Fti 277

Manufactured by Merck Group

Sourced in United States, Germany

FTI-277 is a laboratory research tool developed by Merck Group. It is a farnesyltransferase inhibitor, a class of compounds that target the enzyme farnesyltransferase, which plays a role in cellular processes. The core function of FTI-277 is to serve as a tool for researchers to study the effects of farnesyltransferase inhibition in experimental settings.

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Lab products found in correlation

Ggti 298, by Merck Group (6 mentions) Mevalonate, by Merck Group (4 mentions) Farnesyl pyrophosphate, by Merck Group (4 mentions) Simvastatin, by Merck Group (4 mentions) Atorvastatin, by Merck Group (3 mentions) Geranylgeranyl pyrophosphate, by Merck Group (3 mentions) Ggti 2133, by Merck Group (2 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (2 mentions) Pravastatin, by Merck Group (2 mentions) Zoledronic acid, by Merck Group (2 mentions) Mevalonate, by Santa Cruz Biotechnology (2 mentions) Metformin, by Merck Group (2 mentions) Propidium iodide, by Merck Group (2 mentions) Cholesterol, by Merck Group (2 mentions) Rapamycin, by Merck Group (2 mentions) Zaragozic acid, by Merck Group (1 mentions) Ab16048, by Santa Cruz Biotechnology (1 mentions) Anti synaptophysin, by Thermo Fisher Scientific (1 mentions) Mms 435p, by Abcam (1 mentions) Anti nf68, by Merck Group (1 mentions)

Close spelling variants of this product

FTI-277 trifluoroacetate salt (2 citations) FTI-277 (F9803, (2 citations)

25 protocols using fti 277

Farnesyl Transferase Inhibitor FTI-277 Protocol

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Farnesyl transferase inhibitor-277 (FTI-277) (Sigma-Aldrich) was prepared as a stock at 10 mM. Cells were incubated in media containing 10 µM FTI-277 for 48 h before experimentation. For cells being treated with both FTI-277 and siRNA transfections, cells underwent siRNA transfection 48 h before they started treatment with FTI-277 for 48 h before live cell imaging.

Sears R.M, & Roux K.J. (2022). Mechanisms of A-Type Lamin Targeting to Nuclear Ruptures Are Disrupted in LMNA- and BANF1-Associated Progerias. Cells, 11(5), 865.

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Farnesyltransferase Inhibitor FTI-277 Protocol

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The farnesyltransferase (FTase) inhibitor FTI-277 and farnesylpyrophosphate (FPP) were purchased from Sigma-Aldrich (St. Louis, MO). FTI-277 is a Ras CaaX peptidomimetic (Figure 1) with an IC₅₀ of 50 nM (Sigma-Aldrich, St. Louis, MO). FTI-277 was dissolved in dimethyl sulfoxide (DMSO) at a concentration of 10 mM and stored at −20°C for future application. The 10 mM FTI-277 solution was further diluted using sterile phosphate buffered saline (PBS) at a pH 7.4 for all experiments. For in vivo experiments, the FTI-277 final concentration was 2.5 mg/mL (equivalent to a dose of 20 mg/kg or 0.5 mg per mouse per day). FPP was initially dissolved in a solution of methanol and 10 mM ammonium hydroxide (NH₄OH) to a concentration of 1 μg/μL and stored at −20 °C. FPP was further diluted to the desired concentrations (5, 10, and 20 μM) in sterile PBS for use in cell culture experiments. The vehicle control for FPP was its chemical solvent methanol:NH₄OH (70:30). Previous experiments in our lab showed no evidence of cytotoxicity of this solvent in HBE1 cells using either MTT or Alamar blue assays.

Bratt J.M., Chang K.Y., Rabowsky M., Franzi L.M., Ott S.P., Filosto S., Goldkorn T., Arif M., Last J.A., Kenyon N.J, & Zeki A.A. (2018). Farnesyltransferase Inhibition Exacerbates Eosinophilic Inflammation and Airway Hyperreactivity in Mice with Experimental Asthma: The Complex Roles of Ras GTPase and Farnesylpyrophosphate in Type-2 Allergic Inflammation. Journal of immunology (Baltimore, Md. : 1950), 200(11), 3840-3856.

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Farnesyl Transferase Inhibitor-277 Protocol

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Farnesyl transferase inhibitor-277 (FTI-277) (Sigma) was prepared as a stock at 10 mM. Cells were incubated in media containing 10µM FTI-277 for 48 h before experimentation. For cells being treated with both FTI-277 and siRNA transfections, cells underwent siRNA transfection 48 h before they started treatment with FTI-277 for 48 h before live cell imaging.

Sears R.M., & Roux K.J. (2022). Mechanisms of A-type lamin targeting to nuclear ruptures are disrupted in LMNA- and BANF1-associated progerias.

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Antibody Characterization in Cell Lines

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GGTI-2133, FTI-277, and zaragozic acid were purchased from Sigma. Antibodies (Abs) used in this study were: anti-β-tubulin III (Tuj-1, Covance, MMS-435P), anti-sarcomeric α-actinin (Abcam, ab9465), anti-GAPDH (Millipore, MAB374), anti-synaptophysin (Invitrogen, 18–0130), anti-NF68 (Sigma, N5139), anti-Lamin B1 (Abcam, ab16048) and anti-MYC (Santa Cruz, sc-40). All antibodies were used in 1:1000 dilution.

Okamoto-Uchida Y., Yu R., Miyamura N., Arima N., Ishigami-Yuasa M., Kagechika H., Yoshida S., Hosoya T., Nawa M., Kasama T., Asaoka Y., Alois R.W., Elling U., Penninger J.M., Nishina S., Azuma N, & Nishina H. (2016). The mevalonate pathway regulates primitive streak formation via protein farnesylation. Scientific Reports, 6, 37697.

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Culturing NDF Cell Lines with Doxycycline and FTI-277

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NDF cell lines were provided by the Asian Skin Biobank (A*STAR) and cultured as indicated in Chojnowski et al. (2015 (link)). In short, NDF medium contained 15% fetal calf serum (Invitrogen, SH30071.03), 2 mM glutamine (Invitrogen, 25030081‐P), 0.2 mM non‐essential amino acids (Invitrogen, 10370088) and 50 U/mL Penicillin–Streptomycin (Invitrogen, 15140122) in minimum essential medium (Invitrogen, 10370088). Standard culture conditions were utilised (37°C and 5% CO₂). Whenever cells were sub‐cultured, 0.25% Trypsin with EDTA (Gibco, 25200056) was used and neutralised in dPBS (Cytiva, SH30028.02) with 10% fetal calf serum (Invitrogen, SV30160.03). Working concentration of 1 μg/mL of DOX (Clontech, 631311) and 5 μM of FTI‐277 (FTI‐277 Trifluoroacetate salt Sigma‐Aldrich [cat# F9803]) was used in the indicated experiments.

Foo M.X., Ong P.F., Yap Z.X., Maric M., Bong C.J., Dröge P., Burke B, & Dreesen O. (2024). Genetic and pharmacological modulation of lamin A farnesylation determines its function and turnover. Aging Cell, 23(5), e14105.

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EGF signaling pathway inhibitors

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Cells were starved for 6 h, cultured with DMEM and stimulated with 100 ng/ml EGF for different periods of time. The inhibitors U0126 (Medchem Express, USA, #HY12031), FTI-277 (Sigma, USA, #F9803), Salirasib (Medchem Express, USA, #HY14754), 2BP (Sigma, USA, #238422), tunicamycin (Medchem Express, USA, #HY13585), and simvastatin (Cayman, USA, #10010344) were dissolved in DMSO (Dimethyl sulfoxide). The working concentrations for cells and Drosophila were as follows: U0126 (10 μM), FTI-277 (10 μM), Salirasib (35 μM), 2BP (150 μM), tunicamycin (10 μM), and simvastatin (10 μM). FPP (#63250) and GGPP (#63330) were purchased from Cayman.

Xu Z., Duan F., Lu H., Abdulkadhim Dragh M., Xia Y., Liang H, & Hong L. (2018). UBIAD1 suppresses the proliferation of bladder carcinoma cells by regulating H-Ras intracellular trafficking via interaction with the C-terminal domain of H-Ras. Cell Death & Disease, 9(12), 1170.

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Pharmacological Modulation of Cellular Pathways

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U0126, PD0325901, PD184352, PD98059, KU0063794, Deforolimus, Perifosine, LY294002, GSK429286A, Y-27632 MG-132 and rapamycin were purchased from Selleck Chemicals. FTI-277, U73122, Vinblastine (VBT), Latrunculin B (LB) and Dynasore (Dyn) were purchased from Sigma. PDGF-AA and FGF2 were purchased from PeproTech.

Chen D., Zuo D., Luan C., Liu M., Na M., Ran L., Sun Y., Persson A., Englund E., Salford L.G., Renström E., Fan X, & Zhang E. (2014). Glioma Cell Proliferation Controlled by ERK Activity-Dependent Surface Expression of PDGFRA. PLoS ONE, 9(1), e87281.

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Culturing Human Cell Lines for Osteosarcoma Research

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Human osteosarcoma U-2 OS cells (HTB-96, ATCC), BJ fibroblasts (a gift from S. W Lowe) and fibroblasts from progeria patient (HGADFN003, Progeria Foundation) were cultured in Dulbecco's modified Eagle's medium (Wisent, St-Bruno, QC) supplemented with 10% (for U-2 OS and BJ) or 15% (for HGADFN003) fetal bovine serum (FBS) (Wisent). Flavopiridol was from (Selleckchem, http://www.selleckchem.com/). PD0332991 and FTI-277 were purchased from Sigma-Aldrich.

Moiseeva O., Lopes-Paciencia S., Huot G., Lessard F, & Ferbeyre G. (2016). Permanent farnesylation of lamin A mutants linked to progeria impairs its phosphorylation at serine 22 during interphase. Aging (Albany NY), 8(2), 366-381.

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Statin Drugs and Cholesterol Synthesis

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Nine statin drugs were obtained from commercial sources: Atorvastatin calcium salt trihydrate, simvastatin, pravastatin, mevastatin (PZ0001, S6196, P4498, M2537 Sigma, St Louis, MO, USA); fluvastatin, rosuvastatin, cerivastatin (F601250, R700500, C277000, Toronto Research Chemicals Inc., Toronto, ON, Canada); pitavastatin (S1759, Selleckchem, Boston, MA, USA); lovastatin (430-103-M050, Enzo life sciences, Farmingdale, NY, USA). We prepared 10 mM stock solution in DMSO for in vitro testing. For in vivo testing, pitavastatin was prepared as fresh suspension in methycellulose at 0.4 mg ml⁻¹ (for oral gavage). fluvastatin, cerivastatin, and pitavastatin were prepared as a solution at 0.25 mg ml⁻¹ in PBS for IP injection. GGTI-298 and FTI-277 (G5169, A1393, Sigma) were made into 10 mM stock solution in DMSO. AICAR (#S1802, Selleckchem) was made into 100 mM stock solution in PBS. Intermediate products of cholesterol synthesis were purchased from Sigma: mevalonolactone (M4667), farnesyl pyrophosphate ammonium salt (F6892), geranylgeranyl pyrophosphate ammonium salt (G6025), squalene (S3626), cholesterol solution (S5442), geranylpyrophosphate (G6772), and isopentenyl pyrophosphate triammonium salt solution (I0503).

Jiang P., Mukthavaram R., Chao Y., Nomura N., Bharati I.S., Fogal V., Pastorino S., Teng D., Cong X., Pingle S.C., Kapoor S., Shetty K., Aggrawal A., Vali S., Abbasi T., Chien S, & Kesari S. (2014). In vitro and in vivo anticancer effects of mevalonate pathway modulation on human cancer cells. British Journal of Cancer, 111(8), 1562-1571.

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Pharmacological Interventions in Cell Modeling

Cited 1 time

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The drugs employed in this study were FTI-277, Pravastatin, Zoledronic acid, Rapamycin, Insulin-like growth factor 1, N-acetyl-l-cysteine and GGTI-2133 and were all obtained from Sigma Aldrich, UK. Drugs were added to the media and incubated for fixed periods of time. The final concentration and duration of drug treatments were: FTI-277—2.5 µM for 48 h (Mehta et al. 2011 (link)), Pravastatin—1 µM for 24 h (Varela et al. 2008 (link)), Zoledronic acid—1 µM for 24 h, Rapamycin—10 nM for 24 h (Cao et al. 2011b ), Insulin-like growth factor 1—50.0 ng/mL for 24 h (Mariño et al. 2010 (link)), N-acetyl-l-cysteine—20 µM for 1 h (Richards et al. 2011 (link)), FTI-277 and GGTI-2133—both 2.5 µM for 48 h) (Mehta et al. 2011 (link); Kieran et al. 2007 (link)), Pravastatin and Zoledronic acid—both 1 µM for 24 h (Varela et al. 2008 (link)) and FTI-277—2.5 µM for 48 h, Pravastatin and Zoledronic acid—both 1 µM for 24 h.

Bikkul M.U., Clements C.S., Godwin L.S., Goldberg M.W., Kill I.R, & Bridger J.M. (2018). Farnesyltransferase inhibitor and rapamycin correct aberrant genome organisation and decrease DNA damage respectively, in Hutchinson–Gilford progeria syndrome fibroblasts. Biogerontology, 19(6), 579-602.

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