Mirikizumab for the Treatment of Moderate to Severe Ulcerative Colitis

Abstract

Despite a growing number of available therapeutic options for ulcerative colitis (UC), up to 50% of patients do not respond to initial treatment or lose response over time, highlighting the need for novel therapies. The IL-23 pathway has emerged as an important therapeutic target for UC. Mirikizumab is a humanized IgG4 monoclonal antibody against the p19 subunit of IL-23, dosed intravenously during induction and subcutaneously during maintenance. It is effective for the induction and maintenance of remission in moderately to severely active UC, including patients with prior failure of biological or tofacitinib therapy. Like other IL-23 antagonists, mirikizumab has a favorable safety profile. It is the first agent of its class to receive regulatory approval for moderately to severely active UC in Europe.

Plain language summary

Despite a growing number of available therapeutic options for ulcerative colitis (UC), up to 50% of patients do not respond to initial treatment or lose response over time, highlighting the need for novel therapies. A molecule promoting inflammation in the colon called IL-23 is a promising target for new drugs that treat UC. Mirikizumab is an antibody that works against a portion of IL-23 and thus suppresses inflammation in the colon. Mirikizumab was shown to be effective in alleviating symptoms and resolving inflammation of the colon in patients with UC. The drug was safe and well tolerated by patients. Mirikizumab is the first drug of its kind to receive approval for UC in Europe.

Tweetable abstract

Mirikizumab, an IL-23 inhibitor, is an effective and safe drug to treat moderate-to-severe ulcerative colitis.

Keywords::

• biological therapy
• clinical trials
• inflammatory bowel disease
• IL-23
• therapeutic monoclonal antibodies

Author contributions

Conception and design: J Hanzel, C Ma, V Jairath. Manuscript drafting: J Hanzel, V Jairath. Manuscript editing for important intellectual content: J Hanzel, C Ma, V Jairath. All authors approved the final version of this manuscript for submission.

Financial & competing interests disclosure

J Hanzel has received consulting fees from Alimentiv Inc. and speaker’s fees from Abbvie, Janssen and Takeda. C Ma has received consulting fees from AbbVie, Alimentiv, Amgen, AVIR Pharma Inc, BioJAMP, Bristol Myers Squibb, Celltrion, Ferring, Fresenius Kabi, Janssen, McKesson, Mylan, Pendopharm, Pfizer, Prometheus Biosciences Inc., Roche, Sanofi, Takeda and Tillotts Pharma; speaker’s fees from AbbVie, Amgen, AVIR Pharma Inc, Alimentiv, Bristol Myers Squibb, Ferring, Fresenius Kabi, Janssen, Organon, Pendopharm, Pfizer and Takeda; royalties from Springer Publishing; and research support from Ferring and Pfizer. V Jairath has received consulting/advisory board fees from AbbVie, Alimentiv Inc., Arena Pharmaceuticals, Asahi Kasei Pharma, Asieris, Astra Zeneca, Bristol Myers Squibb, Celltrion, Eli Lilly, Ferring, Flagship Pioneering, Fresenius Kabi, Galapagos, GlaxoSmithKline, Genentech, Gilead, Janssen, Merck, Mylan, Pandion, Pendopharm, Pfizer, Protagonist, Reistone Biopharma, Roche, Sandoz, Second Genome, Takeda, Teva, Topivert, Ventyx and Vividion; and speaker’s fees from Abbvie, Ferring, Galapagos, Janssen, Pfizer, Shire, Takeda and Fresenius Kabi. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.