ST-162
ST-162 is a MAPK/PI3K dual antagonist. ST-162 exhibits antitumor activity and can increase the efficacy of immune checkpoint blockers. ST-162 can be used for the research of cancer, such as melanoma.
For research use only. We do not sell to patients.
- CAS No.: 1883817-83-1
- Formula: C40H44F5IN10O6
- Molecular Weight:982.74
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Chemical Information
-
CAS No. 1883817-83-1
-
Molecular Weight 982.74
-
Formula C40H44F5IN10O6
-
SMILES
O=C(NOCCOCCOCCOCCN1CCN(C2=NC(N3C4=CC=CC=C4N=C3C(F)F)=NC(N5CCOCC5)=N2)CC1)C6=CC=C(F)C(F)=C6NC7=CC=C(I)C=C7F
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
-
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)