Deucravacitinib in plaque psoriasis: 2-year laboratory results from the phase 3 POETYK PSO program
Neil J Korman,1 Thierry Passeron,2 Kenneth B Gordon,3 Yukari Okubo,4 Jerry Bagel,5 Howard Sofen,6 Richard B Warren,7 Neal Bhatia,8 Lynda Spelman,9 Kevin Winthrop,10 Lauren Hippeli,11 Renata M Kisa,11 Subhashis Banerjee,11 Diamant Thaçi12

1Case Western Reserve University, University Hospitals of Cleveland, Cleveland, OH, USA; 2Côte d’Azur University, University Hospital of Nice, Nice, France; 3Medical College of Wisconsin, Milwaukee, WI, USA; 4Tokyo Medical University, Tokyo, Japan; 5Psoriasis Treatment Center of New Jersey, East Windsor, NJ, USA; 6UCLA School of Medicine, Los Angeles, CA, USA; 7Dermatology Centre, 
Salford Royal NHS Foundation Trust, NIHR Manchester Biomedical Research Centre, The University of Manchester, Manchester, UK; 8Therapeutics Clinical Research, San Diego, CA, USA; 9Veracity Clinical Research, Brisbane, QLD, Australia; 10Oregon Health & Science University, Portland, OR, USA; 11Bristol Myers Squibb, Princeton, NJ, USA; 12University of Lübeck, Lübeck, Germany

Presented at the Winter Clinical Dermatology Conference - Hawaii®; January 13-18, 2023; Kohala Coast, HI
This is an encore of the 2022 31st EADV Congress presentation

Email: Neil.Korman@UHhospitals.org Copies of this poster are for personal use only and may not be reproduced without written permission from the authors.

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

(interleukin-23 and Type I interferons) involved in psoriasis pathogenesis1

• Deucravacitinib, an oral, selective, allosteric TYK2 inhibitor, is approved by the US Food and Drug 
Administration for the treatment of adults with moderate-to-severe plaque psoriasis who are 
candidates for systemic therapy or phototherapy2

• Deucravacitinib has a unique mechanism of action, the first in a new class of small molecules1 
(Figure 1)

• The selectivity of deucravacitinib facilitates a more targeted therapeutic approach that avoids 
signature laboratory changes seen with the Janus kinase (JAK) 1/2/3 inhibitors

 — In phase 2 and phase 3 trials (POETYK PSO-1 and PSO-2) in plaque psoriasis, deucravacitinib 
treatment did not result in neutropenia, elevated liver enzyme and serum creatinine levels, and 
dyslipidemia — adverse events that have been associated with JAK 1/2/3 inhibitors3-7

• Deucravacitinib demonstrated a robust efficacy profile, including superiority to placebo and 
apremilast and durability and maintenance of response, in 2 multinational phase 3 trials in patients 
with moderate to severe plaque psoriasis5,6,8

• Patients who completed the POETYK PSO-1 and PSO-2 trials could enroll in the ongoing POETYK 
long-term extension (LTE) trial

Objectives
• To determine whether there were any clinically relevant changes in blood laboratory parameters with up to 2 years of deucravacitinib treatment in the POETYK PSO-1, PSO-2, 

and LTE trials

• To evaluate whether deucravacitinib treatment elicits changes in the blood that are known to occur with JAK 1/2/3 inhibitors

Methods

Study designs
• POETYK PSO-1 (NCT03624127) and PSO-2 (NCT03611751) were 52-week, multinational, phase 3, double-blind trials that randomized patients with moderate to severe plaque 

psoriasis 2:1:1 to deucravacitinib 6 mg once daily, placebo, or apremilast 30 mg twice daily (Figure 2)

• At Week 52, eligible patients were able to enroll in the POETYK LTE trial (NCT04036435) and receive open-label deucravacitinib 6 mg once daily for up to 2 years

Figure 2. POETYK PSO-1, PSO-2, and LTE study designs

100

POETYK PSO-1 and PSO-2

Deucravacitinib 6 mg QDPlacebo (n = 166)

Deucravacitinib 6 mg QD

Apremilast 30 mg BID

Titrate*P
O

E
T

Y
K

 P
SO

-1
1
:2

:1
 r

an
d
o
m

iz
at

io
n

Deucravacitinib 6 mg QD (n = 332)

Apremilast 30 mg BIDa (n = 168)

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

Apremilast 30 mg BIDa (n = 254)

P
O

E
T

Y
K

 P
SO

-2
1
:2

:1
 r

an
d
o
m

iz
at

io
n

Cumulative
exposure (weeks)

Exposure relative
to LTE(weeks)

16 24 520

1
:1

Deucravacitinib 6 mg QDPlacebob

Deucravacitinib 6 mg QDPlacebob

Primary
endpoint

B
LI

N
D

E
D

 S
W

IT
C

H
 T

O
 O

P
E
N

-L
A

B
E
L 

D
E
U

C
R

A
V

A
C

IT
IN

IB

Open-label deucravacitinib 6 mg QD
(N = 1221)

POETYK LTE

14856 60 68 76 88 112 124 1364 8 12 20 28 32 36 40 44 48

480 964 8 16 24 36 60 72 84

≥PASI 75

≥PASI 75

<PASI 50

≥PASI 50

Safety assessed for all available data (currently 2 years)c

POETYK PSO-1: From Armstrong AW, et al. Deucravacitinib versus placebo and apremilast in moderate to severe plaque psoriasis: efficacy and 
safety results from the 52-week, randomized, double-blinded, placebo-controlled phase 3 POETYK PSO-1 trial. J Am Acad Dermatol. 2023;88:29-39. 
This work is licensed under a Creative Commons Attribution License (CC BY-NC-ND 4.0). https://creativecommons.org/licenses/by-nc-nd/4.0/.

POETYK PSO-2: From Strober B, et al. Deucravacitinib versus placebo and apremilast in moderate to severe plaque psoriasis: efficacy and 
safety results from the 52-week, randomized, double-blinded, phase 3 POETYK PSO-2 trial. J Am Acad Dermatol. 2023;88:40-51. This work is 
licensed under a Creative Commons Attribution License (CC BY-NC-ND 4.0). https://creativecommons.org/licenses/by-nc-nd/4.0/.

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. 
cData reported through the cutoff date of October 1, 2021. 
BID, twice daily; LTE, long-term extension; PASI, Psoriasis Area and Severity Index; PASI 50, ≥50% reduction from baseline in PASI; PASI 75, ≥75% reduction from baseline in PASI; QD, once daily.

Laboratory assessments
• Pooled POETYK PSO-1 + PSO-2 data over Weeks 0–52 and pooled POETYK PSO-1 + PSO-2 + LTE data over Weeks 0–100 are presented

• Changes in laboratory parameters that are known to be affected by JAK 1/2/3 inhibitors3 were evaluated in blood over time
 — Hematologic parameters: lymphocytes, neutrophils, platelets, and hemoglobin
 — Lipid parameter: total cholesterol
 — Chemistry parameters: creatinine, creatine phosphokinase (CPK), and alanine aminotransferase (ALT)

• Incidences of grade ≥3 laboratory abnormalities (Common Terminology Criteria for Adverse Events [CTCAE] version 5.0) and treatment discontinuations due to laboratory 
abnormalities were also evaluated through Week 100

Results

Patient population
• This analysis included 1519 patients who received ≥1 dose of deucravacitinib in POETYK 

PSO-1, PSO-2, and/or the LTE through the data cutoff date of October 1, 2021
 — Total deucravacitinib exposure was 2482.0 person-years (PY)

• In total, 1179 (77.6%) and 584 (38.4%) patients had ≥52 weeks and ≥104 weeks, respectively, 
of continuous deucravacitinib exposure at the data cutoff date

 — Median duration of exposure was 682.0 days (97 weeks)

• Baseline patient demographics and disease characteristics are presented in Table 1

Laboratory assessments
• No clinically meaningful changes were observed over Weeks 0–100 in any of the evaluated 

laboratory parameters in the pooled POETYK PSO-1/PSO-2/LTE population (Figure 3)
 — Laboratory parameters remained within normal ranges for most patients throughout  
this period

• Grade ≥3 laboratory abnormalities were rare (Table 2)
 — Frequencies of individual events were comparable across groups over the first 52 weeks 
(POETYK PSO-1 and PSO-2), and no increases were seen with deucravacitinib treatment 
through Week 100 in the POETYK LTE

 — Grade ≥3 CPK elevations occurred rarely, were mostly transient, and were observed at 
a similar incidence in each treatment group over the first 52 weeks; almost all were 
related to recent physical exertion, and none was serious 

• Discontinuations due to laboratory abnormalities were low and balanced across treatment 
groups over the first 52 weeks and were also low through Week 100 in the POETYK LTE 
(Table 3)

 — ALT elevations in deucravacitinib-treated patients (Table 2) were predominantly 
transient, and none was serious or resulted in treatment discontinuation

Figure 3. Changes in hematologic, lipid, and chemistry parameters over 2 years in patients receiving deucravacitinib in POETYK  
PSO-1 + PSO-2 + LTE

0

1

2

3

4

M
e
an

 ±
 S

D
, 

1
0

9
/L

5

Lymphocytes

n=

0

2

4

6

M
e
an

 ±
 S

D
, 

1
0

9
/L

8

Neutrophils

n=

0
100

200

250

150

300

350

400

450

500

M
e
an

 ±
 S

D
, 

1
0

9
/L

Platelets

4 8 12 2016 2824 32 444036 48 5652 6460 68 7672 8480 88 92 10096 104

0 4 8 12 2016 2824 32 444036 48 5652 6460 68 7672 8480 88 92 10096 104 0 4 8 12 2016 2824 32 444036 48 5652 6460 68 7672 8480 88 92 10096 104

0 4 8 12 2016 2824 32 444036 48 5652 6460 68 7672 8480 88 92 10096 104

0 4 8 12 2016 2824 32 444036 48 5652 6460 68 7672 8480 88 92 10096 104

0 4 8 12 2016 2824 32 444036 48 5652 6460 68 7672 8480 88 92 10096 104

0 8 16 24 32 40 48 5652 64 72 80 88 10096 104

0 4 8 12 2016 2824 32 444036 48 5652

Start of LTE Start of LTE

6460 68 7672 8480 88 92 10096 104

LLN

ULN

LLN

ULN

LLN

ULN

n= 7841517 747769 10301075742 113294294695996698810281028 1164 1133 1132 1097 1036

8021519 764793 10611094757 1146963971959989101510511051 1179 1148 1151 1112 1050 8021519 764793 10611094757 1146963972977989101310481050 1178 1148 1151 1112 1050

8031519 765793 10671097758 1146968974982992101610511055 1180 1158 1151 1114 1051

7971518 753779 10381081747 114495095896897099910351038 1170 1146 1141 1108 1048

7921518 750775 10251076739 113994294996296699210311031 1168 1140 1136 1098 1042

1519 790 1064742 962 1042

7921518 750775 10251076739 113994294996296699210311031 1168 1140 1136 1098 1042

12

1.5

1.0

0.5

60

40

20

0

13

14

15

16

17

18

M
e
an

 ±
 S

D
, 

g/
d
L

Hemoglobin

n=

M
e
an

 ±
 S

D
, 

m
g/

d
L

Total cholesterol

n=

M
e
an

 ±
 S

D
, 

m
g/

d
L

Creatinine

n=

0

250

500

750

M
e
an

 ±
 S

D
, 

U
/L

1000

100

150

200

250

300

CPK

n=

M
e
an

 ±
 S

D
, 

U
/L

ALT

n=

LLN

ULN

LLN

ULN

LLN

ULN

LLN

ULN

LLN

ULN

ALT, alanine aminotransferase; CPK, creatine phosphokinase; LLN, lower limit of normal; LTE, long-term extension; SD, standard deviation; ULN, upper limit of normal.

Table 2. CTCAE grades 3 and 4 abnormalities in laboratory parameters over 1 and 2 years

At 1 year
(POETYK PSO-1 + PSO-2, Weeks 0–52)

At 2 years
(POETYK PSO-1 + PSO-2 + LTE,  

Weeks 0–100)

Placebo 
(n = 666)

Deucravacitinib 
(n = 1364)

Apremilast
(n = 422)

Deucravacitinib
(n = 1519)

Parameter Grade
Baseline

n (%)
Week 52

n (%)
Baseline

n (%)
Week 52

n (%)
Baseline

n (%)
Week 52

n (%)
Baseline

n (%)
Week 100

n (%)

Lymphocyte  
count decreased

3 0 1 (0.2)a 0 2 (0.1)b 0 1 (0.2)c 0 2 (0.1)d

4 0 0 0 0 0 0 0 0

Neutrophil  
count decreased 

3 0 1 (0.2)a 1 (0.1)b 4 (0.3)b 0 0 1 (0.1)d 5 (0.3)d

4 0 1 (0.2)a 0 0 0 1 (0.2)c 0 1 (0.1)d

Platelet count 
decreased

3 0 1 (0.2)e 0 0 0 0 0 0

4 0 0 0 0 0 0 0 0

Anemia
3 0 0 0 0 0 1 (0.2)c 0 1 (0.1)d

4 0 0 0 0 0 0 0 0

High cholesterol
3 0 0 0 1 (0.1)f 0 0 0 1 (0.1)g

4 0 0 0 0 0 0 0 0

Creatinine  
increased

3 0 0 0 0 0 0 0 0

4 0 0 0 0 0 0 0 0

CPK increased
3 1 (0.2)a 4 (0.6)a 3 (0.2)b 19 (1.4)b 1 (0.2)h 7 (1.7)h 3 (0.2)i 25 (1.7)i

4 0 3 (0.5)a 0 13 (1.0)b 0 1 (0.2)h 0 26 (1.7)i

ALT increased
3 2 (0.3)a 0 1 (0.1)b 4 (0.3)b 0 0 1 (0.1)i 10 (0.7)i

4 0 0 0 0 0 0 0 0
an = 658. bn = 1351. cn = 418. dn = 1503. en = 657. fn = 1317. gn = 1454. hn = 419. in = 1504. 
ALT, alanine aminotransferase; CPK, creatine phosphokinase; CTCAE, Common Terminology Criteria for Adverse Events; LTE, long-term extension.

Table 3. Laboratory abnormality adverse events leading to treatment discontinuation over 1 and 2 years

At 1 year
(POETYK PSO-1 + PSO-2, Weeks 0–52)

At 2 years
(POETYK PSO-1 + PSO-2 + LTE,  

Weeks 0–100)

Placebo 
(n = 666)

Total exposure = 240.9 PY

Deucravacitinib
(n = 1364)

Total exposure = 969.0 PY

Apremilast
(n = 422)

Total exposure = 221.1 PY

Deucravacitinib
(n = 1519)

Total exposure = 2482.0 PY

Parameter n (%) EAIR/100 PY n (%) EAIR/100 PYa n (%) EAIR/100 PYa n (%) EAIR/100 PYa

Lymphopenia 0 0 1 (0.1) 0.1 0 0 1 (0.1) 0.0

Blood CPK increased 0 0 2 (0.1) 0.2 1 (0.2) 0.4 3 (0.2) 0.1

Hepatic function 
abnormal

1 (0.2)b 0.4 1 (0.1)c 0.1 0 0 1 (0.1) 0.0

AST increased 0 0 0 0 1 (0.2) 0.4 0 0
aIncidences are expressed as EAIRs per 100 PY to account for variable exposure due to treatment switches at Weeks 16 and 24. 
bPatient who received placebo during Weeks 0–16 had ALT >3x ULN on Days 1 and 8; total bilirubin levels remained in the normal range. The patient discontinued placebo and ALT levels improved. 
cPatient who received deucravacitinib during Weeks 0–16 had ALT and AST elevations ≥3x ULN and bilirubin elevation >2x ULN on Day 58. Deucravacitinib treatment was discontinued and ALT, AST, and bilirubin levels improved. 
ALT, alanine aminotransferase; AST, aspartate aminotransferase; CPK, creatine phosphokinase; EAIR, exposure-adjusted incidence rate; LTE, long-term extension; PY, person-years; ULN, upper limit of normal.

Conclusions
• In the large, phase 3 POETYK PSO-1, PSO-2, and LTE trials in patients with plaque psoriasis, no trends or clinically meaningful changes in multiple hematologic, lipid, and 

chemistry parameters were observed in 1519 patients with 2482.0 PY of deucravacitinib exposure
 — Signature laboratory changes associated with JAK 1/2/3 inhibitors were not observed over 2 years of deucravacitinib exposure

• CTCAE grade ≥3 laboratory abnormalities and treatment discontinuations due to laboratory abnormalities in deucravacitinib-treated patients were rare, and were 
comparable to incidence rates observed with placebo and apremilast over the first 52 weeks

• Deucravacitinib, a once-daily oral drug, has the potential to become a treatment of choice and new standard of care for patients who require systemic therapy for their 
moderate to severe plaque psoriasis

References
1. Burke JR, et al. Sci Transl Med. 2019;11:eaaw1736. 2. SOTYKTU™ (deucravacitinib) [package insert]. Princeton, NJ: Bristol-Myers Squibb Company; September 2022. 3. Papp K, et al. N Engl J Med. 2018;379:1313-1321. 4. Winthrop KL. Nat Rev Rheumatol. 2017; 
13:234-243. 5. Armstrong AW, et al. J Am Acad Dermatol. 2023;88:29-39. 6. Strober B, et al. J Am Acad Dermatol. 2023;88:40-51. 7. Thaçi D, et al. Presented at the 30th EADV Congress; September 29–October 2, 2021. 8. Warren RB, et al. Presented at the EADV 
Spring Symposium; 12–14 May 2022; Ljubljana, Slovenia. 9. Wrobleski ST, et al. J Med Chem. 2019;62:8973-8995. 

Acknowledgments
• This study was sponsored by Bristol Myers Squibb
• Writing and editorial assistance was provided by Liz Rockstein, PhD, of Peloton Advantage, LLC, an OPEN Health company, Parsippany, NJ, USA, funded by Bristol Myers Squibb

Disclosures
• NJK: Advisory board and 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 Kirin, Leo Pharma, Menlo, Principia, Prothena, Rhizen, Syntimmune, Trevi, and XBiotech; Speaker: AbbVie, Eli Lilly, Janssen, Novartis, Regeneron, and Sanofi Genzyme
• TP: Advisory board and consulting fees: AbbVie, Almirall, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Galderma, Incyte, Janssen, Leo Pharma, Novartis, Pfizer, Sanofi Genzyme, Sun Pharma, and UCB
• KBG: Grant support and consulting fees: AbbVie, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Janssen, Novartis, and UCB; Consulting fees: Almirall, Amgen, Dermira, Leo Pharma, Pfizer, and Sun Pharma
• YO: Research grants: Eisai, Maruho, Shiseido, and Torii; Current consulting/advisory board agreements: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Janssen, and Sun Pharma; Speakers bureau: AbbVie, Amgen, Boehringer Ingelheim, Bristol 

Myers Squibb, Celgene, Eisai, Eli Lilly, Janssen Pharma, Jimro, Kyowa Kirin, Leo Pharma, Maruho, Novartis, Pfizer, Sanofi, Sun Pharma, Taiho, Tanabe-Mitsubishi, Torii, and UCB; Clinical trials: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli 
Lilly, Janssen, Leo Pharma, Maruho, Pfizer, Sun Pharma, and UCB 

• JB: Research funds payable to the Psoriasis Treatment Center of New Jersey: AbbVie, Amgen, Arcutis, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, CorEvitas’ (Corrona) Psoriasis Registry, Dermavant, Dermira/UCB, Eli Lilly, Glenmark, Janssen Biotech, 
Kadmon, Leo Pharma, Lycera, Menlo Therapeutics, Novartis, Pfizer, Regeneron, Sun Pharma, Taro, and Valeant; Consultant: AbbVie, Amgen, Celgene, Eli Lilly, Janssen Biotech, Novartis, Sun Pharma, and Valeant; Speaker: AbbVie, Celgene, Eli Lilly, Janssen Biotech, 
and Novartis

• HS: Clinical investigator: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Janssen, Leo Pharma, Novartis, and Sun Pharma
• RBW: Research grants: AbbVie, Almirall, Amgen, Celgene, Eli Lilly, Janssen, Leo Pharma, Novartis, Pfizer, and UCB; Consulting fees: AbbVie, Almirall, Amgen, Biogen, Boehringer Ingelheim, Celgene, DICE Therapeutics, Eli Lilly, Janssen, Leo Pharma, Novartis, Pfizer, 

Sanofi, UCB, and UNION
• NB: Advisor and consultant investigator: AbbVie, Almirall, Arcutis, Arena, Boehringer Ingelheim, Bristol Myers Squibb, Dermavant, InCyte, ISDIN, Johnson & Johnson, Leo Pharma, Lilly, Ortho, Pfizer, Regeneron, Sanofi, Stemline, and Sun Pharma; Investigator: 

Arcutis, Biofrontera, Boehringer Ingelheim, Bristol Myers Squibb, Dermavant, Galderma, Leo Pharma, Lilly, and Ortho
• LS: Consultant, paid investigator, and/or speaker: AbbVie, Amgen, Anacor, 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, Merck-Serono, Novartis, Otsuka, Pfizer, Phosphagenics, Photon MD, Regeneron, Roche, Samumed, Sanofi Genzyme, SHR, Sun Pharma ANZ, Trius, UCB, and Zai Lab
• KW: Consulting: AbbVie, AstraZeneca, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead, GlaxoSmithKline, Novartis, Pfizer, Regeneron, Roche, Sanofi, and UCB; Research: Bristol Myers Squibb and Pfizer
• LH, RMK, and SB: Employees and shareholders: Bristol Myers Squibb
• DT: Grant/research support, consultant, scientific advisory board, and 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

Figure 1. Mechanism of action of deucravacitinib

• ≥100-fold greater selectivity for TYK2 vs JAK 1/3
• ≥2000-fold greater selectivity for TYK2 vs JAK 2

Deucravacitinib
(allosteric inhibitor class)

Unique TYK2 
regulatory 

domain

Catalytic domain
(highly conserved
across JAK family)

ATP-binding active site
(approved JAK inhibitor class)

TYK2

Selectivity in cells1,9:

ATP, adenosine 5′-triphosphate; JAK, Janus kinase; TYK2, tyrosine kinase 2.

Table 1. Baseline patient demographics and disease 
characteristics

Parameter

POETYK PSO-1 + PSO-2 + LTE 
Deucravacitinib

(N = 1519)

Age, mean (SD), y 46.6 (13.4)

Weight, mean (SD), kg 90.6 (21.6)

Body mass index, mean (SD), kg/m2 30.5 (6.8)

Female, n (%) 493 (32.5)

Race, n (%)

White 1325 (87.2)

Asian 153 (10.1)

Black or African American 23 (1.5)

Other 18 (1.2)

Age at disease onset, mean (SD), y 28.8 (14.9)

Disease duration, mean (SD), y 18.7 (12.7)

PASI, mean (SD) 21.1 (8.1)

sPGA, n (%)

3 (moderate) 1211 (79.7)

4 (severe) 308 (20.3)

BSA involvement, mean (SD), % 26.2 (15.8)

BSA, body surface area; LTE, long-term extension; PASI, Psoriasis Area and Severity Index; SD, standard deviation; sPGA, static 
Physician’s Global Assessment.