The oral Janus kinase/spleen tyrosine kinase inhibitor ASN 002 demonstrates efficacy and improves associated systemic inflammation in patients with moderate‐to‐severe atopic dermatitis: results from a randomized double‐blind placebo‐controlled study

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Article first published online: 06 May 2019
DOI: 10.1111/bjd.17932

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ASN 002 is an oral dual inhibitor of Janus kinase and spleen tyrosine kinase, which are involved in the pathogenesis of atopic dermatitis ( AD ) through their regulatory role on T helper (Th)1, Th2 and Th17/Th22 pathways.


The objectives of this study were to evaluate the efficacy, safety, pharmacokinetics and effects on systemic biomarkers of ASN 002 in patients with moderate‐to‐severe AD .

Methods A total of 36 patients with moderate‐to‐severe AD were randomized (3 : 1) to ASN 002 or placebo in the phase Ib study. Three dosage cohorts were studied over a 28‑day period (20 mg, 40 mg and 80 mg once daily).


ASN 002 was superior to placebo for the proportion of patients achieving Eczema Area and Severity Index ( EASI ) 50 (20 mg 20%, P = 0·93; 40 mg 100%, P = 0·003; 80 mg 83%, P = 0·03; placebo 22%), EASI 75 (20 mg 0%, P = 0·27; 40 mg 71%, P = 0·06; 80 mg 33%, P = 0·65; placebo 22%) and in change from baseline in pruritus (20 mg −1·3 ± 2·1, P = 0·81; 40 mg −3·1 ± 2·7, P = 0·27; 80 mg −4·7 ± 2·1, P = 0·01; placebo −1·6 ± 1·8). Adverse events were generally mild and similar across all groups. ASN 002 showed dose‐dependent plasma exposure with low interpatient variability, significantly downregulated several serum biomarkers involved in Th1, Th2 and Th17/Th22 immunity, and decreased the atherosclerosis‐associated biomarker E selectin/ SELE .


In patients with moderate‐to‐severe AD , ASN 002 showed strong efficacy with rapid onset of action and associated improvements in systemic inflammation.

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bjd17932-sup-0006-SupInfo.pptxPowerpoint S1 Journal Club Slide Set.
bjd17932-sup-0007-VideoS1.mp4Video S1 Author video.

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