in pictures and a few words
What it is and why it matters
Deucravacitinib is a tablet for psoriasis in adults. It is prescribed for moderate and severe plaque psoriasis, when ointments and creams are no longer enough.
- One tablet a day, with or without food
- Acts on inflammation in a new way: it sits not in the “lock”, but next to it
- A doctor prescribes and manages the treatment
What happens in psoriasis
Psoriasis is not dry skin and not a cosmetic issue, but long-lasting inflammation started by the immune system itself.
- Signal substances of inflammation make skin cells divide many times faster
- Inside the cell, this signal is passed on by one messenger protein
- If it is blocked, the pathway that keeps psoriasis inflammation going switches off
Not in the lock, but beside it
Similar medicines sit in the “lock” — the protein’s working site. This tablet sits next to it, on a “lever”, and holds it in the “off” position.
- The “locks” of related proteins are alike, so ordinary tablets also hit the neighbours
- Their “levers” differ, so this tablet finds the right protein more precisely
More precise than related tablets
At the treatment dose, this tablet barely touches the neighbouring pathways needed for making blood and protecting against infections.
- That is why it does not carry the strictest warning that related tablets have
- It covers serious infections, blood clots, heart and blood vessel disease, and tumours
- This does not mean there are no risks at all — they are just different
What the studies showed
The tablet was tested in adults with moderate and severe psoriasis.
- Improvement began early and lasted
- With use over many years, the benefit and safety were maintained
Tested in people. Tested in people: clear or almost clear skin was seen in more people than on a dummy pill.
Compared with another tablet
There is another tablet for psoriasis. In studies the two were compared head to head — on the new one, more people had clear or almost clear skin.
- A simpler routine: one tablet a day, no need to build up the dose gradually
- The other tablet more often causes stomach and bowel complaints and headache
- Both are needed: the doctor chooses, taking other illnesses and tolerability into account
How to take it
One 6 mg tablet once a day, with or without food. You start straight away with the working dose — no need to increase it gradually.
- Psoriasis is a chronic disease: once treatment stops, it comes back
- So treatment is long-term; the dermatologist decides how long to take it
Its place in treatment
This is treatment in tablet form for when ointments and creams are no longer enough, but it has not yet come to injections.
- Suits those for whom injections are unacceptable or unavailable
- In severe psoriasis and joint involvement, injections remain stronger
- So in severe forms the tablet does not replace injections
Who should see a doctor first
The tablet is prescribed by a doctor. Before starting, hidden infections are ruled out and vaccinations are reviewed.
- Testing for tuberculosis, including latent, and for viral hepatitis B and C
- Live vaccines are given before treatment starts; they are not used during it
- Blood and liver tests — before starting and later as the doctor decides
In one sentence
A once-a-day tablet that precisely switches off the inflammation pathway in psoriasis. It is prescribed by a doctor — after testing for hidden infections.
In brief
What happens in psoriasis
Psoriasis is not "dry skin" or a cosmetic problem but chronic immune inflammation. The key players are the cytokines interleukin-23 and interleukin-12, along with type I interferons. They drive a cascade that makes skin cells divide many times faster than normal and sustains inflammation within the plaque.
The signal from those cytokines is carried into the cell by TYK2, a member of the Janus kinase family. Blocking it means switching off precisely the pathway on which psoriatic inflammation depends.
Why ordinary JAK inhibitors are a blunt instrument
Classic kinase inhibitors (tofacitinib, baricitinib, upadacitinib) bind the active site — where ATP docks to make the enzyme work.
The problem is that active sites are built similarly across related kinases. A drug that fits one inevitably engages its neighbours: JAK1, JAK2 and JAK3 govern haematopoiesis, immune surveillance and interferon signalling. Hence the FDA's class-wide boxed warning about serious infections, thrombosis, cardiovascular events and malignancy.
What was done differently
Besides its working domain, TYK2 has a regulatory (pseudokinase) domain — a part that normally holds the enzyme switched off.
Deucravacitinib binds precisely there. It does not occupy the keyhole; it fixes the adjacent lever in the "off" position.
| Classic JAK inhibitors | Deucravacitinib | |
|---|---|---|
| Binding site | Active site (ATP pocket) | Regulatory domain |
| Similarity of target across neighbouring kinases | High — hence cross-activity | Low — hence selectivity |
| Affects JAK1/2/3 | Yes | Essentially not at therapeutic doses |
| FDA boxed warning | Present | Absent |
| Formulation | Tablets | Tablets |
The design intent: obtain the anti-inflammatory effect along the required pathway without disturbing everything else.
What the trials showed
▸POETYK PSO-1 and PSO-2 (JAAD, 2023) — two phase 3 trials. Deucravacitinib outperformed both placebo and apremilast on the proportion of patients achieving PASI 75 (at least 75% improvement in the psoriasis severity index) and clear or almost clear skin on sPGA [1]. ▸Five-year open-label extension (Am J Clin Dermatol, 2026) — efficacy and safety profile maintained with long-term use [2]. ▸A separate analysis showed improvement begins early and holds through the maintenance phase [3].
How it is taken
| Parameter | Detail |
|---|---|
| Dose | 6 mg once daily |
| Titration | Not required |
| Food | Irrelevant |
| Formulation | Tablet |
The absence of titration is a practical advantage: the patient starts at the working dose without a build-up period.
What to check before and during
▸tuberculosis screening, including latent infection; ▸hepatitis B and C markers; ▸vaccination: live vaccines before starting, not during therapy; ▸baseline blood counts and liver tests before initiation, thereafter at the clinician's discretion.
There is no rigid laboratory schedule of the kind classic JAK inhibitors demand — a direct consequence of the different selectivity.
Where it sits in psoriasis treatment
| Step | Treatment |
|---|---|
| Mild psoriasis | Topicals: corticosteroids, vitamin D analogues, calcineurin inhibitors |
| Moderate to severe | Phototherapy, methotrexate, apremilast, deucravacitinib |
| Severe when tablets are not enough, or with joint involvement | Injectable biologics: IL-17, IL-23 and TNF inhibitors |
Deucravacitinib occupies the oral systemic niche: stronger than apremilast on trial comparisons and simpler to take, though in severe disease and psoriatic arthritis injectable biologics remain the more powerful option.
Summary
▸Allosteric mechanism: binding TYK2's regulatory domain rather than its active site. ▸Hence selectivity and the absence of the boxed warning typical of JAK inhibitors. ▸Efficacy above placebo and apremilast on PASI 75 and sPGA in phase 3 trials. ▸Convenience: 6 mg once daily, no titration, food irrelevant. ▸Monitoring lighter than for the JAK class, though tuberculosis and hepatitis screening is mandatory. ▸Does not replace injectable biologics in severe psoriasis and arthritis.
Treatment can be discussed at a consultation; the product can be ordered here.
References
1. Armstrong AW, et al. Deucravacitinib versus placebo and apremilast in moderate to severe plaque psoriasis: efficacy and safety results from the 52-week, randomized, double-blinded, placebo-controlled phase 3 POETYK PSO-1 trial. J Am Acad Dermatol. 2023;88(1):29–39. PMID 35820547
2. Armstrong AW, et al. Deucravacitinib 5-year safety and efficacy results in plaque psoriasis: a phase 3 open-label extension. Am J Clin Dermatol. 2026. PMID 42563042
3. Korman NJ, et al. Deucravacitinib onset of action and maintenance of response in phase 3 plaque psoriasis trials. J Dermatolog Treat. 2024. PMID 38945549
4. SOTYKTU (deucravacitinib) US Prescribing Information, Bristol Myers Squibb.
Key facts
- Deucravacitinib (brand name Sotyktu, Bristol Myers Squibb) is the first allosteric TYK2 inhibitor, approved by the FDA on 9 September 2022 for moderate-to-severe plaque psoriasis in adults.
- The key difference from ordinary JAK inhibitors: it binds the regulatory (pseudokinase) domain rather than the active site. Active sites are similar across related kinases while regulatory domains differ far more — hence the high selectivity.
- The practical consequence of that selectivity: the drug does not carry the FDA boxed warning about serious infections, thrombosis, cardiovascular events and malignancy that applies to the JAK inhibitor class.
- TYK2 transmits signals from interleukins 12 and 23 and type I interferons — precisely the cytokines that sustain psoriatic inflammation. Before this, blocking them required injectable biologics.
- POETYK PSO-1 and PSO-2 (JAAD, 2023): deucravacitinib outperformed both placebo and apremilast on PASI 75 response and on clear or almost clear skin by sPGA.
- A five-year open-label extension confirms that efficacy and the safety profile are maintained with long-term use.
- Dosing is simple and needs no titration: 6 mg once daily, with or without food — a practical advantage over drugs requiring dose escalation.
- Laboratory monitoring is lighter than for classic JAK inhibitors, but tuberculosis and viral hepatitis screening precedes treatment, and live vaccines are not given during therapy.
- Where it belongs: moderate-to-severe psoriasis when topical therapy is insufficient. It is an oral alternative to injectable biologics, not a replacement for them in severe disease.
- Apremilast is the direct competitor in the oral niche: deucravacitinib performed better in trials, but the choice still rests with the clinician given comorbidity and tolerability.
