Inflammation and disease research
Human ex vivo models for inflammatory skin disease research
Generate human-relevant data for better-informed dermatology drug development


Inflammatory skin diseases such as psoriasis and atopic dermatitis (AD) involve complex interactions between immune signaling, resident immune cells and epidermal biology. Capturing these mechanisms in a physiologically relevant human tissue environment can help drug developers make more informed decisions before clinical studies.
Genoskin provides human ex vivo skin models and research services designed to reproduce key disease-relevant features of inflammatory skin disorders while preserving native human skin architecture and resident immune cells.
Our platforms enable the study of distinct inflammatory mechanisms, from T cell–driven Th1/Th17 psoriasis-like inflammation to type 2 cytokine–driven barrier impairment in atopic dermatitis. Both allow therapeutic candidates to be evaluated using relevant human tissue and multi-parametric readouts.
Explore our inflammatory skin disease models


Psoriasis
Evaluate anti-psoriasis biologics and small molecules, including topical formulations and injected drugs, using InflammaSkin®. It is a T cell–driven human ex vivo model designed to reproduce key features of early Th1/Th17-mediated psoriatic inflammation.


Atopic dermatitis
Evaluate topical therapeutics in a type 2–driven human skin barrier impairment model. IL-4 and/or IL-13 stimulation reproduces key features of AD-associated barrier dysfunction.
From mechanism to efficacy, generate human data that helps you select, rank and advance your next dermatology candidate.
Psoriasis and atopic dermatitis involve distinct immune pathways and biological changes in the skin, requiring different approaches to evaluate therapeutic efficacy. Our human ex vivo induction models reproduce key disease-relevant features of each condition to generate translational data for drug development. They do not reproduce the full complexity of either disease in vivo, including systemic immunity.
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