A chemical investigation of the Arctic-derived fungus Eutypella sp. D-1 based on the OSMAC (one strain many compounds) approach resulted in the isolation of five cytosporin polyketides (compounds 1–3 and 11–12) from rice medium and eight cytosporins (compounds 2 and 4–11) from solid defined medium. The structures of the seven new compounds, eutypelleudesmane A (1), cytosporin Y (2), cytosporin Z (3), cytosporin Y₁ (4), cytosporin Y₂ (5), cytosporin Y₃ (6), and cytosporin E₁ (7), were elucidated by analyzing their detailed spectroscopic data. Structurally, cytosporin Y₁ (4) may be a key intermediate in the biosynthesis of the isolated cytosporins, rather than an end product. Compound 1 contained a unique skeleton formed by the ester linkage of two moieties, cytosporin F (12) and the eudesmane-type sesquiterpene dihydroalanto glycol. Additionally, the occurrence of cyclic carbonate moieties in compounds 6 and 7 was found to be rare in nature. The antibacterial, immunosuppressive, and cytotoxic activities of all compounds derived from Eutypella sp. D-1 were evaluated. Unfortunately, only compounds 3, 6, 8, and 10–11 displayed immunosuppressive activity, with inhibitory rates of 62.9%, 59.5%, 67.8%, 55.8%, and 68.7%, respectively, at a concentration of 5 μg/mL.

Acute myeloid leukemia (AML) is a heterogeneous hematological malignancy with historically high mortality rates. The treatment strategies for AML is still internationally based on anthracyclines and cytarabine, which remained unchanged for decades. With the rapid advance on sequencing technology, molecular targets of leukemogenesis and disease progression related to epigenetics are constantly being discovered, which are important for the prognosis and treatment of AML. Traditional Chinese medicine (TCM) is characterized by novel pharmacological mechanisms, low toxicity and limited side effects. Several biologically active ingredients of TCM are effective against AML. This review focuses on bioactive compounds in TCM targeting epigenetic mechanisms to address the complexities and heterogeneity of AML.

Acute myeloid leukemia (AML) remains a formidable therapeutic challenge, with high relapse rates rooted not only in genetic heterogeneity, but also in dynamic and reversible epigenetic dysregulation that drive resistance to conventional and targeted small-molecule therapies. Although small-molecule inhibitors targeting epigenetic regulators have demonstrated preclinical efficacy and initial clinical activity, therapeutic gains are often limited by transient responses, intra- and inter-patient heterogeneity, and an incomplete understanding of predictive biomarkers. Besides, clinical outcomes have often been less robust than preclinical data suggested, partly due to the complexity of AMLs genetic and epigenetic heterogeneity, the limitations of model systems, and intrinsic resistance mechanisms. Combination approaches, such as pairing epigenetic agents with chemotherapy, immunotherapy, or other targeted drugs are under investigation. However, clinical efficacy remains inconsistent and requires a mechanistic rationale to avoid antagonism. To move forward, it is essential to delineate specific epigenetic dependencies in resistance-prone AML subtypes, design rational, biomarker-guided combination regimens, and enhance specificity and pharmacodynamic profiles of epigenetic inhibitors. Such an integrated strategy holds promise for elevating the effectiveness of epigenetic therapies in AML. Continued research is essential to refine epigenetic-based precision medicine and ultimately improve patient outcomes.

Radiation exposure initiates a cascade of reactions, including the release of reactive oxygen species, DNA double-strand breaks, and cellular apoptosis, leading to cell death, tissue damage, and potentially the development of cancer. Consequently, there is an urgent need to develop highly effective and low-toxicity radioprotective agents. Traditional chemically synthesized protective agents face significant limitations in clinical applicability due to their pronounced off-target toxicity, narrow therapeutic window, and high production costs. In recent years, bioactive natural compounds, including polysaccharides, polyphenols, saponins, alkaloids, and peptides, have emerged as key research targets for the next-generation of radioprotective drugs due to their low toxicity and multi-target synergistic effects. Notably, each class of compounds demonstrates distinct characteristics in its mechanisms of action. In comparison to synthetic drugs, these natural compounds exert protective effects primarily through three mechanisms: antioxidant activity, anti-apoptotic effects, and immune modulation. Additionally, they offer advantages such as abundant availability and high safety profiles. Current research must further elucidate the mechanisms of action of their active ingredients to establish a theoretical foundation for radiation protection in contexts involving radiation workers and potential nuclear emergencies. This article systematically elucidates the molecular mechanisms underlying radiation damage, summarizing the multidimensional protective effects and action pathways of natural products. Its objective is to provide both a theoretical foundation and technical insights for the development of novel radioprotectants.