Lung cancer continues to be the foremost cause of cancer-related mortality globally, with non-small cell lung cancer (NSCLC) accounting for nearly 85% of cases. Historically, the prognosis for NSCLC was grim, but advancements in targeted therapies and immunotherapy are transforming treatment paradigms. This review encapsulates significant developments in molecularly targeted agents and immune checkpoint inhibitors, emphasising their clinical efficacy, resistance mechanisms, and innovative therapeutic combinations. A thorough literature search was conducted across PubMed, ClinicalTrials.gov, and other global intellectual property databases to highlight pivotal advancements in lung cancer therapies. Each section focuses on therapies targeting key molecular drivers such as Epidermal Growth Factor Receptor (EGFR), Anaplastic Lymphoma Kinase (ALK), and others, alongside immunotherapies targeting critical pathways like PD-1 and PD-L1. In genetically defined NSCLC subsets, targeted therapies such as Osimertinib and Lorlatinib have significantly enhanced progression-free survival. Similarly, immune checkpoint inhibitors like Nivolumab have redefined care standards, particularly in PD-L1-positive tumours. Nevertheless, challenges such as acquired resistance persist, prompting ongoing exploration of combination strategies and next-generation agents. This article also reviews pivotal clinical trials and newly filed patents, reflecting current and emerging commercial interests. The integration of molecular diagnostics and precision therapies is reshaping lung cancer treatment, with prospective directions aiming to overcome resistance and broaden access to innovative therapies worldwide, including from India and other developing regions.
Background: Chronic Pseudomonas aeruginosa infection is one of the major chal-lenges in the management of cystic fibrosis (CF) and is often associated with reduced lung function and increased complications. With the rising trend of antibiotic resistance, research-ers' attention has increasingly shifted toward complementary therapies. In this case report, the use of honey–thyme oxymel, a traditional Persian medicine preparation, was evaluated as an adjunctive treatment in a pediatric patient with CF. Case Presentation: The patient was an 11-year-old girl diagnosed with CF in infancy who had been affected by chronic P. aeruginosa infection for the past eight years. Despite strict adher-ence to standard antibiotic regimens, her throat cultures consistently remained positive. Anti-microbial susceptibility testing demonstrated resistance to multiple antibiotics. In addition to standard CF treatment, including inhaled and oral medications, vitamins, and chest physio-therapy, oral honey–thyme oxymel was added to her regimen at a dose of 5 mL twice daily for two months. Throat cultures obtained in the second, fourth, and sixth months were all negative for P. aeruginosa, representing the first microbiological eradication in the past eight years. Clinically, during six months of follow-up, the patient experienced easier sputum expectora-tion, fewer episodes of dyspnea, and no need for hospitalization. Her pulmonary function also showed significant improvement, with FEV₁ increasing from 73.3% to 83.2% in the second month. The treatment was generally well tolerated, with only a mild, transient cough reported as an adverse effect. Conclusion: This case suggests that adjunctive use of honey–thyme oxymel may be effective in achieving microbiological eradication and improving symptoms in patients with CF. How-ever, given the nature of a case report and the concurrent continuation of standard therapy, these improvements cannot be definitively attributed solely to oxymel consumption. There-fore, further studies, particularly controlled clinical trials, are warranted to accurately evaluate the safety and efficacy of this intervention.
Nowadays, diabetic wounds are a major concern in the medical and animal fields due to delayed wound healing, as reactive oxygen species play a crucial role in the healing process. Pro-inflammatory molecules, such as tumor necrosis factor (TNF-α), matrix metalloproteinase 9 (MMP-9), and interleukin (IL)-1 β, are most prevalent in diabetic wounds, along with anti-inflammatory mediators and cytokines, which exhibit dysregulated macrophage responses. Although various plants exhibit strong anti-inflammatory, antibacterial, and antidiabetic properties, only a few have been used as effective therapeutic agents for diabetic wounds. More plants need to be explored for their effects on diabetic wounds. Alstonia scholaris (L.) R. Br. is Devil’s tree, which is a rich source of various alkaloids, such as tubotaiwine, picralinal, and 16-formyl-5-methoxystrictamine, making it a potential therapeutic agent against diabetic wounds. The relevant articles showing the pharmacological effects of the tree, A. scholaris (L.) R. Br. were searched in search engines like Google Scholar, Web of Science databases, and PubMed. It also shows numerous biological properties, such as antioxidant, anti-inflammatory, antibacterial, antifungal, stimulant, carminative, stomachic, hemostatic, inhibitory cytokine, wound-healing, hypoglycemic, improving collagen and hydroxyproline synthesis, repair of skin tears, increasing granulation strength, and helping in wound contraction in models. More research on A. scholaris is needed to prove it as a potential therapeutic regimen against diabetic wounds. Therefore, this review highlights the pharmacological properties and biological effects of A. scholaris, demonstrating its potential as a candidate for the treatment of diabetic wounds.
Differences among individuals in susceptibility to adverse drug reactions are strongly influenced by genetic variation affecting drug metabolism, transport, immune response, and pharmacodynamics pathways, presenting both challenges and opportunities for drug discovery and development. Genetic and genomic variation can modify pharmacokinetics, pharmacodynamics, immunemediated toxicity, treatment resistance, and biomarker-defined therapeutic benefit, making pharmacogenetics and pharmacogenomics central components of precision medicine. The primary aim of this review is to synthesize how pharmacogenetics and pharmacogenomics function as enabling technologies across the pharmaceutical and clinical domains, with emphasis on biomarker-guided drug development, patient stratification, safety optimization, regulatory translation, precision oncology, sex-related variability, population diversity, artificial intelligence, and multi-omics integration. The review also elucidates the distinction between single-gene pharmacogenetics and genome-wide pharmacogenomics and discusses the practical requirements, procedures, advantages, and challenges associated with implementation. Future progress will depend on harmonized standards, diverse population datasets, preemptive testing linked to electronic health records, explainable artificial intelligence, multi-omics validation, and equitable access to genomic prescribing tools, ensuring that precision therapeutics improve drug safety and efficacy across populations.
INTRODUCTION:Multiple sclerosis (MS) involves chronic inflammation driven by dysregulation of the JAK-STAT pathway. This study aimed to evaluate the potential interaction of natural cannabinoids with TYK2, with a focus on cannabidiol (CBD), using computational in silico approaches. METHODS:A combined molecular docking and molecular dynamics (MD) workflow was used. Cannabinoid ligands and the TYK2 structure (JH2 domain) were prepared and docked in MOE, followed by 20 ns MD simulations under NVT and NPT conditions in GROMACS. Complex stability and ligand-protein interactions were analysed. RESULTS:CBD showed a competitive docking score (-7.31 kcal/mol) and a refined RMSD of 0.9198 Å. MD simulations revealed a stable CBD-TYK2 complex, with RMSD fluctuations of 0.15-0.20 nm, which were lower than those observed for the reference inhibitor, deucravacitinib. RMSF analysis revealed a slight increase in local flexibility in specific regions without affecting the overall stability of the protein. The radius of gyration remained stable throughout the simulation, indicating that the protein's compactness was preserved. Hydrogen bond analysis showed fewer but transient interactions for CBD, consistent with a binding mode dominated by hydrophobic interactions. DISCUSSION:These computational results suggest that CBD interacts stably with TYK2 through a distinct binding mode compared to the reference inhibitor, deucravacitinib, while maintaining the structural integrity of the protein. CONCLUSION:CBD showed a stable predicted interaction with TYK2, supporting its potential as a candidate for further in vitro and in vivo studies in the context of MS-related inflammation.
