Psoriasis and atopic dermatitis (the most common kind of eczema) are both chronic inflammatory skin diseases, driven by an immune system that keeps attacking the skin. Fisetin has been tested against models of both, and the laboratory results are encouraging: less skin cell overgrowth, lower levels of the immune signals behind each disease, and calmer skin in mice [1][2].
Before reading further, one fact shapes everything. The strongest psoriasis result came from fisetin applied to the skin of mice, and the rest comes from human skin cells and lab-grown skin. No fisetin product, oral or topical, has been tested in people with psoriasis or eczema. A 2025 review states plainly that clinical trials are lacking [3].
Key Takeaways
- Applied to the skin of mice with imiquimod-induced psoriasis, fisetin reduced the inflammation more than rapamycin did [1].
- In human skin cells and a 3D model of psoriatic skin, fisetin slowed cell overgrowth and lowered IL-17A and IFN-gamma [4].
- In an eczema-like mouse model, fisetin lowered IgE and immune cell infiltration in the skin [2], and it reduced scratching in mice [5].
- No human trial has tested fisetin, oral or topical, for psoriasis or eczema.
Important: This article describes laboratory and animal research and is not medical advice. Do not stop a prescribed cream, biologic or other psoriasis or eczema treatment in favour of a supplement. Psoriasis is linked to joint and heart problems that need medical follow-up. Fisetin can affect enzymes that clear many drugs, so speak to a doctor or pharmacist before adding it.
Why researchers look at fisetin for skin inflammation
Psoriasis is driven largely by IL-17A and related signals from Th17 immune cells, which push skin cells called keratinocytes to multiply far too fast and form thick, scaly plaques. Inside those cells, a growth pathway called PI3K/Akt/mTOR is switched on in psoriatic lesions [1]. Fisetin binds mTOR and a partner enzyme, S6K1, directly, which is why psoriasis researchers took an interest in it.
A 2025 review of 85 studies on psoriasis signalling named fisetin as one of several flavonoids that act on both the PI3K/Akt/mTOR and the JNK pathways [6]. That is a summary of mechanism, not a test of treatment. Our page on fisetin and inflammation explains these pathways more broadly.
Human skin cells and lab-grown psoriatic skin
A 2019 study used normal human keratinocytes, human blood immune cells, and a full-thickness 3D model of human skin built to resemble psoriatic lesions [4]. In keratinocytes, fisetin pushed the cells toward normal maturation and blocked the overgrowth triggered by IL-22, a psoriasis cytokine. It reduced activity in the PI3K/Akt/mTOR pathway and in two stress pathways, p38 and JNK, while having an enhancing effect on ERK1/2.
In stimulated keratinocytes and activated human blood immune cells, fisetin cut the release of IFN-gamma and IL-17A [4]. In the 3D psoriatic skin model, it improved the psoriasis-like features and reduced IL-17 from T cells grown alongside the skin. A 3D model is a better stand-in for a patient than a flat layer of cells, but it has no blood supply, no liver and no whole immune system, so it cannot say what a swallowed dose would do.
The 2022 mouse study, and how to read it
A 2022 study compared fisetin with rapamycin, a drug that blocks mTOR [1]. In human keratinocytes activated with Th1 and Th17 cytokines, fisetin changed the activity of 12,713 genes compared with cells exposed to cytokines alone, against 7,374 for rapamycin. That number describes how broad the effect was. It does not mean fisetin worked better: a wider footprint can equally mean the compound is less selective. Fisetin also blocked mTOR activity, switched on autophagy markers (the cell’s recycling system), and cut IL-17A release from activated T cells.
The animal part used imiquimod, a cream that causes psoriasis-like inflammation on mouse skin. Fisetin was applied to the skin, and it reduced the psoriasis-like inflammation more than rapamycin did, lowered Akt/mTOR activity in the lesions, and reduced T cell and macrophage infiltration [1]. This is the single strongest result for fisetin in psoriasis, and it is a topical result in mice. It says nothing directly about a capsule.
Atopic dermatitis and itch
Eczema has a different immune profile from psoriasis, with more allergic, IgE-driven inflammation. In NC/Nga mice, a strain prone to eczema, repeated application of the chemical DNFB to the skin causes eczema-like lesions [2]. Fisetin reduced the infiltration of eosinophils, mast cells and T cells into those lesions, lowered cytokines and chemokines in the skin, and markedly reduced total IgE in the blood. In activated T cells, it lowered IFN-gamma and IL-4 and raised IL-10, an anti-inflammatory signal.
Itch in eczema is partly driven by IL-31, a signal that works independently of histamine. In human mast cells grown in the lab, fisetin reduced IL-31 production and histamine release, and in mice it reduced scratching behaviour [5]. The authors suggest it could matter for itch that does not respond to antihistamines, but that has not been tested in people. For mast cells and allergy more broadly, see our page on fisetin, allergies and mast cells.
The delivery problem
Fisetin is poorly soluble and does not get into skin easily, which is why a 2025 review of the field focuses on nanoformulations: polymer nanoparticles, liposomes, lipid nanoparticles, nanogels and micelles designed to carry it into the skin [3]. The review reports that these improve skin penetration and reduce redness and scaling in animal psoriasis models, and it concludes that clinical trials are lacking and studies of safety and efficacy in patients are needed.
That also explains why oral supplements are a weak fit for this evidence. Plain fisetin taken by mouth reaches low blood levels; our page on fisetin bioavailability goes through the numbers, and nobody has measured how much reaches the skin.
What this does and does not mean for you
The laboratory picture is coherent: fisetin acts on mTOR and IL-17A in psoriasis models and on IgE and IL-31 in eczema models. Reviewers call it a candidate for development, particularly in nanoparticle form [3].
For people with psoriasis or eczema, the treatments with outcome data are the creams, light therapy, tablets and biologics a dermatologist can explain. Fisetin is not one of them. If you take it for other reasons, do not expect it to clear your skin, and check fisetin drug interactions first, particularly if you use immune-suppressing medicine. For fisetin’s effects on ageing skin rather than inflammatory disease, see fisetin and skin aging.
Common questions
Does fisetin help psoriasis?
In mice, fisetin applied to the skin reduced psoriasis-like inflammation [1], and it calmed human psoriasis skin models in the lab [4]. It has not been tested in people with psoriasis.
Does fisetin help eczema?
In an eczema-like mouse model it lowered IgE and immune cell infiltration in the skin [2]. There are no human studies.
Is oral fisetin useful for skin conditions?
Unknown. The psoriasis mouse study applied fisetin to the skin [1], and no fisetin product, oral or topical, has been tested in people with psoriasis or eczema.
Is fisetin better than rapamycin for psoriasis?
In one mouse study, topical fisetin reduced psoriasis-like inflammation more than rapamycin [1]. That is a single animal comparison, not evidence for people.
Can fisetin stop eczema itch?
In lab-grown human mast cells it lowered IL-31, an itch signal, and it reduced scratching in mice [5]. That has not been tested in people.
References
- Dual targeting of mTOR/IL-17A and autophagy by fisetin alleviates psoriasis-like skin inflammation. Front Immunol (2022). PMID 36741386
- Immunosuppressive effects of fisetin against dinitrofluorobenzene-induced atopic dermatitis-like symptoms in NC/Nga mice. Food Chem Toxicol (2014). PMID 24525099
- Recent advancement of fisetin-based nanoformulations in the management of psoriasis. Discov Nano (2025). PMID 40622453
- Fisetin, a 3,7,3′,4′-Tetrahydroxyflavone Inhibits the PI3K/Akt/mTOR and MAPK Pathways and Ameliorates Psoriasis Pathology in 2D and 3D Organotypic Human Inflammatory Skin Models. Cells (2019). PMID 31540162
- Fisetin inhibits IL-31 production in stimulated human mast cells: Possibilities of fisetin being exploited to treat histamine-independent pruritus. Life Sci (2018). PMID 29604269
- Exploring the Interplay of PI3K/AKT/mTOR and JNK Signaling Pathways in Psoriasis: Insights from Systematic Review and Network Pharmacology Approach. Curr Pharm Biotechnol (2025). PMID 41047673
These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease. Content is for informational purposes only and is not medical advice; consult a qualified healthcare provider before starting any supplement. As an Amazon Associate we earn from qualifying purchases.