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Chemical Compound Review

Mafosfamid     2-[[2-[bis(2- chloroethyl)amino]-2-oxo-1...

Synonyms: Mafosfamida, Mafosfamide, Mafosfamidum, CHEMBL59990, AG-L-65965, ...
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Disease relevance of Mafosfamide


High impact information on Mafosfamide

  • The induction of apoptosis (a cell death program) in vitro in primary CML-BC cells following treatment with bcr/abl antisense [S]ODNs plus or minus prior treatment with mafosfamide was monitored by use of a commercial assay [6].
  • Selective eradication of these cells in vitro can be achieved by combined treatment with antisense phosphorothioate oligodeoxynucleotides ([S]ODNs) specifically targeted to this oncogene (bcr/abl [S]ODNs) and a suboptimal (for use as a single agent) dose of mafosfamide (the in vitro active form of cyclophosphamide) [6].
  • Our results indicate that a combination of a conventional chemotherapeutic agent and a tumor-specific antisense oligodeoxynucleotide is highly effective in killing leukemic cells and in sparing a much higher number of normal progenitor cells as compared with high-dose mafosfamide treatment [7].
  • Quantitation of mafosfamide-resistant pre-colony-forming units in allogeneic bone marrow transplantation: relationship with rate of engraftment and evidence for long-lasting reduction in stem cell numbers [8].
  • We have used a limiting dilution assay of mafosfamide-resistant progenitors (pre-colony-forming units [CFU]), which are ancestral to committed progenitors such as CFU-granulocyte-macrophage (GM) to analyze the kinetics of myeloid engraftment after BMT and to assess the size of the stem cell pool at intervals up to 66 months thereafter [8].

Chemical compound and disease context of Mafosfamide


Biological context of Mafosfamide


Anatomical context of Mafosfamide

  • A total of 125 acute leukemia adult patients were autografted with bone marrow (BM) purged by mafosfamide (ASTA Z) during the period of January 1983 to January 1993 [13].
  • Since grafted bone marrows were pretreated in vitro with the cyclophosphamide derivative ASTA Z 7557, circulating T cells had to be regenerated from reinfused hematopoietic progenitor cells [14].
  • Whereas CFU-L, CFU-GM, and BFU-e grown in semisolid cultures disclosed similar sensitivities to Asta Z 7557, long-term culture (LTC) studies (n = 41) indicated a higher resistance of early progenitors [15].
  • High-dose selection with mafosfamide results in sensitivity to DNA cross-linking agents: characterization of hypersensitive cell lines [3].
  • These data indicate that in vitro treatment with mafosfamide does not select cells resistant to the action of activated lymphocytes and that, given the right experimental conditions, these immune effectors can completely lyse tumor cells [5].

Associations of Mafosfamide with other chemical compounds


Gene context of Mafosfamide


Analytical, diagnostic and therapeutic context of Mafosfamide


  1. Amifostine improves the antileukemic therapeutic index of mafosfamide: implications for bone marrow purging. Douay, L., Hu, C., Giarratana, M.C., Bouchet, S., Conlon, J., Capizzi, R.L., Gorin, N.C. Blood (1995) [Pubmed]
  2. Phase I clinical trial of mafosfamide in infants and children aged 3 years or younger with newly diagnosed embryonal tumors: a pediatric brain tumor consortium study (PBTC-001). Blaney, S.M., Boyett, J., Friedman, H., Gajjar, A., Geyer, R., Horowtiz, M., Hunt, D., Kieran, M., Kun, L., Packer, R., Phillips, P., Pollack, I.F., Prados, M., Heideman, R. J. Clin. Oncol. (2005) [Pubmed]
  3. High-dose selection with mafosfamide results in sensitivity to DNA cross-linking agents: characterization of hypersensitive cell lines. Fritz, G., Hengstler, J.G., Kaina, B. Cancer Res. (1997) [Pubmed]
  4. Intracavitary chemotherapy with activated cyclophosphamides and simultaneous systemic detoxification with protector thiols in Sarcoma 180 ascites tumor. Wagner, T., Mittendorff, F., Walter, E. Cancer Res. (1986) [Pubmed]
  5. Lysis by activated lymphocytes of melanoma and small cell lung cancer cells surviving in vitro treatment with mafosfamide. Gambacorti-Passerini, C., Radrizzani, M., Erba, E., Fossati, G., Parmiani, G. Cancer Res. (1987) [Pubmed]
  6. Treatment of Philadelphia leukemia in severe combined immunodeficient mice by combination of cyclophosphamide and bcr/abl antisense oligodeoxynucleotides. Skorski, T., Nieborowska-Skorska, M., Wlodarski, P., Perrotti, D., Hoser, G., Kawiak, J., Majewski, M., Christensen, L., Iozzo, R.V., Calabretta, B. J. Natl. Cancer Inst. (1997) [Pubmed]
  7. Highly efficient elimination of Philadelphia leukemic cells by exposure to bcr/abl antisense oligodeoxynucleotides combined with mafosfamide. Skorski, T., Nieborowska-Skorska, M., Barletta, C., Malaguarnera, L., Szcyzlik, C., Chen, S.T., Lange, B., Calabretta, B. J. Clin. Invest. (1993) [Pubmed]
  8. Quantitation of mafosfamide-resistant pre-colony-forming units in allogeneic bone marrow transplantation: relationship with rate of engraftment and evidence for long-lasting reduction in stem cell numbers. Kirkland, M.A., Spencer, A., Davidson, R.J., McDonald, C., Goldman, J.M. Blood (1996) [Pubmed]
  9. Antineoplastic activity of ASTA Z 7557 (INN mafosfamide) in transplanted and autochthonous experimental rodent tumors. Zeller, W.J., Berger, M.R., Matys, R., Schuhmacher, J. Investigational new drugs. (1984) [Pubmed]
  10. Efficacy and toxicity of 4-(2-sulfonatoethylthio)-cyclophosphamide cyclohexylamine salt (ASTA Z 7557, INN mafosfamide) after intraperitoneal administration to mice. Roberts, J.D., Hacker, M.P., Newman, R.A., McCormack, J.J., Krakoff, I.H. Investigational new drugs. (1984) [Pubmed]
  11. Limiting-dilution analysis for the determination of leukemic cell frequencies after bone marrow decontamination with mafosfamide or merocyanine 540. Porcellini, A., Talevi, N., Marchetti-Rossi, M.T., Palazzi, M., Manna, A., Sparaventi, G., Delfini, C., Valentini, M. Blood (1987) [Pubmed]
  12. Cyclophosphamide induces caspase 9-dependent apoptosis in 9L tumor cells. Schwartz, P.S., Waxman, D.J. Mol. Pharmacol. (2001) [Pubmed]
  13. One hundred twenty-five adult patients with primary acute leukemia autografted with marrow purged by mafosfamide: a 10-year single institution experience. Laporte, J.P., Douay, L., Lopez, M., Labopin, M., Jouet, J.P., Lesage, S., Stachowiak, J., Fouillard, L., Isnard, F., Noel-Walter, M.P. Blood (1994) [Pubmed]
  14. T-cell ontogeny after autologous bone marrow transplantation: failure to synthesize interleukin-2 (IL-2) and lack of CD2- and CD3-mediated proliferation by both CD4- and CD8+ cells even in the presence of exogeneous IL-2. Cayeux, S., Meuer, S., Pezzutto, A., Körbling, M., Haas, R., Schulz, R., Dörken, B. Blood (1989) [Pubmed]
  15. Autologous bone marrow transplantation using marrow incubated with Asta Z 7557 in adult acute leukemia. Gorin, N.C., Douay, L., Laporte, J.P., Lopez, M., Mary, J.Y., Najman, A., Salmon, C., Aegerter, P., Stachowiak, J., David, R. Blood (1986) [Pubmed]
  16. In vitro drug sensitivity of cells from children with leukemia using the MTT assay with improved culture conditions. Pieters, R., Loonen, A.H., Huismans, D.R., Broekema, G.J., Dirven, M.W., Heyenbrok, M.W., Hählen, K., Veerman, A.J. Blood (1990) [Pubmed]
  17. Human Monocytes, but not Dendritic Cells Derived from Them, Are Defective in Base Excision Repair and Hypersensitive to Methylating Agents. Briegert, M., Kaina, B. Cancer Res. (2007) [Pubmed]
  18. Dependence of aldehyde dehydrogenase-mediated oxazaphosphorine resistance on soluble thiols: importance of thiol interactions with the secondary metabolite acrolein. Bunting, K.D., Townsend, A.J. Biochem. Pharmacol. (1998) [Pubmed]
  19. Regulation of early hematopoiesis in serum-deprived cultures of mafosfamide-treated and untreated CD34-enriched bone marrow cells. Ottmann, O.G., Stella, C.C., Eder, M., Reutzel, P., Ströcker, S., Hoelzer, D., Ganser, A. Exp. Hematol. (1991) [Pubmed]
  20. Induction of "in vitro" apoptosis by fludarabine in freshly isolated B-chronic lymphocytic leukemia cells. Zinzani, P.L., Buzzi, M., Farabegoli, P., Tosi, P., Fortuna, A., Visani, G., Martinelli, G., Zaccaria, A., Tura, S. Leuk. Lymphoma (1994) [Pubmed]
  21. Three different stable human breast adenocarcinoma sublines that overexpress ALDH3A1 and certain other enzymes, apparently as a consequence of constitutively upregulated gene transcription mediated by transactivated EpREs (electrophile responsive elements) present in the 5'-upstream regions of these genes. Sreerama, L., Sládek, N.E. Chem. Biol. Interact. (2001) [Pubmed]
  22. Xrcc2 deficiency sensitizes cells to apoptosis by MNNG and the alkylating anticancer drugs temozolomide, fotemustine and mafosfamide. Tsaryk, R., Fabian, K., Thacker, J., Kaina, B. Cancer Lett. (2006) [Pubmed]
  23. Disease-free survival after autologous bone marrow transplantation in patients with acute myelogenous leukemia. Körbling, M., Hunstein, W., Fliedner, T.M., Cayeux, S., Dörken, B., Fehrentz, D., Haas, R., Ho, A.D., Keilholz, U., Knauf, W. Blood (1989) [Pubmed]
  24. Mafosfamide: a new intra-CSF chemotherapy? Chamberlain, M.C. J. Clin. Oncol. (2005) [Pubmed]
  25. Intrathecal mafosfamide: a preclinical pharmacology and phase I trial. Blaney, S.M., Balis, F.M., Berg, S., Arndt, C.A., Heideman, R., Geyer, J.R., Packer, R., Adamson, P.C., Jaeckle, K., Klenke, R., Aikin, A., Murphy, R., McCully, C., Poplack, D.G. J. Clin. Oncol. (2005) [Pubmed]
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