Deucravacitinib in moderate to severe plaque psoriasis: liver transaminase results from the phase 3 POETYK PSO program Mark Lebwohl,1 Alexander Egeberg,2 Misti Linaberry,3 Kim Hoyt,3 Subhashis Banerjee,3 Renata M Kisa,3 Bruce Strober4 1Icahn School of Medicine at Mount Sinai, New York, NY, USA; 2Bispebjerg Hospital, Copenhagen, Denmark; 3Bristol Myers Squibb, Princeton, NJ, USA; 4Yale University School of Medicine, New Haven, and Central Connecticut Dermatology Research, Cromwell, CT, USA Presented at the Winter Clinical Dermatology Conference - Hawaii®, January 13-18, 2023, Kohala Coast, HI, and Winter Clinical - MiamiTM, February 17-20, 2023, Miami, FL This is an encore of the 2022 Fall Clinical Dermatology Conference poster Email: lebwohl@aol.com 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 essential to intracellular signaling of cytokines (interleukin-23 and Type I interferons) involved in psoriasis pathogenesis1 (Figure 1) • Deucravacitinib, an oral, selective, allosteric TYK2 inhibitor, is approved in the US and other countries for the treatment of adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy2 Figure 1. Mechanism of action of deucravacitinib TY K2 Deucravacitinib (allosteric inhibitor class) Unique TYK2 regulatory domain Catalytic domain (highly conserved across JAK family) ATP-binding active site (approved JAK inhibitor class) •  ≥100-fold greater selectivity for TYK2 vs JAK 1/3 • ≥2000-fold greater selectivity for TYK2 vs JAK 2 Selectivity in cells1,3: ATP, adenosine 5′-triphosphate; JAK, Janus kinase; TYK2, tyrosine kinase 2. • In two phase 3 pivotal trials in patients with moderate to severe plaque psoriasis, deucravacitinib demonstrated a robust safety and efficacy profile, including superiority to placebo and apremilast4,5 • Deucravacitinib treatment did not result in clinically relevant mean changes over time across multiple laboratory parameters, including in measures of liver transaminases6 — Mean alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels remained unchanged and within normal limits over Weeks 0-166 — Increases in liver transaminases have been observed with Janus kinase 1/2/3 inhibitors in patients with autoimmune diseases, including plaque psoriasis7 • However, increases ≥3× the upper limit of normal (ULN) in ALT and AST were observed over 16 weeks in individual patients2 — ALT elevations ≥3× ULN were reported in 9 patients (3.6/100 person-years [PY]) treated with deucravacitinib and in 2 patients (1.6/100 PY) receiving placebo who did not have ALT elevation at baseline — AST elevations ≥3× ULN were reported in 13 patients (5.2/100 PY) treated with deucravacitinib and in 2 patients (1.6/100 PY) receiving placebo Objective • To assess laboratory measures of liver function in the POETYK PSO-1 and PSO-2 trials, including changes over 52 weeks in patients who experienced an elevation ≥3× ULN for ALT or AST in the first 16 weeks of treatment Methods Study designs • POETYK PSO-1 and PSO-2 were 52-week, multinational, phase 3, double-blind, randomized, placebo- and active comparator- controlled trials (Figure 2) • Patients with moderate to severe plaque psoriasis (Psoriasis Area and Severity Index [PASI] ≥12, static Physician’s Global Assessment [sPGA] ≥3, body surface area involvement ≥10%) were randomized 1:2:1 to oral placebo, deucravacitinib 6 mg once daily, or apremilast 30 mg twice daily during Weeks 0–16 — Patients receiving placebo crossed over to deucravacitinib at Week 16 Figure 2. POETYK PSO-1 and PSO-2 study designs Deucravacitinib 6 mg QDPlacebo (n = 166) Deucravacitinib 6 mg QD1× ULN) and AST 33 U/L discontinued treatment on Day 18 due to increased CPK and increased AST. Values at the time of discontinuation were CPK 11,878 U/L (grade 4: reference range, 39-308 U/L), ALT 117 U/L (>2× ULN), and AST 226 U/L (>5× ULN). All values returned to within baseline range on Day 53. bPatient with a relevant history of fatty liver and baseline ALT 110 U/L (>2× ULN), AST 80 U/L (>2× ULN), and bilirubin 0.9 mg/dL discontinued treatment on Day 59 due to “hepatic function abnormal.” Bilirubin levels ranged from 0.9-2.0 mg/dL (reference range, 0-1.2 mg/dL) prior to the reported AE. Values on Day 58 were: ALT 119 U/L (>2× ULN), AST 119 U/L (>3× ULN), and bilirubin 4.2 mg/dL (>3× ULN). The event resolved on Day 92. cPatient with a relevant history of fatty liver, increased liver function test, and screening ALT 73 U/L (>1× ULN) and AST 44 U/L (>1× ULN) discontinued treatment on Day 2 due to “liver function test abnormal.” Values on Day 1 were: ALT 387 U/L (>5× ULN) and AST 177 U/L (>3× ULN). Values returned to within screening range on Day 36. AE, adverse event; ALT, alanine aminotransferase; AST, aspartate aminotransferase; CPK, creatine phosphokinase; IR, incidence rate; PY, person-years; ULN, upper limit of normal. Shifts in CTCAE grade • Definitions of CTCAE grades for increased ALT and increased AST are defined in Table 2 • Across treatment arms, maximum increases from baseline in ALT and AST rarely exceeded 1 CTCAE grade during Weeks 0-16 (Table 3) — Shifts of 1 grade from baseline: • ALT: placebo, 11.4%; deucravacitinib, 11.3%; apremilast, 14.6% • AST: placebo, 9.4%; deucravacitinib, 8.6%; apremilast, 6.7% — Shifts of ≥2 grades from baseline: • ALT: placebo, 0%; deucravacitinib, 0.4%; apremilast, 0.5% • AST: placebo, 0%; deucravacitinib, 0.5%; apremilast, 0.5% Table 2. Definitions of CTCAE grades for ALT and AST elevations Laboratory parameter Grade 1 Grade 2 Grade 3 Grade 4 ALT • ULN–3× ULN if baseline normal • 1.5×–3× baseline if baseline abnormal • >3×-5× ULN if baseline normal • >3×-5× baseline if baseline abnormal • >5×–20× ULN if baseline normal • >5×–20× baseline if baseline abnormal • >20× ULN if baseline normal • >20× baseline if baseline abnormal AST • ULN–3× ULN if baseline normal • 1.5×–3× baseline if baseline abnormal • >3×-5× ULN if baseline normal • >3×-5× baseline if baseline abnormal • >5×–20× ULN if baseline normal • >5×-20× baseline if baseline abnormal • >20× ULN if baseline normal • >20× baseline if baseline abnormal ALT, alanine aminotransferase; AST, aspartate aminotransferase; CTCAE, Common Terminology Criteria for Adverse Events; ULN, upper limit of normal. Table 3. Shifts in transaminase elevations from baseline during Weeks 0-16 by CTCAE grade CTCAE term, n (%) BL grade POETYK PSO-1 and PSO-2 Placebo Deucravacitinib 6 mg QD Apremilast 30 mg BID Maximum grade (Weeks 0-16) Maximum grade (Weeks 0-16) Maximum grade (Weeks 0-16) 0 1 2 3 4 0 1 2 3 4 0 1 2 3 4 ALT increased n = 413 n = 833 n = 419 0 297 (86.3) 47 (13.7) 0 0 0 579 (85.0) 92 (13.6) 3 (0.4) 0 0 287 (82.0) 61 (17.4) 2 (0.6) 0 0 1 55 (87.3) 8 (12.7) 0 0 0 143 (89.9) 14 (8.8) 2 (1.3) 0 0 64 (94.1) 4 (5.9) 0 0 0 2 3 (75.0) 1 (25.0) 0 0 0 0 0 0 0 0 1 (100) 0 0 0 0 3 2 (100) 0 0 0 0 0 0 0 0 0 0 0 0 0 0 4 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 AST increased n = 413 n = 833 n = 419 0 342 (90.0) 38 (10.0) 0 0 0 687 (90.4) 69 (9.1) 3 (0.4) 1 (0.1) 0 344 (92.0) 28 (7.5) 1 (0.3) 1 (0.3) 0 1 27 (90.0) 2 (6.7) 1 (3.3) 0 0 60 (82.2) 10 (13.7) 3 (4.1) 0 0 44 (97.8) 1 (2.2) 0 0 0 2 2 (100) 0 0 0 0 0 0 0 0 0 0 0 0 0 0 3 1 (100) 0 0 0 0 0 0 0 0 0 0 0 0 0 0 4 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 Light pink shading indicates shifts of 1 grade from baseline; dark pink shading indicates shifts of ≥2 grades from baseline. Values sum to 100% across rows for each treatment group. ALT, alanine aminotransferase; AST, aspartate aminotransferase; BID, twice daily; BL, baseline; CTCAE, Common Terminology Criteria for Adverse Events; QD, once daily. Maximum elevations over time • Postbaseline incidences of ALT >3× ULN during Weeks 0-16 were low (<2%) and comparable in all 3 treatment arms (Table 4) — Similar findings were observed for the Weeks 0-52 period (Table 5) • Postbaseline incidences of AST >3× ULN and AST >5× ULN during Weeks 0-16 were low across treatment groups (<2% and <0.5%, respectively) but greater with deucravacitinib vs placebo or apremilast (Table 4) — Similar findings were observed for the Weeks 0-52 period (Table 5) Table 4. Maximum elevations in ALT and AST, Weeks 0–16 Abnormality Placebo (n = 413) Deucravacitinib (n = 833) Apremilast (n = 419) Baseline Weeks 0–16 Baseline Weeks 0–16 Baseline Weeks 0–16 n (%) n (%) n (%) n (%) n (%) n (%) ALT >3×->20× ULN 6 (1.5) 5 (1.2) 0 9 (1.1) 1 (0.2) 2 (0.5) >5×->20× ULN 2 (0.5) 3 (0.7) 0 0 0 0 >10×->20× ULN 0 0 0 0 0 0 >20× ULN 0 0 0 0 0 0 AST >3×->20× ULN 3 (0.7) 2 (0.5) 0 13 (1.6) 0 3 (0.7) >5×->20× ULN 1 (0.2) 1 (0.2) 0 3 (0.4) 0 1 (0.2) >10×->20× ULN 0 0 0 0 0 0 >20× ULN 0 0 0 0 0 0 Patients are counted once in each relevant category. Includes data from POETYK PSO-1 and PSO-2. For ALT, the ULN was defined as 33 U/L for women and 41 U/L for men. For AST, the ULN was defined as 31 U/L for women and 37 U/L for men. ALT, alanine aminotransferase; AST, aspartate aminotransferase; ULN, upper limit of normal. Table 5. Maximum elevations in ALT and AST, Weeks 0–52 Abnormality Placebo (n = 658) Deucravacitinib (n = 1351) Apremilast (n = 419) n (%) PY IR/100 PY n (%) PY IR/100 PY n (%) PY IR/100 PY ALT >3×->20× ULN 11 (1.7) 247.0 4.5 21 (1.6) 977.0 2.1 4 (1.0) 225.8 1.8 >5×->20× ULN 2 (0.3)a 249.9 0.8 6 (0.4) 983.8 0.6 0 ― ― >10×->20× ULN 0 ― ― 1 (0.1) 984.7 0.1 0 ― ― >20× ULN 0 ― ― 0 ― ― 0 ― ― AST >3×->20× ULN 5 (0.8) 249.1 2.0 25 (1.9) 973.3 2.6 3 (0.7) 226.4 1.3 >5×->20× ULN 1 (0.2) 250.2 0.4 7 (0.5) 981.9 0.7 1 (0.2) 226.8 0.4 >10×->20× ULN 0 ― ― 2 (0.1) 984.4 0.2 0 ― ― >20× ULN 0 ― ― 0 ― ― 0 ― ― aOne patient who had an ALT elevation during Weeks 0-16 had a higher elevation after switching to deucravacitinib treatment and is counted with the deucravacitinib patients for the Weeks 0-52 treatment period. Patients are counted once in each relevant category. Includes data from POETYK PSO-1 and PSO-2. For ALT, the ULN was defined as 33 U/L for women and 41 U/L for men. For AST, the ULN was defined as 31 U/L for women and 37 U/L for men. ALT, alanine aminotransferase; AST, aspartate aminotransferase; IR, incidence rate; PY, person-years; ULN, upper limit of normal. Patient-level data in patients who experienced an elevation ≥3× ULN during Weeks 0-16 • Most ALT elevations ≥3× ULN were transient and were often related to underlying liver conditions or concomitant medications (Figure 3; Table 6) • Most AST elevations ≥3× ULN were transient and were often related to underlying liver conditions or concomitant medications (Figure 4; Table 6) Figure 3. ALT levels over Weeks 0-16 in patients with ALT ≥3× ULNa during Weeks 0-16 400 300 100 A n al ys is v al u e ( U /L ) 200 Placebo Patient 12 Patient 11 Patient 10 Patient 13 Patient 14 Visit 3× ULN: Men: 123 U/L Women: 99 U/L Screening Baseline Week 1 Week 2 Week 4 Week 8 Week 12 Week 16 400 300 100 0 A n al ys is v al u e ( U /L ) 200 Apremilast Patient 16 Patient 15 Visit Screening Baseline Week 1 Week 2 Week 4 Week 8 Week 12 Week 16 3× ULN: Men: 123 U/L Women: 99 U/L 400 300 200 100 0 A n al ys is v al u e ( U /L ) Screening Baseline Week 1 Week 2 Week 4 Week 8 Week 12 Week 16 Visit Deucravacitinib Patient 2 Patient 3 Patient 1 Patient 4 Patient 6 Patient 5 Patient 7 Patient 8 Patient 9 3× ULN: Men: 123 U/L Women: 99 U/L Squares represent men; circles represent women. aNormal adult laboratory ranges vary by test assay. For ALT, the ULN was defined as 33 U/L for women and 41 U/L for men. ALT, alanine aminotransferase; ULN, upper limit of normal. Figure 4. AST levels over Weeks 0-16 in patients with AST ≥3× ULNa during Weeks 0-16 300 200 100 0 A n al ys is v al u e ( U /L ) Deucravacitinib Patient 5 Patient 7 Patient 8 Patient 9 Patient 17 Patient 18 Patient 19 Patient 20 Patient 21 Patient 22 Patient 23 Patient 24 Patient 25 3× ULN: Men: 111 U/L Women: 93 U/L Visit Screening Baseline Week 1 Week 2 Week 4 Week 8 Week 12 Week 16 3× ULN: Men: 111 U/L Women: 93 U/L 300 200 100 50 A n al ys is v al u e ( U /L ) Placebo Patient 11 Patient 14 Visit Screening Baseline Week 1 Week 2 Week 4 Week 8 Week 12 Week 16 300 200 100 0 A n al ys is v al u e ( U /L ) Visit Screening Baseline Week 1 Week 2 Week 4 Week 8 Week 12 Week 16 Apremilast Patient 15 Patient 26 Patient 27 3× ULN: Men: 111 U/L Women: 93 U/L Squares represent men; circles represent women. aNormal adult laboratory ranges vary by test assay. For AST, the ULN was defined as 31 U/L for women and 37 U/L for men. AST, aspartate aminotransferase; ULN, upper limit of normal. Table 6. Summary of relevant medical history and prior and concomitant medications in patients with ALT or AST elevations ≥3× ULN through Week 16 Patient ID Treatment Timing of ≥3× ULN ALT increase, weeks Timing of ≥3× ULN AST increase, weeks Relevant medical history and prior and concomitant medications through Week 16 ● Patient 1 Deucravacitinib 12-16 ― • History of liver disease, including fatty liver disease, jaundice, possible hepatitis A, previous elevated ALT, and obesity (BMI 32.3 kg/m2) • Prior use of infliximab, etanercept, and methotrexate ■ Patient 2 Deucravacitinib 12 ― • Patient BMI 32.7 kg/m2, no other relevant medical history or medications available ● Patient 3 Deucravacitinib Screening, 1 ― • History of coronary artery disease, myocardial infarction, hypertriglyceridemia, Type 2 diabetes, hypertension, BMI 33.4 kg/m2, and previous left nephrectomy • Previous treatment with etanercept, clobetasol, and betamethasone dipropionate; previous and continuing treatment with metformin, aspirin, losartan, lorazepam ● Patient 4 Deucravacitinib 1 ― • History of hepatic steatosis and obesity (BMI 38.6 kg/m2) • No relevant medications taken before or during the event at Week 1 ■ Patient 5 Deucravacitinib Baseline 2 • History of fatty liver disease and alcohol use, BMI 30.8 kg/m2 • Prior treatment with olopatadine and betamethasone butyrate propionate; prior and continuing treatment with triazolam, zolpidem tartrate ■ Patient 6 Deucravacitinib 8 ― • History of adipositas, BMI 37.0 kg/m 2 • Previous treatment with Fumaderm ■ Patient 7 Deucravacitinib 4 4 • BMI 29.5 kg/m 2 • Previous and continuing treatment with sildenafil, beclomethasone dipropionate inhaler ● Patient 8 Deucravacitinib 16 16 • History of Kawasaki’s disease and hypertension, BMI 17.0 kg/m2 • Alcohol use was not reported in the parent study, but during the long-term extension study the investigator reported an AE of alcohol dependence syndrome • An abdominal CT done for AE of acute abdomen on Day 74 revealed hepatic steatosis • History of clobetasol propionate, betamethasone butyrate propionate, prednisolone valerate acetate, metroclopramine hydrochloride, Solyugen, acetaminophen, iohexol, esomeprazole magnesium hydrate ● Patient 9 Deucravacitinib 16 16 • BMI 37.4 kg/m2 • Previous treatment with acetic acid, dexamethasone, neomycin sulfate, Otomize ear spray; previous and continuing treatment with Depo-Provera ■ Patient 10 Placebo Baseline, 1 ― • History of fatty liver disease, latent tuberculosis, tinea versicolor, liver function elevations, prediabetes mellitus, gout, and hyperlipidemia, BMI 26.0 kg/m2 • Previous treatment with methotrexate, cyclosporine, neotigason; previous and continuing treatment with Legalon, tiropramide hydrochloride, febuxostat, cilostazol, crovatin, trimebutine maleate, buspirone hydrochloride, pyridoxine, isoniazid ● Patient 11 Placebo Screening, 12 12 • History of transaminitis, BMI 37.6 kg/m2 • Previous and ongoing use of intrauterine contraception device ● Patient 12 Placebo Screening, 1, 4 ― • History of elevated ALT and AST, hypertension, BMI 35.8 kg/m2 • Previous treatment with secukinumab; previous and ongoing treatment with nedal, karnidin, Jaydess, Hepa-Merz 3000, and furaginum ● Patient 13 Placebo Baseline, 1, 2, 4 ― • History of hepatic steatosis, latent tuberculosis, intermittent elevated liver function tests, HAIR-AN syndrome, and obesity (BMI 37.0 kg/m2) • Previous treatment with rifampin; previous and continuing treatment with ibuprofen ■ Patient 14 Placebo Screening, baseline, 1, 2, 4, 8 Baseline, 1, 2, 4, 8 • History of elevated ALT and AST, and benign prostatic hyperplasia, BMI 26.6 kg/m2 • Previous treatment with ixekizumab, guselkumab, amitriptyline, ciprofloxacin; treatment with sulfamethoxazole and trimethoprim (Days 11-16 and Days 29-39) ● Patient 15 Apremilast Screening, 12 12 • BMI 33.0 kg/m2, no other relevant medical history or medications available ■ Patient 16 Apremilast 16 ― • BMI 28.1 kg/m 2 • Prior treatment with levocetirizine dihydrochloride ● Patient 17 Deucravacitinib ― Screening, 8 • History of Helicobacter pylori-positive serum antibody, Type 2 diabetes, and hypertension, BMI 32.6 kg/m2 • Previous treatment with tepilamide fumarate or placebo (as part of a clinical trial), omeprazole, clarithromycin, amoxicillin; previous and continuing treatment with Ancef, lisinopril, amitriptyline, metformin ■ Patient 18 Deucravacitinib ― 8 • BMI 33.0 kg/m 2 • Previous treatment with adalimumab and ustekinumab ■ Patient 19 Deucravacitinib ― 12 • BMI 50.7 kg/m2, no other relevant medical history or medications available ■ Patient 20 Deucravacitinib ― 16 • BMI 43.4 kg/m2, no other relevant medical history or medications available ■ Patient 21 Deucravacitinib ― 4 • BMI 27.2 kg/m 2 • Previous treatment with methotrexate ● Patient 22 Deucravacitinib ― 2 • BMI 26.4 kg/m2 • Previous and continuing treatment with ethinyl estradiol/etonogestrel ■ Patient 23 Deucravacitinib ― 12 • History of penicillin allergy, hypercholesterolemia, occasional heavy alcohol consumption, and hypertension, BMI 25.7 kg/m2 • Previous treatment with guselkumab, doxycycline (taken from Day 72 to Day 81); previous and continuing treatment with aspirin, amlodipine/benazepril, rosuvastatin ■ Patient 24 Deucravacitinib ― 2 • History of coronary artery disease, smoking, stent insertion (3 stents total), and arterial hypertension, BMI 27.6 kg/m2 • Previous and continuing treatment with Coversyl, bisoprolol, Lipitor, and acetylsalicylic acid ■ Patient 25 Deucravacitinib ― 8, 12 • BMI 28.9 kg/m2 • Previous and ongoing treatment with lisinopril, patient-reported excessive alcohol intake while in the long-term extension study ■ Patient 26 Apremilast ― 2 • BMI 31.2 kg/m 2 • Previous treatment with brodalumab ■ Patient 27 Apremilast ― 1, 8, 12 • History of hepatic steatosis, high liver function tests, hyperlipidemia, hypertension, BMI 35.3 kg/m2, and renal cyst (left) • Previous treatment with neotigason; previous and continuing treatment with perindopril and indapamide Squares represent men; circles represent women. AE, adverse event; ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMI, body mass index; CT, computed tomography; ULN, upper limit of normal. Conclusions • In the POETYK PSO-1 and PSO-2 trials in patients with moderate to severe plaque psoriasis, shifts >1 CTCAE grade from baseline in ALT and AST were infrequent over Weeks 0–16 with deucravacitinib treatment — There were no shifts to grade 4 and only 2 shifts to grade 3 (1 each with deucravacitinib and apremilast treatment) • In patients treated with deucravacitinib, increases in ALT and AST >3× ULN were observed in <2% of patients over 52 weeks • ALT and AST increases to >3× ULN were mainly transient, and most were related to underlying liver conditions or concomitant medications • There were no cases of drug-induced liver injury 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. Wrobleski ST, et al. J Med Chem. 2019;62:8973-8995. 4. Armstrong AW, et al. J Am Acad Dermatol. 2023;88:29-39. 5. Strober B, et al. J Am Acad Dermatol. 2023;88:40-51. 6. Thaçi D, et al. Presented at the 30th EADV Congress; September 29–October 2, 2021. 7. Winthrop KL. Nat Rev Rheumatol. 2017;13:234-243. 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 • 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 Therapeutics, 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 • AE: Research funding: AbbVie, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Janssen, Novartis, and Pfizer; Honoraria as consultant and/or speaker: AbbVie, Almirall, Boehringer Ingelheim, Bristol Myers Squibb, Dermavant, Eli Lilly, Galápagos NV, Galderma, Horizon Therapeutics, Janssen, Leo Pharma, McNeil Consumer Healthcare, Mylan, Novartis, Pfizer, Samsung Bioepis Co, Sun Pharma, UCB, UNION, and Zuellig Pharma Ltd • ML, SB, and RMK: Employees and shareholders: Bristol Myers Squibb • KH: Consultant: Bristol Myers Squibb • 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 Therapeutics, CorEvitas' (Corrona) Psoriasis Registry, Dermavant, Dermira, and Novartis mailto:lebwohl%40aol.com?subject=