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Antitumor agent
BML-L108-0005 5 mg 79.00 USD
BML-L108-0025 25 mg 334.00 USD
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Replaces Prod. #: ALX-300-004

Produces strong antitumor and antimetastatic activities. Inhibits phosphatidylinositol specific phospholipase C (PLC, IC50=0.4-9.6μM) and protein kinase C from various leukemic cells. Inhibits CoA-independent transacylase (IC50=0.5μM). Induces apoptosis in HeLa cells and HL-60 cells. Antineoplastic activity.

Product Specification

Alternative Name:2-O-Methyl-PAF-C-18, sn-ET-18-OCH3, Edelfosine
Purity:≥98% (TLC)
Identity:Determined by FAB-MS.
Appearance:White waxy solid.
Solubility:Soluble in 100% ethanol (15mg/ml), DMSO or dimethyl formamide.
Long Term Storage:-20°C
Use/Stability:Stable for at least 1 year after receipt when stored, as supplied, at -20°C. Stock solutions are stable for up to 3 months at -20°C.
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Product Literature References

Intracellular triggering of Fas, independently of FasL, as a new mechanism of antitumor ether lipid-induced apoptosis: C. Gajate, et al.; Int. J. Cancer 85, 674 (2000), Abstract;
Involvement of mitochondria and caspase-3 in ET-18-OCH(3)-induced apoptosis of human leukemic cells: C. Gajate, et al.; Int. J. Cancer 86, 208 (2000), Abstract;
Alkyl-lysophospholipids activate the SAPK/JNK pathway and enhance radiation-induced apoptosis: G.A. Ruiter, et al.; Cancer Res. 59, 2457 (1999), Abstract;
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: C. Cabaner, et al.; Br. J. Pharmacol. 127, 813 (1999), Abstract;
Liposomal ET-18-OCH(3) induces cytochrome c-mediated apoptosis independently of CD95 (APO-1/Fas) signaling: O. Cuvillier, et al.; Blood 94, 3583 (1999), Abstract;
Apoptosis triggered by 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine is prevented by increased expression of CTP:phosphocholine cytidylyltransferase: I. Baburina & S. Jackowski; J. Biol. Chem. 273, 2196 (1998), Abstract;
Cytotoxic etherphospholipid analogues: D. Berkovic; Gen Pharmacol. 31, 511 (1998), Abstract;
Involvement of c-Jun NH2-terminal kinase activation and c-Jun in the induction of apoptosis by the ether phospholipid 1-O-octadecyl-2-O- methyl-rac-glycero-3-phosphocholine: C. Gajate, et al.; Mol. Pharmacol. 53, 602 (1998), Abstract;
The anticancer drug edelfosine is a potent inhibitor of neovascularization in vivo: W.R. Vogler, et al.; Cancer Invest. 16, 549 (1998), Abstract;
The inhibition of cell signaling pathways by antitumor ether lipids: G. Arthur & R. Bittman; Biochim. Biophys. Acta. 1390, 85 (1998), Abstract;
Ether lipids enhance the cytotoxic effect of teniposide and paclitaxel in liposomes against leukaemic cells in culture: B.B. Lundberg; Anticancer Drug Des. 12, 503 (1997), Abstract;
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): F. Mollinedo, et al.; Cancer Res. 57, 1320 (1997), Abstract;
Inhibitors of coenzyme A-independent transacylase induce apoptosis in human HL-60 : J.D. Winkler, et al.; J. Pharmacol. Exp. Ther. 279, 956 (1996), Abstract;
The ether lipid 1-octadecyl-2-methyl-rac-glycero-3-phosphocholine induces expression of fos and jun proto-oncogenes and activates AP-1 transcription factor in human leukaemic cells: F. Mollinedo, et al.; Biochem. J. 302, 325 (1994), Abstract;
Early and selective induction of apoptosis in human leukemic cells by the alkyl-lysophospholipid ET-18-OCH3: F. Mollinedo, et al.; Biochem. Biophys. Res. Commun. 192, 603 (1993), Abstract;
Selective inhibition of phosphatidylinositol phospholipase C by cytotoxic ether lipid analogues: G. Powis, et al.; Cancer Res. 52, 2835 (1992), Abstract;
HL-60 cells become resistant towards antitumor ether-linked phospholipids following differentiation into a granulocytic form: D.S. Vallari, et al.; BBRC 156, 1 (1988), Abstract;
Purging leukemic cells from simulated human remission marrow with alkyl- lysophospholipid: S. Okamoto, et al.; Blood 69, 1381 (1987), Abstract;
Phospholipid-sensitive Ca2+-dependent protein phosphorylation system in various types of leukemic cells from human patients and in human leukemic cell lines HL60 and K562, and its inhibition by alkyl- lysophospholipid: D.M. Helfman, et al.; Cancer Res. 43, 2955 (1983), Abstract;
Disturbance of phospholipid metabolism during the selective destruction of tumor cells induced by alkyl-lysophospholipids: M. Modolell, et al.; Cancer Res. 39, 4681 (1979), Abstract;
Selective destruction of human leukemic cells by alkyl- lysophospholipids: R. Andreesen, et al.; Cancer Res. 38, 3894 (1978), Abstract;

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