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Biomedicines
Special Issues
Drug Development in Gastrointestinal Disorders
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Drug Development in Gastrointestinal Disorders

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Drug Discovery, Development and Delivery".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 1182

Special Issue Editors

Dr. Miglena Milusheva

E-Mail Website
Guest Editor
1. Department of Bioorganic Chemistry, Faculty of Pharmacy, Medical University of Plovdiv, 4002 Plovdiv, Bulgaria 2. Department of Organic Chemistry, Faculty of Chemistry, University of Plovdiv, 4000 Plovdiv, Bulgaria
Interests: medicinal chemistry; organic synthesis; drug design and discovery; SAR; antispasmodics; gastrointestinal pharmacology; multitarget agents; hybrid molecules; memory modulation; neurogastroenterology
Dr. Stoaynka Atanasova Nikolova

E-Mail Website
Guest Editor
Department of Organic Chemistry, Faculty of Chemistry, University of Plovdiv, 4000 Plovdiv, Bulgaria
Interests: synthesis; drug discovery; medicinal chemistry; heterocyclic compounds; organic synthesis; hybrid molecules; nanoparticles; drug-delivery systems; drug-design

Special Issue Information

Dear Colleagues,

Gastrointestinal (GI) disorders encompass a broad spectrum of conditions affecting the digestive tract, liver, and pancreas, ranging from inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) to gastrointestinal cancers, functional dyspepsia, and non-alcoholic fatty liver disease (NAFLD). These disorders collectively represent a significant and growing global health burden, contributing to substantial morbidity, reduced quality of life, and escalating healthcare costs. Despite advances in understanding the pathophysiology of many GI diseases—including the roles of immune dysregulation, gut microbiome imbalance, epithelial barrier dysfunction, and neural-immune crosstalk—therapeutic development has faced persistent challenges.

This Special Issue aims to compile high-quality research and comprehensive reviews that address key challenges and opportunities in GI drug development. Focus areas include

  • Mechanism-driven target discovery and validation in disease-relevant models;
  • Innovative therapeutic modalities, including biologics, small molecules, cell-based therapies, and microbiome-targeted interventions;
  • Advanced drug delivery systems designed for the GI tract;
  • Biomarker development for therapeutic monitoring;
  • Clinical trial strategies for complex GI disorders.

We look forward to receiving your contributions to this important collection.

Dr. Miglena Milusheva
Dr. Stoaynka Atanasova Nikolova
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 250 words) can be sent to the Editorial Office for assessment.

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. Biomedicines 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 2600 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

  • inflammatory bowel disease (IBD)
  • crohn's disease
  • gastrointestinal disorders
  • biologics
  • small-molecule inhibitors
  • drug delivery system
  • therapeutic target
  • drug resistance
  • biomarker
  • multitarget therapy
  • nanoparticles

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Published Papers (2 papers)

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Research

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15 pages, 6382 KB  
Article
Polydeoxyribonucleotide Mitigates Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice Through the PKA/CREB/NF-κB Signaling Pathway
by SeungHwan Lee, Lakkyong Hwang, Sang Hoon Kim, Sang Hoon Lee, Jin Hee Han, Jung Won Jeon, Hyeong Chan Shin and Il-Gyu Ko
Biomedicines 2026, 14(6), 1241; https://doi.org/10.3390/biomedicines14061241 - 29 May 2026
Abstract
Background/Objectives: Ulcerative colitis (UC) is a type of inflammatory bowel disease characterized by abdominal pain, diarrhea, and bleeding. Polydeoxyribonucleotide (PDRN), an adenosine A2A receptor (A2AR) agonist, exhibits anti-inflammatory properties. In the present study, we evaluated the therapeutic effects of PDRN [...] Read more.
Background/Objectives: Ulcerative colitis (UC) is a type of inflammatory bowel disease characterized by abdominal pain, diarrhea, and bleeding. Polydeoxyribonucleotide (PDRN), an adenosine A2A receptor (A2AR) agonist, exhibits anti-inflammatory properties. In the present study, we evaluated the therapeutic effects of PDRN in a dextran sodium sulfate (DSS)-induced murine model of UC. Methods: UC was induced by administering 2% DSS in drinking water for 7 days. One day after DSS administration, mice received intraperitoneal injections of PDRN (8 mg/kg) for 7 days. To investigate the involvement of A2AR, the selective antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 8 mg/kg) was co-administered with PDRN. Results: DSS administration induced colonic tissue damage and increased disease activity index (DAI) and histological scores. DSS also elevated pro-inflammatory cytokines while reducing anti-inflammatory cytokine levels. PDRN treatment reduced histological damage, restored body weight, colon weight, and colon length, and decreased DAI scores. Furthermore, PDRN treatment inhibited nuclear factor kappa B (NF-κB) activation through suppression of NF-κB inhibitor-α phosphorylation and was associated with activation of the cAMP/PKA/CREB signaling pathway. PDRN treatment attenuated inflammation and was associated with increased expression of vascular endothelial growth factor (VEGF) in colonic tissues. Given the context-dependent role of VEGF in inflammatory bowel disease, this increase is interpreted as contributing to mucosal repair rather than exacerbating inflammation. Co-administration of DMPX abolished these effects, suggesting the involvement of A2AR-dependent signaling pathways. Conclusions: PDRN attenuated colonic inflammation and improved disease outcomes in DSS-induced UC, potentially through modulation of the PKA/CREB/NF-κB signaling pathway and VEGF-mediated tissue repair mechanisms. Full article
(This article belongs to the Special Issue Drug Development in Gastrointestinal Disorders)

Review

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15 pages, 801 KB  
Review
Therapeutic Potential of Probiotics in the Modulation of Antibiotic Resistance in Helicobacter pylori
by Lazzat Zhussupbekova, Alina Bulatova, Dinara Nurkina, Klara Kurmangaliyeva, Venera Rakhmetova, Aigyul Izhanova, Kaergeldy Makhambetov and Elmira Akhmedyarova
Biomedicines 2026, 14(5), 1044; https://doi.org/10.3390/biomedicines14051044 - 4 May 2026
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Abstract
Over the past decade, the growth of Helicobacter pylori antibiotic resistance has had an increasingly significant impact on the choice of eradication therapy regimens, significantly limiting the number of effective treatment options. The Maastricht VI guidelines consider the use of probiotics as one [...] Read more.
Over the past decade, the growth of Helicobacter pylori antibiotic resistance has had an increasingly significant impact on the choice of eradication therapy regimens, significantly limiting the number of effective treatment options. The Maastricht VI guidelines consider the use of probiotics as one way to optimise therapy and increase the likelihood of successful eradication. In this regard, the study of the possible mechanisms of action of probiotic preparations on antibiotic-resistant strains of H. pylori, as well as their possible role in preventing the development of resistance, is of considerable interest and may contribute to improving the quality of eradication therapy in the near future. The aim of the study is to determine the role of probiotics in modifying the microbiota during and after eradication therapy, as well as to assess their potential impact on the development of antibiotic resistance. A search for scientific publications was conducted in international and national bibliographic databases: PubMed, Embase, Scopus, Web of Science Core Collection, Google Scholar, and eLIBRARY.ru. The search was conducted in English, Russian, and Kazakh for the period from 26 April 2015 to 14 July 2025. The review includes 41 publications. Eradication therapy has a pronounced negative effect on the intestinal microbiota, leading to disruption of its composition and the development of side effects that reduce treatment tolerability. A number of studies in recent years have demonstrated a link between antibiotic therapy and the development of antibiotic resistance caused by genetic rearrangements and mutations in the gut microbiota genome. As an additional approach to correcting these adverse effects, special attention is paid to the use of probiotics. According to the research results, probiotic preparations help reduce the frequency of side effects of eradication therapy and may increase its effectiveness against antibiotic-resistant strains of H. pylori. The use of probiotic preparations in the treatment of resistant strains of Helicobacter pylori is a promising direction that opens up new opportunities for optimising eradication regimens. However, this approach requires further clinical and experimental studies to confirm its effectiveness and form reasonable prognostic conclusions. Full article
(This article belongs to the Special Issue Drug Development in Gastrointestinal Disorders)
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