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Br J Dermatol. 2019 Mar 28. doi: 10.1111/bjd.17932. [Epub ahead of print]

The oral Janus kinase/spleen tyrosine kinase inhibitor ASN002 demonstrates efficacy and improves associated systemic inflammation in patients with moderate-to-severe atopic dermatitis: results from a randomized double-blind placebo-controlled study.

Author information

1
Innovaderm Research Inc., 1851 Sherbrooke Street East, Suite 502, Montreal, H2K 4L5, Quebec, Canada.
2
Forward Clinical Trials, Inc., 4915 Ehrlich Road, Tampa, 33624, FL, U.S.A.
3
Therapeutics Clinical Research, 9025 Balboa Avenue, Suite 105, San Diego, 92123, CA, U.S.A.
4
Progressive Clinical Research, P.A., LLC, 1973 North West Loop 410, Suite 106, San Antonio, 78213, TX, U.S.A.
5
Dermatology Specialists Research, 3810 Springhurst Boulevard, Suite 130, Louisville, 40241, KY, U.S.A.
6
Center for Clinical Studies, University of Texas Health Science Center, 451 North Texas Avenue, Houston, 77598, TX, U.S.A.
7
Department of Dermatology, Eastern Virginia Medical School and Virginia Clinical Research Inc., 6160 Kempsville Circle, Suite 200A, Norfolk, 23502, VA, U.S.A.
8
Dermatology Research Associates, 8930 South Sepulveda Boulevard, Los Angeles, 90045, CA, U.S.A.
9
Center for Dermatology Clinical Research Inc., 2557 Mowry Avenue, Suite 21 and 25, Fremont, 94538, CA, U.S.A.
10
Olympian Clinical Research, 1201 South Myrtle Avenue, Clearwater, 33756, FL, U.S.A.
11
Asana BioSciences, LLC, 997 Lenox Drive, Suite 220, Princeton Pike Corporate Center, Lawrenceville, 08648, NJ, U.S.A.
12
Icahn School of Medicine at Mount Sinai, 1425 Madison Avenue, Icahn Building 13-76, New York, 10029, NY, U.S.A.

Abstract

BACKGROUND:

ASN002 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.

OBJECTIVES:

The objectives of this study were to evaluate the efficacy, safety, pharmacokinetics and effects on systemic biomarkers of ASN002 in patients with moderate-to-severe AD. Methods A total of 36 patients with moderate-to-severe AD were randomized (3 : 1) to ASN002 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).

RESULTS:

ASN002 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. ASN002 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.

CONCLUSIONS:

In patients with moderate-to-severe AD, ASN002 showed strong efficacy with rapid onset of action and associated improvements in systemic inflammation.

PMID:
30919407
DOI:
10.1111/bjd.17932

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