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Chemical Compound Review

NHNPODA     N'-hydroxy-N-phenyl- octanediamide

Synonyms: Zolinza, Vorinostat, SAHA, vorinostatum, CHEMBL98, ...
 
 
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Disease relevance of SAHA cpd

 

Psychiatry related information on SAHA cpd

 

High impact information on SAHA cpd

  • HDAC inhibitors, such as trichostatin A (TSA) and suberoylanilide hydroxamic acid (SAHA), have anti-tumour effects, as they can inhibit cell growth, induce terminal differentiation and prevent the formation of tumours in mice models, and they are effective in the treatment of promyelocytic leukemia [9].
  • Studies (x-ray crystallographic) showed that the catalytic site of HDAC has a tubular structure with a zinc atom at its base and that these HDAC inhibitors, such as suberoylanilide hydroxamic acid and trichostatin A, fit into this structure with the hydroxamic moiety of the inhibitor binding to the zinc [10].
  • We found striking differences among these cancer cells in constitutive expression and response to suberoylanilide hydroxamic acid in levels of antiapoptotic and proapoptotic proteins, mitochondria membrane integrity, activation of caspases, ROS accumulation, and expression of thioredoxin, the major scavenger of ROS [3].
  • Although p16(INK4A) did not affect the genome-wide transcription changes mediated by SAHA, a small number of apoptotic genes, including BCLXL and B-MYB, were differentially regulated in a manner consistent with attenuated HDACi-mediated apoptosis in arrested cells [11].
  • Transfection of transformed cells with Trx small interfering RNA caused a marked decrease in the level of Trx protein with an increase in ROS, a decrease in cell proliferation, and an increase in sensitivity to SAHA-induced cell death [12].
 

Chemical compound and disease context of SAHA cpd

 

Biological context of SAHA cpd

  • We found that MM cells are irreversibly committed to cell death within few hours of incubation with SAHA [4].
  • Within 1 h, SAHA caused modifications in acetylation and methylation of core histones and increased DNase I sensitivity and restriction enzyme accessibility in the p21(WAF1) promoter [18].
  • Thus, this study identifies effects of SAHA on p21(WAF1)-associated proteins that explain, at least in part, the selective effect of HDACi in altering gene expression [18].
  • Here we studied SAHA-induced changes in the p21(WAF1) promoter of ARP-1 cells to better understand the mechanism of HDACi gene activation [18].
  • We demonstrate that the HDACis suberoylanilide hydroxamic acid (SAHA) and depsipeptide regulate a highly overlapping gene set with at least 22% of genes showing altered expression over a 16-h culture period [11].
 

Anatomical context of SAHA cpd

 

Associations of SAHA cpd with other chemical compounds

 

Gene context of SAHA cpd

 

Analytical, diagnostic and therapeutic context of SAHA cpd

References

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  3. Intrinsic apoptotic and thioredoxin pathways in human prostate cancer cell response to histone deacetylase inhibitor. Xu, W., Ngo, L., Perez, G., Dokmanovic, M., Marks, P.A. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  4. Transcriptional signature of histone deacetylase inhibition in multiple myeloma: biological and clinical implications. Mitsiades, C.S., Mitsiades, N.S., McMullan, C.J., Poulaki, V., Shringarpure, R., Hideshima, T., Akiyama, M., Chauhan, D., Munshi, N., Gu, X., Bailey, C., Joseph, M., Libermann, T.A., Richon, V.M., Marks, P.A., Anderson, K.C. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
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  7. Phase I Study of Vorinostat as a Radiation Sensitizer with 131I-Metaiodobenzylguanidine (131I-MIBG) for Patients with Relapsed or Refractory Neuroblastoma. DuBois, S.G., Groshen, S., Park, J.R., Haas-Kogan, D.A., Yang, X., Geier, E., Chen, E., Giacomini, K., Weiss, B., Cohn, S.L., Granger, M.M., Yanik, G.A., Hawkins, R., Courtier, J., Jackson, H., Goodarzian, F., Shimada, H., Czarnecki, S., Tsao-Wei, D., Villablanca, J.G., Marachelian, A., Matthay, K.K. Clin. Cancer Res. (2015) [Pubmed]
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  11. Identification and functional significance of genes regulated by structurally different histone deacetylase inhibitors. Peart, M.J., Smyth, G.K., van Laar, R.K., Bowtell, D.D., Richon, V.M., Marks, P.A., Holloway, A.J., Johnstone, R.W. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  12. Role of thioredoxin in the response of normal and transformed cells to histone deacetylase inhibitors. Ungerstedt, J.S., Sowa, Y., Xu, W.S., Shao, Y., Dokmanovic, M., Perez, G., Ngo, L., Holmgren, A., Jiang, X., Marks, P.A. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  13. Synergistic induction of oxidative injury and apoptosis in human multiple myeloma cells by the proteasome inhibitor bortezomib and histone deacetylase inhibitors. Pei, X.Y., Dai, Y., Grant, S. Clin. Cancer Res. (2004) [Pubmed]
  14. Cotreatment with Vorinostat (Suberoylanilide Hydroxamic Acid) Enhances Activity of Dasatinib (BMS-354825) against Imatinib Mesylate-Sensitive or Imatinib Mesylate-Resistant Chronic Myelogenous Leukemia Cells. Fiskus, W., Pranpat, M., Balasis, M., Bali, P., Estrella, V., Kumaraswamy, S., Rao, R., Rocha, K., Herger, B., Lee, F., Richon, V., Bhalla, K. Clin. Cancer Res. (2006) [Pubmed]
  15. The histone deacetylase inhibitor suberoylanilide hydroxamic Acid induces growth inhibition and enhances gemcitabine-induced cell death in pancreatic cancer. Arnold, N.B., Arkus, N., Gunn, J., Korc, M. Clin. Cancer Res. (2007) [Pubmed]
  16. In vitro and ex vivo evaluation of second-generation histone deacetylase inhibitors for the treatment of spinal muscular atrophy. Hahnen, E., Eyüpoglu, I.Y., Brichta, L., Haastert, K., Tränkle, C., Siebzehnrübl, F.A., Riessland, M., Hölker, I., Claus, P., Romstöck, J., Buslei, R., Wirth, B., Blümcke, I. J. Neurochem. (2006) [Pubmed]
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  22. Coadministration of the heat shock protein 90 antagonist 17-allylamino- 17-demethoxygeldanamycin with suberoylanilide hydroxamic acid or sodium butyrate synergistically induces apoptosis in human leukemia cells. Rahmani, M., Yu, C., Dai, Y., Reese, E., Ahmed, W., Dent, P., Grant, S. Cancer Res. (2003) [Pubmed]
  23. Photoaffinity labeling and mass spectrometry identify ribosomal protein S3 as a potential target for hybrid polar cytodifferentiation agents. Webb, Y., Zhou, X., Ngo, L., Cornish, V., Stahl, J., Erdjument-Bromage, H., Tempst, P., Rifkind, R.A., Marks, P.A., Breslow, R., Richon, V.M. J. Biol. Chem. (1999) [Pubmed]
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