GRWD5769
GRWD5769 is an orally potent ERAP1 inhibitor. GRWD5769 regulates the peptide repertoire presented by MHC-I, alters TCR diversity/clonality, reprograms antigen-experienced T cells, induces novel T cell responses, drives tumor cell killing, and alleviates T cell exhaustion. GRWD5769 can be used in the research of advanced solid malignancies, microsatellite-stable colorectal cancer, non-small cell lung cancer, bladder cancer, hepatocellular carcinoma, head and neck squamous cell carcinoma, and cervical cancer.
For research use only. We do not sell to patients.
- CAS No.: 2420554-24-9
- Formula: C22H22ClN3O4S
- Molecular Weight:459.95
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
MHC I |
ERAP1 |
In Vitro
Combination treatment with GRWD5769 and anti-PD-1 mAb (HY-P99144) increases intratumoral TCR repertoire diversity, promotes T cell infiltration, upregulates markers associated with immune responses as well as recently activated, non-exhausted T cells, and inhibits tumor growth across multiple syngeneic tumor models in different mouse strains.
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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CAS No. 2420554-24-9
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Molecular Weight 459.95
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Formula C22H22ClN3O4S
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SMILES
ClC(C=C1N2CCCCC2)=C(C#N)C=C1NS(C3=CC(C(O)=O)=CC=C3C4CC4)(=O)=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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Liver Cancer Modeling
Liver cancer can be classified into primary liver cancer and secondary liver cancer. Secondary liver cancer is the metastatic liver cancer. Primary liver cancer includes hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (ICC) and fibrolamellar HCC, of which HCC is the most common form, accounting for approximately 90% of primary liver cancers[1]. HCC mouse models include chemical agent-induced models, transplanted tumor models, and genetic engineered models.
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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)