22TYK2083_Fall Clin NPPA 22_POETYK High Impact Areas PO_CP_v03.indd


Deucravacitinib, an oral, selective tyrosine kinase 2 inhibitor, versus placebo in scalp, nail, and palmoplantar 
psoriasis: subset analyses of the phase 3 POETYK PSO-1 and PSO-2 trials
Andrew Blauvelt,1 Phoebe Rich,2 Howard Sofen,3 Jo Lambert,4 Joseph F Merola,5 Mark Lebwohl,6 Lauren Hippeli,7 Renata M Kisa,7 Subhashis Banerjee,7 Alexa B Kimball8
1Oregon Medical Research Center, Portland, OR, USA; 2Oregon Dermatology and Research Center, Portland, OR, USA; 3UCLA School of Medicine, Los Angeles, CA, USA; 4Ghent University, Ghent, Belgium; 5Harvard Medical School, Boston, MA, USA; 6Icahn School of Medicine at Mount Sinai, New York, NY, USA;  
7Bristol Myers Squibb, Princeton, NJ, USA; 8Beth Israel Deaconess Medical Center, Boston, MA, USA

Presented at the Fall Clinical Dermatology Conference for NPs and PAs®; June 3−5, 2022; Scottsdale, AZ
This is an encore of the 2022 Maui Derm for Dermatologists poster

This poster may not be reproduced without written permission from the authors.Email for Andrew Blauvelt, MD, MBA: ABlauvelt@oregonmedicalresearch.com 

Synopsis
• Deucravacitinib 

 — Oral, selective tyrosine kinase 2 (TYK2) inhibitor that acts via an allosteric 
mechanism by uniquely binding to the regulatory domain instead of the 
catalytic domain of TYK21

•  ≥100-fold greater selectivity for TYK2 vs Janus kinase (JAK) 1/3 and  
≥2000-fold greater selectivity for TYK2 vs JAK 2 in cells1,2

 — Inhibits TYK2-mediated cytokine signaling involved in psoriasis pathogenesis 
(eg, interleukin-23, Type I interferons)1

• Two 52-week, phase 3 psoriasis trials (POETYK PSO-1 and POETYK PSO-2) 
previously demonstrated that deucravacitinib was superior to placebo and 
apremilast at Week 16 based on the coprimary endpoints3:

 — ≥75% reduction from baseline in Psoriasis Area and Severity Index (PASI 75)
 — A static Physician’s Global Assessment score of 0 or 1 (sPGA 0/1; clear or 
almost clear skin)

Objectives
• Efficacy of deucravacitinib vs placebo at Week 16 in patients with moderate to 

severe involvement at baseline in the pooled PSO-1 and PSO-2 population of:

 — Scalp

 — Fingernail

 — Palms and soles (palmoplantar psoriasis)

• Efficacy in these high impact areas through Week 52 in PSO-1 patients: 
 — With continuous deucravacitinib treatment from Day 1 

 — After switching from placebo to deucravacitinib at Week 16

Methods
Study designs
• The study designs for POETYK PSO-1 and PSO-2 are summarized in Figure 1
• Key eligibility criteria included the following:

 — Age ≥18 years
 — Diagnosis of moderate to severe plaque psoriasis 

 — PASI ≥12, sPGA ≥3, body surface area involvement ≥10% 
• Patient randomization was stratified by geographic region, body weight, and prior 

biologic use

Figure 1. 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

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)

≥PASI 75

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.

Efficacy endpoints
• Moderate to severe scalp psoriasis (scalp-specific PGA [ss-PGA] ≥3) at baseline

 — ss-PGA 0/1 

 — ≥90% reduction from baseline in Psoriasis Scalp Severity Index (PSSI 90)
• Moderate to severe fingernail psoriasis (PGA-Fingernails [PGA-F] ≥3) at baseline

 — PGA-F 0/1

• Moderate to severe palmoplantar psoriasis (palmoplantar PGA [pp-PGA] ≥3) at 
baseline

 — pp-PGA 0/1 

 — Palmoplantar PASI (pp-PASI) improvements from baseline

Evaluation time points 
• Weeks 0−16 in the pooled PSO-1 and PSO-2 population
• Weeks 0−52 in PSO-1 (allowed continuous treatment with deucravacitinib for 

Weeks 0−52)

Statistical analysis
• None of the statistical comparisons of deucravacitinib vs placebo were 

mutiplicity controlled except for ss-PGA 0/1 vs placebo at Week 16 in PSO-1

Results
Baseline patient demographics and disease characteristics
• In the pooled PSO-1 and PSO-2 population (N = 1264; Table 1):

 — 64% (n = 808) had moderate to severe scalp psoriasis

 — 15% (n = 184) had moderate to severe fingernail psoriasis

 — 7% (n = 82) had moderate to severe palmoplantar psoriasis

• Presence of moderate to severe disease in these special areas was balanced 
overall in the deucravacitinib vs placebo group 

Table 1. Baseline patient demographics and disease characteristics

POETYK PSO-1 and PSO-2

Placebo Deucravacitinib 

(n = 421) (n = 843)

Age, mean (SD), y 47.5 (13.7) 46.5 (13.5)

Weight, mean (SD), kg 90.6 (21.1) 90.6 (21.9)

Female, n (%) 127 (30.2) 277 (32.9)

Race, n (%)

White 360 (85.5) 741 (87.9)

Asian 42 (10.0) 83 (9.8)

Other 19 (4.5) 19 (2.3)

Disease duration, mean (SD), y 18.9 (12.9) 18.6 (12.7)

Prior systemic treatment use, n (%)

Yes 248 (58.9) 474 (56.2)

Nonbiologic (± biologic) 183 (43.5) 326 (38.7)

Biologic 146 (34.7) 295 (35.0)

No prior systemic therapy 173 (41.1) 369 (43.8)

sPGA, n (%)

3 (moderate) 345 (81.9) 665 (78.9)

4 (severe) 75 (17.8) 178 (21.1)

PASI, mean (SD) 20.9 (8.6) 21.1 (8.0)

BSA, mean (SD), % 25.3 (16.1) 26.4 (15.8)

ss-PGA ≥3, n (%) 294 (69.8) 514 (61.0)

PGA-F ≥3, n (%) 72 (17.1) 112 (13.3)

pp-PGA ≥3, n (%) 25 (5.9) 57 (6.8)

PSSD symptom score, mean (SD) 50.6 (25.6) 52.1 (25.9)

DLQI, mean (SD) 11.6 (6.7) 11.9 (6.6)
BSA, body surface area; DLQI, Dermatology Life Quality Index; PASI, Psoriasis Area and Severity Index; PGA-F, Physician’s Global Assessment-Fingernails;  
pp-PGA, palmoplantar Physician’s Global Assessment; PSSD, Psoriasis Symptoms and Signs Diary; sPGA, static Physician’s Global Assessment; ss-PGA, scalp-specific 
Physician’s Global Assessment.

Scalp psoriasis
• In the pooled PSO-1 and PSO-2 population, significantly more patients receiving 

deucravacitinib vs placebo achieved ss-PGA 0/1 at Week 16 (Figure 2)
 — Efficacy was significantly greater with deucravacitinib vs placebo by Week 1 

Figure 2. ss-PGA 0/1a responses through Week 16 (pooled PSO-1 and PSO-2; 
NRI)

0

10

20

30

40

50

60

70

80

90

100

0 4 8 12 16

†

†

†

†

64.0% †

17.3%

ss
-P

G
A

 0
/1

 r
es

po
ns

e 
ra

te
, %

1 2

Weeks

*

Deucravacitinib 6 mg QD (n = 514)Placebo (n = 294)

aIncluded patients with a baseline ss-PGA score ≥3. 
*P < 0.05 vs placebo. †P < 0.0001 vs placebo. Missing data were imputed with NRI. 
NRI, nonresponder imputation; QD, once daily; ss-PGA 0/1, scalp-specific Physician’s Global Assessment score of 0 or 1.

• In the pooled PSO-1 and PSO-2 population, significantly more patients receiving 
deucravacitinib vs placebo achieved PSSI 90 at Week 16 (Figure 3)

 — Efficacy was significantly greater with deucravacitinib vs placebo by Week 1

Figure 3. PSSI 90a responses through Week 16 (pooled PSO-1 and PSO-2; NRI)

0
10
20
30
40
50
60
70
80
90

100

0 4 8 12 16

P
S

S
I 9

0 
re

sp
on

se
 r

at
e,

 %

Weeks

†

†

†
50.6% †

10.5%
*

1 2

*

Deucravacitinib 6 mg QD (n = 514)Placebo (n = 294)

aIncluded patients with a baseline ss-PGA score ≥3. 
*P ≤ 0.05 vs placebo. †P < 0.0001 vs placebo. Missing data were imputed with NRI. 
NRI, nonresponder imputation; PSSI 90, ≥90% reduction from baseline in Psoriasis Scalp Severity Index; QD, once daily; ss-PGA, scalp-specific Physician’s 
Global Assessment.

• In PSO-1, ss-PGA 0/1 responses at Week 16 were maintained through Week 52 
with continuous deucravacitinib treatment (Figure 4)

 — Patients who crossed over from placebo to deucravacitinib at Week 16 
achieved comparable ss-PGA 0/1 responses at Week 52 to those who had 
received continuous deucravacitinib treatment from Day 1

Figure 4. ss-PGA 0/1a responses through Week 52 (PSO-1; NRI) 

0

10

20

30

40

50

60

70

80

90

100

0 4

Primary endpoint

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

ss
-P

G
A

 0
/1

 r
es

po
ns

e 
ra

te
, %

Weeks

70.3%* 69.7%

65.6%

17.4%

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

aIncluded patients with a baseline ss-PGA score ≥3. 
*P < 0.0001 vs placebo. Missing data were imputed with NRI. 
NRI, nonresponder imputation; ss-PGA 0/1, scalp-specific Physician’s Global Assessment score of 0 or 1.

Fingernail psoriasis
• In the pooled PSO-1 and PSO-2 population, significantly more patients receiving 

deucravacitinib vs placebo achieved PGA-F 0/1 at Week 16 (Figure 5) 
• In PSO-1, PGA-F 0/1 responses at Week 16 were increased through Week 52 

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

Figure 5. PGA-F 0/1a responses through Week 16 (pooled PSO-1 and PSO-2; NRI)

0

10

20

30

40

50

60

70

80

90

100

0 4 8 12 16

20.5%*

8.3%

P
G

A
-F

 0
/1

 r
es

po
ns

e 
ra

te
, %

Weeks
Deucravacitinib 6 mg QD (n = 112)Placebo (n = 72)

aIncluded patients with a baseline PGA-F score ≥3. 
*P = 0.0272 vs placebo. Missing data were imputed with NRI. 
NRI, nonresponder imputation; PGA-F 0/1, Physician’s Global Assessment-Fingernails score of 0 or 1; QD, once daily.

Figure 6. PGA-F 0/1a responses through Week 52 (PSO-1; NRI)

P
G

A
-F

 0
/1

 r
es

po
ns

e 
ra

te
, %

0

10

20

30

40

50

60

70

80

90

100

0 4

Primary endpoint

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

Deucravacitinib (n = 43) Placebo (n = 34) Placebo-deucravacitinib (n = 29)

20.9%

51.7%

46.5%

8.8%

aIncluded patients with a baseline PGA-F score ≥3. 
Missing data were imputed with NRI. 
NRI, nonresponder imputation; PGA-F 0/1, Physician’s Global Assessment-Fingernails score of 0 or 1.

Palmoplantar psoriasis
• In the pooled PSO-1 and PSO-2 population, significantly more patients receiving 

deucravacitinib vs placebo achieved pp-PGA 0/1 at Week 16 (Figure 7)

Figure 7. pp-PGA 0/1a responses through Week 16 (pooled PSO-1 and PSO-2; 
NRI)

Deucravacitinib 6 mg QD (n = 57)Placebo (n = 25)

0

10

20

30

40

50

60

70

80

90

100

0 4 8 12 16

49.1%*

16.0%

pp
-P

G
A

 0
/1

 r
es

po
ns

e 
ra

te
, %

1 2
Weeks

aIncluded patients with a baseline pp-PGA score ≥3. 
*P = 0.0052 vs placebo. Missing data were imputed with NRI. 
NRI, nonresponder imputation; pp-PGA 0/1, palmoplantar Physician’s Global Assessment score of 0 or 1; QD, once daily.

• In the pooled PSO-1 and PSO-2 population, mean change from baseline in 
pp-PASI, adjusted for baseline covariates, was significantly greater with 
deucravacitinib vs placebo at Week 16 (Figure 8)

 — Greater efficacy with deucravacitinib vs placebo was observed as early as 
Week 4

Figure 8. Change from baseline in pp-PASIa through Week 16 (pooled PSO-1 
and PSO-2; mBOCF)

Deucravacitinib 6 mg QD (n = 57)Placebo (n = 25)

Placebo
(n = 25)

Deucravacitinib
(n = 57)

Baseline pp-PASI, mean (SD) 17.5 (12.5) 15.9 (10.9)

* *

-20

-10

0 4 8 12 16

M
ea

n 
C

FB
 in

 p
p-

P
A

S
I

Weeks

*

3.3*

4.2

1 2
20

aIncluded patients with a baseline pp-PGA score ≥3. 
*P ≤ 0.0097 vs placebo. Missing data were imputed with the modified baseline observation carried forward method. 
CFB, change from baseline; mBOCF, modified baseline observation carried forward; pp-PASI, palmoplantar Psoriasis Area and Severity Index; QD, once daily.

• In PSO-1, pp-PGA 0/1 responses at Week 16 were maintained through Week 52 
with continuous deucravacitinib treatment (Table 2)

 — Patients who crossed over from placebo to deucravacitinib at Week 16 
achieved comparable pp-PGA 0/1 responses at Week 52 to those who 
received continuous deucravacitinib treatment

Table 2. pp-PGA 0/1a responses through Week 52 (PSO-1; NRI)
pp-PGA 0/1 response rate, %

Week
Deucravacitinib

(n = 18)
Placebo-deucravacitinib

(n = 7)
16 55.6 0
24 66.7 42.9
52 55.6 42.9

aIncluded patients with a baseline pp-PGA score ≥3. 
Missing data were imputed with NRI. 
NRI, nonresponder imputation; pp-PGA 0/1, palmoplantar Physician’s Global Assessment score of 0 or 1.

Conclusions
• In patients with moderate to severe scalp, fingernail, or palmoplantar 

psoriasis at baseline in PSO-1 and PSO-2, deucravacitinib was significantly 
more efficacious than placebo in improving disease burden in these high 
impact areas through Week 16

• Clinical responses were maintained or increased in PSO-1 patients who 
received continuous deucravacitinib treatment from Day 1 through Week 52

 — Patients who crossed over from placebo to deucravacitinib at Week 16 
achieved comparable responses at Week 52 to those who had received 
continuous deucravacitinib treatment from baseline

• These findings support the use of deucravacitinib, an oral, selective 
TYK2 inhibitor, in patients with moderate to severe scalp, fingernail, or 
palmoplantar 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.

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
AB: Scientific adviser and/or clinical study investigator: AbbVie, Abcentra, Aligos, Almirall, Amgen, Arcutis, Arena, Aslan, Athenex, 
Boehringer Ingelheim, Bristol Myers Squibb, Dermavant, EcoR1, Eli Lilly, Evommune, Forte, Galderma, Incyte, Janssen, Landos, Leo 
Pharma, Novartis, Pfizer, Rapt, Regeneron, Sanofi Genzyme, Sun Pharma, UCB, and Vibliome. PR: Research (principal investigator 
on pharmaceutical trials): AbbVie, Arcutis, Bristol Myers Squibb, Dermavant, Eli Lilly, Janssen, Novartis, Sun Pharma, and UCB.  
HS: Clinical investigator: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Janssen, Leo Pharma, Novartis,  
and Sun Pharma. 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, Amgen, Bristol Myers Squibb, 
Celgene, Eli Lilly, Janssen-Cilag, Leo Pharma, Novartis, and UCB. JFM: Consultant and/or investigator: AbbVie, Amgen, Biogen, 
Bristol Myers Squibb, Dermavant, Eli Lilly, Janssen, Leo Pharma, Novartis, Pfizer, Regeneron, Sanofi, Sun Pharma, and UCB. 
ML: Research funds on behalf of Mount Sinai: AbbVie, Amgen, Arcutis, Avotres, Boehringer Ingelheim, Dermavant, Eli Lilly, Incyte, 
Janssen, Ortho Dermatologics, Regeneron, and UCB; Consultant: Aditum Bio, Almirall, AltruBio AnaptysBio, Arcutis, Arena, Aristea, 
Arrive Technologies, Avotres, BiomX, Boehringer Ingelheim, Brickell Biotech, Bristol Myers Squibb, Cara, Castle Biosciences, 
CorEvitas’ (Corrona) Psoriasis Registry, Dermavant, Dr. Reddy’s Laboratories, Evelo Biosciences, Evommune, Forte Biosciences, 
Helsinn Therapeutics, Hexima, Leo Pharma, Meiji Seika Pharma, Mindera, Pfizer, Seanergy, and Verrica. LH, RMK, and SB: 
Employees and shareholders: Bristol Myers Squibb. ABK: Consultant and investigator: AbbVie, Eli Lilly, Janssen, Novartis, Pfizer, and 
UCB; Investigator: Anapyts Bio, Bristol Myers Squibb, and Incyte; Consultant: Bayer, Concert, EvoImmune, Moonlake, and Ventyx; 
Fellowship funding: AbbVie and Janssen; Previous member of board of directors and past president: International Psoriasis Council; 
Board of directors: Almirall and HS Foundation.