Progress in Immunopharmacy

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 479

Special Issue Editors


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Guest Editor
Department of Medical Research, E-Da Hospital, Kaohsiung 824410, Taiwan
Interests: inflammation pharmacology; drug discovery; cancer biology
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Guest Editor
School of Nursing, Fooyin University, Kaohsiung 831301, Taiwan
Interests: cancer physiology; immunopharmacology; translational medicine
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Special Issue Information

Dear Colleagues,

This Special Issue, "Progress in Immunopharmacy", aims to explore recent advancements and emerging trends in the field of immunopharmacy and immunopharmacology, encompassing the study of immune system-targeting pharmacological interventions, including immunomodulatory drugs, vaccines, and immunotherapies. It seeks to provide a platform for researchers to showcase their innovative research findings, methodologies, and discoveries related to immunopharmacy and immunopharmacology. The topics of interest may include but are not limited to the development of novel immunotherapeutic agents, immunopharmacological mechanisms, drug interactions with the immune system, personalized immunopharmacotherapy approaches, and clinical immunopharmacy applications in various disease settings. By highlighting the latest progress in immunopharmacy, this Special Issue aims to stimulate further research, foster collaboration, and contribute to the advancement of pharmacotherapy tailored to immune response modulation for improved health outcomes.

Dr. Po-Jen Chen
Dr. Shun-Hua Chen
Guest Editors

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Keywords

  • immunopharmacy
  • immunopharmacology
  • immunomodulation
  • pharmacological intervention
  • immunotherapy
  • drug–immune system interaction
  • vaccine development
  • personalized pharmacotherapy

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Published Papers (1 paper)

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Research

19 pages, 16275 KiB  
Article
Targeting the ZMYM2-ANXA9 Axis with FLT3 Inhibitor G749 Overcomes Oxaliplatin Resistance in Colorectal Cancer
by Dezheng Lin, Yucheng Xu, Huanmiao Zhan, Yufan Liang, Riyun Liu, Jun Liu, Dandong Luo, Xiaochuan Chen, Jiawei Cai and Yifeng Zou
Biomedicines 2025, 13(5), 1247; https://doi.org/10.3390/biomedicines13051247 - 20 May 2025
Viewed by 157
Abstract
Background: Chemoresistance and tumor recurrence remain major obstacles in colorectal cancer (CRC) therapy. Elucidating the molecular mechanisms underlying treatment resistance is critical for improving therapeutic outcomes. Methods: We analyzed transcriptomic profiles from public datasets (TCGA and GSE39582) to identify differentially expressed genes [...] Read more.
Background: Chemoresistance and tumor recurrence remain major obstacles in colorectal cancer (CRC) therapy. Elucidating the molecular mechanisms underlying treatment resistance is critical for improving therapeutic outcomes. Methods: We analyzed transcriptomic profiles from public datasets (TCGA and GSE39582) to identify differentially expressed genes associated with a poor response to neoadjuvant chemotherapy in CRC patients. Among 298 candidate genes, ANXA9 emerged as significantly overexpressed in chemoresistant tumors and associated with a poor prognosis. These findings were further validated in an independent cohort of 146 Stage III CRC patients using immunohistochemistry and survival analysis. The expression of ANXA9 was evaluated in oxaliplatin acquired-resistant CRC cell lines via qPCR and Western blot. Functional studies, including RNA interference, colony formation, apoptosis assays, and drug sensitivity testing, were performed in vitro and in vivo to assess the role of ANXA9. A high-throughput drug screen identified G749, a FLT3 inhibitor, as a potential therapeutic agent. Results: ANXA9 expression was significantly elevated in non-responders to chemotherapy and oxaliplatin-resistant CRC cell lines. The knockdown of ANXA9 reduced proliferation and enhanced oxaliplatin sensitivity. G749 was found to suppress ANXA9 expression in a dose-dependent manner and inhibit CRC cell growth in vitro and in patient-derived organoids. In a CRC xenograft mouse model, G749 reduced the tumor burden without observable toxicity. Mechanistically, we identified ZMYM2 as a transcriptional regulator of ANXA9. ChIP-qPCR confirmed ZMYM2 binding to the ANXA9 promoter, especially in resistant cells. Silencing ZMYM2 suppressed tumor cell growth and restored chemosensitivity. Conclusions: The ZMYM2-ANXA9 signaling axis drives chemoresistance and tumor progression in CRC. FLT3 inhibition by G749 effectively downregulates ANXA9 and sensitizes tumors to chemotherapy, highlighting a novel therapeutic approach for chemoresistant CRC. Full article
(This article belongs to the Special Issue Progress in Immunopharmacy)
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