Background:Routine Assessment of Patient Index Data 3 (RAPID3) is a pooled index of 3 patient-reported measures: patient global assessment, pain, and physical function. RAPID3 was shown to correlate with other composite measures of disease activity1 and is recommended by the American College of Rheumatology for use in clinical practice.2Objectives:To evaluate the impact of upadacitinib (UPA) versus comparators on RAPID3 over 60 weeks, as well as the correlation of RAPID3 scores with other disease measures in the UPA phase 3 SELECT clinical program.Methods:This post hoc analysis included placebo-controlled (SELECT-NEXT, -BEYOND, and -COMPARE) and active comparator-controlled (SELECT-EARLY, -MONOTHERAPY, and -COMPARE) trials. Patients received UPA as monotherapy or in combination with conventional synthetic disease-modifying antirheumatic drugs (csDMARDs). Mean change from baseline in RAPID3 and the proportion of patients reporting RAPID3 remission (≤3), low (LDA, >3 to ≤6), moderate (MDA, >6 to ≤12), and high disease activity (HDA, >12) were assessed. Correlations between absolute scores for RAPID3 and Clinical Disease Activity Index (CDAI), Simplified Disease Activity Index (SDAI), and 28-joint Disease Activity Score with C-reactive protein (DAS28[CRP]) were assessed using Spearman correlation coefficients. All data are as observed.Results:A total of 661, 498, 648, 1629, and 945 patients were included from SELECT-NEXT, -BEYOND, -MONOTHERAPY, -COMPARE, and -EARLY. At baseline, the majority of patients across all studies were in RAPID3 HDA (mean baseline RAPID3 [across all studies], 17.2–19.2) (Table 1 and Figure 1). Improvements from baseline in RAPID3 were observed with UPA 15 mg and 30 mg through Week 60, with numerically greater improvements observed with UPA compared with active comparators (Table 1). Across studies, mean improvements in RAPID3 exceeded the minimal clinically important difference (MCID) with UPA and adalimumab (ADA) treatment (MCID=3.83). By Week 60, approximately one-half of UPA-treated patients were in RAPID3 remission or LDA, with only 10–25% remaining in HDA, except for the more refractory population in SELECT-BEYOND, in which ~38% of patients remained in HDA (Figure 1). RAPID3 scores moderately to strongly correlated with CDAI (ρ=0.69–0.83), SDAI (ρ=0.69–0.82), and DAS28(CRP) (ρ=0.58–0.77), across all studies, at Week 60 (all pConclusion:UPA, as monotherapy or in combination with csDMARDs, was associated with improvements in patient-reported disease activity, pain, and physical function, as assessed by RAPID3 over 60 weeks in the phase 3 SELECT clinical program. RAPID3 continues to be an important tool in clinical practice to assess disease activity, as it was shown to correlate to other disease activity measures and allows for rapid scoring.References:[1]Pincus T, et al. Arthritis Care Res (Hoboken) 2010;62:181–9.[2]England BR, et al. Arthritis Care Res (Hoboken) 2019;71:1540–55.[3]Ward MM, et al. J Rheumatol 2019;46:27–30.Table 1.Change from BL in RAPID3 at Week 60 (as observed)Phase 3 studyGroupnaMean (SD) BL scoreMean (SD) change from BLbSELECT-EARLYc(MTX-naïve)MTX23618.5 (5.6)−9.6 (7.5)UPA 15 mg QD26918.9 (5.6)−12.0 (7.6)UPA 30 mg QD25318.2 (5.6)−13.4 (7.2)SELECT-NEXT(csDMARD-IR)UPA 15 mg QD17217.7 (5.1)−11.1 (7.3)UPA 30 mg QD17217.6 (5.3)−10.4 (6.8)SELECT-MONOTHERAPY(MTX-IR)UPA 15 mg QD17217.4 (5.8)−9.6 (7.4)UPA 30 mg QD18017.2 (5.9)−10.6 (7.2)SELECT-COMPAREc(MTX-IR)UPA 15 mg QD55218.5 (5.5)−10.2 (7.1)ADA 40 mg EOW26418.7 (5.4)−8.8 (6.7)SELECT-BEYOND(bDMARD-IR)UPA 15 mg QD13319.2 (5.1)−8.6 (6.8)UPA 30 mg QD11818.5 (5.3)−9.3 (7.3)b, biologic; BL, baseline; EOW, every other week; IR, inadequate response; MTX, methotrexate; QD, once daily; SD, standard deviationaNumber of patients with RAPID3 values at both BL and Week 60. bNegative values indicate improvement from BL. cObserved data include patients rescued to UPA and/or ADA; treatment effect may include both the randomized and switch treatments in these patientsAcknowledgements:AbbVie funded this study; contributed to its design; participated in data collection, analysis, and interpretation of the data; and participated in the writing, review, and approval of the abstract. No honoraria or payments were made for authorship. Medical writing support was provided by Grant Kirkpatrick, MSc, of 2 the Nth (Cheshire, UK), and was funded by AbbVie.Disclosure of Interests:Martin Bergman Shareholder of: Johnson & Johnson, Speakers bureau: AbbVie, Celgene, GSK, MSD, Novartis, Pfizer, and Sanofi/Regeneron, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Genentech/Roche, Gilead, Horizon, Janssen, MSD, Novartis, Pfizer, Sandoz, Sanofi/Regeneron, and Scipher, Maya H Buch Consultant of: AbbVie, Eli Lilly, Merck-Serono, Pfizer, Sandoz, and Sanofi, Grant/research support from: Pfizer, Roche, and UCB, Yoshiya Tanaka Speakers bureau: AbbVie, Asahi Kasei, Astellas, Bristol-Myers Squibb, Chugai, Daiichi Sankyo, Eisai, Eli Lilly, GSK, Janssen, Mitsubishi Tanabe, Novartis, Pfizer, Sanofi, Takeda, UCB, and YL Biologics, Grant/research support from: AbbVie, Astellas, Bristol-Myers Squibb, Chugai, Daiichi Sankyo, Eisai, Mitsubishi Tanabe, MSD, Ono, Taisho Toyama, and Takeda, Gustavo Citera Consultant of: AbbVie, Bristol-Myers Squibb, Eli Lilly, Genzyme, Pfizer, and Roche, Sami Bahlas: None declared, Ernest Wong Consultant of: AbbVie, Chugai, Eli Lilly, MSD, Novartis, Pfizer, Roche, and UCB, Grant/research support from: AbbVie, Chugai, Novartis, and UCB, Yanna Song Shareholder of: May own stock or options in AbbVie, Employee of: AbbVie, Namita Tundia Shareholder of: May own stock or options in AbbVie, Employee of: AbbVie, Jessica Suboticki Shareholder of: May own stock or options in AbbVie, Employee of: AbbVie, Vibeke Strand Consultant of: AbbVie, Amgen, Arena, AstraZeneca, Bayer, Bristol-Myers Squibb, Boehringer Ingelheim, Celltrion, Eli Lilly, Gilead, Ichnos, Inmedix, Janssen, Kiniksa, MSD, Myriad Genetics, Novartis, Pfizer, Regeneron, Samsung, Sandoz, Sanofi, Scipher, Setpoint, and UCB.