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Introduction In a real-world cohort of rheumatoid arthritis (RA) patients who were unable to discontinue glucocorticoids (GCs) despite prior therapies, we aimed to evaluate the GC-sparing effect of baricitinib (BARI) and to identify clinical factors associated with GC reduction. Materials and methods This single-center retrospective observational study included RA patients who initiated BARI while receiving systemic GCs between 2018 and 2024. Disease activity and daily GC dose were assessed at baseline and at weeks 4, 12, and 24. The primary outcome was the percent reduction in daily GC dose at week 24. Linear and logistic regression analyses were performed to identify factors associated with GC reduction and discontinuation, with two-variable multivariable models constructed to avoid overfitting. Results Among 177 patients who initiated BARI, 39 (22%) were receiving GCs at treatment initiation and were included in the analysis. After prior exposure to biologic or targeted synthetic DMARDs in 31 patients (79%), 34 (87%) had moderate or higher disease activity by the Clinical Disease Activity Index at baseline, and 27 (69%) had comorbid interstitial lung disease. The median daily GC dose decreased from 3.0 mg/day at baseline to 1.0 mg/day at week 24 ( P < 0.001), with a significant reduction observed as early as week 4. The median GC reduction rate at week 24 was 66%, with 18 of 39 patients (46%) achieving a ≥ 50% reduction and 10 patients (26%) discontinuing GCs entirely. Disease activity improved significantly, with 62% of patients achieving remission or low disease activity by week 24. In linear regression analysis, refractoriness to ≥ 2 prior biologic or targeted synthetic DMARDs was independently associated with a smaller degree of GC reduction. No unexpected safety signals were observed. Conclusion In this real-world cohort of GC-dependent RA patients with persistent disease activity and frequent ILD comorbidity despite prior therapies, BARI enabled clinically meaningful GC reduction and improved disease activity within 24 weeks. Resistance to multiple prior b/tsDMARDs emerged as a key barrier to GC tapering, highlighting the importance of introducing JAK inhibitors before progression to a difficult-to-treat state.