Introduction • Tyrosine kinase 2 (TYK2) is an intracellular enzyme that mediates signaling of cytokines (eg, interleukin-23, Type I interferons) that are involved in psoriasis pathogenesis 1 • Deucravacitinib, an oral, selective, allosteric TYK2 inhibitor, is approved in the US, EU, and other countries for the treatment of adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy 2-6 • Deucravacitinib uniquely binds to the regulatory domain of TYK2 rather than to the catalytic domain where Janus kinase (JAK) 1,2,3 inhibitors bind 1,7 (Figure 1), representing the frst in a new class of small molecules Figure 1. Mechanism of action of deucravacitinib TYK2 Selectivity in cells 1,7 : • ≥100-fold greater selectivity for TYK2 vs JAK1 and JAK3 • ≥2000-fold greater selectivity for TYK2 vs JAK2 Deucravacitinib (approved allosteric TYK2 inhibitor class) Unique TYK2 regulatory domain Catalytic domain (highly conserved across JAK family) ATP-binding active site (approved JAK inhibitor class) ATP, adenosine 5′-triphosphate; JAK, Janus kinase; TYK2, tyrosine kinase 2. • Deucravacitinib was superior to placebo and apremilast in the global, 52-week, phase 3 POETYK PSO-1 (NCT03624127) and POETYK PSO-2 (NCT03611751) trials in moderate to severe plaque psoriasis 8,9 • Patients completing POETYK PSO-1 and PSO-2 could enroll in the POETYK long-term extension (LTE; NCT04036435) trial and receive open-label deucravacitinib 6 mg once daily (QD) • Deucravacitinib maintained long-term effcacy through 2 years with no new safety signals 10 Objective • To evaluate clinical effcacy for up to 3 years (148 weeks) in a subset of patients who received continuous deucravacitinib treatment from Day 1 in the parent trials and entered the POETYK LTE trial Methods Study design • In POETYK PSO-1 and PSO-2, eligible patients were randomized 1:2:1 to oral placebo, deucravacitinib 6 mg QD, or apremilast 30 mg twice daily (BID) (Figure 2) 8,9 • At Week 52, patients could enter the POETYK LTE trial and receive open-label deucravacitinib 6 mg QD Patient population • Patients pooled from POETYK PSO-1 and PSO-2 who received continuous deucravacitinib from Day 1, achieved ≥75% reduction from baseline in Psoriasis Area and Severity Index (PASI 75) at Week 16 (primary endpoint) or at Week 24 (peak response), and enrolled in the POETYK LTE trial Outcomes • Effcacy of deucravacitinib and maintenance of response through Week 148 (3 years) • Achievement of PASI 75, ≥90% reduction from baseline in PASI (PASI 90), and static Physician Global Assessment score of 0 (clear) or 1 (almost clear) with a ≥2-point improvement from baseline (sPGA 0/1) Figure 2. POETYK PSO-1, PSO-2, and LTE analysis populations a Key eligibility criteria in the parent studies: • Age ≥18 years • Moderate to severe plaque psoriasis: - PASI ≥12 - sPGA ≥3 - BSA involvement ≥10% Deucravacitinib 6 mg QD n = 1221 Deucravacitinib 6 mg QD PSO-1: n = 332 PSO-2 b : n = 511 Apremilast 30 mg BID c,d PSO-1: n = 168 PSO-2: n = 254 Placebo PSO-1: n = 166 PSO-2: n = 255 Deucravacitinib 6 mg QD PSO-1: n = 126 PSO-2: n = 203 Deucravacitinib 6 mg QD Apremilast 30 mg BID Placebo Week 16 Week 52 Week 148 e Week 24 Baseline a Includes patients with ≥1 dose of deucravacitinib 6 mg QD (N = 1519). b In POETYK PSO-2, patients randomized to deucravacitinib on Day 1 who achieved PASI 75 at Week 24 were rerandomized to deucravacitinib or placebo; for patients who were rerandomized to placebo, upon relapse (≥50% loss of Week 24 PASI percent improvement from baseline), they were to cross over to deucravacitinib; however, due to a programming error, these patients continued to receive placebo until Week 52. c In POETYK PSO-1, patients who responded to apremilast remained on apremilast. In POETYK PSO-2, patients who responded to apremilast crossed over to placebo and were to cross over to deucravacitinib upon relapse; however, due to a programming error, these patients continued to receive placebo until Week 52. d Apremilast was titrated from 10 mg QD to 30 mg BID over the frst 5 days of dosing. e Data were reported through the cutoff date of June 15, 2022. BID, twice daily; BSA, body surface area; LTE, long-term extension; PASI, Psoriasis Area and Severity Index; PASI 75, ≥75% reduction from baseline in PASI; QD, once daily; sPGA, static Physician Global Assessment. Statistical analysis • Effcacy was analyzed through the data cutoff date of June 15, 2022 • The Clopper-Pearson method was used to calculate 95% confdence intervals (CIs) • In addition to as-observed analysis, two methods of imputation for missing data were used to evaluate long-term effcacy, as recently done with other agents 11,12 — Treatment failure rules (TFR) 11 : patients who discontinued treatment due to lack of effcacy or worsening of psoriasis were imputed as nonresponders; all other missing data were not imputed — Modified nonresponder imputation (mNRI) 12 : patients who either discontinued prior to Week 148 or reached Week 148 were included; patients with missing data who discontinued treatment due to worsening of psoriasis were imputed as nonresponders; all other missing data were imputed by multiple imputation — Only patients who discontinued or reached Week 148 by the cutoff date were included Results • 513 patients completed 52 weeks in the parent trials and received continuous deucravacitinib treatment from Day 1 (Table 1) • 313 (61.4%) patients treated with deucravacitinib achieved PASI 75 at Week 16 and 336 (66.5%) patients achieved PASI 75 at Week 24 Table 1. Baseline patient demographics and disease characteristics Parameter Total (N = 513) Deucravacitinib Week 16 PASI 75 responders (n = 313) Deucravacitinib Week 24 PASI 75 responders (n = 336) Age, mean (SD), y 46.9 (13.3) 46.3 (13.9) 46.3 (13.8) Weight, mean (SD), kg 89.9 (22.2) 86.7 (21.7) 86.6 (22.1) Body mass index, mean (SD), kg/m 2 30.3 (7.0) 29.5 (6.6) 29.5 (7.0) Female, n (%) 159 (31.0) 110 (35.1) 122 (36.3) Race, n (%) White 440 (85.8) 262 (83.7) 284 (84.5) Asian 64 (12.5) 45 (14.4) 47 (14.0) Black or African American 5 (1.0) 2 (0.6) 1 (0.3) Other 4 (0.8) 4 (1.3) 4 (1.2) Age at disease onset, mean (SD), y 29.0 (14.7) 29.1 (15.3) 28.8 (15.3) Disease duration, mean (SD), y 18.8 (12.6) 18.0 (12.4) 18.3 (13.0) PASI score, mean (SD) 21.1 (7.9) 21.8 (8.2) 21.3 (8.0) sPGA score, n (%) 3 (moderate) 401 (78.2) 241 (77.0) 265 (78.9) 4 (severe) 112 (21.8) 72 (23.0) 71 (21.1) BSA involvement, mean (SD), % 26.9 (15.8) 28.1 (16.1) 27.0 (15.8) BSA, body surface area; PASI, Psoriasis Area and Severity Index; PASI 75, ≥75% reduction from baseline in PASI; SD, standard deviation; sPGA, static Physician Global Assessment. • PASI 75 response rates were maintained from the start of the POETYK LTE trial to Week 148 in Week 16 and Week 24 PASI 75 responders (Figure 3; Figure 4) • PASI 90 response rates were maintained from the start of the POETYK LTE trial in more than half of the Week 16 and Week 24 PASI 75 responders (Figure 5; Figure 6) • sPGA 0/1 response rates were also maintained from Week 52 to Week 148 in Week 16 and Week 24 PASI 75 responders (Figure 7; Figure 8) • Results were consistent regardless of imputation method • Deucravacitinib demonstrated a consistent safety profle through 3 years with no increases in adverse events (AEs) or serious AE rates over time and no emergence of any new safety signals 13 Figure 3. PASI 75 response rates in Week 16 PASI 75 responders 87.0% (82.5%-90.7%) 89.6% (85.8%-93.4%) 84.5% (79.8%-89.2%) 86.5% (82.2%-90.1%) 89.3% (85.1%-92.7%) 87.7% (82.6%-91.7%) 86.5% (82.2%-90.1%) 87.7% (83.3%-91.3%) 84.6% (79.2%-89.0%) 16 20 24 28 32 36 40 44 48 52 56 60 64 68 72 76 80 84 88 92 96 100 104 108 112 116 120 124 128 132 136 140 144 148 0 20 40 60 80 100 Response rate, % of patients c Study week PASI 75 Start of LTE 3-year data 2-year data Week 16 PASI 75 responders Patients, n TFR mNRI As observed 312 291 302 227 300 304 304 301 300 308 308 308 313 277 277 277 277 277 277 277 277 277 277 277 277 277 312 291 302 219 300 304 304 301 300 308 308 308 313 293 277 292 287 277 285 285 277 280 278 277 273 269 277 262 297 277 297 303 277 302 TFR a As observed mNRI b Imputation method: a TFR analysis captures discontinuations coded as "lack of effcacy." b For mNRI analyses, if there are no missing data (ie, no imputed values in the dataset), 95% CI was obtained using the Clopper-Pearson method based on the observed data. c Data callouts represent the response rate (95% CI). CI, confdence interval; LTE, long-term extension; mNRI, modifed nonresponder imputation; PASI 75, ≥75% reduction from baseline in Psoriasis Area and Severity Index; TFR, treatment failure rules. Figure 4. PASI 75 response rates in Week 24 PASI 75 responders 24 28 32 36 40 44 48 52 56 60 64 68 72 76 80 84 88 92 96 100 104 108 112 116 120 124 128 132 136 140 144 148 319 317 243 335 311 322 326 326 320 325 331 336 308 300 296 292 281 321 319 317 248 335 311 322 326 326 320 325 331 336 309 302 300 296 286 322 305 305 305 305 305 305 305 305 305 305 305 305 305 305 305 305 305 305 90.2% (86.3%-93.3%) 90.2% (86.6%-93.8%) 86.0% (81.6%-90.3%) 89.9% (86.1%-92.9%) 90.5% (86.6%-93.6%) 88.1% (83.3%-91.9%) 89.9% (86.1%-92.9%) 89.3% (85.3%-92.6%) 86.3% (81.4%-90.3%) 0 20 40 60 80 100 Response rate, % of patients c Study week PASI 75 Start of LTE 3-year data 2-year data Week 24 PASI 75 responders Patients, n TFR mNRI As observed TFR a As observed mNRI b Imputation method: a TFR analysis captures discontinuations coded as "lack of effcacy." b For mNRI analyses, if there are no missing data (ie, no imputed values in the dataset), 95% CI was obtained using the Clopper-Pearson method based on the observed data. c Data callouts represent the response rate (95% CI). CI, confdence interval; LTE, long-term extension; mNRI, modifed nonresponder imputation; PASI 75, ≥75% reduction from baseline in Psoriasis Area and Severity Index; TFR, treatment failure rules. Figure 5. PASI 90 response rates in Week 16 PASI 75 responders 57.8% (51.7%-63.6%) 60.6% (54.6%-66.4%) 59.2% (53.3%-65.2%) 60.0% (53.9%-66.1%) 55.9% (50.2%-61.5%) 60.6% (54.9%-66.0%) 59.6% (53.6%-65.4%) 63.0% (56.2%-69.4%) 55.9% (50.2%-61.5%) 60.6% (54.9%-66.0%) 58.6% (52.6%-64.4%) 60.8% (54.1%-67.2%) 16 20 24 28 32 36 40 44 48 52 56 60 64 68 72 76 80 84 88 92 96 100 104 108 112 116 120 124 128 132 136 140 144 148 0 20 40 60 80 100 Response rate, % of patients c Study week PASI 90 Start of LTE 3-year data 2-year data Week 16 PASI 75 responders Patients, n TFR As observed 312 291 302 227 300 304 304 301 300 308 308 308 313 312 291 302 219 300 304 304 301 300 308 308 308 313 293 292 287 285 285 280 278 273 269 262 297 297 303 mNRI 277 277 277 277 277 277 277 277 277 277 277 277 277 277 277 277 277 277 277 277 302 TFR a As observed mNRI b Imputation method: a TFR analysis captures discontinuations coded as "lack of effcacy." b For mNRI analyses, if there are no missing data (ie, no imputed values in the dataset), 95% CI was obtained using the Clopper-Pearson method based on the observed data. c Data callouts represent the response rate (95% CI). CI, confdence interval; LTE, long-term extension; mNRI, modifed nonresponder imputation; PASI 75/90, ≥75%/≥90% reduction from baseline in Psoriasis Area and Severity Index; TFR, treatment failure rules. Figure 6. PASI 90 response rates in Week 24 PASI 75 responders 63.3% (57.6%-68.7%) 61.6% (55.9%-67.1%) 61.7% (56.0%-67.3%) 60.4% (54.6%-66.3%) 62.8% (57.4%-68.0%) 61.8% (56.4%-67.0%) 63.2% (57.4%-68.7%) 63.4% (57.0%-69.4%) 62.8% (57.4%-68.0%) 61.8% (56.4%-67.0%) 62.3% (56.6%-67.8%) 62.1% (55.7%-68.2%) 24 28 32 36 40 44 48 52 56 60 64 68 72 76 80 84 88 92 96 100 104 108 112 116 120 124 128 132 136 140 144 148 0 20 40 60 80 100 Response rate, % of patients c Study week PASI 90 Start of LTE 3-year data 2-year data Week 24 PASI 75 responders Patients, n TFR mNRI As observed 319 317 243 335 311 322 326 326 320 325 331 336 308 300 296 292 281 321 319 317 248 335 311 322 326 326 320 325 331 336 309 302 300 296 286 322 305 305 305 305 305 305 305 305 305 305 305 305 305 305 305 305 305 305 TFR a As observed mNRI b Imputation method: a TFR analysis captures discontinuations coded as "lack of effcacy." b For mNRI analyses, if there are no missing data (ie, no imputed values in the dataset), 95% CI was obtained using the Clopper-Pearson method based on the observed data. c Data callouts represent the response rate (95% CI). CI, confdence interval; LTE, long-term extension; mNRI, modifed nonresponder imputation; PASI 75/90, ≥75%/≥90% reduction from baseline in Psoriasis Area and Severity Index; TFR, treatment failure rules. Figure 7. sPGA 0/1 response rates in Week 16 PASI 75 responders 16 20 24 28 32 36 40 44 48 52 56 60 64 68 72 76 80 84 88 92 96 100 104 108 112 116 120 124 128 132 136 140 144 148 312 291 302 227 300 304 304 301 300 309 308 308 313 277 277 277 277 277 277 277 277 277 277 277 277 277 312 291 302 219 300 304 304 301 300 309 308 308 313 293 277 292 287 277 285 285 277 280 278 277 273 269 277 262 297 277 297 303 277 302 84.1% (79.3%-88.2%) 70.8% (65.0%-76.0%) 68.4% (62.8%-74.1%) 62.8% (56.7%-68.9%) 83.1% (78.4%-87.1%) 70.2% (64.8%-75.2%) 67.9% (62.0%-73.3%) 64.8% (58.1%-71.2%) 83.1% (78.4%-87.1%) 70.2% (64.8%-75.2%) 66.7% (60.9%-72.1%) 62.6% (55.9%-68.9%) 0 20 40 60 80 100 Response rate, % of patients c Study week sPGA 0/1 Start of LTE 3-year data 2-year data Week 16 PASI 75 responders Patients, n TFR mNRI As observed TFR a As observed mNRI b Imputation method: a TFR analysis captures discontinuations coded as "lack of effcacy." b For mNRI analyses, if there are no missing data (ie, no imputed values in the dataset), 95% CI was obtained using the Clopper-Pearson method based on the observed data. c Data callouts represent the response rate (95% CI). CI, confdence interval; LTE, long-term extension; mNRI, modifed nonresponder imputation; PASI 75, ≥75% reduction from baseline in Psoriasis Area and Severity Index; sPGA 0/1, static Physician Global Assessment score of 0 (clear) or 1 (almost clear) with a ≥2-point improvement from baseline; TFR, treatment failure rules. Figure 8. sPGA 0/1 response rates in Week 24 PASI 75 responders 83.0% (78.3%-87.0%) 74.1% (68.6%-78.9%) 70.1% (64.7%-75.5%) 64.5% (58.7%-70.7%) 82.4% (77.9%-86.4%) 73.4% (68.4%-78.1%) 70.3% (64.7%-75.4%) 65.8% (59.5%-71.8%) 82.4% (77.9%-86.4%) 73.4% (68.4%-78.1%) 69.3% (63.8%-74.5%) 64.5% (58.2%-70.5%) 24 28 32 36 40 44 48 52 56 60 64 68 72 76 80 84 88 92 96 100 104 108 112 116 120 124 128 132 136 140 144 148 0 20 40 60 80 100 Response rate, % of patients c Study week sPGA 0/1 Start of LTE 3-year data 2-year data Week 24 PASI 75 responders Patients, n TFR mNRI As observed 319 317 243 335 311 322 326 326 320 325 332 336 308 300 296 292 281 321 319 317 248 335 311 322 326 326 320 325 332 336 309 302 300 296 286 322 305 305 305 305 305 305 305 305 305 305 305 305 305 305 305 305 305 305 TFR a As observed mNRI b Imputation method: a TFR analysis captures discontinuations coded as "lack of effcacy." b For mNRI analyses, if there are no missing data (ie, no imputed values in the dataset), 95% CI was obtained using the Clopper-Pearson method based on the observed data. c Data callouts represent the response rate (95% CI). CI, confdence interval; LTE, long-term extension; mNRI, modifed nonresponder imputation; PASI 75, ≥75% reduction from baseline in Psoriasis Area and Severity Index; sPGA 0/1, static Physician Global Assessment score of 0 (clear) or 1 (almost clear) with a ≥2-point improvement from baseline; TFR, treatment failure rules. Conclusions • Clinical effcacy was maintained for up to 148 weeks with continuous deucravacitinib treatment in the majority of patients who achieved PASI 75 at Week 16 or Week 24 in the parent trials and had enrolled in the POETYK LTE trial • These fndings further support the long-term use of once-daily oral deucravacitinib as an effective treatment for patients with moderate to severe plaque psoriasis References 1. Burke JR, et al. Sci Transl Med. 2019;11:eaaw1736. 2. Sotyktu [package insert]. Princeton, NJ: Bristol Myers Squibb; September 2022. 3. Sotyktu [summary of product characteristics]. 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Acknowledgments • This study was sponsored by Bristol Myers Squibb • Writing and editorial assistance was provided by Regina Kelly, MA, of Peloton Advantage, LLC, an OPEN Health company, funded by Bristol Myers Squibb Disclosures • 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 Health, Novartis, Ortho Dermatologics, Pfzer, Regeneron, Sanof Genzyme, Sun Pharma, UCB, Ventyx Biosciences, and vTv Therapeutics; Speaker: AbbVie, Eli Lilly, Janssen, and Sanof Genzyme; Co-scientifc director (consulting fee): CorEvitas Psoriasis Registry; Investigator: AbbVie, Cara Therapeutics, CorEvitas Psoriasis Registry, Dermavant, Dermira, and Novartis • HS: Clinical investigator: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Janssen, Leo Pharma, Novartis, and Sun Pharma • 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), Boehringer Ingelheim, Bristol Myers Squibb, Daiichi Sankyo, Eli Lilly, GlaxoSmithKline, Novartis, and UCB • CP: Grants and consultant: AbbVie, Almirall, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Janssen, Leo Pharma, Merck, Mylan, Novartis, Pfzer, Sandoz, and UCB • MG: Advisory board, principal investigator, and consulting/lecture fees: AbbVie, Amgen, Arcutis, Bausch Health, Boehringer Ingelheim International GmbH, Celgene, Eli Lilly, Janssen, Novartis, Sanof Genzyme, Sun Pharma, and UCB; Advisory board, primary investigator, and lecture fees: Galderma SA, Leo Pharma, Pfzer, and Regeneron; Advisory board, primary investigator and consultant fees: Aslan; Primary investigator and consultant fees: Akros Pharma and Kyowa Kirin; Primary investigator: Aristea, AnaptysBio, Bristol Myers Squibb, Coherus Biosciences, GlaxoSmithKline, Incyte, Dermira, MedImmune, Meiji Seika, Merck, MoonLake, and Nimbus Therapeutics; Advisory board: Asana Biosciences • LS: Consultant, paid investigator, and/or speaker: AbbVie, Amgen, Anacor, Ascend, Astellas, AstraZeneca, Blaze Bioscience, Boehringer Ingelheim, Botanix, Bristol Myers Squibb, Celgene, Dermira, Eli Lilly, Galderma, Genentech, GlaxoSmithKline, Hexima, Janssen, Leo Pharma, Mayne Pharma, MedImmune, Merck, Merck-Serono, Novartis, Otsuka, Pfzer, Phosphagenics, Photon MD, Regeneron, Roche, Samumed, Sanof Genzyme, SHR Pharmacy, Sun Pharma ANZ, Trius, UCB, and Zai Lab • SJS: Nothing to disclose • TP: Advisory board and consulting fees: AbbVie, Almirall, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Galderma, Incyte, Janssen, Leo Pharma, Novartis, Pfzer, Sanof Genzyme, Sun Pharma, and UCB • RMK, VB, EV, MJC, and SB: Employees and shareholders: Bristol Myers Squibb • KH: Consultant: Bristol Myers Squibb via Syneos Health • MA: Advisory boards: AbbVie, Amgen, Boehringer Ingelheim, Janssen Biotech, and Leo Pharma; Consulting fees: AbbVie, Amgen, Eli Lilly, Janssen Biotech, Leo Pharma, Novartis, Sun Pharma, and UCB; Honoraria: AbbVie, Amgen, Boehringer Ingelheim, Eli Lilly, Janssen Biotech, Leo Pharma, Novartis, Sun Pharma, and UCB; Investigator: AbbVie, Amgen, Boehringer Ingelheim, Celgene, Eli Lilly, Janssen Biotech, Leo Pharma, Merck, Novartis, Sun Pharma, and UCB; Research grants: AbbVie, Amgen, Boehringer Ingelheim, Celgene, Janssen Biotech, Leo Pharma, Merck, and Sun Pharma; Speaker: AbbVie, Amgen, Janssen Biotech, Leo Pharma, Sun Pharma, and UCB • LSG: Consultant, advisory board member, and/or speaker: AbbVie, Amgen, Arcutis, Aslan, Bausch Health, Boehringer Ingelheim, Bristol Myers Squibb, Dermavant, Dermira, Eli Lilly, Galderma, Incyte, Janssen, Leo Pharma, Novartis, Pfzer, Regeneron, Sanof Genzyme, Sun Pharma, and UCB • AA: Grants (funds to institution): AbbVie, Almirall, Amgen, Arcutis, Bristol Myers Squibb, Cara Therapeutics, Castle Biosciences, Dermavant, Galderma, Leo Pharma, Novartis, Valeant (Bausch Health), and Vyne; Advisory board/consulting: AbbVie, Allergan, Almirall, Amgen, Arcutis, Bausch Health, Beiersdorf, Bristol Myers Squibb, Cara Therapeutics, Castle Biosciences, Cutera, Dermavant, Eli Lilly, EPI Health, Galderma, Incyte, Janssen, Leo Pharma, L’Oreal, Ortho, Pfzer, Sanof-Regeneron, Swiss American, UCB, VisualDx, and Vyne; Speaker: Bristol Myers Squibb, Pfzer, Regeneron, and Sanof Genzyme; Royalties: Springer, Wiley-Blackwell, Wolters Kluwer Health • DT: Research support and principal investigator (clinical trial funds to institution): AbbVie, Almirall, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Galderma, Janssen-Cilag, Leo Pharma, Novartis, Pfzer, Regeneron, Roche, Sandoz-Hexal, Sanof, and UCB; Consultant: AbbVie, Almirall, Boehringer Ingelheim, Bristol Myers Squibb, Galapagos, Leo Pharma, Novartis, Pfzer, and UCB; Lecturer: AbbVie, Almirall, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Janssen, Eli Lilly, Leo Pharma, Novartis, Pfzer, Roche-Posay, Sanof, Target RWE, and UCB; Scientifc advisory board: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Janssen-Cilag, Leo Pharma, Novartis, Pfzer, Sanof, and UCB • AB: Speaker (with honoraria): AbbVie, Bristol Myers Squibb, Eli Lilly, Pfzer, Regeneron, and Sanof; Scientifc adviser (with honoraria): AbbVie, Abcentra, Aclaris, Affbody, Aligos, Almirall, Alumis, Amgen, AnaptysBio, Apogee, Arcutis, Arena, Aslan, Athenex, Bluefn Biomedicine, Boehringer Ingelheim, Bristol Myers Squibb, Cara Therapeutics, CTI BioPharma, Dermavant, EcoR1, Eli Lilly, Escient, Evelo Biosciences, Evommune, Forte Biosciences, Galderma, HighlightII Pharma, Incyte, InnoventBio, Janssen, Landos, Leo Pharma, Lipidio, Merck, Nektar, Novartis, Pfzer, Rani, Rapt, Regeneron, Sanof Genzyme, Spherix Global Insights, Sun Pharma, Takeda, TLL Pharmaceutical, TrialSpark, UCB, Union, Ventyx Biosciences, Vibliome, and Xencor; Clinical study investigator (institution has received clinical study funds): AbbVie, Acelyrin, Allakos, Almirall, Alumis, Amgen, Arcutis, Athenex, Boehringer Ingelheim, Bristol Myers Squibb, Concert, Dermavant, Eli Lilly, Evelo Biosciences, Evommune, Galderma, Incyte, Janssen, Leo Pharma, Merck, Novartis, Pfzer, Regeneron, Sanof, Sun Pharma, UCB, and Ventyx Biosciences • ML: Research funds on behalf of Mount Sinai: AbbVie, Amgen, Arcutis, Avotres, Boehringer Ingelheim, Cara Therapeutics, Dermavant, Eli Lilly, Incyte, Janssen, Ortho Dermatologics, Regeneron, and UCB; Consultant: Aditum Bio, Almirall, AltruBio, AnaptysBio, Arcutis, Aristea, Avotres, Boehringer Ingelheim, Brickell Biotech, Bristol Myers Squibb, Cara Therapeutics, Castle Biosciences, Celltrion, CorEvitas Psoriasis Registry, Dermavant, Dr. Reddy's Laboratories, EPI Health, Evommune, Forte Bioscience, Galderma, Genentech, Incyte, Leo Pharma, Meiji Seika Pharma, Mindera Health, Pfzer, Seanergy, Strata, Trevi, and Verrica Presented at the 43rd Annual Fall Clinical Dermatology Conference; October 19-22, 2023; Las Vegas, NV This is an encore of the 2023 European Academy of Dermatology & Venereology poster Email: brucestrober30@me.com Deucravacitinib in plaque psoriasis: maintenance of response over 3 years in the phase 3 POETYK PSO-1 and PSO-2 trials Bruce Strober, 1 Howard Sofen, 2 Shinichi Imafuku, 3 Carle Paul, 4 Melinda Gooderham, 5 Lynda Spelman, 6 Seong Jun Seo, 7 Thierry Passeron, 8 Renata M. Kisa, 9 Victoria Berger, 9 Eleni Vritzali, 9 Kim Hoyt, 9 Matthew J. Colombo, 9 Subhashis Banerjee, 9 Matthias Augustin, 10 Linda Stein Gold, 11 Andrew Alexis, 12 Diamant Thaçi, 13 Andrew Blauvelt, 14 Mark Lebwohl 15 1 Yale University School of Medicine, New Haven, and Central Connecticut Dermatology Research, Cromwell, CT, USA; 2 UCLA School of Medicine and Dermatology Research Associates, Los Angeles, CA, USA; 3 Fukuoka University Hospital Faculty of Medicine, Fukuoka, Japan; 4 Toulouse University and CHU, Toulouse, France; 5 SKiN Centre for Dermatology, Peterborough, Queen’s University, Kingston, and Probity Medical Research, Waterloo, ON, Canada; 6 Veracity Clinical Research, Brisbane, QLD, Australia; 7 Chung-Ang University Hospital, Seoul, South Korea; 8 Université Côte d’Azur, University Hospital of Nice, Nice, France; 9 Bristol Myers Squibb, Princeton, NJ, USA; 10 Institute for Health Services Research in Dermatology and Nursing, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; 11 Henry Ford Health System, West Bloomfeld, MI, USA; 12 Weill Cornell Medicine, New York, NY, USA; 13 Institute and Comprehensive Center for Infammation Medicine, University of Lübeck, Lübeck, Germany; 14 Oregon Medical Research Center, Portland, OR, USA; 15 Icahn School of Medicine at Mount Sinai, New York, NY, USA Copies of this poster obtained through QR (Quick Response) and/or text key codes are for personal use only and may not be reproduced without written permission of the authors. 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