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Taltz ® (ixekizumab) injection
This information is provided in response to your request. Resources may contain information about doses, uses, formulations and populations different from product labeling. See Prescribing Information above, if applicable.
What is the mechanism of action of TALTZ® (ixekizumab)?
Ixekizumab is a humanized immunoglobulin G subclass 4 (IgG4) monoclonal antibody that binds with high affinity (<3pM) and specificity to interleukin (IL)-17A, a proinflammatory cytokine and inhibits its interaction with the IL-17 receptor.
How Ixekizumab Works, Ixekizumab Structure and Pharmacology
Ixekizumab is a humanized IgG4 monoclonal antibody that binds with high affinity (<3 pM) and specificity to IL-17A, a proinflammatory cytokine and inhibits its interaction with the IL-17 receptor.1,2
Ixekizumab Structure and Pharmacology
Ixekizumab is a humanized immunoglobulin G subclass 4 monoclonal antibody that selectively binds with the interleukin (IL)-17A cytokine and inhibits its interaction with the IL-17 receptor. Interleukin-17A is a naturally occurring cytokine involved in normal inflammatory and immune responses. By inhibiting IL-17A, ixekizumab inhibits the release of proinflammatory cytokines and chemokines.1,3
Interleukin-17A is a proinflammatory cytokine by virtue of its ability to activate and recruit neutrophils. As shown in , IL-17A can be produced by many cell types.4-6
Elevated levels of IL-17A have been implicated in the pathogenesis of a variety of autoimmune diseases.6
Interleukin-17A Family Members
Ixekizumab selectively binds to IL-17A, without cross-reactivity to other IL-17 family members.1,9,10 Ixekizumab does not bind to ligands IL-17B, IL-17C, IL-17D, IL-17E, or IL-17F.10
The IL-17A cytokine can be composed of either IL-17A homodimers or IL-17A-IL-17F heterodimers. Interleukin-17A binds to receptor interleukin-17 receptor-A (IL-17RA) which consists of 2 IL-17RA subunits and 1 IL-17RC subunit.9 Interleukin-17A belongs to a broader family, which includes IL-17A, IL-17B, IL-17C, IL-17D, and IL-17E ().
Enclosed Prescribing Information
The published references below are available by contacting 1-800-LillyRx (1-800-545-5979).
1Taltz [package insert]. Indianapolis, IN: Eli Lilly and Company; 2021.
2Liu L, Lu J, Allan BW, et al. Generation and characterization of ixekizumab, a humanized monoclonal antibody that neutralizes interleukin-17A. J Inflamm Res. 2016;9:39-50. http://dx.doi.org/10.2147/JIR.S100940
3Data on file, Eli Lilly and Company and/or one of its subsidiaries.
4Cua DJ, Tato CM. Innate IL-17-producing cells: the sentinels of the immune system. Nat Rev Immunol. 2010;10(7):479-489. http://dx.doi.org/10.1038/nri2800
5Gaffen SL. Structure and signalling in the IL-17 receptor family. Nat Rev Immunol. 2009;9(8):556-567. http://dx.doi.org/10.1038/nri2586
6Lin AM, Rubin CJ, Khandpur R, et al. Mast cells and neutrophils release IL-17 through extracellular trap formation in psoriasis. J Immunol. 2011;187(1):490-500. http://dx.doi.org/10.4049/jimmunol.1100123
7Krueger JG, Fretzin S, Suárez-Fariñas M, et al. IL-17A is essential for cell activation and inflammatory gene circuits in subjects with psoriasis. J Allergy Clin Immunol. 2012;130(1):145-154.e9. http://dx.doi.org/10.1016/j.jaci.2012.04.024
8Maddur MS, Miossec P, Kaveri SV, Bayry J. Th17 cells: biology, pathogenesis of autoimmune and inflammatory diseases, and therapeutic strategies. Am J Pathol. 2012;181(1):8-18. http://dx.doi.org/10.1016/j.ajpath.2012.03.044
9Chiricozzi A, Krueger JG. IL-17 targeted therapies for psoriasis. Expert Opin Investig Drugs. 2013;22(8):993-1005. http://dx.doi.org/10.1517/13543784.2013.806483
10Tham LS, Tang CC, Choi SL, et al. Population exposure–response model to support dosing evaluation of ixekizumab in patients with chronic plaque psoriasis. J Clin Pharmacol. 2014;54(10):1117-1124. http://dx.doi.org/10.1002/jcph.312
11Martin DA, Towne JE, Kricorian G, et al. The emerging role of IL-17 in the pathogenesis of psoriasis: preclinical and clinical findings. J Invest Dermatol. 2013;133(1):17-26. http://dx.doi.org/10.1038/jid.2012.194
Date of Last Review: July 22, 2021