Current Research in Pharmacology and Drug Discovery最新文献

{"title":"Desloratadine attenuates renal ischemia-reperfusion injury through activation of the Nrf2-GCL-GSH antioxidant pathway","authors":"Firouzeh Gholampour,&nbsp;Atefeh Maghsoodi,&nbsp;Khojasteh Malekmohammad","doi":"10.1016/j.crphar.2026.100255","DOIUrl":"10.1016/j.crphar.2026.100255","url":null,"abstract":"<div><div>Renal ischemia–reperfusion injury (IRI) is a major cause of acute kidney injury (AKI) in transplantation and major surgery, with limited effective pharmacological interventions. This study evaluated the prophylactic effect of desloratadine, a second-generation H1-receptor antagonist with anti-inflammatory and antioxidant properties, on renal IRI. Twenty-one male Sprague–Dawley rats were randomly assigned to three groups (n = 7 each): Sham, I/R (45 min ischemia followed by 24 h reperfusion), and I/R + desloratadine (5 mg/kg, orally, 1 h prior to ischemia). After 24 h of reperfusion, renal function, oxidative stress markers, histopathology, and antioxidant gene expression were assessed. I/R significantly impaired renal function (increased plasma creatinine and urea, decreased creatinine clearance; <em>P</em> &lt; 0.001), reduced effective free-water reabsorption, and increased oxidative stress (elevated TOS, reduced TAC and GSH; <em>P</em> &lt; 0.01–0.001). Desloratadine significantly improved renal function, restored tubular concentrating ability, reduced oxidative stress, and increased GSH levels (<em>P</em> &lt; 0.05–0.001 vs. I/R). At the molecular level, I/R upregulated Nrf2 and HO-1 expression but downregulated Gclc and Gclm, while desloratadine further enhanced Nrf2/HO-1 expression and restored Gclc/Gclm levels. Histological analysis confirmed attenuation of tubular injury. In conclusion, desloratadine pretreatment is associated with protection against renal IRI, potentially through modulation of the Nrf2–GCL–GSH antioxidant pathway and preservation of tubular function. These findings support its potential repurposing as an adjuvant strategy in settings at risk of renal ischemic injury.</div></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"10 ","pages":"Article 100255"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147747519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-Shigella activity and killing kinetics of compounds from MMV Pathogen and COVID Boxes: Identifying leads against Shigellosis","authors":"Lauve Rachel Tchokouaha Yamthe ,&nbsp;Francine Kengne Mediesse ,&nbsp;Yanick Kevin Melogmo Dongmo ,&nbsp;Sonia Raissa Matchuenkam Gayap ,&nbsp;Darline Dize ,&nbsp;Patrick Valere Tsouh Fokou ,&nbsp;Fabrice Fekam Boyom","doi":"10.1016/j.crphar.2026.100251","DOIUrl":"10.1016/j.crphar.2026.100251","url":null,"abstract":"<div><h3>Background</h3><div>Shigellosis is a leading diarrheal disease, posing critical public health challenges in low- and middle-income countries. Rising antibiotic resistance exacerbates treatment limitations.</div></div><div><h3>Methods</h3><div>We screened 560 compounds from the MMV Pathogen and COVID Boxes for <em>in vitro</em> activity against <em>Shigella flexneri</em>, <em>S. sonnei</em>, and <em>S. dysenteriae</em> via resazurin-based microdilution. Cytotoxicity (RAW 264.7 cells) and killing kinetics against <em>S. flexneri</em> were assessed.</div></div><div><h3>Results</h3><div>From the primary screen, 13 compounds (9 from the Pathogen Box, 4 from the COVID Box) showed potent anti-<em>Shigella</em> activity against <em>S. flexneri</em> (MIC ≤10 μM). Among these, seven non-antibiotic Pathogen Box compounds exhibited low-micromolar MICs (0.31–5 μM) and low cytotoxicity (CC₅₀ &gt; 100 μM). The known antibiotic levofloxacin (MMV687798) showed broad-spectrum activity (MIC 0.15–2.5 μM). MMV1804312 (salinomycin) was the most active COVID Box hit (MIC 1.25 μM). Time-kill assays revealed rapid, concentration-dependent bactericidal activity (≥3-log reduction within 4–6 h) for Pathogen Box compounds MMV675997 and MMV021660, while MMV000858 displayed bacteriostatic action.</div></div><div><h3>Conclusion</h3><div>This study identifies several novel, non-antibiotic leads from the MMV Pathogen Box with potent anti-<em>Shigella</em> activity and favorable cytotoxicity profiles, offering promising starting points for further development against drug-resistant shigellosis.</div></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"10 ","pages":"Article 100251"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146184664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of G protein-coupled receptor 40 alleviates STAT6 activation, airway inflammation and mucus hypersecretion in allergic asthma","authors":"Chantapol Yimnual,&nbsp;Jenjira Sontikun,&nbsp;Vanason Yaovakhan,&nbsp;Suhaibee Kuno,&nbsp;Phattarin Pothipan,&nbsp;Chatchai Muanprasat,&nbsp;Virawudh Soontornniyomkij,&nbsp;Aekkacha Moonwiriyakit","doi":"10.1016/j.crphar.2026.100260","DOIUrl":"10.1016/j.crphar.2026.100260","url":null,"abstract":"<div><div>G-protein coupled receptor 40 (GPR40), also termed free fatty acid receptor 1 (FFAR1) is a promising molecular target for treating chronic metabolic and inflammatory diseases. Despite the antiasthmatic benefit of GPR40 agonists such as omega-3 polyunsaturated fatty acids, it remains unclear whether GPR40 activation improves allergic asthmatic outcomes. The present study investigated the ameliorative effect of GPR40 activation on IL-13-induced allergic inflammation in human bronchial epithelial 16HBE14o-cells and in the ovalbumin-induced asthmatic murine model. The increasing concentration of GPR40 agonists GW9508 and TAK875, markedly mitigated IL-13–induced STAT6 phosphorylation and MUC5AC hypersecretion, suggesting mitigated type 2 inflammation in 16HBE14o-cells. The selective GPR40 antagonists DC260126 and GW1100 both strikingly abolished the anti-inflammatory effect of GW9508. In the asthmatic mouse model, intraperitoneal administration of GW9508 (10 mg/kg) alleviated ovalbumin-induced mucus hypersecretion and airway inflammation, with a reduction in STAT6 phosphorylation in lung tissue. Our findings suggest that GPR40 activation represents a novel therapeutic strategy for STAT6-mediated or type-2-inflammation mediated diseases such as allergic asthma.</div></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"11 ","pages":"Article 100260"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13310601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148344074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting telomere dynamics with plant-derived compounds: Molecular strategies against aging","authors":"Raushanara Akter,&nbsp;Adwiza Chakraborty Bishakha,&nbsp;Raisha Rajib,&nbsp;Asef Raj,&nbsp;Mashwiyat Samrin Roja,&nbsp;Fouzia Noor","doi":"10.1016/j.crphar.2025.100238","DOIUrl":"10.1016/j.crphar.2025.100238","url":null,"abstract":"<div><div>Telomeres, the repetitive DNA–protein complexes capping eukaryotic chromosomes, preserve genomic stability and regulate cellular replicative capacity. Progressive telomere shortening, coupled with diminished telomerase activity, is a hallmark of aging and contributes to cellular senescence, tissue degeneration, and the onset of age-related diseases. Conversely, telomerase overactivation in malignant cells enables uncontrolled proliferation, positioning telomere biology as a dual therapeutic target in longevity and oncology. Plant-derived compounds possess diverse structural classes such as polyphenols, flavonoids, triterpenoid saponins, polysaccharides, lignans, alkaloids, carotenoids, amino acids, and fatty acids that can modulate telomere length and telomerase activity via multiple molecular pathways. These include antioxidant and anti-inflammatory actions, regulation of key genes such as hTERT, SIRT1, and c-Myc, modulation of PI3K/Akt, JAK/STAT, and ERK signaling, and stabilization or destabilization of G-quadruplex DNA structures. Compounds such as resveratrol, epigallocatechin gallate, astragaloside IV, cycloastragenol, and ginsenoside Rg1 have demonstrated telomerase activation or inhibition in a context-dependent manner, influenced by concentration, cell type, and disease state. This review categorizes plant-derived positive and negative telomere/telomerase modulators, detailing their sources, mechanisms of action, experimental evidence, and the formulation challenges that hinder clinical translation, such as low bioavailability, instability, and variability in phytochemical content. By integrating molecular insights with pharmacological perspectives, this review highlights the potential of plant-derived agents as multi-target interventions in aging and cancer. Advancing this field will require rigorous pharmacokinetic profiling, standardized preparations, and longitudinal clinical studies to bridge the gap between laboratory findings and real-world therapeutic outcomes.</div></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"9 ","pages":"Article 100238"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145516511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Metabolic and clinical effect of alpha-lipoic acid administration in schizophrenic subjects stabilized with atypical antipsychotics: A 12-week, open-label, uncontrolled study” [Curr. Res. Pharmacol. Drug Discov. 3 (2022) 100116]","authors":"Fiammetta Iannuzzo ,&nbsp;Gianpaolo Antonio Basile ,&nbsp;Domenica Campolo ,&nbsp;Giovanni Genovese ,&nbsp;Gianluca Pandolfo ,&nbsp;Loretta Giunta ,&nbsp;Domenica Ruggeri ,&nbsp;Antonino Di Benedetto ,&nbsp;Antonio Bruno","doi":"10.1016/j.crphar.2025.100215","DOIUrl":"10.1016/j.crphar.2025.100215","url":null,"abstract":"","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"8 ","pages":"Article 100215"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143600711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic effects of vitamin D and omega-3 supplementation on HFHS diet-induced endothelial dysfunction in Wistar rats","authors":"Dylan Le Jan ,&nbsp;Sandrine Destrumelle ,&nbsp;Chantal Thorin ,&nbsp;Jean-Claude Desfontis ,&nbsp;Eric Betti ,&nbsp;Mohamed Yassine Mallem","doi":"10.1016/j.crphar.2025.100240","DOIUrl":"10.1016/j.crphar.2025.100240","url":null,"abstract":"<div><h3>Background</h3><div>Obesity impairs cardiovascular health through endothelial dysfunction, which is exacerbated by high-fat high-sugar (HFHS) diets through mechanisms involving chronic inflammation, oxidative stress, and insulin resistance. Nutritional interventions, specifically vitamin D (VD) and omega-3 fatty acids (ω3), have emerged as potential therapies to improve endothelial function and mitigate cardiovascular risks associated with obesity.</div></div><div><h3>Objective</h3><div>This study investigated the effects of VD, ω3 and their combination on endothelial dysfunction induced by an HFHS diet in Wistar rats.</div></div><div><h3>Methods</h3><div>Sixty-four male Wistar rats were fed either a Standard (S) or HFHS diet for 26 weeks. After 13 weeks, rats were supplemented with VD (600 IU/kg/day), ω3 (300 mg/kg/day), both (VD/ω3), or a control (C) for an additional 13 weeks. Endothelial function was assessed using aortic ring assays, focusing on acetylcholine (ACh)-mediated endothelium-dependent vasorelaxation, phenylephrine (Phe)-mediated vasoconstriction, and insulin responsiveness.</div></div><div><h3>Results</h3><div>VD and/or ω3 supplementation effectively improved ACh-mediated vasorelaxation and counteracted HFHS-induced endothelial dysfunction. VD enhanced insulin-mediated vasorelaxation, while ω3 showed a non-significant trend towards improved Phe-mediated vasoconstriction.</div></div><div><h3>Conclusion</h3><div>VD and ω3 supplementation, alone or in combination, significantly improved endothelial function and mitigated the adverse effects of an HFHS diet. The combination did not show clear additive effects. These findings suggest their potential as therapeutic strategies for managing obesity-related cardiovascular issues.</div></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"9 ","pages":"Article 100240"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145681173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin combined with antineoplastic drugs or natural products for cancer treatment: An update","authors":"Cristina Trejo-Solís ,&nbsp;Irma Susana Rojas-Tomé ,&nbsp;Helgi Jung-Cook ,&nbsp;Francisca Palomares-Alonso","doi":"10.1016/j.crphar.2025.100239","DOIUrl":"10.1016/j.crphar.2025.100239","url":null,"abstract":"<div><div>Drug combinations have shown promise in suppressing drug resistance, improving drug efficacy, and reducing side effects in anticancer therapy. Considering that the anticancer activity of melatonin may be due to its antiproliferative, antioxidant, and immunomodulatory activities, the combined administration of this endogenous indoleamine with anticancer drugs has been extensively explored. This review provides an overview of the advances in the last five years in the anticancer activity of melatonin in combination with synthetic drugs and natural products. Papers on this topic were searched in PubMed, Google Scholar, Cochrane, and Scopus within the period 2018–2024. A total of 47 papers were retrieved showing a synergistic antitumor effect of melatonin combined with different drugs in the treatment of breast, colorectal, prostate, gastric, thyroid, and pancreatic cancer, as well as in head and neck squamous cell carcinoma, melanoma, and glioblastoma. The evidence gathered in this review will contribute to our knowledge of the use of melatonin. In addition, it may allow us to develop novel approaches to the treatment of cancer to be evaluated in preclinical and/or clinical trials.</div></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"9 ","pages":"Article 100239"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145568491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fragment-based drug discovery: A graphical review","authors":"Dana F. AlKharboush ,&nbsp;Frank Kozielski ,&nbsp;Geoffrey Wells ,&nbsp;Exequiel O.J. Porta","doi":"10.1016/j.crphar.2025.100233","DOIUrl":"10.1016/j.crphar.2025.100233","url":null,"abstract":"<div><div>Three decades after its introduction, fragment-based drug (or lead) discovery (FBDD or FBLD) has become a mature and powerful strategy for generating novel leads, offering distinct advantages for challenging or previously “undruggable” targets where traditional screening (e.g., high throughput screening) often fails. The FBDD approach identifies low molecular weight fragments (MW &lt; 300 Da) that bind weakly to a target; these interactions are detected using highly sensitive biophysical methods such as NMR, X-ray crystallography, and SPR. These initial hits are then optimised into potent leads through structure-guided strategies, including fragment growing, linking, or merging. This graphical review illustrates the modern FBDD workflow, highlighting the critical integration of experimental and computational methods. We discuss how innovations in library design, hybrid screening platforms, and the application of AI/ML are accelerating discovery cycles and improving hit validation. The power of this approach is demonstrated through case studies of FDA-approved drugs, including Vemurafenib and Venetoclax, which progressed from simple fragments to transformative medicines. Finally, we provide an outlook on the future of FBDD as it continues to evolve with emerging technologies to push the boundaries of drug discovery.</div></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"9 ","pages":"Article 100233"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145044499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The suppression of the SPHK1/S1P/S1PR3 signaling pathway diminishes EGFR activation and increases the sensitivity of non-small cell lung cancer to gefitinib","authors":"Jing Zhang ,&nbsp;Zequn Wang ,&nbsp;Xihua Wei ,&nbsp;Mengyuan Han ,&nbsp;Ribai Yan ,&nbsp;Lijie Ma ,&nbsp;Yan Pan","doi":"10.1016/j.crphar.2024.100212","DOIUrl":"10.1016/j.crphar.2024.100212","url":null,"abstract":"<div><div>Non-small-cell lung cancer (NSCLC) represents a predominant histological subtype of lung cancer, characterized by high incidence and mortality rates. Despite significant advancements in therapeutic strategies and a deeper understanding of targeted therapies in recent years, tumor resistance remains an inevitable challenge, leading to poor prognostic outcomes. Several studies have indicated that sphingosine kinase 1 (SPHK1) plays a regulatory role in epidermal growth factor receptor (EGFR) signaling, and its elevated expression may be associated with resistance to EGFR tyrosine kinase inhibitors (EGFR-TKIs). Furthermore, the catalytic product of SPHK1, sphingosine 1-phosphate (S1P), along with its receptor, sphingosine 1-phosphate receptor 3 (S1PR3), plays a regulatory role in the function of the EGFR. However, the specific effects of the SPHK1/S1P/S1PR3 axis on EGFR in NSCLC, as well as the combined effects of SPHK1/S1P/S1PR3 inhibitors with the EGFR-TKI gefitinib, remain to be elucidated. In the present study, we investigated the correlation between SPHK1 expression levels and the survival rates of NSCLC patients, the relationship between SPHK1 or S1PR3 and EGFR, and the impact of SPHK1 expression on the half-maximal inhibitory concentration (IC₅₀) of gefitinib in NSCLC. In A549 cells, the phosphorylation of EGFR was significantly reduced following SPHK1 knockdown. Utilizing SPHK1/S1P/S1PR3 inhibitors, namely PF543, TY52156, and FTY720, we established that the SPHK1/S1P/S1PR3 axis modulates EGFR activation in NSCLC. Furthermore, these signaling inhibitors enhanced the anti-proliferative efficacy of the EGFR-TKI gefitinib. RNA sequencing analysis revealed substantial alterations in 85 differentially expressed genes in NSCLC cells treated with the combination of FTY720 and gefitinib. These genes were predominantly associated with pathways such as axon guidance, microRNAs in cancer, and the JAK-STAT signaling pathway, among others. Overall, targeting the SPHK1/S1P/S1PR3 signaling pathway represents a promising therapeutic strategy to enhance gefitinib sensitivity in NSCLC.</div></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"8 ","pages":"Article 100212"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11787445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ABCC1 and ABCC10 as predictive biomarkers of docetaxel treatment response in prostate cancer","authors":"Nandi Ngesi ,&nbsp;Beynon Abrahams ,&nbsp;Aubrey Shoko ,&nbsp;Mamello Sekhoacha","doi":"10.1016/j.crphar.2025.100216","DOIUrl":"10.1016/j.crphar.2025.100216","url":null,"abstract":"<div><div>Prostate cancer (PCa) is a leading global health burden, with a particularly high prevalence in South Africa. Despite therapeutic advancements, chemoresistance remains a major challenge, limiting the efficacy of docetaxel and contributing to treatment failure and disease progression. Multidrug resistance (MDR), primarily mediated by ATP-binding cassette (ABC) transporters such as ABCC1 and ABCC10, has been implicated in reduced chemotherapy effectiveness. This study aimed to evaluate the association between ABCC1 and ABCC10 expression levels and docetaxel treatment response in PCa patients. A retrospective case-control study was conducted using pre-treated formalin-fixed paraffin-embedded (FFPE) tissue biopsies from PCa patients. Patients were classified into good responders (cases) and poor responders (cases) based on treatment outcomes. For each patient, tumour and adjacent normal sections were excised from FFPE samples, with normal sections serving as the control group. RNA was extracted and subjected to quantitative real-time PCR (qRT-PCR) to assess ABCC1 and ABCC10 expression levels. ABCC1 and ABCC10 were significantly upregulated in tumour sections of poor responders, whereas good responders exhibited downregulated expression in tumour sections. Importantly, normal tissue sections (controls) displayed significantly lower expression levels of both transporter genes compared to tumour sections. The overexpression of ABCC1 and ABCC10 in tumour tissues, particularly in poor responders, suggests their potential role in mediating docetaxel resistance. These findings highlight ABCC1 and ABCC10 as potential predictive biomarkers for docetaxel treatment response in PCa, warranting further investigation in prospective clinical studies.</div></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"8 ","pages":"Article 100216"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143705523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}