Introduction

Upadacitinib, a selective JAK inhibitor, has demonstrated efficacy in clinical trials for ulcerative colitis (UC), but real-world data in refractory populations remain limited. This study evaluates its effectiveness, safety, and differential response based on prior advanced therapy failures in a real-world cohort.

Aims & Methods

Ambispective analysis of 80 UC patients initiating upadacitinib across 13 centers. Clinical remission (CR: partial Mayo score <3), clinical-biochemical remission (CBR: Mayo <3 + CRP <5 mg/L + calprotectin <250 μg/g), and steroid-free remission (SFR) were assessed at weeks 8, 16, and 6 months. Subgroup analyses compared outcomes by prior biologic/small molecule exposure.

Results

A total of 80 patients with ulcerative colitis were included, with a mean age of 38 years (range 17–69) and a predominance of males (62.5%). Most patients had extensive colitis (57%), and the average disease duration was 9 years. Extraintestinal manifestations were present in 26.6% (mainly articular). The cohort was highly refractory, with a mean of 2.3 prior advanced therapies; 84.6% had previously received infliximab, 37.2% ustekinumab, and nearly one-third had tried tofacitinib. At induction, 54.5% received upadacitinib 45 mg for 8 weeks, and at 6 months, 69.7% were maintained on 30 mg, while 24.2% required 45 mg.
At week 8, a rapid improvement in disease activity was observed, with the mean partial Mayo score dropping from 5.8 at baseline to 2.0. Clinical remission was achieved in 62.3% of patients at this timepoint, and 23.2% reached combined clinical-biochemical remission. These benefits were largely maintained over time: at 6 months, 51.3% of patients remained in clinical remission, 23.1% in combined remission, and 28.2% achieved steroid-free remission. Inflammatory markers also improved, with CRP decreasing from 15.0 mg/L at baseline to 4.8 mg/L at 6 months, and calprotectin showing a downward trend. (Table 1)
When analyzing effectiveness by prior treatment exposure, patients with only one previous advanced therapy achieved higher rates of clinical remission at 6 months (64.3%) compared to those with two or more prior biologic failures (44.0%). A similar pattern was seen for steroid-free remission (35.7% vs. 24.0%). Nonetheless, even among multi-refractory patients, a substantial proportion achieved and maintained remission with upadacitinib.
Treatment was generally well tolerated. Ten patients (12.6%) discontinued upadacitinib before 6 months, mainly due to primary non-response. Adverse events were reported in 23.8% of patients, most commonly mild (acne, herpes zoster, mild infections). Only three discontinuations were attributed to adverse events (herpes zoster, pneumonia, and acne), and no serious safety signals were identified.

Table 1: Effectiveness Outcomes

Timepoint	Baseline (n=79)	8 Weeks (n=69)	16 Weeks (n=44)	6 Months (n=32)	p¹
Partial Mayo Index	5.8	2.0 (<0.001)²	2.5 (<0.001)²	2.0 (<0.001)²	<0.001
CRP (mg/L)	15.0	6.5 (0.032)²	10.0 (0.121)²	4.8 (0.760)²	0.018
Calprotectin (μg/g)	2,992.4	1,760.6	1,149.9	2,035.9	0.087
Clinical Remission (%)	5.1%	62.3% (<0.001)³	58.7% (<0.001)³	51.3% (<0.001)³	-
Clinical-Biochemical Remission (%)	1.3%	23.2% (<0.001)³	32.6% (<0.001)³	23.1% (0.013)³	-
Steroid-Free Remission (%)	-	53.6%	39.1% (0.074)³	28.2% (0.021)³	-

Notes:
¹ Friedman test; ² Pairwise Friedman comparisons; ³ McNemar test.

Conclusion

Upadacitinib demonstrates rapid and sustained effectiveness in refractory UC, even in multi-refractory patients. While response rates diminish with prior treatment failures, clinically meaningful benefits persist, supporting its use in advanced therapy-experienced populations. The safety profile aligns with clinical trial data, with manageable adverse events.

Clinical Case Summary

27-year-old male with penetrating Crohn's disease (CD; A1, L2, pB3), diagnosed at the age of 9, with multiple hospitalizations. The patient was treated with infliximab + azathioprine for three years. Colonoscopy at 16 years showed pancolitis and was complicated with perforation, being submitted to total colectomy with rectal preservation and ileostomy. Therapy was switched to adalimumab+methotrexate, with partial clinical response. After seven years, due to severe complex fistulizing perianal disease, adalimumab was switched to ustekinumab. After 2 years of Ustekinumab monotherapy, he presented disabling symptoms and developed an enterocutaneous fistula peri-ileostomy. Combination therapy with ustekinumab+vedolizumab was started. The patient still maintained discharge from the enterocutaneous and perianal fistulas. After 1 year, a painful circumferential penile ulcer with swelling and seropurulent discharge was noted. Other causes, namely infections were excluded. Biopsies were performed and revealed non-caseous granulomatous inflammation with lymphocytic and eosinophilic infiltrates, compatible with CD. Topical therapy with tacrolimus ointment was applied, with no response. Ustekinumab+vedolizumab was switched to upadacitinib. There was a substantial improvement of the penile lesion, the enterocutaneous fistula discharge reduced, and perianal symptoms resolved on maintenance therapy with Upadacitinib.
Genital metastatic CD is uncommon and mainly occurs in the setting of colonic involvement and perianal disease. Treatment options for MCD remain underwhelming due to the limited available evidence and varying responses of reported therapeutic methods. Optimization of biologic therapy is mandatory.

References

For this case we'll include:
- Pictures ​of the penile ulcers before and during maintenance therapy with upadacitinib
- Endoscopic evaluation during follow-up
- Histological specimen of colectomy and from multiple endoscopic evaluations performed
- Radiological evidence of perianal and peri-ileostomy enterocutaneous fistula

Introduction

Mirikizumab (MIRI), a p19-directed antibody against interleukin-23, demonstrated improvements in fatigue, abdominal pain (AP) and stool frequency (SF) at Week (W) 12 and W52 in the VIVID-1 clinical trial.¹

Aims & Methods

The aim of this analysis is to show the effect of MIRI on fatigue, AP, SF and achievement of clinical remission by Patient-Reported Outcome (PRO; SF ≤3 and AP ≤1 and neither worse than baseline) in the VIVID-2 open-label extension study through W104. This analysis includes data from primary analysis set in patients with Crohn’s disease (CD) randomised to the MIRI treatment arm in VIVID-1 who achieved endoscopic response (≥50% reduction from baseline in Simple endoscopic score for CD) at W52 and continued the MIRI subcutaneous dosing (300 mg) in VIVID-2. Change from VIVID-1 baseline was measured for continuous endpoints. Endpoints included fatigue measured using FACIT-Fatigue (measured as change from baseline, and clinically-meaningful improvement of ≥6-points among patients with baseline ≤46), AP improvement (measured as change from baseline, and achievement of ≤1 among patients with baseline >1), SF improvement (measured as change from baseline, and achievement of ≤3 among patients with baseline >3) and clinical remission by PRO, assessed at W64 and 104. Missing data were handled using observed case (OC) and modified non-responder imputation (mNRI) for response rates, while using modified baseline observation carried forward (mBOCF) for change from baseline. Response rates were presented as unadjusted proportions with 2-sided 95% confidence intervals using the Rubin's Rules (mNRI). ANCOVA models were used for continuous variables, adjusting for baseline values and intervention group.

Results

Fatigue mean (standard error [SE]) change from baseline was 10.7 (0.56) at W64; 9.4 (0.59) at W104, (observed response, n [%]: 152 [67.6%] at W64; 136 [64.8%] at W104; Table). AP improved (mean [SE] change: −1.5 [0.04] at W64; −1.6 [0.05] at W104), with response rates increasing from 174 (77.3%) to 161 (84.7%). SF showed sustained improvement (mean [SE] change: −4.3 [0.14] at W64; −4.3 [0.16] at W104), with response rates reaching 155 (89.6%) at W104 (Table). Similar rates of achievement of clinical remission by PRO were observed (178 [73.6%] at W64; 165 [80.1%] at W104) (Table).

Table: Improvement in fatigue, abdominal pain, stool frequency and achievement of clinical remission by PRO up to Week 104

	FACIT-Fatigue (N=251)		Abdominal pain (N=251)		Stool frequency (N=251)		Clinical remission by PRO (N=251)
	Week 64	Week 104	Week 64	Week 104	Week 64	Week 104	Week 64	Week 104
Change from baselinea (mBOCF), LSM (SE)	10.7 (0.56)	9.4 (0.59)	−1.5 (0.04)	−1.6 (0.05)	−4.3 (0.14)	−4.3 (0.16)	NA	NA
Response (observed)b, n (%) (95% CI)	152 (67.6) (61.2–73.3)	136 (64.8) (58.1–70.9)	174 (77.3) (71.4–82.3)	161 (84.7) (78.9–89.2)	175 (86.6) (81.3–90.6)	155 (89.6) (84.2–93.3)	178 (73.6) (67.7–78.7)	165 (80.1) (74.1–85.0)
Responseb (mNRI), % (95% CI)	67.1 (61.0–73.3)	60.8 (54.4–67.2)	76.7 (71.2–82.2)	79.2 (73.7–84.7)	85.8 (80.9–90.6)	84.0 (78.8–89.2)	72.6 (66.9–78.2)	75.0 (69.4–80.7)

CI, confidence interval; LSM, least squares mean; mBOCF, modified baseline observation carried forward; mNRI, modified non-responder imputation; n, no of patients; NA, not applicable; PRO, Patient-Reported Outcome; SE, standard error
^aBaseline of VIVID-1 study
^bFACIT-Fatigue: ≥6-point improvement for baseline score ≤46; Abdominal pain: achievement of ≤1 for baseline score >1; Stool frequency: achievement of ≤3 for baseline score >3; Clinical remission by PRO: SF ≤3 and AP ≤1 and neither worse than baseline

Conclusion

MIRI sustained improvement in fatigue, AP, SF and clinical remission by PRO through 104 weeks of continuous treatment. These consistent findings support the long-term treatment with MIRI to address key symptoms of CD.

References

1. Ferrante, MarcTron, Emiliano, et al. The Lancet. 404 (10470):2423-2436.

Disclosure

PB: Received financial support for research from AbbVie, EG; lecture fees from AbbVie, AMC ICP, Amgen, Bristol Myers Squibb, Celltrion, Dr Falk Benelux, EG, Galapagos, Globalport, Lilly, Medtalks, Materia Prima, Pentax, Springer Media; served on an advisory board for AbbVie, Bristol Meyers Squibb, CIRC, Galapagos, Janssen, Lilly, Pentax, PSI-CRO, Roche, Takeda, Tetrameros. AA: Consultant for Geneoscopy; received research support from Takeda. AV, GY and JW: Employee and shareholder of Eli Lilly and Company. NL: Consultant for Eli Lilly and Company. JRA: Consultant for Janssen, Pfizer, Abbvie, Vedanta, Geneteche, Seres Therapeutics, Ferring, GSK, Merck, Bristol Myer Squibb, Roivant, Celltrion, and TRXBio, Xencor, Shattuck Labs; Speaker for Abbvie, Janssen. MC: Provided educational activities for AbbVie, China Medical System, IPSEN, Janssen, and Takeda; served on an advisory board for Boehringer Ingelheim and Janssen; and has support for clinical research from Janssen and Takeda.

Introduction

Mirikizumab, a p19-directed interleukin-23 monoclonal antibody, is efficacious in inducing clinical response at Week(W) 12 and maintaining clinical remission through W52 in patients with moderately-to-severely active Crohn’s disease (CD) as shown in the phase 3 treat-through trial VIVID-1 (NCT03926130).¹ Here, we present analysis of maintenance outcomes through W52 for Patient-Reported Outcome (PRO) clinical responders and nonresponders at W12.

Aims & Methods

The analysis set includes patients randomized to mirikizumab at baseline, who did or did not achieve PRO clinical response at W12 after intravenous (IV) induction treatment (900 mg mirikizumab IV every 4 weeks [Q4W]) before entering subcutaneous (SC) maintenance treatment (300 mg mirikizumab SC Q4W). Descriptive statistics are used to summarize the data, applying nonresponder imputation for missing binary endpoints. As a treat-through study, no rerandomization was applied.

Results

From a total of 551 patients who entered SC maintenance treatment, baseline characteristics of age, duration of CD, and baseline Crohn’s Disease Activity Index (CDAI) were similar between W12 PRO responders (n=402, 73.0%) and W12 PRO nonresponders (n=149, 27.0%). PRO responders at W12 had a higher objective inflammatory burden at baseline (faecal calprotectin, c-reactive protein, and Simple Endoscopic Score-CD), whereas concomitant or prior medication usage was similar between the groups. For W12 PRO responders, SC mirikizumab treatment from W12 to W52 resulted in an increase in CDAI clinical remission from 52.2% to 65.4%, PRO clinical remission from 53.2% to 65.4%, and endoscopic response from 35.1% to 54.7%, respectively (Table 1). Among W12 PRO nonresponders, PRO response was achieved by 39.6% at W16, 45.6% at W20, 44.3% at W24, and 56.4% at W52 with continued mirikizumab SC treatment, while CDAI clinical remission and PRO clinical remission were achieved by 33.6% and 31.5% at W52, respectively. Endoscopic response increased from 30.2% at W12 to 40.3% at W52 among W12 PRO nonresponders (Table 1).

		PRO Nonresponders at W12 (N=149)	PRO Responders at W12 (N=402)
CDAI clinical remission, n (%)a	W12	8 (5.4%)	210 (52.2%)
	W16	16 (10.7%)	208 (51.7%)
	W20	28 (18.8%)	243 (60.4%)
	W24	35 (23.5%)	242 (60.2%)
	W52	50 (33.6%)	263 (65.4%)
Endoscopic response, n (%)a	W12	45 (30.2%)	141 (35.1%)
	W52	60 (40.3%)	220 (54.7%)
aPercentage of response is calculated by n/Nx*100%. CDAI, Clinical Disease Activity Index; PRO, patient-reported outcome

Table 1.

Conclusion

Subcutaneous mirikizumab maintenance treatment over 40 weeks leads to incremental and sustained improvements in rates of clinical and endoscopic response regardless of PRO clinical response status after induction. A substantial proportion of clinical nonresponders at W12 improved early during maintenance treatment suggesting continued treatment with mirikizumab can be beneficial and lead to long-term response.

References

1. Ferrante, Marc et al. Efficacy and safety of mirikizumab in patients with moderately-to-severely active Crohn's disease: a phase 3, multicentre, randomised, double-blind, placebo-controlled and active-controlled, treat-through study. Lancet. 2024;404(10470):2423-2436. doi:10.1016/S0140-6736(24)01762-8

Introduction

Autoimmune hepatitis (AIH) and its variants are uncommon causes of chronic liver disease (CLD) in India [1]. Concomitant metabolic dysfunction-associated steatotic liver disease (MASLD) in patients with autoimmune hepatitis (AIH) is a distinct entity [2]. We aimed to explore the frequency and impact of concomitant MASLD in patients with AIH [3].

Aims & Methods

This is a retrospective study conducted at Sanjay Gandhi Post Graduate Institute of Medical Sciences and King George Medical University, Lucknow, India. Data of patients with AIH who underwent treatment between 2013-2022 were collected from a prospectively filled-up electronic database. Standard criteria were used to diagnose AIH and MASLD [3][4]. Patients presenting with acute severe-AIH, acute-on-chronic-liver-failure, simple steatosis without any metabolic dysfunction, and hepatocellular carcinoma HCC) were excluded.Criteria to diagnose MASLD were applied to patients with AIH. Their demographic, clinical, biochemical, serological parameters, treatment response and long-term outcomes were measured and compared.

Results

Of 175 patients with AIH, 51 were excluded. A total of 122 patients [median age: 46 (34-54) years; 69.6% female] were included in the final analysis. The median follow-up period was 61 (50-76) months. Of the 122 patients, 38 (31%) had concomitant MASLD (AIH-MASLD). Patients withAIH-MASLD had higher baseline liver enzymes [aspertate aminotranferase 226 (121-278) vs 174 (113-225); p= 0.033, alanine aminotranferase: 115 (113-189) vs 97 (47-169); p=0.041]. A higher number of patients with AIH-MASLD presented with advanced fibrosis and decompensation (20.4% vs 10.7%; p=<0.001,30.3% vs 25%; p=0.030, respectively). Following immunosuppression, Patients with MASLD-AIH had attenuated remission rates compared to AIH alone (34.2% vs 77.4%; p=<0.001) [table: 1].

Table: 1
Outcome of patients with AIH and MASLD-AIH

Outcome	Overall	AIH	MASLD-AIH	p-value
Biochemical Remission at six months	82 (67.2%)	62 (74%)	20 (52.6%)	0.016
Non-response to steroid after two weeks	32 (26.2%)	12 (14.2%)	20 (52.6%)	0.001
Advanced fibrosis	25 (20.4%)	9 (10.7%)	16 (42.1%)	<0.001
Steatohepatitis	13 (10.6%)	5 (5.9%)	8 (21%)	0.012
Adverse events to steroid	44 (44.2%)	34 (47.6%)	21 (55.2%)	0.068
Presentation with Decompensation	37 (30.3%)	21 (25%)	16 (42.1%)	0.030
New Decompensation among patients with c-ACLD	26 (30.5%)	14 (16.7%)	12 (31.5%)	0.002
HCC	2 (1.6%)	0	2 (5.2%)	0.034
Mortality	25 (20.4%)	13 (15.4%)	12 (31.5%)	0.012

On multivariate analysis, liver biopsy suggestive of concomitant Metabolic dysfunction-associated steatohepatitis (MASH) [OR 5.25 (95% CI 2.27 - 12.16); p<0.001), concomitant MASLD [OR: 3.07 (95% CI1.02 - 9.24); p=0.045], advanced fibrosis [ OR: 2.69 (95% CI1.07 - 6.59); p=0.035], and presentation with decompensation [OR: 2.66 (95% CI:1.07 - 6.59); p=0.035] were associated with non-responsiveness to steroid.

Conclusion

About a third of patients with biopsy-proven AIH have concomitant MASLD. A significant number of patients with AIH-MASLD present with higher liver enzymes, advanced fibrosis, and decompensation compared to AIH alone. Patients with AIH-MASLD respond poorly to steroids and have a lower remission rate. Proper work-up is necessary in patients with steroid non-responsive-AIH to rule out concomitant MASLD.

References

1. Choudhuri G, Somani SK, Baba CS, et al. Autoimmune hepatitis in India: profile of an uncommon disease. BMC Gastroenterol. 2005 Aug 15;5:27. doi: 10.1186/1471-230X-5-27. PMID: 16098234; PMCID: PMC1236920.
2. Zachou K, Azariadis K, Lytvyak E, et al; International Autoimmune Hepatitis Group (IAIHG). Treatment responses and outcomes in patients with autoimmune hepatitis and concomitant features of non-alcoholic fatty liver disease. JHEP Rep. 2023 Apr 22;5(8):100778. doi: 10.1016/j.jhepr.2023.100778. PMID: 37456672; PMCID: PMC10339258.
3. Wang G, Tanaka A, Zhao H, et al. The Asian Pacific Association for the Study of the Liver clinical practice guidance: the diagnosis and management of patients with autoimmune hepatitis. Hepatol Int. 2021 Apr;15(2):223-257. doi: 10.1007/s12072-021-10170-1. Epub 2021 May 4. PMID: 33942203; PMCID: PMC8144150.
4. Eslam M, Newsome PN, Sarin SK, et al. A new definition for metabolic dysfunction-associated fatty liver disease: An international expert consensus statement. J Hepatol. 2020 Jul;73(1):202-209. doi: 10.1016/j.jhep.2020.03.039. Epub 2020 Apr 8. PMID: 32278004.

Introduction

Vedolizumab (VDZ), a monoclonal antibody therapy approved for moderate-to-severe ulcerative colitis (UC) and Crohn’s disease (CD) in China in 2020¹ has a unique, gut-selective, anti-lymphocyte trafficking (GSALT) mechanism of action.² However, there is limited data on VDZ's real-world effectiveness and safety in Chinese IBD patients.³ Interim results from the VALUE study that enrolled patients with UC have been published ^3,4 and final results are reported here.

Aims & Methods

VALUE (NCT04872491), a multicenter, single-arm, prospective, observational study evaluated the safety and effectiveness of VDZ in adult Chinese patients with IBD (N = 500) over 72 weeks. Clinical response, clinical remission, and endoscopic remission were assessed at Weeks 14, 30, and 54. Partial Mayo and Mayo endoscopic subscores at baseline and Weeks 14, 30, and 54 were calculated. Clinical response was defined as ≥2-point reduction in Partial Mayo Clinic score and ≥25% decrease from baseline score accompanied with ≥1-point decrease in the rectal bleeding or absolute rectal bleeding subscore ≤1. Clinical remission was defined as Partial Mayo Clinic score ≤2 with no subscore >1, endoscopic remission as Mayo endoscopic subscore ≤1, and complete endoscopic remission as Mayo endoscopic subscore 0. Safety results and CD patients’ data are presented in separate VALUE abstracts (IDs: AS-UEG-2025-01329 and AS-UEG-2025-01324).

Results

Among 409 UC patients enrolled in the final analysis, 91.9% (376/409) were included in the effectiveness analysis set. Mean age (±standard deviation [SD]) of patients was 46.3 (±15.1) years, and 59.4% (n=243) were male. At baseline, 30.8% (126/409) of patients had moderate UC, and 29.8% (122/409) had severe UC. The median duration of UC was 2.5 years, concomitant steroids were prescribed in 18.9% (71/376). Mean (±SD) partial Mayo score was 5.1 (2.1) at baseline, which declined to 1.7 (1.7), 1.5 (1.7) and 1.3 (1.5) by Weeks 14, 30 and 54, respectively, post-VDZ treatment. Patients achieving clinical response, clinical remission, endoscopic remission, and complete endoscopic remission were 76.9% (220/286), 71.1% (207/291), 63.6% (35/55), and 21.8% (12/55) at Week 14; 78.1% (193/247), 76.3% (190/249), 63.6% (28/44), and 27.3% (12/44) at Week 30; and 80.3% (155/193), 83.3% (165/198), 71.4% (20/28), and 50.0% (14/28) at Week 54, respectively. Patients with moderate and severe UC; biologic naïve patients and patients with prior exposure to biologics at baseline also achieved clinical response, clinical remission, and endoscopic remission (Table). Compared with baseline, mean (±SD) reduction of C-reactive protein (mg/L) at Weeks 14, 30, and 54 were 7.8 (20.2), 6.5 (22.2), and 3.4 (24.8), respectively; mean (±SD) reduction of fecal calprotectin (mu g/g) was 42.7 (150.7) at Week 14 and 212.6 (480.1) at Week 30. The proportion of patients achieving clinical remission without steroid use by Week 14 was 37.7% (23/61), which increased to 60.6% (20/33) by Week 54.

Data are presented as % (n/N). N, number of patients having clinical response/remission/endoscopic remission data. n, number of patients achieving clinical response/remission and endoscopic remission data.
	Moderate UC			Severe UC
	Clinical response	Clinical remission	Endoscopic remission	Clinical response	Clinical remission	Endoscopic remission
Week 14	89.8 (79/88)	65.9 (58/88)	57.1 (12/21)	90.0 (72/80)	63.8 (51/80)	56.3 (9/16)
Week 30	87.7 (64/73)	69.9 (51/73)	30.8 (4/13)	91.2 (62/68)	66.2 (45/68)	90.9 (10/11)
Week 54	92.2 (59/64)	81.3 (52/64)	62.5 (5/8)	88.5 (46/52)	73.1 (38/52)	60.0 (3/5)
	Biologic-exposed UC: 10.9% (41/376)			Biologic-naïve UC: 89.1% (335/376)
Week 14	69.0 (20/29)	66.7 (20/30)	16.7 (1/6)	77.8 (200/257)	71.7 (187/261)	69.4 (34/49)
Week 30	74.2 (23/31)	71.0 (22/31)	83.3 (5/6)	78.7 (170/216)	77.1 (168/218)	60.5 (23/38)
Week 54	60.0 (15/25)	81.5 (22/27)	83.3 (5/6)	83.3 (140/168)	83.6 (143/171)	68.2 (15/22)

Conclusion

This study indicated that VDZ demonstrated a good effectiveness profile in Chinese UC patients in the real-world setting.

References

1. Yan J et al., Medicine (Baltimore). 2024; 103: e38759.
2. Soler D et al. J Pharmacol Exp Ther. 2009; 330: 864-875.
3. Baili C et al. Am J Gastroenterol. 2023; 118: S213-S214.
4. Yan C et al. Am J Gastroenterol. 2023; 119: S894-S895.

Disclosure

This study was funded by Takeda (China) International Trading Co. Ltd. Xiuli Zuo, Ye Chen, and Yingchao Li have no conflicts of interest. Lifei Gu and Fang Zhou are Takeda employees and hold Takeda stock options. Minhu Chen received speaker honorariums from Takeda China, AstraZeneca China, Xian Janssen, and Eisai China.
Medical writing support for the development of this abstract under the direction of the authors was provided by Vibhuti Singh, Ph.D., of Cactus Life Sciences (part of Cactus Communications), funded by Takeda (China) International Trading Co., Ltd.