Introduction

Tofacitinib, filgotinib, and upadacitinib, are Janus kinase inhibitors (iJAKs) approved for inflammatory bowel disease (IBD) treatment. Although no direct comparative studies exist, potential differences in efficacy and safety are attributed to in vitro-demonstrated affinity of each molecule for different JAK isoforms. JAK1 plays a crucial role in modulating cytokine-mediated immune responses, such as IL-6 and interferon, which are involved in inflammation and skin homeostasis. Its inhibition can promote conditions that may trigger acne.
Acne may be increased in iJAK-treated patients, meaning a clinical challenge for gastroenterologists.

Aims & Methods

A retrospective study was conducted at ten referral centers in Spain, including all IBD patients who had received iJAK therapy and had at least 3 months of follow-up. Demographic data, disease-related variables, and acne characteristics when appropriate, were collected. Univariate and multivariate logistic regressions were used to identify risk factors for acne; model discrimination was assessed by AUC.

Results

A total of 549 patients included: 258 (47%) were women; 354 (64%) had ulcerative colitis, 191 (35%) had Crohn’s disease and 1% had indeterminate colitis. Mean age was 41 years (IQR 30-52). 219 patients (40%) were treated with tofacitinib, 281 (51%) with upadacitinib, and 49 (9%) with filgotinib.
Ninety patients (16%) developed acne during iJAK treatment: 69% were mild, with only 4 severe cases (4%). Acne occurred early (median onset 42 days, IQR 7-122), predominantly on the face (56%), trunk (13%) or both (31%). Acne morphology included comedones (60%), papules (59%), pustules (39%), nodular-cystic (12%), scarring (9%); 48% showed more than one morphology.
Thirty-six patients received specific acne treatment: 89% topical (antiseptics, benzoyl peroxide, retinoids), 69% systemic (antibiotics, retinoids, antiandrogens), and 44% combined treatment. 83% of those patients responded to acne specific treatment, and only 8 patients (9% of those with acne; 1.5% overall) had to discontinue iJAK treatment, with acne resolving in all cases.
Acne developed in 26%, 6% and 6% of upadacitinib, tofacitinib and filgotinib treated patients respectively (p=0.001). Multivariate analysis showed that acne development was associated with upadacitinib (OR 10.28;IC95%=4,7–22,6; p<0,001) and history of acne (OR 3.52; IC95%=1,5–8,3; p=0,004), while older age (>35 years, OR 0.31; IC95% 0,11–0,83; p=0,02) and Crohn’s disease (OR 0.47; IC95% 0,25–0,90; p=0,02) showed to be protective. This model was reliable in predicting acne development (AUC 0.79). Additionally, univariate analysis showed high dose of iJAK was also associated with acne development, which could not be confirmed in multivariate analysis.

Conclusion

Acne occurred in a relevant proportion of iJAK-treated patients, was generally mild and manageable with dermatological care, and rarely required treatment discontinuation. Risk factors for iJAK-associated acne included use of upadacitinib (probably reflecting a greater affinity for JAK1) and history of acne, while older age and Crohn’s disease were protective.
Gastroenterologists should be aware of both likelihood and management of this specific adverse event when considering iJAK therapy.

Disclosure

Y G-L, MC, GB, ER, IB, DC, M B-dA, LM, I M-J, DG, IV have provided scientific advisory / participated in educational activities / received unrestricted research grants / received payments for lecturing from Johnson & Johnson, ​Takeda, Pfizer, Amgen, AbbVie, Lilly, AlfaSigma, Ferring, Gilead.

Introduction

C-reactive protein (CRP) and fecal calprotectin (FeCal) are non-invasive inflammatory biomarkers used to assess disease activity in UC. The Phase 3 QUASAR induction study evaluated the efficacy and safety of guselkumab (GUS), an IL-23 p19 subunit antagonist, in patients (pts) with moderately to severely active UC. Here, we analyze the effect of GUS treatment on CRP and FeCal through Week (Wk) 12 in pts with elevated CRP and/or FeCal.

Aims & Methods

Pts with a modified Mayo score of 5-9 and a Mayo endoscopy subscore ≥2 at baseline (BL) were randomized 3:2 to receive either GUS 200mg IV or placebo (PBO) IV at Wks0, 4, and 8. CRP and FeCal were assessed at BL, Wk4, Wk8 (for CRP only), and Wk12.

Results

A total of 701 pts were evaluated and approximately 50% of randomized pts had a history of inadequate response/intolerance to advanced therapies (ADT) for UC; 47.4% of these pts had inadequate response/intolerance to ≥2 ADT classes. Median BL concentrations of CRP and FeCal were similar between the GUS-treated and PBO-treated pts (4.34 vs 3.83mg/L and 1651 vs 1606mg/kg, respectively). Among pts with elevated CRP and/or FeCal at BL, greater reductions in CRP and FeCal were observed at the earliest timepoint assessed (Wk4) with GUS and continued through Wk12 compared with PBO (Table).
At BL, 248 GUS-treated pts and 160 PBO-treated pts had elevated CRP (>3mg/L); the proportions were similar between treatment groups (58.9% vs 57.1%, respectively). Among these pts, median change from BL in CRP concentration (mg/L) at Wk12 for the GUS and PBO cohorts were -3.99 and -0.51mg/L, respectively (nominal p<0.001); the proportions of pts achieving 50% and 75% reduction in CRP levels (or ≤3mg/L) at Wk12 were higher for GUS-treated pts than those receiving PBO (59.7% vs 28.1% and 47.2% vs 19.4%, respectively; both nominal p<0.001). Similarly, a higher proportion of GUS-treated pts achieved CRP≤3mg/L at Wk12 than PBO-treated pts (40.3% vs 16.3%, nominal p<0.001).
At BL, 333 GUS-treated pts and 225 PBO-treated pts had elevated FeCal (>250mg/kg); the proportions were similar between treatment groups (79.1% vs 80.4%, respectively). Median change from BL in FeCal concentration (mg/kg) for pts with elevated FeCal at BL at Wk12 were -800 and -86mg/kg for the GUS and PBO cohorts, respectively (nominal p<0.001); the proportions of pts achieving 50% and 75% reduction in FeCal levels (or ≤250 mg/kg) at Wk12 were higher for GUS-treated pts than those receiving PBO (51.1% vs 33.8% and 41.4% vs 23.6%, respectively; both nominal p<0.001). A larger percentage of pts treated with GUS achieved FeCal≤250mg/kg at Wk12 than pts treated with PBO (29.4% vs 17.3%, nominal p<0.001).

Table. Change from baseline in CRP and FeCal through Week 12 among patients with elevated CRP (>3mg/L) or FeCal (>250mg/kg) at baseline
	Placebo IV	Guselkumab 200 mg IV
CRP (mg/L) Baseline, N Median [IQR]	160 8.02 [5.40; 16.85]	248 9.26 [5.31; 18.05]
Wk 4, N Median change from baseline [IQR]	158 -2.06 [-5.70; 1.58]	245 -3.35 [-8.60; -0.23]***
Wk 8, N Median change from baseline [IQR]	156 -1.75 [-5.68; 1.46]	239 -3.80 [-10.77; -0.19]***
Wk 12, N Median change from baseline [IQR]	153 -0.51 [-4.64; 2.72]	239 -3.99 [-11.46; -0.85]***
FeCal (mg/kg) Baseline, N Median [IQR]	225 1743 [1120; 3395]	333 1787 [920; 4009]
Wk 4, N Median change from baseline [IQR]	213 -227 [-1041; 658]	308 -603 [-1866; 230]***
Wk 12, N Median change from baseline [IQR]	201 -86 [-1254; 504]	293 -800 [-2532; 0]***
***Nominal P≤0.001. Patients who had a prohibited change in UC medication, an ostomy or colectomy, or discontinued study agent due to lack of efficacy or an AE of worsening of UC or other reasons except for COVID-19 related reasons (excluding COVID-19 infection) or regional crisis in Russia and Ukraine prior to the designated timepoint had their baseline value carried forward from the time of the event onward. The p-values of treatment comparison were based on the mixed-effect model repeated measures with CRP and FeCal values being log-transformed.

Conclusion

In this phase 3 induction study, pts with moderately to severely active UC and elevated inflammatory markers treated with GUS 200mg IV induction showed greater improvement from BL in both CRP and FeCal levels compared with PBO. Differences were observed as early as the first assessments at Wk4 and continued through Wk12.

Disclosure

Tadakazu Hisamatsu received consulting fees from Janssen Research & Development, LLC.
Laurent Peyrin-Biroulet reports personal fees from Janssen.
Axel Dignass reports fees for participation in clinical trials, review activities such as data monitoring boards, statistical analysis and end point committees from Janssen; consultancy fees from Janssen; and payment from lectures including service on speakers bureaus from Janssen.
Kuan-Hsiang G. Huang, Matthew Germinaro, Nicole Houck,Ye Miao, and Hongyan Zhang are employees of Johnson & Johnson and own company stock/stock options.
Marjorie Argollo reports consulting fees from Janssen.
Ken Takeuchi has served as a speaker for Janssen.
Rafal Filip reports lecture fees and research/education support from Janssen.
Jessica R. Allegretti is a consultant and speaker for Janssen.
Brian G. Feagan received consulting fees from Janssen; a member of the speakers bureau for Janssen; support for attending meetings and/or travel from Janssen; and participation on a Data Safety Monitoring Board or Advisory Board from Janssen.
Bruce E. Sandsreports grants, consulting and speaking fees and other support from Janssen.

Introduction

Pancreatic cysts are a common finding in imaging studies, and, considering the different malignant potentials of mucinous and non-mucinous cysts, it is necessary to develop accurate methods and algorithms to differentiate between them. We conducted this study to compare the diagnostic performance of glucose levels and CEA levels in the diagnosis of mucinous pancreatic cysts.

Aims & Methods

We conducted a retrospective study of patients who underwent EUS-FNA of pancreatic cystic lesions between September 2020 and March 2023 at a tertiary referral center. We included patients whose glucose and CEA levels had been measured. Indicators of mucinous cysts include glucose levels less than 2.7 mmol/l and CEA levels greater than 192 ng/ml. It was compared to the final pathology (obtained after surgery or by EUS-FNB) result to determine their accuracy.

Results

	Non-mucinous	Mucinous
Gender (%male)	47.3%	33.3%
Age ( Median)	50.2	58.3
Cyst location
head	9	3
body	2	5
tail	8	4

A total of 31 patients were included in the study, 13 males and 18 females. The mean age was 55.7 years. Of the 31 patients, 12 (38.7%) were diagnosed with mucinous cysts (6 mucinous cystic neoplasms, 6 intraductal papillary mucinous neoplasms), and 19 (61.2%) were diagnosed with non-mucinous cysts (9 serous cystic neoplasm, 8 pseudocysts, 1 solid pseudopapillary neoplasm, and 1 lymphoepithelial cyst). There was a female prevalence in patients with mucinous cysts (8 females and 4 males) with a mean age of 59,6 years. From the cyst fluid analysis, the sensitivity, specificity, and accuracy of glucose in diagnosing mucinous cysts were 91.7%, 89.5%, and 90.3%, respectively. CEA’s sensitivity, specificity, and accuracy were 81.8%, 85.0%, and 83.9%, respectively.

Conclusion

In the diagnosis of pancreatic cystic lesions, glucose levels have high diagnostic performance with high sensitivity and accuracy. In contrast, CEA levels have a lower diagnostic performance. The findings of our study support the use of EUS-FNA and glucose levels in the diagnosis of pancreatic cystic lesions, as well as EUS-FNB to obtain histological specimens for a more accurate diagnosis of pancreatic cysts. Further studies are needed to validate these findings and explore the potential of other biomarkers in diagnosing and managing pancreatic cystic lesions.

Introduction

There is growing awareness of the importance of histological outcomes in ulcerative colitis (UC). However, direct comparisons of histological endpoints are lacking. Thus, we aimed to conduct a network meta-analysis (NMA) to compare the effectiveness of various biologics and small molecules in achieving histological endpoints in UC.

Aims & Methods

We searched four online databases to identify all randomized controlled trials (RCTs) investigating advanced therapies for moderate-to-severe UC that reported histological outcomes. The analysis focused on the proportion of patients achieving histological improvement, histological remission, and histo-endoscopic improvement during induction and maintenance therapy. Using a random-effects frequentist model, we conducted a NMA, presenting the results as odds ratios (OR) with 95% confidence intervals. To evaluate the relative effectiveness of each treatment, we calculated the P-score, which ranges from 0 to 1. We also assessed the risk of bias and evidence certainty using established scoring systems.

Results

Twenty-four RCT were included, comprising 15 different therapies, and enrolling over 8800 patients. Of these trials, 19 provided data on induction therapy, while 10 assessed histological outcomes during maintenance treatment. Outcome definitions were similar among studies. We found that etrasimod 2 mg/day ranked highest in achieving histologic response (P-score 0.98) and remission (P-score 0.90) following induction, while guselkumab ranked first for histoendoscopic improvement. In maintenance trials, upadacitinib 30 mg/day ranked highest in achieving histologic and histo-endoscopic outcomes (P-score 0.88 for both endpoints). Etrasimod 2 mg/day ranked second for histologic remission (P-score 0.70) and histo-endoscopic improvement (P-score 0.73), while mirikizumab 200 mg/month ranked second for histologic response.

Conclusion

Our findings underscore the importance of small molecules in treating moderate-to-severe UC, particularly etrasimod and upadacitinib. Nonetheless, additional head-to-head RCTs are imperative to better inform clinical practice and to address unanswered questions.

Introduction

The Phase 3 QUASAR Maintenance Study is a randomized-withdrawal, double-blind, placebo (PBO)-controlled, study that evaluated the efficacy and safety of maintenance treatment with subcutaneous (SC) guselkumab (GUS), a dual-acting IL-23p19 subunit inhibitor that binds to CD64, in patients (pts) with moderately to severely active ulcerative colitis (UC) who had prior inadequate response or intolerance to conventional or advanced therapy (ADT) and demonstrated a clinical response to GUS IV induction.

Aims & Methods

At maintenance baseline, clinical responders to 12 weeks of GUS IV induction from QUASAR Phase 2b and Phase 3 induction studies (NCT04033445) were randomized 1:1:1 to SC GUS 200mg q4w, GUS 100mg q8w, or PBO (GUS withdrawal). The primary endpoint was clinical remission at Week (Wk) 44. Major secondary endpoints included corticosteroid-free clinical remission, maintenance of clinical remission, maintenance of clinical response, symptomatic remission, endoscopic improvement, histo-endoscopic mucosal improvement, and endoscopic normalization (remission) at Wk44.

Results

The primary analysis population included 568 pts (mean age, 40.7yr; mean UC duration, 7.8yr; mean modified Mayo score, 6.9 [63.9% with severe disease]; Mayo endoscopy subscore of 3, 66.4%; baseline oral corticosteroid use, 40.0%). Approximately 42% had prior inadequate response or intolerance to ADT (TNF antagonists, vedolizumab, or tofacitinib), and 48.3% of these pts failed ≥2 ADT. Disease characteristics were similar across treatment groups at induction and maintenance baseline.
With both GUS SC maintenance regimens, a significantly higher proportion of pts achieved the primary endpoint and all the major secondary endpoints at Wk44 compared with GUS withdrawal (Table 1).
The proportion of pts with ≥1 adverse events (AEs) was similar across treatment groups: GUS 200mg q4w, 70.0%; GUS 100mg q8w, 64.5%, and GUS withdrawal, 68.2%. The most common AEs in the combined GUS group vs withdrawal group were COVID-19 (11.2% vs 14.1%), UC (11.2% vs 29.7%), and arthralgia (6.1% vs 6.8%), respectively.
No cases of death, active tuberculosis, opportunistic infection, anaphylaxis, serum sickness, Hy’s Law, or serious hepatic AEs were reported. Two cases of malignancy (clear cell renal carcinoma, rectal adenocarcinoma) and 1 major adverse cardiovascular event (hemorrhagic stroke) were reported among GUS-treated pts (primary safety population).

Table 1. Primary and major secondary endpoints at Week 44: Primary analysis population

	GUS Withdrawal (Placebo) (N=190)	GUS 100 mg q8w (N=188)	GUS 200 mg q4w (N=190)
Clinical remission (primary endpoint), n (%)a Adjusted treatment difference (95% CI)	36 (18.9%)	85 (45.2%) 25.2 (16.4, 33.9), P<0.001	95 (50.0%) 29.5 (20.9, 38.1), P<0.001
Corticosteroid-free clinical remission, n (%)b Adjusted treatment difference (95% CI)	35 (18.4%)	85 (45.2%) 25.7 (17.0, 34.5), P<0.001	93 (48.9%) 29.0 (20.5, 37.6), P<0.001
Maintenance of clinical remission, n/N (%)c Adjusted treatment difference (95% CI)	20/59 (33.9%)	40/66 (60.6%) 25.9 (9.2, 42.5), P=0.004	50/69 (72.5%) 38.4 (22.7, 54.1), P<0.001
Maintenance of clinical response, n (%)d Adjusted treatment difference (95% CI)	82 (43.2%)	146 (77.7%) 33.6 (24.5, 42.7), P<0.001	142 (74.7%) 30.7 (21.5, 40.0), P<0.001
Symptomatic remission, n (%)e Adjusted treatment difference (95% CI)	71 (37.4%)	132 (70.2%) 31.9 (22.5, 41.2), P<0.001	131 (68.9%) 30.5 (21.2, 39.9), P<0.001
Endoscopic improvement, n (%)f Adjusted treatment difference (95% CI)	36 (18.9%)	93 (49.5%) 29.5 (20.7, 38.3), P<0.001	98 (51.6%) 31.1 (22.5, 39.8), P<0.001
Histo-endoscopic mucosal improvementg Adjusted treatment difference (95% CI)	32 (16.8%)	82 (43.6%) 25.7 (17.1, 34.3), P<0.001	91 (47.9%) 29.6 (21.1, 38.0), P<0.001
Endoscopic normalization (remission), n (%)h Adjusted treatment difference (95% CI)	29 (15.3%)	65 (34.6%) 18.5 (10.2, 26.8), P<0.001	64 (33.7%) 16.8 (9.0, 24.7), P<0.001
Primary Analysis Population included randomized patients with a modified Mayo score of 5-9 at induction baseline who received at least 1 maintenance study treatment dose. Adjusted treatment difference (Δ) was based on the Wald statistic with Cochran-Mantel-Haenszel (CMH) weight. P-values were based on the CMH test, stratified by clinical remission status at maintenance baseline and induction treatment, except for the maintenance of clinical remission, which was based on the CMH test stratified by induction treatment. a Clinical remission: A Mayo stool frequency subscore of 0 or 1 and not increased from induction baseline, a Mayo rectal bleeding subscore of 0, and a Mayo endoscopy subscore of 0 or 1 with no friability. b Corticosteroid-free clinical remission: Not requiring any treatment with corticosteroids for at least 8 weeks prior to Week 44 and also meeting the criteria for clinical remission (98.9% of guselkumab-treated patients who achieved clinical remission at Week 44 were not taking corticosteroids for at least 8 weeks prior to Week 44). c Maintenance of clinical remission: Clinical remission at Week 44 among patients in clinical remission at maintenance baseline. d Clinical response: A decrease from induction baseline in the modified Mayo score by ≥30% and ≥2 points, with either a ≥1-point decrease from induction baseline in the rectal bleeding subscore or a rectal bleeding subscore of 0 or 1. e Symptomatic remission: A stool frequency subscore of 0 or 1 and not increased from induction baseline, and a rectal bleeding subscore of 0. f Endoscopic improvement: An endoscopy subscore of 0 or 1 with no friability present on the endoscopy. g Histo-endoscopic mucosal improvement: Achieving a combination of histologic improvement (neutrophil infiltration in <5% of crypts, no crypt destruction, and no erosions, ulcerations or granulation tissue per Geboes grading system) and endoscopic improvement. h Endoscopic normalization (remission): An endoscopy subscore of 0.

Conclusion

Among pts with moderately to severely active UC who responded to GUS IV induction, maintenance therapy with both GUS SC regimens was safe and efficacious. The primary endpoint of clinical remission and all secondary endpoints across clinical, symptomatic, endoscopic, and histologic measures were met with statistical significance by both GUS SC maintenance regimens. Safety results through maintenance Wk44 were consistent with the known and favorable safety profile of GUS in approved indications.

Disclosure

DTR: AbbVie, Altrubio, Allergan, Inc., Arena Pharmaceuticals, Aslan Pharmaceuticals, Athos Therapeutics, Bellatrix Pharmaceuticals, Boehringer Ingelheim, Ltd., Bristol Myers Squibb, Celgene Corp/Syneos, Connect BioPharma, GalenPharma/Atlantica, Genentech/Roche, InDex Pharmaceuticals, Ironwood Pharmaceuticals, Iterative Scopes, Janssen Pharmaceuticals, Eli Lilly, Materia Prima, Pfizer, Prometheus Biosciences, Reistone, Takeda, Techlab, Inc and is a co-founder of Cornerstones Health, Inc.
JRA: Finch Therapeutics, Artugen, Pfizer, Takeda, Janssen, and Iterative Scopes, Merck and BMS.
JP: 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.
NS, SY, KGH, MG, RW, and HZ: Employees of Johnson & Johnson.
BGF: AbbVie Inc., Amgen Inc., AdMIRx Inc., Akebia Therapeutics, Allergan, AstraZeneca/MedImmune Ltd., Applied Molecular Transport, Aptevo Therapeutics, Asta Pharma, Atlantic Pharmaceuticals Ltd., Avaxia Biologics Inc., Avir Pharma, Biogen Idec, BioMx Isreal, Boehringer -Ingelheim, Boston Pharmaceuticals, Bristol-Myers Sqibb, Calypso Biotech, Celgene Corporation, Celltech, Centocor Inc, Elan/Biogen, Ferring Pharma, Genentech Inc/Hoffmann-La Roche Ltd., Galapagos, Galen/Atlantica, GiCare Pharma, Gilead Sciences Inc., Gossamer Pharma, GlaxoSmithKline (GSK), Inception IBD Inc, Intact Therapeutics, Janssen Research & Development LLC., Kyowa Kakko Kirin Co Ltd., Lexicon, Lilly, Lycera BioTech, merck, Mesoblast Pharma, Millennium, Nestles, Nextbiotix, Novonordisk, ParImmune, Parvus Therapeutics, Pfizer Inc., Prometheus Therapeutics and Diagnostics, Progenity, Protagonist, Qu Biologics, Rebiotix, Receptos Inc. / Celgene International, Salix Pharma, Sanofi, Santarus Inc., Shire, Sienna Biologics, Sihmoid Pharma, Sterna Biologics, Synergy Pharma Inc., Takeda Development Center Americas Inc., Teva Pharam, TiGenix, Tillotts Pharma AG, UCB, Vertex Pharma, Vivelix Pharma, VHsquared Ltd., Zyngenia and Senior Scientific Officer – Robarts Clinical Trials Inc.
TH: AbbVie, Daiichi-Sankyo, EA Pharma Co, Ltd. Janssen Research & Development LLC., JIMRO, Mitsubishi Tanabe Pharma Corporation, Mochida Pharmacuetical Co., Ltd., Nippon Kayaku Co., Ltd., Pfizer Inc., and Takeda Pharmaceutical Co., Ltd.,
GRL: Abbvie, Allergan, American College of Gastroenterology, American Gastroenterological Association, American Regent, Celgene, Chemed, Eli Lilly, Endo Pharmaceuticals, Ferring, Gastroenterology and Hepatology, Gilead, IMEDEX, Ironwood, Janssen/ Janssen Orthobiotech, MedEd Consultants, Merck, Morphic Therapeutics, Pfizer Pharmaceuticals, Professional Communications, Inc., Prometheus Laboratories, Inc, Romark, Sandoz, Salix Pharmaceuticals/Valeant, Shire Pharmaceuticals, SLACK, Inc, Springer Science and Business Media, Takeda, University of Kentucky, UCB, Up-To-Date, Vindico, and Virgo.
BB: Abbvie, Amgen, BI, BMS, Ferring, Janssen, Merck, Novartis, Organon, Pfizer, Sandoz, Takeda, Alimentiv, Allergan, AMT, Bausch Health, Celgene, Celltrion Healthcare, Eupraxia, Fresenius Kabi, Genentech, GSK, Gilead, Iterative Scopes, Jamp Pharma, Merck Amgen, Microbiome Insights, Mylan, Pendopharm, Protagonist, Qu Biologic, and Viatrisgen.
LPB: AbbVie, Allergan, Alma, Amgen, Applied Molecular Transport, Arena, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Celltrion, CTMA, Enterome, Enthera, Ferring, Fresenius, Genentech, Gilead, Hikma, Index Pharmaceuticals, Janssen, Lilly, MSD, Mylan, Nestlé, Norgine, Oppilan Pharma, OSE Immunotherapeutics, Pfizer, Pharmacosmos, Roche, Samsung Bioepis, Sandoz, Sterna, Sublimity Therapeutics, Takeda, Tillots and Vifor; grants from AbbVie, MSD and Takeda.
BES: Abbvie, Abbivax, Alimentiv, Amgen, Arena Pharmaceuticals, Artugen Therapeutics, Astra Zeneca, Boehringer Ingelheim, Boston Pharmaceuticals, Bristol Myers Squibb, Calibr, Celgene, Celltrion, ClostraBio, Equillium, Enthera, Evommune, Fresenius Kabi, Galapagos, Genentech (Roche), Gilead Sciences, GlaxoSmithKline, Gossamer Bio, Index Pharmaceuticals, Innovation Pharmaceuticals, Inotrem, Janssen, Kaleido, Kallyope, Lilly, Merck, Morphic Therapeutics, MRM Health, Pfizer, Progenity, Prometheus Biosciences, Prometheus Laboratories, Protagonist Therapeutics, Q32 Bio, Sun Pharma, Surrozen, Takeda, Target RWE, Teva, Theravance Biopharma, TLL Pharmaceutical, and Ventyx Biosciences.
AD: Abivax, AbbVie, Amgen, Arena Pharmaceuticals, Biogen, Boehringer Ingelheim, Bristol Myers Squibb/Celgene, CED Service GmbH, Celltrion, Dr Falk Foundation, Ferring Pharmaceuticals, Fresenius Kabi, Galapagos, Gilead, High5MD, Janssen, Lilly, Materia Prima, MedToday, MSD, Pfizer, Pharmacosmos, Roche/Genetech, Sandoz/Hexal, Takeda, Thieme, Tillotts, UniMed Verlag, and Vifor Pharma.