FTI-277 TFA
Based on 2 publication(s) in Google Scholar
FTI-277 TFA is a farnesyltransferase (FTase) inhibitor. FTI-277 TFA inhibits Ras farnesylation, blocks the phosphorylation of downstream ERK1/2 and mTOR, and reduces membrane-bound active N-ras protein. FTI-277 TFA activates caspase 3, upregulates Bim expression, induces cell apoptosis, suppresses regulatory T cell expansion, enhances macrophage phagocytosis, and improves bacterial clearance. FTI-277 TFA activates the PI3K/Akt signaling pathway, inhibits osteoblast differentiation, and reduces the proliferation ability of neuroblastoma cells. FTI-277 TFA can be used in research related to head and neck squamous cell carcinoma, neuroblastoma, sepsis, and vascular calcification.
For research use only. We do not sell to patients.
- CAS No.: 1217447-06-7
- Formula: C24H30F3N3O5S2
- Molecular Weight:561.64
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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
- Purity & Documentation
- References
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Publications Citing Use of MedChemExpress (MCE) FTI-277 TFA
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Biological Activity
FTI-277 (1-40 μM; 24-72 h) TFA decreases the viability of HEp-2 head and neck squamous cell carcinoma cells in a concentration-dependent manner, with a 58.5% reduction in viability at the highest tested concentration (40 μM) after 72 h of treatment[1].
FTI-277 (0.5-10 μM; 24-72 h) TFA decreases the viability of HSC-3 head and neck squamous cell carcinoma cells in a concentration-dependent manner, with a 77.0% reduction in viability at the highest tested concentration (10 μM) after 72 h of treatment, and exhibits greater potency against HSC-3 cells than HEp-2 cells[1].
FTI-277 (40 μM; 36 h) TFA significantly increases caspase-3 activity in HEp-2 head and neck squamous cell carcinoma cells[1].
FTI-277 (5 μM; 36 h) TFA significantly increases caspase-3 activity in HSC-3 head and neck squamous cell carcinoma cells, demonstrating greater potency than against HEp-2 cells[1].
FTI-277 (40 μM; 36 h) TFA significantly increases the percentage of annexin V-positive HEp-2 head and neck squamous cell carcinoma cells, indicating induction of apoptosis[1].
FTI-277 (5 μM; 36 h) TFA significantly increases the percentage of annexin V-positive HSC-3 head and neck squamous cell carcinoma cells, indicating induction of apoptosis with greater potency than against HEp-2 cells[1].
FTI-277 (40 μM; 48 h) TFA suppresses Ras membrane localization, reduces phosphorylation of ERK1/2 and mTOR, and increases Bim protein expression in HEp-2 head and neck squamous cell carcinoma cells[1].
FTI-277 (5 μM; 48 h) TFA suppresses Ras membrane localization, reduces phosphorylation of ERK1/2 and mTOR, and increases Bim protein expression in HSC-3 head and neck squamous cell carcinoma cells, demonstrating greater potency than against HEp-2 cells[1].
FTI-277 (5 μM; 72 h) TFA significantly decreases the viability of NW7 v-H-Ras-transfected NIH3T3 cells but has no significant effect on NV20 empty vector-transfected NIH3T3 cells, indicating selective activity against Ras-overexpressing cells[1].
FTI-277 (1-20 μM; 8-10 days) TFA inhibits osteogenic differentiation and βGP-induced mineralization in primary bovine vascular smooth muscle cells, with significant effects observed at concentrations ≥10 μM, and even when added up to 6 days post-βGP initiation[3].
FTI-277 (10 μM; 77 h) TFA enhances Akt phosphorylation in primary bovine vascular smooth muscle cells when followed by serum starvation and short-term serum stimulation[3].
FTI-277 (10-20 μM; 9-10 days) TFA maintains Akt phosphorylation during βGP-induced mineralization in primary bovine vascular smooth muscle cells, and this Akt activation is required for FTI-277's inhibitory effect on mineralization[3].
FTI-277 (10 μM) TFA inhibits phosphate-induced apoptosis in human coronary artery vascular smooth muscle cells, and this effect depends on Akt activation[3].
FTI-277 (10 μM; 96 h) TFA reduces farnesylated N-Ras protein levels by approximately 50% in IMR-5 neuroblastoma cells[4].
FTI-277 (10 μM; 96 h) TFA reduces basal MAP-kinase activity by ~47% and blunts BDNF-induced MAP-kinase activation to 35% of control levels in IMR-5 neuroblastoma cells[4].
FTI-277 (10 μM; 96 h) TFA reduces basal N-myc expression to 70% of controls and blunts BDNF-induced N-myc expression to 53% of control-stimulated levels in IMR-5 neuroblastoma cells[4].
FTI-277 (10 μM; 96 h) TFA significantly reduces cell proliferation across complete, serum-free, and BDNF-supplemented media, and abolishes BDNF-induced proliferation in IMR-5 neuroblastoma cells[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HEp-2 head and neck squamous cell carcinoma cells
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Concentration:1 μM, 5 μM, 10 μM, 20 μM, 40 μM
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Incubation Time:24 h, 48 h, 72 h
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Result:Decreased HEp-2 cell viability in a concentration-dependent manner.
Reduced cell viability to 97.9% with 1 μM, 98.9% with 5 μM, 89.1% with 10 μM, 78.3% with 20 μM, and 41.5% with 40 μM after 72 h treatment.
Induced statistically significant viability reductions with 20 μM and 40 μM at 48 h, and with 10 μM, 20 μM, and 40 μM at 72 h relative to controls.
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Cell Line:HSC-3 head and neck squamous cell carcinoma cells
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Concentration:1 μM, 5 μM, 10 μM, 20 μM, 40 μM
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Incubation Time:24 h, 48 h, 72 h
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Result:Decreased HSC-3 cell viability in a concentration-dependent manner, with greater potency than in HEp-2 cells.
Reduced cell viability to 89.7% with 0.5 μM, 69.1% with 1 μM, 52.9% with 2.5 μM, 33.4% with 5 μM, and 23.0% with 10 μM after 72 h treatment.
Induced statistically significant viability reductions with all tested concentrations at 24, 48, and 72 h relative to controls.
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Cell Line:HEp-2 head and neck squamous cell carcinoma cells
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Concentration:40 μM
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Incubation Time:36 h
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Result:Increased the percentage of annexin V-positive HEp-2 cells to approximately 42%, relative to control cells with approximately 7% annexin V-positive cells.
Induced statistically significant elevation of annexin V-positive cells, indicating apoptosis induction.
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Cell Line:HSC-3 head and neck squamous cell carcinoma cells
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Concentration:5 μM
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Incubation Time:36 h
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Result:Increased the percentage of annexin V-positive HSC-3 cells to approximately 47%, relative to control cells with approximately 9% annexin V-positive cells.
Induced statistically significant elevation of annexin V-positive cells, indicating apoptosis induction with greater potency than against HEp-2 cells.
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Cell Line:HEp-2 head and neck squamous cell carcinoma cells
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Concentration:40 μM
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Incubation Time:48 h
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Result:Inhibited Ras membrane localization and increased Ras cytoplasmic localization in HEp-2 cells.
Decreased the expression of phosphorylated ERK1/2 and phosphorylated mTOR.
Increased the expression of Bim protein, relative to control cells.
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Cell Line:HSC-3 head and neck squamous cell carcinoma cells
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Concentration:5 μM
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Incubation Time:48 h
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Result:Inhibited Ras membrane localization and increased Ras cytoplasmic localization in HSC-3 cells.
Decreased the expression of phosphorylated ERK1/2 and phosphorylated mTOR.
Increased the expression of Bim protein, relative to control cells.
Demonstrated greater potency than against HEp-2 cells.
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Cell Line:NV20 empty vector-transfected NIH3T3 cells, NW7 v-H-Ras-transfected NIH3T3 cells
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Concentration:5 μM
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Incubation Time:72 h
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Result:Had no significant effect on the viability of NV20 empty vector-transfected NIH3T3 cells.
Significantly reduced the viability of NW7 v-H-Ras-transfected NIH3T3 cells to approximately 35%, relative to untreated NW7 cells.
Exhibited selective activity against Ras-overexpressing cells.
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Cell Line:IMR-5 neuroblastoma cells
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Concentration:10 μM
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Incubation Time:96 h
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Result:Reduced farnesylated N-Ras protein levels by 47%.\nReduced basal MAP-kinase activity by 47% compared to untreated controls.
Blunted BDNF-induced MAP-kinase activation to 35% of control levels.
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Cell Line:IMR-5 neuroblastoma cells
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Concentration:10 μM
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Incubation Time:96 h
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Result:Reduced basal N-myc expression to 70% of untreated control levels.
Blunted BDNF-induced N-myc expression to 53% of control-stimulated levels.
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Cell Line:IMR-5 neuroblastoma cells
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Concentration:10 μM
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Incubation Time:96 h
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Result:Decreased cell numbers by 10% in complete medium over 48 hours, compared to an ~80% increase in untreated controls.
Resulted in significantly lower cell numbers than controls in serum-free medium.
Abolished BDNF-induced 22% proliferation increase seen in control cells in serum-free medium.
Reduced cell proliferation significantly across all three media conditions.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (male, 7 weeks of age, sepsis induced by cecal ligation and puncture)[2]
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Dosage:25 mg/kg
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Administration:i.p.; single dose
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Result:Increased survival rate of septic mice to 67% (10/15 survived to 7 days) compared to 7% (1/15) in vehicle-treated group.
Significantly reduced bacterial colony-forming units in blood and peritoneal cavity at 16 hours post-CLP.
Almost completely blocked sepsis-induced increase in serum HMGB1 concentration at 16 hours post-CLP.
Reduced percentage of TUNEL-positive apoptotic cells in spleen from ~7% to ~2% and in thymus from ~9% to ~1% at 16 hours post-CLP.
Reversed sepsis-induced increase in splenic farnesylated protein levels and farnesyltransferase activity to sham-equivalent levels at 16 hours post-CLP.
Partially reversed sepsis-induced increase in splenic CD4+Foxp3+ regulatory T cells from ~22% to ~15% of total CD4+ cells without altering total CD4+ splenocyte counts.
Restored IFN-γ secretion from ~30 pg/mL to ~100 pg/mL and splenocyte proliferative response to sham-equivalent levels, and reversed sepsis-induced decrease in IFN-γ to IL-4 ratio.
Reduced sepsis-induced increases in PD-L1 and PD-1 expression on splenic CD4+ T cells and macrophages.
Increased phagocytotic activity of peritoneal F4/80+ macrophages, with percentage of fluorescent microsphere-positive cells rising from ~45% to ~65% and mean fluorescence intensity per cell rising from ~220 to ~300.
Chemical Information
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CAS No. 1217447-06-7
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Molecular Weight 561.64
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Formula C24H30F3N3O5S2
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SMILES
OC(C(F)(F)F)=O.CSCC[C@@H](C(OC)=O)NC(C1=C(C2=CC=CC=C2)C=C(C=C1)NC[C@@H](N)CS)=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.
Publications (2)
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Journal Impact Factor
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Most Recent
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Fish Shellfish Immunol
Involvement of H-Ras in the adaptive immunity of Nile tilapia by regulating lymphocyte activation. [Abstract]2019 Apr 3;89:281-289. PMID: 30953781 -
Oncotarget
2017 Nov 22;8(65):109135-109150. PMID: 29312596
FTI-277 TFA purchased from MedChemExpress. Usage Cited in: Oncotarget. 2017 Nov 22;8(65):109135-109150. [Abstract]
MCF-7 cells are pretreated with the indicated chemical inhibitors for 30min, followed by 15 min treatment with RA (20 μM) + EPA (80 μM).Cell extracts are prepared and subjected to western blotting analysis.
Purity & Documentation
References
[1]. Tateishi K, et al. FTI-277 and GGTI-289 induce apoptosis via inhibition of the Ras/ERK and Ras/mTOR pathway in head and neck carcinoma HEp-2 and HSC-3 cells. J BUON. 2021;26(2):606-612. [Content Brief]
[2]. Yang W, et al. Farnesyltransferase inhibitor FTI-277 reduces mortality of septic mice along with improved bacterial clearance. J Pharmacol Exp Ther. 2011;339(3):832-841. [Content Brief]
[3]. Ponnusamy A, et al. FTI-277 inhibits smooth muscle cell calcification by up-regulating PI3K/Akt signaling and inhibiting apoptosis. PLoS One. 2018;13(4):e0196232. Published 2018 Apr 24. [Content Brief]
[4]. Girgert R, et al. Farnesyltransferase inhibitor FTI-277 prevents autocrine growth stimulation of neuroblastoma by BDNF. J Cancer Res Clin Oncol. 2003;129(4):227-233. [Content Brief]
Calculators
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