If you live with ulcerative colitis, you have probably heard both versions of the story. One says there are more UC medicines than ever. The other says people still cycle through drug after drug looking for one that keeps them in remission. Both are true. There is no cure for UC yet, and not every approved medicine works for every person. But the list of options keeps growing, and the research pipeline behind it is one of the busiest in medicine.
It helps to know how short that list used to be. The first advanced therapy for UC was approved in 2005. Before that, doctors worked with three older groups of medicines and, when those failed, surgery. Everything else on the list below has arrived since. Here is the full picture: what is approved today, what is being tested right now, and why new UC drugs still take so long to arrive.
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What is approved today
Doctors have used three older groups of medicines for decades:
- Aminosalicylates. Medicines that calm inflammation in the lining of the colon.
- Corticosteroids. Medicines that lower inflammation across the body.
- Immunomodulators. Medicines that turn down the immune system's activity.
Then there are the advanced therapies. These are newer drugs approved specifically for moderately to severely active UC, and the FDA has cleared about a dozen of them since 2005:
- TNF blockers. They block a protein called TNF that drives inflammation. Infliximab was approved for UC in 2005, adalimumab in 2012, and golimumab in 2013.
- Vedolizumab (2014). An antibody that targets a protein immune cells use to get into the gut, so it works mostly in the intestine.
- Ustekinumab (2019). An antibody that blocks two inflammation proteins, IL-12 and IL-23.
- JAK inhibitors. Pills that block inflammation signals inside cells. Tofacitinib was approved in 2018 and upadacitinib in 2022.
- S1P modulators. A newer class of pills. Ozanimod was approved in 2021 and etrasimod in October 2023.
- IL-23 blockers. The newest wave. These antibodies block the IL-23 protein specifically. Mirikizumab (Omvoh) was approved in October 2023, risankizumab (Skyrizi) in June 2024, and guselkumab (Tremfya) in September 2024. In September 2025 guselkumab also became the first IL-23 blocker with a fully subcutaneous UC regimen, meaning both the starting doses and the maintenance doses come as injections under the skin, with no infusions.
Two things stand out when you lay that list out by year. More than half of the approvals happened in the last eight years. And they hit very different targets: TNF, gut trafficking, IL-12 and IL-23, JAK signalling, S1P. The field has not settled on one mechanism, because none of them works for everybody.
None of this is a recommendation. Which medicine fits a given person depends on their disease, their history, and their doctor.
What researchers are studying now
The UC drug pipeline is busy, and that's a good thing. By one industry count, more than 70 companies are developing over 75 drug candidates for UC. Here are a few examples of where the field is heading.
Obefazimod (Abivax). This is a pill with a completely new approach: instead of targeting inflammation directly, it raises levels of a natural molecule (called miR-124) that helps control inflammation on its own. In July 2025, early trial results were positive, and by June 2026, the longer-term results came in too: after 44 weeks, about half of patients taking the drug were in remission, compared to only about 1 in 10 on placebo. The trial included 580 people, and both doses tested worked. The company plans to file for FDA approval in late 2026. If approved, it would be the first drug of its kind, and the first taken as a simple once-daily pill.
Afimkibart (Roche). This is an antibody that blocks a protein called TL1A, again, a target no approved UC drug currently uses. It's being tested in several large trials right now: a 350-person study in adults with moderate to severe UC, and a separate study in about 100 children and teens testing the same drug in younger patients, something that's still rare in this field. Both are currently recruiting.
Combining drugs. Some researchers are moving past testing one drug at a time. Eli Lilly is running a 252-person trial that combines a new drug (LY4268989) with mirikizumab, a UC drug that's already approved, to see if hitting two different targets works better than just one. For years, the main question was "which single drug works best?" Now, some researchers are starting to ask a different question: maybe the reason more people aren't reaching remission isn't the drug. It's that we've only ever used one at a time.
Why new UC drugs take time
The colonoscopy factor. The FDA requires UC remission to be measured with a colonoscopy, not just how a patient says they feel. An independent expert, one who doesn't know which treatment the patient received, has to look at the colon and confirm it's actually healing. That's what makes the results trustworthy, but it also means participants get scoped at set points during the trial. That's a real commitment, worth knowing about before you sign up, not after.
The two-stage design. UC trials run in two phases: first, does the drug work quickly (induction), and second, does it keep working for months (maintenance)? A drug has to succeed at both stages. That's the right standard for a disease people live with for life, but it's also why these trials take years instead of months. You can see this play out in a study that's currently recruiting: Gilead's 176-person trial of tilpisertib fosmecarbil still has to clear this two-stage bar before anything bigger can follow.
The placebo factor. Some people get better in UC trials even without the real drug. In one recent trial, about 1 in 10 people on placebo reached remission after 44 weeks. That's exactly why trials need a placebo group for comparison, a roughly 5-in-10 result on the actual drug only means something when you can see it against that 1-in-10 baseline. It's also why a handful of convincing stories online aren't the same as real evidence.
The representation gap. IBD affects people of every background, but not equally in research. Recent US data shows it affects roughly 1 in 120 White Americans, 1 in 200 Black Americans, 1 in 220 Hispanic Americans, and 1 in 250 Asian Americans, yet non-White patients are still underrepresented in IBD studies. Many trials today are working to close that gap, which matters for making sure future treatments are well understood across all groups.
Curious why representation in clinical trials matters? Here's the full picture.
The stages of ulcerative colitis and what care usually looks like
Doctors describe UC by how far the inflammation extends:
Proctitis. Inflammation limited to the rectum. This is where UC often starts, and the affected area is small enough that treatment commonly works locally, with medicines delivered directly to the rectum rather than swallowed.
Left-sided colitis. Inflammation extends up the left side of the colon. Beyond the reach of most local treatments, so care here usually combines something taken by mouth with something delivered rectally.
Extensive colitis, or pancolitis. Inflammation covers most or all of the colon. With more of the colon involved, care typically means medicines that work throughout the body, and this is the group where advanced therapies come up most often.
Separately, doctors grade how active the disease is, from mild to severe, using symptoms plus what an endoscopy shows. Extent tells you how much colon is involved, activity tells you how badly. All of the above describes typical practice, not a plan for anyone in particular. Your gastroenterologist decides based on your case.
These labels also do real work in research. Advanced therapies are approved specifically for moderately to severely active UC, and most trial titles state the activity level they enroll, like "moderately to severely active" or "mild to moderate". So knowing your extent and activity level tells you which studies you could qualify for, often from the title alone.
One thing to clear up, because people search for it constantly: there is no official four stage ladder for UC. Unlike cancer, UC has no numbered stages 1 through 4 that every doctor uses. A four stage list you find online is usually someone tidying the severity grades into a neat sequence. It is not a standard your medical record or a trial protocol will use.
Surgery for ulcerative colitis
Surgery has a scary reputation when it comes to UC, so let's put real numbers on it. Among people diagnosed since 2000, fewer than 1 in 10 had their colon removed within 10 years of diagnosis. That number comes from a large analysis combining 26 different population studies, and it also shows this rate has been falling compared to past decades. Most people with UC never need this surgery.
When surgery does happen, it's usually for a specific reason: the medications stopped working (or never worked), colon cancer, precancerous changes in the colon, or a dangerous complication. Surgeons typically remove the colon and rectum, then create a new way for the body to store and pass stool, either an internal pouch built from part of the small intestine, or an ileostomy (an opening in the abdomen where waste collects in a small bag worn outside the body).
Here's the important part: this isn't a cure. Removing the colon does remove the organ that UC attacks, but health authorities still call this a treatment, not a cure. It's major surgery with a real, significant recovery, which is exactly why all the research happening right now matters so much.
Does UC affect more than the colon?
It can. UC is linked to inflammation beyond the intestine. Recognized associations include primary sclerosing cholangitis, a condition of the bile ducts, and joint inflammation. A large Canadian population study also found that people with IBD are more likely than others to be diagnosed with cancer, heart disease, and arthritis.
The same Canadian research looked at life expectancy. People with IBD live longer than they used to, with clear gains between 1996 and 2011, while still averaging several years less than people without IBD. Those are population averages covering IBD as a whole, not UC alone, and they say nothing about any one person's future.
A rare but serious complication of UC itself is toxic megacolon, where the colon swells dangerously and needs urgent care. And because long term colon inflammation raises colorectal cancer risk over time, doctors monitor for it with regular colonoscopies. If any of this worries you, bring it to your doctor. Screening and monitoring plans are individual.
Common myths about ulcerative colitis
"UC is contagious."
It is not. You cannot catch it or pass it on. It comes from abnormal immune reactions inside the body.
"UC is caused by stress or something you ate."
The exact cause is unknown, but researchers point to a mix of an overactive immune response, genes, the community of bacteria living in the gut, and things in the environment. Nothing you ate caused your UC, and it is not your fault.
"If it runs in your family you will get it, and if it does not you will not."
Neither half holds up. About 1 in 10 people with UC have a family member with IBD, which means most have none. Close relatives, meaning a parent, sibling, or child, do carry about four times the risk, and that is worth knowing. But four times a small number is still a small number.
"UC and Crohn's disease are the same thing."
They are both forms of IBD, but they are different diagnoses. The next section explains how.
Crohn's disease vs. ulcerative colitis: what actually differs
The clearest difference is where the disease shows up. UC stays in the large intestine, the colon and rectum, and only affects the inner lining. It starts in the rectum and spreads upward in one continuous stretch. Crohn's disease can affect any part of the digestive tract, from the mouth all the way to the anus, though it most often shows up in the small intestine and the start of the large intestine.
There's a second difference doctors can see during a colonoscopy: in Crohn's, the tissue right around a sore (ulcer) can look completely healthy. In UC, sores always sit inside inflamed tissue. That's one of the ways doctors tell the two apart when symptoms overlap, which they often do.
Timing differs too. On average, UC gets diagnosed faster (around 3 to 4 months after symptoms start) than Crohn's (around 8 months). And while UC is the more common of the two in adults, that flips in children, Crohn's is actually more common in kids and teens.
Does diet cause ulcerative colitis, or fix it?
No, on both counts. Researchers haven't found that specific foods cause UC, and they haven't found specific foods that make it worse either. Eating healthier overall does seem to be linked to a lower chance of developing IBD in the first place, but that's different from a food causing or curing a case someone already has.
There's also no single diet that's been proven to work for everyone with UC. A major IBD organization reviewed the evidence and said plainly: there isn't enough data to recommend one diet for all patients. What doctors do often suggest is keeping a food diary, because personal triggers are real, even if there's no single food that affects everyone the same way. Two people with the exact same diagnosis can react completely differently to the same meal.
How to find a UC study
AllClinicalTrials.com lists ulcerative colitis studies that are recruiting across the United States, from large Phase 3 drug programs to smaller academic studies. A couple of examples show that range: Genentech is running a Phase 2 study of RO7837195 in moderately to severely active UC, while on the smaller end, UCLA is studying the impact of prebiotics on ulcerative colitis, no drug involved at all.
You can filter by city and state, read what each study involves, and check the basic eligibility. The application takes about 5 minutes, and the study team contacts you if you look like a match. Participation is always voluntary, and you can leave a study at any time.
Common questions
What is ulcerative colitis, in simple terms? UC is one of the two main types of inflammatory bowel disease. The immune system mistakenly attacks the colon and rectum, causing ongoing inflammation and small sores (ulcers). Most people notice this as loose, bloody stools and cramping, which comes in flares, periods where symptoms flare up, then calm down, then come back. Most people are diagnosed young, in their teens or twenties, though it can happen at any age.
What is the modified Mayo score? It's the scoring system most UC trials use to define remission, and the FDA's guidance for UC trials is built around it. It includes a score based on what a colonoscopy or sigmoidoscopy shows, which is why those procedures are a regular part of trial visits.
How many treatments are approved for UC? About a dozen advanced therapies have been approved for moderate to severe UC since 2005, plus three older groups of medicines that have been around much longer: aminosalicylates, corticosteroids, and immunomodulators.
How is ulcerative colitis diagnosed? Usually with a colonoscopy and biopsies. A doctor examines the lining of the colon and takes small tissue samples. UC tends to get diagnosed faster than Crohn's disease: about half of people are diagnosed within 3 to 4 months of their first symptoms, compared to about 8 months for Crohn's.
Will I need surgery for ulcerative colitis? Most people won't. Among people diagnosed since 2000, fewer than 1 in 10 had their colon removed within 10 years of diagnosis, and that rate has been going down over time. When surgery does happen, it's usually because medications stopped working, or because of colon cancer, precancerous changes, or a serious complication. Surgeons typically remove the colon and rectum, then create a new way to pass stool, either an internal pouch made from part of the small intestine, or an opening in the abdomen. These are general statistics, not a prediction for you personally, so talk through your own situation with your doctor.
Is ulcerative colitis an autoimmune disease? UC is considered an immune-mediated disease. The immune system's abnormal reactions cause the inflammation and ulcers in the colon. What actually triggers those reactions in the first place is still being studied, but researchers are looking at genetics, the balance of bacteria in the gut, and environmental factors.
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