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Efficacy DataVELSIPITY helped patients calm their UC1*

A proportion of patients achieved clinical remission,* including improvements in stool frequency and rectal bleeding.1

In adults with moderately to severely active UC1: Significant clinical remission*VELSIPITY vs placebo at week 12 and at week 52 (co-primary endpoints)1

See the Data

Meaningful clinical response†VELSIPITY vs placebo at week 12 (other prespecified secondary endpoint)1

See the Data

Significant endoscopic improvement‡VELSIPITY vs placebo at week 12 and at week 52 (key secondary endpoint)1

See the Data

Trial design1,2: A 52-week and a 12-week, randomized, multicenter, double-blind, placebo-controlled trial that evaluated adults with moderate to severe UC who failed ≥1 predefined UC therapies.§ Concomitant use of stable doses of select UC therapies was permitted. See Trial Design.

Clinical remission was defined as an SF subscore of 0 or 1, an RB subscore of 0, and an ES ≤1 (excluding friability). Proportion of patients in clinical remission in UC-1: 27% (74/274) with VELSIPITY vs 7% (9/134) with placebo at week 12; 32% (88/274) with VELSIPITY vs 7% (9/134) with placebo at week 52 (P<0.001). Proportion of patients in clinical remission in UC-2: 26% (57/221) with VELSIPITY vs 15% (17/112) with placebo at week 12 (P<0.05).1Clinical response was defined as a ≥2-point and a ≥30% decrease from baseline in an mMS and a ≥1-point decrease from baseline in an RB subscore or an absolute RB subscore ≤1 at week 12. Proportion of patients in clinical response: 62% (171/274) with VELSIPITY vs 34% (46/134) with placebo in UC-1; 62% (137/221) with VELSIPITY vs 41% (46/112) with placebo in UC-2.1,3Endoscopic improvement was defined as an ES ≤1 (excluding friability). Proportion of patients with endoscopic improvement in UC-1: 35% (96/274) with VELSIPITY vs 14% (19/134) with placebo at week 12; 37% (101/274) with VELSIPITY vs 10% (13/134) with placebo at week 52 (P<0.001). Proportion of patients with endoscopic improvement in UC-2: 30% (66/221) with VELSIPITY vs 19% (21/112) with placebo at week 12 (P<0.05).1Failed=inadequate response, loss of response, or intolerance.1Explore clinical data

Clinical Remission

Clinical Response

Endoscopic Improvement

Symptomatic Improvement

Isolated Proctitis

Example

Clinical remission with VELSIPITY vs placebo

UC-1

UC-2

Significant clinical remission in the overall population1*

Data show proportion of patients who met endpoints

of patients in clinical remission with VELSIPITY at week 52 (88/274) were also corticosteroid free1†

3× as many biologic/JAKi-naive patients achieved clinical remission1*

Data show proportion of patients who met endpoints

 Clinical remission was defined as an SF subscore of 0 or 1, an RB subscore of 0, and an ES ≤1 (excluding friability).1Corticosteroid-free remission was defined as clinical remission at week 52 without receiving corticosteroids for ≥12 weeks prior to week 52.1Advanced therapies include S1P receptor modulators, biologics, and JAKi.2ES=endoscopy score; IL=interleukin; RB=rectal bleeding; SF=stool frequency.

   ES=endoscopy score; IL=interleukin; RB=rectal bleeding; SF=stool frequency.

Significant clinical remission in the overall population1*

Data show proportion of patients who met endpoint

Nearly 2× as many biologic/JAKi-naive patients achieved clinical remission1*

Data show proportion of patients who met endpoint

 Clinical remission was defined as an SF subscore of 0 or 1, an RB subscore of 0, and an ES ≤1 (excluding friability).1Advanced therapies include S1P receptor modulators, biologics, and JAKi.2
Clinical response with VELSIPITY vs placebo

UC-1

UC-2

Meaningful clinical response in the overall population at week 121,4*

Data show proportion of patients who met endpoint

2 out of 3 biologic/JAKi-naive patients had a clinical response at week 123*

Data show proportion of patients who met endpoint

 Clinical response was defined as a ≥2-point and a ≥30% decrease from baseline in an mMS and a ≥1-point decrease from baseline in an RB subscore or in an absolute RB subscore ≤1 at week 12.1Clinical response at week 52

Clinical response in the overall population3,4*

Data show proportion of patients who met endpoint

Clinical response in biologic/JAKi-naive patients3*

Data show proportion of patients who met endpoint

 Clinical response was defined as a ≥2-point and a ≥30% decrease from baseline in an mMS and a ≥1-point decrease from baseline in an RB subscore or in an absolute RB subscore ≤1 at week 12 and week 52.1,2

Meaningful clinical response in the overall population at week 121,4*

Data show proportion of patients who met endpoint

Nearly 2 out of 3 biologic/JAKi-naive patients had a clinical response at week 123*

Data show proportion of patients who met endpoint

 Clinical response was defined as a ≥2-point and a ≥30% decrease from baseline in an mMS and a ≥1-point decrease from baseline in an RB subscore or in an absolute RB subscore ≤1 at week 12.1
Endoscopic improvement with VELSIPITY vs placebo

UC-1

UC-2

Significant endoscopic improvement in the overall population1*

Data show proportion of patients who met endpoint

Additionally, more patients achieved endoscopic remission† by week 12 (15% VELSIPITY vs 4% placebo) and week 52 (26% VELSIPITY vs 6% placebo)1

More than 2× as many biologic/JAKi-naive patients achieved endoscopic improvement1*

Data show proportion of patients who met endpoint

 Endoscopic improvement was defined as an ES ≤1 (excluding friability).1Normalization of the endoscopic appearance of the mucosa, or endoscopic remission, was defined as an ES of 0. At both week 12 and week 52, endoscopic normalization was seen in 11% of VELSIPITY patients vs 1% on placebo.1Advanced therapies include S1P receptor modulators, biologics, and JAKi.2

Significant endoscopic improvement in the overall population1*

Data show proportion of patients who met endpoint

Additionally, more patients achieved endoscopic remission† by week 12 (17% VELSIPITY vs 8% placebo)1

Nearly 2× as many biologic/JAKi-naive patients achieved endoscopic improvement1*

Data show proportion of patients who met endpoint

 Endoscopic improvement was defined as an ES ≤1 (excluding friability).1Normalization of the endoscopic appearance of the mucosa, or endoscopic remission, was defined as an ES of 0.1Advanced therapies include S1P receptor modulators, biologics, and JAKi.3
Symptomatic improvement with VELSIPITY vs placebo1

UC-1

UC-2

Patients experienced symptomatic improvement as early as week 21-3 Nearly half of patients achieved symptomatic remission* at week 121-3 Symptomatic remission was defined as an SF subscore of 0 (or an SF subscore of 1 with a ≥1-point decrease from baseline) and an RB subscore of 0.2RB=rectal bleeding; SF=stool frequency.Additional symptomatic data in UC-1LIMITATIONS: While Rectal Bleeding and Symptomatic Remission were prespecified, Stool Frequency was not prespecified, and was a POST HOC analysis that potentially introduced inherent biases. Also, results at all time points were not controlled for multiplicity, except for Symptomatic Remission at week 12 and at week 52. Therefore, the analyses should be viewed cautiously.Percentage of patients with a ≥1-point decrease from baseline in Stool Frequency3* Patients with an SF subscore of 0 at baseline were considered nonresponders.3

Percentage of patients with a ≥1-point decrease from baseline in Rectal Bleeding3†

 All patients had an RB subscore of ≥1 at baseline.3Significant Symptomatic Remission was achieved at week 12 and at week 52 with VELSIPITY vs placebo3‡ Symptomatic Remission was defined as an SF subscore of 0 (or an SF subscore of 1 with a ≥1-point decrease from baseline) and an RB subscore of 0.2
Patients experienced symptomatic improvement as early as week 21-3 Nearly half of patients achieved symptomatic remission* at week 121-3 Symptomatic remission was defined as an SF subscore of 0 (or an SF subscore of 1 with a ≥1-point decrease from baseline) and an RB subscore of 0.2RB=rectal bleeding; SF=stool frequency.Additional symptomatic data in UC-2LIMITATIONS: While Rectal Bleeding and Symptomatic Remission were prespecified, Stool Frequency was not prespecified, and was a POST HOC analysis that potentially introduced inherent biases. Also, results at all time points were not controlled for multiplicity, except for Symptomatic Remission at week 12. Therefore, the analyses should be viewed cautiously.Percentage of patients with a ≥1-point decrease from baseline in Stool Frequency3* Patients with an SF subscore of 0 at baseline were considered nonresponders.3

Percentage of patients with a ≥1-point decrease from baseline in Rectal Bleeding3†

 All patients had an RB subscore of ≥1 at baseline.3Significant Symptomatic Remission was achieved at week 12 with VELSIPITY vs placebo3‡ Symptomatic Remission was defined as an SF subscore of 0 (or an SF subscore of 1 with a ≥1-point decrease from baseline) and an RB subscore of 0.2
Do you see patients with isolated proctitis in your practice?According to an expert panel discussing their own systematic literature review:

LIMITATIONS: Systematic literature reviews include different trial designs and types, different practice types and regions (some ex-US), different definitions for and severity of ulcerative proctitis across the trials studied, and some missing trials during the selection process.

Based on a meeting of 35 IOIBD experts in September 2021. They convened to make recommendations from their recent systematic literature review to address the unmet needs of ulcerative proctitis because of its exclusion from UC RCTs to date. It is an expert consensus with recommendations as opposed to conclusions based on predefined study endpoints.5IOIBD=International Organization for the Study of Inflammatory Bowel Diseases; RCTs=randomized controlled trials.

VELSIPITY is the first advanced therapy† to include patients with isolated proctitis in UC clinical trials2

8% of patients (n=56) in the VELSIPITY clinical trial program had isolated proctitis confirmed by centrally read colonoscopy or proctosigmoidoscopy at baseline1,3

Advanced therapies include S1P receptor modulators, biologics, and JAKi.2

See data in patients with isolated proctitis

Clinical Remission

Clinical Response

Endoscopic Improvement

Symptomatic Remission

Tab Number 5

Clinical remission data in isolated proctitis subgroup population1-3

UC-1

UC-2

Tab Number 3

Tab Number 4

Tab Number 5

LIMITATIONS: Clinical remission analyses in patients with isolated proctitis were not controlled for multiplicity and patient numbers were small. Therefore, efficacy conclusions cannot be drawn and the data should be viewed cautiously.

Patients with isolated proctitis in clinical remission3*

  • Patients with isolated proctitis (<10 cm rectal involvement) at baseline who met other eligibility criteria could enroll in UC-1 and UC-2, with enrollment capped at 15% of total patients2
  • These subgroup analyses included 56 patients across UC-1 and UC-2 with isolated proctitis confirmed by centrally read colonoscopy or proctosigmoidoscopy at baseline from both trials (N=741)1,3
Clinical remission was defined as an SF subscore of 0 or 1, an RB subscore of 0, and an ES ≤1 (excluding friability).1

LIMITATIONS: Clinical remission analyses in patients with isolated proctitis were not controlled for multiplicity and patient numbers were small. Therefore, efficacy conclusions cannot be drawn and the data should be viewed cautiously.

Patients with isolated proctitis in clinical remission3*

  • Patients with isolated proctitis (<10 cm rectal involvement) at baseline who met other eligibility criteria could enroll in UC-1 and UC-2, with enrollment capped at 15% of total patients2
  • These subgroup analyses included 56 patients across UC-1 and UC-2 with isolated proctitis confirmed by centrally read colonoscopy or proctosigmoidoscopy at baseline from both trials (N=741)1,3
Clinical remission was defined as an SF subscore of 0 or 1, an RB subscore of 0, and an ES ≤1 (excluding friability).1

Clinical response data in isolated proctitis subgroup population1-3

UC-1

UC-2

Tab Number 3

Tab Number 4

Tab Number 5

LIMITATIONS: Clinical response analyses in patients with isolated proctitis were not controlled for multiplicity and patient numbers were small. Therefore, efficacy conclusions cannot be drawn and the data should be viewed cautiously.

Patients with isolated proctitis in clinical response3*

  • Patients with isolated proctitis (<10 cm rectal improvement) at baseline who met other eligibility criteria could enroll in UC-1 and UC-2, with enrollment capped at 15% of total patients2
  • These subgroup analyses included 56 patients across UC-1 and UC-2 with isolated proctitis confirmed by centrally read colonoscopy or proctosigmoidoscopy at baseline from both trials (N=741)1,3
Clinical response was defined as a ≥2-point and a ≥30% decrease from baseline in an mMS and a ≥1-point decrease from baseline in an RB subscore or in an absolute RB subscore ≤1 at week 12 and week 52.1,2

LIMITATIONS: Clinical response analyses in patients with isolated proctitis were not controlled for multiplicity and patient numbers were small. Therefore, efficacy conclusions cannot be drawn and the data should be viewed cautiously.

Patients with isolated proctitis in clinical response3*

  • Patients with isolated proctitis (<10 cm rectal improvement) at baseline who met other eligibility criteria could enroll in UC-1 and UC-2, with enrollment capped at 15% of total patients2
  • These subgroup analyses included 56 patients across UC-1 and UC-2 with isolated proctitis confirmed by centrally read colonoscopy or proctosigmoidoscopy at baseline from both trials (N=741)1,3
Clinical response was defined as a ≥2-point and a ≥30% decrease from baseline in an mMS and a ≥1-point decrease from baseline in an RB subscore or in an absolute RB subscore ≤1 at week 12.1

Endoscopic improvement data in isolated proctitis subgroup population1,2,4

UC-1

UC-2

Tab Number 3

Tab Number 4

Tab Number 5

LIMITATIONS: Endoscopic improvement analyses in patients with isolated proctitis were not controlled for multiplicity and patient numbers were small. Therefore, efficacy conclusions cannot be drawn and the data should be viewed cautiously.

Patients with isolated proctitis with endoscopic improvement3*

  • Patients with isolated proctitis (<10 cm rectal improvement) at baseline who met other eligibility criteria could enroll in UC-1 and UC-2, with enrollment capped at 15% of total patients2
  • These subgroup analyses included 56 patients across UC-1 and UC-2 with isolated proctitis confirmed by centrally read colonoscopy or proctosigmoidoscopy at baseline from both trials (N=741)1,3
Endoscopic improvement was defined as an ES ≤1 (excluding friability).1

LIMITATIONS: Endoscopic improvement analyses in patients with isolated proctitis were not controlled for multiplicity and patient numbers were small. Therefore, efficacy conclusions cannot be drawn and the data should be viewed cautiously.

Patients with isolated proctitis with endoscopic improvement3*

  • Patients with isolated proctitis (<10 cm rectal improvement) at baseline who met other eligibility criteria could enroll in UC-1 and UC-2, with enrollment capped at 15% of total patients2
  • These subgroup analyses included 56 patients across UC-1 and UC-2 with isolated proctitis confirmed by centrally read colonoscopy or proctosigmoidoscopy at baseline from both trials (N=741)1,3
Endoscopic improvement was defined as an ES ≤1 (excluding friability).1

Symptomatic remission data in isolated proctitis subgroup population1-3

UC-1

UC-2

Tab Number 3

Tab Number 4

Tab Number 5

LIMITATIONS: Symptomatic remission analyses in patients with isolated proctitis were not controlled for multiplicity and patient numbers were small. Therefore, efficacy conclusions cannot be drawn and the data should be viewed cautiously.

Patients with isolated proctitis in symptomatic remission3*

  • Patients with isolated proctitis (<10 cm rectal improvement) at baseline who met other eligibility criteria could enroll in UC-1 and UC-2, with enrollment capped at 15% of total patients2
  • These subgroup analyses included 56 patients across UC-1 and UC-2 with isolated proctitis confirmed by centrally read colonoscopy or proctosigmoidoscopy at baseline from both trials (N=741)1,3
Symptomatic remission was defined as an SF subscore of 0 (or an SF subscore of 1 with a ≥1-point decrease from baseline) and an RB subscore of 0.2

LIMITATIONS: Symptomatic remission analyses in patients with isolated proctitis were not controlled for multiplicity and patient numbers were small. Therefore, efficacy conclusions cannot be drawn and the data should be viewed cautiously.

Patients with isolated proctitis in symptomatic remission3*

  • Patients with isolated proctitis (<10 cm rectal improvement) at baseline who met other eligibility criteria could enroll in UC-1 and UC-2, with enrollment capped at 15% of total patients2
  • These subgroup analyses included 56 patients across UC-1 and UC-2 with isolated proctitis confirmed by centrally read colonoscopy or proctosigmoidoscopy at baseline from both trials (N=741)1,3
Symptomatic remission was defined as an SF subscore of 0 (or an SF subscore of 1 with a ≥1-point decrease from baseline) and an RB subscore of 0.2
Trial Design

Read about the trial design for VELSIPITY.

 See Trial Design LoadingReferences:VELSIPITY [prescribing information]. New York, NY: Pfizer Inc.; June 2024.Sandborn WJ, Vermeire S, Peyrin-Biroulet L, et al. Etrasimod as induction and maintenance therapy for ulcerative colitis (ELEVATE): two randomised, double-blind, placebo-controlled, phase 3 studies [published correction appears in Lancet. 2023;401(10381):1000]. Lancet. 2023;401(10383):1159-1171.Data on file. Pfizer Inc.Sandborn WJ, Vermeire S, Peyrin-Biroulet L, et al. Etrasimod as induction and maintenance therapy for ulcerative colitis (ELEVATE): two randomised, double-blind, placebo-controlled, phase 3 studies [published correction appears in Lancet. 2023;401(10381):1000]. Lancet. 2023;401(10383):1159-1171. Supplementary appendix available at: https://www.thelancet.com/cms/10.1016/S0140-6736(23)00061-2/attachment/cdbbc759-490f-4b2a-a3a2-93bc9918b29f/mmc1.pdf. Accessed August 2, 2024.Caron B, Abreu MT, Siegel CA, et al. IOIBD recommendations for clinical trials in ulcerative proctitis: the PROCTRIAL consensus. Clin Gastroenterol Hepatol. 2022;20(11):2619-2627.e1.Peyrin-Biroulet L, Dubinsky MC, Sands BE, et al. Efficacy and safety of etrasimod in patients with moderately to severely active isolated proctitis: results from the phase 3 ELEVATE UC clinical programme [published correction appears in J Crohns Colitis. 2024. https://academic.oup.com/ecco-jcc/advance-article/doi/10.1093/ecco-jcc/jjae098/7696859] [published online ahead of print April 2024]. J Crohns Colitis. 2024. https://academic.oup.com/ecco-jcc/advance-article/doi/10.1093/ecco-jcc/jjae038/7645267. Accessed August 2, 2024.

Forms and resources to help eligible patients access their prescribed medication

Efficacy

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PP-V1A-USA-0857
IndicationVELSIPITY® (etrasimod) is indicated for the treatment of moderately to severely active ulcerative colitis (UC) in adults.
Important Safety Information Contraindications
  • Patients in the last 6 months who experienced myocardial infarction, unstable angina, stroke, transient ischemic attack, decompensated heart failure requiring hospitalization, or Class III or IV heart failure
  • Patients with a history or presence of Mobitz type II second-degree or third-degree AV block, sick sinus syndrome, or sino-atrial block, unless the patient has a functioning pacemaker
Infections 

VELSIPITY may increase the susceptibility to infections. Life-threatening and rare fatal infections have been reported in association with other sphingosine 1-phosphate (S1P) receptor modulators. Before starting VELSIPITY, obtain a recent (i.e., within 6 months) CBC, including lymphocyte count. Delay initiation of VELSIPITY in patients with an active infection until the infection is resolved. Consider interruption of treatment with VELSIPITY if a patient develops a serious infection. Continue monitoring for infections up to 5 weeks after discontinuing VELSIPITY.

  • Progressive multifocal leukoencephalopathy (PML) is an opportunistic viral infection of the brain that typically occurs in patients who are immunocompromised, and usually leads to death or severe disability. PML has been reported in multiple sclerosis (MS) patients treated with S1P receptor modulators and has been associated with risk factors and duration of use. Longer treatment duration (≥18 months) increases the risk of PML. VELSIPITY is not indicated in MS. If PML is suspected, suspend VELSIPITY and discontinue if PML is confirmed by appropriate diagnostic evaluation. Immune reconstitution inflammatory syndrome (IRIS) has been reported in patients with MS treated with S1P receptor modulators who developed PML and discontinued treatment. Clinical decline may be rapid, can lead to serious neurological complications or death, and is often associated with characteristic MRI changes. Onset was generally within a few months after S1P receptor modulator discontinuation. Monitoring for IRIS should be undertaken.
  • Herpes simplex encephalitis, varicella zoster meningitis, and localized herpes viral infections have been reported with S1P receptor modulators. In UC-1, herpes zoster was reported in 0.7% of subjects treated with VELSIPITY and in none of the subjects who received placebo. Patients without a healthcare professional-confirmed history of varicella (chickenpox), or without documentation of a full course of vaccination against varicella zoster virus (VZV), should be tested for antibodies to VZV before initiating VELSIPITY. A full course of VZV vaccination for antibody-negative patients is recommended prior to commencing treatment with VELSIPITY.
  • Cases of fatal cryptococcal meningitis (CM) and disseminated cryptococcal infections have been reported with S1P receptor modulators. VELSIPITY treatment should be suspended until a cryptococcal infection has been excluded. If CM is diagnosed, appropriate treatment should be initiated.
  • VELSIPITY has not been studied in combination with anti-neoplastic, immune-modulating, or non-corticosteroid immunosuppressive therapies. Avoid concomitant administration of these therapies with VELSIPITY. 
  • Update immunizations according to current guidelines prior to VELSIPITY treatment. Avoid the use of live attenuated vaccines during and for 5 weeks after treatment with VELSIPITY. If live attenuated vaccine immunizations are required, administer at least 4 weeks prior to initiation of VELSIPITY.
Bradyarrhythmia and Atrioventricular (AV) Conduction Delays 
Initiation of VELSIPITY may result in a transient decrease in heart rate and AV conduction delays. Before starting VELSIPITY, obtain an ECG to assess for preexisting cardiac conduction abnormalities. Seek advice of a cardiologist for patients with: significant QT prolongation; arrhythmia requiring treatment with Class Ia or Class III anti-arrhythmic drugs or QT prolonging drugs; unstable ischemic heart disease, Class I or Class II heart failure, history of cardiac arrest, cerebrovascular disease, or uncontrolled hypertension; resting HR<50bpm; history of symptomatic bradycardia, recurrent cardiogenic syncope, or severe untreated sleep apnea; history of Mobitz type I second-degree AV block in the absence of a functioning pacemaker.

Liver Injury 
Elevations of aminotransferases may occur in patients receiving VELSIPITY. Obtain transaminase and bilirubin levels, if not recently available (i.e., within the last 6 months), before initiation of VELSIPITY or in patients who develop symptoms suggestive of hepatic dysfunction. Discontinue VELSIPITY if significant liver injury is confirmed. Use of VELSIPITY in patients with severe hepatic impairment is not recommended.

Macular Edema 
S1P receptor modulators have been associated with an increased risk of macular edema. Obtain baseline evaluation of the fundus, including the macula near the start of VELSIPITY treatment. Periodically assess the fundus, including the macula, during treatment or if there is a change in vision. Consider discontinuing VELSIPITY if macular edema develops. 

Increased Blood Pressure 
VELSIPITY patients in clinical trials had average increases of 1 to 4 mm Hg systolic and 1 to 2 mm Hg diastolic blood pressure (BP). Increases were first detected after 2 weeks of treatment and remained within the specified average range of BP increases throughout treatment. Monitor BP during treatment with VELSIPITY and manage appropriately.

Fetal Risk 
Based on animal studies, VELSIPITY may cause fetal harm. Advise pregnant females and females of reproductive potential of the potential risk to a fetus and to use effective contraception to avoid pregnancy during and for one week after stopping VELSIPITY. Pregnant females exposed to VELSIPITY are encouraged to contact the pregnancy registry by calling 1-800-616-3791.

Cutaneous Malignancies 
Risk of cutaneous malignancies is increased in patients treated with S1P receptor modulators in clinical trials and cutaneous malignancies have been reported in the postmarketing setting. Skin examinations are recommended prior to or shortly after the start of treatment and periodically thereafter for all patients, particularly those with risk factors for skin cancer. Monitor for suspicious skin lesions. Limit UV exposure including phototherapy.

Posterior Reversible Encephalopathy Syndrome
Rare cases of posterior reversible encephalopathy syndrome (PRES) have been reported in patients receiving S1P receptor modulators. If a patient develops neurological or psychiatric symptoms/signs or any symptom/sign suggestive of an increase of intracranial pressure, or accelerated neurological deterioration, complete a physical and neurological examination promptly and consider an MRI. Symptoms of PRES are usually reversible but may evolve into ischemic stroke or cerebral hemorrhage. Delay in diagnosis and treatment may lead to permanent neurological sequelae. If PRES is suspected, discontinue treatment with VELSIPITY.

Respiratory Effects 
VELSIPITY may cause a decline in pulmonary function. Spirometric evaluation should be conducted during therapy if clinically indicated.

Unintended Additive Immune System Effects from Prior Treatment with Immunosuppressive or Immune-Modulating Drugs 
When switching to VELSIPITY from drugs with prolonged immune effects, consider the half-life and mode of action of these drugs to avoid unintended additive immunosuppressive effects.

Immune System Effects After Stopping VELSIPITY 
After stopping VELSIPITY, lymphocyte counts returned to the normal range in 90% of subjects within 4 to 5 weeks. Use of immunosuppressants within this period may lead to an additive effect on the immune system, and therefore monitor patients receiving concomitant immunosuppressants for infectious complications up to 5 weeks after the last dose of VELSIPITY.

Most Common Adverse Reactions 
Most common adverse reactions reported in ≥ 2% of subjects and at a higher rate than placebo included: headache, elevated liver tests, dizziness, arthralgia, nausea, hypertension, bradycardia, UTI, hypercholesterolemia, and herpes viral infection.

Please see full Prescribing Information, including Medication Guide.Indication

VELSIPITY is indicated for the treatment of moderately to severely active ulcerative colitis (UC) in adults.