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Chemical Compound Review

EDELFOSINE     2-[(2-methoxy-3-octadecoxy- propoxy)-oxido...

Synonyms: Edelfosina, Edelfosinum, ET-18-O-Methyl, CHEMBL28509, ET18-Ome, ...
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Psychiatry related information on ALKYL-LYSOPHOSPHOLIPID


High impact information on ALKYL-LYSOPHOSPHOLIPID

  • Normal cells, including human and rat hepatocytes, did not incorporate ET-18-OCH(3) and were spared [6].
  • Unlike normal lymphocytes, leukemic T cells incorporated ET-18-OCH(3) into rafts coaggregating with Fas and underwent apoptosis [6].
  • In comparison to an approximate sevenfold to elevenfold (ID50 and LD50, respectively) difference in the susceptibility of the above leukemia cell lines to ET-18-OCH3, no significant difference in the specific activities (0.13-0.21 nmol/min/mg) of the O-alkyl cleavage enzyme was found in the above leukemia cell lines [7].
  • Experiments with radiolabeled ET-18-OCH3 in Raji cells suggest, rather, a critical role for phospholipases C and/or D in ALP metabolism [7].
  • We have found that synthetic alkyl-lysophospholipids (ALPs) edelfosine and perifosine induced apoptosis in MM cell lines and patient MM cells, whereas normal B and T lymphocytes were spared [1].

Chemical compound and disease context of ALKYL-LYSOPHOSPHOLIPID


Biological context of ALKYL-LYSOPHOSPHOLIPID

  • Of six platelet activating factor antagonists tested, four were found to protect WEHI-3B leukemic cells against cell death induced by ET-18-OCH3 [12].
  • The concentration of ET-18-OCH3 with continuous exposure to inhibit cell growth 50% was 19 microM [13].
  • The 50% inhibitory concentration for ET-18-OCH3 decreased from 18.4 microM in the control cells to 9.83 microM in the supplemented cells [14].
  • After a 4-h exposure with 75 micrograms/ml ET-18-OCH3 at a cell density of 2 x 10(5)/ml the number of colonies of HTB 19 decreased from 75 +/- 10/10(3) cells (100%) to 1 +/- 0/10(3) cells (1%), and after subsequent cryopreservation no remaining colonies were found [15].
  • We have investigated the hypothesis that the antiproliferative effect of 1-O-octadecyl-2-O-methylglycero-3-phosphocholine (ET-18-OCH3) is mediated through the inhibition of cellular acylation processes that control the unsaturated fatty acid complement of phospholipids [16].

Anatomical context of ALKYL-LYSOPHOSPHOLIPID

  • Since O-alkyl cleavage enzyme previously was suggested as being important in the detoxification of cytotoxic ALPs, the enzyme activity was compared with the susceptibility to ET-18-OCH3 in the distinct cell lines [7].
  • Results of this study showed that ET-18-OCH(3) induces cocapping of Fas and membrane rafts, specialized plasma membrane regions involved in signaling, before the onset of apoptosis in human leukemic cells [17].
  • Simulated remission bone marrow containing 2% leukemic cells treated in vitro with 20 and 100 micrograms/mL of ET-18-OCH3 (1-octadecyl-2-methyl-sn-glycerol-3-phosphocholine) significantly prolonged survival of lethally irradiated transplanted recipients [18].
  • Sensitivity of K562 and HL-60 cells to edelfosine, an ether lipid drug, correlates with production of reactive oxygen species [19].
  • Here we study two human leukemia cell lines (HL-60 and K562) that have different sensitivities to edelfosine; HL-60 cells are more sensitive than K562 cells [19].

Associations of ALKYL-LYSOPHOSPHOLIPID with other chemical compounds



  • Small cell lung carcinoma exhibits greater phospholipase C-beta1 expression and edelfosine resistance compared with non-small cell lung carcinoma [23].
  • Moreover, treatment with Et-18-OCH3 significantly attenuated serum stimulated MAPK activity in both cultured hepatocytes and H4IIE cells [24].
  • Cells with enfeebled endocytosis and vacuolar protease activities prevented edelfosine-mediated (i) mobilization of sterols, (ii) loss of Pma1p from lipid rafts, and (iii) cell death [25].
  • Our data showed that gat1 and gat2 yeast were resistant and sensitive to lysoplatelet activating factor, platelet activating factor, and the anti-tumor lipid edelfosine, respectively, indicating that their sensitivity to these compounds was not because of differences in rates of phosphatidylcholine deacylation [26].
  • ET-18-OMe inhibited the E-cadherin functions of MCF-7/AZ cells as measured by inhibition of fast and slow aggregation and by the induction of collagen invasion [27].

Analytical, diagnostic and therapeutic context of ALKYL-LYSOPHOSPHOLIPID


  1. Edelfosine and perifosine induce selective apoptosis in multiple myeloma by recruitment of death receptors and downstream signaling molecules into lipid rafts. Gajate, C., Mollinedo, F. Blood (2007) [Pubmed]
  2. Inhibition of estradiol uptake and transforming growth factor alpha secretion in human breast cancer cell line MCF-7 by an alkyl-lysophospholipid. Kosano, H., Yasutomo, Y., Kugai, N., Nagata, N., Inagaki, H., Tanaka, S., Takatani, O. Cancer Res. (1990) [Pubmed]
  3. Cytotoxic interactions of heat and an ether lipid analogue in human ovarian carcinoma cells. Fujiwara, K., Modest, E.J., Welander, C.E., Wallen, C.A. Cancer Res. (1989) [Pubmed]
  4. Enhanced therapeutic effects of liposome-associated 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphocholine. Ahmad, I., Filep, J.J., Franklin, J.C., Janoff, A.S., Masters, G.R., Pattassery, J., Peters, A., Schupsky, J.J., Zha, Y., Mayhew, E. Cancer Res. (1997) [Pubmed]
  5. Biological activities, mechanisms of action and biomedical prospect of the antitumor ether phospholipid ET-18-OCH(3) (edelfosine), a proapoptotic agent in tumor cells. Gajate, C., Mollinedo, F. Curr. Drug Metab. (2002) [Pubmed]
  6. Intracellular triggering of Fas aggregation and recruitment of apoptotic molecules into Fas-enriched rafts in selective tumor cell apoptosis. Gajate, C., Del Canto-Jañez, E., Acuña, A.U., Amat-Guerri, F., Geijo, E., Santos-Beneit, A.M., Veldman, R.J., Mollinedo, F. J. Exp. Med. (2004) [Pubmed]
  7. Sensitivity of leukemia cell lines to cytotoxic alkyl-lysophospholipids in relation to O-alkyl cleavage enzyme activities. Unger, C., Eibl, H., Kim, D.J., Fleer, E.A., Kötting, J., Bartsch, H.H., Nagel, G.A., Pfizenmaier, K. J. Natl. Cancer Inst. (1987) [Pubmed]
  8. The differential susceptibility of A427 and A549 cell lines to the growth-inhibitory effects of ET-18-OCH3 does not correlate with the relative effects of the alkyl-lysophospholipid on the incorporation of fatty acids into cellular phospholipids. Lu, X., Arthur, G. Cancer Res. (1992) [Pubmed]
  9. Increased generation of lipid-derived and ascorbate free radicals by L1210 cells exposed to the ether lipid edelfosine. Wagner, B.A., Buettner, G.R., Burns, C.P. Cancer Res. (1993) [Pubmed]
  10. Induction of apoptosis in human mitogen-activated peripheral blood T-lymphocytes by the ether phospholipid ET-18-OCH3: involvement of the Fas receptor/ligand system. Cabaner, C., Gajate, C., Macho, A., Muñoz, E., Modolell, M., Mollinedo, F. Br. J. Pharmacol. (1999) [Pubmed]
  11. Influence of the alkyllysophospholipid ET-18-OCH3 on methylnitrosourea-induced rat mammary carcinomas. Berger, M.R., Munder, P.G., Schmähl, D., Westphal, O. Oncology (1984) [Pubmed]
  12. Role of endocytosis in the action of ether lipids on WEHI-3B, HL60, and FDCP-mix A4 cells. Bazill, G.W., Dexter, T.M. Cancer Res. (1990) [Pubmed]
  13. Inhibition of growth factor-dependent inositol phosphate Ca2+ signaling by antitumor ether lipid analogues. Seewald, M.J., Olsen, R.A., Sehgal, I., Melder, D.C., Modest, E.J., Powis, G. Cancer Res. (1990) [Pubmed]
  14. Correlation of ether lipid content of human leukemia cell lines and their susceptibility to 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine. Chabot, M.C., Wykle, R.L., Modest, E.J., Daniel, L.W. Cancer Res. (1989) [Pubmed]
  15. Removal of breast cancer cells from bone marrow by in vitro purging with ether lipids and cryopreservation. Dietzfelbinger, H.F., Kühn, D., Zafferani, M., Hanauske, A.R., Rastetter, J.W., Berdel, W.E. Cancer Res. (1993) [Pubmed]
  16. Perturbations of cellular acylation processes by the synthetic alkyl-lysophospholipid 1-O-octadecyl-2-O-methylglycero-3-phosphocholine do not correlate with inhibition of proliferation of MCF7 and T84 cell lines. Lu, X., Arthur, G. Cancer Res. (1992) [Pubmed]
  17. The antitumor ether lipid ET-18-OCH(3) induces apoptosis through translocation and capping of Fas/CD95 into membrane rafts in human leukemic cells. Gajate, C., Mollinedo, F. Blood (2001) [Pubmed]
  18. Purging murine leukemic marrow with alkyl-lysophospholipids. Glasser, L., Somberg, L.B., Vogler, W.R. Blood (1984) [Pubmed]
  19. Sensitivity of K562 and HL-60 cells to edelfosine, an ether lipid drug, correlates with production of reactive oxygen species. Wagner, B.A., Buettner, G.R., Oberley, L.W., Burns, C.P. Cancer Res. (1998) [Pubmed]
  20. Selective inhibition of phosphatidylinositol phospholipase C by cytotoxic ether lipid analogues. Powis, G., Seewald, M.J., Gratas, C., Melder, D., Riebow, J., Modest, E.J. Cancer Res. (1992) [Pubmed]
  21. Antiinvasive effect of racemic 1-O-octadecyl-2-O-methylglycero-3-phosphocholine on MO4 mouse fibrosarcoma cells in vitro. Storme, G.A., Berdel, W.E., van Blitterswijk, W.J., Bruyneel, E.A., De Bruyne, G.K., Mareel, M.M. Cancer Res. (1985) [Pubmed]
  22. Apoptosis triggered by 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine is prevented by increased expression of CTP:phosphocholine cytidylyltransferase. Baburina, I., Jackowski, S. J. Biol. Chem. (1998) [Pubmed]
  23. Small cell lung carcinoma exhibits greater phospholipase C-beta1 expression and edelfosine resistance compared with non-small cell lung carcinoma. Strassheim, D., Shafer, S.H., Phelps, S.H., Williams, C.L. Cancer Res. (2000) [Pubmed]
  24. Altered Gq/G11 guanine nucleotide regulatory protein expression in a rat model of hepatocellular carcinoma: role in mitogenesis. McKillop, I.H., Schmidt, C.M., Cahill, P.A., Sitzmann, J.V. Hepatology (1999) [Pubmed]
  25. Cytotoxicity of an anti-cancer lysophospholipid through selective modification of lipid raft composition. Zaremberg, V., Gajate, C., Cacharro, L.M., Mollinedo, F., McMaster, C.R. J. Biol. Chem. (2005) [Pubmed]
  26. Differential partitioning of lipids metabolized by separate yeast glycerol-3-phosphate acyltransferases reveals that phospholipase D generation of phosphatidic acid mediates sensitivity to choline-containing lysolipids and drugs. Zaremberg, V., McMaster, C.R. J. Biol. Chem. (2002) [Pubmed]
  27. Alkyl-lysophospholipid 1-O-octadecyl-2-O-methyl- glycerophosphocholine induces invasion through episialin-mediated neutralization of E-cadherin in human mammary MCF-7 cells in vitro. Steelant, W.F., Goeman, J.L., Philippé, J., Oomen, L.C., Hilkens, J., Krzewinski-Recchi, M.A., Huet, G., Van der Eycken, J., Delannoy, P., Bruyneel, E.A., Mareel, M.M. Int. J. Cancer (2001) [Pubmed]
  28. Purging of acute myeloid leukemic cells by ether lipids and hyperthermia. Okamoto, S., Olson, A.C., Berdel, W.E., Vogler, W.R. Blood (1988) [Pubmed]
  29. Selective induction of apoptosis in cancer cells by the ether lipid ET-18-OCH3 (Edelfosine): molecular structure requirements, cellular uptake, and protection by Bcl-2 and Bcl-X(L). Mollinedo, F., Fernández-Luna, J.L., Gajate, C., Martín-Martín, B., Benito, A., Martínez-Dalmau, R., Modolell, M. Cancer Res. (1997) [Pubmed]
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