EULAR 2019 Review

Enhancing knowledge of the clinical importance of cytokine signalling 

The Cytokine Signalling Forum 

www.cytokinesignalling.com 

EULAR 2019 

Conference Highlights

EULAR 2019 

Conference Highlights 

Chairman’s Welcome 

Dear CSF Member, 

It is my pleasure to welcome you to the CSF’s review of the EULAR 2019 highlights, which includes my ‘Chairman’s picks’. 

As in previous years, there continues to be an intense focus on the Janus kinase (JAK) inhibitors, with late stage trial results 

from upadacitinib, filgotinib and peficitinib – as well as a host of real-world data and further trial data for the more wellestablished 

baricitinib and tofacitinib. 

Probably the largest number of trial abstracts concerned upadacitinib. Key among them were the 48-week data from the 

SELECT-EARLY study [THU0197; THU0192], SELECT-MONOTHERAPY [THU0191], and SELECT-COMPARE [FRI0137; 

FRI0147], and 60-week data from SELECT-BEYOND [THU0172]. There was an interesting study analysing the clinical and 

functional outcomes of switching between upadacitinib and adalimumab following initial non-response [OP0029] and another 

looking into structural joint damage inhibition with upadacitinib use [THU0188]. 

For filgotinib, Combe et al and Westhovens et al gave us late-breaking data from the FINCH trials [LB0001; LB0003], and for 

peficitinib, Tanaka et al and Takeuchi et al brought us two abstracts from the Phase 3 trials of peficitinib [FRI0134; OP0026], 

in patients with either an inadequate response to DMARDs or MTX. 

There was new clinical data for both tofacitinib and baricitinib – with a phase 3 study comparing early and delayed start of 

baricitinib in methotrexate-naïve patients [THU0075], and a look at MTX-withdrawal in patients taking the extended-release 

formulation of tofacitinib [LB0004]. Real-world studies examined the utility of these two drugs in clinical practice, and several 

registries shared their latest data cuts. Of note, the British Society for Rheumatology shared their data into early use of JAK 

inhibitors in patients with RA [AB0434]. With these new studies, we also saw the most up-to-date safety data for both 

baricitinib [THU0078] and tofacitinib [OP0028]. 

All these new data provided us with a better insight into the use of JAK inhibitors in clinical practice. However, it was also 

good to see a wide breadth of basic science data for all these agents, including biomarker results from Phase 3 studies with 

upadacitinib [THU0181] and in-depth analyses into upadacitinib and its impact on cholesterol [THU0166]. 

At this year’s congress we also saw Phase 2 data from two Bruton’s tyrosine kinase (BTK) inhibitors – fenebrutinib and 

LY3337641 [OP0025; SAT0089]. It will be important to see how these agents progress over the coming years, and to find 

out what hope they can offer to patients who do not succeed on current therapies. 

Within the following pages, we share our review of the congress highlights, including my ‘Chairman’s picks’. As always, 

thank you for your continued support, and we hope you enjoyed your time in Madrid at EULAR 2019! 

Kind regards, 

Prof. Iain McInnes

Highlights from EULAR 2019 

During the EULAR 2019 annual meeting, many presentations and posters reported on cytokine 

signalling and related drugs. This document reviews the highlights. 

NEW AGENTS – Clinical Trials 

Filgotinib 

Phase III studies of filgotinib in RA patients – FINCH1 and FINCH3 

Combe and colleagues presented the primary outcome results from the Phase 3, double-blind, 

active- and placebo-controlled FINCH1 study evaluating filgotinib versus adalimumab or placebo in 

patients with active RA and an inadequate response to MTX. The study randomised 1,759 patients, of 

whom 1,755 received study drug and were analysed (filgotinib 200 mg QD, n=475; filgotinib 100 mg QD, 

n=480; adalimumab 40 mg Q2W, n=325; placebo, n=475). At Week 12, significantly more patients in the 

filgotinib 200 mg and 100 mg arms achieved an ACR20 response (primary outcome) compared with 

placebo (76.6%, 69.8% and 49.9%, respectively). Similarly, compared to placebo, more patients 

receiving filgotinib achieved ACR50 and ACR70 responses, DAS28-CRP scores ≤3.2 and

ackground csDMARDs for 24 weeks. Similar efficacy outcomes, including the primary outcome ACR20 

response at Week 12, were similar in older (≥65 years) and younger (

Peficitinib 

Peficitinib Phase III results 

Efficacy and safety data from a Phase III randomised, placebo-controlled study (NCT02308163) of 

peficitinib (a novel oral JAK inhibitor) were presented by Tanaka and colleagues. Patients with RA and 

an inadequate response to DMARDs received peficitinib alone or in combination with DMARDs. A total 

of 507 patients were randomised and treated: placebo (n=101), peficitinib 100 mg/day (n=104), 

peficitinib 150 mg/day (n=102) and etanercept (n=200). Significant differences were observed with 

peficitinib 100 mg/150 mg versus placebo (P

Fleishmann and colleagues presented 48-week results of the upadacitinib Phase 3 SELECT-COMPARE 

study, which assessed safety and efficacy versus adalimumab in patients with active RA despite 

treatment with MTX. A total of 1629 patients were randomised to upadacitinib 15 mg QD, placebo, or 

adalimumab 40 mg EOW, while continuing stable background MTX. Rescue therapy was offered based 

on predefined clinical criteria at Weeks 14 to 26 and all patients receiving placebo who were not rescued 

were switched to upadacitinib at Week 26. Between Weeks 14 and 26, 38.7% of patients randomised to 

upadacitinib and 48.6% of patients randomised to adalimumab were rescued. At Week 26, and Week 

48, significantly more patients in the upadacitinib versus adalimumab group achieved ACR20/50/70, low 

disease activity and remission; this was also true for visits between Weeks 26 and 48. Similarly, 

improvements in pain and function were significantly greater in the upadacitinib versus adalimumab 

group through week 48. At Week 26, there was significantly less radiographic progression for 

upadacitinib versus placebo, which was maintained through Week 48 based on linear extrapolation. 

Safety was consistent with observations in the first 26 weeks. The rate of AEs leading to discontinuation 

was higher with “any adalimumab” versus “any upadacitinib”, while the rate of herpes zoster was higher 

with “any upadacitinib” exposure. In summary, upadacitinib continued to demonstrate superior clinical 

and functional responses compared with adalimumab through Week 48 [FRI0147]. 

Forty-eight-week results from a long-term extension of the SELECT-MONOTHERAPY study were 

presented by Smolen and colleagues. Of 648 patients randomised at baseline, 92% completed 14 

weeks and continued on to the extension period. Starting from Week 26, background csDMARDs were 

initiated for approximately 18% of patients. Clinical and functional outcomes continued to improve, or 

were maintained through 48 weeks for patients receiving upadacitinib 15 mg and 30 mg. For patients 

continuing upadacitinib 15 and 30 mg, DAS28-CRP

venous thromboembolism, MACE, and malignancy versus comparators. In summary, these data support 

that upadacitinib has an acceptable safety profile in the treatment of moderately-to-severely active RA 

[THU0167]. 

An evaluation of structural joint damage progression through Week 48 in patients with moderately to 

severely active RA treated with upadacitinib monotherapy or in combination with MTX was presented by 

Peterfy and colleagues. The analysis included patients from two trials where MTX-naïve patients were 

randomised to upadacitinib 15 or 30 mg QD or MTX monotherapy (SELECT-EARLY, N=945), or to 

upadacitinib 15 mg QD or adalimumab 40 mg EOW or placebo, with continuous background MTX 

(SELECT-COMPARE, N=1629). At Weeks 24/26, upadacitinib as monotherapy and in combination with 

background MTX significantly inhibited radiographic progression (measured by mean ΔmTSS) and the 

proportion of patients with no radiographic progression versus MTX and placebo, respectively. The 

significant inhibition of radiographic progression with upadacitinib was maintained through Week 48 

versus MTX in SELECT-EARLY and versus placebo in SELECT-COMPARE. Following the switch of all 

placebo patients to upadacitinib in SELECT-COMPARE by Week 26, no further change in mean mTSS 

was observed through Week 48. In summary, upadacitinib both as monotherapy, and in combination 

with background MTX, was effective in inhibiting the progression of structural joint damage through 

Week 48 in MTX-naïve, and MTX-IR patients, respectively [THU0188*]. 

Weinblatt and colleagues presented clinical responses in the Phase 3 SELECT-BEYOND study 

according to the number and mechanism of action of prior bDMARDs. The study randomised 498 

patients to receive upadacitinib 15 or 30 mg QD or placebo for 12 weeks, after which patients on 

placebo received upadacitinib 15 or 30 mg QD. At Week 12, clinical responses were numerically, and 

often statistically, better for patients receiving either dose of upadacitinib versus placebo, irrespective of 

their prior bDMARD exposure or the number of prior bDMARDs received; responses at Week 24 were 

generally consistent with those at Week 12. TEAEs across the subgroups were consistent with the 

overall study population. In summary, at Week 12, treatment with upadacitinib at either 15 or 30 mg QD 

led to significantly better clinical responses versus placebo in a treatment-refractory population, including 

in patients with lack of efficacy to anti-TNF or anti-IL-6 therapies, and those who had an inadequate 

response or intolerance to 1, 2 or ≥3 prior bDMARDs [FRI0171]. 

Remission rates in patients with RA treated with upadacitinib or comparators were presented by Hall and 

colleagues. The analyses included patients who were MTX naïve (SELECT-EARLY, n=945), MTX-IR 

(SELECT-COMPARE, n=1629) and bDMARD-IR (SELECT-BEYOND, n=498). At 12 weeks, in 

SELECT-EARLY and SELECT-COMPARE, a significantly greater proportion of patients receiving 

upadacitinib 15 or 30 mg QD achieved remission by all four definitions versus MTX, placebo or 

adalimumab. In SELECT-BEYOND, (a refractory population many of whom had an inadequate response 

to multiple bDMARDs), a significantly greater proportion of patients receiving upadacitinib 30 mg 

achieved all remission definitions versus placebo within the first 12 weeks and rates of remission further 

increased through Week 24 for both dose groups. All disease activity components of each remission 

definition were significantly improved in patients receiving upadacitinib compared to MTX or placebo, 

and all Boolean components were significantly improved in patients receiving upadacitinib 15 mg 

compared to adalimumab [THU0174]. 

Kremer and colleagues reported the comparative efficacy of upadacitinib in combination with MTX 

versus upadacitinib in combination with other csDMARDs. Analyses were performed using data from the 

SELECT-NEXT and SELECT-BEYOND trials, in which 535 and 410 patients, respectively, received 

concomitant MTX (mean dose 17 mg/week), and 124 and 82 patients received non-MTX csDMARDs. 

Across all subgroups, the proportion of patients achieving efficacy outcomes was higher with both 

upadacitinib doses compared with placebo. There were no significant differences between efficacy 

outcomes (ACR20, LDA, DAS28-CRP remission, CDAI remission) with upadacitinib in combination with 

MTX versus upadacitinib in combination with non-MTX csDMARDs in either patient population. In 

*Chairman’s Pick

summary, the efficacy of upadacitinib in patients with RA appeared comparable whether administered in 

combination with MTX or non-MTX csDMARDs [FRI0155]. 

Genovese et al reported outcomes associated with a treatment switch from upadacitinib to adalimumab 

and vice-versa among RA patients who did not achieve an initial response in a Phase III study of 

upadacitinib 15 mg QD versus placebo or adalimumab 40 mg injection EOW. Of the 651 and 327 

patients randomised to receive upadacitinib and adalimumab, 19% and 24%, were considered 

non-responders and switched to adalimumab and upadacitinib, respectively. Patients switched to 

adalimumab achieved 59%, 26%, 12% improvements in ACR20/50/70 responses, and 35% achieved 

DAS28-CRP≤3.2 at 6 months post-switching. Patients switched to upadacitinib achieved 75%, 49%, 

24% improvements in ACR20/50/70, and 54% achieved DAS28-CRP≤3.2 at 6 months. The proportion of 

patients with infection and serious infection through 6 months post-switching appeared consistent with 

those observed for adalimumab and upadacitinib during comparable periods. The authors concluded 

that patients with initial non-response to either upadacitinib or adalimumab can benefit from switching to 

the other therapy [OP0029*]. 

A poster reporting a comparative analysis of upadacitinib monotherapy and upadacitinib combination 

therapy for the treatment of RA from the Phase 3 SELECT-NEXT (n=661) and SELECT- 

MONOTHERAPY (n=648) trials was presented by Buch and colleagues. In these cohorts of patients 

with RA and an inadequate response to MTX, both upadacitinib monotherapy and upadacitinib 

combination therapy led to significant improvements in efficacy outcomes versus continued MTX or 

placebo. No significant differences were observed between upadacitinib monotherapy and upadacitinib 

combination therapy across a range of clinical endpoints including ACR20/50/70 responses and 

measures of LDA and remission. In addition, improvements in quality of life as measured by HAQ-DI 

were similar with upadacitinib monotherapy and combination therapy. The authors concluded that in 

patients with RA and an inadequate response to MTX, the efficacy of upadacitinib appears comparable 

when administered as monotherapy or when given in combination with MTX [THU0165]. 

Upadacitinib patient-reported outcomes (PROs) in RA 

Strand et al presented two posters on PROs with upadacitinib in the SELECT-COMPARE and 

SELECT-EARLY studies. 

At Week 12 in SELECT-COMPARE, upadacitinib treatment resulted in statistically significant changes from 

baseline versus placebo across all evaluated PROs (PtGA-VAS, pain-VAS, HAQ-DI, FACIT-F, severity and 

duration of AM stiffness, RA-WIS and SF-36). Statistically significant changes from baseline versus 

adalimumab were observed for PtGA, pain, HAQ-DI, AM stiffness severity, FACIT-F, and SF-36 PCS and 

6/8 domain scores. Compared with placebo, significantly more upadacitinib-treated patients reported 

improvements greater or equal to the minimal clinically important difference (MCID) and scores greater or 

equal to normative values across all PROs, with numbers needed to treat less than 10. Importantly, the 

proportion of upadacitinib- versus adalimumab-treated patients reporting improvements greater or equal to 

normative values were significantly greater (all P

SF-36 General Health (both upadacitinib doses) domains [THU0192]. 

Tofacitinib versus upadacitinib in RA – comparative analyses of RCTs 

Lee and Song reported the results of a Bayesian network meta-analysis of efficacy and safety with 

tofacitinib and upadacitinib in combination with MTX in csDMARD-IR or bDMARD-IR patients with RA. 

Nine randomised controlled trials including 5,794 patients were included in the analysis. Upadacitinib 

15 mg plus MTX and upadacitinib 30 mg plus MTX were among the most effective treatments for active 

RA with an inadequate csDMARD or bDMARD response, followed by tofacitinib 10 mg plus MTX, 

tofacitinib 5 mg plus MTX, and adalimumab 40 mg plus MTX. No significant differences were observed 

in the incidence of serious adverse events between treatment groups. The authors concluded that in 

patients with RA and an inadequate response to csDMARDs or bDMARDs, upadacitinib 15 mg plus 

MTX and upadacitinib 30 mg plus MTX were the most efficacious interventions and were not associated 

with significant risks of serious adverse events [FRI0158]. 

New BTK inhibitors 

Fenebrutinib in RA – Phase II results 

Findings from a Phase 2 study of fenebrutinib in RA were presented by Cohen and colleagues. The 

multicentre, randomised, double-blind study enrolled patients with moderate-to-severe active RA with 

an inadequate response to either MTX (Cohort 1) or TNF inhibitors (Cohort 2). Cohort 1 patients were 

randomised to fenebrutinib at 50 mg QD (n=40), 150 mg QD (n=109), 200 mg BID (n=110), or 40 mg 

adalimumab injections SC Q2W (n=111), or placebo n=110). Cohort 2 patients were randomised to 

fenebrutinib 200 mg (n=48) or placebo (n=50). In cohort 1, ACR50 response rates increased with 

increasing fenebrutinib dose (18%, 28%, and 35% for fenebrutinib 50, 150, and 200 mg, respectively). 

Fenebrutinib 150 mg and 200 mg were superior to placebo (15%), and numerically similar to 

adalimumab (36%). In cohort 2, the response for fenebrutinib 200 mg was higher than placebo (25% 

versus 12%). AEs were generally balanced across cohort 1; there were 9 serious AEs in 7 patients and 

one death in the fenebrutinib 200 mg group. In cohort 2, more patients in the placebo arm reported AEs, 

and no serious AEs were reported [OP0025*]. 

LY3337641 in RA – Phase 2 RA-JUVENATE results 

Findings from Part B of the RA-JUVENATE study were presented by Genovese and colleagues. This 

was a 2-part multicentre, randomised, double-blind, placebo-controlled, Phase 2 trial with long-term 

extension in adult patients with RA. In Part B, 250 patients with active moderate-to-severe RA were 

randomised to receive oral LY3337641 5 mg (n=63), 10 mg (n=62), or 30 mg (n=63) or placebo (n=62) 

QD for 12 weeks. After an interim analysis showed a low likelihood of demonstrating significant efficacy 

at the conclusion of the trial, the sponsor discontinued Part B of the study, including the long-term 

extension. Of the 250 patients randomised in Part B, 189 completed 12 weeks and 180 entered the 

long-term extension. There was no statistically significant difference in the ACR20 response between 

any treatment group of LY3337641 and placebo at Week 12; a high placebo rate was noted, but no 

underlying reason was identified in post-hoc analyses. There were 5 SAEs (placebo, n=2; LY3337641 

30 mg, n=3) and one death (LY3337641 30 mg). The study sponsor concluded that the observed 

benefit-risk profile of LY3337641 in the study did not warrant its continuation [SAT0089]. 

*Chairman’s Pick

New Tofacitinib and Baricitinib Data - Clinical Trials 

Tofacitinib 

Efficacy in RA patients with early versus established disease 

Takeuchi and colleagues presented findings from a post-hoc analysis of ORAL Strategy evaluating the 

efficacy and safety of tofacitinib monotherapy, tofacitinib plus MTX and adalimumab plus MTX, stratified 

by baseline RA duration. A total of 241 patients had early RA (≤2 years duration) and 905 patients had 

established RA (>2 years duration). ACR50 and ΔDAS28-4(ESR) were generally similar for tofacitinib 

monotherapy and tofacitinib plus MTX up to Month 12 in early RA but were significantly greater with 

tofacitinib plus MTX in established RA (P

demonstrating that tofacitinib monotherapy was non-inferior to tofacitinib + MTX. Remission rates were 

also similar between arms and generally did not change after MTX withdrawal. In the double-blind 

phase, rates of AEs, SAEs, discontinuations due to AEs, and AEs of special interest, were generally 

comparable between arms. In summary, patients receiving tofacitinib modified-release 11 mg QD + MTX 

who achieve LDA may withdraw MTX up to Week 48 without significant worsening of disease activity, 

and patients in remission tend to remain in remission after MTX withdrawal [LB0004]. 

Baricitinib 

Early- versus delayed-treatment initiation in RA 

Fleischmann and colleagues presented an analysis of the RA-BEGIN trial to examine whether patients 

initially randomised to baricitinib monotherapy (i.e. early initiation) attained enhanced clinical, functional 

and radiographic outcomes compared with patients who initiated MTX and switched to baricitinib at 

Week 52 (i.e. delayed initiation). The analysis included a total of 588 patients with active RA who were 

randomised to MTX, baricitinib 4 mg QD, or combination MTX and baricitinib 4 mg. At Week 52, patients 

could enter a long-term extension study in which all patients received open-label baricitinib 4 mg. In 

early MTX-naïve patients, improved clinical, functional, and radiographic efficacy with baricitinib 4 mg 

versus MTX was observed in most outcome measures up to 52 weeks. Switching from MTX to baricitinib 

at Week 52 provided a rapid clinical response, allowing the majority of patients to achieve similar results 

4 weeks post-switch. The authors noted that if the goal of therapy is to achieve rapid and sustained 

control of disease activity, the differences reported for HAQ-DI and especially structural progression 

support an earlier switch to baricitinib for patients who do not obtain disease control with MTX 

[THU0075*]. 

Cost-effectiveness in a treat-to-target strategy for RA 

Van der Laar and colleagues reported a cost-effectiveness comparison of the DREAM treat-to-target 

strategy csDMARD combination therapy (csDMARDs)→ first bDMARD (adalimumab)→ next bDMARD 

(TNFi/non-TNFi) with the comparable strategy in which baricitinib is placed instead of adalimumab in 

csDMARDs IR, using a Markov model. A probabilistic sensitivity analysis showed the baricitinib strategy 

yielded lower costs (€13431 versus €14288) and higher utility (3.5643 versus 3.5605) over a 5-year 

period and is cost-effective and dominant over the DREAM T2T strategy. Scenario analyses showed the 

baricitinib strategy to be cost-effective in both the moderate and severe at baseline RA populations when 

analysed together and separately. In summary, the results suggest the use of a JAK1/JAK2-inhibitor 

(baricitinib) instead of a 1st bDMARD (adalimumab) in a treat-to-target strategy is cost-effective in 

treating RA patients [OP0313]. 

Real-world and National Data on Approved JAK Inhibitors 

Tofacitinib 

Efficacy and safety in RA patients with high disease activity 

Menshikova and colleagues presented findings of an open study that examined the efficacy of tofacitinib 

treatment in rheumatoid arthritis patients with high disease activity after 12 months of treatment and 

follow-up in real world practice. A total of 30 patients with severe RA and an inadequate response to 

MTX were enrolled and started tofacitinib 5 mg BID. By Month 3, the average mean DAS28-ESR and 

-CRP returned to normal range, the number of painful and swollen joints decreased by two times, 

reductions were observed in DAS28 and SDAI, and 6 patients achieved remission. The aim of a 

treat-to-target strategy was achieved by Month 12, with average DAS28-ESR and -CRP normalised 

and 33% of patients achieving remission according to DAS28 and SDAI. At 12 months, one patient had 

*Chairman’s Pick

a severe herpes zoster infection; no other infections occurred. The authors concluded that tofacitinib is 

an effective and safe treatment option for severe RA in real-world practice, noting that the treatment 

effect develops by 3 months and continues to grow to 12 months [AB0429]. 

Predictors of effectiveness 

Shmidt and colleagues presented data from the Moscow Unified Arthritis Registry for 48 patients 

treated with tofacitinib. Predictors of tofacitinib effectiveness were evaluated. Sex was found to be an 

independent predictor of achieved DAS28 (0.49 lower in men, P

treated with NSAIDs, 12.6% with 5–10 mg/day of prednisolone, 68.9% with MTX (10-25 mg/week) and 

6.7% with sulfasalazine (2.0–3.0 g/day). At visit 3, DAS28

after MTX in 99% of patients and was started prior to a biologic DMARD in 38% of patients. At both 12 

and 24 weeks, a significant reduction of disease activity scores was observed (DAS28-CRP mean 3.07, 

SD 1.36, and 2.85, SD 1.35, respectively; P values

JAKinibs 

JAKinibs versus DMARDs in RA 

Zuccaro and colleagues presented findings from a retrospective evaluation of patients with RA, 

according to 2010 ACR/EULAR Criteria, who began JAKinibs or biologic drugs from December 2017. 

Data were sourced from the Apulian registry BIOPURE. Of a total of 189 patients, 143 (75.6%) were 

treated with bDMARDs, whereas 46 (24.3%) were on JAKinibs, namely baricitinib or tofacitinib. 

Considering the whole cohort, mean DAS28 at baseline significantly decreased at 3 months (P

Update on JAK Inhibitor Safety Data 

JAKinib 

Cardiovascular safety in RA 

Xie and colleagues presented a meta-analysis of randomised controlled trials that examined 

cardiovascular safety in adult patients with RA who received JAKinib therapies. A total of 26 trials 

involving 11,800 patients were included. No statistically significant difference was observed in risk of 

cardiovascular events associated with the use of JAKinibs in general (P=0.89) or individually: tofacitinib 

(P=0.31), baricitinib (P=0.66), upadacitinib (P=0.18), peficitinib (P=0.35), decernotinib (P=0.92). 

Regarding frequently-used dosage, a dose-ranging impact of JAKinibs on the risk of cardiovascular 

events was not observed in tofacitinib (5 mg versus 10 mg, BID) or upadacitinib (15 mg versus 30 mg, 

QD); however, baricitinib at 2 mg QD was found to be safer than 4 mg (P=0.03). The authors concluded 

that existing evidence from randomised controlled trials indicate that JAKinib-based therapies are not 

related to a statistically significant risk of cardiovascular events in RA patients during the limited 

randomised, controlled periods. However, a special focus on baricitinib 4 mg QD is needed concerning 

the cardiovascular safety in the future [FRI0127]. 

Real-world safety and efficacy 

Hernández-Cruz and colleagues presented a case series from a Rheumatology service in the south of 

Spain to examine safety and efficacy of JAKinib in patients with RA. Between September 2018 and 

January 2019, 33 patients were treated with JAKinib and 31 patients were included in the analysis (74% 

female; median age at JAKinib initiation, 63.3 years). The disease duration at the start of JAKinib 

treatment was 14.7 (8.6–27.5) years. All the patients had received csDMARDs, 26% had been treated 

with bDMARDs (84%, baricitinib; 16%, tofacitinib) and 52% were treated with MTX (mean 15 mg/week). 

The baseline DAS28-ESR was 4.9 and the final DAS28-ESR was 2.6 (P

Chen and colleagues presented a second analysis of the long-term safety of baricitinib, evaluating the 

overall and geographical incidence, time to first event and risk factors for herpes zoster. Of 3770 RA 

patients treated with baricitinib, median age at study entry was 54 years, approximately one-quarter 

were each from North America (22%), EU (21%), Asia (25%) and Central America (20%); 47% were on 

concomitant MTX or corticosteroids, respectively. Herpes zoster was reported in 9% of patients over 

9892 patient-years of observation (median baricitinib exposure of 1115 days). The median time to first 

herpes zoster event was 538 days and the overall incidence rate was 3.3/100 person-years of 

observation, which did not increase significantly over time. The majority of events were 

monodermatomal and uncomplicated. Multivariate analyses showed that older age and geographical 

region (Asia, especially Japan, Taiwan and South Korea) were associated with a higher risk of herpes 

zoster [FRI0164]. 

Tofacitinib 

Comparative safety versus bDMARDs in RA 

Kremer and colleagues compared adverse event incidence rates in patients starting tofacitinib versus 

bDMARDs using data from the US Corrona registry. In total, 1544 tofacitinib (2138.2 patient years) and 

7083 bDMARD (9904.9 patient years) initiators were included. Rates of MACE and serious infection 

events were similar in both cohorts. Herpes zoster incidence rate was higher for tofacitinib versus 

bDMARDs and hazard ratios (HR) for herpes zoster were significantly increased with tofacitinib versus 

bDMARDs (adjusted HR 2.12 [95% CI: 1.22, 3.66]). All herpes zoster events were non-serious with 

tofacitinib. Similar results were observed in propensity score-matched populations. In summary, patients 

starting tofacitinib or bDMARDs for RA had similar rates of MACE and serious infections, whereas 

tofacitinib initiators had higher incidence rate of herpes zoster compared with bDMARD initiators 

[OP0028*]. 

Mode of Action / Basic Science 

Tofacitinib 

Biomarker changes with or without MTX or glucocorticoids 

A post-hoc analysis of pooled data from one Phase 2 [NCT00687193] and two Phase 3 (ORAL Scan; 

ORAL Start) studies of tofacitinib were presented by Lee and colleagues. The authors examined 

whether treatment of RA with tofacitinib plus MTX or glucocorticoids (GC) suppressed IFN pathway 

proteins to a greater extent than treatment with tofacitinib monotherapy. In total, 659 serum samples 

were collected from 321 patients. There was no strong evidence suggesting statistical differences 

between tofacitinib monotherapy and tofacitinib plus MTX or GC in changes in levels of the four 

detectable IFN pathway proteins (CXCL10, CXCL9, CXCL11 and IL-12) from baseline to Week 12 

and/or Week 24. Significant differences were observed for two of the 370 other proteins examined: 

MMP-1 (P=0.08) and IL1Ra (P=0.09), where levels decreased from baseline to Week 12 for tofacitinib 

plus MTX to a greater extent than for tofacitinib monotherapy. The results suggest that tofacitinib plus 

MTX or GC may not suppress circulating serum levels of IFN pathway proteins to a greater extent than 

tofacitinib monotherapy. It is not clear if the differences observed for MMP-1 and IL1Ra may be 

attributable to differences in the ethnicities of the study populations (global versus Japan) [AB0072]. 

Pain reduction with or without pain medication 

Taylor and colleagues evaluated the effect of tofacitinib monotherapy with or without pain medication on 

pain. The pooled post-hoc analysis included 676 patients who received tofacitinib 5 mg BID 

monotherapy in Phase 2 (NCT00550446), Phase 3 (ORAL Solo) and Phase 3b/4 (ORAL Strategy) 

*Chairman’s Pick

studies. Eighty-nine percent of patients received ‘any pain therapy’ comprising either pure analgesics 

(21%) or adjuvant analgesics (87%). Reductions in pain (△Pain VAS) at Month 3 and Month 6 were 

generally similar for patients who received tofacitinib with ‘any pain therapy’ versus those who did not 

receive ‘any pain therapy’. There was a trend for a numerically greater reduction in pain at Month 3 and 

Month 6 in patients who received tofacitinib with ‘any pain therapy’ and who achieved LDA at Month 3 

and Month 6 versus those who received tofacitinib with ‘any pain therapy’ and did not achieve LDA (95% 

CI overlapped). In contrast, pain reductions were similar for patients who received tofacitinib without ‘any 

pain therapy’, irrespective of LDA status [AB0449]. 

Baricitinib 

Disease trajectories in MTX-IR patients 

An analysis of RA-BEAM was presented by Taylor and colleagues, who examined treatment trajectories 

based on CDAI improvement in baricitinib 4-mg-treated patients over 52 weeks. A total of 487 patients 

were included in the analyses, which showed that baseline disease severity was associated with 

different treatment trajectories. Although the majority of patients achieved LDA and had no structural 

progression, patients with high baseline disease activity were associated with longer time to achieve 

LDA. Patients with higher baseline structural damage in addition to high disease activity were less likely 

to achieve LDA, but consistent with the other groups, had a similarly low rate of joint damage 

progression [THU0102]. 

Filgotinib 

Modulation of disease-associated cytokines 

Taylor and colleagues also reported data from a longitudinal study of cytokines in FINCH2. Plasma, 

serum, and urine samples were analysed from 449 RA patients who received filgotinib (100 mg, 200 mg) 

or placebo QD plus MTX. At 12 weeks, 18 of 42 cytokines significantly decreased with filgotinib 100-mg 

treatment relative to placebo, and filgotinib 200 mg decreased these cytokines to a similar or greater 

degree. Biomarkers most significantly modulated by filgotinib 200 mg (P

Upadacitinib 

Exposure-response analyses 

Analyses to characterise relationships between upadacitinib plasma exposures and different efficacy 

and safety endpoints were presented by Mohamed and colleagues. Data were included from 3685 (for 

efficacy) and 4577 (for safety) patients with RA enrolled in Phase 2 and Phase 3 studies. The 

percentage of subjects achieving ACR20, ACR50, ACR70, DAS28(CRP)≤3.2, and DAS28(CRP)

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Taylor PC, Emery P, Weinblatt ME, Mysler E, Rubbert-Roth A, Jia B, Sun L, Liu Y, Chen Y-F, Cardoso A, Tanaka Y. Patient disease 

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assessment with TNF inhibitors. Ann Rheum Dis. 2019; 78 (suppl 2):A757. 

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clinical data. Ann Rheum Dis. 2019; 78 (suppl 2):A1375. 

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van Vollenhoven R, Takeuchi T, Pangan A, Friedman A, Chen S, Rischmueller M, Blanco R, Xavier R, Strand V. Monotherapy with 

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78 (suppl 2):A376. 

*Chairman’s Pick

Weinblatt M, Thomson G, Chen K, Meerwein S, Schlacher C, Cush J. Clinical responses in patients with inadequate response to 

bDMARDs upon treatment with upadacitinib. Ann Rheum Dis. 2019; 78 (suppl 2):A759. 

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Xie W, Xiao S, Huang Y, Sun X, Fan Y, Zhang Z. Impact of janus kinase inhibitors on risk of cardiovascular events in patients with 

rheumatoid arthritis: systematic review and meta-analysis of randomized controlled trials. Ann Rheum Dis. 2019; 78 (suppl 2):A732. 

Zuccaro C, Santo L, Quarta L, Maruotti N, Carlino G, Bucci R, Semeraro A, Marsico A, Mazzotta D, Falappone PCF, Iannone F. Short term 

effectiveness of janus kinase inhibitors and biologic drugs in rheumatoid arthritis patients from the Apulian registry Biuopure. Ann Rheum 

Dis. 2019; 78 (suppl 2):A1603. 

*Chairman’s Pick

EULAR 2019 Review

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