Cited by 813Chronic Lymphocytic Leukemia ResearchT-cell and B-cell ImmunologyProtein Degradation and Inhibitors

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Ibrutinib is an irreversible molecular inhibitor of ITK driving a Th1-selective pressure in T lymphocytes

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Dubovsky, Jason A., Beckwith, Kyle A., Natarajan, Gayathri, Woyach, Jennifer A., Jaglowski, Samantha, Zhong, Yiming, Hessler, Joshua D., Liu, Ta-Ming, Chang, Betty Y., Larkin, Karilyn M., Stefanovski, Matthew R., Chappell, Danielle L., Frissora, Frank W., Smith, Lisa L., Smucker, Kelly A., Flynn, Joseph M., Jones, Jeffrey A., Andritsos, Leslie A., Maddocks, Kami, Lehman, Amy M., Furman, Richard, Sharman, Jeff, Mishra, Anjali, Caligiuri, Michael A., Satoskar, Abhay R., Buggy, Joseph J., Muthusamy, Natarajan, Johnson, Amy J., Byrd, John C.·2013·Blood

DOI 10.1182/blood-2013-06-507947PMC PMC3795457

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Abstract

Given its critical role in T-cell signaling, interleukin-2-inducible kinase (ITK) is an appealing therapeutic target that can contribute to the pathogenesis of certain infectious, autoimmune, and neoplastic diseases. Ablation of ITK subverts Th2 immunity, thereby potentiating Th1-based immune responses. While small-molecule ITK inhibitors have been identified, none have demonstrated clinical utility. Ibrutinib is a confirmed irreversible inhibitor of Bruton tyrosine kinase (BTK) with outstanding clinical activity and tolerability in B-cell malignancies. Significant homology between BTK and ITK alongside in silico docking studies support ibrutinib as an immunomodulatory inhibitor of both ITK and BTK. Our comprehensive molecular and phenotypic analysis confirms ITK as an irreversible T-cell target of ibrutinib. Using ibrutinib clinical trial samples along with well-characterized neoplastic (chronic lymphocytic leukemia), parasitic infection (Leishmania major), and infectious disease (Listeria monocytogenes) models, we establish ibrutinib as a clinically relevant and physiologically potent ITK inhibitor with broad therapeutic utility. This trial was registered at www.clinicaltrials.gov as #NCT01105247 and #NCT01217749.

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Additional file 2 of Ibrutinib protects T cells in patients with CLL from proliferation-induced senescence
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Authors: Dubovsky, J. A., Beckwith, K. A., Natarajan, G., Woyach, J. A., Jaglowski, S., Zhong, Y., Hessler, J. D., Liu, T.-M., Chang, B. Y., Larkin, K. M., Stefanovski, M. R., Chappell, D. L., Frissora, F. W., Smith, L. L., Smucker, K. A., Flynn, J. M., Jones, J. A., Andritsos, L. A., Maddocks, K., Lehman, A. M., Furman, R., Sharman, J., Mishra, A., Caligiuri, M. A., Satoskar, A. R., Buggy, J. J., Muthusamy, N., Johnson, A. J., & Byrd, J. C.
Affiliations: Department of Internal Medicine, Division of Hematology,
The Ohio State University (US)
Pharmacyclics (United States) (US)
Weill Cornell Medicine (US)
Willamette Valley Cancer Institute and Research Center (US)
Department of Pathology, and
ORCID: Beckwith, Kyle A.
Natarajan, Gayathri
Woyach, Jennifer A.
Jaglowski, Samantha
Chang, Betty Y.
Chappell, Danielle L.
Smith, Lisa L.
Flynn, Joseph M.
Jones, Jeffrey A.
Andritsos, Leslie A.
Maddocks, Kami
Furman, Richard
Sharman, Jeff
Mishra, Anjali
Caligiuri, Michael A.
Satoskar, Abhay R.
Muthusamy, Natarajan
Johnson, Amy J.
Byrd, John C.
Venue: Blood
Publisher: American Society of Hematology
Published: 2013-10-10
Volume: 122
Issue: 15
Pages: 2539-2549
ISSN: 0006-4971 (ISSN-L)
1528-0020
DOI: 10.1182/blood-2013-06-507947
PMC: PMC3795457
OpenAlex: W2089103836
Cited by: 810
References: 49
Citations by year: 2026: 30 · 2025: 43 · 2024: 55 · 2023: 51 · 2022: 70 · 2021: 98 · 2020: 68 · 2019: 71 · 2018: 71 · 2017: 70 · 2016: 65 · 2015: 67 · 2014: 43 · 2013: 5
FWCI: 29.54
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Blood (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (4p01ca081534-16)
National Cancer Institute (P01CA095426, P50CA140158, T32CA009338, 5 T32 CA009338-33-03, P30CA016058, K12CA133250, P01-CA-081534)
Topics: Health Sciences › Medicine › Hematology › Chronic Lymphocytic Leukemia Research
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Degradation and Inhibitors
Keywords: ibrutinib, irreversible kinase inhibitors, Bruton's tyrosine kinase, T cell signaling, Th1 response, Th2 immune response, chronic lymphocytic leukemia, Leishmania major, Listeria monocytogenes, immunomodulation
MeSH terms: Adenine, Animals, Disease Models, Animal, Enzyme Inhibitors, Humans, Leukemia, Listeriosis, Lymphocyte Activation, Piperidines, Protein-Tyrosine Kinases, Pyrazoles, Pyrimidines, Leishmaniasis, Cutaneous, CD8-Positive T-Lymphocytes, Th1 Cells, Th2 Cells, Jurkat Cells, Mice, Primary Cell Culture

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Ibrutinib is an irreversible molecular inhibitor of ITK driving a Th1-selective pressure in T lymphocytes

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