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Chemical Compound Review

SureCN94663     (4R)-4-benzyl-6-(3H-imidazol- 4-ylmethyl)-3...

Synonyms: CHEMBL351706, SureCN134853, CHEBI:374775, BMS-214662, CID448545, ...
 
 
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Disease relevance of BMS 214662

 

High impact information on BMS 214662

  • Phase I pharmacokinetic and pharmacodynamic study of weekly 1-hour and 24-hour infusion BMS-214662, a farnesyltransferase inhibitor, in patients with advanced solid tumors [5].
  • BMS-214662 induced apoptosis in tumors but did not inhibit MAPK signaling [5].
  • Clearly distinct patterns of sensitivities in a cell line panel were obtained for the apoptotic FTI BMS-214662 and the cytostatic FTI BMS-225975 [6].
  • A subline of HCT-116, HCT-116/VM46, resistant to many standard cytotoxic agents by means of a multiple drug resistance mechanism, remained quite susceptible to BMS-214662, and borderline activity was achieved against N-87 human gastric carcinoma [2].
  • In rodent fibroblasts transformed by oncogenes, BMS-214662 reversed the H-Ras-transformed phenotype but not that of K-Ras or other oncogenes [2].
 

Chemical compound and disease context of BMS 214662

 

Biological context of BMS 214662

 

Anatomical context of BMS 214662

 

Associations of BMS 214662 with other chemical compounds

 

Gene context of BMS 214662

  • BMS-214662 triggered apoptosis in a small fraction of cells (not higher than 30%) that was paralleled by a slight decrease in the levels of TGF-alpha secreted by treated MPM cells [16].
  • Two different FTI compounds, the clinical compound BMS-214662 and the newly described BMS-225975, inhibit the constitutive activation of mTOR/S6K signaling and block serum-free growth of the Tsc-null mouse embryonic fibroblasts [17].
  • Accumulation of unfarnesylated HDJ-2 in PBMCs of patients was evaluated as a marker of farnesyl transferase inhibition by BMS-214662 [12].
  • They can be characterized functionally as those inhibiting Ras protein expression such as the oligodeoxynucleotide ISIS 2503, those inhibiting Ras processing, in particular the farnesyl transferase inhibitors R115777, SCH 66336 and BMS 214662, and those inhibiting downstream effectors Raf, such as ISIS 5132 and MEK, which is inhibited by CI-1040 [18].
 

Analytical, diagnostic and therapeutic context of BMS 214662

References

  1. Phase I study of BMS-214662, a farnesyl transferase inhibitor in patients with acute leukemias and high-risk myelodysplastic syndromes. Cortes, J., Faderl, S., Estey, E., Kurzrock, R., Thomas, D., Beran, M., Garcia-Manero, G., Ferrajoli, A., Giles, F., Koller, C., O'Brien, S., Wright, J., Bai, S.A., Kantarjian, H. J. Clin. Oncol. (2005) [Pubmed]
  2. Preclinical antitumor activity of BMS-214662, a highly apoptotic and novel farnesyltransferase inhibitor. Rose, W.C., Lee, F.Y., Fairchild, C.R., Lynch, M., Monticello, T., Kramer, R.A., Manne, V. Cancer Res. (2001) [Pubmed]
  3. A phase I pharmacokinetic and pharmacodynamic study of the farnesyl transferase inhibitor BMS-214662 in combination with cisplatin in patients with advanced solid tumors. Mackay, H.J., Hoekstra, R., Eskens, F.A., Loos, W.J., Crawford, D., Voi, M., Van Vreckem, A., Evans, T.R., Verweij, J. Clin. Cancer Res. (2004) [Pubmed]
  4. Therapeutic efficacy of prenylation inhibitors in the treatment of myeloid leukemia. Morgan, M.A., Ganser, A., Reuter, C.W. Leukemia (2003) [Pubmed]
  5. Phase I pharmacokinetic and pharmacodynamic study of weekly 1-hour and 24-hour infusion BMS-214662, a farnesyltransferase inhibitor, in patients with advanced solid tumors. Tabernero, J., Rojo, F., Marimón, I., Voi, M., Albanell, J., Guix, M., Vázquez, F., Carulla, J., Cooper, M., Andreu, J., Van Vreckem, A., Bellmunt, J., Manne, V., Manning, J.A., Garrido, C., Felip, E., Del Campo, J.M., García, M., Valverde, S., Baselga, J. J. Clin. Oncol. (2005) [Pubmed]
  6. Apoptotic and cytostatic farnesyltransferase inhibitors have distinct pharmacology and efficacy profiles in tumor models. Manne, V., Lee, F.Y., Bol, D.K., Gullo-Brown, J., Fairchild, C.R., Lombardo, L.J., Smykla, R.A., Vite, G.D., Wen, M.L., Yu, C., Wong, T.W., Hunt, J.T. Cancer Res. (2004) [Pubmed]
  7. BMS-214662 potently induces apoptosis of chronic myeloid leukemia stem and progenitor cells and synergizes with tyrosine kinase inhibitors. Copland, M., Pellicano, F., Richmond, L., Allan, E.K., Hamilton, A., Lee, F.Y., Weinmann, R., Holyoake, T.L. Blood (2008) [Pubmed]
  8. Farnesyltransferase inhibitor BMS-214662 induces apoptosis in myeloma cells through PUMA up-regulation, Bax and Bak activation, and Mcl-1 elimination. Gómez-Benito, M., Marzo, I., Anel, A., Naval, J. Mol. Pharmacol. (2005) [Pubmed]
  9. Phase I clinical trial of the farnesyltransferase inhibitor BMS-214662 given as a 1-hour intravenous infusion in patients with advanced solid tumors. Ryan, D.P., Eder, J.P., Puchlaski, T., Seiden, M.V., Lynch, T.J., Fuchs, C.S., Amrein, P.C., Sonnichsen, D., Supko, J.G., Clark, J.W. Clin. Cancer Res. (2004) [Pubmed]
  10. Farnesyltransferase inhibitor BMS-214662 induces apoptosis in B-cell chronic lymphocytic leukemia cells. Marzo, I., Pérez-Galán, P., Giraldo, P., López-Royuela, N., Gómez-Benito, M., Larrad, L., Lasierra, P., Rubio-Félix, D., Anel, A., Naval, J. Leukemia (2004) [Pubmed]
  11. Clinical development of farnesyltransferase inhibitors in leukemias and myelodysplastic syndrome. Kurzrock, R., Cortes, J., Kantarjian, H. Semin. Hematol. (2002) [Pubmed]
  12. A phase I trial of the novel farnesyl protein transferase inhibitor, BMS-214662, in combination with paclitaxel and carboplatin in patients with advanced cancer. Dy, G.K., Bruzek, L.M., Croghan, G.A., Mandrekar, S., Erlichman, C., Peethambaram, P., Pitot, H.C., Hanson, L.J., Reid, J.M., Furth, A., Cheng, S., Martell, R.E., Kaufmann, S.H., Adjei, A.A. Clin. Cancer Res. (2005) [Pubmed]
  13. Crystal structures of the anticancer clinical candidates R115777 (Tipifarnib) and BMS-214662 complexed with protein farnesyltransferase suggest a mechanism of FTI selectivity. Reid, T.S., Beese, L.S. Biochemistry (2004) [Pubmed]
  14. Discovery of (R)-7-cyano-2,3,4, 5-tetrahydro-1-(1H-imidazol-4-ylmethyl)-3- (phenylmethyl)-4-(2-thienylsulfonyl)-1H-1,4-benzodiazepine (BMS-214662), a farnesyltransferase inhibitor with potent preclinical antitumor activity. Hunt, J.T., Ding, C.Z., Batorsky, R., Bednarz, M., Bhide, R., Cho, Y., Chong, S., Chao, S., Gullo-Brown, J., Guo, P., Kim, S.H., Lee, F.Y., Leftheris, K., Miller, A., Mitt, T., Patel, M., Penhallow, B.A., Ricca, C., Rose, W.C., Schmidt, R., Slusarchyk, W.A., Vite, G., Manne, V. J. Med. Chem. (2000) [Pubmed]
  15. Phase I trial of weekly paclitaxel and BMS-214662 in patients with advanced solid tumors. Bailey, H.H., Alberti, D.B., Thomas, J.P., Mulkerin, D.L., Binger, K.A., Gottardis, M.M., Martell, R.E., Wilding, G. Clin. Cancer Res. (2007) [Pubmed]
  16. Farnesyltransferase inhibitors and human malignant pleural mesothelioma: a first-step comparative translational study. Cesario, A., Catassi, A., Festi, L., Imperatori, A., Pericelli, A., Galetta, D., Margaritora, S., Porziella, V., Cardaci, V., Granone, P., Dominioni, L., Russo, P. Clin. Cancer Res. (2005) [Pubmed]
  17. Farnesyltransferase inhibitors reverse altered growth and distribution of actin filaments in Tsc-deficient cells via inhibition of both rapamycin-sensitive and -insensitive pathways. Gau, C.L., Kato-Stankiewicz, J., Jiang, C., Miyamoto, S., Guo, L., Tamanoi, F. Mol. Cancer Ther. (2005) [Pubmed]
  18. Agents targeting ras signaling pathway. Dancey, J.E. Curr. Pharm. Des. (2002) [Pubmed]
 
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