Introduction

Fatigue is a debilitating, multifactorial symptom experienced by many patients with Crohn’s disease (CD).¹ Mirikizumab (MIRI), an anti-interleukin-23p19 antibody, demonstrated significant improvement in fatigue in patients with moderately to severely active CD in the Phase 2 AMAG² and Phase 3 VIVID-1³ studies.

Aims & Methods

This analysis examines the association of changes in clinical, endoscopic (endo) and selected patient-reported outcomes with changes in fatigue in MIRI-treated patients in the VIVID-1 study. Co primary and gated secondary outcomes, including comparisons with ustekinumab, have been presented elsewhere^4,5Adult patients (N=1065) with moderately to severely active CD were randomized 6:3:2 to MIRI, ustekinumab or placebo. MIRI was given every 4 weeks (W) as 900 mg intravenous at W0, W4, and W8, then 300 mg subcutaneous from W12 to W52. Fatigue was assessed via the validated Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-F) questionnaire (scale from 0-52, higher scores indicating less fatigue⁶ andat least 6-point increase identified as a clinically meaningful within-patient change). Achievement of ≥6-point increase in FACIT-F at W52 was reported among those with and without clinical remission by Crohn’s Disease Activity Index (CDAI), endo response, endo remission, and Urgency Numeric Rating Scale (NRS) ≤2 at W52. For stool frequency (SF), abdominal pain (AP), fecal calprotectin (FCP), and C-reactive protein (CRP), the association of the change from baseline (CFB) at W52 vs. the CFB in FACIT-F at W52 was assessed by the Pearson correlation coefficient.

Results

At W52, 50.9% (268/527) of MIRI-treated patients achieved FACIT-F ≥6-point increase from baseline. Greater proportions of patients who achieved clinical and endo outcomes had ≥6-point increase in FACIT-F (p<0.05) vs. those who did not achieve the outcome (Table). There was weak/moderate correlation between CFB at W52 in AP, SF and log-transformed FCP and CRP, and the CFB in FACIT-F at W52 (Table).

Table: W52 FACIT-F, A: ≥6-pt Increase From BL by Outcomes at W52 and B: CFB Correlation With CFB at W52 in Outcomes

A. W52 FACIT-F ≥6-point Increase From BL by Outcome at W52a, NRI	Outcome Achieved n/N (%) (95% CI)b	Outcome NOT Achieved n/N (%) (95% CI)b	Risk Difference (95% CI)b	p-Valuec
Clinical remission by CDAId	185/280 (66.1) (60.5-71.6)	83/247 (33.6) (27.7-39.5)	32.5 (24.4-40.6)	<0.0001
Endo responsee	154/256 (60.2) (54.2-66.2)	114/271 (42.1) (36.2-47.9)	18.1 (9.7-26.5)	<0.0001
Endo remissionf	59/96 (61.5) (51.7-71.2)	209/431 (48.5) (43.8-53.2)	13.0 (2.1-23.8)	0.0216
Urgency NRS ≤2g	127/188 (67.6) (60.9-74.2)	127/311 (40.8) (35.4-46.3)	26.7 (18.1-35.4)	<0.0001
B. CFB in FACIT-F vs. CFB in Outcomes at W52	N	Pearson Correlation Coefficient	95% CIh	p-Value
CFB in AP score	574	-0.379	-0.447 to -0.306	<0.0001
CFB in SF score	572	-0.306	-0.378 to -0.230	<0.0001
CFB in log-transformed FCP	461	-0.112	-0.201 to -0.020	0.0166
CFB in log-transformed CRP	576	-0.208	-0.285 to -0.128	<0.0001

^aMIRI-treated patients with baseline (BL) FACIT-F score ≤46 points; ^bConfidence interval (CI) constructed using asymptotic method without continuity correction; ^cChi Square test; ^dCDAI <150; ^eSimple Endoscopic Score for CD (SES-CD) Total Score ≥50% improvement from BL; ^fSES-CD Total Score ≤4, ≥2-point reduction from BL and no subscore >1; ^gIn those with BL Urgency NRS ≥3; ^hPearson correlation with Fisher’s z-transformation. A negative correlation indicates an improvement in outcome is associated with an improvement in FACIT-F. Correlation strength defined as: >0.5=strong, 0.3 to ≤0.5=moderate, 0.1 to <0.3=weak, <0.1=insubstantial⁷
NRI=nonresponder imputation.

Conclusion

In patients with moderately to severely active CD treated with MIRI, improvements in clinical, endoscopic, and selected patient-reported outcomes were associated with clinically meaningful improvements in fatigue at W52.

References

1. D’Silva A, et al. Clin Gastroenterol Hepatol. 2022;20:995-1009.
2. Regueiro MD, et al. Am J Gastroenterol. 2023;118:S816.
3. Travis S, et al. J Crohn's Colitis.2024;18:i21–i23.
4. Ferrante M, et al. J Crohn's Colitis. 2024;18:S1 i7–i9.
5. Jairath V, et al. J Crohn's Colitis. 2024;18:i62–i64.
6. Tinsley A, et al. Aliment Pharmacol Ther. 2011;34:1328-36.
7. Cohen J. Statistical Power Analysis for the Behavioural Sciences, 1988, Routledge.

Disclosure

P. Bossuyt has received financial support for research from: AbbVie, Amgen, Janssen, Pfizer, and Viatris; lecture fees from: AbbVie, Bristol Myers Squibb, CAG, Celltrion, Eli Lilly and Company, EPGS, Galapagos NV, Globalport, Janssen, Materia Prima, Pentax, Scope, and Takeda; and advisory board fees from: AbbVie, Bristol Myers Squibb, Celltrion, CIRC, Dr. Falk Pharma Benelux, Eli Lilly and Company, Galapagos NV, Janssen, Pentax, PSI-CRO, Roche, Takeda, and Tetrameros; M. Regueiro has served as an advisor and/or consultant for: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly and Company, Genentech, Gilead Sciences, Janssen, Organon, Pfizer, Prometheus Therapeutics and Diagnostics, Salix Pharmaceuticals, Takeda, and UCB Pharma; M. Fischer has received consulting fees from: AbbVie, Bristol Myers Squibb, Eli Lilly and Company, Ferring Pharmaceuticals, Janssen, Pfizer, Rebiotix, Scioto Biosciences, and Seres Therapeutics; K. Traxler, G. Yu, M. Protic, K. Tsilkos, and A. Vadhariya are employees and shareholders of: Eli Lilly and Company; T. Hisamatsu has received lecture fees from: AbbVie, EA Pharma, Gilead Sciences, Janssen Pharmaceutical K.K., JIMRO, Kyorin, Mitsubishi Tanabe Pharma, Mochida Pharmaceutical, Pfizer, and Takeda; has received honoraria as an advisory board member or consultant for: AbbVie, Brystol Myers Squibb, EA Pharma, Eli Lilly and Company, Gilead Sciences, Janssen Pharmaceutical K.K., Mitsubishi Tanabe Pharma, Pfizer, and Takeda; and has received pharmaceutical/research grants from: AbbVie, Boston Scientific, Daiichi Sankyo, EA Pharma, Kissei Pharmaceutical, JIMRO, Kyorin, Mitsubishi Tanabe Pharma, Mochida Pharmaceutical, Nichi-lko Pharmaceutical, Nippon Kayaku, Pfizer, Takeda, and Zeria Pharmaceutical; P. Juillerat has received fees for lectures and consulting/advisory board from: AbbVie, Amgen, Bristol Myers Squibb, Eli Lilly and Company, Ferring Pharmaceuticals, Gilead Sciences, Janssen, Merck Sharp & Dohme, Pfizer, Pierre Fabre, Sandoz, Takeda, Tillotts Pharma AG, and UCB Pharma

Introduction

Mirikizumab (miri), an anti-IL-23p19 antibody, has shown efficacy in patients with moderately-to-severely active Crohn’s disease (CD) to Week (W)52. We explored the potential relationship between early histologic and endoscopic responses on long term clinical outcomes after 2 years of miri treatment in a double-blind, placebo (PBO)-controlled Phase 2 trial (NCT02891226) in patients with CD.

Aims & Methods

Patients were randomized 2:1:1:2 to 4 treatment arms: miri 1000mg, 600mg, 200mg, and PBO administered intravenously (IV) at W0, W4, and W8. Patients who received miri and achieved ≥1 point improvement at W12 in Simple Endoscopic Score for Crohn’s disease score were re-randomized to either continue their induction IV dose or receive miri 300mg subcutaneously (SC) every 4 weeks up to W52. Subjects reported to experience clinical benefit received 300mg SC from W52 to W104. Biopsies were obtained during endoscopy at W0, W12 and W52 from the edges of any ulcers or from the most inflamed mucosa in the terminal ileum and 4 colonic segments and were scored by blinded central readers. Endpoints were defined post-hoc and prior to analyses (see Table 1). Among patients receiving miri with active histological disease at baseline, we determined the relationship between histologic and/or endoscopic response or remission at W12 and W52 and with clinical remission based on the Crohn’s Disease Activity Index (CDAI), patient-reported outcomes (PRO), and hospitalization rates at W104. Non-responder imputation for CDAI or PRO at W104 was used for patients who have observed histologic and endoscopic outcome value at W52 or W12. Hospitalizations were summarized by observed value. P-values for categorical values were determined with Fisher’s exact test.

Results

At W104, 56.9% patients (N=137) achieved CDAI remission compared to 41.5% of 176 patients at W52. We observed no association between early (W12) histologic, endoscopic, or combined (histo-endo) response and clinical remission (CDAI & PRO) at 2 years. After 2 years, the percentage of patients achieving remission based on CDAI varied according to their response at W52 by histology (60%), endoscopy (25.9%), both histo-endo (56.3%), or neither (10.5%, p=0.006; Table 1). Similarly, the proportion of patients who achieved 2-year clinical remission (by CDAI) varied according to W52 remission by histology (72.7%), endoscopy (40%), both histo-endo (40%) or neither (19.5%, p=0.007). Hospitalization rates during this period were low and varied according to W52 response by histology (16.7%), endoscopy (0%), both (0%) or neither (3.9%, p=0.021).

Table 1. Week 104 clinical remission and hospitalization rates by histologic and endoscopic response at Week 12 and Week 52, and by histologic and endoscopic remission at Week 52

Week 104	Without Histologic or Endoscopic Response	Histologic and Without Endoscopic Response	Endoscopic response Without Histologic	Histologic and Endoscopic Response	P‑value	Without Histologic or Endoscopic Remission	Histologic Without Endoscopic Remission	Endoscopic Without Histologic Remission	Histologic and Endoscopic Remission	P‑value
	Week 12a					Week 12
CDAI remission	60 (12/20)	57.9 (11/19)	50 (2/4)	61.3 (19/31)	>0.999	Due to the low number of patients with endoscopic or histologic remission at Week 12, no data are shown in this quadrant
PRO remission	55 (11/20)	31.6 (6/19)	50 (2/4)	61.3 (19/31)	0.237
Hospitalizations due to CDb	0 (0/42)	3.9 (1/26)	0 (0/8)	3.2 (1/31)	0.426
	Week 52c					Week 52c
CDAI remission	10.5 (2/19)	60 (6/10)	25.9 (7/27)	56.3 (9/16)	0.006	19.5 (8/41)	72.7 (8/11)	40 (6/15)	40 (2/5)	0.007
PRO remission	10.5 (2/19)	30 (3/10)	11.1 (3/27)	68.8 (11/16)	<0.001	12.2 (5/41)	63.6 (7/11)	33.3 (5/15)	40 (2/5)	0.003
Hospitalizations due to CDb	3.9 (1/26)	16.7 (2/12)	0 (0/39)	0 (0/24)	0.021	3.9 (2/52)	5 (1/20)	0 (0/24)	0 (0/5)	0.809
Note: Data displayed as % (n/N). For categorical outcomes, p-values are based on Fisher’s exact test. Histologic response was defined as: a) absence of neutrophils in epithelium, and absence of epithelial damage, erosions and ulceration or b) decrease of either RHI or modified GHAS ≥50% from baseline. Endoscopic response is defined as a 50% reduction from baseline in SES-CD. Histologic remission was defined as absence of mucosal neutrophils, epithelial damage, erosions, and ulceration. Endoscopic remission is defined as SES-CD of <4 ileal-colonic or <2 for isolated ileal disease, and no subscore of >1. CDAI remission is defined as CDAI Total Score <150; PRO remission is defined as (7-day average of SF ≤2.5 and no worse than baseline) + (7-day average of AP≤1 and no worse than baseline). SF captures number of liquid or very soft stools; AP score is classified as 0=none, 1=mild, 2=moderate, 3=severe. Abbreviations: AP= abdominal pain; CDAI= Crohn’s Disease Activity Index; GHAS= Global Histologic Disease Activity Score; PRO= patient-reported outcomes; N=number of patients in the histologic/endoscopic response group; n = number of patients in the specified category; RHI= Robarts Histologic Index; SES-CD=Simple Endoscopic Score for Crohn’s Disease; SF= stool frequency. a Patients with Active histologic disease at Baseline and with both Endoscopic and Histologic measures at Week 12. b Defined as serious adverse event due to hospitalization. Week 12 columns depict hospitalizations from Weeks 12-52. Week 52 columns depict hospitalizations from Weeks 52-104. c Patients with Active histologic disease at Baseline and with both Endoscopic and Histologic measures at Week 52.

Conclusion

In CD patients treated with miri for 2 years, long term clinical remission (CDAI, PRO) was significantly correlated with histologic response alone as well as combined histologic-endoscopic response at Week 52, but not at Week 12. The small sample size was likely a limitation. This data will be further studied in Phase 3 trials.

Disclosure

VJ reports consulting/advisory board fees from AbbVie, Alimentiv Inc (formerly Robarts Clinical Trials), Arena pharmaceuticals, Asahi Kasei Pharma, Asieris, 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, Vividion; speaker’s fees from, Abbvie, Ferring, Galapagos, Janssen, Pfizer, Shire, Takeda, Fresenius Kabi. 
WR reports lecture fees from AbbVie, Actelion, Alpha Wasserman, AstraZeneca, Cellerix, Cosmo Pharmaceuticals, Ferring, Genentech, Grunenthal, Johnson & Johnson, Millennium, Merck, NovoNordisk, Nycomed, Pfizer, Pharmacosmos, Schering-Plough, Salix, Takeda, UCB Pharma, and Vifor; consultant fees from AbbVie, Actelion, Alpha Wasserman, AstraZeneca, Cellerix, Cosmo Pharmaceuticals, Ferring, Genentech, Grunenthal, Johnson & Johnson, Millennium, Merck, NovoNordisk, Nycomed, Pfizer, Pharmacosmos, Schering-Plough, Salix, Takeda, UCB Pharma, and Vifor; and serves as an advisory board member for AbbVie, Actelion, Alpha Wasserman, AstraZeneca, Cellerix, Cosmo Pharmaceuticals, Ferring, Genentech, Grunenthal, Johnson & Johnson, Millennium, Merck, NovoNordisk, Nycomed, Pfizer, Pharmacosmos, Schering-Plough, Salix, Takeda, UCB Pharma, and Vifor.
GDH reports that his institution has received fees for his clinical trial activities with Centocor J&J.
NH has served as an advisory board member or consultant for Eli Lilly and Company, Abbvie Inc., Bristol Meyer Squibb, Inc., and PathAI, Inc.
RP reports consulting fees from Seres Therapeutics, Eli Lilly, Protagonist, Genentech, and Robarts Clinical Trials.
MP, ZL, RH, HC are employees and minor shareholders of Eli Lilly and company. 
FM served as speaker for Abbvie, Arena, Biogen, Bristol-Myers Squibb, Falk, Ferring, Hospira, Janssen, Laboratórios Vitoria, Pfizer, Lilly, Merck Sharp & Dohme, Sandoz, Takeda, UCB, Vifor.

Introduction

Given the natural history of Crohn’s disease (CD), the beneficial effects of treatments may wane over time and result in loss of response. Treatment escalation may aid in re-capturing clinical benefit and improving markers of inflammation. Upadacitinib (UPA) is an oral reversible Janus kinase inhibitor that demonstrated efficacy compared with placebo in 2 phase 3 induction studies and 1 maintenance study, U‑ENDURE, in CD^1-3 and is approved for patients with moderately to severely active CD.⁴ In this post hoc analysis, we evaluated the effect of UPA 30 mg therapy among patients who experienced loss of response to UPA 15 mg maintenance treatment or upon treatment withdrawal.

Aims & Methods

Patients who achieved clinical response (≥ 30% decrease in average daily very soft/liquid stool frequency [SF] and/or abdominal pain score [APS], neither worse than baseline) to 12 weeks of UPA 45 mg once daily (QD) induction therapy were re-randomized to receive UPA 30 mg, UPA 15 mg, or placebo QD in U‑ENDURE (NCT03345823). Beginning at week 4, patients who experienced loss of response and required medical treatment could receive open‑label (OL) UPA 30 mg QD. Loss of response was defined as having clinical symptoms (average daily very soft/liquid SF ≥ 4.0 and/or average daily APS ≥ 2.0) plus an objective marker of inflammation (protocol-specified criteria for high‑sensitivity C-reactive protein [hsCRP], fecal calprotectin [FCP], or Simple Endoscopic Score for CD). Outcomes were assessed at 12 and 24 weeks after initiation of OL UPA 30 mg QD therapy and included clinical remission and clinical response (both per CD Activity Index [CDAI] and SF/APS), enhanced clinical response, and FCP and hsCRP levels. Safety was also assessed. Analyses were based on as observed data without imputation.

Results

Patients who received OL UPA 30 mg QD therapy had, at baseline, a mean CD duration of 10 years, mean CDAI of 304, median hsCRP of 14.3 mg/L, and median FCP of 1550 µg/g; 83.5% had prior biologic failure. At 12 weeks after initiation of OL UPA 30 mg QD, regardless of group during blinded maintenance, 84.4%–87.6% of patients achieved SF/APS clinical response, 77.2%–78.9% achieved enhanced clinical response, 63.3%–71.3% achieved CDAI clinical response, and 46.7%–53.8% achieved SF/APS or CDAI clinical remission (Table). Reponses were sustained through 24 weeks. Median hsCRP and FCP levels decreased after initiation of OL UPA 30 mg QD therapy. Adverse event rates in either group were consistent with those in the overall population. One major adjudicated cardiovascular event in the placebo group and 2 events of non-melanoma skin cancer in the UPA 15-mg group were reported after receiving UPA 30 mg.

Table. Outcomes After Initiation of Open-Label Upadacitinib 30 mg Rescue Therapy
Outcome	Dose Escalation After Loss of Response to UPA 15 mg		Treatment Re-initiation After Loss of Response with PBO Withdrawal
	12 weeks	24 weeks	12 weeks	24 weeks
SF/APS	n = 90	n = 67	n = 145	n = 114
SF/APS clinical responsea Enhanced clinical responseb SF/APS clinical remissionc	76 (84.4) (77.0,91.9) 71 (78.9) (70.5,87.3) 43 (47.8) (37.5,58.1)	60 (89.6) (82.2,96.9) 59 (88.1) (80.3,95.8) 39 (58.2) (46.4,70.0)	127 (87.6) (82.2,93.0) 112 (77.2) (70.4,84.1) 77 (53.1) (45.0,61.2)	103 (90.4) (84.9,95.8) 95 (83.3) (76.5,90.2) 63 (55.3) (46.1,64.4)
CDAI	n = 90	n = 65	n = 143	n = 111
CDAI clinical responsed CDAI clinical remissione	57 (63.3) (53.4,73.3) 42 (46.7) (36.4,57.0)	46 (70.8) (59.7,81.8) 41 (63.1) (51.3,74.8)	102 (71.3) (63.9,78.7) 77 (53.8) (45.7,62.0)	81 (73.0) (64.7,81.2) 62 (55.9) (46.6,65.1)
hsCRP, mg/dL, median (range)	n = 87 4.4 (0.2,75.3)	n = 69 7.0 (0.2,116.0)	n = 147 3.7 (0.2,176.0)	n = 117 3.0 (0.2,75.4)
FCP, µg/g, median (range)	n = 79 715 (30,10901)	n = 55 655 (30,12425)	n = 143 416 (30,11235)	n = 107 356 (30,24853)
APS, abdominal pain score; CDAI, Crohn’s Disease Activity Index; FCP, fecal calprotectin; hsCRP, high-sensitivity C‑reactive protein; PBO, placebo; SF, stool frequency; UPA, upadacitinib. Unless otherwise noted, all results are presented as n (%) (95% CI). a≥ 30% decrease in average daily very soft or liquid SF and/or ≥ 30% decrease in average daily APS and both not greater than baseline. b≥ 60% decrease in average daily very soft or liquid SF and/or ≥ 35% decrease in average daily APS from baseline and both not greater than baseline, or clinical remission per SF/APS. cAverage daily very soft or liquid SF ≤ 2.8 and average daily APS ≤ 1.0 and both not greater than baseline. dDecrease of ≥ 100 points in CDAI from baseline. eCDAI < 150.

Conclusion

Among patients with CD who responded to UPA 45 mg induction therapy and subsequently lost response during maintenance when randomized to placebo or UPA 15 mg QD, most regained clinical response and many achieved clinical remission 12 weeks after initiating UPA 30 mg QD therapy. These improvements were sustained through 24 weeks. No new safety signals were observed.

References

1. Colombel JF, et al. Gastroenterology. 2022;162:S1394.
2. Loftus EV Jr. United European Gastroenterol J. 2022;10;103–104.
3. Panés J, et al. Am J Gastroenterol. 2022;117:S10.
4. RINVOQ. Summary of Product Characteristics. AbbVie Deutschland GmbH & Co. KG; 2023. Accessed 24 April 2023. https://www.ema.europa.eu/en/documents/product-information/rinvoq-epar-product-information_en.pdf.

Disclosure

RP has received consultancy and/or speaking honoraria from Abbott, AbbVie, Alimentiv (formerly Robarts), Amgen, Arena Pharmaceuticals, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Celltrion, Cosmos, Eisai, Elan, Ferring, Galapagos, Fresenius Kabi, Genentech, Gilead, GSK, JAMP Bio, Janssen, Lilly, Merck, Mylan, Novartis, Oppilan Pharma, Organon, Pandion, Pendopharm, Pfizer, Progenity, Prometheus, Protagonist, Roche, Sandoz, Satisfai Health, Shire, Sublimity, Takeda, Theravance, Trellus, Viatris, and Ventyx, and has received research funding from Abbvie, Janssen, Pfizer, and Takeda.
JOL has received consulting and/or speaker fees from AbbVie, Bristol-Myers Squibb, Celgene, Celltrion, Ferring, Galapagos, Gilead, GSK, Janssen, Lilly, Napp, Pfizer, Shire, Takeda, and Vifor Pharma; and investigator-led research grants from AbbVie, Gilead, Pfizer, Shire, and Takeda.
JP has received financial support for research from AbbVie and Pfizer; consultancy fees/honorarium from AbbVie, Arena, Athos, Atomwise, Boehringer Ingelheim, Celgene, Celsius, Celltrion, Ferring, Galapagos, Genentech/Roche, GSK, Janssen, Mirum, Morphic, Nestlé, Origo, Pandion, Pfizer, Progenity, Prometheus, Protagonist, Revolo, Robarts, Sanofi, Takeda, Theravance, and Wasserman; reports payment for lectures, including service on speaker bureaus, from Abbott, Ferring, Janssen, Pfizer and Takeda; and reports payment for development of educational presentations from Abbott, Janssen, Pfizer, Roche and Takeda.
PS has received honoraria for consulting and/or speaking activities from AbbVie, Ferring, Janssen, Lilly, Roche, Pfizer, and Takeda. He has served as an investigator for clinical trials sponsored by Abbvie, Gilead, Janssen, Pfizer, and Takeda.
MNR has been a principal investigator for studies sponsored by AbbVie.
MDM-A has received consulting and/or speaker fees from AbbVie, Galapagos, Janssen, Pfizer, Takeda, and Tillotts, and has received research funding from AbbVie, Janssen, and Pfizer.
FB has served as an investigator for clinical trials sponsored by AbbVie and Janssen.
APL, ED, SF, SA, and TF are employees or contractors of AbbVie, and may own AbbVie stock and/or stock options.
GD'H has received honoraria for consulting and/or speaking activities from AbbVie, Alimentiv, Boehringer Ingelheim, Celltrion, Ferring, Galapagos, GSK, Gossamer Bio, Janssen, Lilly, Pfizer, Progenity, Takeda, and Tillotts.
Funding
AbbVie Inc. 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 Lisa M Pitchford, PhD, of JB Ashtin, and funded by AbbVie.