Deucravacitinib, an oral, selective tyrosine kinase 2 (TYK2) inhibitor, in moderate to severe plaque psoriasis:  
52-week efficacy results from the phase 3 POETYK PSO-1 and PSO-2 trials 
Richard B Warren,1 April W Armstrong,2 Melinda Gooderham,3 Bruce Strober,4 Diamant Thaçi,5 Shinichi Imafuku,6 Howard Sofen,7 Lynda Spelman,8 Neil J Korman,9 Min Zheng,10 Elizabeth Colston,11 John Throup,11 Sudeep Kundu,11  
Renata M Kisa,11 Subhashis Banerjee,11 Andrew Blauvelt12
1Dermatology Centre, Salford Royal NHS Foundation Trust, Manchester NIHR Biomedical Research Centre, The University of Manchester, Manchester, UK; 2University of Southern California, Los Angeles, CA, USA; 3SKiN Center for Dermatology, Queen’s University, and Probity Medical Research, Peterborough, ON, Canada; 4Yale University, New Haven, CT, 
and Central Connecticut Dermatology Research, Cromwell, CT, USA; 5University of Lübeck, Lübeck, Germany; 6Fukuoka University Hospital, Fukuoka, Japan; 7UCLA School of Medicine, Los Angeles, CA, USA; 8Veracity Clinical Research, Woolloongabba, QLD, Australia; 9Case Western Reserve University and University Hospitals, Cleveland, OH, USA; 
10Second Affiliated Hospital, Zhejiang University School of Medicine, National Key Clinical Department of Dermatology, Hangzhou, Zhejiang Province, China; 11Bristol Myers Squibb, Princeton, NJ, USA; 12Oregon Medical Research Center, Portland, OR, USA

Presented at the 2022 Winter Clinical Dermatology Conference — Hawaii® (WC22); January 14−19, 2022; Kauai, HI, and Virtual
This is an encore of the 2021 EADV 30th Congress presentation

This poster may not be reproduced without written permission from the authors.Email for Richard B Warren, MD, PhD: richard.warren@manchester.ac.uk

Introduction
• Tyrosine kinase 2 (TYK2) is an intracellular enzyme that mediates signaling of cytokines 

(interleukin [IL]-23, IL-12, and Type I interferons) involved in psoriasis pathogenesis1

• Deucravacitinib is an oral agent that selectively inhibits TYK2 via an allosteric mechanism 
by uniquely binding to the regulatory domain rather than to the more conserved active 
domain where Janus kinase (JAK) 1/2/3 inhibitors bind (Figure 1)1

 — ≥100-fold greater selectivity for TYK2 vs JAK 1/3 and ≥2000-fold greater selectivity for 
TYK2 vs JAK 2 in cells1,2

• In the phase 3 POETYK PSO-1 and PSO-2 trials, deucravacitinib was significantly more 
efficacious than placebo and apremilast based on the coprimary endpoints of ≥75% 
reduction from baseline in Psoriasis Area and Severity Index (PASI 75) and static Physician’s 
Global Assessment (sPGA) score of 0/1 at Week 16 and was well tolerated in patients with 
moderate to severe plaque psoriasis3

Figure 1. Mechanism of action of deucravacitinib

Deucravacitinib
(allosteric inhibitor)

Regulatory domain Catalytic domain

ATP-binding active site
(other kinase inhibitors)

TYK2

ATP, adenosine triphosphate; TYK2, tyrosine kinase 2.

Objective
• To evaluate the efficacy of deucravacitinib over 52 weeks in POETYK PSO-1 and PSO-2, 

including:
 — Efficacy of continuous deucravacitinib treatment and switching from placebo to 
deucravacitinib at Week 16 through Week 52 (PSO-1)

 — Maintenance of efficacy on continued treatment and durability of response through 
Week 52 after treatment withdrawal among Week 24 PASI 75 responders (PSO-2)

Methods
Key design elements
• The POETYK PSO-1 and PSO-2 study designs are shown in Figure 2
• Key eligibility criteria

 — Adults with moderate to severe plaque psoriasis 
 — PASI ≥12, sPGA ≥3, body surface area (BSA) ≥10% 
 — Stratified by geographic region, body weight, and prior biologic use

• Coprimary endpoints were the proportion of patients who achieved PASI 75 and sPGA 0/1 
responses vs placebo at Week 16

Figure 2. Study designs

POETYK PSO-1
(N = 666)

POETYK PSO-2
(N = 1020)

Deucravacitinib 6 mg QDPlacebo (n = 166)

Deucravacitinib 6 mg QD<PASI 50

Apremilast 30 mg BID≥PASI 50

Titrate*

1
:2

:1
 R

an
d
om

iz
at

io
n

Weeks 16 24 520

Deucravacitinib 6 mg QDPlacebo (n = 255)

Deucravacitinib 6 mg QD (n = 511)

Deucravacitinib 6 mg QD<PASI 75

Deucravacitinib 6 mg QD<PASI 75

Deucravacitinib 6 mg QD

Deucravacitinib 6 mg QD 

Placebob

≥PASI 75

Apremilast 30 mg BIDa (n = 254)

≥PASI 75

1
:2

:1
 R

an
d
om

iz
at

io
n

Weeks 16 24 520

1:1

Deucravacitinib 6 mg QDPlacebob

Deucravacitinib 6 mg QD (n = 332)

Primary
endpoint

Primary
endpoint

Apremilast 30 mg BIDa (n = 168)

aApremilast was titrated from 10 mg QD to 30 mg BID over the first 5 days of dosing.  
bUpon relapse (≥50% loss of Week 24 PASI percentage improvement from baseline), patients were to be switched to deucravacitinib 6 mg QD. 
BID, twice daily; PASI 50, ≥50% reduction from baseline in Psoriasis Area and Severity Index; PASI 75, ≥75% reduction from baseline in PASI; QD, 
once daily.

Outcome measures
• PSO-1

 — Efficacy of continuous deucravacitinib treatment through Week 52
• PASI 75, PASI 90, PASI 100
• sPGA 0/1, sPGA 0

 — Efficacy of switching from placebo to deucravacitinib treatment at Week 16 through 
Week 52

• PASI 75 and sPGA 0/1
• Percentage change from baseline in PASI
• Scalp-specific Physician’s Global Assessment (ss-PGA) score of 0/1 (clear/almost clear 

scalp psoriasis)
• Dermatology Life Quality Index (DLQI) score of 0/1

• PSO-2
 — Maintenance of deucravacitinib response from Week 24 to Week 52 among Week 24  
PASI 75 responders

• PASI 75
• sPGA 0/1

 — Time to loss of PASI 75 response after deucravacitinib withdrawal among Week 24 PASI 75 
responders

Results
Baseline patient demographics and disease characteristics
• Baseline patient demographics and disease characteristics were largely similar across 

treatment groups in pooled data from the 2 trials (Table 1)

Table 1. Baseline patient demographics and disease characteristics
POETYK PSO-1 POETYK PSO-2

Placebo 
(n = 166)

Deucravacitinib 
(n = 332)

Apremilast
(n = 168)

Placebo 
(n = 255)

Deucravacitinib 
(n = 511)

Apremilast
(n = 254)

Age, y, mean (SD) 47.9 (14.0) 45.9 (13.7) 44.7 (12.1) 47.3 (13.6) 46.9 (13.4) 46.4 (13.3)

Weight, kg, mean (SD) 89.1 (22.3) 87.9 (21.8) 87.5 (21.1) 91.5 (20.2) 92.3 (21.9) 93.5 (22.2)

Female, n (%) 53 (31.9) 102 (30.7) 58 (34.5) 74 (29.0) 175 (34.2) 97 (38.2)

Race, n (%)

White 128 (77.1) 267 (80.4) 139 (82.7) 232 (91.0) 474 (92.8) 229 (90.2)

Asian 34 (20.5) 59 (17.8) 28 (16.7) 8 (3.1) 24 (4.7) 12 (4.7)

Other 4 (2.4) 6 (1.8) 1 (0.6) 15 (5.9) 13 (2.5) 13 (5.1)

Disease duration, y, 
mean (SD)

17.3 (12.8) 17.1 (12.4) 17.7 (11.8) 19.9 (12.8) 19.6 (12.9) 18.9 (12.4) 

Prior systemic 
treatment use, n (%)

Biologic 63 (38.0) 130 (39.2) 66 (39.3) 83 (32.5) 165 (32.3) 79 (31.1)

No prior systemic 
therapy

57 (34.3) 132 (39.8) 59 (35.1) 116 (45.5) 237 (46.4) 114 (44.9) 

sPGA, n (%)

3 = moderate 128 (77.1) 257 (77.4) 139 (82.7) 217 (85.1) 408 (79.8) 196 (77.2)

4 = severe 37 (22.3) 75 (22.6) 29 (17.3) 38 (14.9) 103 (20.2) 58 (22.8)

PASI, mean (SD) 20.7 (8.0) 21.8 (8.6) 21.4 (9.0) 21.1 (9.0) 20.7 (7.5) 21.6 (8.4)

DLQI, mean (SD) 11.4 (6.6) 12.0 (6.7) 12.4 (6.8) 11.8 (6.8) 11.8 (6.5) 12.5 (6.7)

BSA, %, mean (SD) 25.3 (16.9) 26.6 (15.9) 26.6 (16.1) 25.3 (15.7) 26.3 (15.8) 28.3 (16.5)

PSSD symptom score, 
mean (SD) 

51.4 (26.8) 51.7 (25.2) 56.2 (25.2) 50.1 (24.8) 52.3 (26.3) 51.9 (25.4) 

BSA, body surface area; DLQI, Dermatology Life Quality Index; PASI, Psoriasis Area and Severity Index; PSSD, Psoriasis Symptoms and Signs Diary; 
sPGA, static Physician’s Global Assessment.

POETYK PSO-1 and PSO-2 patient disposition over 52 weeks
• The patient disposition for both trials over 52 weeks is listed in Table 2

Table 2. Disposition of patients over 52 weeks
Patients, n

Treatment Week 0 Week 16 Week 24 Week 52

POETYK PSO-1

Continuous deucravacitinib (Week 0−52) 332 307 302 268

Placebo (Week 0−16) − deucravacitinib (Week 16−52) 165 145 140 129

POETYK PSO-2

Deucravacitinib (Week 0−16) 510 456b

Week 24 PASI 75 responders − rerandomized to deucravacitinib 
(Week 24−52)a

148 138

Week 24 PASI 75 responders − rerandomized to placebo (Week 
24−52)a

150 133

a142 patients did not achieve PASI 75 response at Week 24 and continued to receive deucravacitinib treatment until Week 52.  
bAn additional 16 patients discontinued deucravacitinib treatment between Weeks 16 and 24. 
PASI 75, ≥75% reduction from baseline in Psoriasis Area and Severity Index.

POETYK PSO-1 PASI and sPGA responses
• PASI 75 and sPGA 0/1 responses were maintained from Week 16 to Week 52 in patients who 

received continuous deucravacitinib treatment (Figure 3)
• PASI 90, PASI 100, and sPGA 0 responses (secondary efficacy endpoints) were also maintained 

through 52 weeks in patients treated with deucravacitinib 

Figure 3. POETYK PSO-1: PASI and sPGA responses with deucravacitinib through 
Week 52 (NRI)

0

10

20

30

40

50

60

70

80

90

100

0 4 8 12 16 20 24 28 32 36 40 44 48 52

R
e
sp

o
n
se

 r
at

e
, 

%

Weeks

12

65.1%

44.0%

19.3%

58.4%

35.5%

14.2%

PASI 75

PASI 90

PASI 100

0

10

20

30

40

50

60

70

80

90

100

0 4 8 12 16 20 24 28 32 36 40 44 48 52

R
e
sp

o
n
se

 r
at

e
, 

%

Weeks

53.6%

17.5%

12

sPGA 0/1

sPGA 0

52.7%

23.5%

Primary endpoint Primary endpoint

PASI 75 (n = 332) sPGA 0/1a (n = 332)

NRI was used to impute missing data. asPGA response is defined as a score of 0 or 1, with ≥2-point improvement from baseline. 
NRI, nonresponder imputation; PASI, Psoriasis Area and Severity Index; PASI 75, ≥75% reduction from baseline in PASI; PASI 90, ≥90% reduction 
from baseline in PASI; PASI 100, 100% reduction from baseline in PASI; sPGA 0/1, static Physician’s Global Assessment score of 0 or 1.

• Patients who switched from placebo to deucravacitinib at Week 16 demonstrated PASI 75 
and sPGA 0/1 responses at Week 52 comparable to those observed in patients who 
received continuous deucravacitinib treatment from Day 1 (Figure 4)

Figure 4. POETYK PSO-1: PASI 75 and sPGA 0/1 responses through Week 52 in 
patients randomized to deucravacitinib and placebo (NRI)

0

10

20

30

40

50

60

70

80

90

100

0 4 8 12 16 20 24 28 32 36 40 44 48 52
0

10

20

30

40

50

60

70

80

90

100

0 4 8 12 16 20 24 28 32 36 40 44 48 52

58.4%*

12.7%

68.3%

Primary endpoint

PASI 75

Weeks

R
e
sp

o
n
se

 r
at

e
, 

%

1 2

Weeks

sPGA 0/1a

Primary endpoint

R
e
sp

o
n
se

 r
at

e
, 

%

53.6%*

7.2%

12

53.8%

52.7%

65.1%

Deucravacitinib (n = 332) Placebo (n = 166) Placebo-deucravacitinib (n = 145) 

NRI was used to impute missing data. asPGA response is defined as a score of 0 or 1, with ≥2-point improvement from baseline. 
*P < 0.0001 vs placebo. 
NRI, nonresponder imputation; PASI 75, ≥75% reduction from baseline in Psoriasis Area and Severity Index; sPGA 0/1, static Physician’s Global 
Assessment score of 0 or 1.

• Patients who switched from placebo to deucravacitinib at Week 16 demonstrated percentage 
changes from baseline in PASI at Week 52 comparable to those observed in patients who 
received continuous deucravacitinib treatment from Day 1 (Figure 5)

Figure 5. POETYK PSO-1: percentage change from baseline in PASI through  
Week 52 in patients randomized to deucravacitinib and placebo (mBOCF)

Deucravacitinib
(n = 332)

Placebo
(n = 166)

Baseline PASI, mean (SD) 21.8 (8.6) 20.7 (8.0)

-100

-90

-80

-70

-60

-50

-40

-30

-20

-10

0
0 4 8 12 16 20 24 28 32 36 40 44 48 52

M
e
an

 p
e
rc

e
n
ta

ge
 

ch
an

ge
 f

ro
m

 b
as

e
li
n
e
 P

A
SI

Weeks

-80.5%

-24.3%

-71.6%

1 2

-78.4%

Primary endpoint

Deucravacitinib (n = 332) Placebo (n = 166) Placebo-deucravacitinib (n = 145) 

mBOCF was used to impute missing data.  
mBOCF, modified baseline observation carried forward; PASI, Psoriasis Area and Severity Index.

POETYK PSO-1 ss-PGA 0/1 through Week 52
• ss-PGA 0/1 responses at Week 16 were maintained through Week 52 with continuous 

deucravacitinib treatment (Figure 6)
 — Patients who switched from placebo to deucravacitinib at Week 16 achieved comparable 
ss-PGA 0/1 responses at Week 52 to those who received continuous deucravacitinib 
treatment

Figure 6. POETYK PSO-1: scalp psoriasis − ss-PGA 0/1 through Week 52 (NRI)

0

10

20

30

40

50

60

70

80

90

100

0 4 8 12 16 20 24 28 32 36 40 44 48 52

R
e
sp

o
n
se

 r
at

e
, 

%

Weeks

70.3%

17.4%

65.6%

69.7%

Primary endpoint

Deucravacitinib (n = 209) Placebo (n = 121) Placebo-deucravacitinib (n = 109)

1 2

NRI was used to impute missing data. The majority (88.9%) of patients had scalp involvement at baseline; >55% of patients had moderate to 
severe scalp psoriasis (ss-PGA ≥3) at baseline and were evaluated for ss-PGA 0/1 responses.4 
NRI, nonresponder imputation; QD, once daily; ss-PGA 0/1, scalp-specific Physician’s Global Assessment score of 0 or 1. 

• Patients who switched from placebo to deucravacitinib at Week 16 achieved DLQI 0/1 
responses at Week 52 comparable to those observed in patients who received continuous 
deucravacitinib treatment from Day 1 (Figure 7)

Figure 7. POETYK PSO-1: DLQI 0/1 response through Week 52 in patients 
randomized to deucravacitinib and placebo (NRI)

Deucravacitinib
(n = 332)

Placebo
(n = 166)

Baseline DLQI, mean (SD) 12.0 (6.7) 11.4 (6.6)

Weeks

0
10
20
30
40
50
60
70
80
90

100

0 4 8 12 16 20 24 28 32 36 40 44 48 52

43.2%

46.1%

1 2

R
e
sp

o
n
se

 r
at

e
, 

%

41.0%

10.6%

Primary endpoint

Deucravacitinib (n = 332) Placebo (n = 166) Placebo-deucravacitinib (n = 141)

NRI was used to impute missing data. DLQI score of 0 or 1 among patients with a baseline score of 2. DLQI 0/1 is indicative of no impact on a 
patient’s life. 
DLQI 0/1, Dermatology Life Quality Index score of 0 or 1; NRI, nonresponder imputation.

• PASI 75 and sPGA 0/1 responses were maintained on continuous treatment through Week 52 in 
the majority of deucravacitinib-treated patients who achieved PASI 75 at Week 24 (Figure 8) 

• Median time to loss of PASI 75 response was 12 weeks in the randomized withdrawal arm

Figure 8. POETYK PSO-2: maintenance and durability of response through Week 52 
among Week 24 PASI 75 responders (NRI)

0

10

20

30

40

50

60

70

80

90

100

24 28 32 36 40 44 48 52

R
e
sp

o
n
se

 r
at

e
, 

%

Weeks

PASI 75

0

10

20

30

40

50

60

70

80

90

100

24 28 32 36 40 44 48 52

R
e
sp

o
n
se

 r
at

e
, 

%

Weeks

sPGA 0/1a

70.3%

80.4%

31.3%
23.5%

Deucravacitinib (n = 148) Placebo (withdrawal; n = 150) Deucravacitinib (n = 118) Placebo (withdrawal; n = 119)

NRI was used to impute missing data. In total, 58.7% of deucravacitinib-treated patients achieved PASI 75 at Week 24 and 49.8% of 
deucravacitinib-treated patients achieved sPGA 0/1 responses at Week 24. Mean half-life of deucravacitinib is approximately 10 hours.  
asPGA response is defined as a score of 0 or 1, with ≥2-point improvement from baseline. This figure shows data for all sPGA 0/1 responders 
among Week 24 PASI 75 responders.  
NRI, nonresponder imputation; PASI 75, ≥75% reduction from baseline in Psoriasis Area and Severity Index; QD, once daily; sPGA 0/1, static 
Physician’s Global Assessment score of 0 or 1.

Conclusions
• In the phase 3 POETYK PSO-1 and PSO-2 trials, deucravacitinib was efficacious 

through 52 weeks in patients with moderate to severe plaque psoriasis

 — Clinical responses improved through Week 24 and were maintained in 
patients who received continuous deucravacitinib treatment through Week 52

 — Week 52 responses in patients who switched from placebo to deucravacitinib 
treatment at Week 16 were comparable to those observed with continuous 
deucravacitinib treatment from Day 1

• Durable responses were observed after withdrawal of treatment in Week 24 
responders

• The results of this 52-week efficacy analysis are consistent with those of the 
primary analyses of PSO-1 and PSO-2 at Week 163

• Deucravacitinib, a once-daily oral drug, has the potential to become an efficacious 
and well-tolerated treatment choice for patients with moderate to severe plaque 
psoriasis

References
1. Burke JR, et al. Sci Transl Med. 2019;11:1-16. 2. Wrobleski ST, et al. J Med Chem. 2019;62:8973-8995.  
3. Armstrong A, et al. Presented at the Annual Meeting of the American Academy of Dermatology; April 23-25, 
2021. 4. Blauvelt A, et al. Presented at EADV 30th Congress; 29 September−2 October 2021. Poster P1391.

Acknowledgments
• These clinical trials were sponsored by Bristol Myers Squibb

• Writing and editorial assistance were provided by Lisa Feder, PhD, of Peloton Advantage, LLC, an OPEN Health 
company, Parsippany, NJ, USA, funded by Bristol Myers Squibb

Disclosures
• RBW: Consulting fees: AbbVie, Almirall, Amgen, Boehringer Ingelheim, Celgene, Eli Lilly, Janssen, Leo Pharma, 

Novartis, Pfizer, Sanofi, UCB, and Xenoport; Research grants: AbbVie, Almirall, Amgen, Celgene, Eli Lilly, 
Janssen, Leo Pharma, Novartis, Pfizer, and UCB; Honorarium: Biogen

• AWA: Grants and personal fees: AbbVie, Bristol Myers Squibb, Eli Lilly, Janssen, Leo Pharma, and Novartis; 
Personal fees: Boehringer Ingelheim/Parexel, Celgene, Dermavant, Genentech, GlaxoSmithKline, Menlo 
Therapeutics, Merck, Modernizing Medicine, Ortho Dermatologics, Pfizer, Regeneron, Sanofi Genzyme, Science 
37, Sun Pharma, and Valeant; Grants: Dermira, Kyowa Hakko Kirin, and UCB, outside the submitted work

• MG: Advisory board, principal investigator, and lecture fees: AbbVie, Galderma, Leo Pharma, Pfizer, and 
Regeneron; Advisory board and lecture fees: Actelion; Principal investigator and consulting fees: Akros 
Pharma; Advisory board, principal investigator, lecture fees, and consulting fees: Amgen, Boehringer 
Ingelheim, Celgene, Eli Lilly, Janssen, Novartis, Sanofi Genzyme, and Valeant; Principal investigator: Arcutis, 
Bristol Myers Squibb, Dermira, GlaxoSmithKline, MedImmune, Merck, Roche Laboratories, and UCB; Principal 
investigator and lecture fees: Glenmark

• BS: Consultant (honoraria): AbbVie, Almirall, Amgen, Arcutis, Arena, Aristea, Asana, Boehringer Ingelheim, 
Bristol Myers Squibb, Connect Biopharma, Dermavant, Eli Lilly, Equillium, GlaxoSmithKline, Immunic 
Therapeutics, Janssen, Leo Pharma, Maruho, Meiji Seika Pharma, Mindera, Novartis, Ortho Dermatologics, 
Pfizer, Regeneron, Sanofi Genzyme, Sun Pharma, UCB, Ventyxbio, and vTv Therapeutics; Speaker: AbbVie, Eli 
Lilly, Janssen, and Sanofi Genzyme; Co-scientific director (consulting fee): CorEvitas’ (Corrona) Psoriasis 
Registry; Investigator: AbbVie, Cara, CorEvitas’ (Corrona) Psoriasis Registry, Dermavant, Dermira, and Novartis

• DT: Grant/research support, consultant, scientific advisory board speakers bureau: AbbVie, Almirall, Amgen, 
Biogen Idec, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Galapagos, Galderma, Janssen-Cilag, Leo 
Pharma, Novartis, Pfizer, Regeneron, Roche, Sandoz-Hexal, Sanofi, Target-Solution, and UCB

• SI: Grants and personal fees: AbbVie, Eisai, Janssen, Kyowa Kirin, Leo Pharma, Maruho, Sun Pharma, Taiho 
Yakuhin, Tanabe Mitsubishi, and Torii Yakuhin; Personal fees: Amgen (Celgene), Bristol Myers Squibb, Eli Lilly, 
Daiichi-Sankyo, Novartis, and UCB

• HS: Clinical Investigator: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Janssen, Leo 
Pharma, Novartis, and Sun Pharma

• LS: Consultant, paid investigator, and/or speaker: Amgen, Anacor, AbbVie, Ascend, Astellas, AstraZeneca, 
Blaze Bioscience, Bristol Myers Squibb, Boehringer Ingelheim, Botanix, Celgene, Dermira, Eli Lilly, Galderma, 
Genentech, GlaxoSmithKline, Hexima, Janssen, Leo Pharma, Mayne, Medimmune, Merck (MSD), Merck-Serono, 
Novartis, Otsuka, Pfizer, Phosphagenics, Photon MD, Regeneron, Roche, Samumed, Sanofi Genzyme, SHR, Sun 
Pharma ANZ, Trius, UCB, and Zai Lab

• NJK: Advisory board, consulting fees: AbbVie, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, 
Janssen, Leo Pharma, Novartis, Principia, Regeneron, Sanofi Genzyme, Sun Pharma, and UCB; Grant support/
principal investigator: AbbVie, Amgen, Argenx, Bristol Myers Squibb, Celgene, Chemocentryx, Eli Lilly, 
Galderma, Kyowa Hakko Kirin, Leo Pharma, Menlo, Principia, Prothena, Rhizen, Syntimmune, Trevi, and 
Xbiotech; Speaker: AbbVie, Eli Lilly, Janssen, Novartis, Regeneron, and Sanofi Genzyme

• MZ: Consultant (honoraria), clinical investigator, and lecture fees: AbbVie, Boehringer Ingelheim, Bristol Myers 
Squibb, Eli Lilly China, Leo Pharma China, Novartis China, Pfizer, Sanofi China, and Xian-Janssen

• EC, JT, SK, RMK, and SB: Employees and shareholders: Bristol Myers Squibb
• AB: Scientific adviser and/or clinical study investigator: AbbVie, Aligos, Almirall, Arena, Athenex, Boehringer 

Ingelheim, Bristol Myers Squibb, Dermavant, Eli Lilly, Evommune, Forte, Galderma, Incyte, Janssen, Leo 
Pharma, Novartis, Pfizer, Rapt, Regeneron, Sanofi Genzyme, Sun Pharma, and UCB