Risankizumab: an anti-IL-23 antibody for the treatment of psoriasis

被引:45
作者
Haugh, Isabel M. [1 ]
Preston, Allie K. [2 ]
Kivelevitch, Dario N. [1 ]
Menter, Alan M. [1 ]
机构
[1] Baylor Univ, Med Ctr, Dept Dermatol, Dallas, TX USA
[2] Texas A&M Hlth Sci Ctr, Coll Med, Bryan, TX USA
关键词
psoriasis; risankizumab; human monoclonal antibody; interleukin-23; efficacy; safety; INTERLEUKIN-23; P19; PATHOGENESIS; ASSOCIATION; EXPRESSION; CYTOKINES; VULGARIS; IL-23;
D O I
10.2147/DDDT.S167149
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Risankizumab, a fully human IgG monoclonal antibody inhibitor of IL-23, is a therapeutic agent currently in late stage development for use in the treatment of moderate-tosevere plaque psoriasis. It is a biologic agent similar to guselkumab and tildrakizumab which targets IL-23 specifically, and has been primarily developed for use in moderate-to-severe psoriasis. USA-based pharmaceutical company Abbvie submitted it for a Biologics License Application to the US Food and Drug Administration (FDA) in April 2018. Risankizumab is the result of a collaboration between the German company Boehringer Ingelheim and Abbvie, which together are leading the future development and commercialization of risankizumab globally. The results from Phase I to Phase III clinical trials of risankizumab show it is highly effective and its FDA-approval in 2018 is likely. In this article we provide an independent expert opinion on the efficacy and safety of risankizumab in psoriasis based on a full review of the literature.
引用
收藏
页码:3879 / 3883
页数:5
相关论文
共 16 条
[1]   The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-γ, interleukin-2, and tumor necrosis factor-α, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations:: a type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients [J].
Austin, LM ;
Ozawa, M ;
Kikuchi, T ;
Walters, IB ;
Krueger, JG .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1999, 113 (05) :752-759
[2]  
Blauvelt A, 2018, 14 ANN MAUI DERM DER
[3]   A large-scale genetic association study confirms IL12B and leads to the identification of IL23R as psoriasis-risk genes [J].
Cargill, Michele ;
Schrodi, Steven J. ;
Chang, Monica ;
Garcia, Veronica E. ;
Brandon, Rhonda ;
Callis, Kristina P. ;
Matsunami, Nori ;
Ardlie, Kristin G. ;
Civello, Daniel ;
Catanese, Joseph J. ;
Leong, Diane U. ;
Panko, Jackie M. ;
McAllister, Linda B. ;
Hansen, Christopher B. ;
Papenfuss, Jason ;
Prescott, Stephen M. ;
White, Thomas J. ;
Leppert, Mark F. ;
Krueger, Gerald G. ;
Begovich, Ann B. .
AMERICAN JOURNAL OF HUMAN GENETICS, 2007, 80 (02) :273-290
[4]  
Gordon KB, 2018, AM AC DERM ANN M FEB
[5]   Th17 Cytokines Stimulate CCL20 Expression in Keratinocytes In Vitro and In Vivo: Implications for Psoriasis Pathogenesis [J].
Harper, Erin G. ;
Guo, Changsheng ;
Rizzo, Heather ;
Lillis, Joseph V. ;
Kurtz, Stephen E. ;
Skorcheva, Iliyana ;
Purdy, David ;
Fitch, Erin ;
Iordanov, Mihail ;
Blauvelt, Andrew .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2009, 129 (09) :2175-2183
[6]   Psoriasis pathogenesis and the development of novel targeted immune therapies [J].
Hawkes, Jason E. ;
Chan, Tom C. ;
Krueger, James G. .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2017, 140 (03) :645-653
[7]   Highly Effective New Treatments for Psoriasis Target the IL-23/Type 17 T Cell Autoimmune Axis [J].
Kim, Jaehwan ;
Krueger, James G. .
ANNUAL REVIEW OF MEDICINE, VOL 68, 2017, 68 :255-269
[8]   Anti-IL-23A mAb BI 655066 for treatment of moderate-to-severe psoriasis: Safety, efficacy, pharmacokinetics, and biomarker results of a single-rising-dose, randomized, double-blind, placebo-controlled trial [J].
Krueger, James G. ;
Ferris, Laura K. ;
Menter, Alan ;
Wagner, Frank ;
White, Alexander ;
Visvanathan, Sudha ;
Lalovic, Bojan ;
Aslanyan, Stella ;
Wang, Elaine E. L. ;
Hall, David ;
Solinger, Alan ;
Padula, Steven ;
Scholl, Paul .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2015, 136 (01) :116-U231
[9]   Increased expression of interleukin 23 p19 and p40 in lesional skin of patients with psoriasis vulgaris [J].
Lee, E ;
Trepicchio, WL ;
Oestreicher, JL ;
Pittman, D ;
Wang, F ;
Chamian, F ;
Dhodapkar, M ;
Krueger, JG .
JOURNAL OF EXPERIMENTAL MEDICINE, 2004, 199 (01) :125-130
[10]   Immunology of Psoriasis [J].
Lowes, Michelle A. ;
Suarez-Farinas, Mayte ;
Krueger, James G. .
ANNUAL REVIEW OF IMMUNOLOGY, VOL 32, 2014, 32 :227-255