Risankizumab

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Risankizumab
Monoclonal antibody
Type ?
Source Humanized
Target interleukin 23A
Clinical data
Synonyms BI-655066
ATC code
  • none
Identifiers
CAS Number
ChemSpider
  • none
UNII
Chemical and physical data
Formula C6476H9992N1720O2016S44
Molar mass 145.6 kDa

Risankizumab also known as BI-655066 is a humanized monoclonal antibody targeting interleukin 23A (IL-23A).[1] Risankizumab is part of a collaboration between Boehringer Ingelheim and AbbVie. It is an experimental drug that has not been approved for the treatment of any medial conditions. The therapeutic potential of risankizumab was evaluated for the treatment of psoriasis in a preliminary phase 2 clinical trial.

Clinical Drug Trial Information[edit]

Psoriasis[edit]

In a phase II clinical trial, thirty-nine patients received single-dose Risankizumab, 18 of which received the drug intravenously, 13 subcutaneously, and 8 received the placebo drug. There were several instances that adverse effects occurred but in the same frequency for the placebo and the experimental groups. Four considerably serious adverse events occurred, but it was determined that they were not treatment related, in the Risankizumab treated patients. Risankizumab was associated with clinical improvement in individuals treated with the drug, from week 2 and maintained for up to 66 weeks after treatment. At week 12 of treatment, 75%, 90%, and 100% decreases in the psoriasis area and Severity Index were achieved by 87%, 58%, and 16% of Risankizumab treated patients, regardless of dose, respectively, versus individuals receiving placebo. Significant correlation between treatment-associated molecular changes and psoriasis area and severity index improvement was observed.[2]

Mechanism of Action and Pharmacodynamic Effects[edit]

The IL23/IL17 axis plays an important role in the development of chronic inflammation, with potential genetic links between the IL23 receptor (IL23R) or its ligand identified in inflammatory diseases such as psoriasis, inflammatory bowel disease, and graft-versus-host disease. Signaling through the IL23R induces Janus kinase 2 (JAK2) and tyrosine kinase 2 (tyk2) phosphorylation and leads to increased levels of the inflammatory cytokines IL17 and IL22. Risankizumab binds to the p19 sub-unit of IL23, IL23A, preventing receptor activation and thereby disrupting the IL23/IL17 axis.[3]

References[edit]

  1. ^ Singh, Sanjaya (July–August 2015). "Selective targeting of the IL23 pathway: Generation and characterization of a novel high-affinity humanized anti-IL23A antibody". Mabs. 7 (4): 778–791. doi:10.1080/19420862.2015.1032491. PMC 4622456Freely accessible. 
  2. ^ Krueger, J; et al. (July 2015). "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 Allergy Clin Immunol. 136 (1): 116–127. doi:10.1016/j.jaci.2015.01.018. 
  3. ^ Gaffen, S.; et al. (September 2014). "The IL-23-IL-17 immune axis: from mechanisms to therapeutic testing". Nat Rev Immunol. 9 (14): 585–600. doi:10.1038/nri3707. PMC 4281037Freely accessible. 

[1]

  1. ^ "Risankizumab". Drug Spider. Retrieved May 26, 2016.