Chemotherapy-induced peripheral neuropathy (CIPN) represents one of the most challenging dose-limiting toxicities in oncology, affecting 20-85% of patients receiving neurotoxic chemotherapy agents. This debilitating condition significantly impacts quality of life and often necessitates dose reductions or treatment discontinuation, potentially compromising therapeutic outcomes. Among emerging neuroprotective strategies, curcumin (diferuloylmethane), the principal bioactive compound derived from Curcuma longa, has demonstrated remarkable potential in preventing and treating CIPN across multiple chemotherapeutic classes. This comprehensive analysis examines curcumin's differential efficacy against specific chemotherapy agents, elucidating mechanistic pathways and synthesizing clinical evidence to provide a foundation for precision neuroprotection strategies. The review synthesizes mechanistic and clinical data for taxanes, platinums, and vinca alkaloids, highlighting convergent roles of oxidative stress, mitochondrial dysfunction, axonal transport disruption, ion-channel dysregulation, and neuroinflammation in dorsal root ganglia and peripheral nerves. Future clinical success depends on using optimized curcumin formulations and tailoring doses to the specific pathophysiology of each type of CIPN.
Viruses are major pathogenic agents responsible for a wide spectrum of pathological conditions in humans, animals, and plants, ranging from self-limiting illnesses to severe, life-threatening conditions. Viral infections continue to represent a worldwide threat and societal crisis, driving ongoing efforts to develop effective and low-toxicity antiviral therapies. The rapid spread of viral diseases such as COVID-19, influenza, and hepatitis has underscored the urgent need for effective antiviral treatments. Despite significant progress in antiviral drug discovery, the development of safe and efficacious antiviral medications remains a major challenge. This article outlines the paradigm shift in antiviral therapeutics, highlighting novel antiviral targets, newly developed compounds, repurposing existing drugs, and emerging drug delivery systems. We begin by outlining the major classes of viruses and their replication cycle, followed by a historical overview of antiviral drug development. The different ways to classify antiviral agents, whether in accordance with their targets, which may be either viral components or host cell factors, or according to chemical structure, including virus-neutralizing antibodies, CRISPR/Cas-based antiviral therapy, and antiviral nucleic acid polymers, including siRNAs are also discussed. We will also tackle how artificial intelligence and machine learning reshape the future of antiviral combination therapies. The review places particular focus on novel antiviral candidates, advances in drug delivery technologies, and current progress in vaccine development against re-emerging viruses. The article concludes by addressing future directions in antiviral drug discovery, emphasizing the importance of global collaboration and technological innovation to confront emerging viral threats.
Acute myeloid leukemia (AML) is a genetically complex and heterogeneous aggressive cancer in which targeted therapies have improved outcomes but are often limited by induced resistance. This review provides a comprehensive and mechanistically driven overview of the molecular subclasses of AML mutations (including Class I, II, III, and IV mutations) and critically examines how these alterations inform therapeutic vulnerabilities. Moreover, it outlines the molecular subclasses of AML and examines key targeted agents, including FLT3 inhibitors such as Quizartinib and Gilteritinib, as well as IDH inhibitors like Ivosidenib and Enasidenib with BCL-2 inhibition (Venetoclax), and Revumenib as emerging menin-directed agent, highlighting their clinical impact. Emphasis is placed on rational combination strategies designed to simultaneously inhibit primary oncogenic drivers and compensatory survival pathways. By integrating mechanistic insights with clinical data, the review proposes a framework for precision-guided combination therapy aimed at overcoming resistance and achieving more durable remissions in AML with less side effects.
Nobel prizes are usually awarded to major breakthroughs in basic science and are usually inspiring to the researchers world-wide to build new ideas and develop others based on them. This can lead to consecutive breakthroughs in applied sciences through all the fields including the medical field and specifically, the drug delivery one. This editorial sheds the light on three Nobel prizes; two in chemistry and one in physiology or medicine that inspired the drug delivery and nanomedicine scientists to develop novel formulations and medicines for hard-to-treat diseases such as cancer. The first demonstrated Nobel prize was the foundation of the use of conductive polymers as responsive drug delivery systems. The second was the basis for the emergence of the new field of nano-onco-immunotherapy and finally the third paved the way for the use of metallic organic frameworks as successful drug nanocarriers. This editorial encourages pharmaceutics scientists to pay more attention on basic sciences and always get aware of all relevant advancements that can be related to their scientific field.
Radiation therapy, a crucial tool in cancer treatment, delivers precise cytotoxic effects specifically against malignant cells. Despite its therapeutic efficacy, radiation exposure commonly inflicts collateral damage on surrounding healthy tissues. This damage is largely mediated by persistent oxidative stress and chronic inflammation, driven by excessive production of reactive oxygen species (ROS) and the activation of key inflammatory pathways such as nuclear factor kappa B (NF-κB) and inflammasome-mediated pyroptosis. These molecular events not only compromise tissue integrity but also contribute to long-term complications, including fibrosis, organ dysfunction, and impaired healing.Recent advances in pharmacology have highlighted the potential of drug repurposing as a strategic approach to mitigate radiation-induced toxicity. Among these, incretin-based therapies—originally developed for glycemic control in type 2 diabetes—have emerged as promising candidates due to their robust antioxidant and anti-inflammatory properties. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and dipeptidyl peptidase-4 (DPP-4) inhibitors exhibit pleiotropic effects that extend beyond metabolic regulation. These agents have demonstrated neuroprotective, nephroprotective, and cardioprotective actions, primarily through mechanisms that reduce ROS generation, enhance endogenous antioxidant defenses, and suppress pro-inflammatory signaling cascades.Preclinical studies have begun to uncover the radioprotective potential of incretin-based drugs, showing improved survival rates and reduced tissue damage in irradiated models. Their ability to modulate mitochondrial function, preserve endothelial integrity, and inhibit pyroptotic cell death. This review suggests that incretin medications may successfully counter both the initial, severe oxidative stress and the subsequent inflammatory amplification loop associated with radiation exposure.
