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PRMT1 MEDIATED H4R3ME2A RECRUITS SFN TO PROMOTE GASTRIC CANCER PROGRESSION

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Introduction

It is of great significance to expand understanding of the development mechanism and improve the therapeutic effect of gastric cancer. The protein arginine methyl transferase 1 (PRMT1) catalyzing the asymmetric dimethylation of histone H4 on arginine 3 (H4R3me2a) and activating gene transcription, has been demonstrated to promote cancer development in various tumors. However, the expression and mechanism of PRMT1 in gastric cancer are still poorly understood.

Aims & Methods

Immunohistochemistry was performed on gastric cancer tissue chip to evaluate the expression situation of PRMT1 and its relationship with the prognosis of related patients. shPRMT1 lentivirus, SFN overexpression plasmids or deletion mutant PRMT1(PRMT1Δ, mutating the S-adenosylmethionine binding site) overexpression plasmids were used to interfere the expression of corresponding genes, and CCK8, EDU and transwell experiments were employed to evaluate the functional changes of gastric cancer cells on proliferation, metastasis and invasion. Pull down proteins of H4R3me2a antibody were detected by mass spectrometry, and validated with COIP experiments. Immunofluorescence (IF) and/or nucleocytoplasmic separation experiments were used to evaluate the cellular localization of H4R3me2a and SFN. RNA-seq was performed to detect the mRNA expression differences affected by knocking down PRMT1 or SFN. Western blot and qPCR were employed to verify gene expression changes on protein and mRNA levels.

Results

PRMT1 is significantly overexpressed in gastric cancer compared to adjacent tissues, and its high expression is closely related to poor prognosis. Knocking down PRMT1 could significantly inhibit the proliferation, migration, and invasion of gastric cancer cells, while overexpression of PRMT1Δ had similar effects. These results indicate that PRMT1 promotes the progression of gastric cancer in a methyltransferase activity dependent manner. The results of mass spectrometry of H4R3me2a antibody pull-down protein and further CoIP confirmed the binding relationship of SFN and H4R3me2a. The results of IF showed that SFN and H4R3me2a colocalized in the nucleus of gastric cancer cells, while the nuclear distribution of SFN was also found by the nucleoplasmic separation experiments. In terms of function, overexpression of SFN significantly enhanced the proliferation, migration, and invasion of gastric cancer cells, while simultaneous knocking down PRMT1 or overexpressing PRMT1Δ could reverse these effects. RNA-seq results showed that FOXQ1 was one of the common downstream target genes of PRMT1 and SFN, which was further proved by western bolt and qPCR. More significantly, PRMT1 inhibitor AMI-1could reverse the increase of FOXQ1 mRNA expression caused by SFN overexpression. These above results indicate that SFN is a main associated protein of H4R3me2a, and cooperates with PRMT1 to promote the progression of gastric cancer.

Conclusion

PRMT1 mediated H4R3me2a recruits SFN to co-regulate downstream target genes expression and promote gastric cancer progression.

PRMT1 MEDIATED H4R3ME2A RECRUITS SFN TO PROMOTE GASTRIC CANCER PROGRESSION

Hu Wang 1, HE NIE 2, Qinglin Zhang 3, Zhan Qiang 1

1 The Affiliated Wuxi People'S Hospital Of Nanjing Medical University, Wu Xi, China

2 The Affiliated Wuxi People'S Hospital Of Nanjing Medical University, Wu xi, China

3 Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, China

Event

UEG Week Copenhagen 2023

Topics

Digestive Oncology Mechanisms & Personalised Medicine Oesophagus Stomach & H. Pylori

Submission format

Abstract

Session

Molecular roadway to upper GI cancer

Citation

United European Gastroenterology Journal 2023; 11 (Supplement 8)

Published

2023

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Best of UEG Week - IBD with Bel Kok

Bel Klaartje Kok, Pradeep Mundre

Topics

IBD

Published

2025

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Best of UEG Week - IBD

Pradeep Mundre 1, Julia Mayerle 2, Tim Raine 3

1 Bradford Teaching Hospitals NHS trust, Leeds, United Kingdom

2 Klinikum der LMU München-Grosshadern, München, Germany

3 Cambridge University Hopsital NHS Foundation Trust, Cambridge, United Kingdom

Topics

IBD

Published

2023

UEG Podcast Episode

Journal Podcast

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Episode 1: UEG Journal May spotlight

Mohsan Subhani, Maria Manuela Estevinho

Published

2025

UEG Poster

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Introduction

Risankizumab (RZB) is a high-affinity humanised immunoglobulin (Ig) G1 monoclonal antibody that selectively binds to the p19 subunit of the interleukin-23 (IL-23) cytokine and inhibits its interaction with the IL-23 receptor.^1,2Long-term RZB therapy for 3 years of maintenance showed durable efficacy and a well-tolerated safety profile in patients with ulcerative colitis (UC) in the COMMAND open-label extension (OLE) study.^1,3This post hoc analysis evaluated the long-term efficacy of RZB in improving patient-reported outcomes through week (wk) 96 of the ongoing COMMAND OLE study.

Aims & Methods

COMMAND OLE is a 220-wk study enrolling patients who completed 52-wks maintenance dosing or enrolled directly as responders to induction.^1,3 This analysis included patients who completed 52 wks maintenance and an additional 96 wks of RZB treatment in the OLE. All patients received subcutaneous (SC) RZB180 Q8w starting at OLE wk 0, except patients who had prior rescue therapy (single RZB 1200 mg intravenous dose, then SC RZB360 Q8w) who continued RZB360 in the OLE. The OLE study was not designed to compare RZB180 and RZB360 groups. The data cut-off date for this interim analysis was 30 June 2024. Efficacy outcomes included the percentage of patients who achieved the absence of abdominal pain, bowel urgency, faecal incontinence, nocturnal bowel movements, tenesmus, sleep disruption due to UC symptoms; Inflammatory Bowel Disease Questionnaire (IBDQ) response; a meaningful within-person change (MWPC) in Functional Assessment of Chronic Illness Therapy (FACIT)-Fatigue, Short-Form Health Survey-36 version 2 Mental Component Score (SF-36v2 MCS), and SF-36v2 Physical Component Score (PCS). Results were reported using as-observed (AO; Table) and nonresponder imputation (NRI) methods (Table). Safety was reported previously.³

Results

Of the 1003 patients (RZB180 = 701; RZB360 = 302) who entered the OLE, 398 (39.7%) patients (RZB180 = 262; RZB360 = 136) completed wk 96 at data cut-off date. In the AO analysis, RZB180- or RZB360-treated patients showed sustained improvements from OLE wks 0 to 96 in the absence of abdominal pain, bowel urgency, nocturnal bowel movements, tenesmus, faecal incontinence, sleep disruption due to UC symptoms, IBDQ response, MWPC in FACIT-Fatigue, SF-36 PCSv2, and SF-36v2 MCS (Table). Using the more conservative NRI analysis, similar results were observed for most endpoints through OLE wk 96 (Table). Despite RZB360-treated patients were more likely to have numerically higher clinical and endoscopic activity at OLE wk 0 compared with RZB180-treated patients (Adapted Mayo Score [AMS], mean [standard deviation], RZB180, 2.0 [1.4]; RZB360, 3.5 [2.0]; endoscopic subscore: RZB180, 1.1 [1.0]; RZB360, 1.9 [1.0]; clinical remission per AMS, RZB180, 54.8%; RZB360, 24.8%), at OLE wk 96, both RZB dosing regimens exhibited consistent and similar sustained improvements throughout all investigated patient-reported outcomes.

Endpoint, (n/N) % [95% CI]^a	AO analysis^b		NRI analysis^c
Endpoint, (n/N) % [95% CI]^a	RZB 180 mg SC	RZB 360 mg SC	RZB 180 mg SC	RZB 360 mg SC
No abdominal pain^d Week 0 Week 96 No bowel urgency^d Week 0 Week 96 No nocturnal bowel movement^d Week 0 Week 96 No tenesmus^d Week 0 Week 96 No faecal incontinence^d Week 0 Week 96 No sleep disruptiondue to UC symptoms^d Week 0 Week 96	(441/701) 62.9 [59.3, 66.5] (129/180) 71.7 [65.1, 78.2] (504/701) 71.9 [68.6, 75.2] (129/180) 71.7 [65.1, 78.2] (499/552) 90.4 [87.9, 92.9] (166/179) 92.7 [88.9, 96.5] (423/552) 76.6 [73.1, 80.2] (154/179) 86.0 [81.0, 91.1] (495/549) 90.2 [87.7, 92.7] (160/171) 93.6 [89.9, 97.2] (486/549) 88.5 [85.9, 91.2] (155/171) 90.6 [86.3, 95.0]	(145/302) 48.0 [42.4, 53.6] (49/79) 62.0 [51.3, 72.7] (156/302) 51.7 [46.0, 57.3] (53/79) 67.1 [56.7, 77.5] (195/233) 83.7 [78.9, 88.4] (73/79) 92.4 [86.6, 98.2] (145/233) 62.2 [56.0, 68.5] (63/79) 79.7 [70.9, 88.6] (198/230) 86.1 [81.6, 90.6] (66/74) 89.2 [82.1, 96.3] (181/230) 78.7 [73.4, 84.0] (70/74) 94.6 [89.4, 99.7]	(162/262) 61.8 [55.9, 67.7] (129/262) 49.2 [43.2, 55.3] (175/262) 66.8 [61.1, 72.5] (129/262) 49.2 [43.2, 55.3] (108/262) 41.2 [35.3, 47.2] (166/262) 63.4 [57.5, 69.2] (92/262) 35.1 [29.3, 40.9] (154/262) 58.8 [52.8, 64.7] (100/262) 38.2 [32.3, 44.1] (160/262) 61.1 [55.2, 67.0] (104/262) 39.7 [33.8, 45.6] (155/262) 59.2 [53.2, 65.1]	(63/136) 46.3 [37.9, 54.7] (48/136) 35.3 [27.3, 43.3] (65/136) 47.8 [39.4, 56.2] (51/136) 37.5 [29.4, 45.6] (57/136) 41.9 [33.6, 50.2] (71/136) 52.2 [43.8, 60.6] (42/136) 30.9 [23.1, 38.6] (61/136) 44.9 [36.5, 53.2] (49/136) 36.0 [28.0, 44.1] (64/136) 47.1 [38.7, 55.4] (51/136) 37.5 [29.4, 45.6] (68/136) 50.0 [41.6, 58.4]
IBDQ response^e Week 0 Week 96	(629/689) 91.3 [89.2, 93.4] (182/191) 95.3 [92.3, 98.3]	(266/299) 89.0 [85.4, 92.5] (76/78) 97.4 [93.9, 100.9]	(238/262) 90.8 [87.3, 94.3] (182/262) 69.5 [63.9, 75.0]	(118/136) 86.8 [81.1, 92.5] (76/136) 55.9 [47.5, 64.2]
MWPC in FACIT-Fatigue^f Week 0 Week 96	(494/683) 72.3 [69.0, 75.7] (147/189) 77.8 [71.9, 83.7]	(227/298) 76.2 [71.3, 81.0] (63/77) 81.8 [73.2, 90.4]	(190/262) 72.5 [67.1, 77.9] (147/262) 56.1 [50.1, 62.1]	(105/136) 77.2 [70.2, 84.3] (63/136) 46.3 [37.9, 54.7]
MWPC in SF-36v2 PCS^g Week 0 Week 96 MWPC in SF-36v2 MCS^g Week 0 Week 96	(526/683) 77.0 [73.9, 80.2] (153/188) 81.4 [75.8, 86.9] (472/683) 69.1 [65.6, 72.6] (130/188) 69.2 [62.5, 75.8]	(228/298) 76.5 [71.7, 81.3] (65/77) 84.4 [76.3, 92.5] (197/298) 66.1 [60.7, 71.5] (52/77) 67.5 [57.1, 78.0]	(196/262) 74.8 [69.6, 80.1] (153/262) 58.4 [52.4, 64.4] (177/262) 67.6 [61.9, 73.2] (130/262) 49.6 [43.6, 55.7]	(107/136) 78.7 [71.8, 85.6] (65/136) 47.8 [39.4, 56.2] (87/136) 64.0 [55.9, 72.0] (52/136) 38.2 [30.1, 46.4]
Table. Patient-Reported Outcomes and Health-Related Quality of Life Efficacy Analysis From the COMMAND Open-Label Extension Study. AO, As-observed; CI, confidence interval; FACIT-Fatigue, Functional Assessment of Chronic Illness Therapy-Fatigue, IBDQ, inflammatory bowel disease questionnaire; IV, intravenous; MCS, Mental Component Score; MWPC, meaningful within-person change; NRI, nonresponder imputation; OLE, open-label extension; PCS, Physical Component Score; RZB, risankizumab; SC, subcutaneous; SF-36v2, Short-Form Health Survey-36 version 2; SS, substudy. Efficacy analysis included patients who entered the OLE from SS1 and SS2 and received at least 1 dose of study drug. Analysis included patients who received RZB 180 mg starting at OLE week 0, and patients who had prior rescue therapy (single RZB 1200 mg IV dose, then 360 mg SC Q8w) during SS1 and SS2 and continued with RZB 360 mg in OLE. The data cut-off date was 30 June 2024. Week 0 was defined as the entry of the OLE period, based on the last nonmissing value prior to the first dose of study drug in the OLE. ^a95% CI for response rate was based on the normal approximation to the binomial distribution. ^bData after rescue therapy during the OLE was excluded. ^cMissing data or patients who received rescue therapy during the OLE were imputed as nonresponders. ^dQuantified as the percent of patients who achieved the absence of each symptom. ^eIncrease in IBDQ score ≥ 16 points from baseline of induction. ^fIncrease in FACIT-Fatigue ≥ 5 points from baseline of induction. ^gIncrease in SF-36v2 PCS/MCS ≥ 4.1 point from baseline of induction.

Conclusion

RZB-treated patients who completed OLE wk 96 (3 years of total maintenance therapy) experienced sustained improvement in quality of life and patient-reported outcomes.

References

Louis E, et al. JAMA. 2024; 332:881-97.
Singh S, et al. mAbs. 2015;7:778-91.
Atreya R, et al. J Crohn’s Colitis. 2025;19(S1):i108-i110 [Abstract].

Disclosure

Funding: AbbVie funded this study (COMMAND; NCT03398135) and participated in the study design, research, analysis, data collection, interpretation of data, reviewing, and approval of the publication. All authors had access to relevant data and participated in the drafting, review, and approval of this publication. No honoraria or payments were made for authorship.
Acknowledgments: AbbVie and the authors thank the participants, study sites, and investigators who participated in this clinical trial. Paulette A. Krishack, PhD, of AbbVie, provided medical writing support; S. Michael Austin, of AbbVie, provided editorial support.
Disclosures: Luc Biedermann has received lecture and consulting fees from Takeda, Sanofi, AbbVie, Falk, Bristol Myer Squibb, and Pfizer and is on advisory boards for AbbVie, Amgen, Bristol Myers Squibb, Falk, Janssen, Pfizer, Takeda, and Sanofi.
Julian Panés received consultancy fees/honorarium from AbbVie, Alimentiv, Athos, Atomwise, Boehringer Ingelheim, Celsius, Ferring, Galapagos, Genentech/Roche, GlaxoSmithKline, Janssen, Mirum, Nimbus, Pfizer, Progenity, Prometheus, Protagonist, Revolo, Sanofi, Sorriso, Surrozen, Takeda, and Wasserman, and has served on a data safety monitoring board for Alimentiv, Mirum, Sorriso, Sanofi, and Surrozen.
Silvio Danese has received consultancy fees from AbbVie, Allergan, Amgen, AstraZeneca, Biogen, Boehringer Ingelheim, Celgene, Celltrion, Enthera, Ferring, Gilead, Hospira, Janssen, Johnson & Johnson, Lilly, Merck Sharp and Dohme, Mundipharma, Mylan, Pfizer, Roche, Sandoz, Sublimity Therapeutics, Takeda, TiGenix, UCB and Vifor.
Satoshi Tanida received speaker fees from JIMRO, Mitsubishi Tanabe Pharma, AbbVie, Janssen, Kissei, writing fees from Pfizer, and research funding from AbbVie.
Parambir S. Dulai received research support and/or consulting for AbbVie, Abivax, Adiso, Alimentiv, Bristol Meyer Squibb, Celltrion, Genentech/Roche, Geneoscopy, Janssen, Pfizer, Takeda.
Nidhi Shukla, Jasmina Kalabic, Pierre Morisset, Cecile Holweg, and Dolly Sharma, are employees of AbbVie and may own stock options.
Joana Torres has received grant funding/speaker fees from and/or has participated in advisory boards for AbbVie, Galapagos, Janssen, and Pfizer.

SUSTAINED IMPROVEMENT IN PATIENT-REPORTED OUTCOMES WITH LONG-TERM RISANKIZUMAB TREATMENT IN PATIENTS WITH MODERATELY TO SEVERELY ACTIVE ULCERATIVE COLITIS: INTERIM 2-YEAR RESULTS FROM THE PHASE 3 COMMAND OPEN-LABEL EXTENSION STUDY

Luc Biedermann 1, Julian Panés 2, Silvio Danese 3, Satoshi Tanida 4, Parambir Dulai 5, Nidhi Shukla 6, Jasmina Kalabic 7, Pierre Morisset 6, Cecile Holweg 6, Dolly Sharma 6, Joana Torres 8

1 USZ Zürich, Zürich, Switzerland

2 Hospital Clínic Barcelona, Barcelona, Spain

3 Vita-Salute San Raffaele University - IRCCS San Raffaele Scientific Institute, Milan, Italy

4 Gamagori City Hospital, Nagoya, Japan

5 Northwestern University, Chicago, United States

6 AbbVie, North Chicago, United States

7 AbbVie Deutschland GmbH Co. KG, Ludwigshafen am Rhein, Germany

8 Hospital Beatriz Ângelo & Hospital da Luz, Lisbon, Portugal

Conference

UEG Week Berlin 2025

Topics

IBD

Submission format

Abstract

Session

Patient-reported outcome and quality of life in IBD (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Anti-TNF failure in ulcerative colitis

Ailsa L Hart 1

1 St Mark’s Hospital and Academic Institute, Harrow, United Kingdom

Event

UEG Postgraduate Teaching Programme Vienna 2024

Topics

Education & Training IBD Immunology Mechanisms & Personalised Medicine Surgery

Session

Decision time in IBD: Difficult cases

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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Introduction

Upadacitinib (UPA) is an oral, reversible Janus kinase inhibitor (JAKi) approved for the treatment of patients with moderate-to-severe ulcerative colitis (UC).^1-2Despite substantial evidence from clinical trials supporting the use of UPA for treating UC, real-world (RW) data on its effectiveness and safety remain limited.³ The Prospective Real-World Study of UPA in UC (PROFUNDUS) is an ongoing multi-country, open-label, noninterventional, observational study aimed to evaluate the effectiveness and safety of UPA in patients with moderate-to-severe UC in RW practice (initiated 15 Aug 2022).

Aims & Methods

PROFUNDUS recruited 785 adult patients (18 to 75 years [yrs] of age) with moderate-to-severe UC initiating UPA in 16 countries worldwide. UPA was administered in accordance with the terms of the local marketing authorization, with patient treatment determined by the investigator, and patients followed for up to 3 yrs (156 weeks [wk]). This analysis represents data available after the first 500 patients completed 6 months of treatment or discontinued before 6 months, with a data cut-off of 28 Feb 2025. Of the first 500 patients who provided informed consent and met the inclusion criteria, the full analysis set (FAS) included 490 patients who initiated a once-daily UPA dosing regimen. This analysis reported baseline demographics and disease characteristics among FAS; the time to achievement of first clinical response per daily Partial Adapted Mayo Score (pAMS) and the percentage of patients achieving clinical response per pAMS at the end of UPA induction (wk 8) or extended induction (wk 16) were reported among evaluable patients who took at least 1 dose of UPA and had available scores to define the outcomes, a subset of FAS. Safety outcomes were analysed through week 26 (6 months), with treatment-emergent adverse events (TEAEs) presented as patient numbers and percentages.

Results

Among FAS, the patient age range was 18 to 79 yrs; 43.3% were female. At baseline (defined as the last available assessment on or before the first dose date of UPA), pAMS were as follows: < 2: 26.5%; 2-4: 48.1%; > 4-5: 18.8%; > 5-6: 6.6%; with score 0 indicative of inactive disease, while a score of 6 indicates active disease and spontaneous bleeding.⁴ At baseline, 51.3% of patients had a history of intolerance or inadequate response (IR) to advanced therapies (AT-IR), with 13.1% of patients who failed ≥ 1 JAKi. Among evaluable patients, the median (IQR) time to achieve the first clinical response per daily pAMS was 4 (3.0-8.0) days (N = 373; Table). By the end of induction treatment (wk 8 or 16), 79.6% (258/324) of the evaluable UPA-treated patients achieved clinical response per pAMS (Table). Among UPA-treated patients, the occurrence rates of any treatment-emergent adverse events (TEAEs) and TEAEs possibly related to the study treatment were as follows: any adverse event (AE) (51.2%; 34.9%), serious AEs (5.5%; 2.2%), and severe AEs (5.1%; 2.2%) (Table).

Effectiveness^a	Any UPA dose
Time to first achievement^b of clinical response per Daily pAMS^b Events analysed – n/N (%) Median (IQR), days Clinical response per pAMS^c at week 8 or 16 of induction, n/N (%) [95% CI]	364/373 (97.6) 4.0 (3.0-8.0) 258/324 (79.6) [75.2, 84.0]
Overall TEAEs, Week 26 of Therapy,^d n (%) Any AE AE with a reasonable possibility of being related to study treatment^e Severe TEAE Serious TEAE AE leading to discontinuation of the study drug AE resulting in death^f	Any UPA dose (N = 490) 251 (51.2) 171 (34.9) 25 (5.1) 27 (5.5) 34 (6.9) 1 (0.2)
Overview of TEAEs With Reasonable Possibility of Being Related to Study Treatment Through Week 26,^dn (%) Any AE^e Severe TEAE Serious TEAE AE leading to discontinuation of the study drug AE resulting in death	Any UPA dose (N = 490) 171 (34.9) 11 (2.2) 11 (2.2) 24 (4.9) 0
Table. Summary of PROFUNDUS Interim Effectiveness and Safety Results. FAS, full analysis set; IQR, interquartile range; pAMS, partial Adapted Mayo Score; RBS, rectal bleeding score; SF, stool frequency; TEAE, treatment-emergent adverse event; UPA, upadacitinib. ^aEffectiveness population included evaluable patients who took at least 1 dose of UPA and had available diary scores to define the corresponding outcome among the first 500 patients who provided informed consent and satisfied eligibility criteria. Patients who discontinued due to lack of effectiveness or intolerability were categorised as nonresponders, while those who discontinued due to other reasons were treated as missing data for the responder outcome and censored for the time-to-event outcome. ^bDefined as a decrease in daily pAMS ≥ 1 point and ≥ 30% from baseline, in addition to a decrease in daily RBS ≥ 1 or a daily RBS ≤ 1. Time to first achievement was based on the difference in time between the date of first achievement and first dose of UPA. Only patients with baseline daily pAMS > 0 with at least one post-baseline score are included. If a patient never achieved this outcome within 183 days (week 26), then that patient's time to first achievement was censored at day 183 (week 26), UPA discontinuation, study discontinuation, or cut-off date, whichever comes earlier. Kaplan-Meier nonparametric estimates were reported. ^cDefined as a decrease from baseline in pAMS ≥ 1 point and ≥ 30%, in addition to a decrease from baseline in the RBS ≥ 1 or absolute RBS ≤ 1. Patients with baseline score ≥1 and available score at end of induction are included. ^dIncluded patients with at least 1 dose of UPA among the first 500 patients who provided informed consent and satisfied eligibility criteria. Included events within 26 weeks (183 days) of starting study treatment. ^eAs assessed by study investigator. ^fThere was 1 death due to drowning that was determined to have no reasonable possibility of being related to the study drug. Data cut-off date was 28 Feb 2025.

Conclusion

In this interim analysis of the PROFUNDUS study, UPA demonstrated rapid effectiveness in achieving clinical response in patients with moderate-to-severe UC in RW practice, in a wide variety of age ranges, consistent with the efficacy observed in the UPA UC clinical trials.¹ Overall, UPA was well-tolerated, with few serious AEs reported, and most of these were assessed as unrelated to UPA by the investigator.

References

AbbVie Inc. RINVOQ (Upadacitinib) [package insert] U.S. Food and Drug Administration website. https://www.rxabbvie.com/pdf/rinvoq_pi.pdf. Revised May 2023. Accessed 25 Feb 2025.
AbbVie DG& CoK. RINVOQ. Summary of Product Characteristics. European Medicine Agency website. https://www.ema.europa.eu/en/documents/product-information/rinvoq-epar-product-information_en.pdf. Revised Feb 2025. Accessed 25 Feb 2025.
Seidelin J, et al. J Crohn’s Colitis. 2025;19(1):i1260-i1262. [Abstract].
Louis E, et al. JAMA. 2024;332(11):881-897.

Disclosure

Funding: AbbVie funded this study (PROFUNDUS; NCT05494606) and participated in the study design, research, analysis, data collection, interpretation of data, reviewing, and approval of the publication. All authors had access to relevant data and participated in the drafting, review, and approval of this publication. No honoraria or payments were made for authorship.
Acknowledgments: AbbVie and the authors thank the participants, study sites, and investigators who participated in this clinical trial. Paulette A. Krishack, PhD, of AbbVie, provided medical writing support.
Disclosures: Remo Panaccione has received consulting fees, speaker fees, and research support from Abbott, AbbVie, Abbivax, Alimentiv Amgen, AnaptysBio, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene Corporation, Celltrion, Cosmos Pharmaceuticals, Eisai, Elan, Eli Lilly, Ferring Pharmaceuticals, Galapagos, Fresenius Kabi, Genentech, Gilead Sciences, GlaxoSmithKline, JAMP Bio, Janssen Pharmaceuticals, Merck, Mylan, Novartis, Oppilan Pharma, Organon, Pandion Pharma, Pendopharm, Pfizer, Progenity, Prometheus Biosciences, Protagonist Therapeutics, Roche, Sandoz, Sanofi, Satisfai Health, Sublimity Therapeutics, Takeda Pharmaceuticals, Theravance Biopharma, Trellus, Viatris, Ventyx, and UCB.
Gareth Parkesreports personal payments, honoraria, speaker fees, travel grants and/or fellowships from AbbVie, Allergan, Bristol Myers Squibb, Celltrion, Ferring, Galapagos, Janssen, Napp, Takeda, and Tillotts, and directorship and shareholding with Ampersand Health. TR reports personal grants from AbbVie; personal consulting fees from AbbVie, Arena, Aslan, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Ferring, Galapagos, Gilead, GSK, Heptares, LabGenius, Janssen, MonteRosa, Mylan, MSD, Novartis, Numab, Pfizer, Roche, Sandoz, Takeda, UCB and XAP; membership of the ECCO Scientific Committee, and membership in the UEG Scientific Committee; director of Endoread.
Mathurin Fumery has received lecture and consulting fees from AbbVie, Amgen, Biogen, BI, BMS, Celgene, Celltrion, CTMA, Ferring, Fresenius, Galapagos, Gilead, Janssen, Pfizer, Lilly, MSD, Sandoz, Takeda, Tillots, and Viatris.
Dominik Bettenworth is on the advisory board or consultant for Amgen, AbbVie, Dr. Falk Foundation, Ferring, MSD, Pfizer, Pharmacosmos, Roche, Takeda, Tillotts Pharma, and Vifor. Silvio Danese has served as a speaker, consultant, and advisory board member for Schering-Plough, AbbVie, Actelion, Alphawasserman, AstraZeneca, Cellerix, Cosmo Pharmaceuticals, Ferring, Genentech, Grünenthal, Johnson and Johnson, Millenium Takeda, MSD, Nikkiso Europe GmbH, Novo Nordisk, Nycomed, Pfizer, Pharmacosmos, UCB Pharma and Vifor.
Pierre A Morisset, Madhuja Mallick, Shirley H. Chen, and Smitha Suravaram are employees of AbbVie and may own stock options.

REAL-WORLD EFFECTIVENESS AND SAFETY IN UPADACITINIB-TREATED PATIENTS WITH MODERATE-TO-SEVERE ULCERATIVE COLITIS: INTERIM RESULTS FROM THE PROFUNDUS STUDY

Remo Panaccione 1, Gareth Parkes 2, Mathurin Fumery 3, Dominik Bettenworth 4, Pierre Morisset 5, Madhuja Mallick 5, Shirley H. Chen 5, Smitha Suravaram 5

1 University of Calgary, Calgary, Canada

2 The Royal London Hospital, London, United Kingdom

3 Amiens University Hospital, Amiens, France

4 University of Munster, Munster, Germany

5 AbbVie, North Chicago, United States

Conference

UEG Week Berlin 2025

Topics

IBD

Submission format

Abstract

Session

Real-world evidence in ulcerative colitis (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG's educational platform for gastroenterology education bringing recordings, courses, guidelines, and more together in one place.

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