FTS-MOM
FTS-MOM (Salirasib methoxymethyl ester), a Salirasib (FTS) (HY-14754) derivative, is a selective Rap1 inhibitor with selectivity over Ras. FTS-MOM inhibits GTP loading of Rap1 in quiescent and activated T cells. FTS-MOM inhibits Rap1-dependent T cell adhesion to ICAM-1.
For research use only. We do not sell to patients.
- CAS No.: 1092521-71-5
- Formula: C24H34O3S
- Molecular Weight:402.59
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| PANC-1 | IC50 |
12 μM
Compound: FTS-MOME
|
Cytotoxicity against human PANC1 cells after 5 to 7 days
Cytotoxicity against human PANC1 cells after 5 to 7 days
|
[PMID: 19072665] |
| U-87MG ATCC | IC50 |
10 μM
Compound: FTS-MOME
|
Cytotoxicity against human U87 cells after 5 to 7 days
Cytotoxicity against human U87 cells after 5 to 7 days
|
[PMID: 19072665] |
In Vitro
FTS-MOM (50 μM; overnight) inhibits antigen receptor-induced Rap1 activation in Jurkat T cells by 53%[1].
FTS-MOM (50 μM; overnight) inhibits Rap1-dependent adhesion of anti-CD3-stimulated Jurkat T cells to ICAM-1, reducing adhesion to ~25% of stimulated control levels[1].
FTS-MOM (50 μM; overnight) acts as a Rap1-selective inhibitor in Panc-1 cells, strongly reducing GTP-Rap1 levels while only weakly inhibiting GTP-Ras levels[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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CAS No. 1092521-71-5
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Molecular Weight 402.59
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Formula C24H34O3S
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SMILES
C/C(C)=C/CC/C(C)=C/CC/C(C)=C/CSC1=C(C=CC=C1)C(OCOC)=O
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Synonyms
Salirasib methoxymethyl ester
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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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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)