Introduction

Ulcerative colitis (UC) is a chronic inflammatory bowel disease marked by relapsing symptoms and significant impact on quality of life, with current therapies often limited by suboptimal efficacy or adverse effects. Interleukin-12/23p40 (IL-12/23p40) antagonists have emerged as targeted treatments due to their role in modulating key inflammatory pathways, yet the class-wide efficacy and safety of these agents remain uncertain.

Aims & Methods

To evaluate the effectiveness and safety of IL-12/23p40 antagonists in moderate to severe UC, a systematic review, meta-analysis, and trial sequential analysis were conducted. Databases including PubMed, Embase, Cochrane Central, and ClinicalTrials.gov were searched in December 2024 to identify randomized controlled trials (RCTs) comparing IL-12/23p40 antagonists to placebo. Outcomes included clinical and endoscopic remission and response, adverse events, and additional endpoints such as histologic healing, symptomatic relief, and glucocorticoid-free remission. Risk ratios (RR) and mean differences (MD) with 95% confidence intervals (CI) were pooled using a random-effects model in R software.

Results

Nine RCTs enrolling 3,808 patients in the induction phase and 1,734 in the maintenance phase were included [1–6]. IL-12/23p40 antagonists significantly improved clinical remission during induction (21.8% vs. 8%; RR 2.63, 95% CI 2.05–3.36, p < 0.001) and maintenance (46.8% vs. 23%; RR 1.99, 95% CI 1.63–2.44, p < 0.001), and clinical response (induction: RR 1.94, 95% CI 1.70–2.20, p < 0.001; maintenance: RR 1.51, 95% CI 1.34–1.69, p < 0.001). Endoscopic remission (induction: RR 2.36, 95% CI 1.63–3.41, p < 0.001; maintenance: RR 1.96, 95% CI 1.63–2.37, p < 0.001) and endoscopic response were also significantly improved. Notably, prior biologic or JAK inhibitor failure was linked to higher induction remission rates (RR 3.74, 95% CI 1.60–8.76, p = 0.002), with meta-regression confirming this association (p = 0.008), suggesting enhanced remission in previously treatment-resistant patients. Additionally, IL-12/23p40 antagonists improved histologic, endoscopic, and mucosal healing (RR 2.49; 95% CI 2.01–3.08, p < 0.001), symptomatic remission (RR 2.16, 95% CI 1.66–2.82, p < 0.001), and quality of life as measured by the IBDQ score (MD 16.3, 95% CI 12.2–20.4, p < 0.001). Moreover, IL-12/23p40 antagonists demonstrated a favorable safety profile in both the induction and maintenance phases. During induction, they were associated with a significantly lower risk of serious adverse events (RR 0.40, 95% CI 0.27–0.69, p < 0.001). No significant differences were observed compared to placebo in the overall incidence of adverse events (induction: RR 0.97, 95% CI 0.90–1.04, p = 0.38; maintenance: RR 0.95, 95% CI 0.87–1.03, p = 0.22), headache (induction: RR 1.17, 95% CI 0.82–1.68, p = 0.39; maintenance: RR 1.29, 95% CI 0.60–2.78, p = 0.51), or nasopharyngitis (induction: RR 1.09, 95% CI 0.67–1.76, p = 0.73; maintenance: RR 1.07, 95% CI 0.77–1.50, p = 0.68).

Conclusion

IL-12/23p40 antagonists demonstrate superior efficacy compared to placebo in inducing and maintaining clinical and endoscopic remission in patients with moderate to severe UC, with a favorable safety profile and potential benefits even among biologic-experienced populations. These results support the use of IL-12/23p40 antagonists as an effective and well-tolerated treatment option in the management of UC.

References

1. Louis E, Schreiber S, Panaccione R, Bossuyt P, Biedermann L, Colombel JF, et al. Risankizumab for Ulcerative Colitis: Two Randomized Clinical Trials. JAMA. 2024 Sep 17;332(11):881–97.
2. D’Haens G, Dubinsky M, Kobayashi T, Irving PM, Howaldt S, Pokrotnieks J, et al. Mirikizumab as Induction and Maintenance Therapy for Ulcerative Colitis. N Engl J Med. 2023 Jun 29;388(26):2444–55.
3. Rubin DT, Allegretti JR, Panés J, Shipitofsky N, Yarandi SS, Huang KHG, et al. Guselkumab in patients with moderately to severely active ulcerative colitis (QUASAR): phase 3 double-blind, randomised, placebo-controlled induction and maintenance studies. Lancet. 2024 Dec 17;S0140-6736(24)01927-5.
4. Peyrin-Biroulet L, Allegretti JR, Rubin DT, Bressler B, Germinaro M, Huang KHG, et al. Guselkumab in Patients With Moderately to Severely Active Ulcerative Colitis: QUASAR Phase 2b Induction Study. Gastroenterology. 2023 Dec;165(6):1443–57.
5. Sandborn WJ, Ferrante M, Bhandari BR, Berliba E, Feagan BG, Hibi T, et al. Efficacy and Safety of Mirikizumab in a Randomized Phase 2 Study of Patients With Ulcerative Colitis. Gastroenterology. 2020 Feb;158(3):537-549.e10.
6. Sands BE, Sandborn WJ, Panaccione R, O’Brien CD, Zhang H, Johanns J, et al. Ustekinumab as Induction and Maintenance Therapy for Ulcerative Colitis. N Engl J Med. 2019 Sep 26;381(13):1201–14.

Introduction

For patients with Crohn’s disease (CD), endoscopic healing is an important long-term treatment goal per STRIDE-II consensus recommendations.¹ In this post hoc analysis, the relationships between endoscopic healing and long-term clinical outcomes were assessed in risankizumab (RZB)-treated patients with moderate to severe CD who previously failed tumor necrosis factor antagonist therapy from the phase 3 SEQUENCE trial.²

Aims & Methods

This analysis included RZB-treated patients who completed the week 48 visit in Part 1 of SEQUENCE (NCT04524611) and continued to receive RZB maintenance therapy during Part 2 of the trial. Part 2 is an ongoing open-label extension (OLE) wherein patients who received RZB induction and maintenance treatment during Part 1 could continue to receive RZB (subcutaneous 360mg every 8 weeks up to an additional 220 weeks). All patients in this post hoc analysis completed 100 weeks of RZB treatment (48 weeks in Part 1 and 52 weeks in Part 2). The proportion of patients who achieved week 100 (Part 2) clinical outcomes (including CD activity index [CDAI] response and remission, steroid-free CDAI clinical remission, and normalized fecal calprotectin [FCP] levels) were compared based on week 48 achievement of endoscopic response vs not, endoscopic remission vs not, and steroid-free endoscopic remission vs not (endpoint definitions in Table footnote), using chi-square testing. Patients with missing outcomes were imputed as nonresponders. Endoscopies were scored by a central reviewer. Long-term safety assessments for RZB have been reported elsewhere.³

Results

Of the 224 patients included in the analysis, 114 (50.9%), 80 (35.7%), and 80 (35.7%) patients achieved week 48 endoscopic response, endoscopic remission, and steroid-free endoscopic remission, respectively. A significantly greater proportion of patients who achieved week 48 endoscopic response also achieved week 100 CDAI remission and response, steroid-free CDAI clinical remission, and normalized FCP levels compared to patients who did not achieve week 48 endoscopic response (P≤.05 for all comparisons) (Table). Similar results were observed for patients who achieved week 48 endoscopic remission or steroid-free endoscopic remission (P≤.05 for all endpoints except for CDAI clinical response).

Conclusion

Results from this post hoc analysis of data from SEQUENCE demonstrated that achieving week 48 endoscopic outcomes was associated with sustained clinical improvements after 2 years of RZB treatment.

References

1. Turner D, et al. Gastroenterology. 2021 Apr;160(5):1570–83.
2. Peyrin-Biroulet L, et al. N Engl J Med. 2024 Jul 18;391(3):213–23.
3. Peyrin-Biroulet L, et al. J Crohns Colitis. 2025 Jan 22;19(Supplement_1):i1405–7.

Disclosure

Disclosures
Vipul Jairath has received has received consulting/advisory board fees from AbbVie, Alimentiv Inc, Arena Pharmaceuticals, Asahi Kasei Pharma, Asieris, Astra Zeneca, Bristol Myers Squibb, Celltrion, Eli Lilly, Ferring, Flagship Pioneering, Fresenius Kabi, Galapagos, GlaxoSmithKline, Genentech, Gilead, Janssen, Merck, Mylan, Pandion, Pendopharm, Pfizer, Protagonist, Reistone Biopharma, Roche, Sandoz, Second Genome, Takeda, Teva, Topivert, Ventyx, and Vividion; and speaker’s fees from, AbbVie, Ferring, Galapagos, Janssen Pfizer Shire, Takeda, and Fresenius Kabi.
Christopher Ma has received consulting fees from AbbVie, Alimentiv, Amgen, AVIR Pharma Inc, Bristol Myers Squibb, Celltrion, Eli Lilly, Ferring, Fresenius Kabi, Janssen, McKesson, Mylan, Pendopharm, Pfizer, Prometheus Biosciences Inc., Roche, Sanofi, Takeda, Tillotts Pharma; speaker's fees from AbbVie, Amgen, AVIR Pharma Inc, Alimentiv, Bristol Myers Squibb, Eli Lilly, Ferring, Fresenius Kabi, Janssen, Organon, Pendopharm, Pfizer, Sanofi, Takeda, Tillotts Pharma; royalties from Springer Publishing; research support from AbbVie, Ferring, Pfizer.
Peter Bossuyt received financial support for research from AbbVie, Amgen, Celltrion, Mylan, Pfizer, and Takeda; lecture fees from AbbVie, Celltrion, Janssen, Lilly, and Takeda; and advisory board fees from AbbVie, Arena Pharmaceuticals, BMS, Celltrion, Dr Falk, Galapagos, Janssen, Lilly, Pentax, PSI-CRO, Roche, Takeda, and Tetrameros.
Brian G Feagan has served as a consultant or received speaker’s fees from Abbott/AbbVie, ActoGeniX, Akros, Albireo Pharma, Amgen, AstraZeneca, Avaxia Biologics, Avir Pharma, Axcan, Baxter Healthcare, Biogen, Boehringer Ingelheim, Bristol Myers Squibb, Calypso Biotech, Celgene, Elan/Biogen, enGene, Ferring Pharmaceuticals, gIcare Pharma, Gilead, Given Imaging, GSK, Ironwood Pharmaceuticals, Janssen Biotech (Centocor), Johnson & Johnson/Janssen, Kyowa Hakko Kirin Co, Lexicon, Lilly, Lycera, Merck, Mesoblast, Millennium, Nektar, Nestlé, Novartis, Novo Nordisk, Pfizer, Prometheus Therapeutics and Diagnostics, Protagonist Therapeutics, Receptos, Roche/Genentech, Salix Pharmaceuticals, Serono, Shire, Sigmoid Pharma, Synergy Pharmaceuticals, Takeda, Teva Pharmaceuticals, TiGenix, Tillotts, UCB, Vertex Pharmaceuticals, VHsquared, Warner Chilcott, Wyeth, Zealand Pharma, and Zyngenia, and has received research support from Abbott/AbbVie, Amgen, AstraZeneca, Bristol Myers Squibb, Janssen Biotech (Centocor), Johnson & Johnson/Janssen, Millennium, Pfizer, Receptos, Roche/Genentech, Sanofi, Santarus, Tillotts, and UCB.
Namita Joshi, Nidhi Shukla, Kristina Kligys, Javier Zambrano, Toni Anschutz, and Brooke Kim are full-time employees/contractor of AbbVie and may own AbbVie stock or options.

Acknowledgments
AbbVie funded this study and participated in the study design, research, analysis, data collection, interpretation of data, reviewing, and approval of the abstract. All authors had access to relevant data and participated in the drafting, review, and approval of this abstract. No honoraria or payments were made for authorship. AbbVie and authors thank all the trial investigators and the patients who participated in this clinical trial.
Medical writing support was provided by Stephanie Parsons, PhD, an employee of AbbVie. Editorial support was provided by Amy Kuang, an employee of AbbVie.

Introduction

There is limited real-world evidence regarding the effectiveness and safety of risankizumab in patients with Crohn’s disease. This multicenter observational study aimed to evaluate the clinical outcomes of risankizumab in Crohn’s disease across several hospitals in Andalusia.

Aims & Methods

Clinical and biochemical data were ambvispectively collected from 160 patients who started risankizumab therapy at ten centers participating in the AIRIS-Crohn registry. Clinical remission (CR) was defined as a Harvey-Bradshaw Index (HBI) score below 5. Combined clinical and biochemical remission (CBR) required HBI <5, C-reactive protein (CRP) <5 mg/L, and fecal calprotectin <250 μg/g. Steroid-free remission (SFR) was defined as HBI <5 with no corticosteroid use from week 12 onward. Outcomes were assessed at weeks 12 and 24.

Results

A total of 160 patients were included, with a mean age of 50 years (range 19–84), and 48% were male. Ileal involvement was present in 49%, and upper gastrointestinal involvement in 6%. Extraintestinal manifestations were observed in 38%, and perianal disease in 56%. The average disease duration was 15 years, and 40% had a history of surgery. Patients had previously failed an average of 2.5 advanced therapies. At initiation, 3% were on immunomodulators and 30% on corticosteroids. At week 24, 89% remained on 360 mg every 8 weeks, 6% required dose intensification to every 6 weeks, and 5% to every 4 weeks.
At week 12, among 129 patients, 49% achieved CR (p<0.001) and 8% achieved CBR (p=0.041). At week 24, among 81 patients, 37% achieved CR (p<0.001), 3% achieved CBR (p=0.480), and 34% achieved SFR (p=0.007). The mean baseline HBI was 8, decreasing to 5.4 at week 12 and 6.1 at week 24 (p<0.001). Mean baseline fecal calprotectin was 1761 μg/g, decreasing to 1151 μg/g at week 12 and 1091 μg/g at week 24 (p<0.001). CRP levels also declined, though not significantly (from 12.9 mg/L at baseline to 8.4 mg/L at week 12 and 7.4 mg/L at week 24; p=0.407) (Table 1).
Patients with ≥2 prior advanced treatment failures showed significantly lower 6-month clinical remission (32.9% vs 64.3% in 1-failure group, p=0.029) and steroid-free remission rates (28.9% vs 64.3%, p=0.014).
Treatment discontinuation occurred in 12.5% of patients, primarily due to lack of response. Adverse events were reported in 5.6%, mainly cutaneous reactions, leading to discontinuation in five cases.

Table 1: Effectiveness Outcomes

Conclusion

Risankizumab demonstrated favorable effectiveness and safety in a cohort of highly refractory Crohn’s disease patients, with 88% maintaining therapy through follow-up. Composite remission rates remained low across all groups (<9%), highlighting the challenge of achieving combined clinical and biochemical targets in multirefractory CD. These results align with real-world evidence showing risankizumab maintains effectiveness in patients with multiple biologic failures, though response rates diminish with increasing treatment refractoriness.

Introduction

Risankizumab is an interleukin-23 inhibitor approved for the treatment of Crohn’s disease (CD). Its efficacy and safety have recently been demonstrated in trial-setting but there is yet limited evidence of its real-world effectiveness, especially on the middle- and long-term.

Aims & Methods

Using prospective data from the Dutch Initiative on Crohn and Colitis (ICC) Registry, we aimed to evaluate the effectiveness and adverse events of risankizumab in patients with difficult-to-treat CD, defined as the failure of advanced therapies with at least two different mechanisms of action¹. The primary endpoint was corticosteroid-free (CSF) clinical remission at week (W) 24. CSF clinical remission was defined as Harvey Bradshaw Index (HBI) ≤ 4 and no use of systemic corticosteroids at the time of the visit. As secondary outcomes, we examined clinical remission, biochemical remission (faecal calprotectin (FC) level ≤ 250μg/g) and combined clinical and biochemical remission at W24. Furthermore, remission rates between patients without history of bowel resection (i.e. surgery-naïve) and with bowel resection (i.e. surgery-experienced) at W24, drug survival and adverse events were assessed. Patients were included in the analysis if they received at least one intravenous dose of risankizumab before the 28^th of February 2025. Patients without available remission data at W24 and who remained on treatment were excluded from the W24 analysis population. Patients who discontinued treatment before W24 due to non-response, adverse events or loss to follow-up were considered non-responders.

Results

Eighty-five patients were included in the current analysis; 56 (65.9%) were female. Patients had a median disease duration of 16.0 years (IQR 14.0). Surgery history was available for 83 patients; 33 (39.8%) patients did not undergo surgery, while 50 (60.2%) were considered as surgery-experienced. At baseline, HBI was available for 72 patients; the median HBI was 6 (IQR 5); 24 (33.3%) patients had an HBI ≤ 4. Biochemical data were available for 19 (79.2%) patients in clinical remission: only one (5.3%) was in biochemical remission. At W24, HBI was available for 62 patients; 34 (54.8%) patients were in CSF clinical remission. Independent of CSF status, 62.9% (39/62) of the patients were in clinical remission. FC levels at W24 were available for 55 patients; 17 (30.9%) patients were in biochemical remission. Remission rates were not influenced by surgery history (Table 1). Over time, 16.5% (14/85) patients stopped risankizumab, after a median treatment duration of 182 days (IQR 188). Three (21.4%) patients discontinued risankizumab before W12, three (21.4%) between W12 and W24, and eight (57.2%) between W24 and W52. Reasons for discontinuation were non-response (42.9%), loss of response (42.9%) and adverse events (14.2%). A total of 83 adverse events were reported in 51 patients. Most common adverse events included respiratory infections (13.2%), skin problems (10.8%) and herpes zoster infections (8.4%). No hospitalisation or death were reported.

Conclusion

This prospective real-world study demonstrates the clinical effectiveness and the favourable safety profile of risankizumab at W24 in a difficult-to-treat Crohn’s disease population, including a high proportion of patients with bowel resection.

References

1. Parigi TL, D'Amico F, Abreu MT, Dignass A, Dotan I, Magro F, Griffiths AM, Jairath V, Iacucci M, Mantzaris GJ, O'Morain C, Reinisch W, Sachar DB, Turner D, Yamamoto T, Rubin DT, Peyrin-Biroulet L, Ghosh S, Danese S. Difficult-to-treat inflammatory bowel disease: results from an international consensus meeting. Lancet Gastroenterol Hepatol. 2023 Sep;8(9):853-859. doi: 10.1016/S2468-1253(23)00154-1. Epub 2023 Jul 6. PMID: 37423233.

Disclosure

LMMV - none FDMvS - adviser and/or speaker for Takeda, Galapagos, Dr. Falk, Lilly, and Janssen-Cilag; received an unrestricted grant from Takeda MRN - none ACdV - advisory boards for Takeda, Janssen, Bristol Myers Squibb, Abbvie, Pfizer, and Galapagos; research grants from Takeda, Janssen, and Pfizer AEvdMDJ - speaker fee from AbbVie, Alfasigma, Ferring, Janssen Pharmaceuticals, Takeda, Tramedico, and Vedanta; grants from Norgine, Cablon, Alfasigma, and ZonMW MCV - speaker fees from Janssen-Cilag, Galapagos, and Ferring B.V. WAvD - none WSN - none TER - none RLW - speaker fee from Abbvie, Ferring, and Pfizer BJ - none AGLB - none PV - speaker fee from Takeda, Abbvie, Janssen, Alfa Sigma, Lilly, and BMS BO - advisory boards of Takeda, BMS, Galapagos, Janssen, AbbVie, BMS, and Ferring; grants from Takeda, Pfizer, Galapagos, Ferring, Celltrion, BMS, and AbbVie ML - consultancy/lecture fees from AbbVie, Bristol Myers Squibb, Eli Lilly, Galapagos, Janssen-Cilag, Johnson & Johnson, Medtronic, Pfizer, Takeda, and Tillotts Pharma; grants from Alfasigma, the Netherlands Federation of University Medical Centres, TKI, and ZonMW JELS - none LAAPD - served on advisory boards as a speaker for Abbvie, Alfasigma, Janssen, and Pfizer; independent research funding from Pfizer HHF - none MJP - speaker fee from BMS, Janssen Cilag, and Takeda; non-restricted research grants from Horizon 2020, ZONMW (Dutch national research fund), MLDS, Takeda, Johnson and Johnson, Abbvie, and Galapagos MD - speaking fee from Bristol Meyers Squibb, Takeda, Galapagos, Janssen, and Dr. Falk; advisory board fees from Abbvie, Bristol Meyers Squibb, Celltrion, Galapagos/Alfasigma, Janssen, Takeda; grant/research support from Pfizer, Bristol Meyers Squibb, Galapagos Alfasigma, and Janssen ZM - speaker fee from Friso – Friesland Campina, Galapagos, Eli Lilly, and Takeda (paid to host institution); ; advisory board fees from Johnson & Johnson, Eli Lilly, Pfizer (paid to host institution); grants from ZonMw, Niels Stensen Fellowship, MLDS, Top consortium for Knowledge and Innovation (TKI), and Galapagos

Introduction

The comparable efficacy and safety of both IV and SC induction with guselkumab (GUS), a dual-acting IL-23p19 subunit inhibitor, in pts with moderately to severely active CD has been established in the phase 3 GALAXI and GRAVITI studies.^1,2,3 To determine whether pts with higher baseline disease severity respond differently to IV or SC induction, we compared the efficacy of GUS IV and SC induction in subgroups based on baseline disease characteristics.

Aims & Methods

Pts had moderately to severely active CD (CDAI 220-450 and SES-CD≥6 or if ileal disease only, SES-CD≥4), and a history of inadequate response/intolerance to oral corticosteroids, AZA/6-MP/MTX, or biologics. GUS induction regimen was 200mg IV q4w in GALAXI 2 & 3 (N=582) and 400mg SC q4w in GRAVITI (N=230), while matching IV/SC PBO q4w (N=148 and N=117, respectively) was the comparator regimen. Clinical remission (CDAI<150) and endoscopic response (≥50% improvement from baseline SES-CD) were evaluated at Wk12 for predefined subgroups based on baseline involved disease location, CDAI, SES-CD, C-reactive protein (CRP), and fecal calprotectin (FeCal). Abnormal CRP was defined as >3 mg/L and >5 mg/L for GALAXI and GRAVITI, respectively.

Results

GALAXI and GRAVITI had similar entry criteria, and baseline disease characteristics of the randomized study populations were also similar. Pts treated with IV or SC GUS induction achieved clinical remission at Wk12 in greater proportions than those who received PBO across subgroups of disease location (ileal only [IV: GUS=44%, PBO=13%; SC: GUS=56%, PBO=27%], colon only [IV: GUS=44% vs PBO=18%; SC: GUS=56% vs PBO=18%], and both ileum and colon [IV: GUS=52% vs PBO=24%; SC: GUS=57% vs PBO=22%]), baseline CDAI (≤300 [IV: GUS=52%, PBO=25%; SC: GUS=66%, PBO=26%] and >300 [IV: GUS=40% vs PBO=10%; SC: GUS=41% vs PBO=14%]), baseline SES-CD (≤12 [IV: GUS=43%, PBO=21%; SC: GUS=52%, PBO=24%] and >12 [IV: GUS=53% vs PBO=16%; SC: GUS=62% vs PBO=18%]), baseline CRP (≤3mg/L or ≤5mg/L in GALAXI and GRAVITI, respectively, [IV: GUS=45%, PBO=17%; SC: GUS=53%, PBO=28%] and >3mg/L or >5mg/L [IV: GUS=48% vs PBO=20%; SC: GUS=59% vs PBO=17%]), and baseline FeCal (≤250μg/g [IV: GUS=49%, PBO=25%; SC: GUS=60%, PBO=26%] and >250μg/g [IV: GUS=46% vs PBO=16%; SC: GUS=54% vs PBO=20%]). Endoscopic response at Wk12 was also achieved by greater proportions of GUS- than PBO-induced pts across all subgroups with either IV or SC induction (Table).

Table. Endoscopic Response at Week 12 by Baseline Disease Characteristics

Conclusion

Both IV and SC induction with GUS were similarly effective in pts with moderately to severely active CD across predefined subgroups of disease location and baseline clinical, endoscopic, and inflammatory biomarker disease activity. The treatment effects were consistent in the subgroups following IV and SC induction, particularly in those that represent high disease severity.

References

1. Sachen K, Hammaker D, Sarabia I, et al. Frontiers in Immunology. 2025: doi:10.3389/fimmu.2025.1532852.
2. Panaccione R, Danese S, Feagan BG, et al. Gastroenterology. 2024; 166(5): S1057b.
3. Hart A, Panaccione R, Steinwurz F, et al. Gastroenterology. 2025: doi:10.1053/j.gastro.2025.02.033.

Disclosure

BES reports consulting fees from Abbvie, Adiso Therapeutics, Agomab, Alimentiv , Amgen, AnaptysBio, Arena Pharmaceuticals, Artugen Therapeutics, Astra Zeneca, Biolojic Design, Biora Therapeutics, Boehringer Ingelheim, Boston Pharmaceuticals, Calibr, Celgene, Celltrion, ClostraBio, Equillium, Enthera, Enveda Biosciences, Evommune, Ferring, Fresenius Kabi, Fzatat, Galapagos, Genentech (Roche), Gilead Sciences, GlaxoSmithKline, Gossamer Bio, Imhotex, Index Pharmaceuticals, Innovation Pharmaceuticals, Inotrem, Kaleido, Kallyope, Merck, Microba, Mobius Care, Morphic Therapeutics, MRM Health, Nexus Therapeutics, Nimbus Discovery, Odyssey Therapeutics, Progenity, Prometheus Biosciences, Prometheus Laboratories, Protagonist Therapeutics, Q32 Bio, Rasayana Therapeutics, Recludix Therapeutics, Reistone Biopharma, Sanofi, Spyre Therapeutics, Sun Pharma, Surrozen, Target RWE,Teva, TLL Pharmaceutical, Tr1X, Union Therapeutics, Ventyx Biosciences; consulting and speaking fees from Abivax; consulting and speaking fees and other support from Lilly; research grants, consulting and speaking fees and other support from Bristol Myers Squibb, Janssen, Pfizer, Takeda; research grants and consulting fees from Theravance Biopharma; and stock/stock options from Ventyx Biopharma.
TH received grant support from Mitsubishi Tanabe Pharma Corporation, EA pharma Co. Ltd., AbbVie GK, JIMRO Co. Ltd., Zeria Pharmaceutical Co. Ltd., Kyorin Pharmaceutical Co. Ltd., Nippon Kayaku Co. Ltd., Takeda Pharmaceutical Co. Ltd., Pfizer Inc., Mochida Pharmaceutical Co. Ltd., Boston Scientific Corporation, Kissei Pharmaceutical Co. Ltd., consulting fees from Mitsubishi Tanabe Pharma Corporation, EA pharma Co. Ltd., AbbVie GK, Janssen Pharmaceutical K.K., Pfizer Inc., Nichi-Iko Pharmaceutical Co. Ltd., Eli Lilly, Gilead Sciences, Bristol Myers Squibb, and lecture fee from Mitsubishi Tanabe Pharma Corporation, AbbVie GK, EA pharma Co. Ltd., Kyorin Pharmaceutical Co. Ltd., JIMRO Co., Janssen Pharmaceutical K.K., Mochida Pharmaceutical Co., Ltd., Takeda Pharmaceutical Co. Ltd., Pfizer Inc. Kissei Pharmaceutical Co. Ltd.
AA reports potential conflicts of interest with AbbVie, Bristol Myers Squibb/Celgene, DiaSorin, Eli Lilly, Gilead, IBD Horizons, Janssen, Pfizer, Takeda, and TLL Pharmaceuticals.
NAT, MO, RVR, JY, and WvD are employees of Johnson & Johnson and own company stock/stock options.
AH served as a clinical investigator and consultant for Janssen.
SD reports consultancy fees from AbbVie, Alimentiv, Allergan, Amgen, AstraZeneca, Athos, Biogen, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Enthera, Ferring, Gilead, Hospira, Inotrem, Janssen, Johnson & Johnson, MSD, Mundipharma, Mylan, Pfizer, Roche, Sandoz, Sublimity, Takeda, TiGenix, UCB and Vifor; and reports lecture fees from AbbVie, Amgen, Ferring, Gilead, Janssen, Mylan, Pfizer and Takeda.
RP reports having received consulting fees from Abbivax, Abbott, AbbVie, Alimentiv (formerly Robarts), Amgen, Arena Pharmaceuticals, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Celltrion, Cosmos Pharmaceuticals, Eisai, Elan, Eli Lilly, Ferring,Fresenius Kabi, Galapagos, Genentech, Gilead Sciences, Glaxo-Smith Kline, JAMP Bio, Janssen, Merck, Mylan, Novartis, Oppilan Pharma, Organon, Pandion Pharma, Pendopharm, Pfizer, Progenity, Prometheus Biosciences, Protagonist Therapeutics, Roche, Sandoz, Satisfai Health, Shire, Sublimity Therapeutics, Takeda Pharmaceuticals, Theravance Biopharma, Trellus, Viatris, Ventyx, UCB; Speaker’s Fees from AbbVie, Amgen, Arena Pharmaceuticals, Bristol-Myers Squibb, Celgene, Eli Lilly, Ferring, Fresenius Kabi, Gilead Sciences, Janssen, Merck, Organon, Pfizer, Roche, Sandoz, Shire, Takeda Pharmaceuticals and served on Advisory Boards for: AbbVie, Alimentiv (formerly Robarts), Amgen, Arena Pharmaceuticals, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Eli Lilly, Ferring, Fresenius Kabi, Genentech, Gilead Sciences, Glaxo-Smith Kline, JAMP Bio, Janssen, Merck, Mylan, Novartis, Oppilan Pharma, Organon, Pandion Pharma, Pfizer, Progenity, Protagonist Therapeutics, Roche, Sandoz, Shire, Sublimity Therapeutics, Takeda Pharmaceuticals, and Ventyx.