Introduction

The incidence of colorectal neuroendocrine tumors (NETs) has increased over the past decades with early detection during screening colonoscopy.^1,2 The C-NET STUDY is a Japanese multicenter prospective cohort study, in which patients with colorectal NETs were consecutively enrolled.³

Aims & Methods

The study aimed to evaluate the short-term outcomes of various methods of endoscopic resection for colorectal NETs. Among the C-NET STUDY registrants, patients with colorectal NETs who underwent endoscopic treatment as the initial therapy were included. Patients who received treatment at a previous institution before participating in this study, biopsy diagnosed but the resected lesion was not pathologically diagnosed as NET, and who had defective data were excluded. The study protocol stated that endoscopic treatment should be performed if the tumor size is <10 mm in depth from the mucosa to the submucosa, with no ulceration or depression on the surface. For lesions with no treatment consensus in various guidelines, treatment selection was determined by each physician according to their policy in clinical practice. With respect to endoscopic resection procedures, several techniques were available in clinical practice, including endoscopic mucosal resection with a ligation device (ESMR-L), endoscopic mucosal resection using a cap (EMR-C), and endoscopic submucosal dissection (ESD). The major outcome measurements were short-term treatment outcomes, including en bloc resection rate, complete resection (defined as en bloc resection with tumor-free margin (R0)) rate, need for hospitalization, and treatment-related complications based on treatment modalities. Clinicopathological risk factors of incomplete resection (R1/RX) was also examined.

Results

A total of 472 patients with 477 colorectal NETs received endoscopic treatment. Of these, 418 patients with 421 lesions, who met the eligibility criteria, were included in the analysis. The median patient age was 55 years, and 56.9% of the patients were male. The lower rectum was the most common site (88.6%), and lesions <10 mm accounted for 87% of the cases. Among all cases, en bloc resection and R0 resection were achieved in 421 (100%) and 398 (94.5%) lesions. A total of 267 (63.4%) patients required hospitalization for treatment, with a median hospital stay of 3 days. Endoscopic mucosal resection with a ligation device (ESMR-L, 56.5%) was the most common method, followed by endoscopic submucosal dissection (ESD, 31.4%) and endoscopic mucosal resection using a cap (EMR-C, 8.5%). R0 resection rates <10 mm were 95.5%, 94.8 %, and 94.3% for ESMR-L, ESD, and EMR-C, respectively. All the treatment-related complications observed in 16 (3.8%) patients were treated conservatively. There were no independent clinicopathological risk factors for R1/X resection.

Conclusion

ESMR-L, ESD, and EMR-C were equally effective and safe techniques for colorectal NETs with diameter <10 mm (UMIN000025215).

References

1. Kooyker AI, Verbeek WH, van den Berg JG, et al. Change in incidence, characteristics and management of colorectal neuroendocrine tumours in the Netherlands in the last decade. United European Gastroenterol J 2020;8:59-67.
2. Ito T, Igarashi H, Nakamura K, et al. Epidemiological trends of pancreatic and gastrointestinal neuroendocrine tumors in Japan: a nationwide survey analysis. J Gastroenterol 2015;50:58-64.
3. Sekiguchi M, Hotta K, Takeuchi Y, et al. Characteristics of colorectal neuroendocrine tumors in patients prospectively enrolled in a Japanese multicenter study: a first report from the C-NET STUDY. J Gastroenterol 2022; 57: 547-558.

Introduction

Infection is the main cause of decompensation in liver cirrhosis (LC) and contributes to high mortality. Infection by multidrug-resistant microorganisms (MDRO) is becoming increasingly prevalent, and there is evidence that it reduces survival in LC.

Aims & Methods

A 6-year retrospective analysis was carried out on a cohort of patients with LC admitted due to infection between October 2017 and March 2018. MDRO was defined as resistance to at least 3 antibiotic classes. The survival time in weeks from the date of MDRO isolation or date of hospitalization to the date of death was evaluated. SPSS was used to reproduce Kaplan-Meier (KM) survival curves.

Results

31 patients were included, 17 of whom had MDRO isolation vs. 14 without MDRO isolation (N-MDRO) during the 2017-2018 period. After the analysis period, 30 patients had died. A lower survival rate was observed in patients with MDRO isolation, with a mean survival rate of 37.9 weeks vs. 61.5 weeks for N-MDRO, although without statistical significance (p=0.7). From the subgroup analyses carried out, there was also a statistically non-significant lower average survival in the MDRO group: analyzing patients without a diagnosis of hepatocellular carcinoma (23 patients), there was an average survival of 47.9 weeks in the MDRO (12 patients) vs 75.7 weeks in the N-MDRO group (p=0.74); and in the subgroup with Child Pugh <C (12 patients), there was an average survival of 29.6 weeks in the MDRO (9 patients) vs 110.6 weeks in the N-MDRO group (p=0.18).

Conclusion

The results of this cohort, although not statistically significant, suggest that MDRO infection has an impact on the decreased survival of patients with LC, particularly in patients who would expect a longer survival.

References

Kaplan Meier curves of survival will be presented.

Introduction

Both vedolizumab and ustekinumab can be considered for the treatment of ulcerative colitis (UC) but head-to-head trials are lacking. We aimed to compare the effectiveness of vedolizumab and ustekinumab after anti-TNF failure in UC patients.

Aims & Methods

All consecutive patients with UC treated with ustekinumab or vedolizumab after being exposed to at least one anti-TNF in 10 French centers between January 2019 and August 2022 were included retrospectively. The primary endpoint was clinical remission (Mayo score partial ≤ 2) without corticosteroid (SFCR) at week 16 (W16). Secondary endpoints were endoscopic remission (SFCR and endoscopic Mayo score ≤ 1 or fecal calprotectin < 150 µg/g), and histological healing (endoscopic remission and histological (Nancy index ≤ 1)). All the comparisons were performed using propensity score analyses (inverse probability of treatment weighting) adjusted for age, gender, smoking status, disease duration and extension, number of prior biologics or prior primary failure to biologics, the co-prescription of 5-ASA, corticosteroids or immunosuppressants, and disease severity.

Results

Among a total of 316 patients included, 165 and 151 received ustekinumab and vedolizumab, respectively. Baseline characteristics (gender, age, disease location, co-prescription of 5-ASA or corticosteroids) were similar between the two groups except for disease duration (ustekinumab, 9.3 vs vedolizumab 7.2 year; p=0.003), co-immunosuppressants (5.4% vs 20.5%, <0.001), and prior exposition to > 2 biologics (46.6% vs 5.9%, p<0.001). At W16, SFCR was respectively 40.3% and by 37.9% in the ustekinumab and vedolizumab groups (aOR = 1.10 [0.39-3.12], p=0.085). SFCR rates were 62.2% vs 53.2% (p=0.52) after one failure, 33.7% vs 44.3% (p=0.52) after two biologics and 19.1% vs 2.6% (p=0.03) after 3 biologics failure, in the ustekinumab and vedolizumab groups, respectively.
Endoscopic remission and histologic healing rates at week 16 were respectively of 17.5% vs 5.3% (aOR = 3.77 [1.25-11.36], p=0.018) and 11.1% vs 2.1% (aOR = 5.85 [1.47-23.30], p=0.012) in the groups ustekinumab and vedolizumab.

Conclusion

While no difference in terms of clinical remission was observed, ustekinumab appears to be more effective than vedolizumab to induce endoscopic and histological remission after failure of anti-TNFs in UC.

Disclosure

AbbVie, Ferring, Janssen, MSD, Takeda, Pfizer, Celgene, Biogen, Amgen, Boehringer Ingelheim, Hospira et Celltrion

Introduction

Filgotinib (FIL) is a once-daily, oral, Janus 1 kinase preferential inhibitor approved for the treatment of ulcerative colitis (UC) in Europe and Japan. The efficacy and safety of FIL in patients with moderately to severely active UC was evaluated in the phase 2b/3 randomized, double-blind, placebo (PBO)-controlled SELECTION study (NCT02914522).¹

Aims & Methods

This post hoc analysis aimed to identify characteristics of FIL-treated patients that were associated with achieving corticosteroid (CS)-free remission. Adults aged 18–75 years were randomized 2:2:1 to induction FIL 100 mg, FIL 200 mg or PBO once daily for 11 weeks in induction study A (biologic-naive) and B (biologic-experienced). At week 10, patients in clinical remission or with a Mayo Clinic Score (MCS) response were re-randomized 2:1 to continue their FIL regimen or PBO for 47 weeks in the maintenance study. This analysis included only data from patients receiving CSs at baseline. Using univariate logistic regression, we analysed characteristics associated with achieving clinical remission at week 58 without using CSs for UC over a continuous period of ≥6 months (CS-free remission). P values <0.05 were considered statistically significant.

Results

At baseline, 81, 37, 92 and 47 patients were receiving CSs in the maintenance FIL 100 mg (n=172), PBO-to-match (PTM) FIL 100 mg (n=89), FIL 200 mg (n=199) and PTM FIL 200 mg (n=98) groups, respectively. The rates of CS-free remission in the FIL 100 mg, PTM FIL 100 mg, FIL 200 mg and PTM FIL 200 mg groups were 13.6%, 5.4%, 27.2% and 6.4%, respectively. Age, body mass index, history of pancolitis, duration of UC, faecal calprotectin and C-reactive protein levels, MCS and concomitant use of systemic CSs, immunomodulators and aminosalicylates had no significant effect on CS-free remission in the FIL 200 mg group. Mean baseline Robarts Histopathology Index (RHI) (odds ratio [OR]=0.949, p=0.023) was significantly associated with 6-month CS-free remission in the FIL 200 mg group. A baseline Mayo endoscopic subscore (MES) of 2 (vs 3) was associated with significantly increased odds of 6-month CS-free remission in the FIL 200 mg and FIL 100 mg groups (Table). Being male, a former (vs current) smoker or biologic-experienced was associated with significantly reduced odds of 6-month CS-free remission in the FIL 200 mg group.

Table. Association between 6-month CS-free clinical remission (dependent variable) and baseline characteristics^a by treatment groups.

Conclusion

Most baseline characteristics analysed had no statistically significant effect on 6-month CS-free remission under FIL 200 mg treatment. Low baseline MES and RHI, female sex, being a current (vs former) smoker and biologic-naive may predict higher likelihood of sustained CS-free remission in patients receiving FIL 200 mg.

References

1. Feagan BG et al. Lancet 2021;397:2372–84.

Disclosure

TK has served as an advisory board member, consultant or speaker for AbbVie, Activaid, Ajinomoto Bio-Pharma, Alfresa Pharma, Astellas Pharma, Bristol Myers Squibb, Celltrion, Covidien, EA Pharma, Eisai, Eli Lilly, Ferring Pharmaceuticals, Gilead Sciences, Janssen Pharmaceuticals, JIMRO, JMDC, Kissei Pharmaceutical, Kyorin Pharmaceutical, Mitsubishi Tanabe Pharma, Mochida Pharmaceutical, Nippon Kayaku, Pfizer, Takeda, Thermo Fisher Scientific and Zeria Pharmaceutical, and has received research funding from AbbVie, Alfresa Pharma, EA Pharma, Kyorin Pharmaceutical, Mochida Pharmaceutical, Nippon Kayaku, Otsuka Holdings, Sekisui Medical, Takeda, Thermo Fisher Scientific and Zeria Pharmaceutical.
AD reports fees for participation in clinical trials, review activities such as data monitoring boards, statistical analysis and end point committees from Abivax, AbbVie, Arena Pharmaceuticals, Falk Foundation, Gilead/Galapagos, Janssen and Pfizer; consultancy fees from AbbVie, Amgen, Arena Pharmaceuticals, Biogen, Boehringer Ingelheim, Bristol Myers Squibb/Celgene, Celltrion, Falk Foundation, Ferring Pharmaceuticals, Fresenius Kabi, Galapagos, Janssen, MSD, Pfizer, Pharmacosmos, Roche/Genentech, Sandoz/Hexal, Takeda, Tillotts, and Vifor Pharma; payment from lectures, including service on speakers bureaus from AbbVie, Biogen, Celltrion, the Falk Foundation, Ferring Pharmaceuticals, Gilead/Galapagos, High5ImmunoTV, Janssen Pharmaceuticals, MSD, Pfizer, Takeda, Tillotts Pharma and Vifor Pharma; and payment for manuscript preparation from the Falk Foundation, Takeda, Thieme Medical Publishers and UNI-MED Verlag.
XR has served as an advisory board member, consultant or speaker for AbbVie, Amgen, Biogen, Celltrion, Ferring Pharmaceuticals, Galapagos NV, Janssen Pharmaceuticals, MSD, Pfizer, Sandoz and Takeda.
YF is an employee of Gilead Sciences K.K.
AO is an employee and shareholder of Galapagos NV.
CJ is a contractor for Galapagos NV.
TH has received lecture fees from Aspen Japan K.K., Janssen Pharmaceuticals, JIMRO, Mitsubishi Tanabe Pharma, Mochida Pharmaceutical Co., Ltd., Pfizer and Takeda; research grants from AbbVie GK, Activaid, Alfresa Pharma Corporation, Bristol Myers Squibb, Eli Lilly Japan K.K., Ferring Pharmaceuticals, Gilead Sciences, Inc., Janssen Pharmaceutical K.K., JMDC Inc., Mochida Pharmaceutical Co., Ltd., Nippon Kayaku Co., Ltd., Pfizer Japan Inc. and Takeda; scholarship contributions from Mitsubishi Tanabe Pharma Corporation, Nippon Kayaku Co., Ltd. and Zeria Pharmaceutical Co., Ltd.; and study group sponsorship from AbbVie GK, EA Pharma Co., Ltd., JIMRO Co., Ltd., Kyorin Pharmaceutical Co., Ltd., Mochida Pharmaceutical Co., Ltd., Otsuka Holdings and Zeria Pharmaceutical Co., Ltd.
This study was funded by Gilead Sciences K.K.
The SELECTION trial was sponsored by Gilead Sciences Inc (Foster City, CA, USA). Galapagos NV (Mechelen, Belgium) was a collaborator for the SELECTION trial.
Writing support for the development of this abstract was provided by Tamsyn Stanborough, PhD, and Georgii Filatov of Oxford PharmaGenesis, Melbourne, Australia, and funded by Gilead Sciences K.K.

Introduction

Among patients with functional gastrointestinal disorders (FGID), food intake is often identified as a symptom trigger. Common foods known to cause gastrointestinal (GI) symptoms include fatty foods (1) and fermentable carbohydrates (FODMAPs) (2), but the evidence is limited and may vary among different FGID.

Aims & Methods

The aim of this study was to explore if certain foods are considered more tolerable, and which specific foods are identified as triggers of GI symptoms among participants with irritable bowel syndrome (IBS) and functional dyspepsia (FD). An online survey was conducted including n=537 participants from the Swedish general population with symptoms compatible with a functional bowel disorder. The survey included questions on demographics and an adapted food frequency questionnaire that assessed intakes of 38 different food items or aggregated food groups. For each food, participants had to answer whether or not they considered the specific food to be a trigger for GI symptoms.

Results

Among the respondents, a total of 220 participants with IBS and/or FD (mean age 34.7 years, body mass index 26.8 kg/m², women: 78.2%) were included in the analyses, of whom n=128 fulfilled criteria for FD and n=136 for IBS. Foods that were least commonly reported to cause GI symptoms included hard bread, fish and shellfish, berries, nuts, and seeds (Figure). The most frequently reported food triggers included pizza, crisps, confectionery, candy, ice cream, white bread, dairy, french fries, pie, and sausages. White bread, more often than whole grain bread, was reported to cause GI symptoms. Most vegetables and fruits were well tolerated in FD. A few FODMAP-rich vegetables, such as onion, garlic, beans, lentils, cauliflower and cabbage were more often reported as food triggers in IBS compared with FD. Having overlapping IBS and FD increased the prevalence of foods that were considered to cause symptoms.

Conclusion

In individuals with IBS and/or FD, foods traditionally associated with a healthy dietary pattern were less commonly reported to cause GI symptoms, whereas foods associated with western food/junk food were more commonly reported to cause GI symptoms. Promoting healthy food choices seem compatible with dietary treatment of patients with IBS and FD.

References

1, Feinle-Bisset C, Azpiroz F. Dietary and lifestyle factors in functional dyspepsia. Nature reviews Gastroenterology & hepatology. 2013 Mar;10(3):150-7.
2. van Lanen AS, de Bree A, Greyling A. Efficacy of a low-FODMAP diet in adult irritable bowel syndrome: a systematic review and meta-analysis. European journal of nutrition. 2021 Sep;60:3505-22.

Introduction

Filgotinib is an oral Janus kinase 1 selective inhibitor licensed for the treatment of moderate to severe ulcerative colitis (UC) following the successful UC-SELECTION registration trials.¹ However, no real-world data have been published since filgotinib first received marketing authorisation in November 2021.

Aims & Methods

The aim of this study was to assess the short-term safety and effectiveness of filgotinib for the treatment of UC. The primary outcome was post-induction clinical remission, defined as a Simple Clinical Colitis Activity Index (SCCAI) of ≤2. A retrospective, observational cohort study was conducted at a tertiary IBD referral centre using prospectively maintained records between August 2022 and February 2023. Clinical disease activity was assessed at baseline and following induction at week 10 using paired SCCAI scores, faecal calprotectin (FCAL), and C-reactive protein (CRP). Quality of life was assessed using the IBD-Control questionnaire. Non-responder imputation was used for analyses.

Results

Thirty-four patients were initiated on filgotinib during the study period, with post-induction outcome data available for 32 patients; 56% male, median age 38 (IQR range 26–53), 41% with prior biologic and/or tofacitinib exposure. Patients were treated for a median duration of 20 weeks (IQR 13–25) with treatment persistence of 69% at the time of analysis; eight patients were switched to alternative treatments due to non-response and two patients underwent colectomy.
At the end of induction, nine patients (28%) were in clinical remission; all patients were corticosteroid-free. Median SCCAI decreased significantly from a baseline of 7 (IQR 4-10) to 1 (IQR 0-6) at week 10, p<0.01, n=25. Median FCAL fell numerically from a baseline of 464 mcg/g (IQR 183-1245) to 125mcg/g (IQR 30-502) following induction, p=0.06, n=20. There was no significant change in CRP, haemoglobin, serum albumin, or lipid profile components following induction. There was a significant improvement in pre- and post-treatment quality of life scores from a median of 5 (IQR 2-9) to 16 (IQR 4-16), p<0.01.
Thirteen patients described a mild self-resolving coryzal illness, sore throat, or headaches during treatment. There was one reported case of oral herpes simplex infection requiring treatment interruption. There were no serious adverse events.

Conclusion

Filgotinib was well tolerated and clinically effective in the short term with improvements in quality of life but larger prospective cohorts with longer follow up are needed.

References

1. Feagan BG, Danese S, Loftus EV, et al. Filgotinib as induction and maintenance therapy for ulcerative colitis (SELECTION): a phase 2b/3 double-blind, randomised, placebo-controlled trial. The Lancet. 2021 Jun 19;397(10292):2372–84.

Disclosure

FD has received honoraria for educational meetings and speaker fees for Dr Falk. Received advisory board/nurse consultation fees for for Dr Falk, Galapagos, Pfizer and Takeda. Travel grants received from Pharmacosmos, Celtrion, and Tillotts.
KP has received honoraria for educational meetings and speaker fees from AbbVie, Janssen, Takeda, Pfizer, DrFalk, PredictImmune and Ferring and has received advisory board fees from AbbVie, Galapagos, Pfizer and Janssen.
SH served as a speaker, a consultant, and/or an advisory board member for Pfizer, Janssen, AbbVie, and Takeda. Travel grants received from Ferring, Falk Pharma, and Pharmacosmos.
RH, AA and SK have no disclosures.

Introduction

Most clinical trials of systemic ulcerative colitis (UC) therapies exclude patients (pts) with isolated proctitis, who are considered a more treatment-refractory population, creating a need for clinical evidence. Etrasimod is an investigational, oral, once-daily, selective sphingosine 1‑phosphate (S1P)_1,4,5 receptor modulator in development for the treatment of moderately to severely active UC. The phase 3 etrasimod ELEVATE UC trials included pts with isolated proctitis (< 10 cm rectal involvement), provided they met all other eligibility criteria.¹

Aims & Methods

This post hoc analysis assessed predefined efficacy and safety outcomes in subgroups of pts with isolated proctitis and more extensive colitis (proctosigmoiditis/left-sided colitis/pancolitis). In ELEVATE UC 52 (NCT03945188) and ELEVATE UC 12 (NCT03996369), pts (aged 16–80 years) with moderately to severely active UC were randomised 2:1 to etrasimod 2 mg once daily or placebo. ELEVATE UC 52 comprised a 12-week (wk) induction period followed by a 40-wk maintenance period with a treat-through design. ELEVATE UC 12 comprised a 12-wk induction period. Clinical endpoints were assessed in pts with isolated proctitis (data pooled from both trials) and in pts with more extensive colitis (individual trial data). Sustained and corticosteroid-free clinical remission were assessed at Wk 52 (ELEVATE UC 52 only). Bowel urgency Numeric Rating Scale (NRS) was assessed at Wks 12 and 52. Safety was assessed up to Wk 52.

Results

This analysis included 64 (pooled; Wk 12) and 36 (ELEVATE UC 52; Wk 52) pts with isolated proctitis, and 397 (ELEVATE UC 52; Wks 12 and 52) and 326 (ELEVATE UC 12; Wk 12) pts with more extensive colitis. Similar proportions of pts with isolated proctitis achieved the predefined efficacy endpoints vs those with more extensive colitis (Table). Pts with isolated proctitis receiving etrasimod had similar improvements in urgency NRS scores vs those with more extensive colitis (mean change from baseline: Wk 12, -2.8 vs -2.9 [both trials]; Wk 52, -5.0 vs -4.1). Safety in pts with isolated proctitis was generally similar to that in the overall trial population.¹

Conclusion

Etrasimod treatment had similar efficacy in pts with isolated proctitis and in those with more extensive colitis. Prospective confirmation in larger pt cohorts with isolated proctitis is necessary. Safety was consistent with the overall population.¹

References

1. Sandborn WJ et al. Lancet 2023: Epub ahead of print

Disclosure

LPB: research: Takeda, Fresenius Kabi, Celltrion; consultancy: AbbVie, Alimentiv, Alma, Amgen, Applied MolecularTransport, Arena, Biogen, BMS, Celltrion, CONNECTBiopharm, Cytoki, Enthera, Ferring, Fresenius Kabi, Galapagos, Genentech, Gilead, Gossamer, GSK, HAC, IAG ImageAnalysis, Index, Inotrem, Janssen, Eli Lilly, Medac, Mopac, Morphic, MSD, Norgine, Novartis, OM, ONO, OSE, Pandion, Par'Immune, Pfizer, Prometheus, Protagonist, Roche, Sandoz, Takeda, Theravance, Thermo Fisher, TiGenix, Tillotts, Viatris, Vifor, Ysopia, Abivax; speaker: Galapagos, AbbVie, Janssen, Genentech, Ferring, Tillotts, Celltrion, Takeda, Pfizer, Sandoz, Biogen, MSD, Amgen, Vifor, Arena, Eli Lilly, Gilead, Viatris, Medac, Sanofi; stock: CTMA.
MCD: research: Janssen; consultancy: AbbVie, Arena, BMS, Celgene, Eli Lilly, Galapagos, Genentech, Gilead, Janssen, Pfizer, Prometheus, Takeda, Trellus Health, UCB; shares/royalties: Trellus; directorship/ownership interests: Trellus.
BES: research/grants: Arena, Janssen. Lecture/Speakers Bureau: BMS, Janssen, Lilly, Pfizer, Takeda. Consultancy: AbbVie, Alimentiv, Amgen, Arena, AstraZeneca, Boehringer-Ingelheim, BMS, Celltrion, Fresenius Kabi, Genentech, GSK, Janssen, Lilly, Merck, Pfizer, Prometheus Biosciences, Sun Pharma Global, Takeda Pharmaceuticals International, Teva Branded Pharmaceutical Products R&D. Shareholder/Stock Options: Ventyx Biosciences. Other non-financial support: Janssen, Lilly, Pfizer, Takeda.
JP: personal: AbbVie, Arena, Athos, Atomwise, Boehringer Ingelheim, Celgene, Celltrion, Ferring, Galapagos, Genentech/Roche, GSK, Immunic, Janssen, Mirum, Morphic, Nestlé, Origo, Pandion, Pfizer, Progenity, Revolo, Takeda, Theravance, Wassermann; grants: AbbVie, Pfizer.
SS: speaker: AbbVie, Arena, Biogen, BMS, Celgene, Celltrion, Dr. Falk, Fresenius, Janssen, MSD, Pfizer, Takeda; consultancy/advisory: AbbVie, Arena, Biogen, BMS, Celgene, Celltrion, Dr. Falk, Fresenius, Gilead, IMAB, Janssen, MSD, Mylan, Pfizer, Protagonist, Provention, Takeda, Theravance.
WR: speaker: AbbVie, Celltrion, Dr. Falk, Ferring, Janssen, Galapagos, MSD, Roche, Pfizer, Pharmacosmos, Shire, Takeda, Therakos; consultant: AbbVie, Amgen, AOP Orphan, Arena, Astellas, AstraZeneca, Bioclinica, Boehringer Ingelheim, BMS, Calyx, Celgene, Celltrion, Eli Lilly, Dr. Falk, Ferring, Galapagos, Gatehouse, Genentech, Gilead, Grünenthal, ICON, Index, Inova, Janssen, Landos Biopharma, Medahead, MedImmune, Microbiotica, Mitsubishi Tanabe, MSD, Novartis, OMass, Otsuka, Parexel, Periconsulting, Pharmacosmos, Pfizer, Protagonist, Provention, Quell, Sandoz, Seres, Setpointmedical, Sigmoid, Sublimity, Takeda, Teva, Therakos, Theravance, Zealand; advisory board: AbbVie, Amgen, AstraZeneca, Boehringer Ingelheim, BMS, Celgene, Celltrion, Galapagos, Janssen, Mitsubishi Tanabe, MSD, Pharmacosmos, Pfizer, Sandoz, Takeda; research: AbbVie, Janssen, MSD, Sandoz, Sanofi, Takeda.
BGF: consultant/advisory: AbbVie, AbolerIS, AgomAB, AllianThera, Amgen, AnaptysBio, Applied Molecular Transport, Arena, Avoro Capital, Atomwise, BIOJAMP, Biora, Boehringer Ingelheim, Boxer, Celsius, BMS, Connect, Cytoki, Disc Medicine, Duality, EcoR1, Eli Lilly, Equillium, Ermium, First Wave, FirstWord, Galapagos, Galen Atlantica, Genentech/Roche, Gilead, Gossamer, GSK, Hinge, HotSpot, InDex, Imhotex, Immunic, JAK, Janssen, Japan Tobacco, Kaleido, Landos, Leadiant, L.E.K., Lenczner Slaght, LifeSci, Lument AB, Millennium, MiroBio, Morgan Lewis, Morphic, Mylan, OM, Origo, Orphagen, Pandion, Pendopharm, Pfizer, Prometheus, Diagnostics, Play to Know AG, Progenity, Protagonist, PTM, Q32, Rebiotix, REDX, Roche, Sandoz, Sanofi, Seres, Silverback, Surrozen, Takeda, Teva, Thelium, TiGenix, Tillotts, Ventyx, VHSquared, Viatris, Ysios, YSOPIA, Zealand; speaker: AbbVie, Janssen, Takeda; Alimentiv Senior Scientific Director, provides central reading services; not a company employee, no equity stake; shareholder: Gossamer.
SD: consultancy/advisory: AbbVie, Allergan, Amgen, AstraZeneca, Biogen, Boehringer Ingelheim, Celgene, Celltrion, Ferring, Gilead, Hospira, Janssen, J&J, MSD, Mundipharma, Pfizer, Roche, Sandoz, Takeda, TiGenix, UCB Vifor; speaker: AbbVie, Amgen, Ferring, Gilead, Janssen, Mylan, Pfizer, Takeda; directorship/ownership interests: Gastroenterology and Endoscopy.
AJY: consultancy: Pfizer, Arena, Takeda, BMS; speaker: BMS.
GD’H: advisor: AbbVie, AstraZeneca, Alimentiv, BMS, Boehringer Ingelheim, Celltrion, Cosmo, Eli Lilly, Galapagos, GSK, J&J, Takeda, Pfizer, Polpharma, Prometheus, Tillotts, Ventyx; speaker: AbbVie, Boehringer Ingelheim, Celltrion, J&J, Takeda, Pfizer, Tillotts.
MG, KW, JCW, IM, AMcD, LB, CJR: Pfizer employees & shareholders.
SV: research: AbbVie, MSD, Pfizer, Galapagos, Takeda; consultancy: AbbVie, AbolerIS, Alimentiv, Arena, AstraZeneca, Avaxia, BMS, Boehringer Ingelheim, Celgene, CVasThera, Dr. Falk, Eli Lilly, Ferring, Galapagos, Genentech/Roche, Gilead, Hospira, Imidomics, Janssen, J&J, Materia Prima, MiroBio, Morphic, MrMHealth, MSD, Mundipharma, Pfizer, Prodigest, Progenity, Prometheus, Robarts Clinical Trials, Second Genome, Shire, Surrozen, Takeda, Theravance, Tillotts, Zealand; speaker: AbbVie, Dr. Falk, Ferring, Hospira, MSD, Takeda, Tillotts.