EULAR 2017 CS Review

Enhancing knowledge of the clinical 

importance of cytokine signalling 

The Cytokine Signalling Forum 

www.cytokinesignalling.com 

EULAR 2017 

Conference Highlights 

Cytokine Signalling Science 

Register for all this FREE content at 



info@cytokinesignalling.com 

@CytokineForum 

lnkd.in/PyqQPm 

Supported by an unrestricted educational grant 

from Pfizer Italia S.R.L., Lilly and R-Pharm. 

Developed under the auspices of the University of Glasgow

Chairman’s Welcome 

EULAR 2017 Conference Highlights 


Dear CSF Member, 

Thank you for your continued support of the Cytokine Signalling Forum. We are now in our fourth year, and continue to strive to bring 

you the most up-to-date and interesting data in cytokine signalling. To that end, I am delighted to share with you our pick of the EULAR 

highlights for 2017. We have identified the most interesting and impactful abstracts being presented at this year’s meeting on both cytokine 

signalling and IL-6. I have also selected my ‘Chairman’s picks’: those abstracts that I feel are the most significant at this year’s congress. 

Cytokine Signalling 

Again, this year there is an interesting range of both basic and clinical science. There are several baricitinib posters covering durability 

and maintenance of efficacy [FRI0096], switching to monotherapy [SAT0058], and dose reduction [SAT0072]. The possibility of an 

anti-inflammatory biomarker profile in patients treated with filgotinib monotherapy is examined [THU0182], and the results of the DARWIN-3 

open label extension study up to 144 weeks are presented in Thursday’s poster session and tour [THU0173]. 

Tofacitinib posters in RA concentrate on long-term safety and efficacy over eight years [THU0197] as well as an examination of 

cardiovascular risk factors [SAT0686], and safety and efficacy in patients with an inadequate response to conventional synthetic or biologic 

DMARDs [THU0185]. Real-world tofacitinib drug-retention data are also shared as a poster from the Swiss SCQM registry [THU0174]; 

and real-world tofacitinib monotherapy data from the US CORRONA registry as an oral presentation [OP0022]. Three further oral 

presentations on Thursday and Friday will share exciting new data from the Phase 3 tofacitinib studies in psoriatic arthritis [OP0202; 

OP0216] as well as long-term effectiveness of live zoster vaccine in patients with RA, subsequently treated with tofacitinib [OP0230]. 

IL-6 

Several abstracts showcase key data from the clinical programmes of sarilumab, sirukumab and tocilizumab. 

There are three key presentations on sarilumab, including patient-reported (PROs) from two Phase 3 studies in RA [FRI0240], and efficacy 

and patient-reported benefits of sarilumab monotherapy versus adalimumab monotherapy in the MONARCH study [SAT0202; OP0102]. 

Sirukimab posters focus on Phase 3 data in RA, with efficacy and safety from the SIRROUND-T study [FRI0214], analyses of health-related 

quality of life and work productivity from SIRROUND-D and -T, respectively [FRI0246; FRI0251], and an integrated safety analysis of the 

SIRROUND programme [SAT0194]. 

Tocilizumab oral presentations examine tapering and dose reduction strategies [OP0104] as well as the long-term safety profile seen in 

clinical trials and post-marketing populations [OP0105]. Tocilizumab posters look at real-world data, with clinical remission in the TOSPACE 

trial [SAT0183], and a pooled analysis of Phase 4 data across 22 countries [SAT0199]. 

The following pages provide an overview of these topics and highlight my ‘Chairman’s picks’. Once again, thank you for your support and 

I hope you enjoyed EULAR 2017! 

Yours, 

Prof. Iain McInnes



Highlights from EULAR 2017: Cytokine Signalling 

During the EULAR 2017 annual meeting, many presentations and posters reported on 

cytokine signalling and related drugs. This document reviews the highlights. 

A separate highlights document covering interleukin 6 (IL-6) and related drugs is 

also available. 

ABT-494 

There were four posters and one publication-only abstract on ABT-494, a selective janus 

kinase (JAK)-1 inhibitor currently being evaluated in Phase 3 trials in rheumatoid arthritis 

(RA) at doses of 15 mg and 30 mg QD in an extended-release tablet formulation. 

Clinical efficacy in RA 

Strand, et al. presented a post hoc analysis from two Phase 2b trials (BALANCE-1 

and BALANCE-2), looking at changes in haemoglobin with ABT-494, and its relation to 

baseline levels of C-reactive protein (CRP). In 210 patients with RA, higher baseline CRP 

was associated with smaller mean decreases in haemoglobin at Week 12. They also 

found that ACR20 or DAS28-CRP ≤3.2 responders had smaller decreases in haemoglobin 

versus non-responders at Week 12. The authors concluded that effective treatment of 

RA-associated inflammation with ABT-494 may counterbalance the small haemoglobin 

reduction associated with JAK inhibition [THU0210]. 

A second presentation from Strand, et al. shared early patient-reported outcomes (PROs) 

and clinical outcomes in inadequate responders (IR) to methotrexate (MTX; n=150) or 

tumour necrosis factor inhibitors (TNFi; n=166) from a post hoc analysis of Phase 2 trials. 

In both trials, significantly more patients receiving the 12 mg dose of ABT-494 reported 

improvements greater than the minimal important difference (MID) in RAPID3 (Routine 

Assessment of Patient Index Data) versus placebo at Week 2. Significantly more MTX-IR patients 

receiving 6 mg BID ABT-494 versus placebo also had improvements ≥MID in RAPID3 

(54% versus 30%). These responses were sustained through both trials in patients 

receiving the 12 mg dose. DAS28 and Clinical Disease Activity Index (CDAI) also showed 

fast and sustained responses to Week 12 in both MTX-IR and TNF-IR populations 

[SAT0217].



Pharmacokinetics 

Mohamed, et al. presented a poster on the pharmacokinetics of the extended-release 

compared to immediate-release formulations of ABT-494 in 24 healthy individuals. 

At steady-state, ABT-494 AUC 0-24 

ratio was 0.94, C max 

ratio was 0.91 and C min 

ratio was 

1.09 for the 15 mg QD regimen of the extended-release formulation relative to the 6 mg 

BID regimen of the immediate-release formulation. Similar results were shown for the 30 mg 

QD regimen of the extended-release formulation relative to the 12 mg BID regimen. 

All evaluated regimens were well-tolerated [THU0177]. 

Mohamed, et al. also shared an abstract evaluating ABT-494 QT prolongation potential 

using an exposure-response analysis of data collected in early Phase 1 studies. 

They found no statistically significant relationship between the change from baseline in 

the QTcF interval and ABT-494 plasma concentrations at the expected therapeutic and 

supra-therapeutic plasma exposures for the doses being used in Phase 3 trials in 

RA patients [AB0432]. 

Baricitinib 

Baricitinib had a strong presence, with a focus on Phase 3 efficacy results and the 

long-term extension studies. 


Efficacy and safety of 423 patients switching to baricitinib monotherapy upon entering the 

long-term extension study (RA-BEYOND) was reported by Fleischmann, et al. At Week 

24 of the extension period, 47% of patients remained on monotherapy. Most of those 

who initiated MTX did so within 4 weeks. These patients tended to have worse disease 

control upon entry and during the study. No statistically significant changes in disease 

activity were observed in patients who were switched from combination to monotherapy. 

Clinically significant or consistent differences in serious infectious events, serious adverse 

event (SAEs), or AEs leading to study drug discontinuation were not seen in any of the 

arms, whether MTX was added or not [SAT0058]. 

Smolen, et al. examined durability and maintenance of efficacy following prolonged 

treatment with baricitinib in the long-term extension. Approximately half the patients in 

the durability analyses had low disease activity (LDA) by Week 24, with similar proportions 

at Week 96. Three-quarters of patients demonstrated Health Assessment Questionnaire 

Disability Index (HAQ-DI) improvement by Week 12 and more than half achieved the 

minimum clinically important difference at Week 96. Most responders at entry into the 

long-term extension maintained response to Week 96 [FRI0096].



Takeuchi, et al. also presented results from the long-term extension, showing that among 

patients who achieved sustained disease control with baricitinib 4 mg, dose reduction to 

2 mg resulted in significant increases in disease activity at 12, 24, and 48 weeks; however, 

most patients in both groups maintained the state of LDA or remission. Rescue rates were 

7.3% for 4 mg and 17.1% for the 2 mg dose, and most rescued patients could regain LDA 

or remission. Dose reduction was associated with a lower rate of non-serious infections; 

rates of SAEs and AEs leading to discontinuation were similar across groups. The authors 

concluded that 4 mg QD was the most efficacious dose of baricitinib for patients with RA 

[SAT0072]. 

52-week EULAR responses from 1305 patients in RA-BEAM were presented in a poster 

by Kvien, et al. At Week 4, moderate EULAR responses were experienced by 37.3%, 

62.0%, and 60.3% of patients on placebo, baricitinib, and adalimumab, respectively. 

The mean MTX dosage was 15 mg/week, and 59% were taking concomitant oral 

glucocorticoids. The cumulative incidence for first transition to good EULAR response at 

Weeks 12, 24, and 52 was higher in patients who reached moderate response at Week 

4 on baricitinib than those who reached moderate response on adalimumab; cumulative 

incidence for first transitions to subsequent no response was higher in patients who 

achieved moderate response at Week 4 on adalimumab than baricitinib [SAT0070]. 

In a post hoc analysis of Phase 3 data, Curtis, et al. showed that patients with CDAI 

≤35–36 at baseline achieved sustained LDA more frequently and more rapidly than those 

in the higher disease category at baseline. In patients with higher disease activity at 

baseline, a more robust response was observed with the baricitinib 4 mg dose than with 

the 2 mg dose [AB0235]. 

Combe, et al. also performed a post hoc analysis of 5 studies to establish the impact 

of comorbidities on clinical outcomes. Treatment with baricitinib 4 mg showed similar 

effect in terms of efficacy and safety in patients with selected comorbidities, including 

depression, osteoporosis, cardiovascular events, and hepatic impairment. No trends 

were noted in each comorbidity subgroup for increased risk of events after treatment with 

baricitinib compared with placebo [FRI0086]. 

A further post hoc analysis from Curtis, et al. assessed disease activity in patients who 

achieved CDAI ≤10 at ≥1 visit (LDA) or at ≥2 consecutive visits (sustained LDA) within 

the 24-week originating study and continued into the long-term extension. The most 

robust benefit was observed with baricitinib 4 mg treatment, which required shorter time 

to response, than the 2 mg dose. This was observed in both the short- and long-term 

in patients with an inadequate response to conventional systemic disease-modifying 

antirheumatic drugs (csDMARD-IR) or biologic DMARDs (bDMARD-IR) patients [FRI0089].



Emery, et al. reported on temporary interruptions of treatment during the Phase 3 studies, 

caused by AEs, abnormal laboratory results, or at the investigator’s discretion. There were 

modest symptom increases during interruption compared to the last pre-interruption 

value, with a return to pre-interruption values or better after resumption of study drug 

[FRI0124]. 

Pincus, et al. shared a post hoc analysis of RA-BEAM in MTX-IR patients, designed to 

compare improvement according to RAPID3, DAS 28-ESR (erythrocyte sedimentation 

rate), and CDAI. Improvement from baseline to Week 24 ranged from 19.2–37.0% 

in placebo patients, 40.0–65.9% in baricitinib-treated patients, and 37.6–60.9% in 

adalimumab-treated patients. Changes according to RAPID3-like, DAS28-ESR and CDAI 

were similar in the three treatment groups. The authors concluded that RAPID3 is feasible 

to provide quantitative, standard medical history data [SAT0069]. 

Kavanaugh, et al. analysed data from RA-BEAM and RA-BUILD to assess whether 

concomitant use of csDMARDs altered the response or safety outcomes to baricitinib in 

patients with RA, and evaluated the effect of concomitant corticosteroid use on efficacy. 

The differences in clinical efficacy between baricitinib 4 mg and placebo at 12 weeks 

was similar regardless of the number or type of csDMARDs concomitantly used, or 

concomitant use of corticosteroids. Rates of SAEs and discontinuation due to AEs were 

comparable regardless of the number or type of csDMARDs used or corticosteroid use 

[THU0078]. 

Curtis, et al. also looked at RA-BEAM and RA-BUILD to ascertain the effects of smoking 

on the efficacy of baricitinib in 290 patients. They found that smoking status at baseline 

did not affect clinical outcomes over 24 weeks with baricitinib; conversely, smokers who 

received placebo were numerically less likely than non-smokers receiving placebo to 

achieve most clinical outcomes. The effect of baricitinib on modified total Sharp score 

was more pronounced among non-smokers [THU0114]. 

In a network meta-analysis, Lee, et al. examined the efficacy and safety of baricitinib in 

patients with active RA using direct and indirect evidence from 3461 patients in 7 clinical 

trials. ACR20 response was significantly higher for baricitinib 4 mg in combination with 

DMARDs than in the placebo plus DMARD group. A ranking probability calculation 

indicated that baricitinib 4 mg plus DMARD was likely to elicit the best ACR20 response 

rate, followed by (in order) baricitinib 4 mg monotherapy, baricitinib 2 mg plus DMARD, 

adalimumab 40 mg plus MTX, and lastly placebo plus DMARD. By contrast, the safety 

based on the number of treatment-emergent AEs did not differ significantly among the 

5 interventions [THU0213].



Structural efficacy in RA 

Structural results from RA-BEGIN were reported by van der Heijde, et al. Patients were 

classified into two groups based on their DAS28-CRP. In patients who achieved sustained 

low DAS28-CRP scores, progression rates compared with MTX were reduced to a similar 

degree with baricitinib monotherapy or in combination with MTX. Compared with MTX in 

patients who did not achieve sustained low DAS28-CRP scores, progression rates were 

reduced most markedly with combination therapy [THU0088]. 

van der Heijde, et al. also presented 2-year structural results from the long-term extension 

study. At Year 2, progression was significantly lower in those who received initial baricitinib 

(including monotherapy) in the Phase 3 trial versus initial MTX in DMARD-naïve patients. 

In MTX/csDMARD-IR patients, progression with initial baricitinib was significantly lower 

than initial placebo, and similar to initial adalimumab [FRI0087]. 

Patient-reported outcomes in RA 

Taylor, et al. evaluated the effect of baricitinib on pain reduction compared with adalimumab 

or placebo in MTX-IR and bDMARD-IR patients in RA-BEAM and RA-BEACON. 

A significantly greater proportion of patients treated with baricitinib 4 mg achieved ≥30% 

and ≥50% pain improvement as early as Week 1 compared with placebo, and as early 

as Week 4 compared with adalimumab. A significant pain improvement of ≥70% was 

achieved at Week 12 for 4 mg baricitinib-treated patients compared with placebo and 

adalimumab. Pain improvement of ≥30%, ≥50%, and ≥70% with the baricitinib 2 mg 

dose was significant compared with placebo by Week 12, and sustained through Week 24 

[SAT0055]. 

Fautrel, et al. presented the PROs in patients who achieved LDA or remission in the 

Phase 3 RA-BEAM study. Among patients in LDA or remission, significantly greater 

improvements in Pain and HAQ-DI scores were observed with baricitinib than 

adalimumab or placebo, and significantly greater improvements in morning joint stiffness 

were observed with baricitinib or adalimumab than placebo. Patients in remission or LDA 

showed greater numerical improvement and less residual impairment in other PROs with 

baricitinib or adalimumab than with placebo [THU0081].



Safety in RA 

Takeuchi, et al. analysed changes in absolute lymphocyte count and cell subsets (LCS) 

in the Phase 3 RA-BEGIN study. Low B and NK cell counts were common at baseline, 

and post-baseline changes within normality occurred in all treatment groups. Compared 

with MTX, baricitinib was not associated with an increase in the percentage of patients 

with low NK or CD8+ cell counts, while baricitinib in combination with MTX did show an 

increase in the percentage of patients with a low NK cell count. Changes appeared to 

be distinct for LCS, suggesting different mechanisms may underscore the effect of JAK 

inhibition. The authors noted that whether low NK or CD8+ cell counts predispose to 

increased risk for serious infections or Herpes zoster was difficult to assess owing to few 

patients with low counts experiencing these events [AB0281]. 

Changes in absolute neutrophil counts (ANC), absolute leukocyte counts (ALC), and platelet 

counts following once-daily oral administration of baricitinib were characterised by Kremer, 

et al. using pooled data from 6 Phase 2 and 3 studies. Treatment with baricitinib 

was associated with a decrease in ANC and an increase in ALC and platelets, which 

stabilised over time and returned to baseline with prolonged treatment (ALC) or treatment 

discontinuation (ANC and platelets). No associations were observed between either ANC 

decreases and infections, or between thrombocytosis and thromboembolic events [FRI0090]. 

Kay, et al. evaluated baseline and subsequent changes in haemoglobin and related 

laboratory parameters in patients with RA treated with baricitinib 2 mg or 4 mg QD, 

placebo, or active comparator (MTX or adalimumab). The proportions of RA patients with 

treatment-emergent abnormally low haemoglobin did not differ significantly between 

baricitinib and placebo. Reductions in haemoglobin (including to Grade 3 or higher), 

were generally not associated with adverse outcomes. Despite concerns about the 

impact of JAK2 inhibition on erythropoietin signalling, following initial declines incident 

to phlebotomy, dose-dependent increases in erythropoietin, total iron, and total iron 

binding capacity with return to baseline in reticulocyte and haemoglobin were observed 

with baricitinib. The authors concluded that this suggests that homeostatic mechanisms 

counterbalance the pharmacologic effect of JAK inhibition on erythropoietin signalling, 

and that baricitinib treatment enhances iron utilisation markers associated with anaemia 

of chronic disease [FRI0092]. 

A meta-analysis of serious infections with baricitinib, tofacitinib and bDMARDs was 

presented as a poster, by Strand, et al. The results showed no significant difference from 

control for both doses of baricitinib, consistent with analyses of tofacitinib and bDMARDs. 

There were limited data to assess the incidence of serious infectious events for baricitinib 

(4 mg) monotherapy versus barictinib in combination with MTX. Incidence rates for 

baricitinib were for 2 mg and 3.67 for the 4 mg dose [THU0211].



Filgotinib 

Filgotinib is a selective JAK1 inhibitor (previously known as GLPG0634 or GS-6034). 

There were a handful of posters looking at basic science, and one showcasing clinical 

efficacy data from the Phase 2b DARWIN studies. 

Clinical efficacy and safety in RA 

Alten, et al. presented the long-term data from DARWIN-3 in 739 patients who entered 

the long-term extension after initial treatment for 24 weeks. Based on an observed case 

analysis, 84%, 65%, 44% and 51% of patients reached ACR20, ACR50, ACR70 and 

DAS28(CRP) remission at Week 60, respectively. Treatment-emergent AEs (157.7 per 

100 patient-years), SAEs (5.3 per 100 patient-years) and serious infections (1.9 per 

100 patient-years) occurred at similar rates as seen in the core studies; however, 

infections decreased from 15% (Weeks 0–12) to 5% (Weeks 85–96). Sixteen cases of 

Herpes zoster were reported (1.2 per 100 patient-years), 6 non-non-melanoma skin 

cancer (NMSC) malignancies (0.5 per 100 patient-years) and 1 major adverse cardiac 

event (MACE) 

(0.1 per 100 patient-years) [THU0173]. 

Basic science 

Kavanaugh, et al. investigated the mode of action of filgotinib when used as monotherapy 

in RA patients by analysing the impact of the drug on a broad panel of immune 

modulators in the serum. Following treatment with filgotinib 100 mg QD and 200 mg 

QD, there were significant reductions in cytokines important in expansion and activity of 

multiple T-cell subsets and innate immunity, including proinflammatory cytokines (IL-6, 

IL-1β, and TNFα), TH1-related (IL-2, IFN-γ and IL-12), TH2-related (IL-4, IL-5, and IL-13) 

and TH17-related cytokines (IL-1β, IL-6, IL-17A, IL-21 and IL-23). All doses of filgotinib 

also reduced the B- and T-cell development cytokine IL-7. In contrast, IL-8 was not 

affected by filgotinib [THU0182]. 

Taylor, et al. used serum samples to assess the effect of filgotinib on markers of 

inflammation in patients with RA taking background MTX. They found that filgotinib 

induced a dose-dependent and significant decrease in a variety of biomarkers implicated 

in the pathogenesis of RA, including inflammation (IL-1β, IL-6, TNFα and SAA), matrix 

degradation and cartilage destruction (MMP1 and MMP3), immune cell trafficking 

(CXCL10, ICAM-1 and VCAM-1) and angiogenesis (VEGF). Cytokines involved in TH1 

(IFN-γ, IL-2, IL-12) and TH17 (IL-1β, IL-6, IL-21, IL-23) cell subset differentiation and 

activity were significantly decreased. Additionally, decrease in the B-cell chemoattractant 

CXCL13 and the myeloid growth factor GM-CSF support theanti-inflammatory effects of 

filgotinib treatment [THU0206].



The effect of filgotinib on multi-biomarker disease activity (MBDA) scores in MTX-IR 

patients with active RA were presented by Genovese, et al. Filgotinib-treated patients 

had reductions in MBDA from baseline at both 100 mg and 200 mg QD. At Weeks 4 and 

12, these reductions were significantly different from the placebo group. Most individual 

components contributed to the decrease in MBDA, but the largest reductions were 

observed for serum amyloid A (SAA), CRP, and IL-6, and biomarkers of joint damage. 

The authors concluded that these findings were consistent with the filgotinib efficacy 

observed in patients with RA over 12 weeks [THU0205]. 

Blanqué, et al. presented a mouse model, where systemic expression of IL-23 generated 

a PsA phenotype that was associated with altered gene expression in diseased tissues. 

The authors found that a strong interferon signature was reversed by filgotinib, as were 

several inflammation and disease markers [FRI0428]. 

A second mouse model in PsA was detailed by Robin-Jagerschmidt, et al. in an oral 

presentation. The authors found that high levels of IL-23 were maintained during the timecourse 

of the study and were correlated with severity of finger and paw swelling. 

Filgotinib significantly improved clinical scoring and tended to prevent neutrophil or 

granulocyte infiltrate in paw, with a significant effect being showed at an earlier timepoint. 

Filgotinib reversed some up-regulated inflammatory genes in enthesis and/or fingers 

(CCL20, CXCL1, IL‐22, MMP9 and TNFa) and reduced the target-related gene Mx2. 

Filgotinib significantly counteracted pSTAT3 induction in the subcutaneous area, further 

demonstrating target engagement in the diseased tissue. Finally, they noted that – in line with 

previous findings – Mx2 expression in colon was slightly reversed by filgotinib [OP0161]. 

Tofacitinib 

As in previous years, there continued to be large numbers of presentations on the JAK 

inhibitor tofacitinib. The vast majority related to long-term and real-world use in RA, but 

there were also data in psoriatic arthritis (PsA) and ankylosing spondylitis (AS). 


Fleischmann, et al. gave a late-breaking oral presentation of the results from ORAL 

STRATEGY, a Phase 3b/4 trial of tofacitinib versus adalimumab head-to-head, 

non-inferiority trial in 1146 patients. At Month 6, non-inferiority was demonstrated for 

tofacitinib 5 mg BID plus MTX versus adalimumab plus MTX (P



Wollenhaupt, et al. presented the efficacy and safety data up to 8 years. In total, 4967 

patients were treated with tofacitinib 5- or 10 mg BID, either as monotherapy or with 

background DMARDs. Over a mean of 1215 days, 77.4% of patients maintained their 

initial dose, and clinical responses were sustained from Month 1 to Month 90 [THU0197]. 

Phase 3 data from ORAL Solo, ORAL Start, ORAL Step, ORAL Scan, ORAL Sync, ORAL 

Standard were also pooled in an analysis by Schwartzman, et al. Tofacitinib 5- and 

10 mg BID demonstrated efficacy in patients with moderate and severe RA with more 

than 7 years’ mean disease duration. By Month 3, patients with severe versus moderate 

baseline disease activity had greater improvements in disease activity and physical 

functioning. Higher proportions of patients with moderate versus severe baseline disease 

activity achieved remission, LDA or normal physical functioning [AB0436]. 

Tesser, et al. evaluated tofacitinib efficacy and safety using pooled data from 8 Phase 2 

and 6 Phase 3 trials in non-MTX csDMARD-IR and MTX-IR (second-line) populations. 

Tofacitinib 5- and 10 mg BID achieved higher ACR responses and greater changes 

from baseline in DAS28-4(ESR) and HAQ-DI scores versus placebo at Month 3 in both 

populations. Numerically higher proportions of non-MTX csDMARD-IR patients achieved 

efficacy outcomes versus second-line population. AE frequency was generally lower in 

non-MTX csDMARD-IR patients versus the second-line population [THU0195]. 

Kaine, et al. demonstrated the re-establishment of efficacy after temporary withdrawal 

of tofacintib in 199 patients in a sub-study of an open-label vaccine study. Laboratory, 

clinical and PRO results suggested that the efficacy of tofacitinib 10 mg BID can be 

re-established following loss of efficacy during temporary 2-week treatment discontinuation. 

AEs were experienced by 35.4% and 49.5% of patients receiving interrupted and 

continuous treatment, respectively [THU0193]. 

Structural efficacy in RA 

Gaylis, et al. reported on clinical and structural responses using step-up doses in a 

treat-to-target approach in 20 patients with RA. Over a 12-week period, six patients 

remained at 5 mg BID and 14 escalated to 10 mg BID. In the 5 mg group, there was no 

change in erosions. However, in the 10 mg group, nine patients showed no change in 

erosions, one regression and one progression. Overall, five patients showed no change 

in synovitis and six showed regression, and seven showed no change in osteitis, three 

showed regression and one showed progression [AB0261].



Patient-reported outcomes in RA 

Aletaha, et al. presented the magnitude and duration of early response with tofacitinib in a 

post hoc analysis of ORAL Solo and ORAL Sync. DMARD-IR patients with active RA 

receiving tofacitinib with or without csDMARDs appeared to show greater improvements 

compared with placebo in HAQ-DI, and Pain as early as Week 2. Responses were 

maintained or improved through Month 3 for those receiving monotherapy, or Month 6 for 

those receiving background csDMARDs [THU0186]. 

PROs were also examined by Yamanaka, et al. in Japanese patients with RA. Data for 

238 patients from 2 12-week randomised dose-finding Phase 2 studies found that 

tofacitinib 5- and 10 mg BID demonstrated significantly greater improvements from 

baseline versus placebo in Patient’s Global Assessment of Arthritis (PtGA), Physician’s 

Global Assessment of Arthritis (PGA), HAQ-DI, Pain, Functional Assessment of Chronic 

Illness Therapy – Fatigue (FACIT-F), Medical Outcomes Study (MOS) Sleep Scale and in 

four of the eight Short-Form Health Survey (SF-36) domain scores [THU0191]. 

Li, et al. also looked at PROs in RA, this time in 216 Chinese patients in the Phase 3 

study ORAL Sync study. At Month 3, tofacitinib resulted in significantly greater changes 

in HAQ-DI, PtGA, Pain and SF-36 Physical Component Summary scores versus placebo 

[THU0215]. 

Efficacy and patient-reported outcomes in PsA 

Gladman, et al. and Mease, et al. gave oral presentations of recent Phase 3 data in PsA 

[OP0202; OP0216]. Gladman, et al. covered TNFi-IR patients from the OPAL Beyond 

study. Superior ACR20 responses were seen as early as Week 2, and both ACR20 and 

HAQ-DI significantly improved with both tofacitinib doses versus placebo at Month 3, 

which were maintained to Month 6. No new safety risks were identified compared to 

those seen in previous studies in other indications [OP0202]. Mease, et al. presented 

similar results in csDMARD-IR, TNFi-naïve patients [OP0216]. 

Strand, et al. presented PROs from two Phase 3 studies in PsA (OPAL Broaden and 

OPAL Beyond). Patients receiving tofacitinib 5- and 10 mg BID reported improved PROs 

compared with placebo. Greater improvements in PtGA and Arthritis Pain were observed 

as early as Week 2 through Month 3 with both tofacitinib doses compared with placebo in 

both studies (P≤0.05) [AB0794].



Phase 3 data from OPAL Balance, an open-label long-term extension trial in PsA, 

were presented in a poster by Nash, et al. Efficacy was maintained to Month 15, with 

improvements reported in joint, skin and quality of life measures [FRI0509]. 

Nash, et al. also presented an integrated efficacy analysis of pooled data from OPAL 

Broaden and OPAL Beyond. In these csDMARD-IR/TNFi-naïve and TNFi-IR patients, 

tofacitinib 5- and 10 mg BID were superior to placebo at Month 3 across four PsA disease 

domains: peripheral arthritis, psoriasis, enthesitis and dactylitis [SAT0469]. 

Efficacy in AS 

Maksymowych, et al. showed that tofacitinib treatment is associated with attainment of 

the minimally important reduction in axial MRI inflammation in 164 patients with AS in a 

16-week Phase 2 dose-ranging study. Tofacitinib 2-, 5- and 10 mg BID improved mean 

SPondyloArthritis Research Consortium of Canada (SPARCC) scores versus placebo, 

and approximately three-times more patients achieved minimally important changes in 

sacroiliac joint or spine in the pooled tofacitinib group versus placebo [THU0352]. 

Safety in RA 

In the Wollenhaupt, et al. 8-year analysis reported above [THU0197], 47.7% of patients 

discontinued. The most common AE classes were infections and infestations (68.9%) 

and musculoskeletal/connective tissue disorders (39.0%). Overall, safety was consistent 

through to Month 105 [THU0197]. 

Charles-Schoeman, et al. reported on the risk factors for major AEs in the pooled Phase 3 

and long-term extension studies. In 4076 patients, 52 MACE cases occurred over 12 873 

patient-years of exposure (incidence rate: 0.4 patients with events per 100 patient-years). 

At baseline, patients with MACE were older, had a higher mean body mass index (BMI), 

longer mean RA disease duration, and were more likely to have a history of diabetes and 

hypertension compared with patients without MACE events. Increases in LDL-c and total 

cholesterol (TC) after 24 weeks of tofacitinib therapy were not associated with future MACE 

risk. Increases in HDL-c and decreases in TC:HDL-c ratio after 24 weeks of tofacitinib 

therapy were associated with a reduced future MACE risk. The authors found that increases 

in ESR after 24 weeks may be associated with an increased future MACE risk [SAT0686]. 

In a second poster from Charles-Schoeman, et al., tofacitinib was examined in 

inadequate responders to csDMARDs or one or more bDMARDs. Prior to initiating 

tofacitinib, bDMARD-IR patients had longer RA disease duration, greater disease burden 

and more corticosteroid use compared with csDMARD-IR patients. SAEs were more 

common among bDMARD-IR versus csDMARD-IR patients, but SAE rates were not 

higher in those who had failed two or more bDMARDs compared with those who had 

failed only one [THU0185].



Winthrop, et al. showed the long-term effectiveness of live zoster vaccine in 100 patients 

who continued to receive tofacitinib in ORAL Sequel. Five cases (not adjudicated) of 

Herpes zoster occurred up to 741 days post vaccine after initiation of tofacitinib. 

Four cases were monodermatomal, and 1 involved five dermatomes, but all cases 

resolved with treatment. Three cases had undetectable ELISPOT measures at baseline 

and Week 6 post vaccination, indicating a lack of varicella zoster virus (VZV) specific 

immunity. Two cases responded adequately to vaccination by both immunoglobulin 

G (IgG) and ELISPOT measures, but had lower than average VZV IgG levels, both at 

baseline and at Week 6. Overall, live zoster vaccine prior to treatment with tofacitinib is 

effective at boosting IgG levels and cell-mediated immunity towards VZV [OP0230]. 

The first report of an increase in BMI with tofacitinib was presented by Novikova, et al. 

in a report of 28 patients with RA. There was an increase in BMI of less than 5% in 39% 

of patients, 5–10% increase in 25% of patients, and greater than 10% increase in 21% 

of patients, respectively. These changes in BMI correlated negatively with DAS-28 and 

Simple Disease Activity Index (SDAI) at baseline, and were independent of tofacitinib dose 

or use of cardioprotective therapy. An increase in TC from 4.60 to 5.45 (P=0.001) was 

observed in patients who were not receiving statins; co-administration of tofacitinib and 

statins resulted in significant favourable changes in LDL-and HDL-c [FRI0231]. 

Gomez-Reino, et al. shared the results of a systematic review and meta-analysis of 

malignancies, excluding NMSC, in patients with RA treated with tofacitinib or bDMARDs. 

The authors used the tofacitinib clinical trial dataset of 6194 patients with a total exposure 

of 19385 patient-years and compared it to 64 bDMARD articles, representing 58 unique 

studies and approximately 27000 patients. The incidence rate of malignancy for tofacitinib 

was 0.89 (95% CI 0.76, 1.04) compared with estimated incidence rates of 0.75 (0.56, 

1.01) for abatacept, 1.06 (0.41, 2.74) for rituximab, 1.02 (0.69, 1.52) for tocilizumab and 

0.95 (0.79, 1.14) for TNFi – suggesting that the incidence of non-NMSC malignancies in 

patients treated with tofacitinib is within a similar range to those reported in published 

interventional studies of similar RA populations treated with approved bDMARDs [THU0196]. 

Post-marketing surveillance data from Japan was shared by Mimori, et al. In this 6-month 

interim analysis of 2387 tofacitinib-treated patients, 594 patients (24.9%) discontinued 

treatment, mainly due to AEs (9.9%) or lack of effectiveness (9.4%). In total, 1793 patients 

continued treatment for 6 months. At least one AE was observed in 34.1% of patients, 

the most frequent of which was Herpes zoster (3.3%), including 12 serious cases. SAEs 

occurred in 8.0%; the most frequent were pneumonia (0.8%), interstitial lung disease 

(0.6%) and a definition of ‘condition aggravated’ (0.5%). Infections (12.7%) were serious 

in 3.7% of patients. Thirteen patients reported malignancy, including ovarian cancer 

(0.1%), diffuse large B-cell lymphoma (0.1%) and lymphoproliferative disorder (0.04%).



Sixteen (0.7%) deaths were reported. Overall, there were no new or unexpected safety 

signals compared to results from the tofacitinib RA clinical programme. The target sample 

size for the final analysis of this 3-year post-marking study is 6000 patients [AB0431]. 

Gennadjevna, et al. presented a poster on the increase of night QT-interval duration seen 

during 12-month ECG follow-up. In patients treated with tofacitinib there was a significant 

decrease in heart rate and an increase in QRS, night QTc interval duration, number 

of ventricular premature beats by 24-hour ECG. The authors found that QTc duration 

correlated with dynamic of disease activity, type 2 diabetes and diastolic blood pressure 

[THU0148]. 

In Schneeberger, et al.’s retrospective data from 10 centres in Latin America, there were 

no new safety signals. Serious infection events and Herpes zoster were uncommon; 

no cases of tuberculosis or other opportunistic infections occurred [AB0419]. 

Safety in PsA 

Curtis, et al. compared the safety profile of tofacitinib seen in 2 Phase 3 clinical studies 

in PsA (n=1257) with real-world data from a comparison cohort of 5799 patients initiating 

therapy with a systemic agent. Incidence rates of serious infection events were lower 

for tofacitinib versus the comparison cohort. The tofacitinib group had a higher rate of 

Herpes zoster, with incidence rates of 1.96 and 2.66 for 5- and 10 mg doses, respectively, 

compared with 1.26 for any bDMARD, and 2.62 for apremilast. Incidence rates for 

malignancies and MACE were similar between cohorts [FRI0496]. 

Phase 3 data from OPAL Balance, an open-label long-term extension trial in PsA, were 

presented in a poster by Nash, et al. To Month 24, 860 AEs were reported in 367 (54.0%) 

patients, SAEs in 41 (6.0%); 24 patients (3.5%) discontinued due to AEs. Overall, the 

safety profile of tofacitinib was generally similar to that of the pivotal Phase 3 studies, 

and no new safety signals were identified. [FRI0509]. 

An integrated safety summary of pooled data from the OPAL Broaden and OPAL Beyond 

trials was presented in a poster by Burmester, et al. Across all tofacitinib-treated patients, 

serious infections occurred in 11 (incidence rate 1.40). Herpes zoster was reported in 

16 patients (incidence rate 2.05) and 3 cases of multidermatomal Herpes zoster were 

adjudicated as opportunistic infections. Two deaths occurred and were considered 

unrelated to the study drug. MACE were reported in three patients (incidence rate 0.38), 

malignancies (excluding NMSC) in five patients (incidence rate 0.63) and NMSC in four 

patients (incidence rate 0.51). Overall, tofacitinib was well tolerated in patients with PsA, 

with a safety profile consistent to that seen in RA [SAT0439].



Real-world use 

Moura, et al. examined the comparative effectiveness of tofacitinib, bDMARDs and 

traditional DMARDs in RA, using data from MarketScan ® databases (2011–2014) to study 

individuals previously treated with MTX and newly prescribed one of the medications 

under investigation. 16 305 patients with RA were included: 2879 began therapy with 

DMARD, 13345 with bDMARDs and 81 with tofacitinib. Similar effectiveness was 

observed among groups. Fewer patients initiating bDMARDs were non-adherent 

compared with DMARD and tofacitinib therapy, but switching tended to be higher in the 

bDMARD group [SAT0149]. 

Adherence and access to tofacitinib and bDMARDs was examined by Machado-Alba, 

et al. in a retrospective cohort of 1102 Colombian patients. The most commonly 

prescribed drugs were adalimumab (31.9%), etanercept (22.2%) and tofacitinib (12.5%). 

Global adherence was 66.3%, with better adherence reported for self-administered 

subcutaneous drugs given every week or longer, compared with daily dosing of oral 

drug. 42.4% of patients experienced at least one delay per year in the application or 

dispensation of their medication, resulting in 36.1% experiencing dose losses due to 

difficulties in access [AB0403]. 

Reed, et al. compared TNFi and tofacitinib monotherapy in clinical practice as captured 

in the US CORRONA registry. The presentation included data from 7976 eligible TNFi 

initiations (31% monotherapy) and 555 tofacitinib initiations (61% monotherapy). 

Overall, TNFi combination therapy was more effective than TNFi monotherapy in 

second-line therapy, but the difference diminished with third- and fourth-line treatments. 

Tofacitinib combination therapy was similar to monotherapy in the matched thirdand 

fourth-line populations combined. Tofacitinib monotherapy was similar to TNFi 

combination therapy in the matched third- and fourth-line populations combined [OP0022]. 

Schneeberger, et al. shared retrospective data from 10 centres in Latin America, looking 

at 288 patients with severe active RA. Overall, tofacitinib usage corresponded to 13% 

of advanced therapies (JAK inhibitors, bDMARDs and biosimilars). Tofacitinib was 

given as second-line therapy after csDMARD in 44% of patients, after one bDMARD in 

18% and after two or more bDMARDs in 38% of patients. 41% received tofacitinib as 

monotherapy, and the remainder in combination with a csDMARD. There were no new 

safety signals. Serious infection events and Herpes zoster were uncommon; no cases of 

tuberculosis or other opportunistic infections occurred [AB0419].



Sansinanea, et al. described the real-life experience with tofacitinib in 62 patients in 

Argentina. Most patients (87%) received the drug in combination with another DMARD 

– most commonly MTX. During the time of exposure to tofacitinib, the following AEs 

were observed: 2 Herpes Zoster infections (monometameric, no visceral involvement in 

unvaccinated patients), 1 upper airway infection, 1 transient increase in liver enzymes, 

1 case of peripheral facial paralysis, and 1 case of tachycardia. There were no cases of 

serious infections, opportunistic infections, cytopenias, dyslipidemia, or increased CPK 

[AB0434]. 

Luchikhina, et al. presented the efficacy and safety of open-label tofacitinib in 129 

Russian patients with RA who did not respond to csDMARDs or bDMARDs in clinical 

practice. At Month 3, SDAI decreased to 14.6 (P



Pérez Baos, et al. examined the lipid paradox in a rabbit model, showing that tofacitinib 

restores the inhibition of reverse cholesterol transport (RCT) induced by inflammation. 

The results suggest that active inflammation could be associated with lipid accumulation 

in macrophages in the synovium and other tissues, thereby inducing a decrease in serum 

lipid levels. Tofacitinib may prevent this phenomenon, at least partially, by increasing RCT 

pathways in macrophages. The authors concluded that these findings further explain how 

serum lipid levels are diminished in RA, and partially justify the effect of tofacitinib on the 

lipid profile in patients with RA [FRI0071]. 

It is known that tocilizumab improves left ventricular mass (LVM) or cardiac output (CO) 

independently of effects on disease activity. Kume, et al. found that tofacitinib also LVM 

and CO in 24 patients with RA. LVM index and CO were attenuated significantly by 

tofacitinib over a 24-week period, and DAS28 and CRP improved significantly (P



References 

• Aletaha D, Kivitz A, Valenzuela G, et al. MAGNITUDE AND DURATION OF EARLY RESPONSE WITH TOFACITINIB: 

POST-HOC ANALYSIS OF TWO PHASE 3, PLACEBO-CONTROLLED STUDIES. Presented at: EULAR; 14–17 June 

2017, Madrid, Spain. Abstract THU0186. 

• Alten R, Westhovens R, Kavanaugh A, et al. LONG TERM SAFETY AND EFFICACY OF FILGOTINIB IN A PHASE 2B 

OPEN LABEL EXTENSION STUDY IN PATIENTS WITH RHEUMATOID ARTHRITIS: RESULTS UP TO 144 WEEKS. 

Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract THU0173. 

• Blanqué R, Ongenaert M, David C, et al. THE JAK1-SELECTIVE INHIBITOR, FILGOTINIB, INHIBITS INFLAMMATION 

PATHWAYS OBSERVED IN AN IL23-INDUCED PSORIATIC ARTHRITIS MOUSE MODEL. Presented at: EULAR; 

14–17 June 2017, Madrid, Spain. Abstract FRI0428. 

• Burmester G, FitzGerald O, Winthrop K, et al. INTEGRATED SAFETY SUMMARY OF TOFACITINIB IN PSORIATIC 

ARTHRITIS CLINICAL STUDIES. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract SAT0439. 

• Charles-Schoeman C, Kremer J, Krishnaswami S, et al. COMPARISON OF TOFACITINIB SAFETY AND EFFICACY 

IN RHEUMATOID ARTHRITIS PATIENTS WITH INADEQUATE RESPONSE TO CONVENTIONAL SYNTHETIC 

DMARDS, OR TO ONE OR MORE BIOLOGICAL DMARDS. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. 

Abstract THU0185. 

• Charles-Schoeman C, Valdez H, Soma K, et al. MAJOR ADVERSE CARDIOVASCULAR EVENTS: RISK FACTORS IN 

PATIENTS WITH RA TREATED WITH TOFACITINIB. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract 

SAT0686. 

• Combe B, Balsa A, Sarzi-Puttini P, et al. EFFICACY AND SAFETY DATA BASED ON HISTORICAL OR PRE-EXISTING 

CONDITIONS AT BASELINE FOR PATIENTS WITH ACTIVE RHEUMATOID ARTHRITIS WHO WERE TREATED WITH 

BARICITINIB. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract FRI0086. 

• Conaghan PG, Bowes MA, Østergaard M, et al. INFLAMMATION DETECTED WITH MODERN SENSITIVE 

MRI ANALYSIS DEMONSTRATES THAT THERAPEUTIC RESPONSE AS EARLY AS ONE MONTH PREDICTS 

12-MONTH RADIOGRAPHIC PROGRESSION: DATA FROM A STUDY USING TOFACITINIB AND METHOTREXATE 

IN METHOTREXATE-NAÏVE PATIENTS WITH EARLY RA. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. 

Abstract THU0175. 

• Curtis J, Emery P, Burmester G, et al. EFFECTS OF SMOKING ON BARICITINIB EFFICACY IN PATIENTS WITH 

RHEUMATOID ARTHRITIS: POOLED ANALYSIS FROM TWO PHASE 3 CLINICAL TRIALS. Presented at: EULAR; 

14–17 June 2017, Madrid, Spain. Abstract THU0114. 

• Curtis JR, Kavanaugh A, van der Heijde D, et al. EFFECT OF BASELINE DISEASE ACTIVITY ON ACHIEVING 

SUSTAINED LOW DISEASE ACTIVITY IN BARICITINIB PHASE 3 STUDIES. Presented at: EULAR; 14–17 June 2017, 

Madrid, Spain. Abstract AB0235. 

• Curtis JR, Kavanaugh A, van der Heijde D, et al. EFFECT OF STARTING DOSE OF BARICITINIB IN ACHIEVING 

SUSTAINED LOW DISEASE ACTIVITY. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract FRI0089. 

• Curtis JR, Yun H, FitzGerald O, et al. COMPARING TOFACITINIB SAFETY PROFILE IN PATIENTS WITH PSORIATIC 

ARTHRITIS IN CLINICAL STUDIES WITH REAL-WORLD DATA. Presented at: EULAR; 14–17 June 2017, Madrid, 

Spain. Abstract FRI0496. 

• Emery P, Tanaka Y, Cardillo TE, et al. TEMPORARY INTERRUPTIONS OF STUDY DRUG DURING THE BARICITINIB 

PHASE 3 RHEUMATOID ARTHRITIS PROGRAM. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract 

FRI0124. 

• Fautrel B, van de Laar M, Kirkham B, et al. DIFFERENCES IN PATIENT-REPORTED OUTCOMES BETWEEN 

BARICITINIB AND COMPARATORS AMONG PATIENTS WITH RHEUMATOID ARTHRITIS WHO ACHIEVED LOW 

DISEASE ACTIVITY OR REMISSION. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract THU0081. 

• Finckh A, Herzog L, Scherer A, et al. DRUG RETENTION OF TOFACITINIB VERSUS BIOLOGIC ANTIRHEUMATIC 

AGENTS IN RHEUMATOID ARTHRITIS: OBSERVATIONAL DATA FROM THE SWISS SCQM REGISTRY. Presented 

at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract THU0174.



• Fleischmann R, Mysler E, Hall S, et al. TOFACITINIB WITH AND WITHOUT METHOTREXATE VERSUS 

ADALIMUMAB WITH METHOTREXATE FOR THE TREATMENT OF RHEUMATOID ARTHRITIS: RESULTS FROM 

ORAL STRATEGY, A PHASE 3B/4 RANDOMISED TRIAL. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. 

Abstract LB0003. 

• Fleischmann R, Takeuchi T, Schiff M, et al. EFFECTS OF BARICITINIB ON PATIENTS WHO STOP METHOTREXATE 

MONOTHERAPY AND SWITCH TO BARICITINIB MONOTHERAPY. Presented at: EULAR; 14–17 June 2017, Madrid, 

Spain. Abstract SAT0058. 

• Gaylis NB, Sagliani J, Needell S. CLINICAL AND STRUCTURAL RESPONSES OF PATIENTS WITH ACTIVE 

RHEUMATOID ARTHRITIS (RA) USING STEP-UP DOSAGES OF TOFACITINIB IN A TREAT TO TARGET APPROACH. 

Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract AB0261. 

• Gennadjevna Kirillova I, Novikova D, Luchikhina E, et al. INCREASE OF NIGHT QT-INTERVAL DURATION IN 

RHEUMATOID ARTHRITIS PATIENTS TREATED WITH TOFACITINIB DURING 12-MONTH FOLLOW-UP. Presented 

at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract THU0148. 

• Genovese MC, Li W, Goyal L, et al. EFFECTS OF THE JAK1-SELECTIVE INHIBITOR FILGOTINIB ON 

MULTIBIOMARKER DISEASE ACTIVITY SCORES IN PATIENTS WITH ACTIVE RHEUMATOID ARTHRITIS AND AN 

INADEQUATE RESPONSE TO METHOTREXATE. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract 

THU0205. 

• Gladman DD, Rigby WFC, Azevedo VF, et al. EFFICACY AND SAFETY OF TOFACITINIB, AN ORAL JANUS KINASE 

INHIBITOR, IN PATIENTS WITH ACTIVE PSORIATIC ARTHRITIS AND AN INADEQUATE RESPONSE TO TUMOUR 

NECROSIS FACTOR INHIBITORS: OPAL BEYOND, A RANDOMISED, DOUBLE-BLIND, PLACEBO-CONTROLLED, 

PHASE 3 TRIAL. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract OP0202. 

• Gomez-Reino JJ, Checchio T, Geier J, et al. SYSTEMATIC REVIEW AND META-ANALYSIS OF MALIGNANCIES, 

EXCLUDING NON-MELANOMA SKIN CANCER, IN PATIENTS WITH RHEUMATOID ARTHRITIS TREATED WITH 

TOFACITINIB OR BIOLOGIC DISEASE-MODIFYING ANTIRHEUMATIC DRUGS. Presented at: EULAR; 14–17 June 

2017, Madrid, Spain. Abstract THU0196. 

• Harrold LR, Reed GW, Best J, et al. COMPARATIVE EFFECTIVENESS OF TOCILIZUMAB (TCZ) MONOTHERAPY 

WITH TUMOR NECROSIS FACTOR INHIBITORS (TNFI) IN COMBINATION WITH VARYING DOSES OF 

METHOTREXATE (MTX) IN PATIENTS WITH RHEUMATOID ARTHRITIS. Presented at: EULAR; 14–17 June 2017, 


• Kaine J, Tesser J, DeMasi R, et al. REESTABLISHMENT OF EFFICACY OF TOFACITINIB, AN ORAL JANUS KINASE 

INHIBITOR, IN RHEUMATOID ARTHRITIS PATIENTS AFTER TEMPORARY DISCONTINUATION. Presented at: 

EULAR; 14–17 June 2017, Madrid, Spain. Abstract THU0193. 

• Kavanaugh A, Helt C, Muram D, et al. CONCOMITANT USE OF CONVENTIONAL SYNTHETIC DMARDS AND 

RESPONSE TO BARICITINIB. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract THU0078. 

• Kavanaugh A, Van der Aa A, Jamoul C, et al. MONOTHERAPY WITH THE JAK1-SELECTIVE INHIBITOR FILGOTINIB 

DISPLAYS AN ANTI-INFLAMMATORY BIOMARKER PROFILE IN RHEUMATOID ARTHRITIS PATIENTS. Presented 


• Kay J, Harigai M, Rancourt J, et al. EFFECTS OF BARICITINIB ON HAEMOGLOBIN AND RELATED LABORATORY 

PARAMETERS IN RHEUMATOID ARTHRITIS PATIENTS. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. 

Abstract FRI0092. 

• Kremer J, Huizinga TWJ, Chen L, et al. ANALYSIS OF NEUTROPHILS, LYMPHOCYTES, AND PLATELETS IN 

POOLED PHASE 2 AND PHASE 3 STUDIES OF BARICITINIB FOR RHEUMATOID ARTHRITIS. Presented at: EULAR; 

14–17 June 2017, Madrid, Spain. Abstract FRI0090. 

• Kume K, Amano K, Yamada S, et al. TOFACITINIB IMPROVES LEFT VENTRICULAR MASS AND CARDIAC OUTPUT 

IN PATIENTS WITH RHEUMATOID ARTHRITIS. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract 

THU0199. 

• Kvien TK, van Riel P, Rubbert-Roth A, et al. BARICITINIB VERSUS ADALIMUMAB IN PATIENTS WITH ACTIVE 

RHEUMATOID ARTHRITIS: ANALYSIS OF PATIENTS ACHIEVING A MODERATE EULAR RESPONSE AT WEEK 4. 

Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract SAT0070.



• Lee YH, Seo YH, Song GG. COMPARATIVE EFFICACY AND SAFETY OF BARICITINIB 2 MG AND 4 MG IN 

PATIENTS WITH ACTIVE RHEUMATOID ARTHRITIS: A BAYESIAN NETWORK META-ANALYSIS OF RANDOMIZED 

CONTROLLED TRIALS. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract THU0213. 

• Li Z, An Y, Li G, et al. EFFECTS OF TOFACITINIB ON PATIENT-REPORTED OUTCOMES IN A PHASE 3 STUDY OF 

CHINESE PATIENTS WITH ACTIVE RHEUMATOID ARTHRITIS AND AN INADEQUATE RESPONSE TO DMARDS. 

Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract THU0215. 

• Luchikhina EL, Karateev D, Misiyuk A, et al. EFFICACY AND SAFETY OF TOFACITINIB IN PATIENTS WITH 

RHEUMATOID ARTHRITIS WHO DID NOT RESPOND TO SYNTHETIC AND BIOLOGICAL DMARDS IN CLINICAL 

PRACTICE. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract THU0188. 

• Machado-Alba JE, Machado-Duque ME, Granada S. ADHERENCE AND ACCESS TO BIOLOGICAL THERAPY AND 

TOFACITINIB IN A COHORT OF COLOMBIAN PATIENTS WITH RHEUMATOLOGICAL DISEASES. Presented at: 

EULAR; 14–17 June 2017, Madrid, Spain. Abstract AB0403. 

• Maksymowych WP, van der Heijde D, Baraliakos X, et al. TOFACITINIB TREATMENT IS ASSOCIATED WITH 

ATTAINMENT OF THE MINIMALLY IMPORTANT REDUCTION IN AXIAL MRI INFLAMMATION IN PATIENTS WITH 

ANKYLOSING SPONDYLITIS. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract THU0352. 

• Mease PJ, Hall S, FitzGerald O, et al. FFICACY AND SAFETY OF TOFACITINIB, AN ORAL JANUS KINASE 

INHIBITOR, OR ADALIMUMAB IN PATIENTS WITH ACTIVE PSORIATIC ARTHRITIS AND AN INADEQUATE 

RESPONSE TO CONVENTIONAL SYNTHETIC DISEASE-MODIFYING ANTIRHEUMATIC DRUGS (CSDMARDS): A 

RANDOMISED, PLACEBO-CONTROLLED, PHASE 3 TRIAL. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. 

Abstract OP0216. 

• Mimori T, Harigai M, Atsumi T, et al. POST-MARKETING SURVEILLANCE OF TOFACITINIB IN JAPANESE PATIENTS 

WITH RHEUMATOID ARTHRITIS: AN INTERIM REPORT OF SAFETY DATA. Presented at: EULAR; 14–17 June 2017, 


• Mohamed M-E, Zeng J, Jiang P, et al. ABT-494 HAS NO EFFECT ON THE QT INTERVAL AT THE DOSES BEING 

EVALUATED IN RHEUMATOID ARTHRITIS PHASE 3 TRIALS. Presented at: EULAR; 14–17 June 2017, Madrid, 

Spain. Abstract AB0432. 

• Mohamed M-E, Zeng J, Song IH, et al. ABT-494 PHARMACOKINETICS FOLLOWING ADMINISTRATION OF THE 

ONCE-DAILY EXTENDED-RELEASE TABLET FORMULATION BEING UTILIZED IN THE ONGOING RHEUMATOID 

ARTHRITIS PHASE 3 TRIALS. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract THU0177. 

• Moura CS, Machado MA, Behlouli H, et al. COMPARATIVE EFFECTIVENESS OF TOFACITINIB, BIOLOGIC DRUGS 

AND TRADITIONAL DISEASE-MODIFYING ANTIRHEUMATIC DRUGS IN RHEUMATOID ARTHRITIS. Presented at: 

EULAR; 14–17 June 2017, Madrid, Spain. Abstract SAT0149. 

• Nash P, Coates LC, Fleischmann R, et al. INTEGRATED EFFICACY ANALYSIS OF TOFACITINIB, AN ORAL JANUS 

KINASE INHIBITOR, IN PATIENTS WITH ACTIVE PSORIATIC ARTHRITIS. Presented at: EULAR; 14–17 June 2017, 

Madrid, Spain. Abstract SAT0469. 

• Nash P, Coates LC, Kivitz AJ, et al. SAFETY AND EFFICACY OF TOFACITINIB, AN ORAL JANUS KINASE 

INHIBITOR, UP TO 24 MONTHS IN PATIENTS WITH ACTIVE PSORIATIC ARTHRITIS: INTERIM DATA FROM OPAL 

BALANCE, AN OPEN-LABEL, LONG-TERM EXTENSION STUDY. Presented at: EULAR; 14–17 June 2017, Madrid, 

Spain. Abstract FRI0509. 

• Novikova D, Kirillova I, Luchikhina E, et al. THE FIRST REPORT OF SIGNIFICANT INCREASE OF BODY MASS 

INDEX IN RHEUMATOID ARTHRITIS PATIENTS TREATED WITH TOFACITINIB DURING 12-MONTH FOLLOW-UP. 

Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract FRI0231. 

• Pérez Baos S, Barrasa JI, Gratal P, et al. OFACITINIB RESTORES THE INHIBITION OF REVERSE CHOLESTEROL 

TRANSPORT INDUCED BY INFLAMMATION: UNDERSTANDING THE LIPID PARADOX ASSOCIATED WITH 

RHEUMATOID ARTHRITIS. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract FRI0071. 

• Pincus T, Zhu B, Larmore CJ, et al. RAPID3-LIKE INDEX DOCUMENTS SUPERIOR EFFICACY OF BARICITINIB TO 

ADALIMUMAB AND PLACEBO, SIMILAR TO DAS28 AND CDAI IN THE RA-BEAM CLINICAL TRIAL IN PATIENTS 

WITH RHEUMATOID ARTHRITIS. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract SAT0069.



• Reed GW, Gerber RA, Shan Y, et al. TNFI AND TOFACITINIB MONOTHERAPY AND COMPARATIVE 

EFFECTIVENESS IN CLINICAL PRACTICE: RESULTS FROM CORRONA REGISTRY. Presented at: EULAR; 14–17 

June 2017, Madrid, Spain. Abstract OP0022. 

• Robin-Jagerschmidt C, Lavazais S, Marsais F, et al. THE JAK1 SELECTIVE INHIBITOR FILGOTINIB REGULATES 

BOTH ENTHESIS AND COLON INFLAMMATION IN A MOUSE MODEL OF PSORIATIC ARTHRITIS. Presented at: 

EULAR; 14–17 June 2017, Madrid, Spain. Abstract OP0161. 

• Sansinanea P, Costi AC, Vulcano A, et al. TOFACITINIB IN RHEUMATOID ARTHRITIS: REAL LIFE EXPERIENCE. 


• Schneeberger EE, Salas A, Medina LF, et al. REAL WORLD USE OF TOFACITINIB IN RHEUMATOID ARTHRITIS: 

DATA FROM LATIN AMERICA. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract AB0419. 

• Schwartzman S, Sunkureddi P, Takiya L, et al. COMPARISON OF TOFACITINIB EFFICACY IN PATIENTS WITH 

MODERATE VS SEVERE RHEUMATOID ARTHRITIS: POOLED ANALYSIS OF PHASE 3 STUDIES. Presented at: 


• Smolen J, Li Z, Klar R, et al. DURABILITY AND MAINTENANCE OF EFFICACY FOLLOWING PROLONGED 

TREATMENT WITH BARICITINIB. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract FRI0096. 

• Strand S, de Vlam K, Covarrubias-Cobos JA, et al. EFFECT OF TOFACITINIB ON PATIENT-REPORTED OUTCOMES 

IN PATIENTS WITH ACTIVE PSORIATIC ARTHRITIS: RESULTS FROM TWO PHASE 3 STUDIES. Presented at: 


• Strand V, Ahadieh S, DeMasi R, et al. META-ANALYSIS OF SERIOUS INFECTIONS WITH BARICITINIB, 

TOFACITINIB AND BIOLOGIC DMARDS IN RHEUMATOID ARTHRITIS. Presented at: EULAR; 14–17 June 2017, 

Madrid, Spain. Abstract THU0211. 

• Strand V, Genovese M, Kremer J, et al. CHANGES IN HEMOGLOBIN LEVELS UPON TREATMENT WITH ABT-494, 

A SELECTIVE JAK-1 INHIBITOR, AND RELATION TO BASELINE LEVELS OF C-REACTIVE PROTEIN. Presented at: 

EULAR; 14–17 June 2017, Madrid, Spain. Abstract THU0210. 

• Strand V, Tundia N, Song IH, et al. EARLY PATIENT-REPORTED OUTCOMES AND CLINICAL OUTCOMES 

WITH ABT-494 IN PATIENTS WITH ACTIVE RHEUMATOID ARTHRITIS WHO ARE INADEQUATE RESPONDERS 

TO METHOTREXATE OR TUMOR NECROSIS FACTOR INHIBITORS: POST-HOC ANALYSIS OF PHASE 2 

RANDOMIZED CONTROLLED TRIALS. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract SAT0217. 

• Takeuchi T, Fleischmann R, Schiff M, et al. CHARACTERIZATION OF CHANGES IN LYMPHOCYTE SUBSETS IN 

BARICITINIB-TREATED PATIENTS WITH EARLY, DMARD NAÏVE, RHEUMATOID ARTHRITIS IN A PHASE 3 STUDY. 


• Takeuchi T, Genovese M, Haraoui B, et al. DOSE REDUCTION OF BARICITINIB IN PATIENTS WITH RHEUMATOID 

ARTHRITIS ACHIEVING SUSTAINED DISEASE CONTROL: RESULTS OF A PROSPECTIVE STUDY. Presented at: 

EULAR; 14–17 June 2017, Madrid, Spain. Abstract SAT0072. 

• Taylor P, Westhovens R, Van der Aa A, et al. THE JAK1-SELECTIVE INHIBITOR FILGOTINIB REDUCES MULTIPLE 

MARKERS OF INFLAMMATION LINKED TO VARIOUS PATHOLOGIC CELL TYPES AND PROCESSES IN 

RHEUMATOID ARTHRITIS PATIENTS. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract THU0206. 

• Taylor P, Zhu B, Gaich C, et al. BARICITINIB SHOWED RAPID AND GREATER REDUCTION IN PAIN COMPARED 

TO ADALIMUMAB OR PLACEBO IN PATIENTS WITH RHEUMATOID ARTHRITIS. Presented at: EULAR; 14–17 June 

2017, Madrid, Spain. Abstract SAT0055. 

• Tesser J, Gül A, Olech E, et al. CONSISTENT EFFICACY AND SAFETY OF TOFACITINIB IN RHEUMATOID 

ARTHRITIS PATIENTS WITH INADEQUATE RESPONSE OR INTOLERANCE TO NON-MTX CSDMARDS. Presented 


• van der Heijde D, Durez P, Schett G, et al. STRUCTURAL DAMAGE PROGRESSION IN PATIENTS TREATED WITH 

METHOTREXATE, BARICITINIB MONOTHERAPY OR BARICITINIB + METHOTREXATE BASED ON THEIR LEVEL OF 

CLINICAL RESPONSE IN THE PHASE 3 RA-BEGIN STUDY. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. 

Abstract THU0088.



• van der Heijde D, Schiff M, Tanaka Y, et al. LOW RATES OF RADIOGRAPHIC PROGRESSION OF STRUCTURAL 

JOINT DAMAGE OVER 2 YEARS OF BARICITINIB TREATMENT IN PATIENTS WITH RHEUMATOID ARTHRITIS. 

Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract FRI0087. 

• Vidal B, Cascão R, Finnilä M, et al. EFFECTS OF TOFACITINIB IN EARLY ARTHRITIS BONE LOSS. Presented at: 


• Winthrop KL, Wouters A, Choy EH, et al. THE EFFECTIVENESS OF ZOSTER VACCINE IN RA PATIENTS 

SUBSEQUENTLY TREATED WITH TOFACITINIB. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract 

OP0230. 

• Wollenhaupt J, Silverfield J, Lee EB, et al. TOFACITINIB, AN ORAL JANUS KINASE INHIBITOR, IN THE TREATMENT 

OF RHEUMATOID ARTHRITIS: SAFETY AND EFFICACY IN OPEN-LABEL, LONG-TERM EXTENSION STUDIES 

OVER 8 YEARS. Presented at: EULAR; 14–17 June 2017, Madrid, Spain. Abstract THU0197. 

• Yamanaka H, Tanaka Y, Takeuchi T, et al. EFFECTS OF TOFACITINIB, AN ORAL JANUS KINASE INHIBITOR, ON 

PATIENT-REPORTED OUTCOMES IN JAPANESE PATIENTS WITH RHEUMATOID ARTHRITIS. Presented at: EULAR; 

14–17 June 2017, Madrid, Spain. Abstract THU0191.

Register for all this FREE content at 



info@cytokinesignalling.com 

@CytokineForum 

lnkd.in/PyqQPm 

Supported by an unrestricted educational grant 

from Pfizer Italia S.R.L., Lilly and R-Pharm. 

Developed under the auspices of the University of Glasgow

EULAR 2017 CS Review

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?