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This information is intended for US healthcare professionals to access current scientific information about J&J Innovative Medicine products. It is prepared by Medical Information and is not intended for promotional purposes, nor to provide medical advice.

STELARA® (ustekinumab)

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STELARA - Use in Combination with a Janus Kinase Inhibitor in Adult Patients With Crohn’s Disease or Ulcerative Colitis

Last Updated: 04/16/2025

Summary

The company cannot recommend any practices, procedures, dosing, or usage that deviate from the approved labeling.
The efficacy and safety of STELARA in combination with Janus kinase inhibitors (JAKis) for the treatment of Crohn’s disease (CD) or ulcerative colitis (UC) have been reported in a retrospective study, case series, and case reports.¹^-⁸

clinical data

Retrospective Study - CD or UC

Alayo et al (2021)¹ conducted a retrospective study in the United States in patients with CD or UC who received tofacitinib in combination with biologic therapies, including STELARA.

A total of 35 patients with inflammatory bowel disease were included in this study; 5 patients were receiving concomitant therapy with STELARA.
For efficacy outcomes of STELARA in combination with tofacitinib, see Table: Efficacy Outcomes.

Efficacy Outcomes¹

Outcome	N	STELARA + Tofacitinib (%)
Clinical response at week 8^a	3	66.7
Clinical response at week 16^a	3	66.7
Clinical response at LDA^a	5	60.0
Endoscopic/radiographic response^b	4	100
Abbreviations: CD, Crohn’s disease; HBI, Harvey-Bradshaw Index; LDA, last documented assessment; MARIAs, simplified magnetic resonance index of activity; PGA, physician global assessment; SCCAI, Simple Clinical Colitis Activity Index; SES-CD, Simple Endoscopic Score for Crohn’s Disease; TBT, tofacitinib in combination with a biologic therapy; UC, ulcerative colitis. Note: Clinical response was assessed by HBI for CD, SCCAI for UC, or PGA for patients with ostomy at weeks 8, 16, 26, 39, and 52 (4 weeks) after initiation of TBT. ^aClinical response was deﬁned as either a decrease in HBI by ≥3 or SCCAI by ≥3 from baseline. ^bEndoscopic/radiographic response was defined as a ≥1 point reduction in the Mayo endoscopic subscore for UC, >50% reduction in SES-CD, or ≥50% reduction in the global MARIAs score for CD.

Case Series

Miyatani et al (2024)² conducted a retrospective, observational case series of 10 patients with CD who received STELARA and upadacitinib from April 2021 to July 2022.

The median age was 35.5 years (interquartile range [IQR], 28.3-43.8), with a median age at diagnosis of 18.5 years (IQR, 16-24.3). The median number of previous biologic therapies was 4 (IQR, 4-5).
STELARA was administered either at 90 mg every 4 weeks subcutaneous (SC, n=8; 80%) or every 8 weeks SC (n=2; 20%).
The median follow-up was 10 months (IQR, 7.3-12). Efficacy and safety outcomes of the STELARA and updacitinib combination therapy are presented in Table: Efficacy and Safety Outcomes.
No patients required surgery following combination treatment.
Mild infections occurred in 4 patients (40%), all of which were resolved within a week.
No cases of herpes zoster infection, thromboembolism, major adverse cardiovascular events, or malignancy were reported.

Efficacy and Safety Outcomes²

Case	Outcome (3-6 Months)	Steroid-Free After DTT	Adverse Effect	Follow-up Period (Months)	Continue DTT
1	Joint pain improved (Active EIM)	Yes	None	12	Yes
2	Joint pain improved (Active EIM)	NA	Nausea	2	Yes^a
3	Clinical remission^b	NA	None	12	Yes
4	Clinical remission^b	Yes	Small bowel obstruction^c	4	Yes
5	Perianal fistula closed	NA	Sinusitis	17	Yes
6	Clinical response^d	NA	Upper respiratory infection	7	Yes
7	Clinical remission^b, joint pain improved (Active EIM)	NA	Upper respiratory infection	9	Yes
8	Clinical remission^b	NA	Acne	11	Yes
9	Clinical remission^b	Yes	None	17	Yes
10	NA^e	No	Nausea, cutaneous fungal infection	8	No
Abbreviations: EIM, extraintestinal manifestations; DTT, dual-targeted therapy; HBI, Harvey-Bradshaw Index; NA, not applicable. ^aThis patient required de-escalation from upadacitinib 15 mg daily to 15 mg every other day. Clinical remission was defined as HBI ≤4, and clinical response was defined as a decrease in HBI by ≥3 or by physician assessment of clinical response. ^bClinical remission was defined as HBI <5. ^cThe patient in case 4 developed a small bowel obstruction requiring hospitalization and bowel rest; however, stenosis had been identified prior to treatment. ^dClinical response was defined as a decrease in HBI by ≥3 or by physician assessment of clinical response. ^ePatient did not tolerate combination therapy due to nausea.

Case Reports

Case reports of adult patients with CD or UC treated with STELARA and JAKis are described in Table: Summary of Case Reports Among Adults with CD or UC who Received Combination Therapy of STELARA and JAKi.

Summary of Case Reports Among Adults with CD or UC who Received Combination Therapy of STELARA and JAKi²^-⁸

Author/Year	Patient Characteristics	Treatment Outcomes
Case report - CD
Owings et al (2020)³	A 40-year-old African American male patient with CD and severe cutaneous granulomatous. CD affected both the large and small intestine, complicated by perianal fistulae, lymphopenia, cutaneous lesions, bowel resection, colostomy, total proctocolectomy, and end ileostomy. Prior treatment for CD included anti-TNFs, AZA, and steroids.	Mostly recently, the patient had been receiving STELARA and AZA for over a year but continued to experience flares with minimal improvement in the skin lesions. A biopsy examination confirmed the diagnosis of granulomatous dermatitis with vasculitis; furthermore, abnormal results from 2 DHR tests raised strong concerns for CGD AZA was discontinued due to concerns of CGD and the patient was started on tofacitinib in combination with STELARA. The patient showed significant overall improvement, with substantial healing of the granulomatous rash.
Case report - UC
Rowan et al (2024)⁴	A 28-year-old pregnant patient with UC (pancolitis, duration of 5 years) received combination therapy with STELARA and tofacitinib and 5-ASA. Patient was receiving STELARA 90 mg Q4W, with a prior secondary loss of response to infliximab. Despite achieving endoscopic remission 3 months before conception, the patient was symptomatic by 8 weeks gestation, with FCP levels >10,000 μg/g. Intestinal sonography revealed increased left colonic wall thickness and hyperemia.	Treatment was initiated with oral corticosteroids and 5-ASA suppositories; however, the inability to taper prednisone <20 mg daily required STELARA reinduction. Tofacitinib 10 mg BID was initiated, due to a Mayo score of 2 at 15 weeks gestation. By 34 weeks of gestation, the patient achieved corticosteroid-free clinical and sonographic remission while continuing on tofacitinib 10 mg BID, STELARA Q4W, and 5-ASA suppositories. Tofacitinib 10 mg twice daily was discontinued at delivery due to anticipated breastfeeding. At the time of this report, the patient was in remission (calprotectin, 145 μg/g) while continuing STELARA and 5-ASA suppositories.
Bucheeri et al (2024)⁵	A 35-year-old male patient with severe UC received STELARA and tofacitinib. The patient was refractory to multiple therapies, including 5-ASA, AZA, infliximab with methotrexate, vedolizumab, STELARA, and tofacitinib.	Due to disease progression requiring hospitalization and parenteral steroid rescue therapy, the patient was switched back to STELARA, which provided minimal symptom improvement; repeated steroid courses were required for disease control. Tofacitinib was added to the treatment regimen. Combination therapy led to remission of symptoms and inflammatory markers, with reduction in FCP (3728 μg/g to 46 μg/g), as well as endoscopic and histologic remission. The patient also weaned off his oral steroid. After 4 years of combination therapy, the patient remained in remission without any reported AEs or infections.
Thurston et al (2023)⁶	A 20-year-old Caucasian male patient with UC received STELARA, vedolizumab, and tofacitinib. In August 2015, the patient was hospitalized for Clostridium difficile infection and received 2 infusions of infliximab 10 mg/kg, which he continued post-discharge along with mesalamine, 6MP, and a prednisone taper. A colonoscopy in November 2015 revealed severe Mayo score of 3 pancolitis. Vedolizumab was initiated following discontinuation of 6MP and infliximab due to insufficient response.	Steroids were started and his vedolizumab dose was escalated to q4w based on August 2016 colonoscopy findings of chronic colitis, with Mayo 2 inflammation of ascending, transverse, descending and rectosigmoid colon. The patient exhibited a clinical response, leading to steroid tapering by October 2016. A colonoscopy in November 2016 indicated resolution of right-sided colitis with residual proctosigmoiditis (Mayo score of 2), while colonoscopy on May 2017 showed persistent rectosigmoid inflammation (Mayo score of 2) with chronic active colitis. Due to recurring inflammation, STELARA q8w was added. A colonoscopy in December 2017 showed no improvement, which led to STELARA dose escalation to q4w along with increased steroid dose and addition of budesonide and mesalamine. The steroid was tapered off by February 2020 following clinical improvement. A colonoscopy in December 2020 revealed severe (Mayo score of 3) recto-sigmoiditis with mild colitis in the descending to transverse colon. Tofacitinib was added and budesonide was discontinued in February 2021 due to clinical improvement. A colonoscopy in November 2021 demonstrated complete endoscopic remission (Mayo score of 0), prompting de-escalation by initially discontinuing mesalamine and increasing STELARA to q8w, then adjusting vedolizumab to q8w interval. Subsequently, STELARA and tofacitinib were discontinued, and the patient remained in remission on vedolizumab q8w monotherapy at the time of this report.
Hickman et al (2022)⁷	A 25-year-old Caucasian male patient with refractory UC. During 4 years after the initial diagnosis, the patient experienced treatment failure, intolerance, and secondary nonresponse to various biologic therapies and could not be tapered-off of prednisone. Prior to admission, the patient was on 14 weeks of infliximab without any clinical improvement. Colonoscopy revealed Mayo score of 2-3 disease with discrete ulcerations.	The patient was initiated on STELARA due to primary nonresponse. However, despite dose escalation to Q4W and continued prednisone use, the symptoms persisted. Tofacitinib was initiated; the patient initially experienced clinical improvement, but the condition worsened after 3 months. The tofacitinib dose was increased from BID to TID, and repeat colonoscopy revealed pancolitis with Mayo score of 2 disease. The patient was switched to combination therapy with STELARA and tofacitinib twice daily. The patient experienced progressive clinical improvement. After a year, colonoscopy showed no signs of disease activity, and biopsy examinations showed no evidence of cryptitis, crypt abscesses, or an active inflammatory infiltrate.
Costiniuk et al (2021)⁸	A 36-year-old female patient with severe UC and comorbid HIV receiving antiretroviral therapy in 2008. Later in 2012, the patient experienced frequent episodes of bloody diarrhea. Colonoscopy revealed severe pancolitis, with biopsy findings consistent with active UC.	Along with mesalamine suppositories and enemas, the patient received oral prednisone, IV methylprednisolone, oral mesalamine, 6MP. The patient was also treated with infliximab (2012-2013) until the development of antibodies. In 2014, UC remained refractory despite administration of maximum doses of adalimumab. Dose tapering led to disease flare ups and a cushingoid feature. The patient declined colectomy. In 2015, colonoscopy revealed severe inflammation with ulcerations and friability. The patient received vedolizumab, but experienced rectal bleeding and weight loss, requiring continuation of prednisone. By March 2016, prednisone was discontinued as clinical remission was achieved. In 2016, three months after stopping steroids, colonoscopy revealed worsening disease with Mayo 3 colitis. Consequently, the patient switched to vedolizumab, and prednisone oral dose was increased. The patient experienced bright red rectal bleeding, frequent stools, lower abdominal cramping, and rectal pain. The patient was initiated with tofacitinib while prednisone dose was maintained. Symptoms persisted and required hospitalization for IV prednisolone, but the patient continued to decline surgical colectomy. Following tofacitinib, the patient received STELARA from March to September 2017, during which the patient gained 30 pounds in 1 year (BMI, 37), developed increased abdominal fat, and bilateral cataracts due to cortisone. Attempts to taper the prednisone dose to <30 mg daily led to bloody diarrhea, with 12 to 17 bowel movements per day. By June 2018, the patient agreed to undergo subtotal abdominal colectomy with rectal stump and temporary end ileostomy. Postoperatively, the patient initially showed improvement but presented with right lower quadrant pain and elevated CRP a month later. In March 2019, surveillance sigmoidoscopy revealed chronic active proctitis with ulceration, consistent with chronic idiopathic IBD.

Abbreviations: 5-ASA, 5-aminosalicylic acid; AZA, azathioprine; 6MP, 6-mercaptopurine; AE, adverse event; BID, two times a day; BMI, body mass index; CD, Crohn’s disease; CGD, chronic granulomatous disease; CRP, C-reactive protein; DHR, dihydro rhodamine; FCP, fecal calprotectin; HIV, human immunodeficiency virus; IBD, inflammatory bowel disease; IV, intravenous; Q4W, every 4 weeks; Q8W, every 8 weeks; TID, thrice times a day; TNF, tumor necrosis factor; UC, ulcerative colitis.

Abbreviations: 5-ASA, 5-aminosalicylic acid; AZA, azathioprine; 6MP, 6-mercaptopurine; AE, adverse event; BID, two times a day; BMI, body mass index; CD, Crohn’s disease; CGD, chronic granulomatous disease; CRP, C-reactive protein; DHR, dihydro rhodamine; FCP, fecal calprotectin; HIV, human immunodeficiency virus; IBD, inflammatory bowel disease; IV, intravenous; Q4W, every 4 weeks; Q8W, every 8 weeks; TID, thrice times a day; TNF, tumor necrosis factor; UC, ulcerative colitis.

LITERATURE SEARCH

A literature search of MEDLINE^®, EMBASE^®, BIOSIS Previews^®, and DERWENT^® (and/or other resources, including internal/external databases) was conducted on 15 March 2025.

References

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1	Alayo QA, Khatiwada A, Patel A, et al. Effectiveness and safety of combining tofacitinib with a biologic in patients with refractory inflammatory bowel diseases. Inflamm Bowel Dis. 2021;27(10):1698-1702.
2	Miyatani Y, Choi D, Choi NK, et al. Dual-targeted therapy with upadacitinib and ustekinumab in medically complex Crohn’s disease. Dig Dis Sci. 2024;69(2):355-359.
3	Owings AH, Glover SC. Severe cutaneous lesions in Crohn’s disease responsive to combination therapy, ustekinumab and tofacitinib [abstract]. Am J Gastroenterol. 2020;115(1):S1211. Abstract S2291.
4	Rowan C, Yeaman F, Ernest-Suarez K, et al. Tofacitinib as a rescue therapy for ulcerative colitis in pregnancy. Inflamm Bowel Dis. 2024;30(5):868-870.
5	Bucheeri MA, Alabdulkarim B, Wolman S. Combining tofacitinib and ustekinumab for refractory ulcerative colitis: a case report [abstract]. J Can Assoc Gastroenterol. 2024;7(Suppl. 1):52-53. Abstract A76.
6	Thurston T, Moskow J, Glassner K, et al. Vedolizumab, ustekinumab and tofacitinib as triple therapy for ulcerative colitis [abstract]. Inflamm Bowel Dis. 2023;29(Suppl. 1):S81-S82. Abstract izac247.0156.
7	Hickman K, Jordan R, Sonnier W. Combination biologic and small molecule therapy for refractory ulcerative colitis. Gastroenterology. 2022;162(3):S103.
8	Costiniuk CT, Bessissow T, Isnard S, et al. Use of various immunotherapies for refractory ulcerative colitis in a person living with HIV: a case report. Oxf Med Case Rep. 2021;2021(1):40-42.