Corticosteroids
Corticosteroids
Corticosteroids
Information included in this Introduction to IBD Medication Classes is for educational purposes only and is intended for US-based healthcare providers (HCPs).
This information does not represent medical advice or endorse any specific product. It should not be the basis for clinical diagnoses or treatment decisions.
Use this information in conjunction with a clinical assessment and independent research from other relevant sources.
This information was last updated 1/2026.
Medication Class Introduction
Corticosteroids are naturally occurring molecules in the human body that can be synthetically produced for therapeutic use.1 Synthetic corticosteroids were first used for the treatment of inflammatory bowel disease (IBD) in the 1950s.2,3
IBD Treatment Landscape3–13
JAK=Janus kinase; S1P=sphingosine-1-phosphate; TNF=tumor necrosis factor.
Role in IBD Pathogenesis
The pathogenesis of IBD involves chronic inflammation in the gastrointestinal tract, driven by an imbalance between pro-inflammatory and anti-inflammatory cytokines.14–17 The expression of both pro- and anti-inflammatory proteins is regulated by genes located in the cell nucleus.14,18–20 Elevated levels of pro-inflammatory cytokines can maintain an exaggerated immune response and sustained inflammation, leading to the clinical manifestations of IBD.15,16
DNA=deoxyribonucleic acid.
Mechanism of Action in IBD
When administered, corticosteroid molecules bind to glucocorticoid receptors within the cytoplasm of immune cells, forming an active glucocorticoid receptor-corticosteroid complex that is transported to the nucleus.1–3,18 Once inside the nucleus, this complex binds to glucocorticoid-responsive elements on DNA, activating anti-inflammatory gene transcription.1–3,17,18 Additionally, the complex interferes with specific pro-inflammatory transcription factors (such as nuclear factor-κB).1–3,17,18 This results in the suppression of pro-inflammatory gene expression and down-regulation of pro-inflammatory proteins.1–3,17,18
DNA=deoxyribonucleic acid.
Resources
Current IBD Treatment Guidelines
Guidelines for managing IBD are available from the American College of Gastroenterology (ACG) and the American Gastroenterological Association (AGA). You can access them through the following links:
- ACG Clinical Guideline: Management of Crohn’s Disease in Adults
- ACG Clinical Guideline Update: Ulcerative Colitis in Adults
- AGA Living Clinical Practice Guideline on the Pharmacologic Management of Moderate-to-Severe Crohn’s Disease
- AGA Clinical Practice Guidelines on the Management of Mild-to-Moderate Ulcerative Colitis
- AGA Living Clinical Practice Guideline on Pharmacological Management of Moderate-to-Severe Ulcerative Colitis
Resources to Help Explain Medication Options for IBD to Patients
The Crohn’s & Colitis Foundation resources below may help you explain medication options, including the mechanism of action of IBD medication classes and how they are designed to work in the body, to your patients with IBD.
Resources to Help Understand Medical Management of IBD From UpToDate®
The UpToDate® resources below may help you understand medical management of IBD in adults including but not limited to disease activity, severity, and risk, as well as medication options for induction and maintenance.
- Medical management of mild Crohn’s disease
- Medical management of moderate to severe Crohn’s disease
- Medical management of mild to moderate ulcerative colitis
- Medical management of moderate to severe ulcerative colitis
For More Information on IBD Medications
To learn more about the medications commonly used to treat IBD—including potential side effects and safety considerations—please refer to the following resource:
Links to third-party websites are provided as resources and not intended to be an endorsement. Takeda is not responsible for their content.
- Bruscoli S, Febo M, Riccardi C, Migliorati G. Front Immunol. 2021;12:691480.
- Cai Z, Wang S, Li J. Front Med (Lausanne). 2021;8:765474.
- Dorrington AM, Selinger CP, Parkes GC, Smith M, Pollok RC, Raine T. J Crohns Colitis. 2020;14(9):1316-1329.
- Murray A, Nguyen TM, Parker CE, Feagan BG, MacDonald JK. Cochrane Database Syst Rev. 2020;8(8):CD000544.
- de Boer NKH, Peyrin-Biroulet L, Jharap B, et al. J Crohns Colitis. 2018;12(5):610-620.
- Lichtenstein GR, Loftus EV, Afzali A, et al. Am J Gastroenterol. 2025;120(6):1225-1264.
- Actis GC, Pellicano R, Fagoonee S, Ribaldone DG. J Clin Med. 2019;8(11):1970.
- Santiago P, Braga-Neto MB, Loftus EV Jr. Gastroenterol Hepatol (N Y). 2022;18(8):453-465.
- Pérez-Jeldres T, Tyler CJ, Boyer JD, et al. Front Pharmacol. 2019;10:212.
- Fudman DI, McConnell RA, Ha C, Singh S. Clin Gastroenterol Hepatol. 2025;23(3):454-469.
- Moschen AR, Tilg H, Raine T. Nat Rev Gastroenterol Hepatol. 2019;16(3):185-196.
- Choden T, Cohen NA, Rubin DT. Gastroenterol Hepatol (N Y). 2022;18(5):265-271.
- Martinez-Molina C, González-Suárez B. J Clin Med. 2025;14(11):3890.
- Neurath MF. Nat Rev Immunol. 2024;24(8):559-576.
- Kaluzna A, Olcyzk P, Komosinska-Vassev K. J Clin Med. 2022;11(2):400.
- Vebr M, Pomahacová R, Sýkora J, Schwarz J. Biomedicines. 2023;11(12):3229.
- Dubois-Camacho K, Ottum PA, Franco-Munoz D, et al. World J Gastroenterol. 2017;23(36):6628-6638.
- van der Goes MC, Jacobs JW, Bijlsma JW. Arthritis Res Ther. 2014;16(suppl 2):S2.
- Neurath MF. Nat Rev Immunol. 2014;14(5):329-342.
- Liu T, Zhang L, Joo D, Sun S-C. Signal Transduct Target Ther. 2017;2:17023.
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