Current drug targets最新文献

{"title":"(E)-Labda dial-Loaded Nanoparticles for Triple Negative Breast Cancer.","authors":"Anum Munir, Muhammad Rizwan, Alan Janbey","doi":"10.2174/0113894501439423251224072750","DOIUrl":"https://doi.org/10.2174/0113894501439423251224072750","url":null,"abstract":"<p><strong>Introduction: </strong>Triple-negative breast cancer (TNBC) is the most aggressive kind of breast cancer, with no hormone receptors and resistance to targeted therapy. Chemotherapy is the current standard; however, it is limited by toxicity, poor response, and high recurrence, emphasising the need for innovative methods.</p><p><strong>Methods: </strong>This study investigates the therapeutic potential of (E)-labda-8(17), 12-diene-15,16-dial ((E)-labda dial), a bioactive chemical found in Curcuma amada (mango ginger) that was formulated into nanoparticles to increase transport and effectiveness. Whole-genome sequencing of TNBC cell lines was used to detect protein-altering mutations, which were then assessed using molecular docking and dynamics simulations to assess (E)-labda dial interactions with key mutant proteins (BRCA1, BRCA2, BARD1, PALB2, TP53, CHEK2). Lipid-based nanoparticles (LNPs) and polymeric nanoparticles (PNPs) were developed and tested for drug encapsulation, release kinetics, and stability. MTT and other functional tests were used to assess cytotoxic effects, and in silico pharmacokinetic models were carried out to anticipate treatment results.</p><p><strong>Results: </strong>Results showed that PNPs outperformed LNPs in terms of encapsulation efficiency, sustained drug release, and tumour inhibition. Docking investigations demonstrated that mutant CHEK2, BARD1, and PALB2 bind to (E)-labda dial more strongly, indicating that carcinogenic pathways may be disrupted.</p><p><strong>Discussion: </strong>These data, taken together, emphasise the abilities of (E)-labda dial-loaded nanoparticles as a targeted treatment method for TNBC, with potential effectiveness and toxicity benefits over traditional chemotherapy.</p><p><strong>Conclusion: </strong>This work lays the basis for precision and personalised treatment for TNBC patients. However, future optimisation and clinical validation of these nanoparticles can be done in future to determine their translational potential for use in practice.</p>","PeriodicalId":10805,"journal":{"name":"Current drug targets","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Review on Chalcone as Carbonic Anhydrase Inhibitors.","authors":"Sapna Sivanthie Suresh Kumar, Sachithra Thazhathuveedu Sudevan, Sunil Kumar, Naseer Maliyakkal, Leena K Pappachen, Bijo Mathew","doi":"10.2174/0113894501446010260319103143","DOIUrl":"https://doi.org/10.2174/0113894501446010260319103143","url":null,"abstract":"<p><p>Over the last decade, research on Carbonic Anhydrases (CAs) has focused on designing and developing novel inhibitors that are specific to certain isoforms to prevent non-specific binding. Many studies have employed computer-assisted drug design to develop selective inhibitors, including non-zinc binding inhibitors. Discrimination of selectivity and bioavailability, along with decreased toxicity optimization, is still lacking. Understanding of isoform-specific structural variation and the lack of corresponding resistance mechanisms, as well as further studies on allosteric modulation and novel binding interactions, are needed. The aim of this review is to investigate the link between chalcone structures and CA inhibition and explore their potential as selective inhibitors. Structural modifications with diverse functional groups are thought to bridge gaps in the discovery of chalcone-based carbonic anhydrase inhibitors. The study emphasizes further exploration of the development of chalcone-based carbonic anhydrase inhibitors.</p>","PeriodicalId":10805,"journal":{"name":"Current drug targets","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147627284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Glues for Undruggable Targets: Mechanisms, Clinical Applications, and AI-driven Design.","authors":"Zike Chen, Wenying Meng, Mengyan Chen, Chen Wang, Min Shi","doi":"10.2174/0113894501451027260305032128","DOIUrl":"https://doi.org/10.2174/0113894501451027260305032128","url":null,"abstract":"","PeriodicalId":10805,"journal":{"name":"Current drug targets","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147618552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PTP1B Inhibitors for Type 2 Diabetes: From Natural Products, Synthetic Inhibitors, and Multi-Target Drug Design Strategies to Clinical Translation.","authors":"Pallavi Joshi, Avijit Mazumder, Bhavani Pentela, Abhijit Debnath","doi":"10.2174/0113894501447162260311053819","DOIUrl":"https://doi.org/10.2174/0113894501447162260311053819","url":null,"abstract":"<p><strong>Introduction: </strong>Type 2 Diabetes Mellitus (T2DM) still exists as a worldwide health problem, and the current therapeutic options have selectivity and bioavailability issues. Protein Tyrosine Phosphatase 1B (PTP1B) emerged as an important therapeutic target for T2DM.</p><p><strong>Methods: </strong>In this study, we analyzed all publications between 2021 and 2025 available in the Scopus database, and the search was limited to English-language articles that were also indexed in PubMed. The search strategy employed multiple keyword combinations, including \"PTP1B\" OR \"Protein Tyrosine Phosphatase 1B\" OR \"PTPN1\", combined with inhibitor, drug discovery, type 2 diabetes, insulin resistance, and structural biology terms.</p><p><strong>Results: </strong>Natural products from plant, marine, and microbial sources demonstrate diverse PTP1B inhibitory mechanisms through their active compounds, which include terpenoids, flavonoids, alkaloids, and diarylheptanoids. The development of synthetic approaches that combine thiazole derivatives with coumarin-based compounds and peptide inhibitors has produced promising scaffolds. The researchers used computational methods to find new allosteric binding sites through molecular docking and molecular dynamics simulations. The four clinical candidates Ertirprotafib, Trodusquemine, ISIS-113715, and JTT-551 all failed because their selectivity and efficacy were insufficient, but the dual PTPN2/PTPN1 inhibitor ABBV-CLS-484 shows oncology treatment potential.</p><p><strong>Discussion: </strong>Beyond diabetes, PTP1B inhibition shows medical value for cancer immunotherapy treatment, together with neurodegenerative disorders, inflammation, and cardiovascular diseases. The development of PROTAC degraders, glycosylation-lipidation modifications, and multi-target inhibitors represents a new approach to solving past problems.</p><p><strong>Conclusion: </strong>The development of PTP1B inhibitors requires integrated approaches that include allosteric modulation, tissue-specific delivery, and patient stratification to achieve successful clinical translation across multiple disease indications.</p>","PeriodicalId":10805,"journal":{"name":"Current drug targets","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in Target Identification and Drug Development for Depression.","authors":"Kaixuan Hu, Xinmin Wang, Wentong Yu, Qiyue Liu, Yan Cheng, Yuting Song, Li Liang, Wei Liu, Junping Zhang, Shan Chang, Jianping Hu","doi":"10.2174/0113894501438555260211105139","DOIUrl":"https://doi.org/10.2174/0113894501438555260211105139","url":null,"abstract":"<p><p>Depression is a prevalent mental disorder that is devastating to mental health. The high prevalence and multifactorial nature of causation pose significant challenges for developing effective treatment strategies. This review provides a first approach survey of the epidemiological nature of depression. It then attempts to delineate the interrelated biological, psychological, and environmental factors that stimulate its pathogenesis. Both traditional and new clinical and basic research therapeutic targets that are taking center stage today are highlighted. A review of the evolution of different antidepressant drugs targeting these molecular targets is provided. Emphasis is placed on current developments in Quantitative Structure-Activity Relationship (QSAR) modeling. A detailed study of representative compounds shows critical structure-activity relationships useful for designing effective drugs. We also consider some of the murine models of depression that are not particularly new, their applicability, and their limitations across various research environments. A particular barrier that is highlighted as an issue in the delivery of new antidepressant agents is the Blood-Brain Barrier (BBB). Creative methods of enhancing penetration of the central nervous system are also discussed. In general, this review provides a rational and prospective review of mechanistic literature and treatment innovation in non-depression studies.</p>","PeriodicalId":10805,"journal":{"name":"Current drug targets","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147608373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systematic Identification and Characterization of Causal Risk Genes Implicated in Colorectal Cancer by Integrating GWAS, eQTL, and mQTL Data.","authors":"Shuai Xu, Guanglin Guo, Jie Gao, Zhou Fang, Lu Chai, Yuanyuan Gao, Junjie Liu, Jun Wang, Siqinbateer, Lirong Zhang","doi":"10.2174/0113894501444884260130225445","DOIUrl":"https://doi.org/10.2174/0113894501444884260130225445","url":null,"abstract":"<p><strong>Introduction: </strong>Knowledge of the mechanisms through which common single-nucleotide polymorphisms (SNPs) modulate colorectal cancer (CRC) susceptibility is central to elucidating the molecular basis of this disease. Genome-wide association studies (GWAS) reveal noncoding SNPs influencing CRC susceptibility, yet their functional mechanisms, particularly through gene expression dysregulation, DNA methylation alterations, and interactions with gut microbiota, remain uncharacterized. Through integrative analysis, systematically exploring the effects of genetic variations on gene expression heterogeneity, DNA methylation, and gut microbiome is expected to yield potential biomarkers for early diagnosis and intervention of CRC.</p><p><strong>Methods: </strong>An integrative framework is developed to prioritize causal risk genes at CRC-associated GWAS loci, applying the SMR&HEIDI (Summary-data-based Mendelian randomization and heterogeneity in dependent instruments) and TSMR (Two-sample Mendelian Randomisation) methods. The findings were validated via gene expression and TF binding affinity.</p><p><strong>Results: </strong>10 tissue-specific gene-SNP pairs, 3 blood eQTL-gene pairs, 26 gene-CpG-SNP regulatory modules, and 39 microbiota-associated gene-SNP pairs are identified. A few potential regulatory influences on CRC development associated with genes and variants, such as POU5F1B and rs10797801, were identified. Moreover, the genetic variants disrupted TF binding affinity while only a few promoted the binding of transcription factors (TFs).</p><p><strong>Discussion: </strong>The data integration enabled us to prioritize genes according to different regulatory mechanisms, such as gene expression and DNA methylation, and bridge the gap between statistical associations and biological functionality.</p><p><strong>Conclusion: </strong>Multi-omics integration reveals some causal risk genes and variants implicated in CRC. These findings offer novel insight into the molecular mechanisms underlying CRC susceptibility and provide valuable clues for diagnosis and therapeutic intervention strategies.</p>","PeriodicalId":10805,"journal":{"name":"Current drug targets","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147608337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating Alternative Treatments for Dyslipidemia Using Bioactive Compounds Derived from Kiwifruit (Actinidia chinensis): A Network Pharmacology, Molecular Docking, and Molecular Dynamics Simulation Analysis.","authors":"Itzel Zamudio-Felix, Karina González-Becerra, Fernando Martínez-Esquivias, Oscar Daniel Oviedo-Tapia, Antistio Anibal Alviz-Amador, Mario Isiordia-Espinoza, Juan Manuel Guzmán-Flores","doi":"10.2174/0113894501424607260119062949","DOIUrl":"https://doi.org/10.2174/0113894501424607260119062949","url":null,"abstract":"<p><strong>Introduction: </strong>Kiwi has many bioactive compounds that may improve blood lipid levels and help treat dyslipidemia, but its molecular mechanism is not fully understood. This study explores these mechanisms using pharmacological network analysis.</p><p><strong>Methods: </strong>Bioactive compounds of kiwi were obtained from the IMPPAT website, and molecular targets were identified using Swiss Target Prediction and PharmMapper. Genes associated with dyslipidemia were searched in the DISGENET database. Subsequently, an enrichment analysis was conducted, and a protein-protein interaction network was constructed. Hub genes were identified. Subsequently, a molecular docking analysis was performed, followed by a molecular dynamics simulation.</p><p><strong>Results: </strong>Six bioactive compounds in kiwifruit showed good oral bioavailability and drug-likeness. Thirty-five genes linked to dyslipidemia and kiwi's targets were identified. Enrichment analysis highlighted the PPAR signaling pathway, lipid metabolism, and atherosclerosis. Hub genes included ALB, PPARG, AKT1, MMP9, PPARA, HMGCR, GSK3B, NOS3, PPARD, ACE, JAK2, and DPP4, with their interactions verified by molecular docking. Interactions between JAK2, ACE, and bioactive compounds (quinic acid and citric acid) involved spontaneous binding. Molecular dynamics simulations assessed conformational stability, mobility, solvation, and compaction of top-scoring protein-compound complexes.</p><p><strong>Discussion: </strong>Bioactive compounds in kiwifruit can modulate dyslipidemia via PPAR pathways, JAK2, and ACE, supported by docking analyses and simulations. They show therapeutic potential, pending experimental validation.</p><p><strong>Conclusion: </strong>Our findings suggest how kiwi affects dyslipidemia. In silico analysis is a first step in exploring food compounds like kiwi as potential alternative treatments.</p>","PeriodicalId":10805,"journal":{"name":"Current drug targets","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147608360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E2 Protein of Chikungunya Virus: A Narrative Review of Its Potential as a Therapeutic Target.","authors":"Kelly Megumi Yaekashi, Jessica Aparecida Carneiro, Geovana Martelossi-Cebinelli, Mariana Marques Bertozzi, Mariana Stinglin Rosa Ribas, Camila Zanluca, Claudia N Duarte Dos Santos, Rubia Casagrande, Waldiceu A Verri","doi":"10.2174/0113894501436868260120100843","DOIUrl":"https://doi.org/10.2174/0113894501436868260120100843","url":null,"abstract":"<p><strong>Introduction: </strong>Chikungunya Virus (CHIKV), an enveloped RNA virus transmitted by Aedes mosquitoes, has become an increasing global health concern, particularly in South America, where cases and fatalities have risen (PAHO, 2023). This review focuses on therapeutic strategies targeting the CHIKV E2 protein, including vaccines, antibodies, and antiviral approaches tested in vitro and in vivo.</p><p><strong>Methods: </strong>Literature reporting on the E2 protein, including studies on viral structure, host interactions, symptoms, and treatments under development, was analyzed.</p><p><strong>Results: </strong>The E2 protein, a major structural component of CHIKV, is critical for viral entry and virulence, mediating interactions with host factors (Glycosaminoglycans (GAGs) and C-type lectins) and receptors (Matrix Remodeling-Associated Protein 8 (Mxra8) and Prohibitin-1 (PHB1)). It also elicits robust antibody responses, making it a key target for therapeutic intervention.</p><p><strong>Discussion: </strong>The E2 protein is essential for CHIKV entry and virulence, making it a key target for vaccines, antibodies, and antivirals. While preclinical studies show promise, efficacy varies and clinical translation remains limited. Challenges include viral diversity, immune escape, and the need for integrated strategies combining different therapeutic approaches.</p><p><strong>Conclusion: </strong>Given the absence of licensed vaccines and antivirals for alphaviruses, the E2 protein represents a promising therapeutic target while inhibiting E2 could block viral entry and infection. However, current strategies show variable efficacy and inconclusive results, highlighting the need for further research to validate and optimize E2-targeted therapies.</p>","PeriodicalId":10805,"journal":{"name":"Current drug targets","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147510310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research on the Anti-breast Hyperplasia Mechanism of Liqi Sanjie Granules Based on Network Pharmacological Analysis and Experimental Verification.","authors":"Xionghui Hu, Xun Liu, Rensong Yan, Xianhai Li, You Zhou, Fei Chen, Min Xu, Cheng Xiao, Yi Wang, Zhang Wang, Yao Liu, Bingguang Zhong, Xiaoqi Hu, Qing Zhou, Tanjun Wei","doi":"10.2174/0113894501441176260118230500","DOIUrl":"https://doi.org/10.2174/0113894501441176260118230500","url":null,"abstract":"<p><strong>Background: </strong>Breast hyperplasia has become a major public health challenge due to changes in dietary patterns. However, there is still a lack of effective pharmacotherapy for Breast hyperplasia.</p><p><strong>Methods: </strong>The chemical components of Liqi Sanjie Granules (LSG) were quantified through HPLC. Three key components were screened out by combining network pharmacology methods and experimental determination methods, whereas key components in sera were quantified through LC-MS. The potential molecular mechanisms of LSG and these three blood-entering chemicals for the treatment of breast hyperplasia were predicted by network pharmacology. Estradiol benzoate and progesterone were injected intramuscularly to establish a breast hyperplasia model. Serum estradiol (E2), progesterone (P), testosterone (T), and prolactin (PRT) were detected by ELISA. H&E was used in monitoring the hyperplasia of rat mammary gland tissues. Immunohistochemistry and RT-PCR were used to detect the protein and mRNA expression levels of estrogen receptors (ERs) and progesterone receptors (PR) in rat mammary glands.</p><p><strong>Results: </strong>The contents of seven components in LSG were quantified. After administration, the levels of paeoniflorin, glycyrrhizin, and ferulic acid were 280.16 ± 64.77, 101.87 ± 7.88, and 253.28 ± 17.64 μg per 200 μL, respectively. Network pharmacology studies have shown that LSG treats breast hyperplasia by acting on 63 targets in 36 signaling pathways, and the blood-entering chemicals of LSG involve 18 potential targets and 5 signaling pathways. Histopathological analysis revealed that rats in the LSG group had fewer mammary lobules and acini. Additionally, the proliferation of glandular epithelial cells was reduced. No significant changes were found in the serum levels of E2, P, PRT, and T in the LSG group. Concurrently, LSG can reduce the expression levels of PR protein and the mRNA of ESR1 and PGR in the rat mammary glands.</p><p><strong>Discussion: </strong>This study suggests that the blood-entering chemicals paeoniflorin, glycyrrhizin, and ferulic acid may alleviate breast hyperplasia through decreasing the expression levels of ER, ESR1, and PGR in the mammary tissues, reducing the number of mammary lobules and alveoli, and inhibiting pathological changes in vacuolar degeneration, hyperplasia, and detachment of glandular epithelial cells.</p><p><strong>Conclusions: </strong>This study quantitatively analysed the seven chemical components of LSG and determined the contents of paeoniflorin, glycyrrhizin, and ferulic acid in the medicated serum. Furthermore, it demonstrates that LSG improves breast hyperplasia by regulating ER and PR expression levels.</p>","PeriodicalId":10805,"journal":{"name":"Current drug targets","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147510373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bee Venom and Cancer: A Mini-review Focusing on Melittin Antitumoral Effects.","authors":"Ana Maria Boaventura de Oliveira, Tatiane Roquete Amparo, Morena Brazil Martins Sant'Anna, Gisele Picolo, Tamires Cunha Almeida","doi":"10.2174/0113894501424902260115203324","DOIUrl":"https://doi.org/10.2174/0113894501424902260115203324","url":null,"abstract":"<p><p>Cancer remains a major concern, accounting for one in six deaths globally. Developing effective treatments is challenging due to the complex mechanisms involving environmental, genetic, and epigenetic factors. Animal toxins have been utilized as pharmacological agents for treating several diseases. Among these compounds, melittin, derived from bee venom, exhibits significant therapeutic potential against cancer. This efficacy is attributed to its multifaceted nature, enabling it to function as a multi-target modulator of oncogenic signaling pathways and exert a broad spectrum of anticancer effects. In vitro studies have demonstrated that melittin treatment reduces cell viability, adhesion, clonogenic survival, migration, and invasion in various cancer cell types. Additionally, in vitro experiments have demonstrated that melittin induces apoptosis through multiple mechanisms, such as upregulating TNF-α and BAX, triggering ferroptosis, activating the mitochondrial pathway, initiating endoplasmic reticulum stress, and inhibiting METTL3. Furthermore, in vivo assays indicate that melittin reduces angiogenesis and tumor growth, enhances the effects of chemotherapy, and prolongs survival. The effects of melittin on the tumor microenvironment, modulation of the epigenetic process, and inhibition of the epithelial-mesenchymal transition have also been demonstrated. Overall, melittin shows potential as a therapeutic agent for breast, lung, gastric, cervical, colorectal, and bladder cancers by targeting multiple pathways involved in cancer progression. Moreover, other bee venom components, such as apamin and bee venom phospholipase A2, also exhibit potential anticancer effects. In this review, a comprehensive overview of the various actions of melittin and other components of bee venom on different types of cancer is provided. The research discusses their mechanisms of action and potential strategies to enhance efficacy and minimize toxicity.</p>","PeriodicalId":10805,"journal":{"name":"Current drug targets","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147510337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}