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Chemical Compound Review

Tocris-1401     8-hydroxy-2-methyl-1H- quinazolin-4-one

Synonyms: PubChem15449, CHEMBL123904, SureCN215529, SureCN215530, AG-H-70863, ...
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Disease relevance of NU1


High impact information on NU1

  • The potentiation of growth inhibition by NU1025 and NU1085 varied between the cell lines from 1.5- to 4-fold for TM and 1- to 5-fold for TP and was unaffected by p53 status [4].
  • In studies with L1210 cells in vitro, a concentration of 200 microM 8-hydroxy-2-methylquinazolinone (6, NU1025) (IC50 value 0.40 microM) potentiated the cytotoxicity of the monomethylating agent 5-(3-methyltriazen-1-yl)imidazole-4-carboxamide and gamma-radiation 3.5- and 1.4-fold, respectively, at the 10% survival level [5].
  • Differential effects of the poly (ADP-ribose) polymerase (PARP) inhibitor NU1025 on topoisomerase I and II inhibitor cytotoxicity in L1210 cells in vitro [6].
  • The potent novel poly(ADP-ribose) polymerase (PARP) inhibitor, NU1025, enhances the cytotoxicity of DNA-methylating agents and ionizing radiation by inhibiting DNA repair [6].
  • Taken together, these data suggest that potentiation of camptothecin cytotoxicity by NU1025 is a direct result of increased DNA strand breakage, and that activation of PARP by camptothecin-induced DNA damage contributes to its repair and consequently cell survival [6].

Chemical compound and disease context of NU1


Biological context of NU1

  • Investigation of DNA strand breakage and repair in gamma-irradiated cells by alkaline elution demonstrated that NU1025 caused a marked retardation of DNA repair [7].
  • Neuroprotection with NU1025 was associated with reduction in PAR accumulation, reversal of brain NAD depletion and reduction in DNA fragmentation [2].
  • Analysis of cell growth and cell cycle kinetics showed a synergistic anti-proliferative effect of 10nM TPT and 10muM NU1025 and a G(2)/M block of the cell cycle [3].
  • Conversely, in U251(p53mut) cells we found that NU1025 incremented the TPT-dependent apoptosis characterised by PARP-1 proteolysis [3].

Associations of NU1 with other chemical compounds

  • Pretreatment with NU1025 (0.2 mM) restored cell viability to approximately 73 and 82% in H(2)O(2) and SIN-1 injured cells, respectively [2].
  • It has recently been suggested that our results might be limited to certain BRCA2 mutations as the CAPAN-1 cell line, which carries a naturally occurring 6174delT mutation in one BRCA2 allele accompanied by loss of the wild-type allele, is apparently insensitive to two PARP inhibitors 3-aminobenzamide (IC50 33 microM) and NU1025 (IC50 400 nM) [8].

Gene context of NU1

  • There were no significant changes in NMNAT activity in response to MNNG treatment over 24 h, either in the presence or in the absence of NU1025 [9].

Analytical, diagnostic and therapeutic context of NU1

  • NU1025 at 1 and 3 mg/kg reduced total infarct volume to 25% and 45%, respectively, when administered 1 h before reperfusion [2].


  1. Targeted disruption of FANCC and FANCG in human cancer provides a preclinical model for specific therapeutic options. Gallmeier, E., Calhoun, E.S., Rago, C., Brody, J.R., Cunningham, S.C., Hucl, T., Gorospe, M., Kohli, M., Lengauer, C., Kern, S.E. Gastroenterology (2006) [Pubmed]
  2. Neuroprotective effects of NU1025, a PARP inhibitor in cerebral ischemia are mediated through reduction in NAD depletion and DNA fragmentation. Kaundal, R.K., Shah, K.K., Sharma, S.S. Life Sci. (2006) [Pubmed]
  3. Poly(ADPR)polymerase-1 signalling of the DNA damage induced by DNA topoisomerase I poison in D54(p53wt) and U251(p53mut) glioblastoma cell lines. Cimmino, G., Pepe, S., Laus, G., Chianese, M., Prece, D., Penitente, R., Quesada, P. Pharmacol. Res. (2007) [Pubmed]
  4. Potentiation of temozolomide and topotecan growth inhibition and cytotoxicity by novel poly(adenosine diphosphoribose) polymerase inhibitors in a panel of human tumor cell lines. Delaney, C.A., Wang, L.Z., Kyle, S., White, A.W., Calvert, A.H., Curtin, N.J., Durkacz, B.W., Hostomsky, Z., Newell, D.R. Clin. Cancer Res. (2000) [Pubmed]
  5. Resistance-modifying agents. 5. Synthesis and biological properties of quinazolinone inhibitors of the DNA repair enzyme poly(ADP-ribose) polymerase (PARP). Griffin, R.J., Srinivasan, S., Bowman, K., Calvert, A.H., Curtin, N.J., Newell, D.R., Pemberton, L.C., Golding, B.T. J. Med. Chem. (1998) [Pubmed]
  6. Differential effects of the poly (ADP-ribose) polymerase (PARP) inhibitor NU1025 on topoisomerase I and II inhibitor cytotoxicity in L1210 cells in vitro. Bowman, K.J., Newell, D.R., Calvert, A.H., Curtin, N.J. Br. J. Cancer (2001) [Pubmed]
  7. Potentiation of anti-cancer agent cytotoxicity by the potent poly(ADP-ribose) polymerase inhibitors NU1025 and NU1064. Bowman, K.J., White, A., Golding, B.T., Griffin, R.J., Curtin, N.J. Br. J. Cancer (1998) [Pubmed]
  8. BRCA2-deficient CAPAN-1 cells are extremely sensitive to the inhibition of Poly (ADP-Ribose) polymerase: an issue of potency. McCabe, N., Lord, C.J., Tutt, A.N., Martin, N.M., Smith, G.C., Ashworth, A. Cancer Biol. Ther. (2005) [Pubmed]
  9. Low nicotinamide mononucleotide adenylyltransferase activity in a tiazofurin-resistant cell line: effects on NAD metabolism and DNA repair. Boulton, S., Kyle, S., Durkacz, B.W. Br. J. Cancer (1997) [Pubmed]
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