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Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by progressive joint erosion. Tumor necrosis factor (TNF) antagonists are the most widely used biological disease-modifying anti-rheumatic drug in RA. However, there continue to be one third of RA patients who have poor or no response to TNF antagonists. Following consideration of the uncertainty of therapeutic effects and the high price of TNF antagonists, it is worthy to predict the treatment responses before anti-TNF therapy. According to the comparisons between the responders and non-responders to TNF antagonists by omic technologies, such as genomics, transcriptomics, proteomics, and metabolomics, rheumatologists are eager to find significant biomarkers to predict the effect of TNF antagonists in order to optimize the personalized treatment in RA.
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http://dx.doi.org/10.1007/s10067-017-3639-0 | DOI Listing |
APMIS
September 2025
Cancer Cytogenomic Laboratory, Center for Research and Drug Development (NPDM), Federal University of Ceara, Fortaleza, Ceara, Brazil.
Toll-like receptors (TLRs) are essential components of the innate immune system, functioning as pattern recognition receptors (PRRs) to detect pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). In hematological malignancies, particularly myelodysplastic syndromes (MDS), acute myeloid leukemia (AML), and chronic myeloid leukemia (CML), TLRs influence inflammation, disease progression, and therapeutic response. This review highlights the prognostic relevance of TLR expression, the role of the MyD88 signaling pathway in clonal evolution, and the dual nature of TLR-mediated immune responses, either promoting antitumor activity or contributing to leukemogenesis.
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December 2025
Office of Pharmaceutical Quality Research, Office of Pharmaceutical Quality, Center for Drug Evaluation and Research, Food and Drug Administration, Silver Spring, MD, USA.
The analytical comparability of biologic products and their biosimilars, including higher-order structure (HOS) assessment, ensures product quality and is required for regulatory approval. In this study, nuclear magnetic resonance (NMR) spectroscopy was used to evaluate the HOS of Humira (adalimumab) and its biosimilars under normal and photo-stressed conditions. Under normal conditions, 1D and 2D NMR spectra showed strong structural similarity among all products.
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August 2025
Department of Allergy, Immunology and Rheumatology, Chung Shan Medical University Hospital, Taichung, Taiwan.
Objective: We aim to evaluate the malignancy risk between Janus kinase inhibitors (JAKi) users and tumor necrosis factor inhibitors (TNFi) users in rheumatoid arthritis (RA) patients, using a large real-world electronic health record database (TriNetX).
Methods: In this retrospective cohort study, we identified adult RA patients initiating JAKi or TNFi therapy between January 1, 2018, and December 31, 2022, within the TriNetX global federated network. The hazard ratio (HR) and confidence intervals (CI) of incident-specific cancers, overall cancer incidence, and all-cause mortality, were calculated between the propensity score matched JAKi and TNFi cohorts.
Drug Des Devel Ther
September 2025
The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, 310053, People's Republic of China.
Purpose: To assess the pharmacodynamic effects and therapeutic mechanisms of modified Fuzi decoction (MFZD) in osteoarthritis (OA), particularly OA-related inflammation.
Methods: The main components of MFZD were identified using Ultra Performance Liquid Chromatography-Tandem Mass Spectrometry (UPLC-MS/MS). An OA model was established in Sprague-Dawley rats via intra-articular injection of monoiodoacetate (MIA) to evaluate the anti-OA efficacy of MFZD via gavage.
Bioorg Med Chem Lett
September 2025
Department of Chemistry and Biochemistry, University of Notre Dame, Notre Dame, IN 46556, United States. Electronic address:
The mitochondrial Hsp90 isoform, Tumor Necrosis Factor Receptor Associated Protein 1 (TRAP1), is central to the pathogenesis of disease states that include cancer, ischemic retinopathy, and diabetic kidney disease among others. TRAP1 contributes to these diseases through the regulation of mitochondrial metabolism, apoptosis, oxidative stress, cell signaling and angiogenesis through interactions with client proteins. Numerous TRAP1-selective inhibitors have been developed to limit the toxicities associated with Hsp90 pan-inhibition, while leveraging the therapeutic benefits of TRAP1 inhibition.
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