Haiyun Fan

The effect of tofacitinib on pneumococcal and influenza vaccine responses in rheumatoid arthritis

Objective To evaluate tofacitinibs effect upon pneumococcal and influenza vaccine immunogenicity. Methods We conducted two studies in patients with rheumatoid arthritis using the 23-valent pneumococcal polysaccharide vaccine (PPSV-23) and the 2011–2012 trivalent influenza vaccine. In study A, tofacitinib-naive patients were randomised to tofacitinib 10 mg twice daily or placebo, stratified by background methotrexate and vaccinated 4 weeks later. In study B, patients already receiving tofacitinib 10 mg twice daily (with or without methotrexate) were randomised into two groups: those continuing (‘continuous’) or interrupting (‘withdrawn’) tofacitinib for 2 weeks, and then vaccinated 1 week after randomisation. In both studies, titres were measured 35 days after vaccination. Primary endpoints were the proportion of patients achieving a satisfactory response to pneumococcus (twofold or more titre increase against six or more of 12 pneumococcal serotypes) and influenza (fourfold or more titre increase against two or more of three influenza antigens). Results In study A (N=200), fewer tofacitinib patients (45.1%) developed satisfactory pneumococcal responses versus placebo (68.4%), and pneumococcal titres were lower with tofacitinib (particularly with methotrexate). Similar proportions of tofacitinib-treated and placebo-treated patients developed satisfactory influenza responses (56.9% and 62.2%, respectively), although fewer tofacitinib patients (76.5%) developed protective influenza titres (≥1:40 in two or more of three antigens) versus placebo (91.8%). In study B (N=183), similar proportions of continuous and withdrawn patients had satisfactory responses to PPSV-23 (75.0% and 84.6%, respectively) and influenza (66.3% and 63.7%, respectively). Conclusions Among patients starting tofacitinib, diminished responsiveness to PPSV-23, but not influenza, was observed, particularly in those taking concomitant methotrexate. Among existing tofacitinib users, temporary drug discontinuation had limited effect upon influenza or PPSV-23 vaccine responses. Trial registration numbers NCT01359150, NCT00413699.

Herpes Zoster and Tofacitinib: Clinical Outcomes and the Risk of Concomitant Therapy

Patients with rheumatoid arthritis (RA) are at increased risk of herpes zoster (HZ), and the risk appears to be increased in patients treated with tofacitinib. The aim of this study was to evaluate whether concomitant treatment with conventional synthetic disease‐modifying antirheumatic drugs (csDMARDs) or glucocorticoids (GCs) contributes to the increased risk of HZ in RA patients treated with tofacitinib.

Effect of Glucocorticoids on the Clinical and Radiographic Efficacy of Tofacitinib in Patients with Rheumatoid Arthritis: A Posthoc Analysis of Data from 6 Phase III Studies

Objective. Tofacitinib has been investigated for the treatment of rheumatoid arthritis (RA) in phase III studies in which concomitant glucocorticoids (GC) were allowed. We analyzed the effect of GC use on efficacy outcomes in patients with RA receiving tofacitinib and/or methotrexate (MTX) or conventional synthetic disease-modifying antirheumatic drugs (csDMARD) in these studies. Methods. Our posthoc analysis included data from 6 phase III studies (NCT01039688; NCT00814307; NCT00847613; NCT00853385; NCT00856544; NCT00960440). MTX-naive patients or patients with inadequate response to csDMARD or biological DMARD received tofacitinib 5 or 10 mg twice daily alone or with csDMARD, with or without concomitant GC. Patients receiving GC (≤ 10 mg/day prednisone or equivalent) before enrollment maintained a stable dose throughout. Endpoints included the American College of Rheumatology (ACR) 20/50/70 response rates, rates of Clinical Disease Activity Index (CDAI)-defined low disease activity (LDA; CDAI ≤ 10) and remission (CDAI ≤ 2.8), and changes from baseline in CDAI, 28-joint count Disease Activity Score (DAS28-4)–erythrocyte sedimentation rate (ESR), Health Assessment Questionnaire–Disability Index (HAQ-DI), pain visual analog scale (VAS), and modified total Sharp score. Results. Of 3200 tofacitinib-treated patients, 1258 (39.3%) received tofacitinib monotherapy and 1942 (60.7%) received tofacitinib plus csDMARD; 1767 (55.2%) received concomitant GC. ACR20/50/70 response rates, rates of CDAI LDA and remission, and improvements in CDAI, DAS28-4-ESR, HAQ-DI, and pain VAS with tofacitinib were generally similar with or without GC in monotherapy and combination therapy studies. GC use did not appear to affect radiographic progression in tofacitinib-treated MTX-naive patients. MTX plus GC appeared to inhibit radiographic progression to a numerically greater degree than MTX alone. Conclusion. Concomitant use of GC with tofacitinib did not appear to affect clinical or radiographic efficacy. MTX plus GC showed a trend to inhibit radiographic progression to a greater degree than MTX alone.

SAT0229 Herpes Zoster and Tofacitinib: The Risk of Concomitant Nonbiologic Therapy

Background Rheumatoid arthritis (RA) patients are at increased risk for herpes zoster (HZ), and treatment with tofacitinib, an oral janus kinase (JAK) inhibitor, appears to increase this risk.1 Prior analysis from the RA development programme for tofacitinib identified Japanese and Korean patients to be at increased risk within the clinical development programme.1 There is a need to understand whether patients using concomitant nonbiologic disease-modifying antirheumatic drugs (DMARDs; ie methotrexate [MTX]) are at higher risk than tofacitinib monotherapy patients. Objectives To evaluate the incidence of HZ in patients receiving tofacitinib and to investigate the incidence rates (IRs) among patients using tofacitinib monotherapy and those using concomitant nonbiologic DMARDs or corticosteroids. Methods We identified reports of serious and non-serious HZ from Phase (P)1/P2/P3 and long-term extension (LTE) studies of tofacitinib in RA patients (data cut April 2014), and calculated crude IRs for all HZ (serious and non-serious; unique patients with events per 100 patient-years [py]) with 95% CI. One of the LTE studies was ongoing at the time of the analysis (database not locked). Patients were censored at study withdrawal, development of HZ or death. In addition, within P3 studies where dose groups were balanced, we described HZ rates in stratified fashion according to concomitant nonbiologic DMARDs and baseline corticosteroid use. Results In pooled P1/P2/P3 and LTE studies (19 studies; 6192 patients; 16 839 py of exposure) HZ was reported in 636 tofacitinib-treated patients: IR 4.0 (3.7, 4.4). IRs for tofacitinib-associated HZ varied widely across regions of enrolment, being lowest in Eastern and Western Europe (2.4 [2.0, 2.9] and 3.3 [2.4, 4.40], respectively) and highest among patients enrolled in Japan/Korea: IR 8.1 (7.0, 9.4). Within P3 studies, HZ incidence varied according to tofacitinib dose and background therapy with nonbiologic DMARDs: tofacitinib 5 mg twice daily (BID) monotherapy, 14 cases (IR 2.0 [1.2, 3.3]); tofacitinib 10 mg BID monotherapy, 22 cases (IR 2.9 [1.9, 4.5]); tofacitinib 5 mg BID with nonbiologic DMARDs, 43 cases (IR 4.4 [3.2, 5.9]); tofacitinib 10 mg BID with nonbiologic DMARDs, 50 cases (IR 5.0 [3.8, 6.6]). Crude IRs for HZ in patients enrolled outside Japan/Korea were lower, but similar trends in rates, according to background nonbiologic DMARDs and tofacitinib dose, were observed. In addition, crude HZ IRs were higher in patients using corticosteroids vs those not using corticosteroids, although total exposure time for these groups was limited (Figure 1). Conclusions From univariate analysis within the P3 database of the tofacitinib RA clinical development programme, numerically higher crude IRs, with overlapping CIs, were observed for HZ in patients using higher dose of tofacitinib, combination nonbiologic DMARD therapy and corticosteroids. However, further analysis, including multivariable analysis, is necessary to thoroughly evaluate the risk of these and other factors for HZ development. References Winthrop KL, et al. Arthritis Rheumatol 2014; 66: 2675-84. Acknowledgements All aspects of this study were funded by Pfizer Inc. Editorial support was provided by Claire Cridland of Complete Medical Communications, and funded by Pfizer Inc. Disclosure of Interest K. Winthrop Grant/research support from: Pfizer Inc, S. Lindsey Speakers bureau: Pfizer Inc, H. Fan Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, L. Wang Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, D. Gelone Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, A. Mendelsohn Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, E. Bananis Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, J. Curtis Grant/research support from: Pfizer Inc, Consultant for: Pfizer Inc

THU0193 Reestablishment of efficacy of tofacitinib, an oral janus kinase inhibitor, in rheumatoid arthritis patients after temporary discontinuation

Background Tofacitinib is an oral Janus kinase inhibitor for the treatment of rheumatoid arthritis (RA). Objectives To assess the efficacy and safety of tofacitinib after temporary discontinuation and reinitiation of therapy in RA patients (pts). Methods Data were collected from a randomised, parallel-group (grp), controlled, open label, vaccine sub-study in RA pts participating in a long-term extension (LTE) study (NCT00413699). Pts were ≥18 years of age with active RA and had received tofacitinib 10 mg BID for ≥3 months. The sub-study included 2 treatment (tx) grps: “continuous tx” (tofacitinib 10 mg twice daily [BID] as monotherapy or with methotrexate [MTX]) and “interrupted tx” (tofacitinib withdrawn for 2 weeks post-randomisation [Day 1–Day 15; Visits 1–3], then tofacitinib 10 mg BID reinitiated as monotherapy or with MTX at Visit 3); randomisation was stratified by MTX use. Pneumococcal and influenza vaccines were administered to all pts on Day 8 (Visit 2; vaccine titers reported previously1). Blood samples were taken on Days 8, 15 (Visit 3) and 43 (Visit 4). Efficacy endpoints included change from baseline in C-reactive protein (CRP), Health Assessment Questionnaire Disability Index (HAQ-DI) and Disease Activity Score in 28 joints, erythrocyte sedimentation rate (DAS28-4[ESR]) at each visit. A mixed-effects model with repeated measures was used to evaluate treatment effect at each visit. Analyses for efficacy were exploratory, with no multiplicity adjustment for comparisons. Results Of the 199 pts in this analysis (continuous, n=100; interrupted, n=99), 117 received concomitant MTX. At LTE study baseline (BL) in the continuous and interrupted grps, respectively: 81.8/83.8% of pts were white, 84.8/86.9% were female and mean age was 55.0/53.9 years. BL (Day 1) values for CRP, HAQ-DI and DAS28-4(ESR) were generally similar between groups. At Day 8, mean CRP and DAS28-4(ESR) significantly increased from BL for interrupted vs continuous tx; HAQ-DI values were similar between grps (Figure). As expected at Day 15, mean CRP, HAQ-DI and DAS28-4(ESR) significantly increased from BL for interrupted vs continuous tx. After tofacitinib reinitiation for 28 days (Day 43), changes in CRP, HAQ-DI and DAS28-4(ESR) were similar between grps and approached BL levels. Adverse events (AEs) were experienced by 35.4% and 49.5% of pts receiving interrupted and continuous tx, respectively. The most frequent treatment-emergent AEs were bronchitis and upper respiratory tract infection (each AE: 6 pts) and vaccination-related immunisation reaction, myalgia and rash (each AE: 5 pts). Serious AEs occurred in 3 pts (3%) in each grp. In total, 1 pt (1%), in the interrupted tx grp, discontinued due to a study-drug related AE; no pts discontinued due to disease flare. Conclusions Efficacy of tofacitinib 10 mg BID can be reestablished following loss of efficacy during temporary (2 weeks) tx discontinuation in pts with RA. Pts receiving continuous tx maintained efficacy throughout the study. Further investigations are required. References Winthrop KL et al. Ann Rheum Dis 2016; 75: 687–695. Acknowledgements This study was sponsored by Pfizer Inc. Editorial support was provided by K Haines of CMC and was funded by Pfizer Inc. Disclosure of Interest J. Kaine Speakers bureau: Bristol-Myers Squibb, Pfizer Inc, J. Tesser Grant/research support from: Pfizer Inc, Consultant for: Pfizer Inc, Speakers bureau: Pfizer Inc, R. DeMasi Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, L. Takiya Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, L. Wang Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, M. Snyder Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, H. Fan Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, J. Wollenhaupt Consultant for: Pfizer Inc, Speakers bureau: Pfizer Inc

A pooled analysis of the safety of tofacitinib as monotherapy or in combination with background conventional synthetic disease-modifying antirheumatic drugs in a Phase 3 rheumatoid arthritis population

OBJECTIVE This post-hoc, pooled analysis of Phase 3 studies of tofacitinib examined the safety of tofacitinib 5 and 10 mg twice daily (BID) when used as monotherapy versus combination therapy with conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) in patients with rheumatoid arthritis (RA). METHODS Pooled data from six double-blind, randomized controlled Phase 3 studies of tofacitinib 5 and 10 mg BID in patients with RA were analyzed for safety and stratified by administration as monotherapy (ORAL Solo: NCT00814307 and ORAL Start: NCT01039688) or in combination with csDMARDs (ORAL Sync: NCT00856544, ORAL Standard: NCT00853385, ORAL Scan: NCT00847613, and ORAL Step: NCT00960440), and by glucocorticoid use at baseline. Safety assessments included incidence rates (IRs) for serious adverse events (SAEs), discontinuations due to AEs, serious infection events, and herpes zoster (HZ), and were evaluated throughout the duration of the Phase 3 studies. RESULTS In total, 3881 patients were included in the safety analysis (monotherapy studies: n = 1380; combination therapy studies: n = 2501). IRs for selected AEs of interest were generally numerically lower in patients who received tofacitinib 5 and 10 mg BID as monotherapy than as combination therapy (SAEs: IR [range] 6.21-6.72 versus IR 10.17-13.46; discontinuations due to AEs: IR 5.53-6.18 versus IR 10.80-11.01; serious infections: IR 1.57-1.66 versus IR 3.39-3.56; HZ: IR 1.95-2.93 versus IR 4.37-4.99, respectively), irrespective of tofacitinib dose or glucocorticoid use. There were too few patients and events within the placebo group to fully evaluate effect between combination therapy and monotherapy. CONCLUSIONS Safety profiles were generally similar between patients receiving monotherapy and combination therapy; however, selected safety events of interest, including HZ and serious infections, showed lower IRs with non-overlapping 95% confidence intervals for tofacitinib all monotherapy versus combination therapy. Tofacitinib monotherapy may, therefore, have fewer safety events compared with combination therapy, and have a favorable risk-benefit profile in patients with active RA who are intolerant to csDMARDs.

Modified- versus immediate-release tofacitinib in Japanese rheumatoid arthritis patients: a randomized, phase III, non-inferiority study

Abstract Objective Tofacitinib is an oral Janus kinase inhibitor for treatment of RA. We compared tofacitinib modified-release (MR) 11 mg once daily (QD) with tofacitinib immediate-release (IR) 5 mg twice daily (BID) in Japanese patients with RA and inadequate response to MTX. Methods Phase III, randomized, double-blind, double-dummy, 12-week study. Patients were randomized to tofacitinib MR 11 mg QD (n = 104) or IR 5 mg BID (n = 105), with stable MTX. Compliance was based on returned pill counts. The primary objective was to demonstrate non-inferiority of MR 11 mg QD to IR 5 mg BID. Non-inferiority was declared if the upper bound of the two-sided 95% CI for the difference in change from baseline in DAS28-4(CRP) at week 12 was <0.6. Results At week 12, with tofacitinib MR 11 mg QD and IR 5 mg BID, respectively, the change from baseline in least squares mean DAS28-4(CRP) was −2.43 and −2.85; the mean difference was 0.43 (95% CI 0.17, 0.69). Non-inferiority of MR 11 mg QD to IR 5 mg BID was not met. Improvement of DAS28-4(CRP) ⩾1.2 was observed in 89 and 85% of patients, respectively, corresponding to a clinically important, significant change in both groups. The frequency of adverse events (52.9 and 51.4%, respectively) and serious adverse events (4.8 and 3.8%, respectively) was generally similar between treatments. No deaths were reported. Conclusion Non-inferiority of MR 11 mg QD to IR 5 mg BID was not met in this study. However, clinically meaningful improvements in RA were observed with both tofacitinib formulations in Japanese patients. The safety profile was similar with both formulations. Trial registration ClinicalTrials.gov, http://clinicaltrials.gov, NCT02281552.

SAT0252 Clinical and functional response to tofacitinib and adalimumab in patients with rheumatoid arthritis: probability plot analysis of results from the oral strategy trial

Background: Tofacitinib is an oral Janus kinase inhibitor for the treatment of rheumatoid arthritis (RA). ORAL Strategy (NCT02187055), a 12-month, global, Phase 3b/4 study, demonstrated that in patients with RA and an inadequate response to methotrexate (MTX), tofacitinib + MTX was non-inferior to adalimumab + MTX, while tofacitinib monotherapy was not non-inferior to either combination based on American College of Rheumatology (ACR)50 response rates at Month 6.1 Objectives: To assess clinical and functional efficacy across treatments in the ORAL Strategy trial using cumulative probability plots. Methods: Efficacy was evaluated between patients who received tofacitinib 5 mg twice daily (BID) as monotherapy (N=384), tofacitinib 5 mg BID + MTX (N=376) and adalimumab 40 mg subcutaneously once every 2 weeks + MTX (N=386) based on ACR responses and changes from baseline in Health Assessment Questionnaire-Disability Index (ΔHAQ-DI) score at Month 12. Cumulative probability plots for ACR-n (where ACR is the % improvement from baseline in ACR components, and n represents the mimimum % achieved by each patient) and ΔHAQ-DI are presented. The area under the curve (AUC) was calculated for ACR-n up to Month 12 (in months), and an analysis of covariance model was used to assess treatment effects in terms of the AUC of ACR-n at Month 12; there was no adjustment for multiplicity for this post hoc analysis. Results: The cumulative probability plots of ACR responses at Month 12 indicated that the proportion of patients who achieved responses of ACR20, ACR50 and ACR70 was similar for tofacitinib + MTX and adalimumab + MTX, but was numerically smaller for tofacitinib monotherapy (figure, A). Responses of approximately ≥ACR80 were achieved by a similar proportion of patients in each treatment group. Least squares mean (standard error) AUC of ACR-n up to Month 12 (in months) was similar for tofacitinib + MTX (437 [35]) and adalimumab + MTX (402 [35]), but was smaller for tofacitinib monotherapy (319 [35]; p<0.05). The cumulative probability plots of ΔHAQ-DI suggested that, in general, reductions from baseline in HAQ-DI were similar across treatment groups (figure, B), although a slightly higher proportion of patients who received tofacitinib monotherapy reported an increase in HAQ-DI vs other treatments. Figure 1 Cumulative probability plot of A) ACR response and B) VHAQ-DI at Month 12 Two outlets for ACR response are not shown: tofacitinib 5 mg BID monotherapy, ACR-n-1700, cumulative probability-0.0003; adailmumab 40 mg SC Q2W + MTX, ACR-n-463, cumulative probability-0.003 Conclusions: These data support the primary ORAL Strategy findings,1 indicating that in patients with RA, clinical efficacy, based on ACR response, was generally similar for tofacitinib + MTX and adalimumab + MTX, while a smaller proportion of patients who received tofacitinib monotherapy achieved ACR response in general, and particularly for <ACR80. Functional efficacy, based on ΔHAQ-DI, was generally similar across all treatment groups. Cumulative probability analyses for CDAI will be further evaluated. Reference [1]Fleischmann R, et al. Lancet2017;390:457–68. Acknowledgements: Study sponsored by Pfizer Inc. Medical writing support was provided by A MacLachlan of CMC and funded by Pfizer Inc. Disclosure of Interest: T. Takeuchi Grant/research support from: AbbVie, Asahi Kasei, Astellas, AstraZeneca, AYUMI, Bristol-Myers Squibb, Chugai, Daiichi Sankyo, Eisai, Eli Lilly Japan, Janssen, Mitsubishi Tanabe, Nippon Kayaku, Novartis, Pfizer Japan Inc, Taiho, Taisho Toyama, Takeda, Teijin, Consultant for: AbbVie, Asahi Kasei, Astellas, AstraZeneca, AYUMI, Bristol-Myers Squibb, Chugai, Daiichi Sankyo, Eisai, Eli Lilly Japan, Janssen, Mitsubishi Tanabe, Nippon Kayaku, Novartis, Pfizer Japan Inc, Taiho, Taisho Toyama, Takeda, Teijin, Speakers bureau: AbbVie, Asahi Kasei, Astellas, AstraZeneca, AYUMI, Bristol-Myers Squibb, Chugai, Daiichi Sankyo, Eisai, Eli Lilly Japan, Janssen, Mitsubishi Tanabe, Nippon Kayaku, Novartis, Pfizer Japan Inc, Taiho, Taisho Toyama, Takeda, Teijin, J. Smolen Grant/research support from: AbbVie, Eli Lilly, Janssen, MSD, Pfizer Inc, Roche, Consultant for: AbbVie, Amgen, AstraZeneca, Astro, Celgene, Celtrion, Eli Lilly, GSK, ILTOO, Janssen, MedImmune, MSD, Novartis-Sandoz, Pfizer Inc, Roche, Samsung, Sanofi, UCB, Speakers bureau: AbbVie, Amgen, AstraZeneca, Astro, Celgene, Celtrion, Eli Lilly, GSK, ILTOO, Janssen, MedImmune, MSD, Novartis-Sandoz, Pfizer Inc, Roche, Samsung, Sanofi, UCB, R. Fleischmann Consultant for: AbbVie, Amgen, AstraZeneca, Bristol-Myers Squibb, Celltrion, Eli Lilly, Genentech, GSK, Janssen, Novartis, Pfizer Inc, Sanofi-Aventis, UCB, N. Iikuni Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, H. Fan Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, K. Soma Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, E. Akylbekova Consultant for: Pfizer Inc, Employee of: IQVIA, T. Hirose Shareholder of: Pfizer Japan Inc, Employee of: Pfizer Japan Inc

OP0037 Efficacy of tofacitinib after temporary discontinuation in patients with rheumatoid arthritis: analysis of data from open-label long-term extension studies

Background Tofacitinib is an oral Janus kinase inhibitor for the treatment of rheumatoid arthritis (RA). Given the chronic nature of RA, there may be situations when therapy is temporarily discontinued. It is important to understand loss of response during temporary discontinuation and the ability to regain disease control following treatment reinitiation. Re-establishment of tofacitinib efficacy following temporary discontinuation/reinitiation has been previously demonstrated in patients (pts) with RA participating in the vaccine sub-study of the long-term extension (LTE) study ORAL Sequel.1 Objectives To further assess tofacitinib efficacy and safety after temporary discontinuation and reinitiation in pts with RA in LTE studies. Methods Data were pooled from two open-label LTE studies (NCT00413699 [database lock: March 2017] and NCT00661661) of pts with RA who had completed qualifying Phase 1/2/3 index studies. Pts received tofacitinib 5 or 10 mg twice daily as monotherapy or with conventional synthetic disease-modifying antirheumatic drugs. Pts who received continuous tofacitinib for ≥4 months, temporarily discontinued tofacitinib for 14–30 days and then resumed treatment were included in the analysis. Efficacy outcomes were analysed at the pre-interruption visit (≤90 days before discontinuation) and at the post-interruption visit (within 14–42 days of resuming treatment); data from the interruption period were not analysed. Efficacy outcomes included: ACR20/50/70 response rates, mean tender and swollen joint counts, mean C-reactive protein levels and mean DAS28–4(ESR), CDAI, HAQ-DI, Patient Global Assessment of arthritis, Pain and Physician Global Assessment of arthritis scores. Safety was analysed from Day 1 of temporary discontinuation to the post-interruption visit and included adverse events (AEs), serious AEs (SAEs) and discontinuations due to AEs that occurred within the time range. Results 261 pts met the criteria for temporary discontinuation. Median (range) duration of temporary discontinuation was 1914–30 days. Pt demographics are shown in table 1. Efficacy outcomes were generally similar at pre- and post-interruption visits (table 2). From Day 1 of discontinuation to the post-interruption visit, AEs, SAEs and discontinuations due to AEs occurred in 142 (54.4%), 29 (11.1%) and 4 (1.5%) pts, respectively.Abstract OP0037 – Table 1 Patients demographics and baseline disease characteristics1 Abstract OP0037 – Table 2 Efficacy endpoints at the pre-interruption visit (≤90 days before temporary discontinuation) and post-interruption visit (within 14–42 days of resuming treatment) Conclusions In pts with RA who temporarily discontinued tofacitinib, similar efficacy responses were observed at pre– and post–interruption visits, suggesting that there is no loss of efficacy after temporary withdrawal and reinitiation of tofacitinib. The safety profile was consistent with previous tofacitinib reports in LTE studies over 9 years.2 References [1] Kaine J, et al. Arthritis Rheumatol2017;69(suppl 10):Abstract 424. [2] Wollenhaupt J, et al. Arthritis Rheumatol2017;69(suppl 10):Abstract 522. Acknowledgements Study sponsored by Pfizer Inc. Medical writing support was provided by AG McCluskey of CMC and funded by Pfizer Inc. Disclosure of Interest J. Kaine Speakers bureau: Bristol-Myers Squibb, Pfizer Inc, J. Tesser Grant/research support from: Pfizer Inc, Consultant for: Pfizer Inc, Speakers bureau: Pfizer Inc, R. DeMasi Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, L. Takiya Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, L. Wang Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, M. Snyder Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, H. Fan Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, V. Bandi Consultant for: Pfizer Inc through Eliassen Group Inc, J. Wollenhaupt Speakers bureau: Pfizer Inc