Risankizumab, sold under the brand name Skyrizi, achieved clinical remission at more than three times the rate of placebo in its pivotal Phase 3 trial — 20.3% versus 6.2% at week 12 — making it one of the most compelling new options for people living with moderate-to-severe ulcerative colitis. The FDA approved it in June 2024, and it became the first IL-23 inhibitor greenlit for both ulcerative colitis and Crohn’s disease. For the millions of patients who have cycled through older therapies without lasting relief, that kind of separation from placebo in a rigorous trial is not a minor statistical footnote. It represents a genuine shift in what targeted treatment can accomplish.
But risankizumab is far from the only drug rewriting expectations. A new class of anti-TL1A antibodies — including tulisokibart and duvakitug — is producing remission numbers in early trials that would have seemed unrealistic five years ago. Meanwhile, mirikizumab (Omvoh) now has four-year data showing sustained corticosteroid-free remission in 78% of patients, and the JAK inhibitor upadacitinib (Rinvoq) is delivering clinical response in over 80% of patients within just eight weeks. This article walks through each of these drugs in detail, examines what the trial data actually shows, addresses limitations and risks, and explores what this evolving landscape means for patients — particularly older adults and those managing overlapping conditions like cognitive decline.
Table of Contents
- Which Ulcerative Colitis Drug Is Achieving Remission 3x Faster Than Standard Therapy?
- The Anti-TL1A Revolution — Why Tulisokibart and Duvakitug Could Change Everything
- Four Years of Sustained Remission — What Omvoh’s Long-Term Data Reveals
- Comparing Speed, Efficacy, and Practical Tradeoffs Across UC Drug Classes
- Safety Signals and Limitations That Rarely Make the Headlines
- The Gut-Brain Connection — Why UC Treatment Matters for Cognitive Health
- Where UC Treatment Is Headed — Precision Medicine and Combination Approaches
- Conclusion
- Frequently Asked Questions
Which Ulcerative Colitis Drug Is Achieving Remission 3x Faster Than Standard Therapy?
The drug most directly matching the “3x faster remission” claim is risankizumab. In the INSPIRE Phase 3 induction trial, which randomized 975 patients with moderate-to-severe ulcerative colitis, 20.3% of those receiving the drug reached clinical remission by week 12, compared to just 6.2% on placebo. that is a ratio of roughly 3.3 to 1. What made this result particularly notable was the speed of early response: 52.2% of risankizumab patients showed clinical response by week 4, compared to 30.5% on placebo. For a disease where flares can be debilitating and unpredictable, shaving weeks off the time to meaningful improvement matters in tangible, daily ways — fewer urgent bathroom trips, less bloody stool, less gut pain interrupting sleep. The maintenance data reinforced the induction results.
In the COMMAND trial, 40.2% of patients receiving the 180 mg dose and 37.6% on the 360 mg dose maintained clinical remission at week 52, versus 25.1% on placebo. This matters because ulcerative colitis is a chronic relapsing condition. A drug that works fast but fails to hold remission is, in practical terms, a temporary reprieve followed by another round of disappointment. Risankizumab’s durability profile suggests it can do both, though no therapy works for everyone, and a meaningful percentage of patients in the trial did not achieve remission at all. It is worth placing these numbers in context. A 20% remission rate at 12 weeks might not sound transformative in isolation, but ulcerative colitis trials consistently show low placebo remission rates because the disease is genuinely difficult to control. The threefold separation from placebo is what distinguishes risankizumab from many older biologics, where the gap was often narrower. For patients who have already failed one or more therapies, even a statistically modest absolute number can represent a real chance at stability they have not had before.
The Anti-TL1A Revolution — Why Tulisokibart and Duvakitug Could Change Everything
If risankizumab represents a strong incremental advance, the anti-TL1A antibodies represent something closer to a new frontier. Tulisokibart, developed by Merck under the designation MK-7240, posted striking results in its Phase 2 ARTEMIS-UC trial, published in the New England Journal of Medicine. Among all enrolled patients, 26.5% achieved clinical remission at week 12 versus just 1.5% on placebo — a roughly 17-fold difference. Among patients who tested positive on a companion diagnostic, the remission rate climbed to 31.6% versus 10.8% on placebo. This is the first anti-TL1A monoclonal antibody with a companion diagnostic, meaning it could eventually allow gastroenterologists to identify which patients are most likely to respond before prescribing. Duvakitug, developed jointly by Sanofi and Teva, is the other anti-TL1A antibody generating serious attention. In the RELIEVE UCCD Phase 2b trial, the high-dose group achieved 47.8% clinical remission at week 14, compared to 20.45% on placebo.
Maintenance data announced in February 2026 showed 58% remission at week 44 on the 900 mg dose, with 50% reaching endoscopic improvement versus 23% on placebo. Sanofi has described the drug’s potential as “best-in-class,” and the numbers — particularly the maintenance figures — justify cautious optimism. However, both tulisokibart and duvakitug remain investigational. Phase 2 trials are designed primarily to assess dosing and safety signals, not to confirm efficacy with the rigor of Phase 3. History is littered with drugs that looked exceptional in Phase 2 and stumbled in larger, more diverse patient populations. Phase 3 trials for both drugs are underway, but until those results are in hand, clinicians and patients should view these numbers as promising signals, not settled science. The companion diagnostic approach for tulisokibart also introduces a layer of complexity — if the test is not widely available or insurance does not cover it, access could be uneven regardless of how well the drug performs.
Four Years of Sustained Remission — What Omvoh’s Long-Term Data Reveals
While newer drugs compete on speed to remission, mirikizumab (Omvoh), manufactured by Eli Lilly, has quietly built what may be the most impressive long-term dataset in the IL-23 class. Data from the LUCENT-3 extension study, presented at United European Gastroenterology Week in October 2025, showed that 78% of patients maintained corticosteroid-free clinical remission after four full years of treatment. Endoscopic remission — meaning the lining of the colon showed healing on direct visualization — was observed in 81% of patients. Perhaps most meaningfully for daily quality of life, 93% reported improvement in bowel urgency, the symptom that many patients describe as the most socially and emotionally disruptive aspect of living with ulcerative colitis.
These are the first four-year sustained outcomes data for any IL-23p19 antagonist in ulcerative colitis, and they address a question that short induction trials cannot: does the benefit last? For older adults in particular — including those managing cognitive changes or early dementia alongside a chronic gut condition — treatment stability is paramount. Frequent medication switches, steroid tapers, and disease flares do not just affect the colon. They disrupt sleep, nutrition, and daily routines in ways that can accelerate cognitive decline or complicate dementia care plans. The FDA has also approved a single-injection, once-monthly maintenance regimen for Omvoh, which simplifies administration considerably. For caregivers managing a loved one’s ulcerative colitis alongside dementia care, the difference between a complicated infusion schedule and a monthly subcutaneous injection at home can be the difference between a treatment that is sustainable and one that gradually falls apart.
Comparing Speed, Efficacy, and Practical Tradeoffs Across UC Drug Classes
Not all of these therapies compete on the same terms, and understanding the tradeoffs matters for making informed decisions with a gastroenterologist. Upadacitinib (Rinvoq), a JAK inhibitor, may be the fastest-acting option currently available — over 80% of patients who had previously failed anti-TNF therapy achieved clinical response or remission within eight weeks. That speed is valuable for patients in acute flares who need rapid stabilization. But JAK inhibitors carry boxed warnings for serious infections, cardiovascular events, blood clots, and malignancies, particularly in patients over 50 and those with cardiovascular risk factors. For an older adult population, that safety profile demands careful risk-benefit discussion.
Risankizumab and mirikizumab, both targeting IL-23, have generally favorable safety profiles in trial data but require longer timelines to reach peak effect. The anti-TL1A drugs offer a different mechanism entirely and may eventually prove effective in patients who do not respond to IL-23 blockade, though head-to-head comparison data does not yet exist. Guselkumab, another IL-23 inhibitor, received FDA approval in September 2025 for moderate-to-severe UC and became the first in its class to offer both subcutaneous and intravenous formulations — a flexibility that may matter for patients or caregivers who have strong preferences about how the drug is administered. The honest reality is that no single drug is best for every patient. Disease severity, prior treatment failures, age, comorbidities, insurance coverage, and even practical factors like whether a patient can reliably get to an infusion center all shape which therapy makes sense. A 45-year-old with newly diagnosed moderate UC and no prior biologic exposure is in a very different situation than a 72-year-old with treatment-refractory disease, cardiovascular risk factors, and a caregiver managing their medication schedule alongside a dementia care plan.
Safety Signals and Limitations That Rarely Make the Headlines
Trial data in press releases tends to emphasize efficacy over risk, and it is worth spending a moment on what these drugs cannot do and where caution is warranted. The remission rates cited above — 20% for risankizumab, 26.5% for tulisokibart, 47.8% for duvakitug — also mean that a substantial proportion of patients in every trial did not achieve remission. These are not cures. They are treatments that shift the odds meaningfully for a subset of patients, and the clinical challenge remains identifying which patients will respond to which drug before cycling through months of trial and error. Immunosuppression is an inherent consequence of all biologic and small-molecule therapies for UC. Drugs that dampen the immune system to reduce colonic inflammation also, by definition, reduce the body’s ability to fight infections and, potentially, surveil for malignancies.
For older adults — particularly those in congregate living settings or those whose immune systems are already compromised — this is not a theoretical concern. Tuberculosis screening, hepatitis B testing, and vaccination status reviews are standard parts of biologic initiation, but they require coordination that can fall through the cracks when multiple providers are involved in a patient’s care. There is also the question of cost. Biologics for ulcerative colitis commonly carry list prices exceeding $20,000 per year, and newer drugs often cost more. Insurance coverage, prior authorization requirements, and step therapy mandates — where a patient must fail cheaper drugs before gaining access to newer ones — create real barriers. A drug that achieves remission 3x faster than placebo is meaningless if a patient cannot access it for six months while navigating a prior authorization appeal. Patients and caregivers should ask about manufacturer patient assistance programs, specialty pharmacy support, and appeal processes before assuming a prescribed drug will be available and affordable.
The Gut-Brain Connection — Why UC Treatment Matters for Cognitive Health
The gut-brain axis is not a metaphor. Chronic intestinal inflammation drives systemic inflammatory signaling that crosses the blood-brain barrier, and emerging research has linked inflammatory bowel disease to modestly elevated risks of neurodegenerative conditions.
For patients already living with mild cognitive impairment or early-stage dementia, uncontrolled ulcerative colitis introduces compounding problems: malnutrition from poor absorption, sleep disruption from nocturnal symptoms, social isolation from bowel urgency, and the cognitive burden of managing a complex medication regimen on top of existing challenges. Achieving and sustaining remission in ulcerative colitis is not just a gastrointestinal goal — it is a strategy for preserving function, independence, and quality of life across multiple domains. When a drug like mirikizumab can deliver corticosteroid-free remission for four years, it also means four years without the cognitive side effects of systemic steroids, four years of more stable nutrition, and four years of one fewer crisis demanding attention from an already-stretched caregiver.
Where UC Treatment Is Headed — Precision Medicine and Combination Approaches
The next chapter in ulcerative colitis treatment is likely to be defined by two themes: precision medicine and combination therapy. Tulisokibart’s companion diagnostic approach — selecting patients based on a biomarker before prescribing — previews a future where gastroenterologists do not rely solely on trial-and-error prescribing. If Phase 3 data confirms the Phase 2 signal, and if the diagnostic becomes widely accessible, it could meaningfully reduce the months of ineffective treatment that many patients currently endure. Combination strategies, pairing drugs from different mechanism classes, are also under active investigation.
The logic is straightforward: if IL-23 inhibitors, anti-TL1A antibodies, and JAK inhibitors all work through different pathways, combining them might produce deeper remission in patients who respond partially to one drug alone. That research is still in early stages, and safety questions about stacking immunosuppressive mechanisms are legitimate and unresolved. But the trajectory is clear. The treatment landscape for ulcerative colitis has changed more in the past two years than in the preceding decade, and the drugs in late-stage development today suggest that the pace of progress is accelerating, not slowing.
Conclusion
The era of settling for marginal improvement in ulcerative colitis is ending. Risankizumab has demonstrated remission at more than three times the placebo rate in its Phase 3 trial, tulisokibart and duvakitug are posting Phase 2 numbers that would have been dismissed as implausible a few years ago, mirikizumab has proven that sustained four-year remission is achievable, and upadacitinib offers rapid response for patients who need immediate stabilization. Each drug carries its own profile of benefits, risks, costs, and practical considerations, and none is a universal solution — but collectively, they represent a fundamentally different conversation between patients and their gastroenterologists than what was possible even in 2022.
For older adults and those navigating ulcerative colitis alongside cognitive decline, these advances matter on multiple levels. Stable remission means fewer hospitalizations, fewer steroid courses with their attendant cognitive side effects, better nutritional status, and one less source of chaos in a care plan that may already be complex. The most important next step for any patient or caregiver reading this is a direct conversation with a gastroenterologist about whether current treatment is achieving true remission — not just tolerability — and whether newer options warrant consideration.
Frequently Asked Questions
Is risankizumab (Skyrizi) a cure for ulcerative colitis?
No. Risankizumab is a maintenance therapy that suppresses inflammation, not a cure. Patients who respond well still require ongoing treatment to maintain remission. In the COMMAND trial, 40.2% of patients on the 180 mg dose maintained remission at one year, meaning the majority either lost response or did not achieve full remission to begin with.
How do anti-TL1A antibodies like tulisokibart differ from existing biologics?
TL1A is a cytokine involved in both inflammation and fibrosis in the gut. Anti-TL1A antibodies target a different pathway than IL-23 inhibitors or anti-TNF drugs, which means they may work in patients who have failed those other classes. Tulisokibart’s companion diagnostic adds another distinction — it can identify patients more likely to respond before treatment begins.
Are these new UC drugs safe for elderly patients?
The biologic therapies — risankizumab, mirikizumab, and the anti-TL1A drugs — generally have more favorable safety profiles than JAK inhibitors for older adults. However, all immunosuppressive therapies carry infection risk, and elderly patients require careful screening and monitoring. JAK inhibitors like upadacitinib carry specific boxed warnings about cardiovascular events and malignancies that are especially relevant for patients over 50.
How long does it take to know if risankizumab is working?
Clinical response can be assessed as early as week 4, when 52.2% of patients in the INSPIRE trial showed improvement. Full clinical remission is typically evaluated at week 12. If no meaningful response is observed by that point, a gastroenterologist will likely consider alternative therapies.
What does “corticosteroid-free remission” mean, and why does it matter?
It means achieving disease remission without relying on steroids like prednisone. This distinction matters because long-term steroid use causes bone loss, weight gain, elevated blood sugar, mood changes, and cognitive effects — all of which are particularly harmful for older adults and those with existing cognitive impairment. Mirikizumab’s four-year data showing 78% corticosteroid-free remission is significant precisely because it demonstrates disease control without these harmful side effects.
Will insurance cover these newer UC treatments?
Coverage varies widely. Most insurers require step therapy, meaning patients must document failure of older, less expensive treatments before gaining access to newer biologics. Prior authorization is almost always required. Manufacturer patient assistance programs exist for most of these drugs and can significantly reduce out-of-pocket costs. A specialty pharmacy or the prescribing gastroenterologist’s office can typically help navigate the approval process.
