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Advances in Yupingfeng San Research: Multi-Target Mechanisms and Clinical Evidence
Drug Des Devel Ther. 2026 May 18;20:603491. doi: 10.2147/DDDT.S603491. eCollection 2026.
ABSTRACT
This review systematically summarizes the chemical composition, mechanisms of action, and recent progress in research and clinical applications of Yupingfeng San (YPFS) in various diseases. Research indicates that YPFS contains abundant active constituents-such as flavonoids, coumarins, and terpenoids, and demonstrates diverse biological activities,including immune modulation, anti-inflammatory, antiviral, antibacterial, and antitumor activities. Recent pharmacological and network pharmacology studies have elucidated that YPFS regulates key signaling pathways - such as PI3K-Akt, NF-ΞΊB, TLR4/MyD88, and JAK-STAT - through multi-target and multi-pathway mechanisms. These effects contribute to its therapeutic role in allergic rhinitis (AR), asthma, atopic dermatitis (AD), liver cancer, lung cancer, and other conditions. Although limited clinical trials and meta-analyses suggest that YPFS, when combined with conventional therapies, can improve treatment efficacy, relieve symptoms, and demonstrate good safety and tolerability, current research is constrained by low evidence quality and the absence of standardized quality control measures. Future research should prioritize large-scale, multi-center clinical trials and integrate multi-omics approaches to identify the main active components and mechanisms of action.
PMID:42182585 | PMC:PMC13196821 | DOI:10.2147/DDDT.S603491
Advances in Yupingfeng San Research: Multi-Target Mechanisms and Clinical Evidence
Drug Des Devel Ther. 2026 May 18;20:603491. doi: 10.2147/DDDT.S603491. eCollection 2026.
ABSTRACT
This review systematically summarizes the chemical composition, mechanisms of action, and recent progress in research and clinical applications of Yupingfeng San (YPFS) in various diseases. Research indicates that YPFS contains abundant active constituents-such as flavonoids, coumarins, and terpenoids, and demonstrates diverse biological activities,including immune modulation, anti-inflammatory, antiviral, antibacterial, and antitumor activities. Recent pharmacological and network pharmacology studies have elucidated that YPFS regulates key signaling pathways - such as PI3K-Akt, NF-ΞΊB, TLR4/MyD88, and JAK-STAT - through multi-target and multi-pathway mechanisms. These effects contribute to its therapeutic role in allergic rhinitis (AR), asthma, atopic dermatitis (AD), liver cancer, lung cancer, and other conditions. Although limited clinical trials and meta-analyses suggest that YPFS, when combined with conventional therapies, can improve treatment efficacy, relieve symptoms, and demonstrate good safety and tolerability, current research is constrained by low evidence quality and the absence of standardized quality control measures. Future research should prioritize large-scale, multi-center clinical trials and integrate multi-omics approaches to identify the main active components and mechanisms of action.
PMID:42182585 | PMC:PMC13196821 | DOI:10.2147/DDDT.S603491
Targeted Therapy-Induced Interstitial Lung Disease in NSCLC: Mechanisms, Clinical Signatures, and a Precision Medicine Roadmap
Drug Des Devel Ther. 2026 Apr 8;20:600434. doi: 10.2147/DDDT.S600434. eCollection 2026.
ABSTRACT
Molecularly targeted therapies have transformed the therapeutic landscape of non-small cell lung cancer (NSCLC), establishing precision oncology as the foundation of modern disease management. However, these advances are increasingly complicated by drug-induced interstitial lung disease (DILD), a potentially life-threatening adverse event that can disrupt treatment continuity and compromise clinical benefit. In this review, we provide a comprehensive evaluation of interstitial lung disease associated with targeted agents in NSCLC, including oncogene-directed tyrosine kinase inhibitors, antibody-drug conjugates (ADCs), and angiogenesis inhibitors. We summarize reported differences in ILD incidence, onset timing, clinical manifestations, and radiographic characteristics across targeted agents, with particular emphasis on high-risk populations and the elevated ILD incidence observed with deruxtecan-based ADCs. We further summarize current mechanistic evidence suggesting that DILD may arise from multiple overlapping processes, including immune-mediated inflammatory activation, direct epithelial cytotoxicity, off-target kinase inhibition, and payload-dependent bystander injury. Finally, we discuss current challenges and future directions for improving pulmonary safety, including real-world datasets, multi-omics approaches, and emerging AI-assisted tools for earlier detection and risk stratification. Importantly, the current evidence base remains limited by the predominance of retrospective studies, case reports, and incomplete mechanistic validation. These insights may help guide safer and more sustained implementation of targeted therapies in NSCLC.
PMID:41978697 | PMC:PMC13070417 | DOI:10.2147/DDDT.S600434