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Chemical Compound Review

GNF-Pf-2453     7-(4-amino-5-hydroxy-6- methyl-oxan-2...

Synonyms: AGN-PC-0067V2, CHEMBL263733, SureCN233853, Neuro_000057, Neuro_000121, ...
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Disease relevance of Adriblastina


Psychiatry related information on Adriblastina

  • Time-response studies showed that the cytotoxic effects of Pro are increased for 3 days in human tumor cells, whereas VCR, Dox and 5-Fu showed decreased cytotoxic action after 24 h [6].

High impact information on Adriblastina

  • These findings indicate that treatment with etoposide, Ara-C, or doxorubicin up-regulates DR5 levels in a p53-independent manner and sensitizes human acute leukemia cells to Apo-2L-induced apoptosis [7].
  • This study suggests the combination of CDDP and Dox is highly effective in BC and SC cancers of the skin and by itself can produce long unmaintained remissions, but when combined with a second modality of therapy, it is capable of producing not only long unmaintained CRs but probable cures in the majority of pts [8].
  • CONCLUSIONS: FLIP, an inhibitor of apoptosis induced by cytokines of TNF family, contributes at least partly to Dox-induced sensitization to Fas-mediated apoptosis in cardiac myocytes [9].
  • Both of N-acetylcysteine (NAC) and the combination of superoxide dismutase and catalase restored the decreased FLIP in Dox-treated cardiac myocytes to the basal level [9].
  • We investigated the molecular mechanism by which Dox sensitizes cardiac myocytes to Fas-induced apoptosis [9].

Chemical compound and disease context of Adriblastina


Biological context of Adriblastina

  • FZ was able to reverse dox intracellular tolerance of C6 0.5 cells and to restore dox accumulation at the IC50 to the level observed in sensitive cells [12].
  • 4. The negative inotropism of 30-100 microM DOX, EPI, or MEN 10755 correlated with cellular levels of both alcohol metabolites (r=0.88, P<0.0001) and carbonyl anthracyclines (r=0.79, P<0.0001) [13].
  • DNA damage induced by DOX was not predictive of cytotoxicity [10].
  • Coordinately, cell growth inhibition induced by amrubicin and amrubicinol, but not that induced by DXR, was antagonized by ICRF-193 [14].
  • Analog AN-207, formed by linking 2-pyrrolino-DOX to [D-Lys6]LH-RH, and analog AN-152, produced by conjugation of DOX to the same carrier, given i.p. as a single injection or repeatedly 2 days apart at their maximum tolerated doses (MTDs) resulted in a 89-93% inhibition of tumor growth [15].

Anatomical context of Adriblastina

  • By confocal microscopy, the subcellular distribution of Ann was identical in sensitive and resistant cells, localizing mostly in the perinuclear structures, while that of Dox was exclusively nuclear in sensitive cells and nuclear and in the cell membrane in resistant cells [16].
  • FZ was able, at a relatively high concentration (30 microM), to completely restore dox sensitivity in both cell lines [12].
  • As compared with Dox, both Ann and L-Ann induced 3 times more DNA double- and single-strand breaks in KB cells [17].
  • The DX content was not modified by amiodarone in the other organs studied (heart, lung, spleen and pancreas) [18].
  • Unlike DOX, flavopiridol (FL) did not protect HCT116 cells [19].

Associations of Adriblastina with other chemical compounds

  • In addition, we designed and synthesized a highly active derivative of DOX, 2-pyrrolino-DOX (AN-201), which is 500-1000 times more potent than DOX in vitro [20].
  • The CDDP resistant tumours were not cross-resistant in vivo to L-PAM, BCNU and Dox, which had been active in vitro, nor to tallimustine, which had been cross-resistant in vitro [21].
  • Moreover, we have recently found that an HPMA conjugate containing a combination of both Dox and the aromatase inhibitor aminoglutethimide (AGM) shows significantly increased anti-tumour activity in vitro [2].
  • In experiments on isolated guinea pig heart, which is considered a highly predictive model of acute anthracycline cardiotoxicity in humans, 4'-deoxy-DXR was found to be significantly less cardiotoxic than DXR [22].
  • 4'-deoxydoxorubicin (4'-deoxy-DXR), a new doxorubicin (DXR) analogue with interesting antineoplastic activity, was tested for its cardiotoxicity in guinea pigs and humans [22].

Gene context of Adriblastina

  • DOX-containing cytotoxic LHRH analog AN-152 is scheduled for clinical phase I/IIa trials in patients with advanced ovarian and breast cancers in 2005 [20].
  • We thus demonstrate that ectopic expression of Daxx substantially increases the rate of apoptosis upon incubation with death receptor agonists such as Fas and TRAIL as well as upon incubation with the cytotoxic drug doxorubicin (DOX) [23].
  • We have tried to elucidate TNF signaling in FLC/DOX [24].
  • Instead, p53-dependent activation and apoptosis were not only induced by PFTalpha itself but were also enhanced by a combination of PFTalpha with UVB or Dox [25].
  • Certain cytokines might be capable of bypassing this process and here we report on the in vitro effects of Tumor Necrosis Factor alpha, (TNF) on a MDR variant (FLC/DOX) of Friend leukemia [24].

Analytical, diagnostic and therapeutic context of Adriblastina

  • To test the efficacy of targeted chemotherapy based on LHRH analogs, we recently developed a cytotoxic analog of LHRH, designated AN-152, which consists of [D-Lys6]LHRH covalently linked to one of the most widely used chemotherapeutic agents, doxorubicin (DOX) [20].
  • These models were subdivided into four subgroups randomly: Doxorubicin (DOX)-treated group, TAM-treated group, DOX and TAM group and control group [26].
  • Moreover, the correlation between DOX sensitivity and P-glycoprotein expression was assessed by flow cytometry [27].
  • Preliminary data indicated a lower percentage of EKG abnormalities in comparison not only with DXR but also with other anthracycline analogues [22].
  • Doxorubicin (DOX) was introduced into the starlike HPMA copolymer to evaluate its potential as a drug delivery system [4].


  1. High incidence of local venous reactions to esorubicin. Lee, K.M., Dorr, R.T., Robertone, A. Investigational new drugs. (1987) [Pubmed]
  2. HPMA copolymer-aminoglutethimide conjugates inhibit aromatase in MCF-7 cell lines. Greco, F., Vicent, M.J., Penning, N.A., Nicholson, R.I., Duncan, R. Journal of drug targeting. (2005) [Pubmed]
  3. The antineoplastic activity of 4'-deoxydoxorubicin in murine solid tumors. Marmonti, L., Jin, X.Q., Filippeschi, S., Spreafico, F. Anticancer Res. (1984) [Pubmed]
  4. Synthesis of starlike N-(2-hydroxypropyl)methacrylamide copolymers: potential drug carriers. Wang, D., Kopecková, J.P., Minko, T., Nanayakkara, V., Kopecek, J. Biomacromolecules (2000) [Pubmed]
  5. The effect of modulation of gamma-glutamyl transpeptidase and nitric oxide synthase activity on GSH homeostasis in HepG2 cells. Kwiecień, I., Rokita, H., Lorenc-Koci, E., Sokolowska, M., Włodek, L. Fundamental & clinical pharmacology (2007) [Pubmed]
  6. Anti-proliferative effects, cell cycle G2/M phase arrest and blocking of chromosome segregation by probimane and MST-16 in human tumor cell lines. Lu, d.a. .Y., Huang, M., Xu, C.H., Yang, W.Y., Hu, C.X., Lin, L.P., Tong, L.J., Li, M.H., Lu, W., Zhang, X.W., Ding, J. BMC Pharmacol. (2005) [Pubmed]
  7. Antileukemic drugs increase death receptor 5 levels and enhance Apo-2L-induced apoptosis of human acute leukemia cells. Wen, J., Ramadevi, N., Nguyen, D., Perkins, C., Worthington, E., Bhalla, K. Blood (2000) [Pubmed]
  8. Cisplatin-based chemotherapy in advanced basal and squamous cell carcinomas of the skin: results in 28 patients including 13 patients receiving multimodality therapy. Guthrie, T.H., Porubsky, E.S., Luxenberg, M.N., Shah, K.J., Wurtz, K.L., Watson, P.R. J. Clin. Oncol. (1990) [Pubmed]
  9. Reactive oxygen species regulate FLICE inhibitory protein (FLIP) and susceptibility to Fas-mediated apoptosis in cardiac myocytes. Nitobe, J., Yamaguchi, S., Okuyama, M., Nozaki, N., Sata, M., Miyamoto, T., Takeishi, Y., Kubota, I., Tomoike, H. Cardiovasc. Res. (2003) [Pubmed]
  10. Ifosfamide metabolism and DNA damage in tumour and peripheral blood lymphocytes of breast cancer patients. Johnstone, E.C., Lind, M.J., Griffin, M.J., Boddy, A.V. Cancer Chemother. Pharmacol. (2000) [Pubmed]
  11. Antiproliferation and apoptosis induction of paeonol in HepG(2) cells. Xu, S.P., Sun, G.P., Shen, Y.X., Wei, W., Peng, W.R., Wang, H. World J. Gastroenterol. (2007) [Pubmed]
  12. Azelastine and flezelastine as reversing agents of multidrug resistance: pharmacological and molecular studies. Hu, Y.P., Robert, J. Biochem. Pharmacol. (1995) [Pubmed]
  13. Impairment of myocardial contractility by anticancer anthracyclines: role of secondary alcohol metabolites and evidence of reduced toxicity by a novel disaccharide analogue. Minotti, G., Parlani, M., Salvatorelli, E., Menna, P., Cipollone, A., Animati, F., Maggi, C.A., Manzini, S. Br. J. Pharmacol. (2001) [Pubmed]
  14. A new antitumor agent amrubicin induces cell growth inhibition by stabilizing topoisomerase II-DNA complex. Hanada, M., Mizuno, S., Fukushima, A., Saito, Y., Noguchi, T., Yamaoka, T. Jpn. J. Cancer Res. (1998) [Pubmed]
  15. Targeted cytotoxic luteinizing hormone releasing hormone (LH-RH) anlalogs inhibit growth of estrogen independent MXT mouse mammary cancers in vivo by decreasing cell proliferation and inducing apoptosis. Szepeshazi, K., Schally, A.V., Nagy, A., Halmos, G., Groot, K. Anticancer Drugs (1997) [Pubmed]
  16. Annamycin circumvents resistance mediated by the multidrug resistance-associated protein (MRP) in breast MCF-7 and small-cell lung UMCC-1 cancer cell lines selected for resistance to etoposide. Perez-Soler, R., Neamati, N., Zou, Y., Schneider, E., Doyle, L.A., Andreeff, M., Priebe, W., Ling, Y.H. Int. J. Cancer (1997) [Pubmed]
  17. Cellular pharmacology of the partially non-cross-resistant anthracycline annamycin entrapped in liposomes in KB and KB-V1 cells. Perez-Soler, R., Ling, Y.H., Zou, Y., Priebe, W. Cancer Chemother. Pharmacol. (1994) [Pubmed]
  18. Serum concentrations of amiodarone required for an in vivo modulation of anthracycline resistance. Genne, P., Coudert, B., Pelletier, H., Girardot, C., Martin, F., Chauffert, B. Anticancer Res. (1989) [Pubmed]
  19. Flavopiridol inversely affects p21(WAF1/CIP1) and p53 and protects p21-sensitive cells from paclitaxel. Blagosklonny, M.V., Darzynkiewicz, Z., Figg, W.D. Cancer Biol. Ther. (2002) [Pubmed]
  20. Targeting of cytotoxic luteinizing hormone-releasing hormone analogs to breast, ovarian, endometrial, and prostate cancers. Nagy, A., Schally, A.V. Biol. Reprod. (2005) [Pubmed]
  21. In vitro and in vivo characterisation of low-resistant mouse reticulosarcoma (M5076) sublines obtained after pulse and continuous exposure to cisplatin. Belvedere, G., Imperatori, L., Damia, G., Tagliabue, G., Meijer, C., de Vries, E.G., D'Incalci, M. Eur. J. Cancer (1996) [Pubmed]
  22. Preliminary evaluation of myocardial toxicity of 4'-deoxydoxorubicin: experimental and clinical results. Villani, F., Comazzi, R., Genitoni, V., Lacaita, G., Guindani, A., Crippa, F., Monti, E., Piccinini, F., Rozza, A., Lanza, E. Drugs under experimental and clinical research. (1985) [Pubmed]
  23. Daxx overexpression in T-lymphoblastic Jurkat cells enhances caspase-dependent death receptor- and drug-induced apoptosis in distinct ways. Boehrer, S., Nowak, D., Hochmuth, S., Kim, S.Z., Trepohl, B., Afkir, A., Hoelzer, D., Mitrou, P.S., Weidmann, E., Chow, K.U. Cell. Signal. (2005) [Pubmed]
  24. The apoptotic signaling of TNF-alpha in multidrug resistant Friend leukemia cells. D'Alessandro, N., Flugy, A., Tolomeo, M., Dusonchet, L. Anticancer Res. (1998) [Pubmed]
  25. Pifithrin-alpha promotes p53-mediated apoptosis in JB6 cells. Kaji, A., Zhang, Y., Nomura, M., Bode, A.M., Ma, W.Y., She, Q.B., Dong, Z. Mol. Carcinog. (2003) [Pubmed]
  26. Tamoxifen can reverse multidrug resistance of colorectal carcinoma in vivo. Shen, L.Z., Hua, Y.B., Yu, X.M., Xu, Q., Chen, T., Wang, J.H., Wu, W.X. World J. Gastroenterol. (2005) [Pubmed]
  27. Tamoxifen circumvents the multidrug resistance in fresh human gastrointestinal cancer cells. Hotta, T., Tanimura, H., Yamaue, H., Iwahashi, M., Tani, M., Tsunoda, T., Tamai, M., Noguchi, K., Mizobata, S., Arii, K., Terasawa, H. J. Surg. Res. (1996) [Pubmed]
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