Background/Objectives: Cancer remains one of the leading causes of mortality globally, underscoring the need for novel therapeutic strategies capable of targeting multiple molecular pathways simultaneously. Natural products, particularly fungal-derived metabolites from the genus Cordyceps, represent promising candidates due to their diverse biological activities. Although previous studies have indicated the anticancer potential of Cordyceps species, systematic characterization of their molecular targets has been limited. This study aimed to comprehensively identify and evaluate Cordyceps metabolites as potential multitarget anticancer agents through a network pharmacology approach. Methods: A total of 129 metabolites previously reported in the literature from polar aqueous, alcoholic, and non-polar extracts of Cordyceps were compiled and chemically classified using ChemMine tools. Structure-based target prediction and pathway enrichment analyses were performed to investigate their potential biological targets. Predicted molecular targets were cross-referenced with differentially expressed genes in breast, colorectal, and lung cancers to identify hub proteins. Molecular docking simulations were conducted to assess binding affinities of metabolites to key oncogenic targets, and SwissADME was utilized for pharmacokinetic profiling. Results: The analysis revealed that Cordyceps metabolites targeted critical oncogenic pathways, including cell cycle regulation, DNA replication, and apoptosis. Hub proteins such as TYMS, AURKA, and CDK1 were identified as primary targets. Docking simulations highlighted metabolites such as cordycepsidone A, jiangxienone, and flazin, demonstrating binding affinities comparable or superior to clinically used inhibitors. Pharmacokinetic profiling identified several metabolites with favorable drug-like properties, supporting their potential as lead compounds. Conclusions:Cordyceps extracts contain structurally diverse metabolites capable of modulating multiple cancer-relevant molecular targets, providing a robust foundation for their development into multitarget anticancer therapies. This integrative network pharmacology approach underscores the potential of fungal metabolites in oncology drug discovery.

Many therapies have been developed against COVID-19 since it first appeared in December 2019. Antivirals, antimalarials, cephalosporins, colchicine, anticoagulants, and corticosteroids, among others, have been evaluated as protecting agents against antibacterial complications due to their anti-inflammatory and immunomodulatory effects against thrombosis and cell death caused by infection with SARS-CoV-2. Nevertheless, the overall balance in their application has not been found to be satisfactory. On the other hand, developing and applying several vaccines against this virus have marked an important watershed in preventive and prophylactic medicine in the new millennium. However, given the regular efficacy reported of some of them, the still scarce affordability, and the emergency of new strains for which no drug has been evaluated, the search for new pharmacological therapy alternatives still represents an essential component in the clinical management of COVID-19, and the rapid identification of drugs with potential antiviral and/or immunomodulatory properties is needed. In the present review, a potential therapeutic effect of metformin and other antidiabetic therapies for the management of COVID-19 are proposed and discussed from the viewpoint of their in vitro and in vivo immunomodulatory effects. Given that acute inflammation is an important component of COVID-19, antidiabetic therapies could be promising alternatives in its management and reducing the disease's severity. In order to understand how metformin and other antidiabetic therapies could work in the context of COVID-19, here we review the possible mechanisms of action through a detailed description of cellular and molecular events.

Objective: The stems from plants of the genus Cissus are used in traditional medicine worldwide. In Mexico Cissus trifoliata is employed for the management of several diseases, however little is known about the active compounds. The present investigation focuses on the extraction, isolation, and characterization of the lipid contents from the stems of C. trifoliata by chromatographic, spectroscopic, and spectrometric techniques. Methods: The hexane extract was fractionated sequentially with hexane and ethanol and visualized by TLC. The compounds were isolated by column chromatography and structurally elucidated using NMR. In addition, the complete extract and solids obtained by fractionations were analyzed by GC-MS. Results: According to NMR signals, solids present in the hexane extract correspond to hentriacontane, octatetracontane, octacosanoic acid, tricosyl tetracosanoate and sitosterol. Furthermore, the analysis by GC-MS found 33 compounds, and the most abundant were hentriacontane, squalene, palmitic acid, oleic acid, β-sitosterol, and nonacosane. Conclusion: This report describes the major constituents in the hexane extract from Cissus trifoliata stems. Our analysis suggests an abundant composition of higher alkanes, fatty acids, and sterols, which are the major lipid components of cuticular waxes and plant cell membranes.

Cancer remains a leading cause of mortality worldwide and continues to challenge therapy due to its biological complexity and metabolic plasticity. Among the pathways supporting malignant progression, L-arginine metabolism has emerged as a key regulator of tumor cell fitness, integrating nutrient sensing, bioenergetics, redox balance, and immune modulation. In cancer, arginine homeostasis is frequently rewired, generating L-arginine auxotrophy and increased dependence on extracellular L-arginine, which contributes to several hallmarks of cancer, including proliferation, metabolic adaptation, angiogenesis, immune evasion, and tumor aggressiveness. This review discusses the molecular mechanisms through which L-arginine metabolism reshapes tumor biology, focusing on signaling pathways such as mTORC1 and on tumor-immune interactions within the tumor microenvironment. Therapeutic strategies targeting this pathway, including L-arginine deprivation therapies and emerging small-molecule modulators, are also examined alongside adaptive resistance mechanisms that may limit their clinical efficacy.