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Cited by 44NF-κB Signaling PathwaysNatural Compounds in Disease TreatmentImmune Response and Inflammation

A novel IRAK4/PIM1 inhibitor ameliorates rheumatoid arthritis and lymphoid malignancy by blocking the TLR/MYD88-mediated NF-κB pathway

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Yoon, Sae-Bom, Hong, Hyowon, Lim, Hee-Jong, Choi, Ji Hye, Choi, Yoon Pyo, Seo, Seong Wook, Lee, Hyuk Woo, Chae, Chong Hak +6 more·2023·Acta Pharmaceutica Sinica B
DOI 10.1016/j.apsb.2022.12.001PMC PMC10031381
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Abstract

Interleukin-1 receptor-associated kinase 4 (IRAK4) is a pivotal enzyme in the Toll-like receptor (TLR)/MYD88 dependent signaling pathway, which is highly activated in rheumatoid arthritis tissues and activated B cell-like diffuse large B-cell lymphoma (ABC-DLBCL). Inflammatory responses followed by IRAK4 activation promote B-cell proliferation and aggressiveness of lymphoma. Moreover, proviral integration site for Moloney murine leukemia virus 1 (PIM1) functions as an anti-apoptotic kinase in propagation of ABC-DLBCL with ibrutinib resistance. We developed a dual IRAK4/PIM1 inhibitor KIC-0101 that potently suppresses the NF-κB pathway and proinflammatory cytokine induction in vitro and in vivo. In rheumatoid arthritis mouse models, treatment with KIC-0101 significantly ameliorated cartilage damage and inflammation. KIC-0101 inhibited the nuclear translocation of NF-κB and activation of JAK/STAT pathway in ABC-DLBCLs. In addition, KIC-0101 exhibited an anti-tumor effect on ibrutinib-resistant cells by synergistic dual suppression of TLR/MYD88-mediated NF-κB pathway and PIM1 kinase. Our results suggest that KIC-0101 is a promising drug candidate for autoimmune diseases and ibrutinib-resistant B-cell lymphomas.

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  • NF-κB inhibitors increase cell sensitivity to toxic stimuli and low-dose chemotherapy.

    “NF-κB inhibitors target tumor cell survival and anti-apoptotic pathways, increasing cell sensitivity to toxic stimuli and low-dose chemotherapy [153–155].”

    From Multiple myeloma: signaling pathways and targeted therapy (2024) · cites this paper as [155]

    The Results section on PIM1 inhibition reports that KIC-0101, which inhibits NF-κB-related signaling, activated apoptosis in B-cell lymphoma cells; another Results section reports greater tumor suppression when it was combined with ibrutinib. The paper does not show increased sensitivity to toxic stimuli or low-dose chemotherapy, so those parts of the attributed claim are unsupported. (LLM, conf=0.84)

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Authors
Yoon, S.-B., Hong, H., Lim, H.-J., Choi, J. H., Choi, Y. P., Seo, S. W., Lee, H. W., Chae, C. H., Park, W.-K., Kim, H. Y., Jeong, D., De, T. Q., Myung, C.-S., & Cho, H.
Affiliations
  • Chungnam National University (KR)
  • Korea Research Institute of Chemical Technology (KR)
Corresponding author
Cho, Heeyeong
ORCID
Venue
Acta Pharmaceutica Sinica B
Publisher
Elsevier BV
Published
2023-03
Volume
13
Issue
3
Pages
1093-1109
ISSN
2211-3835 (ISSN-L)
DOI
10.1016/j.apsb.2022.12.001
PMC
PMC10031381
OpenAlex
W4311564107
Cited by
44
References
3
Citations by year
2026: 7 · 2025: 15 · 2024: 16 · 2023: 5
FWCI
3.79
Type
journal article
Language
en
Open access
Licence
Locations
  • Acta Pharmaceutica Sinica B (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Ministry of Trade, Industry and Energy
  • Korea Research Institute of Chemical Technology (20009774, KK1963-413, SI-2231-40)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
  • Health Sciences › Medicine › Complementary and alternative medicine › Natural Compounds in Disease Treatment
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
IRAK4, PIM-1, rheumatoid arthritis, ABC-DLBCL, NF-κB signaling, ibrutinib resistance, JAK/STAT signaling, B-cell lymphoma, cartilage damage, anti-inflammatory cytokines, dual kinase inhibitors

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