IBA-12
IBA-12 is a IKZF2 molecular glue/PROTAC degrader with a DC50 of 276.2 nM (Jurkat cells) and 461.8 nM (Mino cells), and an IC50 of 179.9 nM. IBA-12 binds to the canonical tryptophan triad pocket of CRBN to form a ternary complex with IKZF2. IBA-12 induces IKZF2 degradation mediated by the CRBN-dependent ubiquitin-proteasome system, with no effect on other CRBN substrates. IBA-12 induces the production of interleukin-2 (IL-2) through degrading IKZF2. IBA-12 is applicable to cancer immunology research.
(Pink: IZKF2 ligand (HY-Y1863); Blue: Cereblon ligand (HY-182807); Black: linker).
For research use only. We do not sell to patients.
- Formula: C24H25ClN4O3
- Molecular Weight:452.93
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All PROTACs Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
IKZF2 276.2 nM (DC50) |
Cereblon |
In Vitro
IBA-12 (0-1000 nM; 24 h) dose-dependently increases IL-2 production in stimulated Jurkat cells, confirming functional modulation of the IKZF2-regulated transcriptional pathway[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:stimulated Jurkat cells
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Concentration:0, 10, 100, 1000 and 1000 nM
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Incubation Time:24 h
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Result:Induced dose-dependent increases in IL-2 production.
Showed statistically significant increases observed at 100 and 1000 nM.
Parmacokinetics
Chemical Information
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Molecular Weight 452.93
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Formula C24H25ClN4O3
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SMILES
O=C1CCC(N2NC(C=C(C3CCN(CC4=CC(Cl)=CC=C4)CC3)C=C5)=C5C2=O)C(N1)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Cancer Immunology
Cancer immunology studies how the immune system recognizes, suppresses, edits, or fails to eliminate malignant cells through tumor antigen release, antigen presentation, T-cell priming, immune trafficking, tumor-cell killing, and feedback inhibition in the tumor microenvironment. The cancer-immunity cycle links tumor antigenicity, dendritic-cell priming, CD8+ T-cell infiltration, cytotoxic function, and immune-checkpoint regulation to tumor rejection or immune escape. Immune-checkpoint pathways such as PD-1/PD-L1 and CTLA-4 suppress antitumor T-cell activity and can be therapeutically blocked, but many tumors remain resistant because of poor antigen presentation, weak T-cell infiltration, suppressive myeloid cells, regulatory T cells, and tumor-intrinsic immune-exclusion programs. Unresolved questions include which immune-cell states predict response, how tumor-intrinsic pathways exclude immune cells, how myeloid suppression limits checkpoint blockade, and which combination strategies
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)