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Identification of a novel Azaspirooxindolinone-based PROTAC for selective BTK degradation and enhanced anticancer activity

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15640%2F25%3A73630464" target="_blank" >RIV/61989592:15640/25:73630464 - isvavai.cz</a>

  • Alternative codes found

    RIV/00098892:_____/25:10159182 RIV/61989592:15110/25:73630464

  • Result on the web

    <a href="https://www.sciencedirect.com/science/article/pii/S0045206825001968?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S0045206825001968?via%3Dihub</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.bioorg.2025.108316" target="_blank" >10.1016/j.bioorg.2025.108316</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Identification of a novel Azaspirooxindolinone-based PROTAC for selective BTK degradation and enhanced anticancer activity

  • Original language description

    Bruton&apos;s Tyrosine Kinase (BTK) is a key driver of hematological malignancies, autoimmune disorders, and neuroinflammation, making it an attractive therapeutic target. Proteolysis targeting chimeras (PROTACs) offer a novel strategy for BTK degradation via the E3 ubiquitin ligase pathway. Here, we evaluated nine azaspirooxindolinone-based PROTAC derivatives for their cytotoxicity and BTK-targeting activity. Several compounds exhibited potent cytotoxicity against BTK-high RAMOS lymphoma cells without affecting non-cancer fibroblasts or normal T/B-cell lymphocytes. Among them, PROTAC 25 emerged as the most effective degraded, achieving a Dmax of 72.84 % and DC50 of 0.27 mu M in a proteasome-dependent manner. Although PROTAC 25 was cytotoxic to IL-2-inducible T cell Kinase (ITK)-positive cells, ITK protein levels remained unaffected. Furthermore, kinase assays revealed that PROTAC 25 inhibited BTK kinase activity (IC50 = 0.44 mu M) with moderate selectivity over ITK (IC50 = 2.16 mu M). Notably, PROTAC 25 suppressed BTK-mediated downstream signaling in RAMOS cells, as evidenced by reduced phosphorylation of BTK and its downstream effector, p38 MAPK. These findings highlight PROTAC 25 as a promising BTK degrader with therapeutic potential and underscore the value of azaspirooxindolinone-based PROTACs in targeting BTK-driven diseases.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10608 - Biochemistry and molecular biology

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2025

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    BIOORGANIC CHEMISTRY

  • ISSN

    0045-2068

  • e-ISSN

    1090-2120

  • Volume of the periodical

    157

  • Issue of the periodical within the volume

    04/2025

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    16

  • Pages from-to

    108316

  • UT code for WoS article

    001439775800001

  • EID of the result in the Scopus database

    2-s2.0-85219022926