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ObjectivesTo evaluate efficacy and safety of abatacept in adults with active primary Sjögren’s syndrome (pSS) in a phase III, randomised, double-blind, placebo-controlled trial.MethodsEligible patients (moderate-to-severe pSS [2016 ACR/European League Against Rheumatism (EULAR) criteria], EULAR Sjögren’s Syndrome Disease Activity Index [ESSDAI] ≥5, anti-SS-related antigen A/anti-Ro antibody positive) received weekly subcutaneous abatacept 125 mg or placebo for 169 days followed by an open-label extension to day 365. Primary endpoint was mean change from baseline in ESSDAI at day 169. Key secondary endpoints were mean change from baseline in EULAR Sjögren’s Syndrome Patient Reported Index (ESSPRI) and stimulated whole salivary flow (SWSF) at day 169. Other secondary clinical endpoints included glandular functions and patient-reported outcomes. Selected biomarkers and immune cell phenotypes were examined. Safety was monitored.ResultsOf 187 patients randomised, 168 completed double-blind period and 165 continued into open-label period. Mean (SD) baseline ESSDAI and ESSPRI total scores were 9.4 (4.3) and 6.5 (2.0), respectively. Statistical significance was not reached for primary (ESSDAI −3.2 abatacept vs −3.7 placebo, p=0.442) or key secondary endpoints (ESSPRI, p=0.337; SWSF, p=0.584). No clinical benefit of abatacept over placebo at day 169 was seen with other clinical and PRO endpoints. Relative to baseline, abatacept was associated with significant differences vs placebo in some disease-relevant biomarkers (including IgG, IgA, IgM-rheumatoid factor) and pathogenic cell subpopulations (post hoc analyses). No new safety signals were identified.ConclusionsAbatacept treatment did not result in significant clinical efficacy compared with placebo in patients with moderate-to-severe pSS, despite evidence of biological activity.

Background:Tyrosine kinase 2 (TYK2) is an intracellular kinase that mediates IL-23, IL-12, and IFNα/β signaling. Deucravacitinib is a novel, oral selective inhibitor of TYK2 acting via the TYK2 regulatory domain. Phase 2 results showed deucravacitinib was efficacious and well tolerated versus placebo (PBO) in patients with active psoriatic arthritis (PsA).Objectives:This analysis further evaluated improvements in musculoskeletal disease manifestations in patients in the Phase 2 PsA trial.Methods:The ongoing Phase 2 trial (NCT03881059) enrolled patients who had a PsA diagnosis for ≥6 months, met CASPAR criteria, had active disease (≥3 tender joints, ≥3 swollen joints, C-reactive protein [CRP] ≥3 mg/L), and had at least 1 active skin lesion. Patients either failed or were intolerant to at least 1 nonsteroidal anti-inflammatory drug, corticosteroid, conventional synthetic disease-modifying antirheumatic drug, and/or 1 TNF inhibitor (TNFi; ≤30%). Patients were randomized 1:1:1 to deucravacitinib 6 mg QD or 12 mg QD or PBO, and stratified by TNFi status (experienced vs naive) and body weight (Results:Patients treated with deucravacitinib were numerically more likely to achieve ACR20 response at Week 16 compared with PBO-treated patients regardless of TNFi experience or body weight, although some of these groups were small (Figure). Improvements for deucravacitinib 6 mg and 12 mg QD versus PBO were observed in all ACR components, with apparent separation occurring as early as Week 4 on, for example, HAQ-DI (mean change from baseline, -0.2 vs -0.2 vs -0.1, respectively) and hCRP (mean change from baseline, -7.4 vs -5.2 vs 0.3, respectively) and maintained through Week 16 (Table).Table 1.Mean (SD) change from baseline for ACR componentsTJCSJCPtGAPainPGAHAQ-DIhCRPBaselineaPBO16.9 (9.8)10.5 (7.7)66.2 (15.8)64.9 (18.2)63.8 (14.8)1.3 (0.6)20.4 (39.1)DEUC 618.1 (10.3)11.9 (7.0)68.2 (16.8)63.6 (21.7)68.2 (14.7)1.3 (0.6)17.6 (23.6)DEUC1219.4 (11.8)11.3 (9.0)63.6 (15.6)63.8 (15.9)63.3 (16.1)1.3 (0.6)16.5 (21.7)Week 16bPBO-4.6 (9.7)-4.3 (8.0)-13.4 (23.5)-13.8 (21.5)-19.9 (21.8)-0.1 (0.4)-3.3 (22.6)DEUC 6-9.3 (9.7)-7.7 (5.8)-28.7 (23.1)-25.3 (26.1)-33.6 (23.0)-0.4 (0.5)-14.2 (24.5)DEUC 12-12.2 (10.2)-8.5 (9.1)-27.6 (25.8)-27.5 (25.0)-32.2 (25.0)-0.4 (0.6)-10.9 (22.8)PBO, n/N=58/66; DEUC 6, n/N=63/70; DEUC 12, n/N=59/67; n/N = number of patients who completed treatment/number of patients randomized; the number of patients with data available for individual components at each time point may vary.aMean (SD). bMean (SD) change from baseline.ACR, American College of Rheumatology; DEUC 6, deucravacitinib 6 mg QD; DEUC 12, deucravacitinib 12 mg QD; HAQ-DI, Health Assessment Questionnaire-Disability Index total score; hCRP, high-sensitivity C-reactive protein; PBO, placebo; PGA, Physician’s Global Assessment of psoriatic arthritis; PtGA, Patients’ Global Assessment of disease activity; QD, once daily; SJC, swollen joint count; TJC, tender joint count.Conclusion:Analyses confirmed the efficacy of deucravacitinib versus PBO across TNFi and body weight subgroups. With deucravacitinib treatment, improvements were displayed in all ACR components.Acknowledgements:This study was sponsored by Bristol Myers Squibb. Professional medical writing assistance was provided by Peloton Advantage, LLC, an OPEN Health company, and funded by Bristol Myers Squibb.Disclosure of Interests:Philip J Mease Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead, GlaxoSmithKline, Janssen, Novartis, Pfizer, SUN Pharma, UCB, Grant/research support from: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead, GlaxoSmithKline, Janssen, Novartis, Pfizer, SUN Pharma, UCB, Atul Deodhar Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Galapagos, GlaxoSmithKline, Janssen, Novartis, Pfizer, UCB, Grant/research support from: AbbVie, Eli Lilly, GlaxoSmithKline, Novartis, Pfizer, UCB, Désirée van der Heijde Consultant of: AbbVie, Amgen, Astellas, AstraZeneca, Bayer, Bristol Myers Squibb, Boehringer Ingelheim, Celgene, Cyxone, Daiichi, Eisai, Eli Lilly, Galapagos, Gilead, GlaxoSmithKline, Janssen, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi, Takeda, UCB Pharma. Director of Imaging Rheumatology BV, Frank Behrens Consultant of: Pfizer, AbbVie, Sanofi, Lilly, Novartis, Genzyme, Boehringer, Janssen, MSD, Celgene, Roche, Chugai, Bristol Myers Squibb, UCB Pharma, Grant/research support from: Pfizer, Janssen, Chugai, Celgene, Roche, Alan Kivitz Shareholder of: Pfizer, Sanofi, GlaxoSmithKline, Gilead Sciences, Inc., Novartis; Paid consultant: AbbVie, Boehringer Ingelheim, Flexion, Janssen, Pfizer, Sanofi, Regeneron, SUN Pharma Advanced Research, Gilead Sciences, Inc, Speakers bureau: Amgen, Horizon, Lilly, Novartis, Pfizer, Sanofi, Genzyme, Flexion, AbbVie, Thomas Lehman Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb, Lan Wei Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb, Marleen Nys Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb, Subhashis Banerjee Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb, Miroslawa Nowak Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb

ObjectivesTo assess the efficacy and safety of abatacept, a selective T-cell costimulation modulator, in a phase III study in psoriatic arthritis (PsA).MethodsThis study randomised patients (1:1) with active PsA (~60% with prior exposure to a tumour necrosis factor inhibitor) to blinded weekly subcutaneous abatacept 125 mg (n=213) or placebo (n=211) for 24 weeks, followed by open-label subcutaneous abatacept. Patients without ≥20% improvement in joint counts at week 16 were switched to open-label abatacept. The primary end point was the proportion of patients with ≥20% improvement in the American College of Rheumatology (ACR20) criteria at week 24.ResultsAbatacept significantly increased ACR20 response versus placebo at week 24 (39.4% vs 22.3%; pConclusionsAbatacept treatment of PsA in this phase III study achieved its primary end point, ACR20 response, showed beneficial trends overall in musculoskeletal manifestations and was well tolerated. There was only a modest impact on psoriasis lesions.Trial registration numberClinicalTrials.gov number, NCT01860976 (funded by Bristol-Myers Squibb).

Background:Maintenance of clinical response over time has been shown in individual patients (pts) with polyarticular-course juvenile idiopathic arthritis (pJIA) treated with SC abatacept (ABA).1It is unknown whether each individual pt with sustained efficacy also consistently maintains the previously reported shorter-term benefits on patient-reported outcomes (PROs)2,3over time.Objectives:Investigate whether combined efficacy and stringent, optimal PRO responses to ABA treatment are maintained by individual pts with pJIA over time.Methods:In this analysis of the intent-to-treat population, pts in two age cohorts (2–5 and 6–17 yrs) who achieved clinical response to weekly SC ABA (10–4) were followed for 2 yrs. Stringent efficacy outcomes (Juvenile Arthritis Disease Activity Score 27 [JADAS27] minimal disease activity [MDA; ≤3.8] and inactive disease [ID; ≤1] status) were combined with optimal PRO endpoints (childhood [C]HAQ-DI=0, Parental Global Assessment [PaGA] ≤1 and Pain visual analogue scale [VAS] Results:219 pts entered the study (46 [21.0%] 2–5 yrs; 173 [79.0%] 6–17 yrs); a subgroup of these pts achieved a clinical response at Mo 4 (Table 1). Many pts who achieved JADAS27 MDA or JADAS27 ID combined with optimal PROs at Mo 4 sustained their response at Mo 13, and at both Mo 13 and Mo 21 in the 2–5-yr and 6–17-yr cohorts (Table 1). Across the cohorts, 33–88% of pts maintained a combined JADAS27 MDA with optimal PRO responses through Mo 21. Where estimable, median times to combined efficacy and specific optimal PRO responses were consistent across the cohorts (Table 2; Figs 1, 2).Table 1.Proportion of pts with combined efficacy and optimal PRO responses at Mos 4, 13 and 21EndpointResponders at Mo 4Responders at Mos 4 and 13*Responders at Mos 4, 13 and 21*2–5 yrs (n=46)6–17 yrs (n=173)2–5 yrs6–17 yrs2–5 yrs6–17 yrsJADAS27 MDA and CHAQ-DI=09 (20)34 (20)5/9 (56)25/34 (74)3/9 (33)16/34 (47)JADAS27 MDA and PaGA ≤18 (17)14 (8)8/8 (100)7/14 (50)7/8 (88)5/14 (36)JADAS27 MDA and Pain VAS 28 (61)70 (41)25/28 (89)58/70 (83)21/28 (75)43/70 (61)JADAS27 ID and CHAQ-DI=07 (15)20 (12)2/7 (29)13/20 (65)1/7 (14)9/20 (45)JADAS27 ID and PaGA ≤16 (13)10 (6)4/6 (67)4/10 (40)4/6 (67)4/10 (40)JADAS27 ID and Pain VAS 17 (37)31 (18)10/17 (59)22/31 (71)8/17 (47)17/31 (55)Data are n (%) or n/N (%). *% based on n of pts who achieved response at Mo 4 (denominator)Table 2.Kaplan–Meier estimates for median (95% CI) times (mos) to achieving combined efficacy and optimal PRO responsesEndpoint2–5 yrs6–17 yrsJADAS27 MDA and CHAQ-DI=021.5 (6.8, NE)21.5 (13.1, 24.4)JADAS27 MDA and PaGA ≤1NE (15.9, NE)24.6 (24.3, NE)JADAS27 MDA and Pain VAS 2.8 (1.9, 2.9)3.8 (3.7, 6.6)JADAS27 ID and CHAQ-DI=0NE (18.4, NE)24.4 (18.7, NE)JADAS27 ID and PaGA ≤1NE (21.3, NE)24.6 (24.3, NE)JADAS27 ID and Pain VAS 3.8 (3.8, 10.3)13.2 (10.3, 15.9)NE=not estimableConclusion:Many individuals with pJIA who achieved stringent efficacy and PRO measures with weekly SC abatacept by Mo 4 sustained them over 2 years. Time to achieve combined efficacy and Pain VAS References:[1]Ruperto N, et al.Ann Rheum Dis2019;78:99–100 (abstr OP0056)[2]Brunner H, et al.Arthritis Rheumatol2019;71(suppl 10):abstr 2707[3]Ruperto N, et al.Ann Rheum Dis2017;76:75 (abstr OP0058)[4]Brunner HI, et al.Arthritis Rheumatol2018;70:1144–54Acknowledgments:Katerina Kumpan, PhD, Caudex; funding: Bristol-Myers SquibbDisclosure of Interests: :Hermine Brunner Consultant of: Hoffman-La Roche, Novartis, Pfizer, Sanofi Aventis, Merck Serono, AbbVie, Amgen, Alter, AstraZeneca, Baxalta Biosimilars, Biogen Idec, Boehringer, Bristol-Myers Squibb, Celgene, EMD Serono, Janssen, MedImmune, Novartis, Pfizer, and UCB Biosciences, Speakers bureau: GSK, Roche, and Novartis, Nikolay Tzaribachev: None declared, Ingrid Louw Consultant of: Amgen, Novartis, Pfizer, Roche (advisory boards), Inmaculada Calvo Grant/research support from: Bristol-Myers Squibb, Clementia, GlaxoSmithKline, Hoffman-La Roche, Merck Sharpe & Dohme, Novartis, Pfizer, Sanofi, Speakers bureau: AbbVie, GlaxoSmithKline, Hoffman-La Roche, Novartis, Francisco Zapata: None declared, Gerd Horneff Grant/research support from: AbbVie, Chugai, Merck Sharp & Dohme, Novartis, Pfizer, Roche, Speakers bureau: AbbVie, Bayer, Chugai, Merck Sharp & Dohme, Novartis, Pfizer, Roche, Ivan Foeldvari Consultant of: AbbVie, Amgen, Bristol-Myers Squibb, Chugai, Eli Lilly, Novartis, Pfizer, Daniel Kingsbury: None declared, Maria Gastanaga Grant/research support from: Amgen, Bristol-Myers Squibb, GlaxoSmithKline, Novartis, Pfizer, Roche, Speakers bureau: AbbVie, Roche, Carine Wouters Grant/research support from: GlaxoSmithKline, Pfizer, Roche, Johannes Breedt: None declared, Robert Wong Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, Marleen Nys Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, Margarita Askelson Consultant of: Bristol-Myers Squibb, Joe Zhuo Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, Alberto Martini Consultant of: AbbVie, Eli Lily, EMD Serono, Janssen, Novartis, Pfizer, UCB, Daniel J Lovell Consultant of: Abbott (consulting and PI), AbbVie (PI), Amgen (consultant and DSMC Chairperson), AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb (PI), Celgene, Forest Research (DSMB Chairman), GlaxoSmithKline, Hoffman-La Roche, Janssen (co-PI), Novartis (consultant and PI), Pfizer (consultant and PI), Roche (PI), Takeda, UBC (consultant and PI), Wyeth, Employee of: Cincinnati Children’s Hospital Medical Center, Speakers bureau: Wyeth, Nicolino Ruperto Grant/research support from: Bristol-Myers Squibb, Eli Lily, F Hoffmann-La Roche, GlaxoSmithKline, Janssen, Novartis, Pfizer, Sobi (paid to institution), Consultant of: Ablynx, AbbVie, AstraZeneca-Medimmune, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lily, EMD Serono, GlaxoSmithKline, Hoffmann-La Roche, Janssen, Merck, Novartis, Pfizer, R-Pharma, Sanofi, Servier, Sinergie, Sobi, Takeda, Speakers bureau: Ablynx, AbbVie, AstraZeneca-Medimmune, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lily, EMD Serono, GlaxoSmithKline, Hoffmann-La Roche, Janssen, Merck, Novartis, Pfizer, R-Pharma, Sanofi, Servier, Sinergie, Sobi, Takeda

Background IV abatacept (ABA) 10 mg/kg every 4 weeks is safe and effective in reducing signs and symptoms of polyarticular forms of juvenile idiopathic arthritis (pJIA) in children and adolescents. 1 SC ABA 125 mg weekly has therapeutically equivalent efficacy and comparable safety to IV ABA in adult RA, but similar data in pJIA are lacking. Objectives To assess the PK, efficacy and safety of SC ABA in children and adolescents with active pJIA. Methods This single-arm, open-label (OL), Phase III study (NCT01844518) enrolled patients (pts) aged 2–17 years (yrs) with pJIA and an inadequate response/intolerance to ≥1 DMARD. Pts received SC ABA weekly OL for 4 months (M), based on body weight tier (10– 50 kg [125 mg ABA]). JIAACR criteria 30 (JIAACR30) responders at 4M could enter a 20M OL extension; JIAACR30 non-responders could continue SC ABA for 3M more and discontinued if JIAACR30 was not achieved by M7. The primary endpoint was steady-state blood trough concentration (C minss ) of ABA at 4M in the 6–17-yr-old pJIA pts (n=173); we report PK, efficacy and safety from the initial 4M OL phase for these pts. Results Baseline characteristics of the 173 pJIA pts were: mean age (SD) =12.3 (3.1) yrs; mean number of active joints (SD) =12.4 (8.3); 78.6% of patients used MTX (mean dose: 12 mg/m 2 /week) and 26.6% failed prior biologic treatment. The target therapeutic C minss of 10 μg/mL was achieved (Figure); at 4M, mean (SD) C minss was 42.1 (14.7) μg/mL and was consistent across all three weight groups. Robust JIAACR responses were seen at 4M (Figure): JIAACR30, 80.9%; inactive disease, 29.5%. Biologic-naive pts had a numerically higher JIAACR30 response than biologic-experienced pts at 4M. The number of pts with serious AEs and those who discontinued study drug due to AEs during the initial 4M were low (n=5 and n=3 [fatigue, exanthematous rash and ovarian germ cell teratoma] pts, respectively). AEs of interest reported included infections (31.8%) with 1 case of sepsis, injection-site reactions (5.2%) and malignancy (0.6%). No laboratory abnormalities or unexpected safety concerns were reported. Conclusions The target therapeutic exposure for SC abatacept was achieved in pts aged 6–17 yrs with pJIA irrespective of weight group. The exposures for SC abatacept were within the range for IV abatacept in pJIA and comparable with SC abatacept in adult RA. Robust efficacy was observed with SC abatacept with no new safety concerns after 4M of treatment. References Ruperto N, et al. Lancet 2008;372:383–91. Disclosure of Interest N. Ruperto Grant/research support from: Gaslini Hospital, Bristol-Myers Squibb, Hoffman-La Roche, Janssen, Novartis, Pfizer, sanofi aventis, Schwarz Biosciences, Sobi, Consultant for: AbbVie, Amgen, Biogen Idec, Baxalta, Boehringer, Bristol-Myers Squibb, Celgene, EMD Serono, Hoffman-La Roche, Janssen, Novartis, Pfizer, Servier, Sinergie,Takeda, Speakers bureau: AbbVie, Amgen, Biogen Idec, Baxalta, Boehringer, Bristol-Myers Squibb, Celgene, EMD Serono, Hoffman-La Roche, Janssen, Novartis, Pfizer, Servier, Sinergie,Takeda, D. J. Lovell Grant/research support from: NIH, Consultant for: AstraZeneca, Bristol-Myers Squibb, AbbVie, Pfizer, Roche, Novartis, UBC, Forest Research Institute, Horizon, Johnson & Johnson, Biogen, Takeda, Genentech, GlaxoSmithKline, Boehringer Ingelheim, Celgene, Janssen, N. Tzaribachev Grant/research support from: UCB, Pfizer, Janssen, Roche, G. Vega-Cornejo: None declared, I. Louw: None declared, A. Berman: None declared, I. Calvo Grant/research support from: Novartis, Speakers bureau: AbbVie, Roche, Novartis, Sobi, R. Cuttica: None declared, G. Horneff Grant/research support from: Pfizer, AbbVie, Roche, F. Avila-Zapata: None declared, J. Anton Grant/research support from: Pfizer, Novartis, Speakers bureau: Pfizer, AbbVie, Novartis, Sobi, Roche, D. Viola: None declared, I. Foeldvari: None declared, V. Keltsev: None declared, D. Kingsbury: None declared, X. Li Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, M. Nys Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, R. Wong Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, S. Banerjee Shareholder of: Bristol-Myers Squibb, Employee of: Bristol-Myers Squibb, A. Martini Grant/research support from: The Gaslini Hospital, which is the public Hospital where I work as full time public employee, has received contributions from the following industries: Abbott, Bristol-Myers Squibb, “Francesco Angelini”, GlaxoSmithKline, Hoffman-La Roche, Italfarmaco, Janssen, Novartis, Pfizer, sanofi aventis, Schwarz Biosciences, Sobi, Xoma, Wyeth, Consultant for: Abbott, AbbVie, Amgen, Biogen, Bristol-Myers Squibb, Astellas, Boehringer, Italfarmaco, Janssen, MedImmune, Novartis, NovoNordisk, H. I. Brunner Consultant for: Pfizer, Bristol-Myers Squibb, UCB, Janssen, Amgen, Celgene, AstraZeneca, Novartis, Genentech, Speakers bureau: Novartis, Genentech

Objective To assess the efficacy and safety of abatacept in biological-naive patients with rheumatoid arthritis and an inadequate response to methotrexate treated in the long-term extension (LTE) of the ATTEST trial. Methods Patients randomly assigned to abatacept, placebo or infliximab completing the 1-year double-blind period were eligible to receive abatacept ∼10 mg/kg in the open-label LTE. Efficacy to year 2 is presented for patients randomly assigned to abatacept or infliximab who switched to open-label abatacept. Safety data are presented for all patients entering LTE regardless of double-blind treatment. Results Of 431 patients randomly assigned, 79.8% remained on abatacept at year 2. At years 1 and 2, 19.7% and 26.1% of abatacept and 13.3% and 28.6% of infliximab-to-abatacept patients achieved disease activity score 28-defined remission (

Background Immunogenicity with therapeutic proteins has been linked to reduction in both efficacy and safety in patients (pts) with RA.1,2 We previously reported in clinical trials that IV abatacept (ABA) demonstrated low (∼3%) and transient immunogenicity that has no apparent impact on efficacy or safety.3 Objectives To evaluate immunogenicity in a large pt group with long-term (up to 8 yrs) IV ABA exposure. Methods Data from 7 ABA RA clinical trials were included in immunogenicity assessments, including double-blind periods from 6 placebo-controlled studies (AIM, ATTEST, ATTAIN, ASSURE, 101 and 100) and 1 non-randomized, open-label study (ARRIVE), and their open-label, long-term extensions. Pts had active RA, inadequate response/intolerance to MTX/DMARDs or biologics and were treated with IV ABA (∼10 mg/kg) every 4 weeks. Anti-ABA antibodies were detected using two ELISA assays: one to whole ABA molecule (CTLA4 and IgG1), and one to CTLA4 “tip” region (T). Positive samples had titers≥400 for anti-ABA or ≥25 for anti-CTLA4-T. Persistent immunogenicity was defined as positive response on ≥2 consecutive visits. Data are as-observed for all ABA-treated pts. Results 3985 pts were included with up to 8 yrs’ ABA exposure. A total of 6.3% of pts demonstrated immunogenicity; titers were low and did not increase with continued treatment. Persistent immunogenicity (2.4%) and immunogenicity with missed doses (3.8% for 1 and 4.6% for ≥2 missed doses) were also low. Serious adverse events (SAEs) attributed as being related to study drug were reported in 32/252 (12.7%) pts who experienced immunogenicity. No relationship was identified between immunogenicity and SAEs, peri-infusional, acute infusional or autoimmune events, or hypersensitivity reactions. No consistent relationship between immunogenicity and efficacy (measured by ACR20) was observed; 83% (55/66) of ACR20 responders maintained ACR20 vs 36% (10/28) of non-responders achieved ACR20 following positive antibody response. Conclusions Abatacept demonstrated low immunogenicity in pts with RA and up to 8 yrs of abatacept exposure. Titers of anti-abatacept and anti-CTLA-4-T antibodies were low and did not persist nor increase with continued treatment. No consistent association was observed between antibody response and clinical efficacy or safety. References Bartelds GM, et al. JAMA 2011;305:1460–8. Pascual-Salcedo D, et al. Rheumatology 2011;50:1445–52. Haggerty HG, et al. J Rheum 2007;34:2365–73. Disclosure of Interest M. Weinblatt Grant/Research support from: Bristol-Myers Squibb, Consultant for: Bristol-Myers Squibb, M. Genovese Consultant for: Bristol-Myers Squibb, M. Schiff Consultant for: Bristol-Myers Squibb, R. Westhovens Grant/Research support from: Roche, UCB, Inc., Consultant for: Bristol-Myers Squibb, Centocor, Inc., Roche, Schering-Plough, Speakers Bureau: Bristol-Myers Squibb, R. Alten Grant/Research support from: BMS, Merck Pharma GmbH, Wyeth Pharmaceuticals, Pfizer, Consultant for: Abbott Laboratories, Horizon Pharma, Merck Pharma GmbH, Nitec Pharma GmbH, Novartis Pharmaceuticals Corporation, Roche, Speakers Bureau: Abbott Laboratories, BMS, Horizon Pharma, Merck Pharma GmbH, Novartis Pharmaceuticals Corporation, Roche, I. Delaet Employee of: Bristol-Myers Squibb, M. Nys Employee of: Bristol-Myers Squibb, J. Manning Employee of: Bristol-Myers Squibb, J. Kremer Grant/Research support from: Bristol-Myers Squibb, Speakers Bureau: Bristol-Myers Squibb