There is no single best medicine for gout because the condition has two distinct phases that require different treatments. During an acute flare, the priority is fast pain relief with anti-inflammatory drugs. Between flares, the goal shifts to lowering uric acid levels so attacks stop happening altogether. Most people with recurring gout need medication for both phases.
Medicines That Stop a Gout Attack
When a flare hits, three types of medication can bring relief: anti-inflammatory painkillers (NSAIDs), colchicine, and corticosteroids. Which one works best for you depends on your other health conditions, how quickly you start treatment, and how your body tolerates each drug.
NSAIDs
Over-the-counter and prescription anti-inflammatory drugs are the most common first choice. Naproxen (500 mg twice daily) and indomethacin (50 mg three times daily) are the ones most often prescribed for gout flares. High-dose ibuprofen (800 mg three times daily) is another option. These work best when you start them within the first 24 hours of symptoms. Most people see meaningful pain reduction within a day or two, and a typical course lasts about a week.
NSAIDs aren’t a good fit if you have kidney disease, stomach ulcers, or are on blood thinners. In those cases, one of the next two options is usually better.
Colchicine
Colchicine is an older drug that targets gout inflammation specifically. The modern low-dose approach is 1.2 mg at the first sign of a flare, followed by 0.6 mg one hour later, for a total of 1.8 mg. That’s it for the first day. The key with colchicine is timing: it works dramatically better when taken within the first 12 hours of an attack. If you wait two or three days into a flare, it’s far less effective. Many people who get recurrent gout keep colchicine on hand so they can take it immediately.
Corticosteroids
When NSAIDs and colchicine aren’t options, corticosteroids fill the gap. An oral course typically lasts several days with a tapering dose. For gout in a single large joint, a steroid injection directly into the joint can provide fast, targeted relief without the body-wide side effects of oral steroids. Corticosteroids are particularly useful for people with kidney problems or those who can’t tolerate the other two options.
Medicines That Prevent Future Attacks
Stopping a flare is only half the picture. If you’ve had two or more attacks in a year, have visible tophi (chalky deposits under the skin), or show joint damage on imaging, urate-lowering therapy is the long-term solution. The goal is to get your blood uric acid level below 6 mg/dL. At that threshold, existing uric acid crystals in your joints gradually dissolve, and new ones stop forming.
How effective is hitting that target? In a clinical trial using a nurse-led approach where medication was carefully adjusted, 95% of patients reached the 6 mg/dL goal. Those patients had a 67% lower risk of future flares compared to a standard care group where only 30% hit the target. The difference between good and mediocre gout management often comes down to whether the dose gets adjusted enough times to actually reach that number.
Allopurinol
Allopurinol is the most widely prescribed urate-lowering drug and the recommended first-line option. It works by blocking the enzyme that produces uric acid. Treatment starts low, at 100 mg daily or less (even lower if you have significant kidney disease), and gets increased every two to five weeks until your uric acid hits the target. Some people need only 200 or 300 mg. Others need as much as 800 mg daily. The dose that works is whatever gets your uric acid below 6 mg/dL.
One important safety note: a small percentage of people carry a gene variant called HLA-B*5801 that puts them at risk for a rare but serious allergic skin reaction to allopurinol. Genetic testing before starting the drug is recommended for all adults of Han Chinese or Thai descent, and for Korean adults with stage 3 or higher chronic kidney disease. If you fall into one of these groups, a simple blood test can identify the risk before you take your first dose.
Febuxostat
Febuxostat works through the same mechanism as allopurinol and is typically used when allopurinol isn’t tolerated or doesn’t bring uric acid down far enough. It carries a cardiovascular caution, though. A major trial found increased mortality in the 30 days after patients abruptly stopped taking febuxostat, possibly because the sudden spike in uric acid triggered crystal formation in the cardiovascular system. Current guidelines recommend against febuxostat for people with a history of cardiovascular disease or a new heart-related event. If you’re on febuxostat and doing well with no heart history, there’s no reason to panic, but never stop it abruptly without medical guidance.
Treatment for Severe, Resistant Gout
A small number of people don’t respond to standard urate-lowering pills or can’t tolerate them. For this group, pegloticase is an option. It’s an infusion given every two weeks in a medical setting, each session lasting at least two hours. Pegloticase is an engineered enzyme that breaks down uric acid directly in the bloodstream, and it can rapidly lower levels that other drugs couldn’t budge.
It’s reserved for patients who’ve truly failed conventional therapy because it carries real risks, including serious allergic reactions. Patients receive antihistamines and corticosteroids before each infusion to reduce that risk, and their uric acid is checked before every session. If levels climb back above 6 mg/dL on two consecutive checks, the treatment is usually stopped because the drug is no longer working and the infusion risk isn’t worth it.
The Flare That Comes Before Things Get Better
One of the most frustrating aspects of gout treatment is that starting urate-lowering therapy can actually trigger flares in the first few months. As uric acid levels drop, existing crystal deposits shift and partially dissolve, irritating the joint lining. This doesn’t mean the medication isn’t working. It means the opposite.
To get through this transition period, doctors typically prescribe a low daily dose of colchicine or an NSAID alongside the urate-lowering drug. This prophylaxis usually continues for three to six months, sometimes longer, until uric acid has been at target long enough for the crystal burden to shrink. Many people who quit their urate-lowering medication do so during this early window because they think it’s making things worse. Sticking with it through the adjustment period is one of the most important things you can do for long-term results.
How the Pieces Fit Together
Gout treatment works in layers. During a flare, you use a fast-acting anti-inflammatory (NSAIDs, colchicine, or steroids) to shut down the pain. Once the flare resolves and you’ve decided with your doctor that long-term prevention makes sense, you start allopurinol or an alternative at a low dose, with a prophylactic anti-inflammatory running alongside it. Over weeks to months, the urate-lowering dose gets titrated upward until your blood uric acid drops below 6 mg/dL. Once it stays there, crystal deposits slowly dissolve, flares become less frequent, and for most people they eventually stop altogether.
The “best” medicine, in practice, is whichever combination gets your uric acid to target and keeps it there. For the majority of people, that’s allopurinol paired with colchicine during the transition, plus an NSAID or steroid kept on hand for breakthrough flares. The specific drug matters less than the strategy: treat attacks fast, lower uric acid to a specific number, and stay on therapy long enough for the crystals to clear.