and Precision Therapy)
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Review

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22 pages, 2743 KiB  
Review
Updates on the Activity, Efficacy and Emerging Mechanisms of Resistance to Cefiderocol
by Gabriele Bianco, Matteo Boattini, Monica Cricca, Lucia Diella, Milo Gatti, Luca Rossi, Michele Bartoletti, Vittorio Sambri, Caterina Signoretto, Rossella Fonnesu, Sara Comini and Paolo Gaibani
Curr. Issues Mol. Biol. 2024, 46(12), 14132-14153; https://doi.org/10.3390/cimb46120846 - 14 Dec 2024
Cited by 4 | Viewed by 1876
Abstract
In recent years, novel antimicrobials have been developed to counter the emergence of antimicrobial resistance and provide effective therapeutic options against multidrug-resistant (MDR) Gram-negative bacilli (GNB). Cefiderocol, a siderophore cephalosporin, represents a novel valuable antimicrobial drug for the treatment of infections caused by [...] Read more.
In recent years, novel antimicrobials have been developed to counter the emergence of antimicrobial resistance and provide effective therapeutic options against multidrug-resistant (MDR) Gram-negative bacilli (GNB). Cefiderocol, a siderophore cephalosporin, represents a novel valuable antimicrobial drug for the treatment of infections caused by MDR-GNB. The mechanism of cefiderocol to penetrate through the outer membrane of bacterial cells, termed “Trojan horse”, makes this antimicrobial drug unique and immune to the various resistance strategies adopted by GNB. Its broad spectrum of action, potent antibacterial activity, pharmacokinetics properties, safety, and tolerability make cefiderocol a key drug for the treatment of infections due to MDR strains. Although this novel antimicrobial molecule contributed to revolutionizing the therapeutic armamentarium against MDR-GNB, the recent emergence of cefiderocol-resistant strains has redefined its role in clinical practice and required new strategies to preserve its antibacterial activity. In this review, we provide an updated discussion regarding the mechanism of action, emerging mechanisms of resistance, pharmacokinetic/pharmacodynamic (PK/PD) properties, and efficacy data of cefiderocol against the major Gram-negative bacteria and future prospects. Full article
(This article belongs to the Special Issue Molecular Biology in Drug Design and Precision Therapy)
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Other

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26 pages, 1409 KiB  
Perspective
Potential Benefits of Adding Alendronate, Celecoxib, Itraconazole, Ramelteon, and Simvastatin to Endometrial Cancer Treatment: The EC5 Regimen
by Richard E. Kast
Curr. Issues Mol. Biol. 2025, 47(3), 153; https://doi.org/10.3390/cimb47030153 - 26 Feb 2025
Viewed by 619
Abstract
Metastatic endometrial cancer continues to be a common cause of death as of 2024, even after maximal use of all currently available standard treatments. To address this problem of metastatic cancer generally in 2025, the drug repurposing movement within oncology identifies medicines in [...] Read more.
Metastatic endometrial cancer continues to be a common cause of death as of 2024, even after maximal use of all currently available standard treatments. To address this problem of metastatic cancer generally in 2025, the drug repurposing movement within oncology identifies medicines in common general medical use that have clinical or preclinical experimental data indicating that they interfere with or inhibit a specific growth driving element identified in a given cancer. The drug repurposing movement within oncology also uses data from large scale in vitro screens of thousands of drugs, looking for simple empirical growth inhibition in a given cancer type. This paper outlines the data showing that five drugs from general medical practice meet these evidence criteria for inhibition of endometrial cancer growth, the EC5 regimen. The EC5 regimen uses the osteoporosis treatment drug, alendronate; the analgesic drug, celecoxib; the antifungal drug, itraconazole; the sleep aid, ramelteon; and the cholesterol lowering drug, simvastatin. Side effects seen with these drugs are usually minimal and easily tolerated by patients. Full article
(This article belongs to the Special Issue Molecular Biology in Drug Design and Precision Therapy)
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