TARGET A SOURCE OF ITCH AND INFLAMMATION1-3

OPZELURA is a topical JAK inhibitor designed to target the signaling of key cytokines believed to be critical to the Th2 response in AD, which contribute to1,2,4,5:
Itch and inflammation: IL-4, IL-13, IL-31, and TSLP
Itch and inflammation:
IL-4, IL-13, IL-31, and TSLP

OPZELURA targets the signaling of key cytokines believed to contribute to inflammation and itch in AD1,3

This video shows how ruxolitinib, a topical JAK inhibitor, was designed to target the signaling of key cytokines believed to be critical to the Th2 response in AD, which contribute to itch and inflammation: IL-4, IL-13, IL-31 and TSLP.

JAKs are intracellular signaling enzymes that act downstream of many inflammatory cytokines involved in AD pathogenesis.2

The relevance of inhibition of specific JAK enzymes to therapeutic effectiveness is not currently known.1

AD=atopic dermatitis; IL=interleukin; JAK=Janus kinase; Th2=T helper 2; TSLP=thymic stromal lymphopoietin.

See how OPZELURA was studied >

References: 1. Opzelura. Prescribing Information. Incyte Corporation; 2021. 2. Kim BS, Howell MD, Sun K, et al. Treatment of atopic dermatitis with ruxolitinib cream (JAK1/JAK2 inhibitor) or triamcinolone cream. J Allergy Clin Immunol. 2020;145(2):572-582. 3. Smith P, Yao W, Shepard S, et al. Developing a JAK inhibitor for targeted local delivery: ruxolitinib cream. Pharmaceutics. 2021;13(7):1044. doi:10.3390/pharmaceutics13071044. 4. Cevikbas F, Wang X, Akiyama T, et al. A sensory neuron-expressed IL-31 receptor mediates T helper cell-dependent itch: involvement of TRPV1 and TRPA1. J Allergy Clin Immunol. 2014;133(2):448-460. 5. Wilson SR, Thé L, Batia LM, et al. The epithelial cell-derived atopic dermatitis cytokine TSLP activates neurons to induce itch. Cell. 2013;155(2):285-295.