POS0447 PHYSICAL FUNCTION IN PATIENTS WITH RA, STRATIFIED BY SEROSTATUS AND TREATMENT LINE, FOLLOWING SC ABATACEPT: POST HOC ANALYSIS OF AN OBSERVATIONAL, 2-YEAR STUDY CONDUCTED IN ROUTINE CLINICAL PRACTICE (ASCORE)

Background: RA is characterised by the production of autoantibodies, including RF and anti-citrullinated protein antibodies (ACPAs).1 Seropositive disease is associated with poorer prognosis in patients with RA,2 and response to different treatments has been shown to vary based on ACPA status.3 ASCORE (Abatacept SubCutaneOus in Routine Clinical PracticE; NCT02090556) was a 2-year, observational, prospective, multicentre study of SC abatacept for the treatment of RA.4 Objectives: This post hoc analysis of the ASCORE study evaluated patient-reported outcomes, assessed using HAQ-DI, by RF/ACPA serostatus and treatment line over 24 months of treatment with abatacept. Methods: Eligible patients, aged ≥18 years, with active moderate-to-severe RA (ACR/EULAR 2010 criteria) who were IV abatacept-naive and initiated SC abatacept 125 mg once weekly, were enrolled into two cohorts: biologic (b)DMARD-naive patients and those with ≥1 prior bDMARD treatment failure. This post hoc analysis assessed mean change from baseline in HAQ-DI score at 6, 12, 18 and 24 months in response to treatment with abatacept stratified by baseline serostatus (RF/ACPA double positive [+/+]; RF/ACPA single positive [+/−; RF+/ACPA– or RF–/ACPA+] or RF/ACPA double negative [–/–]) and by line of therapy (all patients, patients receiving abatacept as a first-line bDMARD or as a ≥ second-line bDMARD [data not shown], and those receiving abatacept following 1 [data not shown] or ≥2 prior bDMARDs). Estimates of mean difference with 95% CIs between patients with different serostatus were calculated using a t-test for all patients and within different lines of therapy. Results: Among 2892 eligible patients in ASCORE, 1748 patients with RF/ACPA status available at baseline were included in this analysis (1079 +/+, 326 +/– and 343 –/–). Of these, 791 patients received abatacept as a first-line bDMARD therapy and 957 as a ≥ second-line bDMARD therapy (505 patients had received ≥2 prior bDMARDs). Among all patients, mean change from baseline in HAQ-DI score at 6 months was greater for patients with +/+ RA (mean difference [95% CI]: –0.2 [–0.3, –0.0]; p=0.0068) or +/– RA (mean difference [95% CI]: –0.2 [–0.3, –0.0]; p=0.0315) versus those with –/– RA at baseline (Figure 1). Similarly, mean change (95% CI) in HAQ-DI score at 6 months was greater for patients with +/+ RA versus –/– RA among those receiving abatacept as first-line therapy (–0.2 [–0.4, –0.0]; p=0.0407) or following treatment with ≥2 bDMARDs (–0.3 [–0.5, –0.0]; p=0.0265) (Figure 1). Among patients treated with abatacept following ≥2 prior bDMARDs, mean change in HAQ-DI score was higher among patients with +/– RA versus –/– RA at 18 months (data not shown) and 24 months (Figure 1). No other significant differences were observed by serostatus or line of therapy at any other time points. Conclusion: Patients with RA who were RF+/ACPA+ at baseline showed an enhanced initial response to abatacept compared with those who were RF–/ACPA–. Over 24 months of treatment in this real-world setting, abatacept was equally effective as a first- or ≥ second-line therapy. References: [1]Scott DL, et al. Lancet 2010;376:1094–1108. [2]Hecht C, et al. Ann Rheum Dis 2015;74:2151–2156. [3]Harrold LR, et al. J Rheumatol 2018;45:32–39. [4]Alten R, et al. Ann Rheum Dis 2019;78(suppl 2):A1639. Acknowledgements: Professional medical writing and editorial assistance was provided by Fiona Boswell, PhD, at Caudex and was funded by Bristol Myers Squibb. This study was funded by Bristol Myers Squibb. Disclosure of Interests: Rieke Alten Speakers bureau: AbbVie, Bristol Myers Squibb, Gilead, Janssen, Lilly, Pfizer, Consultant of: AbbVie, Bristol Myers Squibb, Gilead, Janssen, Lilly, Pfizer, Grant/research support from: AbbVie, Bristol Myers Squibb, Gilead, Janssen, Lilly, Pfizer, Xavier Mariette Consultant of: Bristol Myers Squibb, Galapagos, Gilead, GlaxoSmithKline, Janssen, Pfizer, UCB, Rene-Marc Flipo Speakers bureau: AbbVie, Bristol Myers Squibb, Janssen, Lilly, Medac, Merck Sharp & Dohme, Novartis, Pfizer, Roche-Chugai, Grant/research support from: Amgen, Janssen, Novartis, Pfizer, Roberto Caporali Speakers bureau: AbbVie, Amgen, Bristol Myers Squibb, Celltrion, Fresenius Kabi, Galapagos, Gilead, Lilly, Merck Sharp & Dohme, Pfizer, Roche, Samsung Bioepis, Sanofi, UCB, Consultant of: Galapagos, Gilead, Janssen, Lilly, Merck Sharp & Dohme, Maya H Buch Speakers bureau: AbbVie, Consultant of: AbbVie, Eli Lilly, Gilead, Merck Serono, Pfizer, Roche, Sanofi, Grant/research support from: Gilead, Pfizer, Roche, UCB, Yusuf Patel: None declared, Sara Marsal Speakers bureau: Bristol Myers Squibb, Celgene, Pfizer, Roche, Sanofi, UCB, Consultant of: AbbVie, Bristol Myers Squibb, Celgene, Galapagos, Merck Sharp & Dohme, Pfizer, Roche, Sanofi, UCB, Grant/research support from: AbbVie, Bristol Myers Squibb, Celgene, Janssen, Merck Sharp & Dohme, Novartis, Pfizer, Roche, Sanofi, UCB, M.T. Nurmohamed Speakers bureau: AbbVie, Bristol Myers Squibb, Eli Lilly, Roche, Sanofi, Consultant of: AbbVie, Celgene, Celltrion, Eli Lilly, Janssen, Grant/research support from: AbbVie, Bristol Myers Squibb, Celgene, Eli Lilly, Janssen, Merck Sharp & Dohme, Mundipharma, Novartis, Pfizer, Roche, Sanofi, Hedley Griffiths Consultant of: AbbVie, Gilead, Janssen, Novartis, Peter Peichl: None declared, Bettina Bannert: None declared, Adrian Forster: None declared, Melanie Chartier Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb, Yedid Elbez Consultant of: Bristol Myers Squibb, Christiane Rauch Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb, Karissa Lozenski Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb, Vadim Khaychuk Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb