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IKK family

Unless otherwise stated all data on this page refer to the human proteins. Gene information is provided for human (Hs), mouse (Mm) and rat (Rn).


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The IκB kinase (IKK)-related kinases are central to the induction of the innate type I interferon (IFN) response [7]. A set of rare autoimmune disorders known as type I interferonopathies are caused by disturbance of the homeostatic control of induction, transmission, and resolution of the type I IFN-mediated immune response [6]. Therefore, members of this signaling pathway are subject to investigation as intervention points for pharmacological inhibition [4]. Initial investigations targeted IFN-I downstream signaling, including IFN-I proteins, IFNAR and the JAK/STAT signaling pathway. For example, sifalimumab (anti-IFN-α mAb), anifrolumab (anti-IFNAR1) and the JAK inhibitors ruxolitinib and tofacitinib, can all potentially tackle the effector function of dysregulated IFN by blocking downstream IFN-I signaling, but do not contribute to reducing the production of IFN. Upstream targeting of TBK1 and/or IKKε could be effective at blocking de novo IFN-I induction by a variety of stimuli. Small molecule kinase inhibitors of TBK1/IKKε already in development for cancer may expedite investigation for inflammatory diseases also [9].


IKK-alpha (component of inhibitor of nuclear factor kappa B kinase complex) Show summary » More detailed page

IKK-beta (inhibitor of nuclear factor kappa B kinase subunit beta) Show summary » More detailed page

IKK-epsilon (inhibitor of nuclear factor kappa B kinase subunit epsilon) Show summary » More detailed page

TBK1 (TANK binding kinase 1) Show summary » More detailed page


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How to cite this family page

Database page citation:

IKK family. Accessed on 17/10/2019. IUPHAR/BPS Guide to PHARMACOLOGY,

Concise Guide to PHARMACOLOGY citation:

Alexander SPH, Fabbro D, Kelly E, Marrion NV, Peters JA, Faccenda E, Harding SD, Pawson AJ, Sharman JL, Southan C, Davies JA; CGTP Collaborators. (2017) The Concise Guide to PHARMACOLOGY 2017/18: Enzymes. Br J Pharmacol. 174 Suppl 1: S272-S359.