The rapid clinical validation of messenger RNA (RNA) during the COVID-19 pandemic has catalyzed a shift from traditional vaccine development toward a versatile, programmable therapeutic platform. This review provides a comprehensive analysis of the mRNA landscape, moving beyond historical milestones to critically evaluate the structural biology and synthetic modifications required for therapeutic stabilization. We examine the transition from Lipid Nanoparticle (LNP) dominance toward next-generation delivery vehicles designed to overcome current limitations in tissue targeting and systemic reactogenicity. Furthermore, this article contrasts mRNA with DNA-based modalities, specifically focusing on the safety profiles and rapid design cycles that favor mRNA in acute and personalized indications. A significant portion of this synthesis is dedicated to the shifting intellectual property landscape, interpreting how patent concentration among key industry players influences global innovation and market accessibility. By identifying current gaps in manufacturing scalability and regulatory harmonization, this review previews the transition of mRNA technology from an emergency response tool to a mainstay of chronic disease management and precision oncology. Overall, this work outlines the technical and socio-economic hurdles that must be cleared to realize a new era of adaptable, "on-demand" healthcare solutions.

Cancer is a leading cause of death worldwide and continues to pose significant challenges in treatment. Poor drug solubility, non-specific distribution, MDR, and systemic toxicity remain some of the major concerns regarding treatment efficacy. Emulsomes represent a promising drug delivery platform that helps overcome some of these limitations, acting as hybrid nanocarrier systems that incorporate the advantages of liposomes and solid lipid nanoparticles. This article provides an overview of the composition, structure, and physicochemical properties of emulsomes, their advantages over conventional nanocarriers, and a detailed discussion of their role in cancer treatment. The authors discuss a variety of medicinal substances, including chemotherapeutic drugs and natural chemicals, that are delivered using emulsomes. Current research highlights the potential application of emulsomes across a wide range of cancers, including colon, brain, lung, prostate, breast, and hematologic malignancies. These features are compared with those of other nanocarriers with respect to composition, size (nm), stability, tumor-targeting capacity, biocompatibility, and toxicity. In addition, this work further highlights the current in vitro and in vivo evaluations of emulsomes, along with a thorough discussion of formulation challenges, scaling issues, and regulatory considerations. Lastly, this study covers recent advancements and potential future applications, including AI-enabled surface modification for targeted distribution, personalized medication, theragnostic applications, and emulsome design optimization. Overall, this study provides a strong foundation for understanding the current and future potential of emulsomes in managing various types of cancer.

The use of chitin, chitosan, and Chitooligosaccharides (COS) has advanced rapidly in recent years due to their exceptional physicochemical and biological characteristics. Because of their biocompatibility, biodegradability, low toxicity, and functional flexibility, chitin and chitosan have attracted significant interest from the biomedical, pharmaceutical, agrochemical, culinary, and cosmetic sectors. Tissue engineering, wound healing, medication delivery, and the creation of bioactive substances with antibacterial and antiinflammatory properties are among their uses. When compared to their parent polymers, chitooligosaccharides- low-molecular-weight derivatives of chitosan with a degree of polymerization below 20-show better biological activity and water solubility. Numerous pharmacological benefits, including antioxidant, antiinflammatory, anti-obesity, anti-cancer, neuroprotective, cardioprotective, and anti-aging properties, are demonstrated by COS. Although preclinical research presently provides the majority of the data, these bioactivities make COS attractive candidates for treatments in a variety of disorders. Chemical processes that are frequently toxic to the environment and challenging to regulate with respect to polymerization and acetylation levels have historically been used to produce chitosan and COS. In order to produce well-defined products with enhanced functional properties, recent research has concentrated on enzymatic methods utilizing chitinases, chitosanases, and chitin deacetylases. This review emphasizes recent advancements in our understanding of the structural, physicochemical, and bioactive aspects of chitin-based derivatives and discusses both traditional and novel synthesis methods. Additionally, it highlights the necessity for further in vivo and translational research to fully realize the therapeutic potential of chitosan-based bioactive molecules by examining their creative uses in a variety of fields.

Duchenne Muscular Dystrophy (DMD) is a chronic X-linked recessive neuromuscular disorder with a prevalence of 1 in 3,500 to 5,000 live male births worldwide. Alterations in the dystrophin gene, one of the biggest known human genes with 2.5 million base pairs and 79 exons, located at Xp21.1, are responsible for the disease. The dystrophin protein, an essential structural component that links the muscle cell cytoskeleton actin to the extracellular matrix through the dystrophin-associated protein complex, is either lacking or dysfunctional due to these mutations. Dystrophin deficiency compromises muscle membrane stability, leading to gradual deterioration of muscle fibers, fibrosis, and replacement by adipose tissue. Numerous disrupted physiological pathways, such as calcium dysregulation, faulty nitric oxide signaling, altered PI3K-Akt-mTOR growth signaling, chronic inflammatory responses, and oxidative stress, are implicated in the pathophysiology of DMD. Affected males clinically demonstrate early childhood muscular weakness; characteristic signs such as Gower's maneuver and calf hypertrophy; increasing ambulation loss by adolescence; and potentially lethal cardiorespiratory problems that generally manifest in the third decade of life. Corticosteroids remain the primary therapeutic modality, significantly improving ambulation and quality of life; nevertheless, extended use entails severe adverse effects. Recent treatment advancements provide renewed optimism via diverse innovative strategies, namely CRISPR-Cas9 gene editing, antisense oligonucleotide-mediated exon skipping (eteplirsen, golodirsen, viltolarsen, and casimersen), microdystrophin gene therapy using Adeno-Associated Viral (AAV) vectors, stop codon read-through therapy, and stem cell-based treatments. But difficulties with cost, immunogenicity, efficacy, and mutant specificity persist. Through multidisciplinary treatment and continuous scientific progress, individualized precision medicine that integrates therapies targeting secondary pathogenic pathways with dystrophin-restoration techniques can finally convert this devastating illness into a tolerable chronic ailment.

The nanofiber-based drug delivery systems offer a high surface-area-to-volume ratio, tunable porosity, controllable degradation, and superior drug-loading capacity, making them promising platforms for precision cancer therapy. This review details the engineering design, fabrication methods and biomedical uses of nanofibers for cancer therapeutics, as well as for extracellular matrix (ECM)-mimicking tumor models. The major fabrication techniques such as electrospinning, phase separation, self-assembly, and template synthesis are critically examined, and their impact on the fiber morphology, drug packaging, and drug release are highlighted. Electrospun nanofibers closely replicate the native ECM architecture, which allows for the creation of physiologically relevant 3-D tumor models for the study of tumor progression, metastasis, and therapeutic resistance. Recent studies have shown that nanofibrous platforms can be used to deliver chemotherapeutics, genes, and combination therapies locally and in a stimulus-responsive manner, leading to increased cytotoxicity, extended release times, and decreased systemic toxicity in models of breast cancer, melanoma, pancreatic cancer, and colorectal cancer. The applications of nanofibers in precision oncology are further highlighted by advanced multifunctional systems based on magnetic nanoparticles, pH-responsive carriers, and core-shell architectures. Commercial products, patents, and current clinical trials further highlight the increasing translational importance of nanofiber technologies. However, issues in large-scale manufacturing, residual solvent toxicity, reproducibility, long-term biocompatibility and regulatory standardization remain to be clinically translated. The use of artificial intelligence, computational models and automated manufacturing could further drive the emergence of clinically translatable and scalable nanofiber-based cancer therapeutics.

Short-chain fatty acids (SCFAs), primarily acetate, propionate, and butyrate, are key microbial metabolites generated through the fermentation of indigestible carbohydrates by gut bacteria. Beyond their local actions in the intestinal environment, these metabolites exert far-reaching systemic effects, particularly in shaping neuroimmune communication along the gut-brain axis. Their interaction with free fatty acid receptor 2 (FFAR2), expressed on intestinal epithelial cells, peripheral immune populations, and microglia, has emerged as a central mechanism linking gut microbial activity to neuroinflammatory regulation. Disrupted FFAR2 signalling and altered SCFA production are now implicated in the pathogenesis of key neuroinflammatory and neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. In this narrative review, we synthesize current evidence suggesting that SCFAs can mediate microglial development, cytokine cross-linking, and barrier stability, as well as neuronal-glial communication via FFAR2-mediated and receptor-independent mechanisms, including HDAC inhibition. Importantly, current evidence supports three partially overlapping mechanistic frameworks: (i) direct receptor-dependent signalling, including potential FFAR2-mediated effects on microglia, although such expression and functional relevance in adult microglia remain debated; (ii) receptor-independent intracellular mechanisms, particularly histone deacetylase (HDAC) inhibition and metabolic reprogramming; and (iii) indirect peripheral immune and gut-brain regulatory pathways, involving modulation of systemic cytokine milieus, barrier integrity, and immune cell trafficking, which appear to be more consistently supported in adult in vivo models. Experimental research shows that restoring SCFA supply or activating FFAR2 can suppress neuroinflammation, increase the clearance of pathological proteins by proteases, and promote neuronal survival. Available strategies to increase endogenous SCFA production include dietary fiber consumption, prebiotics, and customized SCFA formulations, and novel synthetic FFAR2 agonists offer a pharmacological approach to targeted therapy. Nonetheless, there remains a significant degree of variability in dosing, route of delivery, bioavailability, and interindividual microbiota profiles, which restricts clinical translation. Combined, the existing knowledge base places the SCFA-FFAR2 axis as an encouraging therapeutic agent regarding altering neuroimmune responses and creating new approaches to the control of neuroinflammatory and neurodegenerative diseases.

Hyperlipidemia, characterized by elevated blood lipid levels, represents a major global health concern due to its strong association with cardiovascular disease, diabetes, and metabolic syndrome. While current therapies - such as statins, fibrates, bile acid sequestrants, and PCSK9 inhibitors - are effective in controlling hyperlipidemia, they are often associated with adverse effects, potential drug resistance, and suboptimal efficacy in certain patient populations. All of the above underscore the urgent need for safer and more effective therapeutic alternatives. Among the major molecular targets involved in the regulation of lipid metabolism are HMG-CoA reductase, PCSK9, peroxisome proliferator-activated receptors (PPARs), cholesteryl ester transfer protein (CETP), and nuclear receptors, including the liver X receptor (LXR) and farnesoid X receptor (FXR), which are also targets for future antihyperlipidemic drug development. Recent advancements in artificial intelligence (AI) and machine learning (ML) have significantly transformed and accelerated drug discovery by enabling the processing of vast amounts of genomic, proteomic, and chemical data. Furthermore, ML tools such as quantitative structure-activity relationship (QSAR) modelling, deep learning, random forest, and support vector machines (SVM) have proven predictive and effective in identifying novel lipid metabolism modulators, thereby enhancing the efficacy and accuracy of virtual screening. Meanwhile, molecular docking has become an integral part of structure-based drug design (SBDD), and software such as AutoDock, Glide, and GOLD have proven effective in generating accurate ligand-target docking models. Molecular docking, together with ML-based approaches, enables the identification of potent and selective drug candidates. Overall, the combination of ML and molecular docking offers an efficient and accurate platform for antihyperlipidemic drug discovery, helping to overcome the limitations of currently available therapeutic strategies.