Psoriasis Treatment Over a Decade: The Best Injections Leave 85–91% of Patients with Almost Clear Skin, Pills 50–58%

In March 2026, the FDA approved ICOTYDE (icotrokinra), the first pill that blocks the IL-23 receptor. Until then, IL-23 itself had been intercepted only by injectable antibodies, while the pill SOTYKTU dampened its signal already inside the cell. Icotrokinra is a peptide of 13 amino acids. In animal studies, only 0.1–0.3% of the dose from the pill reaches the bloodstream. That was enough for it, in two head-to-head trials, to give patients almost clear skin almost twice as often as SOTYKTU, the previous best pill: 55–58% versus 30–34% at week 16. On September 18, 2026, the drug was approved in the EU as well.

Ten years ago the conversation was different. The most widely used biologic, adalimumab (Humira), gave almost clear skin to about half of patients — 47% at week 16. The best modern injection, bimekizumab, gives 85–91% (these are different trials). Between those figures lie ten new drugs, a new understanding of how inflammation reaches the skin, and a new goal of treatment: European guidelines now name PASI 90 as the desired outcome, rather than just “noticeable improvement.”

Over ten years, psoriasis has become a disease that in clinical trials can be almost fully controlled in most patients: the best injections give 85–91% of participants almost clear skin, and pills 50–58%, on a par with older injections but below the best. No drug can yet cure psoriasis for good.

This is a review of studies and the market as of October 23, 2026, not medical advice. The drugs discussed are prescribed by a dermatologist; do not start, change or stop treatment on your own.

01 · Ten years: from “caring for the skin” to “almost clear skin”

Psoriasis is a chronic immune disease. The skin only shows what is happening in the immune system: inflammatory signals make skin cells divide too fast, and thick red scaly plaques appear on the elbows, knees, scalp or nails. According to the Global Burden of Disease model, 43m people had psoriasis in 2021; the WHO in 2016 cited at least 100m, as the models count mild and undiagnosed cases differently. In Western and Central Europe, 1.8–1.9% of adults have psoriasis (BMJ, 2020). Moderate or severe disease, which requires pills or injections, affects 10% to 30% of patients, depending on the definition.

Psoriasis is not only about the skin. Roughly one patient in five (19.7% according to a meta-analysis of 266 studies) has psoriatic arthritis. With severe psoriasis, the risk of heart attack is 1.7 times higher than in people without it (observational studies; causality not proven). Symptoms of depression on questionnaires are found in 28% of patients.

By the mid-2010s, a doctor had few options: corticosteroid creams, phototherapy, methotrexate or cyclosporine as pills, and three TNF-α blockers — etanercept, adalimumab and infliximab — plus, since 2009, ustekinumab. The most widely used of them, adalimumab, gave almost clear skin to fewer than half of patients. The goal of treatment sounded modest: reduce plaques by 75%.

From 2014 to 2026, ten new drugs were approved in the US and EU for plaque psoriasis — seven injections and three pills. Meanwhile the old ones became cheaper: after patents expired, biosimilars of adalimumab and ustekinumab appeared.

The most important change shows in the numbers. Secukinumab (2015) and ixekizumab (2016), the first IL-17 blockers, gave almost clear skin to 59–71% of patients at week 12. Guselkumab (2017) and risankizumab (2019), IL-23 blockers, gave 73–75% at week 16. Bimekizumab (2021), which blocks both forms of IL-17 at once, gave 85–91%. Pills moved along the same path but from a lower starting point: from 20% for apremilast to 55–58% for icotrokinra.

The goal changed along with the drugs. In 2017, the American National Psoriasis Foundation proposed a target: plaques covering no more than 1% of body surface area after three months of treatment. The European EuroGuiDerm guideline (the 2026 German adaptation) treats PASI 75 as the minimum goal and PASI 90, or a residual PASI below 2, as the desirable one. What in 2010 was the best possible result is now the minimum.

Fifteen years ago, the medical record of a psoriasis patient was mostly a history of ointments. Now the patient’s chart counts percentages of clear skin.

02 · Where the new drugs came from: the science of IL-23 and IL-17

Today’s drugs grew out of several discoveries of the early 2000s. In 2000, researchers at the company DNAX described a new signaling protein of the immune system, IL-23. It consists of two parts: its own p19 and the p40 it shares with another protein, IL-12. In 2003–2005 it emerged that IL-23 specifically sustains a distinct type of T cell, Th17, which produces IL-17. And IL-17 acts directly on skin cells: it intensifies inflammation and their division.

In 2007, geneticists confirmed that this chain matters specifically for psoriasis. Variants of the genes for the IL-23 receptor (IL23R) and the p40 subunit (IL12B) changed the risk of the disease: one IL23R variant raised the odds of falling ill 1.44 times, while a protective IL12B variant lowered them by a third. Genetics pointed to the target before the drugs appeared.

Pharmaceutical companies then intercepted this chain at different points. Ustekinumab (2009) blocks the shared p40 part, that is, both IL-12 and IL-23. Guselkumab, tildrakizumab and risankizumab block only p19, that is, only IL-23. Secukinumab and ixekizumab neutralize IL-17A, bimekizumab neutralizes IL-17A and IL-17F, and brodalumab blocks the IL-17 receptor. The new pills hit the same axis: deucravacitinib and its successors block the enzyme TYK2, through which the IL-23 signal passes into the cell, while icotrokinra occupies the IL-23 receptor itself.

Different points of attack produce different dynamics. An IL-17 blocker acts closer to the skin and is therefore faster: in the IXORA-R head-to-head trial, at week 12 ixekizumab produced completely clear skin in 41% of patients versus 25% on guselkumab. But by week 24 the results had evened out — 50% and 52%. And in the ECLIPSE trial, a year later the IL-23 blocker guselkumab had maintained almost clear skin in 84% of patients versus 70% on secukinumab.

Why IL-23 blockers hold the result longer has not been definitively established. One explanation involves memory T cells, which remain in the skin even after a plaque has gone. In 2017, researchers at the Karolinska Institute found, in healed areas of skin, clones of T cells that produce IL-17; some of them were identical across different patients and were not found in healthy people. Possibly they are responsible for plaques returning to the same places, while IL-23 blockade keeps them “switched off” for longer. For now this is a hypothesis: the studies show a link, not a proven mechanism.

03 · Duels: what the head-to-head trials showed

Most of the figures on psoriasis drugs come from trials in which the drug was compared with a placebo. Comparing such results with one another is risky: the patients, the duration and the rules for counting dropouts all differ. A more reliable form of evidence is a direct comparison of two drugs in a single trial. Over ten years, enough such duels have accumulated.

In each of the eight duels the newer injectable won, and by a wide margin: from 14 to 46 percentage points. Risankizumab delivered almost clear skin 25 points more often than adalimumab and 33 points more often than ustekinumab. Bimekizumab did so 39 points more often than adalimumab. Most of these trials were sponsored by the manufacturer of the newer drug.

The broadest picture comes from the Cochrane network meta-analysis, which is updated every year. The 2025 version covered 204 trials and 67,889 participants. By the share of patients reaching PASI 90 early in treatment, the best performers were infliximab, the Chinese IL-17 blocker xeligekimab, bimekizumab, ixekizumab and risankizumab. Deucravacitinib and apremilast ended up below the IL-17 and IL-23 blockers (except tildrakizumab). The authors caution: 157 of the 204 trials were funded by industry, and only the first 8–24 weeks were assessed. Icotrokinra did not make it into this analysis — the search ended in July 2024.

04 · Pills: three generations in twelve years

For many patients an injection is no small matter. Injection pens must be kept in a refrigerator, and some people are afraid of needles. In surveys, most patients choose a pill if all other properties are equal: in China, 87% versus 13%. But in reality the properties are not equal, and in a Japanese study patients ranked long-term efficacy above the route of administration. The history of psoriasis pills is the history of an attempt to catch up with injectables on efficacy.

Apremilast (Otezla, 2014): the first, weak but popular

Apremilast blocks the enzyme PDE4 inside immune cells and reduces the production of several inflammatory signals at once. In the ESTEEM trials at week 16, plaques shrank by at least 75% in only 33% and 29% of patients. Almost clear skin, according to the later POETYK head-to-head trial, was reached by 18–20%.

Despite its modest effect, apremilast became a commercial success. Its sales grew from $70m in 2014 to $2.27bn in 2025: doctors prescribed it to patients with moderate psoriasis who did not want injections. In 2019 Amgen paid $13.4bn for the drug. The sale was forced: the US Federal Trade Commission allowed Bristol Myers Squibb to buy Celgene only on condition that it get rid of Otezla, because BMS already had in development “the most advanced oral treatment for moderate-to-severe psoriasis.” The regulator did not name it; presumably it meant deucravacitinib, BMS’s main oral psoriasis candidate.

Apremilast’s weak spot is retention. In the French PsoBioTeq cohort, after one year only 23% of the patients who had started on apremilast were still taking it, against 56–84% on injectables.

Deucravacitinib (SOTYKTU, 2022): the first TYK2 blocker

TYK2 is one of the four enzymes of the JAK family through which the signals of IL-23, IL-12 and interferons are passed into the cell. Pills that block JAK enzymes in general (tofacitinib, upadacitinib) are effective in arthritis, but after the ORAL Surveillance trial they received a boxed warning in the US. In patients with rheumatoid arthritis aged 50 and over with cardiovascular risk factors, tofacitinib, compared with TNF blockers, was more often accompanied by serious cardiovascular events (hazard ratio 1.33) and cancer (1.48). In 2022 the European Medicines Agency (EMA) restricted the use of such drugs in people over 65, smokers and patients at risk of cancer.

Deucravacitinib works differently. It binds not to the enzyme’s active site, as JAK inhibitors do, but to its regulatory part, which exists only in TYK2. In a human blood assay it suppresses the TYK2 signal at a concentration of 42 nM, and the JAK1/JAK3 and JAK2 signals only at concentrations 40 and more than 200 times higher. Upadacitinib is the mirror image: strong on JAK1 and JAK2, weak on TYK2. It is not yet known whether the risks of the JAK class apply to deucravacitinib: the FDA label explicitly calls the question open, and the five-year follow-up had no comparison group.

Genetics suggested that this approach made sense. A rare variant of the TYK2 gene (P1104A), which weakens the enzyme, protects against autoimmune diseases: carriers’ risk of rheumatoid arthritis is a third lower. But in people with two copies of this variant, in regions where tuberculosis is common, the risk of contracting it is tens of times higher. The pill blocks the enzyme only partially and not for life, yet the prescribing information requires a tuberculosis test before starting deucravacitinib.

In the two main POETYK trials, at week 16 deucravacitinib produced almost clear skin in 36% and 27% of patients, versus 20% and 18% on apremilast and 3–4% on placebo. Among those who took the drug continuously, 67% still had a reduction in plaques of at least 75% after five years — but that is only 513 of 1,519 participants, that is, the ones the drug suited. The most common side effects in the first 16 weeks are upper respiratory tract infections (19% versus 15% on placebo), cold sores, mouth ulcers and acne. There is no boxed warning on the label. In 2026 the drug was also approved for psoriatic arthritis — in the US in March, in the EU in May.

Yet for insurance systems SOTYKTU proved a weak argument. Germany’s G-BA in 2023 judged its added benefit “not proven”: the manufacturer showed superiority over apremilast and placebo, not over the injectables with which the drug was supposed to compete on price. England’s NICE allowed it only after the failure of conventional systemic therapies. Sales for 2025 were $291m, in the US down 5%.

Icotrokinra (ICOTYDE, 2026): a peptide that works as a pill

Protein drugs usually cannot be taken by mouth: the digestive system breaks them down the same way it breaks down food. Even the most successful oral peptide, semaglutide in pill form, gets into the bloodstream at only 0.4–1%, and it needs a special absorption-enhancing substance to do even that. Icotrokinra, which was created by Protagonist Therapeutics and has been developed by Johnson & Johnson since 2017, gets around the problem differently. It is a cyclic peptide of 13 amino acids, about 80 times lighter than an antibody. It is stable in artificial gastric and intestinal fluid for more than a day and binds to the IL-23 receptor extremely tightly (dissociation constant: 7.1 picomolar). So, judging by animal studies, even a tiny fraction of the dose reaching the bloodstream is enough.

How much icotrokinra is absorbed in humans has not been published. What is known instead is that between 37% and 81% of the dose leaves the body unchanged. Hence the dosing rule: the pill is taken immediately after waking, on an empty stomach, with no food for 30 minutes. A fatty breakfast reduces the amount of the drug in the blood by 43%.

A peptide that should have been digested like a piece of meat, and is not. Icotrokinra’s main engineering problem is solved at the level of the ring’s chemistry.

The study results are as follows. In ICONIC-LEAD (684 adults and adolescents), almost clear skin at week 16 was reached by 50% of patients on icotrokinra versus 4% on placebo, and completely clear skin by 27% versus less than 1%. Side effects occurred in 49% of patients in both groups. In adolescents the result was higher, 70% versus 14%, but there were few of them (44 versus 22 patients). The main thing, though, is the two head-to-head trials against SOTYKTU, ICONIC-ADVANCE 1 and 2 (1,505 patients).

At week 16, icotrokinra gave almost clear skin to 55% and 58% of patients versus 30% and 34% on deucravacitinib, and completely clear skin to 31–32% versus 11–14%. Through week 24 the gap held at about 22 points. Over 24 weeks, side effects occurred in 57% of patients on icotrokinra and 65% on deucravacitinib. Over the second half of the first year, 70–75% of patients had almost clear skin and about half had completely clear skin.

The drug was also tested on areas that are hard to treat. On the scalp and genitals the result was convincing. On palms and soles it was not: the difference from placebo turned out to be statistically insignificant.

The safety profile so far looks calm, but it is short. The FDA label has no contraindications other than allergy and no boxed warning. Fungal infections of the skin and mucous membranes occurred in 1.1% of patients versus 0% on placebo, and serious infections in 0.2% versus 0.4%. One patient with risk factors died of gastric bleeding; a link to the drug has not been established. The label recommends “considering” a tuberculosis test, and live vaccines should be avoided. The entire first-year safety record amounts to 1,840 patient-years of observation, whereas for biologics the record is counted in decades.

Approval so far covers only plaque psoriasis. Phase 3 trials in psoriatic arthritis, ulcerative colitis and Crohn’s disease are ongoing.

Three generations: each 1.5–1.8 times better than the previous one

If you take only the head-to-head trials between pills, the picture is consistent. Deucravacitinib gave almost clear skin 1.5–1.8 times more often than apremilast. Icotrokinra did so 1.7–1.8 times more often than deucravacitinib. The same holds for zasocitinib, the next candidate.

05 · Pill or injection: where the line runs

The strongest argument against the thesis “pills will replace injections” is the numbers. Icotrokinra gives almost clear skin to 50–58% of patients at week 16. The best injectables give 73–91%. These are results from different trials, and there is no head-to-head trial of the pill against the best injectables yet. The ICONIC-ASCEND trial, which compares icotrokinra with ustekinumab, completed its main phase in November 2025, but as of October 23, 2026 no results have been published.

Indirect comparisons contradict one another depending on who pays. An analysis conducted with the participation of employees of AbbVie, the maker of risankizumab, gives risankizumab 71.4% of patients with almost clear skin versus 49.9% on icotrokinra. A poster placed on the Johnson & Johnson website puts icotrokinra on a par with risankizumab and guselkumab by the share of completely clear skin. The honest conclusion: icotrokinra works at the level of the older injectables, ustekinumab (42–50%) and adalimumab (47%), but falls short of the best IL-17 and IL-23 blockers.

The second difference is dosing frequency. The pill has to be taken every day; the risankizumab injection, four times a year. For some patients 365 pills are more convenient than four injections, for others they are not. There are as yet no data on how well patients follow the “empty stomach and 30 minutes without food” rule.

The third difference is persistence. The previous pill, apremilast, lost to injectables precisely on this point: after a year, fewer than a quarter of patients were still taking it. Whether the new pills will repeat that fate will be shown only by real-world practice; there are no registry data yet for deucravacitinib and icotrokinra.

The fourth is what happens after discontinuation. Icotrokinra clears from the blood within a day (half-life of about 12 hours), so it works as a switch. In the ICONIC-LEAD trial, patients who had responded to treatment were split at week 24: some continued the pill, others switched to placebo. By week 52, 84% of those who continued kept almost clear skin, and only 21% of those who stopped. The median time to loss of response was 10 weeks.

The antibody risankizumab clears more slowly: its half-life is about 28 days. After its withdrawal in the IMMhance trial, the median time to relapse was 295 days. On retreatment the result returned in most patients: 84% of those on risankizumab and, according to conference data, 85% of those on icotrokinra.

There is also an intermediate option for the best responders. In the German GUIDE trial, patients whose skin had cleared completely on guselkumab received injections every 16 weeks instead of every eight. On the primary endpoint there was no difference: residual PASI below 3 was seen in 91.9% versus 92.6%. Fewer patients, however, had completely clear skin on the less frequent schedule: 69% versus 81%. But this is less frequent dosing, not drug withdrawal. No drug has yet proven remission without medication.

06 · Money: why the best pill is not yet a bestseller

The psoriasis drug market is, above all, a market for injections. Skyrizi (risankizumab) earned $17.6bn in 2025, almost seven times more than both pills combined. The figures cover all indications, not only psoriasis: the same drugs treat arthritis and inflammatory bowel disease.

Over ten years the market has seen two changes of leader. Humira, the world’s best-selling drug of the 2010s, lost 79% of its sales in three years after biosimilars launched in the US in 2023, from $21.2bn to $4.5bn. The revenue was taken over by a new injection from the same manufacturer, AbbVie: Skyrizi overtook Humira as early as 2024. In 2025 biosimilars began taking sales from Stelara (ustekinumab) in the same way: down 41%, to $6.1bn. Bimzelx (bimekizumab) more than tripled its sales in a year, to €2.2bn.

Pills are still secondary in this story. SOTYKTU, the best pill until 2026, sells eight times less than the older and weaker apremilast. The reasons are prosaic: insurance systems admit new pills only after other methods have failed, doctors are used to injections, and a pill is no cheaper.

Even so, companies are putting big money on pills: the three largest deals of 2019–2023 alone come to almost $20bn.

The real savings for payers over ten years came not from new pills but from biosimilars. When Denmark ran an adalimumab tender in October 2018, monthly spending on it fell by 82.8% within three months. NHS England negotiated a price of about a quarter of its previous spending on Humira. In 2025 in the US, Steqeyma, a biosimilar of ustekinumab, launched at an 85% discount to Stelara’s list price.

07 · Price and access: Europe and Ukraine

The EU approves a drug centrally, but each country sets the price and reimbursement itself. So SOTYKTU, on the EU market since 2023, costs different amounts in different countries and is available on different terms. A year of treatment runs from about €8,000 in Bulgaria to €12,000 in Germany. In Germany that is as much as the original Humira, and 2.5 times as much as a ustekinumab biosimilar.

ICOTYDE received authorization in the EU in September 2026, but as of the end of October no country has published a price or a reimbursement decision. In Germany the standard procedure will apply after market launch: a G-BA assessment within roughly six months and price negotiations within a year. In the US, according to reports citing a filing with the Vermont attorney general, the list price is about $8,300 per pack, or roughly $100,000 a year before discounts.

Approval does not yet mean access. In a study of 18 countries in Central, Southern and Eastern Europe (2024), TYK2-blocker pills were available in only three, and drugs approved after 2019 were unavailable in seven. Even in Denmark, where access to medicines is among the best in Europe, 37.7% of patients for whom systemic treatment is indicated never received it. Between 2020 and 2023 Poland tripled the number of patients in the B.47 program, from 1,344 to 4,133, and that is still only a small share of patients with the severe form.

In Ukraine, official statistics record only those who sought care at state facilities: 222.5 per 100,000 population in 2014, or about 0.2%. Expert estimates run to 1.5m patients, 10–15 times more. We found no newer official data. We also found no state program for purchasing psoriasis biologics, as in Poland; as of October 23, 2026, SOTYKTU and ICOTYDE are not listed in Ukrainian pharmacy directories. We did not have access to the State Register of Medicinal Products, so we do not claim that the drugs are unregistered.

In the coming years, competition rather than generics will make the new pills cheaper. SOTYKTU’s basic US patents expire in November 2033, an additional patent on the dosage form in 2043. ICOTYDE’s patents expire in 2039–2041. These dates apply to the US; in Europe the patent situation and court rulings may differ.

08 · The future: what is already in trials and may appear by 2030

The nearest candidate is zasocitinib from Takeda, another TYK2 blocker. Takeda paid $4bn upfront for it and promised up to $2bn more if sales reach $4–5bn a year. In two placebo-controlled trials, zasocitinib gave almost clear skin to 61% and 52% of patients at week 16. In the head-to-head LATITUDE Atlas trial, the result was 62.5% versus 34% on SOTYKTU.

These data are so far known only from Takeda press releases; there is no peer-reviewed publication. Zasocitinib caused side effects more often than placebo: 62% versus 47%; serious ones, 3% versus less than 1%. The FDA accepted the application for priority review in September 2026, and the company expects a decision in the first quarter of 2027. The EMA is also reviewing the application.

The second candidate is envudeucitinib from Alumis. In the ONWARD1 and ONWARD2 trials (more than 1,700 patients), at week 24 it gave almost clear skin to 68% and 62% of patients versus 26% on apremilast, and completely clear skin to 41% and 40%. Among everyone who started treatment with envudeucitinib, 66% had almost clear skin after 48 weeks and 47% had completely clear skin. The drug is taken twice a day, and there is no head-to-head trial against SOTYKTU. The company planned to file with the FDA in the fourth quarter of 2026; on standard review timelines, a decision could be expected in late 2027 or in 2028 — this is our estimate, not a company date.

Pills that block IL-17 lag several years behind. Lilly’s LY4100511, acquired along with DICE Therapeutics, reduced plaques by at least 75% in 31–45% of patients at week 12 in phase 2, versus 4% on placebo, according to results in the ClinicalTrials.gov registry. There is no publication yet, and no phase 3 has been announced. Protagonist’s peptide PN-881, which blocks both forms of IL-17, is only starting phase 2b in early 2027. Neither is likely to go on sale by 2030.

Alongside the candidates there are also drugs that have stalled. Their history shows how far SOTYKTU and ICOTYDE have raised the bar.

Ventyx is an instructive case. Its TYK2 blocker formally met the trial’s primary endpoint, but the company halted the program: in a market that already has SOTYKTU, a “statistically significant” result is not enough. A new pill now has to beat ICOTYDE, not placebo.

Every number in this text is hundreds of people who agreed to a daily pill with an unknown outcome, and some of them to a placebo.

A separate direction is not new molecules but new regimens for old ones. The GUIDE trial has already partly shown whether people whose skin has cleared completely can be treated less often. Whether early treatment can achieve long-term remission without drugs is an open question; there is no evidence yet.

If nothing changes, by 2030 a patient in Europe will have three or four pills (deucravacitinib, icotrokinra, zasocitinib and possibly envudeucitinib), cheap biosimilars of adalimumab and ustekinumab, and expensive modern injectables. The pills will probably approach the level of the best injectables but will not surpass them. Competition among three or four similar pills may bring prices down before generics appear.

09 · What remains unresolved

The main point: psoriasis still has no cure. All current drugs suppress inflammation while they are taken. After withdrawal the disease returns — a few weeks after stopping a pill, a few months after stopping an injection. Memory cells that remain in the skin probably explain why plaques appear in the same places.

The number of patients is growing, although the age-adjusted share of patients has barely changed. From 1990 to 2021 the number of people with psoriasis worldwide rose by 86%, from 23m to 43m. Age-standardized prevalence over the same period rose by only 8%. Most of the increase is a result of aging and population growth.

And the biggest gap is between what is possible and what people actually receive. In the population-based MAPP survey in North America and Europe (around 2012), more than 80% of people with skin involvement covering an area of four palms or more either had no treatment at all or used only creams. There are no more recent comparable data for Europe. For Ukraine there are none at all. We wrote about how the disease looks from the inside and what it says about the state of the body in the article Psoriasis as a Dashboard.

In ten years medicine has done more for psoriasis than in the previous fifty: almost clear skin has become an achievable goal, and powerful treatment has arrived in a pill. But the pill has not yet replaced the best injection, no drug has cured the disease for good, and for most patients in the world, including Ukraine, the new drugs remain drugs from other people’s trials.

Sources

• Regulators: EMA, EPAR — ICOTYDE, SOTYKTU, Bimzelx, Cosentyx, Taltz, Skyrizi; restrictions on JAK inhibitors (2022). FDA labels: ICOTYDE, SOTYKTU, Skyrizi, Cosentyx 2015, Taltz 2016, Tremfya 2017, Ilumya 2018, Otezla 2014, Rybelsus/Ozempic in pill form
• Icotrokinra: ICONIC-ADVANCE 1/2, Lancet 2025, 52-week results, BJD 2026, ICONIC-LEAD, NEJM 2025, ICONIC-TOTAL, registry NCT06143878, NCT06220604, ICONIC-ASCEND NCT06934226; pharmacokinetics and absorption; review by Ferreira, Am J Clin Dermatol 2026; 2-year data, HCPLive; EU approval, J&J; indirect comparison with risankizumab (AbbVie)
• Deucravacitinib: POETYK PSO-1, POETYK PSO-2, 5-year follow-up, selectivity, Chimalakonda 2021; G-BA, 2023, G-BA dossier, 2026, NICE TA907; ORAL Surveillance, NEJM 2022
• Injections and head-to-head trials: UltIMMa-1/2, IMMvent, IMMerge, IMMhance, BE READY, BE VIVID, BE SURE, BE RADIANT, CLEAR, ECLIPSE, IXORA-R, GUIDE, ESTEEM 1; Cochrane — 2023, 2025; drug retention, PsoBioTeq
• Science: discovery of IL-23 (2000), IL-23 and Th17 (2005), IL12B and IL23R genes (2007), TYK2 variants and autoimmune diseases, TYK2 P1104A and tuberculosis, memory cells in healed skin
• Pipeline: Takeda — priority review, LATITUDE Atlas; envudeucitinib — ONWARD1/2, ONWARD3; LY4100511, NCT06602219; PN-881, Protagonist; VTX958; orismilast; piclidenoson
• Money: AbbVie, 2025, AbbVie 10-K, J&J 10-K, BMS, Q4 2025, Amgen, 2025, UCB, 2025, FTC on Otezla, Takeda — Nimbus, Lilly — DICE, Alumis IPO; biosimilars — Denmark, JAMA Internal Medicine, Steqeyma; patents — SOTYKTU, ICOTYDE
• Prices and access: Bulgaria, Greece, Spain, Nomenclator, Netherlands, Poland — Ministry of Health reply, 2024, reimbursement announcement, July 2026; Ukraine — compendium, IL and TNF blockers, JAK/TYK2; access in 18 CEE countries, ISPOR 2025; Denmark, undertreatment
• Prevalence and burden: WHO, 2016, GBD 2021, Parisi, BMJ 2020, psoriatic arthritis, JAAD 2019, cardiovascular risk, JAHA 2013, depression, JID 2014, MAPP, JAAD 2014, EuroGuiDerm, German adaptation 2026, Ukraine — Tkach et al., 2020, Kotvitska, 2013