AHL-7160
AHL-7160 is a molecular glue degrader targeting DGKα, with an IC50 value of 12 nM against the human protein. AHL-7160 rapidly recruits DGKα to the plasma membrane, blocks DGKα-mediated phosphatidic acid production, and induces proteasome-dependent degradation of DGKα with full proteome selectivity. AHL-7160 enhances primary T cell-mediated glioblastoma cell killing. AHL-7160 can be used in related research on glioblastoma.
For research use only. We do not sell to patients.
- Formula: C28H30N8O3S
- Molecular Weight:558.65
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
IL-2 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HEK293-A | EC50 |
39 nM
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Recruitment of endogenous DGKα to the plasma membrane of CRISPR-edited HEK293A cells stably expressing NG-tagged endogenous DGKα, measured via TIRF microscopy over up to 600 seconds post-treatment.
Recruitment of endogenous DGKα to the plasma membrane of CRISPR-edited HEK293A cells stably expressing NG-tagged endogenous DGKα, measured via TIRF microscopy over up to 600 seconds post-treatment.
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PMC12713590 |
| HEK293-A | IC50 |
340 nM
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Inhibition of DGKα-mediated phosphatidic acid production at mitochondrial and plasma membrane subcellular regions in HEK293A cells with a chemically inducible mitochondrial DGKα activation system, monitored via the PILS-Nir1 biosensor over up to 10 minutes post-stimulation with rapamycin.
Inhibition of DGKα-mediated phosphatidic acid production at mitochondrial and plasma membrane subcellular regions in HEK293A cells with a chemically inducible mitochondrial DGKα activation system, monitored via the PILS-Nir1 biosensor over up to 10 minutes post-stimulation with rapamycin.
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PMC12713590 |
In Vitro
AHL-7160 potently and covalently inhibits recombinant human DGKα-HEK293T proteome activity with an IC50 of 12 nM[1].
AHL-7160 (5 µM; 2 hours) stereoselectively engages endogenous DGKα at residues Y669 and K411 in Jurkat T cells without altering DGKα protein abundance[1].
AHL-7160 (1-1000 nM; up to 10 minutes post-stimulation) stereoselectively blocks DGKα-mediated PA production at mitochondrial and plasma membrane subcellular regions in HEK293A cells with an IC50 of 340 nM[1].
AHL-7160 (0.01-10 µM; 24 hours primary T cell cytokine assays) stereoselectively potentiates MAPK signaling and IL-2 production in anti-CD3/CD28-activated Jurkat T cells, and elicits a broad, multi-effector cytokine response in activated primary human CD4+ and CD8+ T cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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Molecular Weight 558.65
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Formula C28H30N8O3S
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SMILES
CN(C1=CC=C(C#N)N=C1C(N2C[C@@H](C)N(CC3=CC=C(S(N4C=NC(C5CC5)=N4)(=O)=O)C=C3)C[C@@H]2C)=C6)C6=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)
AHL-7160 Related Classifications
HY-180898 Related Classifications
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