JAK Inhibitors
JAK Inhibitors
JAK Inhibitors
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
Janus kinase (JAK) inhibitors were first introduced in the 2010s.1,2 They are a class of targeted synthetic small molecules that target Janus kinases (JAKs) and inhibit their interaction with Signal Transducer and Activator of Transcription (STAT) proteins, thereby interrupting the JAK-STAT signaling pathway.2–5 This pathway is involved in the inflammatory processes associated with inflammatory bowel disease (IBD).2,3,5,6
Targeted synthetic small molecule therapies are low-molecular-weight compounds that diffuse through cell membranes.3,4 Unlike biological therapies such as monoclonal antibodies, which are large proteins usually administered by injection, targeted synthetic small molecules are typically administered orally and have a low risk of provoking immunogenicity.3
IBD Treatment Landscape3,7–16
JAK=Janus kinase; S1P=sphingosine-1-phosphate; TNF=tumor necrosis factor.
Role in IBD Pathogenesis
In IBD, binding of a proinflammatory cytokine to its receptor promotes receptor pairing and activation of JAKs through addition of a phosphate group, known as phosphorylation.2,3,5,6,17 JAKs are enzymatic proteins that, once activated, phosphorylate and activate STATs. Activated STATs form dimers, or pairs, and translocate to the cell nucleus, where they regulate transcription of immune and inflammatory genes, leading to the production of inflammatory mediators.
DNA=deoxyribonucleic acid; JAK=Janus kinase; P=phosphate group; STAT=Signal Transducer and Activator of Transcription.
Mechanism of Action in IBD
JAK inhibitors are targeted synthetic small molecules that can diffuse through the cell membranes of immune cells and bind to sites located on JAKs.2,3,6 This binding blocks the phosphorylation and activation of JAKs and subsequently STATs, thereby disrupting intracellular signaling and downstream transcription of genes involved in the production of inflammatory mediators.2,3,5,6
DNA=deoxyribonucleic acid; JAK=Janus kinase; P=phosphate group; STAT=Signal Transducer and Activator of Transcription.
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.
- Imbrizi M, Magro F, Coy CSR. Pharmaceuticals (Basel). 2023;16(9):1272.
- Herrera-deGuise C, Serra-Ruiz X, Lastiri E, Borruel N. Front Med (Lausanne). 2023;10:1089099.
- Pérez-Jeldres T, Tyler CJ, Boyer JD, et al. Front Pharmacol. 2019;10:212.
- Crohn’s & Colitis Foundation. Fact Sheet. October 2023. https://www.crohnscolitisfoundation.org/sites/default/files/2023-10/Targeted Synthetic Small Molecule Fact Sheet FINAL 10.23_2.pdf. Accessed January 5, 2026.
- Honap S, Agorogianni A, Colwill MJ, et al. Frontline Gastroenterol. 2024;15(1):59-69.
- Spiewak TA, Patel A. Curr Res Pharmacol Drug Discov. 2022;3:100096.
- Murray A, Nguyen TM, Parker CE, Feagan BG, MacDonald JK. Cochrane Database Syst Rev. 2020;8(8):CD000544.
- Dorrington AM, Selinger CP, Parkes GC, Smith M, Pollok RC, Raine T. J Crohns Colitis. 2020;14(9):1316-1329.
- 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.
- Santiago P, Braga-Neto MB, Loftus EV Jr. Gastroenterol Hepatol (N Y). 2022;18(8):453-465.
- Actis GC, Pellicano R, Fagoonee S, Ribaldone DG. J Clin Med. 2019;8(11):1970.
- 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.
- Soendergaard C, Bergenheim FH, Bjerrum JT, Nielsen OH. Pharmacol Ther. 2018;192:100-111.
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