Search Results (2,771)

Background: Drug repurposing represents an accelerated and cost-effective approach to discovering novel oncologic therapeutics. Here, we investigated the anticancer potential and underlying mechanisms of marbofloxacin (MBF), a veterinary fluoroquinolone (FQ), against breast cancer (BC) cells. Methods: The cellular impacts of MBF on cell viability, anchorage-dependent growth, tumorigenicity, migration, apoptosis, proliferation, senescence, and mitochondrial function were thoroughly characterized. To further elucidate its mechanistic activity, real-time qRT-PCR, untargeted LC-MS/MS-based metabolomics, network pharmacology, and molecular docking analysis were integrated. Results: MBF suppressed BC cell growth by inhibiting cellular proliferation and migration, disrupting mitochondrial membrane potential, and inducing ROS-mediated apoptosis and irreversible cellular senescence. These phenotypic impacts were accompanied by upregulation of tumor suppressors such as CDKN1A and PUMA and downregulation of oncogenes including MKI67, BIRC5, and BCL-2. Metabolomic analysis revealed broad suppression of biosynthesis-related metabolic pathways, characterized by the depletion of critical polyamines and nucleotide pathways. Network pharmacology and molecular docking analyses identified EGFR and HSP90AA1 as putative hub proteins potentially associated with the observed anticancer phenotype. Conclusions: These results provide initial evidence that MBF induces metabolic and molecular rewiring in BC, highlighting its promise as a repositionable therapeutic candidate. Full article

Pyridopyrimidine is an important heterocyclic scaffold widely explored in anticancer drug discovery. Its structural similarity to purine enables effective interaction with various biological targets, mainly kinases involved in cancer progression. This manuscript presents recent developments reported between 2021 and 2026, focusing on the biological evaluation, and structure–activity relationships of pyridopyrimidine derivatives. Many of these synthesized compounds act as inhibitors of key targets such as EGFR, CDK4/6, and the PI3K/mTOR pathway, which are closely associated with tumor growth, survival, and resistance mechanisms. Other targets such as ATR and PIM are also explored. Recent studies show that structural modifications, including substitution on the core ring and hybridization with pharmacologically active moieties like triazoles and thiazolidinediones, significantly improve anticancer activity. Several derivatives have demonstrated strong antiproliferative effects against different cancer cell lines and are capable of inducing apoptosis and cell cycle arrest. In addition, molecular docking and other computational studies support their binding efficiency and help explain their mechanisms of action. There is also increasing interest in the development of dual-target or multi-target inhibitors to overcome drug resistance and enhance therapeutic effectiveness. Overall, pyridopyrimidine- and pyridopyrimidinones-based compounds continue to show great promise as potential anticancer agents. Further research combining synthetic chemistry, biological studies, and computational approaches may lead to the development of more effective and safer drugs in the future. Full article

Advances in anticancer therapies have substantially improved cancer survival but have also highlighted the growing challenge of cancer therapy-related cardiac dysfunction. Ferroptosis, an iron-dependent form of regulated cell death characterized by iron dysregulation, lipid peroxidation, and impaired antioxidant defense, has emerged as a promising strategy for eliminating therapy-resistant tumors. However, the lack of tissue specificity in ferroptosis regulation raises concerns regarding its potential contribution to cardiovascular injury during anticancer treatment. This review summarizes the dual roles of ferroptosis in cancer biology and cardio-oncology. We first discuss the molecular mechanisms governing ferroptosis, including iron metabolism, lipid peroxidation, and antioxidant defense systems. We then highlight the context-dependent roles of ferroptosis in tumor progression, immune regulation, and metabolic adaptation. Furthermore, we systematically review how chemotherapy, targeted therapy, immunotherapy, and radiotherapy contribute to ferroptosis-associated cardiovascular toxicity. Finally, we discuss emerging approaches to minimize cardiac injury, including tissue-specific ferroptosis-targeting and cardioprotective strategies. Understanding tissue-specific ferroptosis regulation may facilitate the development of safer and more precise therapeutic approaches in cardio-oncology. Full article

Breast cancer cells exhibit a reversed pH gradient and metabolic plasticity that promote proliferation, invasion, and resistance to therapy. Natural products such as chlorogenic acid (CGA) and cinnamaldehyde (CA) have shown emerging anticancer potential. However, their effects on intracellular pH and metabolic transport systems remain undefined. Therefore, the aim of this study was to characterize these parameters in breast cancer and non-tumorigenic breast cells. This study evaluated the physiochemical properties of CGA and CA using LC–MS, under pH conditions (pH 1.2, 7.4, and 9.0) mimicking the gastrointestinal track (GIT). Additionally, LC–MS-based human liver microsome (HLM) assays with NADPH were used to evaluate susceptibility to CYP-mediated metabolism to evaluate first-pass metabolic stability. Intracellular uptake kinetics were quantified at multiple time points using LC–MS. Following CGA:CA treatment, intracellular pH (pH_i) was measured in cancerous MDA-MB-231 and non-tumorigenic MCF-10A breast cell lines using SNARF-1 targeted ratio-metric fluorescence approach. Expression of OATP1B1, GLUT1, and MCT1 were analyzed by Western and immunofluorescence respectively, to assess potential cellular uptake of CGA:CA through OATP1B1 and their effects on glucose uptake and lactate and proton transport. Physiochemical results demonstrated that the compounds ranged from fully stable (pH 1.2 and 7.4) to completely unstable (pH 9.0). HLM incubation indicated no CYP-mediated hepatic metabolism. Treatment results showed that there was rapid intracellular uptake of CGA and CA in cancer cells and that CGA:CA lowered pH_i in both MDA-MB-231 and MCF-7 cells, while pH_i remained mostly unchanged in MCF-10A cells. Protein analysis revealed that CGA:CA treatment downregulated GLUT1 and MCT1 expression in cancer cells, suggesting impaired glycolytic activity and lactate shuttling. OATP1B1 expression was significantly suppressed in cancer cells, suggesting feedback inhibition of the solute carrier protein. Collectively, these findings indicate that CGA and CA exhibit favorable biochemical stability and disrupt intracellular pH regulation and metabolic transporter expression in breast cancer cells. Importantly, normal cells are not significantly affected. Thus, CGA:CA demonstrates therapeutic potential for breast cancer through pH_i and metabolic modulation. Full article

Lupins have been cultivated since ancient times. Poland ranks second in the world in terms of lupin cultivation area (second only to Australia), particularly for narrow-leaved lupin. It is used in various industries. The purpose of this review is to analyze data on the chemical composition of narrow-leaved lupin in comparison with other species of this genus, as well as to identify its potential applications. The literature data characterize narrow-leaved lupin in terms of its content of protein, lectins, fat, carotenoids, phytosterols, fiber, sugars, alkaloids, vitamins, flavonoids, phenolic compounds, volatile organic compounds, and micro- and macronutrients. Due to its interesting qualitative and quantitative composition, this species may play a significant role in human nutrition—not only as an alternative source of protein, but above all as a source of health-promoting compounds. Studies conducted on humans and animals have demonstrated a wide range of biological effects, including anti-inflammatory, antioxidant and cholesterol-lowering effects. In addition, in vitro studies suggest anticancer effects. Among the tangible outcomes of research and commercialization efforts is the availability on the consumer market of food and cosmetic products containing lupin. Due to its properties, this species has a wide range of applications. However, to meet the requirements of various industrial sectors, a collaborative approach is necessary among plant breeders, scientists, and industry representatives working to improve this species. Only through joint efforts can the use of narrow-leaved lupin be expanded. Full article

Quinoline is a bicyclic aromatic heterocycle composed of a fused benzene and pyridine ring, and it has held an important place in medicinal chemistry for nearly two centuries. F. Runge first isolated it from coal tar in 1834, and it was later found to form the structural core of well-known natural products such as quinine, camptothecin, and γ-fagarine. Its asymmetric electron distribution, amphoteric character, and ability to undergo both electrophilic and nucleophilic substitution confer considerable pharmacophoric versatility on the quinoline scaffold. This review covers the chemistry and therapeutic relevance of quinoline derivatives, with an emphasis on their pharmacological significance rather than on their synthesis alone. It begins with a brief account of the scaffold’s structural features and main synthetic routes, then examines the biological activities reported for quinoline-based compounds, including antibacterial, anticancer, anti-inflammatory, antimalarial, antiparasitic, antitubercular, antioxidant, and antiviral activities, together with structure–activity relationships discussed at the level of specific ligand–target interactions where data allow. The last section covers more recent directions in quinoline-based drug discovery, including PROTAC degraders, kinase inhibitors, and multitarget-directed ligands, an area not extensively addressed in earlier reviews of this scaffold. The literature surveyed here shows that quinoline derivatives continue to serve as a versatile scaffold for generating new leads, linking established synthetic chemistry with current mechanistic and computational approaches. The continued diversification of quinoline-based chemotypes and their biological mechanisms reinforces the importance of this scaffold as a versatile platform for medicinal chemistry and drug discovery. Full article

Cancer-associated thrombosis (CAT) is defined as venous or arterial thrombotic events occurring in patients with active malignancy or during anticancer treatment, most commonly presenting as venous thromboembolism and representing a leading cause of morbidity and mortality in oncology. Hormone-sensitive malignancies, including breast, ovarian, and endometrial cancers, are characterized by a complex interaction among tumor biology, endocrine signaling, inflammation, endothelial dysfunction, and coagulation activation. In these malignancies, venous thromboembolism (VTE) risk is influenced not only by intrinsic tumor-related mechanisms but also by patient-specific factors and anticancer therapies, particularly endocrine treatments, chemotherapy, targeted agents, and extensive surgical procedures. Breast cancer is generally associated with an intermediate thrombotic risk, although endocrine therapy—especially tamoxifen—significantly increases VTE incidence. Ovarian cancer represents one of the most thrombogenic solid tumors because of elevated tissue factor expression, inflammatory activation, advanced-stage presentation, and aggressive multimodal treatment strategies. Endometrial cancer exhibits a strong association with obesity, metabolic syndrome, prolonged estrogen exposure, and perioperative thrombotic complications. Emerging evidence highlights the role of immune-thrombosis, extracellular vesicles, inflammatory cytokines, and sex-specific coagulation pathways in cancer-associated hypercoagulability. Current guidelines increasingly support individualized thromboprophylaxis based on tumor biology, patient-specific risk factors, and bleeding risk assessment. This review summarizes the biological mechanisms linking hormones and thrombosis in breast and gynecologic cancers, discusses current evidence regarding VTE risk factors and treatment-related thrombotic complications, and explores modern approaches to biomarkers, risk stratification, and personalized thromboprophylaxis. Full article

Background: Rosuvastatin, a potent lipid-lowering statin, and curcumin, a bioactive naturally occurring polyphenolic phytochemical, both show pleiotropic antioxidant and anti-inflammatory properties. In addition, curcumin shows also antimicrobial, anticancer, hypolipidemic and antifibrotic effects. From the pharmacodynamic point, rosuvastatin and curcumin target overlapping molecular pathways—suggesting possible pharmacodynamic synergy that has emerged as a promising therapeutic approach in the management of various diseases, including cardiovascular, metabolic, kidney, and inflammatory diseases. Objectives: This review aimed to systematically summarize and critically evaluate all available preclinical data concerning the combined use of rosuvastatin and curcumin, emphasizing their possible synergistic effects. Methods: A total of seven preclinical studies that investigated the combination of curcumin and rosuvastatin, three in vitro and four in vivo, conducted between 2017 and 2025, were included in the analysis. Results: While in vitro studies suggested a promising synergy in lipid-lowering, antioxidant, and anti-inflammatory effects, in vivo findings confirmed enhanced lipid-lowering effects, potential hepatoprotection and nephroprotection when two agents are co-administered. In addition to pharmacodynamic interaction, pharmacokinetic studies also revealed that curcumin may increase systemic rosuvastatin exposure by inhibiting hepatic transporters, warranting further investigation into dosing and safety of the combination. Conclusions: While current evidence supports the therapeutic potential of the combined use of rosuvastatin and curcumin, additional pharmacokinetic, mechanistic, and clinical studies are needed to fully assess its translational value. Full article

Chemotherapy-induced neurotoxicity is a major dose-limiting complication of systemic anticancer therapy that adversely affects neurological function, treatment continuity, and long-term quality of life among cancer survivors. Chemotherapy-induced peripheral neuropathy (CIPN) is the most common manifestation, whereas chemotherapy-related cognitive impairment (CRCI) and selected immune-mediated neurological toxicities increasingly contribute to survivorship-related morbidity. Although these immune-mediated syndromes are distinct from conventional chemotherapy-induced neurotoxicity, they are included because they share several downstream pathogenic mechanisms relevant to biomarker discovery and neuroprotective strategies. This structured narrative review critically synthesizes current evidence on the molecular mechanisms, clinical manifestations, biomarkers, and emerging neuroprotective strategies underlying chemotherapy-induced neurotoxicity. A comprehensive PubMed/MEDLINE search was performed, with emphasis on studies published between 2014 and 2026. Evidence from systematic reviews, meta-analyses, clinical guidelines, randomized controlled trials, prospective clinical studies, and high-quality translational research was critically evaluated. Current evidence indicates that chemotherapy-induced neurotoxicity arises through interconnected mechanisms involving oxidative stress, mitochondrial dysfunction, neuroinflammation, calcium dysregulation, blood–brain barrier disruption, and SARM1-mediated programmed axonal degeneration. Among emerging biomarkers, neurofilament light chain (NfL) demonstrates the greatest translational potential for early detection and monitoring, while inflammatory cytokines, circulating microRNAs, pharmacogenomic markers, cerebrospinal fluid biomarkers, and advanced neuroimaging may improve individualized risk stratification. Although duloxetine remains the only guideline-recommended pharmacological treatment for established painful CIPN, mechanism-based therapies targeting mitochondrial dysfunction, neuroinflammation, oxidative stress, and SARM1 signaling, together with structured exercise and biomarker-guided precision medicine, represent promising translational approaches. However, clinical implementation remains limited by incomplete biomarker validation, heterogeneous study methodologies, and the absence of effective disease-modifying neuroprotective therapies, underscoring the need for large biomarker-guided multicenter clinical trials. Full article

Background/Objective: Cinnamaldehyde (CA) is a naturally occurring bioactive compound derived from the leaves, bark, roots, and flowers of the Chinese medicinal plant Cinnamomum cassia. It exhibits a broad spectrum of pharmacological properties, encompassing antioxidant, antibacterial, anti-diabetic, antifungal, and anticancer activities. Notably, it has shown potential therapeutic benefits in the management of type 2 diabetes mellitus (T2DM) and non-alcoholic fatty liver disease (NAFLD). Ochratoxin A (OTA), a common contaminant found in foods such as cereals, coffee, and raisins, is also present in traditional Chinese medicinal materials, including Astragalus and liquorice. T2DM and NAFLD share intertwined pathophysiological pathways, including insulin resistance, dyslipidaemia, chronic low-grade inflammation and oxidative stress, with insulin resistance serving as the common pathological hub for both conditions. Consequently, they frequently co-occur and exacerbate each other. OTA exerts dual-targeted toxicity to the pancreas and liver, which may synergistically drive the development of the comorbidity of T2DM and NAFLD. These two processes are mutually causal and together constitute the pathological basis of metabolic comorbidity. Methods: Network toxicology employs toxicological data, gene expression, and protein–protein interaction (PPI) networks to predict the targets of toxins, while network pharmacology, based on systems biology principles, reveals how drugs exert regulatory effects through multiple targets and pathways. In this study, we employed an integrated network toxicology and network pharmacology approach to jointly decipher the potential mechanisms by which CA intervenes in OTA-induced comorbid T2DM-NAFLD. First, a network toxicology approach was employed to preliminarily screen for core toxicological targets responsible for OTA’s pathogenicity. Subsequently, network pharmacology was used to identify potential targets of CA-mediated intervention in the disease. Finally, the common overlap among the CA intervention targets, OTA toxicity targets, and disease targets was defined as the final set of potential targets for CA-mediated intervention in OTA-induced T2DM-NAFLD comorbidity. A PPI network was constructed using the STRING database, and topological analysis was performed with Cytoscape. Core targets were selected using the median values of six parameters—betweenness centrality, closeness centrality, degree centrality, eigenvector centrality, LAC (local average connectivity) score, and network centrality—as cut-off thresholds, and the top 10 key genes were further identified using the cytoHubba plugin. Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted via the DAVID database, and the results were visualized on the CNSknowall platform. Lastly, molecular docking of the core targets was performed using the CB-DOCK2 platform to validate binding affinity. Results: Based on an integrated analysis of network toxicology, network pharmacology, and molecular docking, 10 key targets were systematically identified. These may serve as potential mediators of cinnamaldehyde in the treatment of OTA-induced T2DM-NAFLD comorbidity. Among these, six targets—albumin (ALB), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), interleukin-6 (IL-6), tumor necrosis factor (TNF), actin beta (ACTB), and estrogen receptor 1 (ESR1)—possess crystal structures amenable to molecular docking. KEGG enrichment analysis revealed that CA and OTA jointly participate in key pathological processes such as the cancer pathway, the lipid and atherosclerosis pathway, the advanced glycation end-products–receptor for advanced glycation end-products (AGE-RAGE) signaling pathway, the phosphatidylinositol 3-kinase–protein kinase B (PI3K-Akt) signaling pathway, the TNF signaling pathway, and the interleukin-17 (IL-17) signaling pathway. OTA exacerbates inflammatory responses, impairs insulin signaling, promotes hepatic steatosis, and disrupts systemic metabolic homeostasis, ultimately contributing to T2DM-NAFLD comorbidity. Conversely, cinnamaldehyde counteracts these pathological processes through multiple mechanisms, including antioxidant and anti-inflammatory effects as well as regulation of glucose and lipid metabolism, thereby restoring metabolic homeostasis. Conclusions: This study has preliminarily identified the toxicological targets of OTA and the potential intervention targets of CA, offering new avenues for preventing and intervening in OTA-induced metabolic toxicity. Furthermore, it provides a theoretical basis for CA as a potential multi-target therapeutic agent and presents novel insights worthy of further investigation into the prevention of T2DM-NAFLD comorbidity. Full article

Background/Objectives: Dermatologic toxicities are among the most common adverse effects of anticancer therapies, including chemotherapy, targeted therapies, and immunotherapies. Although typically non-life-threatening, these conditions can significantly impair quality of life, alter body image, and lead to treatment non-adherence which may compromise health outcomes. This systematic review aims to synthesize the evidence on the incidence, severity, and management of treatment-related dermatologic toxicities, with a focus on pharmaceutical and multidisciplinary care strategies. Methods: This review followed the PRISMA 2020 guidelines. PubMed, ScienceDirect, and Cochrane were searched for studies published between 1 January 2015 and 31 December 2025. Eligibility criteria were defined using the PICO (R) framework. Study selection, data extraction, and risk-of-bias assessment were performed independently by two reviewers. Given study heterogeneity, a narrative synthesis was conducted. Results: Seventeen studies were included. Dermatologic toxicities were frequently reported during cancer treatment and were generally mild to moderate in severity, although they imposed a substantial burden on patients. Supportive dermatologic care strategies were associated with reduced symptom severity and improved quality of life in some studies. Evidence for pharmaceutical care and multidisciplinary management was more limited, and the available data do not allow firm conclusions regarding their effectiveness. Conclusions: Dermatologic toxicities remain an important challenge in oncological care. The evidence suggests potential benefits of supportive care approaches, but the certainty of the evidence is limited, particularly for pharmaceutical care. Further high-quality studies are needed to clarify the impact of these interventions and support standardized recommendations. Full article

Breast cancer remains a major disease burden and a leading cause of cancer-related morbidity and mortality among women, while current therapies are often limited by toxicity, drug resistance, and recurrence. α-Mangostin (AM), a prenylated xanthone derived from Garcinia mangostana L., has attracted considerable interest because of its antioxidant, redox-modulating, and anticancer properties, which may contribute to improved health outcomes and patient well-being. This study systematically reviewed the therapeutic potential of AM against breast cancer based on evidence from in silico, in vitro, and in vivo studies focusing on biomedical and pharmaceutical applications. Relevant articles were retrieved from the Scopus and PubMed databases using predefined keywords and selection criteria. Eligible studies were extracted, categorized, and analyzed using Microsoft Word and EndNote to assess the pharmacological actions, target interactions, delivery systems, and therapeutic outcomes associated with AM, while the quality of animal studies was assessed using the ARRIVE guidelines. Twenty-nine studies met the inclusion criteria. Computational studies demonstrated favorable AM interactions with ERα, STAT3, RXRα, CXCR4, AKT1, CTNNB1, and HSP90AA1. In vitro studies showed that AM inhibited cancer cell viability, induced apoptosis and autophagy, modulated reactive oxygen species, and suppressed metastatic and immune-evasion markers. Furthermore, nano-formulations, radiolabeled derivatives, and combination approaches improved bioavailability, tumor targeting, and efficacy. In vivo studies reported inhibition of tumor-growth and metastasis, improved pharmacokinetic profiles, and prolonged survival. However, no clinical trials evaluating AM in breast cancer patients have been reported to date. Overall, AM represents a promising preclinical candidate for breast cancer treatment. Nevertheless, standardized pharmacokinetic, toxicological, and efficacy studies, followed by well-designed clinical trials, are essential to facilitate its translation into clinical practice. Full article

Head and neck cancer (HNC) remains a major therapeutic challenge due to high recurrence rates, limited efficacy of current treatments, and the frequent emergence of therapeutic resistance. Curcumin and its analogs have gained increasing interest as adjuvant compounds capable of potentiating the efficacy of conventional anticancer strategies, including chemotherapy with cisplatin, paclitaxel, and 5-fluorouracil, as well as radiotherapy. This review summarizes preclinical and translational evidence investigating combination approaches involving curcumin-based compounds and standard therapies in HNC models, highlighting their synergistic effects on tumor growth inhibition, apoptosis induction, modulation of therapy resistance mechanisms, and mitigation of treatment-related toxicity. Strategies aimed at overcoming the pharmacokinetic limitations of curcumin, including nanoformulations, co-delivery systems, and targeted delivery platforms, are also discussed. By integrating current evidence, this review highlights the translational potential of curcumin and its analogs as adjuvant agents in multimodal HNC therapy, while identifying current gaps in clinical validation, and outlining future directions for improving therapeutic efficacy and safety. Full article

Background/Objectives: Cervical cancer (CC) is the most clinically significant HPV-associated malignancy. Platinum-based chemotherapies produce drug resistance and serious adverse effects. Drug repurposing and combinations are promising approaches to improve the antitumor response. Here, we evaluated the antineoplastic potential of loratadine and simvastatin alone and in combination with cisplatin and gefitinib in HPV-positive CC cells. Methods: HeLa and SiHa CC cells were treated with loratadine, simvastatin, cisplatin, gefitinib, or their combinations. Metabolic activity was assessed using the MTT assay to determine drug inhibitory concentrations (IC₂₀, IC₅₀) from concentration–response curves. Apoptosis was assessed by Annexin V-FITC/PI flow cytometry. Clonogenic survival and migratory capacity were evaluated using colony formation and wound-healing assays, respectively. Tumor formation was evaluated in vivo using the chick chorioallantoic membrane model. Results: Metabolic activity decreased in a concentration-dependent manner following drug treatment in both cell lines. Several combination regimens at IC₂₀ significantly improved reductions in metabolic activity and increases in apoptosis compared with monotherapies or two-drug combinations. Notably, some three-drug combinations, with or without cisplatin, had similar effects to the quadruple regimen. Combination treatments also reduced clonogenic survival and migratory capacity, as well as tumor formation and cancer cell dissemination in vivo. Conclusions: Drug combinations at relatively low concentrations (IC₂₀) significantly enhanced the anticancer effects on CC cells in in vitro and in vivo settings. These findings support the potential of drug repurposing and combination strategies as promising approaches to decrease adverse side effects while improving therapeutic efficacy for the benefit of CC patients. Full article

Flax lignans are abundant plant secondary metabolites in flaxseed, with secoisolariciresinol diglucoside (SDG) content reaching 0.61–1.33% of seed dry weight—substantially higher than levels reported for sesame seeds (0.01–0.03%), cereals (<0.01%), and most legumes (<0.005%). These levels make them natural bioactive compounds with considerable application potential. This review summarizes the biosynthetic pathways, key enzymes, and regulatory mechanisms of flax lignans; describes their major biological activities, including antioxidant, anti-inflammatory, anticancer, cardiovascular protective, and metabolic regulatory effects and possible mechanisms of action; and analyzes current progress in extraction, purification, analytical detection, and application. Key limitations in industrial application include complex extraction procedures, high production costs, lack of unified quality standards, and insufficient clinical evidence. Advanced strategies such as synthetic biology approaches for heterologous production, molecular breeding for high-lignan varieties, and green extraction technologies are discussed as promising solutions. This review is intended to serve as a conceptual reference for subsequent mechanistic studies, product development, and industrial translation of flax lignans in food, pharmaceutical, and cosmetic applications. Full article