One line title  two line title


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. Armstrong AW, et al. J Am Acad Dermatol. 2022;S0190-9622(22)02256-3. doi: 10.1016/j.jaad.2022.07.002. Online ahead of print. 4. Strober B, et al. J Am Acad Dermatol. 
2022;S0190-9622(22)02643-3. doi: 10.1016/j.jaad.2022.08.061. Online ahead of print. 5. Warren RB, et al. Presented at the European Academy of Dermatology and 
Venereology 30th Congress; September 29—October 2, 2021. 6. Warren RB, et al. Presented at the European Academy of Dermatology and Venereology Spring Symposium; 
May 12–14, 2022. 7. Wrobleski ST, et al. J Med Chem. 2019;62:8973-8995. 8. Walsh JA, et al. J Am Acad Dermatol. 2013;69:931-937. 9. Merola JF, et al. J Invest Dermatol. 
2018;138:1955-1961.

Deucravacitinib 6 mg QDPlacebo (n = 166)

Deucravacitinib 6 mg QD

Apremilast 30 mg BID≥PASI 50

1
:2

:1
 R

an
d
om

iz
at

io
n

52Weeks

Deucravacitinib 6 mg QD (n = 332)

16 24

<PASI 50

Apremilast 30 mg BIDa (n = 168)

Primary endpoint

0

≥PASI 75

Placebo (n = 255)

Deucravacitinib 6 mg QD (n = 511)

Deucravacitinib 6 mg QD

Deucravacitinib 6 mg QD<PASI 75

Deucravacitinib 6 mg QD

Deucravacitinib 6 mg QD

Apremilast 30 mg BIDa (n = 254)

≥PASI 75

52Weeks

1:1

Placebob Deucravacitinib 6 mg QD

16 24

<PASI 75

Primary endpoint

1
:2

:1
 R

an
d
om

iz
at

io
n

Placebob Deucravacitinib 6 mg QD

0

≥PASI 75

-90

-80

-70

-60

-50

-40

-30

-20

-10

0
0 1 2 4 8 12 16 20 24

M
ea

n 
pe

rc
en

ta
ge

 C
FB

‡

‡§

‡§

‡§
§

§

-11.3%

-43.2%

-60.0%

BSA over 24 weeks
Weeks

-66.6%

-46.1%

‡

0

10

20

30

40

50

60

70

80

90

0 1 2 4 8 12 16 20 24

M
ea

n 
re

sp
on

se
 r

at
e,

 %
 o

f 
pa

ti
en

ts

Weeks

-90
-80
-70
-60
-50
-40
-30
-20
-10

0
0 1 2 4 8 12 16 20 24 28 32 36 40 44 48 52

M
ea

n 
pe

rc
en

ta
ge

 C
FB

-62.9%

• Tyrosine kinase 2 (TYK2) is an intracellular enzyme that mediates cytokine 
signaling (eg, interleukin-23, Type 1 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

– Uniquely binds to the TYK2 regulatory domain with high selectivity and 
inhibits TYK2 via an allosteric mechanism1 (Figure 1)

• The phase 3 POETYK PSO-1 and PSO-2 trials demonstrated that deucravacitinib was 
superior to placebo and apremilast in patients with moderate to severe plaque 
psoriasis based on the coprimary endpoints of a ≥75% reduction from baseline in 
Psoriasis Area and Severity Index (PASI 75) and a static Physician’s Global 
Assessment score of 0 (clear) or 1 (almost clear) with a ≥2-point improvement from 
baseline (sPGA 0/1) at Week 163,4

• Clinical responses were maintained through 52 weeks in patients who 
received continuous deucravacitinib treatment and were improved in 
patients who switched from placebo to deucravacitinib at Week 165

• The 2-year efficacy and safety of deucravacitinib in the POETYK long-term extension 
trial was consistent with Weeks 0–52 of the POETYK PSO-1 and PSO-2 trials6

-90

-80

-70

-60

-50

-40

-30

-20

-10

0
0 1 2 4 8 12 16 20 24

M
ea

n 
pe

rc
en

ta
ge

 C
FB

-72.6%

‡§

‡§

§ §

-55.1%

‡

*‡

‡§

-19.9%

-55.9%

-76.1%

†

Deucravacitinib, an oral, selective tyrosine kinase 2 inhibitor, versus placebo and apremilast in moderate to 
severe plaque psoriasis: analysis of body surface area involvement in the phase 3 POETYK PSO-1 and PSO-2 trials
Jo Lambert,1 Carle Paul,2 Alice B Gottlieb,3 Yves Poulin,4 Diamant Thaçi,5 Stephen Tyring,6 Chien-Hui Hong,7 Lauren Hippeli,8 Renata M Kisa,8 Lluís Puig9
1Ghent University, Ghent, Belgium; 2Toulouse University and CHU, Toulouse, France; 3Icahn School of Medicine at Mount Sinai, New York, NY, USA; 4Université Laval, Hôpital Hotel-Dieu de Québec, and Centre de Recherche Dermatologique du Québec Métropolitain, Québec, QC, Canada; 5University of Lübeck, Lübeck, Germany; 6University of Texas Health Science Center and Center for Clinical Studies, Houston, TX, USA;
7National Yang Ming Chiao Tung University School of Medicine, Taipei City, and Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan; 8Bristol Myers Squibb, Princeton, NJ, USA; 9Hospital de la Santa Creu i Sant Pau and Universitat Autònoma de Barcelona, Barcelona, Spain

Presented at the 2022 Fall Clinical Dermatology Conference; October 20–23, 2022; Las Vegas, NV
This is an encore of the 2022 SPIN poster

Email for Jo Lambert, MD, PhD: Jo.Lambert@uzgent.be This poster may not be reproduced without written permission from the authors.

Figure 1. Mechanism of action of deucravacitinib

ATP, adenosine 5’-triphosphatase; JAK, Janus kinase; TYK2, tyrosine kinase 2.

Figure 3. Mean percentage changes in BSA and BSA × sPGA scores over 24 weeks in POETYK PSO-1 and PSO-2 pooled results

*P < 0.02 vs apremilast. †P = 0.0002 vs placebo. ‡P < 0.0001 vs placebo. §P < 0.0001 vs apremilast.
mBOCF was used to impute missing data; baseline observation was carried forward for patients who discontinued due to lack of efficacy or adverse events.
BSA, body surface area; BSA × sPGA, body surface area × static Physician’s Global Assessment score; CFB, change from baseline; mBOCF, modified baseline observation carried forward. 

Figure 5. Mean change from baseline responses in BSA and BSA × sPGA during POETYK PSO-1: Weeks 0‒52

References

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
JL: Unrestricted grants: AbbVie, Almirall, Celgene, Eli Lilly, Janssen-Cilag, Leo Pharma, Novartis, and UCB; Speaker: AbbVie, Almirall, Bristol Myers Squibb, Janssen-Cilag, 
Pfizer, and UCB; Consultant: AbbVie, Bristol Myers Squibb, Celgene, Eli Lilly, Janssen-Cilag, Leo Pharma, Novartis, and UCB. CP: Grants and consultant: AbbVie, Almirall, 
Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Janssen, Leo Pharma, Merck, Mylan, Novartis, Pfizer, Sandoz, and UCB. ABG: Honoraria 
or consultation fees: AnaptsysBio, Avotres, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Dermavant, Eli Lilly, Janssen, Novartis, Pfizer, Sanofi, Sun Pharma, and 
Xbiotech (stock options for an RA project); Research grants (paid to institution): AnapytsysBio, Janssen, Novartis, Ortho, Sun Pharma, and UCB, and Sun Pharma. YP:
Honoraria or consultation fees: AbbVie, Amgen, Biogen, Boehringer Ingelheim, Celgene, Eli Lilly, Leo Pharma, Merck-Serono, Merck Sharp & Dohme, Novartis, Pfizer, 
Regeneron, Roche, Sandoz, Sanofi, and UCB; Research grants or participation in clinical trials (paid to institution): AbbVie, Amgen, Boehringer Ingelheim, Celgene, Eli Lilly, 
Janssen, Leo Pharma, Novartis, Pfizer, Regeneron, Roche, Sanofi, and UCB. 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. ST: Participation in clinical trials: Bristol Myers Squibb. C-HH: Principal investigator: Bristol Myers Squibb, G&E 
Biotechnology, and Teva; Lecture fees: AbbVie, Bristol Myers Squibb, Eli Lilly, Leo Pharma, Mylan, Novartis, Pfizer, Roche-Posay, and Sanofi. LH and RMK: Employees and 
shareholders: Bristol Myers Squibb. LP: Honoraria or consultation fees: AbbVie, Almirall, Amgen, Baxalta, Biogen, Boehringer Ingelheim, Celgene, Eli Lilly, Fresenius Kabi, 
Gebro, Janssen, Leo Pharma, Merck-Serono, Merck Sharp & Dohme, Mylan, Novartis, Pfizer, Regeneron, Roche, Samsung Bioepis, Sandoz, Sanofi, and UCB; Research grants or 
participation in clinical trials (paid to institution): AbbVie, Almirall, Amgen, Boehringer Ingelheim, Celgene, Eli Lilly, Janssen, Leo Pharma, Novartis, Pfizer, Regeneron, 
Roche, Sanofi, and UCB; Speakers bureau: Celgene, Eli Lilly, Janssen, Merck Sharp & Dohme, Novartis, and Pfizer.

Synopsis

• Responses, including body surface area (BSA) involvement and the composite 
endpoint BSA × sPGA, were also monitored in both POETYK PSO-1 and PSO-2 to 
determine deucravacitinib efficacy in multiple endpoints

– PASI is the standard efficacy outcome for clinical trials but is time consuming 
and less meaningful for clinicians in everyday practice8

– sPGA is also standard for clinical trials but focuses on plaque qualities and 
does not include an assessment of BSA involvement8,9

– Together, BSA and BSA × sPGA can be useful proxies for PASI in clinical 
practice for assessment of disease severity in patients with moderate to 
severe plaque psoriasis9

Objective
• To evaluate the efficacy of deucravacitinib over 52 weeks based on BSA 

involvement and BSA × sPGA

Methods
Study designs
• The study designs for POETYK PSO-1 and PSO-2 are illustrated in Figure 2

• Patients meeting the following criteria were eligible to enroll in one of the 
studies:
– Age ≥18 years
– Diagnosis of moderate to severe plaque psoriasis

• Baseline PASI ≥12, sPGA ≥3, and BSA involvement ≥10%

• Patient randomization in POETYK PSO-1 and PSO-2 was stratified by 
geographic region, body weight, and prior biologic use

• BSA was estimated using the handprint method: the size of the patient’s 
handprint, including fingers and thumb, represented 1% of BSA involvement

Outcomes
• The current analysis examined mean percentage change from baseline in BSA and BSA × sPGA
• Response rates for a ≥75% improvement from baseline in BSA × sPGA (BSA × sPGA 75) were also reported
• Efficacy outcomes for Weeks 0‒24 were evaluated using the pooled POETYK PSO-1/PSO-2 population
• Maintenance of response through Week 52 was examined in the POETYK PSO-1 population only since it allowed assessment of 

continuous deucravacitinib treatment without any changes

Statistical methods
• Modified baseline observation carried forward (mBOCF) was used for change from baseline endpoints

– Baseline observation was carried forward for patients who discontinued due to lack of efficacy or adverse events
– For patients who discontinued the study treatment for other reasons or had a missing value, the last valid observation was 

carried forward (including the baseline value as applicable)
• Nonresponder imputation (NRI) was used for BSA × sPGA 75

– Patients who discontinued the study treatment or study or had missing endpoint data prior to time point of comparison were 
imputed as nonresponders

• Patients were excluded if data were missing solely due to COVID-19

Results
• A total of 1686 patients were randomized across the POETYK PSO-1 and PSO-2 trials (Table 1)
• Mean baseline BSA and BSA × sPGA scores were generally similar in each treatment group in POETYK PSO-1 and PSO-2 (Table 1)

Conclusions
• In the POETYK PSO-1 and PSO-2 trials, deucravacitinib treatment was associated with greater improvements in BSA, BSA ×

sPGA, and BSA × sPGA 75 over time compared with placebo and apremilast in patients with moderate to severe plaque psoriasis

• Deucravacitinib was associated with long-term improvements in response rates and maintenance of response in patients 
continuously treated over 52 weeks and in those who switched to deucravacitinib following 16 weeks of placebo

Deucravacitinib
(allosteric inhibitor)

Unique TYK2
regulatory

domain

Catalytic domain
(highly conserved
across JAK family)

ATP-binding active site
(other kinase inhibitors)

TYK2

Selectivity in cells1,7:
• ≥100-fold greater selectivity for TYK2 vs JAK 1/3
• ≥2000-fold greater selectivity for TYK2 vs JAK 2

Weeks 0‒52 (POETYK PSO-1 population)
• Findings from POETYK PSO-1 demonstrated maintenance of BSA and BSA × sPGA results in patients who received continuous 

deucravacitinib treatment, with mean percentage reductions of 74.6% and 81.4%, respectively, from baseline to Week 52 (Figure 5)

• Patients who switched from placebo to deucravacitinib at Week 16 had similar mean percentage reductions at Week 52 (BSA, 
75.6%; BSA × sPGA, 84.4%) to patients treated continuously with deucravacitinib (Figure 5)

• BSA × sPGA 75 responses were maintained through Week 52 in patients who received continuous deucravacitinib treatment and 
improved in patients who switched from placebo to deucravacitinib at Week 16, with Week 52 response rates that were similar 
between the groups (Figure 6)

*P < 0.0001 vs placebo. 
Nonresponder imputation was used to impute missing data. 
BSA × sPGA 75, ≥75% improvement from baseline in body surface area × static Physician’s Global Assessment score.

Deucravacitinib Placebo Apremilast

Patients, n

843Deucravacitinib

422Apremilast
421Placebo

843

422

421

843

422

421

843

422

421

843

422

421

843

422

421

843

422

421

842

421

NA

836

422

NA

BSA × sPGA over 24 weeks
Weeks

Figure 6. BSA × sPGA 75 response rates during POETYK PSO-1: Weeks 1‒52

0
10
20
30
40
50
60
70
80
90

0 1 2 4 8 12 16 20 24 28 32 36 40 44 48 52

M
ea

n 
re

sp
on

se
 r

at
e

Weeks

*
*

*

*

332
145

332
145

Patients, n

Deucravacitinib
Placebo

332
166

332
166

332
166

332
166

332
166

332
166

332
145

332
144

330
144

326
145

320
142

324
144 145

325

65.1%

15.1%

77.9%

73.5%

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

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, Psoriasis Area and Severity Index; PASI 50, ≥50% reduction from baseline in PASI; PASI 75, ≥75% reduction from baseline in PASI; QD, once daily.

• By Week 16, significantly greater reductions in BSA involvement were observed in patients treated with deucravacitinib (60.0%) 
vs those treated with placebo (11.3%; P < 0.0001) and apremilast (43.2%; P < 0.0001) (Figure 3)
– Significantly greater reductions were also observed with deucravacitinib vs apremilast by Week 24 (66.6% vs 46.1%; P < 0.0001)

• BSA × sPGA scores followed a similar pattern, with a decrease of 72.6% at Week 16 in deucravacitinib-treated patients vs 19.9% 
with placebo (P < 0.0001) and 55.1% with apremilast (P < 0.0001) (Figure 3)
– By Week 24, BSA × sPGA involvement decreased by 76.1% in patients who received deucravacitinib vs 55.9% (P < 0.0001) in 

patients treated with apremilast
• BSA × sPGA 75 response rates were significantly higher in patients treated with deucravacitinib vs those treated with placebo 

(P < 0.0001) and apremilast (P < 0.0001) at Week 16 and vs apremilast at Week 24 (P < 0.0001) (Figure 4)

POETYK PSO-1
(N = 666)

mBOCF was used to impute missing data; baseline observation was carried forward for patients who discontinued due to lack of efficacy or adverse events.
BSA, body surface area; BSA × sPGA, body surface area × static Physician’s Global Assessment score; CFB, change from baseline; mBOCF, modified baseline observation carried forward. 

Deucravacitinib Placebo to deucravacitinib 

BSA over 52 weeks
Weeks

POETYK PSO-2
(N = 1020)

-90
-80
-70
-60
-50
-40
-30
-20
-10

0
0 1 2 4 8 12 16 20 24 28 32 36 40 44 48 52

M
ea

n 
pe

rc
en

ta
ge

 C
FB

-74.2%

BSA × sPGA over 52 weeks
Weeks

-21.1%

-81.4%

-84.4%

-11.1%

-75.6%

-74.6%

332
Patients, n

332 332

145166Placebo

332

166

332

166

332

166

332

166

332

166

332

166 145

332 330

144

326 320 324 332Deucravacitinib

144 145 142 144 145

325

145

Figure 4. BSA × sPGA 75 mean response rates during POETYK PSO-1/PSO-2: Weeks 1‒24

*P < 0.0001 vs placebo. †P < 0.0001 vs apremilast. 
Nonresponder imputation was used to impute missing data.
BSA × sPGA 75, ≥75% improvement from baseline in body surface area × static Physician’s Global Assessment score.

*

*†

*

*†

*†
†

†

68.5%

44.5%

13.3%

43.8%

62.6%

Patients, n

Deucravacitinib

Apremilast

Placebo

843

422

421

843

422

421

843

422

421

843

422

421

843

422

421

843

422

421

836

422

NA

842

421

NA

Deucravacitinib Placebo Apremilast

Deucravacitinib Placebo to deucravacitinib 

Parameter

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, mean (SD), y 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, mean (SD), kg 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)

Disease duration, mean (SD), y 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)

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)

BSA × sPGA, mean (SD) 82.1 (57.3) 86.9 (56.1) 85.4 (54.9) 81.1 (56.3) 85.0 (54.6) 92.4 (58.7)
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)

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

Table 1. Baseline patient demographics and disease characteristics

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