Background: Immune-mediated inflammatory diseases such as giant cell arteritis (GCA) and rheumatoid arthritis (RA) may increase patients' risk for cardiovascular (CV) and thrombotic events [1-4]. The risk for CV or venous thromboembolism (VTE) events in GCA relative to RA is not well known. Objectives: To describe the relative risk of myocardial infarction or stroke (MI/stroke) and VTE events in patients with GCA compared with RA and a matched control cohort unaffected by GCA, and to explore how baseline demographics, comorbidities, and select medications contribute to the underlying risk of such events in patients with GCA. Methods: This retrospective, observational, comparative cohort study used US claims data (Optum Clinformatics® Data Mart; 1 Jan 2014–30 Sep 2022) from adults aged ≥ 50 years with GCA or RA; non-GCA controls were matched 1:1 to patients in the GCA cohort (but not the RA cohort) by age, sex, and cohort entry date (CED). Control patients were not excluded for other comorbidities. Patients had ≥ 12 months of baseline claims data before diagnosis or CED and ≥ 1 day of follow-up data, and were followed until the earliest date of either a MI/stroke or VTE, disenrollment, death, or analysis period end. The primary outcomes were an inpatient (IP) hospitalized MI/stroke or VTE (deep vein thrombosis, pulmonary embolism) diagnosis. A secondary outcome for VTE included diagnoses for IP VTE or outpatient (OP) VTE (2 OP diagnoses within 7–‍185 days of each other, or 1 OP diagnosis and anticoagulant initiation within ≤ 7 days). MI/stroke and VTE cases per 100 person-years (PY) were reported. The relative risk (for GCA vs RA or controls) and the risk by baseline characteristics (in GCA) for MI/stroke and VTE were estimated with the Cox proportional hazards regression model adjusted for baseline demographics, comorbidities, and medications. Results: Data from 17,148 patients with GCA and non-GCA–matched controls (mean [SD] age, 75.1 [8.5] years; 72.1% female), and 379,764 patients with RA (age, 73.0 [9.5] years; 73.2% female) were included. Systemic corticosteroids (SCS) were used in the 90 days before diagnosis or CED by 43.0%, 28.3%, and 13.5% of patients in the GCA, RA, and control groups, respectively. Among the GCA cohort, 2303 IP MI/stroke cases were observed during 45,921 PY of follow-up. The crude IP MI/stroke incidence rate (95% CI) was higher for patients with GCA (5.02 [4.81, 5.22] cases/100 PY) vs RA (3.02 [2.99, 3.05]) and non-GCA–matched controls (3.46 [3.29, 3.64]). Among the GCA cohort, 495 cases of IP VTE were observed during 49,489 PY of follow-up. The crude IP VTE incidence rate was higher for patients with GCA (1.00 [0.91, 1.09] cases/100 PY) vs RA (0.69 [0.68, 0.71]) and non-GCA–matched controls (0.62 [0.55, 0.70]). The adjusted relative IP MI/stroke or VTE risk was higher for patients with GCA than RA and controls (Figure 1). For patients with GCA, the risk for IP MI/stroke was ≥ 30% higher in those with a history of ischemic heart disease, hypertension, diabetes, or congestive heart failure (Figure 2). For patients with GCA, the risk for IP VTE was ≥ 30% higher in those who were obese, had a VTE history, hospitalization in the past year, or received non-steroidal anti-inflammatory drugs or SCS in the 90 days before GCA diagnosis. Trends were similar with both IP and OP VTE. Conclusion: GCA was associated with a higher underlying risk for MI/stroke and VTE relative to RA and non-GCA–matched controls, which persisted after adjusting for baseline demographics, comorbidities, and select medications. This study also investigated baseline risk factors for MI/stroke and VTE in patients with GCA. When evaluating the risk of MI/stroke or VTE in patients with GCA, considering an individual's medical history and comorbidities may inform treatment benefit-risk assessments. REFERENCES: [1] Molander V, et al. Ann Rheum Dis. 2022;81:517–8. [2] del Rincón ID, et al. Arthritis Rheum. 2021;44:2737–45. [3] Michailidou D, et al. J Intern Med. 2022;291:665–75. [4] Tomasson G, et al. Ann Intern Med. 2014;160:73–80. Acknowledgements: AbbVie funded this study and participated in the study design, research, analysis, data collection, interpretation of data, reviewing, and approval of the abstract. All authors had access to relevant data and participated in the drafting, review, and approval of this abstract. No honoraria or payments were made for authorship. AbbVie and authors thank all the trial investigators and the patients who participated in the study. Medical writing support was provided by Morgan A Gingerich, PhD, of JB Ashtin, and funded by AbbVie. Disclosure of Interests: Whitney Krueger WK is a full-time employee of AbbVie and may hold AbbVie stock or stock options., Xiaomeng Yue XY is a full-time employee of AbbVie and may hold AbbVie stock or stock options., Ivan Lagunes IL is a full-time employee of AbbVie and may hold AbbVie stock or stock options., Arathi Setty AS is a full-time employee of AbbVie and may hold AbbVie stock or stock options., Cristina Ponte CP has received research grants and/or consultancy fees from AbbVie, AstraZeneca, GSK, Vifor, and Roche., Ana Romero AR is a full-time employee of AbbVie and may hold AbbVie stock or stock options.

Background: Pain, including inflammatory joint pain, may be debilitating in patients with psoriatic arthritis (PsA). Pain in PsA is multidimensional and can be influenced via reduction of inflammation and potentially by other means, such as a direct analgesic drug effect. Objectives: The objective of this analysis of the SELECT-PsA 1 study was to assess the direct and indirect (ie, by changes in inflammation surrogates) effects of treatment with upadacitinib (UPA), a selective and reversible Janus kinase (JAK) inhibitor, or adalimumab (ADA), a TNF inhibitor, vs placebo (PBO) on pain in patients with PsA. Methods: SELECT-PsA 1 was a randomized, double-blind phase 3 study in patients with PsA who had active disease at baseline. Adults (≥18 years) were randomized 1:1:1:1 to UPA 15 mg once daily, UPA 30 mg once daily, ADA 40 mg every other week, or PBO; for UPA, only UPA 15 mg data are reported here. As observed analysis was used for change from baseline to week 16 in Patient’s Global Assessment (PtGA) of pain (1–100 mm) or tender joint count based on 28 joints (TJC28). Observed case multiple mediation analysis1 for effect of UPA vs PBO and ADA vs PBO on pain (pain assessed as PtGA of pain or TJC28) was conducted. Indirect effect of treatment on pain was assessed based on inflammatory factors including itch, total enthesitis, Leeds Enthesitis Index (LEI), and CRP. Results: 1281 patients were included in this analysis (UPA, n=429, ADA, n=429, PBO, n=423). PtGA of pain significantly improved with UPA vs PBO from baseline to week 16 (–25.0 [n=404] vs –11.0 [n=390]; P<0.05; Figure 1). Improvements in pain were also observed with ADA at week 16 (–23.0 [n=408]). Total effects (15.1 and 12.4) and direct effects (9.8 and 8.3) on improvement in PtGA of pain were significantly greater with both UPA vs PBO and ADA vs PBO, respectively at week 16 (all P<0.001; Figure 2); numerically greater reductions in total effect on pain were observed with UPA vs ADA. Direct and indirect effects on pain assessed as improvement in PtGA of pain were numerically greater with UPA vs ADA (Figure 2). Improvement in elicited pain assessed as TJC28 was also significantly greater with UPA and ADA vs PBO (all P<0.05; Figure 2). Furthermore, UPA reduced pain assessed as TJC28 numerically more than ADA when examining the total effect explained by direct effects and the inflammatory mediators (indirect effects). Conclusion: UPA and ADA produced relevantly higher mean improvements in pain via inflammatory or non-inflammatory mechanisms vs PBO in patients with PsA. Total effects on pain improvement were numerically greater with UPA vs ADA when assessed as PtGA of pain and TJC28. REFERENCES: [1] Preacher, KJ & Hayes, AF. Behavior Research Methods,2008;40(3), 879–891. Acknowledgements: AbbVie funded this study and participated in the study design, research, analysis, data collection, interpretation of data, reviewing, and approval of the publication. All authors had access to relevant data and participated in the drafting, review, and approval of this publication. No honoraria or payments were made for authorship. Medical writing support was provided by M Hovenden and J Matsuura of ICON plc (Blue Bell, PA) and was funded by AbbVie. Disclosure of Interests: Peter C. Taylor AbbVie, Biogen, Galapagos, Gilead, GlaxoSmithKline, Janssen, Lilly, Pfizer, Sanofi, Nordic Pharma, Fresenius, and UCB., AbbVie, Biogen, Galapagos, Gilead, GlaxoSmithKline, Janssen, Lilly, Pfizer, Sanofi, Nordic Pharma, Fresenius, and UCB., AbbVie, Biogen, Galapagos, Gilead, GlaxoSmithKline, Janssen, Lilly, Pfizer, Sanofi, Nordic Pharma, Fresenius, and UCB., David A. Walsh AbbVie and Contura International A/S, Pfizer, Eli Lilly, GlaxoSmithKline Research & Development Limited, and Orion Corporation, Tsutomu Takeuchi AbbVie, Astellas Pharma, Eisai, Eli Lilly Japan, Gilead Sciences, Inc., and Pfizer Japan Inc., AbbVie, Astellas Pharma, Eli Lilly Japan, and Gilead Sciences, Inc, Bruno Fautrel AbbVie, BMS, Chugai, Fresenius Kabi, Galapagos, Lilly, Medac, NORDIC Pharma, Novartis, Pfizer, SOBI, and UCB, Janet Pope advisor/review panel member and consultant for AbbVie, Koji Kato employee of AbbVie and may own AbbVie stock and/or options, employee of AbbVie and may own AbbVie stock and/or options, Arathi Setty employee of AbbVie and may own AbbVie stock and/or options, employee of AbbVie and may own AbbVie stock and/or options, Tianming Gao employee of AbbVie and may own AbbVie stock and/or options, employee of AbbVie and may own AbbVie stock and/or options, Diane Caballero employee of AbbVie and may own AbbVie stock and/or options, employee of AbbVie and may own AbbVie stock and/or options, Ralph Lippe employee of AbbVie and may own AbbVie stock and/or options., employee of AbbVie and may own AbbVie stock and/or options., Arthur Kavanaugh AbbVie, Amgen, BMS, Eli Lilly, Novartis, Pfizer, and UCB

Background: In the phase 3 SELECT-PsA 1 and SELECT-PsA 2 studies, upadacitinib (UPA), an oral Janus kinase inhibitor, met the primary endpoint (≥20% improvement in ACR score at week [wk] 12) and demonstrated efficacy through 24 wks. Objectives: In this post-hoc analysis, the maintenance of clinical response rates with UPA 15 mg (UPA15) were evaluated through nearly 3 years of treatment among patients (pts) who achieved response at wk 24. Methods: Enrolled pts were adults with moderately to severely active PsA with inadequate response to non-biologic DMARDs (non–bDMARD-IR; SELECT-PsA 1, NCT03104400) or biologic DMARDs (bDMARD-IR; SELECT-PsA 2, NCT03104374). Both trials included a 24 wk double-blind, placebo-controlled treatment period followed by 32 wks of blinded UPA. SELECT-PsA 1 also included an active-comparator arm (adalimumab 40 mg [ADA]) in the 56-wk blinded period. Afterwards, pts received open-label UPA (both trials) or ADA (SELECT-PsA 1) through wk 152. This analysis included pts originally randomized to UPA15 or ADA. Assessments included improvement in ACR score by ≥50% (ACR50) or ≥70% (ACR70), reduction in Psoriasis Area and Severity Index score by ≥75% (PASI75) or ≥90% (PASI90), minimal disease activity (MDA), low disease activity (Disease Activity in Psoriatic Arthritis score ≤14 [DAPSA-LDA]), resolution of dactylitis/enthesitis (Leeds Dactylitis/Enthesitis Index=0), and clinically meaningful improvement in HAQ-Disability Index (HAQ-DI, ≥0.35 decrease) or pain (≥1 decrease [0–10 numerical rating scale]). Sustainability of wk 24 responses for each efficacy endpoint was evaluated through wk 152. No imputation on missing data was performed; 95% CIs were based on Wald limits without continuity correction. Only pts with data at both wk 24 and a later visit were included to calculate response sustainability at that visit. Results: This analysis included 1069 pts originally randomized to UPA15 (SELECT-PsA 1, N=429; SELECT-PsA 2, N=211) or ADA (N=429). In UPA15-treated pts who achieved ACR50 at wk 24, most pts sustained the response at wk 152 (non–bDMARD-IR, 88.1% [156/177]; bDMARD-IR, 78.1% [50/64]; Figure 1). Similar results occurred for non–bDMARD-IR and bDMARD-IR, respectively, in ACR70 (77.7% [73/94] and 81.8% [27/33]), PASI75 (80.8% [84/104] and 82.5% [47/57]), and PASI90 (75.0% [48/64] and 66.7% [24/36]; Figure 2). At wk 152, sustained treatment effects were also observed on MDA (79.4% [108/136] and 73.9% [34/46]); DAPSA LDA (88.0% [139/158] and 76.8% [43/56]); resolution of dactylitis (97.7% [86/88] and 100% [28/28]) or enthesitis (87.6% [113/129] and 88.0% [44/50]); and clinically meaningful improvement in HAQ-DI (88.3% [158/179] and 85.3% [58/68]) or pain (94.0% [249/265] and 89.9% [98/109]; Figure 1-2). In SELECT-PsA 1, the maintenance of response for each assessment was similar between UPA15 and ADA (Figure 1-2). Conclusion: Although this analysis only evaluated wk 24 treatment responders who did not discontinue the trials, pts with PsA who were non–bDMARD-IR or bDMARD-IR largely sustained wk 24 responses, achieving durable disease control with UPA15 through nearly 3 years of treatment. Future analyses can assess continuous endpoints rather than categorial response measures to confirm these results. REFERENCES: NIL. Acknowledgements: AbbVie funded this study and participated in the study design, research, analysis, data collection, interpretation of data, reviewing, and approval of the abstract. AbbVie and authors thank all the trial investigators and the patients who participated in the clinical trials. Tianming Gao provided assistance with generation and analysis of data. Medical writing support was provided by Jay Parekh, PharmD, of JB Ashtin, and funded by AbbVie. Disclosure of Interests: Philipp Sewerin AbbVie, Biogen, Bristol Myers Squibb, Celgene, Chugai, Hexal, Janssen-Cilag, Lilly, Novartis, Pfizer, Roche, Sanofi-Genzyme, Swedish Orphan Biovitrum, and UCB, AbbVie, Biogen, Bristol Myers Squibb, Celgene, Chugai, Hexal, Janssen-Cilag, Lilly, Novartis, Pfizer, Roche, Sanofi-Genzyme, Swedish Orphan Biovitrum, and UCB, AbbVie, Celgene, Chugai, Janssen-Cilag, Lilly, Novartis, Pfizer, and UCB, Francisco J. Blanco AbbVie, Amgen, AstraZeneca, Biohope, Boehringer Ingelheim España, Bristol Myers Squibb, Centrexion Therapeutics, Corbus Pharmaceuticals, CSL Behring, FZE, Fundación para la Investigación Biomédica Del Hospital Clínico San Carlos, Galapagos, Gedeon Richter, GlaxoSmithKline Research & Development, Grünenthal, Janssen Cilag, Janssen Research & Development, Kiniksa Pharmaceuticals, Lilly, Merck, Novartis, Pfizer, Sanofi, Sun Pharma Global, TEDEC-MEIJI FARMA, Viela Bio, UCB, and UCB BIOPHARMA SPRL., AbbVie, Amgen, AstraZeneca, Biohope, Boehringer Ingelheim España, Bristol Myers Squibb, Centrexion Therapeutics, Corbus Pharmaceuticals, CSL Behring, FZE, Fundación para la Investigación Biomédica Del Hospital Clínico San Carlos, Galapagos, Gedeon Richter, GlaxoSmithKline Research & Development, Grünenthal, Janssen Cilag, Janssen Research & Development, Kiniksa Pharmaceuticals, Lilly, Merck, Novartis, Pfizer, Sanofi, Sun Pharma Global, TEDEC-MEIJI FARMA, Viela Bio, UCB, and UCB BIOPHARMA SPRL., Ennio Lubrano EL has received honoraria or consulting fees from AbbVie, Alfasigma, Galapagos, Janssen, Lilly, MSD, Novartis, and Pfizer., Rodrigo Garcia Salinas AbbVie, AstraZeneca, Biogen, Bristol Myers Squibb, Genentech, GlaxoSmithKline, Janssen, and Merck Serono, AbbVie, AstraZeneca, Biogen, Bristol Myers Squibb, Genentech, GlaxoSmithKline, Janssen, and Merck Serono, Andra Bălănescu Akros, AstraZeneca, Bristol Myers Squibb, GlaxoSmithKline, MSD, Novartis, Roche, Sandoz, Sanofi, Pfizer, and UCB, AbbVie, AlphaSigma, Angellini, Amgen, AstraZeneca, Berlin-Chemie, Biogen, Bristol Myers Squibb, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, Sandoz, Teva, UCB, and Zentiva, Ralph Lippe employee of AbbVie and may hold AbbVie stock and/or stock options, employee of AbbVie and may hold AbbVie stock and/or stock options, Mira Ali employee of AbbVie and may hold AbbVie stock and/or stock options, employee of AbbVie and may hold AbbVie stock and/or stock options, Arathi Setty employee of AbbVie and may hold AbbVie stock and/or stock options, employee of AbbVie and may hold AbbVie stock and/or stock options, Limei Zhou employee of AbbVie and may hold AbbVie stock and/or stock options, employee of AbbVie and may hold AbbVie stock and/or stock options, Philip J. Mease AbbVie, Amgen, Janssen, Lilly, Novartis, Pfizer, and UCB, AbbVie, Acelyrin, Aclaris, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Galapagos, Gilead, GlaxoSmithKline, Janssen, Lilly, Novartis, Pfizer, Sun, UCB, and Ventyx, AbbVie, Acelyrin, Amgen, Bristol Myers Squibb, Janssen, Lilly, Novartis, Pfizer, Sun, and UCB

Introduction Les corticoïdes (GC) restent la principale option thérapeutique de l’artérite à cellules géantes (ACG). L’upadacitinib (UPA), un inhibiteur oral et sélectif de JAK, approuvé pour traiter plusieurs maladies inflammatoires, a le potentiel de traiter l’ACG. Patients et méthodes SELECT-GCA est une étude randomisée de phase III, en double aveugle contrôlée vs PBO dont l’objectif est d’évaluer l’efficacité et la tolérance d’UPA en association avec une diminution progressive des GC, chez des patients ayant une ACG. Sont rapportés ici les résultats de l’analyse principale à 52 semaines (S). Les patients ont reçu l’UPA 7,5mg (UPA7,5) ou 15mg (UPA15), avec une diminution des GC sur 26S ou un PBO avec une diminution des GC sur 52S. Les patients éligibles avaient≥50 ans, un diagnostic ou une rechute d’ACG, avaient été traités par≥40mg/j de prednisone ou équivalent avant l’inclusion (incl), et étaient traités par prednisone≥20mg/j à l’incl. Les patients traités antérieurement par inhibiteurs de JAK, ayant eu une réponse inadéquate ou traités par des anti-IL-6 au cours des 4S précédant l’incl ou ayant une utilisation chronique de GC systémiques étaient exclus. Le critère principal était la rémission maintenue, définie par l’absence de signes ou symptômes d’ACG entre S12 et S52 et le respect du schéma de réduction des GC prévu au protocole. Les critères secondaires incluaient la rémission complète maintenue (rémission maintenue avec normalisation de la VS et de la CRP), des critères liés aux poussées de la maladie, et l’exposition cumulée aux GC. Les événements indésirables (EI) ont été documentés durant les 52S. Résultats Au total, 428 patients ont été randomisés et traités (PBO : n=112 ; UPA7,5 : n=107 ; UPA15 : n=209). Les caractéristiques à l’incl étaient comparables entre les groupes de traitement. Le critère principal de rémission maintenue à S52 a été atteint avec l’UPA15 vs le PBO (46 % vs 29 %, p=0,0019) et 9/11 critères secondaires contrôlés pour la multiplicité des tests ont été atteints avec l’UPA15, y compris la rémission complète maintenue de S12 à S52 (37 % vs 16 %, p<0,0001). Une diminution du risque de poussées a été observée avec l’UPA15 par rapport au PBO au cours des 52S (Fig. 1). L’exposition médiane cumulée aux GC sur les 52S a été significativement plus faible avec l’UPA15 vs le PBO (1615mg vs 2882mg, p<0,0001). Pour la plupart des critères, une amélioration numériquement supérieure à celle du PBO a été observée avec l’UPA7,5. Les résultats de tolérance étaient généralement similaires dans les groupes UPA et PBO (Tableau 1), avec des taux plus élevés d’infections graves et de MACE rapportés dans le groupe PBO et aucun MACE rapporté dans les groupes UPA. Les taux de zona, lymphopénie, anémie et cancer cutané non-mélanome (CCNM) étaient numériquement plus élevés avec UPA15 vs PBO. Les taux d’évènements thromboemboliques étaient comparables dans tous les groupes de traitement. Les taux d’EI graves et de cancers (hors CCNM) étaient similaires entre UPA15 et le PBO. Quatre décès ont été rapportés : deux dans le groupe PBO et deux dans le groupe UPA15 (un attribuable au COVID-19 et un de cause inexpliquée). Conclusion L’UPA15 a démontré une efficacité supérieure et une utilisation réduite des GC par rapport au PBO. Aucun nouveau signal de tolérance n’a été identifié avec UPA par rapport au profil connu [1]. L’UPA15 a présenté un rapport bénéfice/risque favorable et représente un nouveau traitement ciblé potentiel pour les patients atteints d’ACG.

Background: Advanced targeted therapies for giant cell arteritis (GCA) are limited, and glucocorticoids (GCs) remain a primary treatment option. Interleukin-6 (IL-6) and interferon gamma (IFN-γ) have been strongly implicated in the pathogenesis of GCA. Upadacitinib (UPA), an oral and selective JAK inhibitor approved across multiple inflammatory diseases, is a strong inhibitor of the JAK-dependent cytokines IL-6 and IFN-γ and has the potential to treat GCA. Objectives: To assess the efficacy and safety of UPA vs placebo (PBO), in combination with a GC taper regimen, in patients with GCA. Methods: SELECT-GCA is a double-blind, randomized PBO-controlled phase 3 trial conducted in 24 countries, consisting of two 52-week periods. Results from the first 52-week period (primary analysis) are reported here, in which patients received either UPA 7.5 mg or 15 mg (UPA7.5 or UPA15) once daily in combination with a 26-week GC taper regimen or PBO with a 52-week GC taper regimen. Eligible patients were aged ≥50 yrs, diagnosed with new-onset or relapsing GCA, and had received prior GCA treatment with ≥40 mg prednisone or equivalent daily before baseline (BL) and were taking prednisone ≥20 mg daily at BL. Patients with prior exposure to JAK inhibitors, inadequate response or exposure to IL-6 inhibitors within 4 weeks before BL, or chronic use of systemic GCs were excluded. The primary endpoint was sustained remission, defined as the absence of signs or symptoms of GCA from week 12 through week 52 and adherence to the protocol-defined GC taper regimen. Secondary endpoints included sustained complete remission (defined as achievement of sustained remission with normalization of ESR and CRP), disease flare-related endpoints, several patient-reported outcomes including FACIT-Fatigue, and cumulative GC exposure. Exposure-adjusted treatment-emergent adverse events (TEAEs) were documented through 52 weeks. Results: A total of 428 patients were randomized and treated (PBO, N=112; UPA7.5, N=107; UPA15, N=209). BL characteristics were balanced across treatment groups, with 70% and 30% of patients having new-onset and relapsing GCA, respectively. The primary endpoint of sustained remission at week 52 was achieved with UPA15 vs PBO (46% vs 29%, P=.0019). Additionally, the study met 9 out of 11 multiplicity-controlled secondary endpoints with UPA15 including achievement of sustained complete remission from week 12 through week 52 (37% vs 16%, P<.0001). UPA15 resulted in a decreased risk for flare through 52 weeks relative to those receiving PBO (Figure). Additionally, UPA15 led to significantly greater improvements in FACIT-Fatigue scores from BL to week 52 (least-squares mean change: UPA15, 1.7; PBO, -2.4; P=.0036). Cumulative GC exposure over 52 weeks was significantly lower with UPA15 vs PBO (median exposure of 1615 mg vs 2882 mg, P<.0001). Across most endpoints, UPA7.5 showed numerically better efficacy compared to PBO but did not reach statistical significance. Safety outcomes over 52 weeks were generally similar among the UPA groups and PBO (Table), with numerically higher rates of serious infections and MACE observed in the PBO group and no MACE reported in the UPA groups. Rates of herpes zoster, lymphopenia, anemia, and nonmelanoma skin cancer (NMSC) were numerically higher with UPA15 than PBO. Rates of VTE were comparable across treatment groups. Rates of serious TEAEs and malignancy, excluding NMSC, were similar between UPA15 and PBO. Four treatment-emergent deaths were reported: two in the PBO group and two in the UPA15 group (one of which was attributable to COVID-19 and the other was adjudicated as an unexplained cause). Conclusion: UPA15 combined with a 26-week GC taper demonstrated superior efficacy and reduced GC use compared to PBO with a 52-week GC taper. No new safety signals were identified with UPA as compared to its known safety profile [1]. Overall, UPA15 provided a favorable benefit-risk profile and represents a potential new oral targeted therapy for patients with GCA. REFERENCES: [1] Burmester GR et al. RMD Open 2023:9:e002735. Acknowledgements: AbbVie and the authors thank the patients, study sites, and investigators who participated in this clinical trial (NCT03725202). AbbVie funded this trial and participated in the study design, research, analysis, data collection, interpretation of data, reviewing, and approval of the publication. All authors had access to relevant data and participated in the drafting, review, and approval of this publication. No honoraria or payments were made for authorship. Medical writing support was provided by Matthew Eckwahl, PhD, of AbbVie. We also thank Yang Yang, Charles Phillips, and Aditi Kadakia, of AbbVie, for their contributions. Disclosure of Interests: Daniel Blockmans GSK, Roche, Sara K Penn AbbVie, AbbVie, Arathi Setty AbbVie, AbbVie, Wolfgang Schmidt AbbVie, Chugai, Medac, Novartis, Roche, and Sanofi, Advisory board member for AbbVie, Chugai, GlaxoSmithKline, Novartis, Roche, Fresenius Kabi, and Sanofi, AbbVie, GlaxoSmithKline, Novartis, and Sanofi, Andrea Rubbert-Roth AbbVie, Amgen, BMS, Chugai, Eli Lilly, Gilead, Janssen, Novartis, Pfizer, Roche, and Sanofi, AbbVie, Amgen, BMS, Chugai, Eli Lilly, Gilead, Janssen, Novartis, Pfizer, Roche, and Sanofi, Ellen-Margrethe Hauge Novo Nordic, Novartis, AbbVie, Sanofi, Sobi, MSD, and UCB, Novartis, AbbVie, and Sobi; advisory board for SynACT Pharma, Independent Research Fund Denmark, Novo Nordic Foundation, Danish Rheumatism Association, Aarhus University, Danish Regions Medicine Grants, Galapagos, AbbVie, Roche, and Novartis, Helen Keen Roche and eTherapeutic Guidelines Australia, Board member of Australian Rheumatology Association, Roche, Abbvie, Sun, Emerald, Novartis, Biogen, Sanofi, and Syneos, Tomonori Ishii AbbVie, Asahi Kasei Pharma, Astellas, Ayumi Pharmaceutical, BMS, Chugai Pharmaceutical, Daiichi-Sankyo, Eisai, Janssen, Mitsubishi Tanabe, Ono Pharmaceutical, Pfizer, and Sanofi, Nader Khalidi Travel support from Astra Zeneca, Advisory Board fees from Roche, BMS, Sanofi, and Abbvie, Meng Liu AbbVie, AbbVie, Weihan Zhao AbbVie, AbbVie, Ivan Lagunes AbbVie, AbbVie, Ana Romero AbbVie, AbbVie, Peter K Wung AbbVie, AbbVie, Peter A. Merkel Royalties from UpToDate, AbbVie, AstraZeneca, Boeringher-Ingelheim, BMS, ChemoCentryx, CSL Behring, Dynacure, EMDSerono, Forbius, Genentech/Roche, Genzyme/Sanofi, GlaxoSmithKline, Immagene, InflaRx, Jannsen, Kiniksa, Kyverna, Magenta, MiroBio, Neutrolis, Novartis, Pfizer, Regeneron, Sparrow, Takeda, and Talaris, AbbVie, AstraZeneca, Boeringher-Ingelheim, BMS, ChemoCentryx, Eicos, Forbius, Genentech/Roche, Genzyme/Sanofi, GlaxoSmithKline, InflaRx, Sanofi, and Takeda.

Background Involvement of weight-bearing joints in patients with psoriatic arthritis (PsA) can be associated with reduced activities of daily living and quality of life. Upadacitinib (UPA) is an oral, reversible Janus kinase inhibitor approved for the treatment of active PsA in adults. In the SELECT-PsA 1 and SELECT-PsA 2 trials, treatment with once daily UPA 15 mg (UPA15) or 30 mg (UPA30) resulted in greater improvements in the number of swollen and tender joints as well as other patient- and physician-reported outcomes when compared with placebo.[1-3] Objectives To evaluate the long-term efficacy of UPA in patients with PsA and involvement in 1 or more regions of weight-bearing joints. Methods The SELECT-PsA 1 (NCT03104400) and SELECT-PsA 2 (NCT03104374) phase 3, randomized, controlled trials enrolled patients ≥ 18 years old with active PsA and intolerance or inadequate response to ≥ 1 nonbiologic disease modifying anti-rheumatic drug (DMARD; SELECT-PsA 1) or biologic DMARD (SELECT-PsA 2). This post hoc analysis of the 2 phase 3 trials stratified patients with involvement in 1 to 6 regions of weight-bearing joints (hips, knees, ankles, midfoot, metatarsophalangeal [MTP], or proximal interphalangeal [PIP]) who were randomized at baseline to receive either UPA15, placebo (PBO), or adalimumab (ADA; only in SELECT-PsA 1); at week 24, PBO-treated patients switched to UPA15 (PBO/UPA15). This analysis did not include patients who received UPA30 or PBO/UPA30. A mixed-effects model with repeated measures was used to analyze the change from baseline to week 104 in 4 patient-reported outcome measures (pain, Health Assessment Questionnaire-Disability Index [HAQ-DI], Work Productivity and Activity Impairment [WPAI] questionnaire, and EuroQol 5 Dimension 5 Level [EQ-5D-5L]) and 1 composite outcome measure (Disease Activity in Psoriatic Arthritis [DAPSA]). UPA safety results in patients with PsA have been previously reported.[1-3] Results A total of 1069 patients from the SELECT-PsA 1 trial and 317 patients from the SELECT-PsA 2 trial were included in the pooled analysis. Of all patients with any involvement in regions of weight-bearing joints, > 91% of patients had involvement in ≥ 2 regions. The most common weight-bearing joints with involvement were the PIP (SELECT-PsA 1, 79.8%; SELECT-PsA 2, 84.5%), MTP (71.1%; 73.8%), and knee (62.3%; 64.9%) joints. Improvements from baseline to week 104 were observed with UPA15 treatment in patient-reported outcomes of pain, HAQ-DI, WPAI, EQ-5D-5L, and the DAPSA score across all subgroups of patients with involvement in 1 to 6 regions of weight-bearing joints (Figure 1). In general, the magnitude of improvement in outcome scores with UPA15 was greater in patients with involvement in a higher number of regions. Similar improvements from baseline to week 104 in outcome scores were observed in patients who received PBO/UPA15 or ADA to week 104. Conclusion UPA15 treatment was associated with long-term improvements in pain, disability, work productivity, disease activity, and quality of life in patients with PsA and involvement in 1 or more regions of weight-bearing joints. References [1]McInnes IB, et al. N Engl J Med. 2021;384:1227–1239. [2]McInnes IB, et al. RMD Open. 2021;7:e001838. [3]Mease PJ, et al. Ann Rheum Dis. 2022;80:312–320. Acknowledgements AbbVie funded this study and participated in the study design, research, analysis, data collection, interpretation of data, reviewing, and approving the abstract. All authors had access to relevant data and participated in the drafting, review, and approval of this abstract. No honoraria or payments were made for authorship. All authors agreed to submit this abstract to the EULAR 2023 Congress. Medical writing support was provided by Michael Dyle, PhD, of JB Ashtin, and funded by AbbVie. Disclosure of Interests Kristi Mizelle Speakers bureau: AbbVie, Amgen, Eli Lilly, GSK, Janssen, and Pfizer, Consultant of: AbbVie, Boehringer Ingelheim, Eli Lilly, and UCB, William Tillett Consultant of: AbbVie, Amgen, Celgene, Eli Lilly, GSK, Janssen, MSD, Novartis, Ono-Pharma, Pfizer, and UCB, Grant/research support from: AbbVie, Celgene, Eli Lilly, GSK, Janssen, and Pfizer, Mira Ali Shareholder of: May hold stock or stock options for AbbVie, Employee of: AbbVie, Thomas Iyile Shareholder of: May hold stock or stock options for AbbVie, Employee of: AbbVie, Tianming Gao Shareholder of: May hold stock or stock options for AbbVie, Employee of: AbbVie, Arathi Setty Shareholder of: May hold stock or stock options for AbbVie, Employee of: AbbVie, Jessica A. Walsh Consultant of: AbbVie, Eli Lilly, Janssen, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Eli Lilly, Merck, and Pfizer, Laura Coates Speakers bureau: AbbVie, Amgen, Biogen, Celgene, Eli Lilly, Galapagos, Gilead, GSK, Janssen, Medac, Novartis, Pfizer, and UCB, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Galapagos, Gilead, Janssen, Moonlake, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Amgen, Celgene, Eli Lilly, Janssen, Novartis, Pfizer, and UCB.

Background The efficacy and safety of upadacitinib (UPA) in patients (pts) with psoriatic arthritis (PsA) and inadequate response to ≥1 biologic disease-modifying antirheumatic drug (bDMARD-IR) have been demonstrated up to 56 and 104 weeks of treatment [1,2]. Objectives To assess the long-term safety and efficacy of UPA in bDMARD-IR pts with PsA through 152 weeks of treatment in the SELECT-PsA 2 study. Methods Pts were randomized to receive UPA 15 or 30 mg once daily (QD), or placebo (PBO) for 24 weeks, followed by blinded switch to UPA 15 or 30 mg QD for pts initially randomized to PBO. After 56 weeks, pts continued their assigned dose up to 152 weeks in an open-label extension (OLE). Following approval of the 15 mg QD dose, the protocol was amended and all pts on UPA 30 mg QD were switched to the approved dose (earliest switch at week 116). Endpoints assessed at 152 weeks included: % of pts achieving 20/50/70% improvement in American College of Rheumatology (ACR) criteria, minimal disease activity (MDA), and 75/90/100% improvement in Psoriasis Area and Severity Index, as well as patient-reported outcomes. Efficacy data were evaluated using non-responder imputation (NRI) and as-observed (AO) data (binary endpoints), and mixed effect model for repeated measures (continuous endpoints). Treatment-emergent adverse events (TEAEs) through 3 years (cut-off date, 05 May 2022) are also reported. Results Of the 641 pts randomized to receive UPA 15 or 30 mg QD, or PBO followed by UPA 15 or 30 mg QD (n=211, 218, 106, and 106, respectively), 478 entered the OLE. Improvements in efficacy outcomes with UPA observed at 561 and 1042 weeks were maintained through the OLE, with ACR20 achieved by 43–51% (NRI) and 79–87% (AO) of pts across treatment arms at week 152. The highest % of MDA responders at week 152 (31% [NRI] and 44% [AO]) were in the continuous UPA 15 mg arm (Table 1). UPA was well tolerated through 152 weeks, with no new safety signals identified. The overall exposure-adjusted event rates for any TEAE were higher for UPA 30 vs 15 mg (295 vs 226 events/100 PY, respectively [Figure]). Conclusion Observed improvements in the signs and symptoms of PsA with UPA were maintained through 3 years of treatment in bDMARD-IR pts. The long-term safety profile of UPA in this treatment-refractory population was consistent with its known safety profile across indications. References [1]Mease PJ, et al. Rheumatol Ther 2021;8:903–919[2]Mcinnes I, et al. Rheumatol Ther 2022. doi.org/10.1007/s40744-022-00499-w Acknowledgements AbbVie funded this study; contributed to its design; participated in data collection, analysis, and interpretation; and participated in the writing, review, and approval of the abstract. AbbVie and the authors thank all study investigators for their contributions and the patients who participated in this study. No honoraria or payments were made for authorship. Medical writing support was provided by Katerina Betsista, MD, of 2 the Nth (Cheshire, UK), and was funded by AbbVie. Disclosure of Interests Philip J Mease Grant/research support from: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squib, Celgene, Galapagos, Genentech, Gilead, GlaxoSmithKline, Janssen, Lilly, Novartis, Pfizer, Sun Pharma, and UCB, Arathi Setty Employee of: AbbVie, and may own stock or options, Kim Papp Speakers bureau: AbbVie, Akros, Allergan, Almirall, Amgen, Bausch Health, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Dermavant, Dermira, Eli Lilly and Company, Galderma, Genentech/Roche, Janssen, Kyowa Kirin, LEO, Meiji, Merck Sharp & Dohme, Novartis, Pfizer, Regeneron, Sanofi Genzyme, Sienna Pharmaceuticals, Sun Pharma, Takeda, UCB, and Valeant, Consultant of: AbbVie, Akros, Allergan, Almirall, Amgen, Arcutis, Avillion, Bausch Health, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Dermavant, Dermira, Eli Lilly and Company, Galderma, Genentech/Roche, GlaxoSmithKline, Janssen, Kyowa Kirin, LEO, Meiji, Merck Sharp & Dohme, Novartis, Pfizer, Regeneron, Sanofi Genzyme, Sienna Pharmaceuticals, Sun Pharma, Takeda, UCB, and Valeant, Filip van den Bosch Speakers bureau: AbbVie, Bristol Myers Squibb, Celgene, Eli Lilly, Galapagos, Janssen, Merck, Novartis, Pfizer, Sanofi, and UCB, Consultant of: AbbVie, Bristol Myers Squibb, Celgene, Eli Lilly, Galapagos, Janssen, Merck, Novartis, Pfizer, Sanofi, and UCB, Shigeyoshi Tsuji Speakers bureau: AbbVie, Eli Lilly, Janssen, Novartis, and UCB, Consultant of: AbbVie, Eli Lilly, Janssen, Novartis, and UCB, Grant/research support from: AbbVie, Eli Lilly, Janssen, Novartis, and UCB, MAURO KEISERMAN Speakers bureau: AbbVie, Bristol Myers Squibb, Celgene, Eli Lilly, Roche, Novartis, Pfizer, Janssen, and UCB, Grant/research support from: AbbVie, Bristol Myers Squibb, Celgene, Eli Lilly, Roche, Novartis, Pfizer, Janssen, and UCB, Kyle Carter Employee of: AbbVie, and may own stock or options, Reva McCaskill Employee of: AbbVie, and may own stock or options, Erin McDearmon-Blondell Employee of: AbbVie, and may own stock or options, Peter Wung Employee of: AbbVie, and may own stock or options, William Tillett Speakers bureau: AbbVie, Amgen, Celgene, Eli Lilly, Janssen, Novartis, Pfizer, and UCB, Consultant of: AbbVie, Amgen, Celgene, Eli Lilly, MSD, Novartis, Ono Pharma, Pfizer, and UCB, Grant/research support from: AbbVie, Celgene, Janssen, Eli Lilly, Pfizer, and UCB.Table 1Efficacy endpoints at week 152EndpointUPA 15 mg QD (n=211)UPA 30 mg QDa (n=218)PBO/UPA 15 mg QD (n=106)PBO/UPA 30 mg QDa (n=106)Proportion of patients (%)NRIAONRIAONRIAONRIAOACR20/50/7051/39/2481/60/3649/35/2279/56/3443/29/2087/60/4043/28/1879/53/36MDA3144254116411937PASI75/90/10043/31/2066/46/3041/36/2972/61/4845/34/2379/61/4241/35/3075/63/55Resolution of enthesitis (LEI=0)b3869366824762562Resolution of dactylitis (LDI=0)c4994501003410028100Change from BLMixed effect model for repeated measuresmean (95% confidence interval)Health Assessment Questionnaire – Disability Index-0.4(-0.5, -0.3)-0.5(-0.5, -0.4)-0.5(-0.6, -0.3)-0.3(-0.4, -0.2)Bath Ankylosing Spondylitis Disease Activity Indexd-2.6(-3.1, -2.1)-2.0(-2.5, -1.5)-2.3(-3.1, -1.5)-2.5(-3.2, -1.7)Ankylosing Spondylitis Disease Activity Scored-1.4(-1.6, -1.1)-1.1(-1.4, -0.9)-1.0(-1.4, -0.7)-1.2(-1.5, -0.8)aFollowing a protocol amendment, all pts on UPA 30 mg QD switched to UPA 15 mg QD (earliest switch at week 116).bBL LEI >0.cBL LDI >0.dAmong pts with psoriatic spondylitis at BL, as determined by the investigator.ACR20/50/70, 20/50/70% improvement in American College of Rheumatology Criteria; AO, as observed; BL, baseline; LDI, Leeds Dactylitis Index; LEI, Leeds Enthesitis Index; MDA, minimal disease activity; NRI, non-responder imputation; PASI75/90/100, 75/90/100% improvement in Psoriasis Area and Severity Index; PBO, placebo; pt, patient; QD, once daily; UPA, upadacitinib.

L’upadacitinib (UPA), un inhibiteur de Janus kinase (JAK) par voie orale, a démontré son efficacité et sa sécurité chez des patients atteints de rhumatisme psoriasique (RP) ayant une réponse insuffisante ou une intolérance à ≥ 1 traitement de fond biologique (bDMARD) à la S56 de l’étude de phase III SELECT-PsA 2. Évaluer l’efficacité et la tolérance de l’UPA à S104 de l’extension à long terme en cours de l’étude SELECT-PsA 2. Patients randomisés pour recevoir UPA 15 mg, UPA 30 mg ou placebo (PBO) pendant 24 semaines. Les patients sous PBO passaient ensuite à UPA15 ou UPA30. Évaluation d’efficacité à S104 des patients traités en continu par UPA en NRI (imputation en non-répondeurs) et données observées (critères binaires), ou en MMRM (modèle mixte pour mesures répétées) et données observées (critères continus). Au total, 641 patients ont reçu ≥ 1 dose d’UPA. À S104, 38,4 % de l’ensemble des patients avaient arrêté leur traitement par UPA et les taux d’arrêt les plus élevés ont été observés chez les patients randomisés dans le groupe PBO à l’inclusion (total PBO : 46,7 %). Les motifs les plus fréquents d’arrêt du traitement étaient un manque d’efficacité (UPA15 : 12,3 %, UPA30 : 8,7 %, total PBO : 21,7 %) et la survenue d’un EI (UPA15 : 10,9 %, UPA30 : 13,3 %, total PBO : 12,7 %). La proportion de patients sous UPA ayant obtenu une réponse ACR20/50/70, MDA, PASI75/90/100, et résolution des dactylites/enthésites était similaire voire améliorée à S104 de traitement versus S56 (Tableau 1). La variation moyenne par rapport à l’inclusion du HAQ-DI, de l’évaluation de la douleur par le patient et des scores BASDAI/ASDAS était plus importante avec UPA. À S104, les réponses cliniques étaient similaires sous UPA15 et UPA30. Les données de tolérance à S104 (Fig. 1) concordaient avec celles rapportées à S56. Les infections graves, zonas, affections hépatiques, anémies, neutropénies, lymphopénies et élévations des CPK restaient plus élevés sous UPA30 vs UPA15. Les taux de cancers, d’EICM et de TEV étaient similaires dans les 2 groupes UPA. 1 décès rapporté avec UPA15 (inexpliqué, manque d’informations ; la patiente ayant récemment reçu un diagnostic de cancer de l’ovaire) et 2 avec l’UPA30 (pancytopénie et pneumonie à COVID-19). Chez les patients atteints de RP ayant présenté une réponse insuffisante ou une intolérance à ≥ 1 bDMARD, les réponses cliniques se sont maintenues avec UPA15 et UPA30 jusqu’à 2 ans de traitement. Aucun nouveau signal de sécurité n’a été identifié durant cette période d’extension.

BackgroundThe multifaceted nature of psoriatic arthritis (PsA) can make it challenging to evaluate treatment targets and disease activity. Moreover, most existing assessment tools are time-consuming and not always feasible in routine clinical care, indicating a need for new disease measures that are easy to perform and calculate. Composite measures using 3-visual analog scale (VAS; physician’s global assessment, patient’s global assessment, and skin) or 4-VAS (physician’s global assessment, joints, skin, and pain) have been proposed as simpler alternatives.1 Given potential advantages of numeric rating scales (NRS) over VAS, we here adapted 3/4-VAS for use with NRS components and tested its validity via post hoc analysis of the upadacitinib (UPA) SELECT-PsA program.ObjectivesEvaluate the ability of 3/4-NRS scores to assess treatment response in SELECT-PsA 1 and 2, as well as the correlation of 3/4-NRS with other common disease activity measures.MethodsData are from the SELECT-PsA 1 and 2 phase 3 trials in patients with prior inadequate response or intolerance to ≥1 non-biologic DMARD or ≥1 biologic DMARD, respectively. In both trials, patients received once daily UPA 15 mg, UPA 30 mg, or placebo (PBO); SELECT-PsA 1 also included the active comparator adalimumab (ADA) 40 mg every other week (wk). 3-NRS scores were determined using the mean of SAPS questions 1–10, physician’s global assessment of disease activity, and patient’s global assessment of disease activity; 4-NRS scores were determined using the mean of SAPS questions 1–10, physician’s global assessment of disease activity, patient’s assessment of pain, and BASDAI question 3 related to joint pain and swelling. The 3/4-NRS scale ranges from 0 (no disease activity) to 10 (severe activity). 3/4-NRS and cDAPSA (DAPSA without the CRP component) were assessed at all available visits through wk 56. Correlations between 3/4-NRS with PsA disease activity score (PASDAS), routine assessment of patient index data 3 (RAPID3), DAPSA, cDAPSA, and other disease activity measures were determined by nonparametric Spearman rank correlation coefficient for UPA 15 mg patients from both trials and ADA for SELECT-PsA 1. All data are shown as observed; nominal p-values are provided throughout.ResultsA total of 1281 and 423 patients were included from SELECT-PsA 1 and 2, respectively. For both cDAPSA and 3/4-NRS scores, patients receiving UPA 15 mg showed clear numerical improvements compared with PBO at wk 24 in both trials (Table 1). 3/4-NRS scores were highly correlated with RAPID3 and PASDAS measures (r >0.6, P <0.0001) for UPA 15 mg patients at baseline (Figure 1). Moderate correlations were observed between 3/4-NRS and DAPSA/cDAPSA (r = ~0.4, P <0.0001), as well as physical function (HAQ-DI) and quality of life measures (SF-36). Nominally significant but weaker correlations were detected for joints, skin, and other disease activity assessments. Similar overall results were observed for patients receiving ADA.Table 1.3/4-NRS and cDAPSA Disease Activity Scores at Week 24 and 56 (As Observed)SELECT-PsA 1Wk 24Wk 56Mean score [n]PBOUPA 15 mgADAUPA 15 mgADA3-NRS3.7 [370]2.2 [398]2.4 [398]1.8 [372]2.0 [359]4-NRS3.8 [367]2.3 [392]2.6 [395]1.9 [367]2.2 [357]cDAPSA24.0 [372]14.9 [399]16.6 [400]10.2 [372]11.3 [358]SELECT-PsA 2Wk 24Wk 56Mean score [n]PBOUPA 15 mgUPA 15 mg3-NRS4.7 [172]2.9 [190]2.4 [164]4-NRS4.9 [170]3.1 [188]2.7 [162]cDAPSA37.1 [172]21.6 [190]15.3 [166]3/4-NRS ranges from 0–10; cDAPSA ranges from 0–154. Lower scores indicate decreased disease activity.Conclusion3/4-NRS was able to successfully discriminate between PBO and therapeutic groups in SELECT-PsA 1 and 2. 3/4-NRS scores correlated well with other clinical and patient reported outcome measures, including those focused on joints (DAPSA) or multiple manifestations (PASDAS), supporting 3/4-NRS as a viable and easy to use tool in daily clinical practice.References[1]Tillett W, et al. J Rheumatol 2021; 201675.AcknowledgementsAbbVie and the authors thank the patients, study sites, and investigators who participated in these clinical trials. AbbVie funded these studies and participated in the study design, research, analysis, data collection, interpretation of data, reviewing, and approval of the publication. All authors had access to relevant data and participated in the drafting, review, and approval of this publication. No honoraria or payments were made for authorship. Medical writing support was provided by Matthew Eckwahl, PhD, of AbbVie.Disclosure of InterestsWilliam Tillett Speakers bureau: AbbVie, Amgen, Celgene, Lilly, Janssen, MSD, Novartis, Pfizer, and UCB, Consultant of: AbbVie, Amgen, Celgene, Lilly, Janssen, MSD, Novartis, Pfizer, and UCB., Laura Coates Speakers bureau: AbbVie, Amgen, Biogen, BMS, Boehringer Ingelheim, Celgene, Galapagos, Gilead, GSK, Janssen, Lilly, Medac, Novartis, Pfizer, Serac, and UCB., Consultant of: AbbVie, Amgen, Biogen, BMS, Boehringer Ingelheim, Celgene, Galapagos, Gilead, GSK, Janssen, Lilly, Medac, Novartis, Pfizer, Serac, and UCB., Mitsumasa Kishimoto Consultant of: AbbVie, Amgen-Astellas BioPharma, Asahi-Kasei Pharma, Astellas, Ayumi Pharma, BMS, Celgene, Chugai, Daiichi-Sankyo, Eisai, Eli Lilly, Gilead, Janssen, Kyowa Kirin, Novartis, Ono Pharma, Pfizer, Tanabe-Mitsubishi, Teijin Pharma, and UCB Pharma., Arathi Setty Shareholder of: AbbVie, Employee of: AbbVie, Tianming Gao Shareholder of: AbbVie, Employee of: AbbVie, Ralph Lippe Shareholder of: AbbVie, Employee of: AbbVie, Philip Helliwell Paid instructor for: Educational services: Abbvie, Amgen, Novartis, Janssen, Consultant of: Eli Lilly