The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Chemical Compound Review

Entinostat     pyridin-3-ylmethyl N-[[4-[(2...

Synonyms: SNDX-275, PubChem24433, CHEMBL27759, S1053_Selleck, SureCN148309, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of ms-275

  • Because HDAC modulates chromatin structure and gene expression, parameters considered to influence radioresponse, we have investigated the effects of the HDAC inhibitor MS-275 on the radiosensitivity of two human tumor cell lines (DU145 prostate carcinoma and U251 glioma) [1].
  • PURPOSE: The objective of this study was to define the maximum-tolerated dose (MTD), the recommended phase II dose, the dose-limiting toxicity, and determine the pharmacokinetic (PK) and pharmacodynamic profiles of MS-275 [2].
  • MS-275, a histone deacetylase inhibitor, selectively induces transforming growth factor beta type II receptor expression in human breast cancer cells [3].
  • PATIENTS AND METHODS: Patients with advanced solid tumors or lymphoma were treated with MS-275 orally initially on a once daily x 28 every 6 weeks (daily) and later on once every-14-days (q14-day) schedules [2].
  • In this study, we examined whether RARbeta2 expression is repressed in human renal cell carcinoma (RCC) and whether the HDAC inhibitor MS-275 may revert its epigenetic repression [4].

High impact information on ms-275

  • These results suggest that MS-275 is a potent brain region-selective HDAC inhibitor [5].
  • Whereas this response peaks after a s.c. injection of 15 micromol/kg, the increase in Ac-H3 content in the hippocampus becomes significant only after an injection of 60 micromol/kg, suggesting that MS-275 is 30- to 100-fold more potent than VPA in increasing Ac-H3 in these brain regions [5].
  • A structurally analogous compound to MS-27-275 without HDA-inhibiting activity showed neither the biological effects in cell culture nor the in vivo therapeutic efficacy [6].
  • It behaved in a manner similar to other HDA inhibitors, such as sodium butyrate and trichostatin A; MS-27-275 induced p21(WAF1/CIP1) and gelsolin and changed the cell cycle distribution, decrease of S-phase cells, and increase of G1-phase cells [6].
  • MS-27-275 inhibited partially purified human HDA and caused hyperacetylation of nuclear histones in various tumor cell lines [6].

Chemical compound and disease context of ms-275

  • Unlike another anilide-based HDAC inhibitor, MS-275, which decreases both red and white blood counts and reduces spleen weights in mice, Compound 2 does not exhibit noticeable toxicity [7].
  • In contrast to SAHA, the compounds m-Carboxycinnamic acid bis-Hydroxamide, suberoyl bishydroxamic acid and M344 displayed unfavourable toxicity profiles, whereas MS-275 failed to increase SMN levels [8].
  • Considering the ability of MS-275 to cross the blood-brain barrier, our experimental model identifies the benzamide MS-275 as a promising therapeutic compound for targeting epigenetic chromatin modulation as systemic treatment of metastatic melanomas [9].
  • Among them, the compound having a (3,4-difluorobenzyl)(2-hydroxyethyl)amino group at one end and a 2-aminobenzamide group at the other of molecule showed the most promising profile as an anticancer drug candidate, since it had a comparatively low toxicity as did MS-275 against a normal fibroblast cell CCD-1059SK [10].
  • Implantation of enhanced green fluorescent protein-transfected F98 glioma cells into slice cultures of rat brain confirmed the cytostatic effect of MS-275 without neurotoxic damage to the organotypic neuronal environment in a dose escalation up to 20 micromol/L [11].

Biological context of ms-275

  • Together, these findings demonstrate that MS-275 exerts dose-dependent effects in human leukemia cells, i.e., p21(CIP1/WAF1)-dependent growth arrest and differentiation at low drug concentrations and a marked induction of ROS, mitochondrial damage, caspase activation, and apoptosis at higher concentrations [12].
  • Treatment with MS-275 results in an increase in acetylation of histones within 4 h of drug exposure [13].
  • However, the effects on cell cycle were diverse because in some cases MS-275 induced an increase in G(1) or G(2), whereas in others, there was an induction of apoptosis [13].
  • Treatment of cells with MS-275 for 48 h followed by irradiation had little or no effect on radiation-induced cell death [1].
  • These results indicate that MS-275 can enhance radiosensitivity and suggest that this effect may involve an inhibition of DNA repair [1].

Anatomical context of ms-275


Associations of ms-275 with other chemical compounds


Gene context of ms-275


Analytical, diagnostic and therapeutic context of ms-275


  1. Enhanced radiation-induced cell killing and prolongation of gammaH2AX foci expression by the histone deacetylase inhibitor MS-275. Camphausen, K., Burgan, W., Cerra, M., Oswald, K.A., Trepel, J.B., Lee, M.J., Tofilon, P.J. Cancer Res. (2004) [Pubmed]
  2. Phase I and pharmacokinetic study of MS-275, a histone deacetylase inhibitor, in patients with advanced and refractory solid tumors or lymphoma. Ryan, Q.C., Headlee, D., Acharya, M., Sparreboom, A., Trepel, J.B., Ye, J., Figg, W.D., Hwang, K., Chung, E.J., Murgo, A., Melillo, G., Elsayed, Y., Monga, M., Kalnitskiy, M., Zwiebel, J., Sausville, E.A. J. Clin. Oncol. (2005) [Pubmed]
  3. MS-275, a histone deacetylase inhibitor, selectively induces transforming growth factor beta type II receptor expression in human breast cancer cells. Lee, B.I., Park, S.H., Kim, J.W., Sausville, E.A., Kim, H.T., Nakanishi, O., Trepel, J.B., Kim, S.J. Cancer Res. (2001) [Pubmed]
  4. Epigenetic modulation of retinoic acid receptor beta2 by the histone deacetylase inhibitor MS-275 in human renal cell carcinoma. Wang, X.F., Qian, D.Z., Ren, M., Kato, Y., Wei, Y., Zhang, L., Fansler, Z., Clark, D., Nakanishi, O., Pili, R. Clin. Cancer Res. (2005) [Pubmed]
  5. The benzamide MS-275 is a potent, long-lasting brain region-selective inhibitor of histone deacetylases. Simonini, M.V., Camargo, L.M., Dong, E., Maloku, E., Veldic, M., Costa, E., Guidotti, A. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  6. A synthetic inhibitor of histone deacetylase, MS-27-275, with marked in vivo antitumor activity against human tumors. Saito, A., Yamashita, T., Mariko, Y., Nosaka, Y., Tsuchiya, K., Ando, T., Suzuki, T., Tsuruo, T., Nakanishi, O. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  7. Sulfonamide anilides, a novel class of histone deacetylase inhibitors, are antiproliferative against human tumors. Fournel, M., Trachy-Bourget, M.C., Yan, P.T., Kalita, A., Bonfils, C., Beaulieu, C., Frechette, S., Leit, S., Abou-Khalil, E., Woo, S.H., Delorme, D., MacLeod, A.R., Besterman, J.M., Li, Z. Cancer Res. (2002) [Pubmed]
  8. 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]
  9. Ex vivo therapy of malignant melanomas transplanted into organotypic brain slice cultures using inhibitors of histone deacetylases. Hölsken, A., Eyüpoglu, I.Y., Lueders, M., Tränkle, C., Dieckmann, D., Buslei, R., Hahnen, E., Blümcke, I., Siebzehnrübl, F.A. Acta Neuropathol. (2006) [Pubmed]
  10. Synthesis and cancer antiproliferative activity of new histone deacetylase inhibitors: hydrophilic hydroxamates and 2-aminobenzamide-containing derivatives. Nagaoka, Y., Maeda, T., Kawai, Y., Nakashima, D., Oikawa, T., Shimoke, K., Ikeuchi, T., Kuwajima, H., Uesato, S. European journal of medicinal chemistry. (2006) [Pubmed]
  11. Experimental therapy of malignant gliomas using the inhibitor of histone deacetylase MS-275. Eyüpoglu, I.Y., Hahnen, E., Tränkle, C., Savaskan, N.E., Siebzehnrübl, F.A., Buslei, R., Lemke, D., Wick, W., Fahlbusch, R., Blümcke, I. Mol. Cancer Ther. (2006) [Pubmed]
  12. The histone deacetylase inhibitor MS-275 promotes differentiation or apoptosis in human leukemia cells through a process regulated by generation of reactive oxygen species and induction of p21CIP1/WAF1 1. Rosato, R.R., Almenara, J.A., Grant, S. Cancer Res. (2003) [Pubmed]
  13. MS-27-275, an inhibitor of histone deacetylase, has marked in vitro and in vivo antitumor activity against pediatric solid tumors. Jaboin, J., Wild, J., Hamidi, H., Khanna, C., Kim, C.J., Robey, R., Bates, S.E., Thiele, C.J. Cancer Res. (2002) [Pubmed]
  14. Histone Deacetylase Inhibitors Induce Apoptosis with Minimal Viral Reactivation in Cells Infected with Kaposi's Sarcoma-Associated Herpesvirus. Niedermeier, A., Talanin, N., Chung, E.J., Sells, R.E., Borris, D.L., Orenstein, J.M., Trepel, J.B., Blauvelt, A. J. Invest. Dermatol. (2006) [Pubmed]
  15. Factors affecting the pharmacokinetic profile of MS-275, a novel histone deacetylase inhibitor, in patients with cancer. Acharya, M.R., Karp, J.E., Sausville, E.A., Hwang, K., Ryan, Q., Gojo, I., Venitz, J., Figg, W.D., Sparreboom, A. Investigational new drugs. (2006) [Pubmed]
  16. Histone deacetylase inhibitor pharmacodynamic analysis by multiparameter flow cytometry. Chung, E.J., Lee, S., Sausville, E.A., Ryan, Q., Karp, J.E., Gojo, I., Telford, W.G., Lee, M.J., Kong, H.S., Trepel, J.B. Ann. Clin. Lab. Sci. (2005) [Pubmed]
  17. Blockade of histone deacetylase inhibitor-induced RelA/p65 acetylation and NF-kappaB activation potentiates apoptosis in leukemia cells through a process mediated by oxidative damage, XIAP downregulation, and c-Jun N-terminal kinase 1 activation. Dai, Y., Rahmani, M., Dent, P., Grant, S. Mol. Cell. Biol. (2005) [Pubmed]
  18. The histone deacetylase inhibitor MS-275 interacts synergistically with fludarabine to induce apoptosis in human leukemia cells. Maggio, S.C., Rosato, R.R., Kramer, L.B., Dai, Y., Rahmani, M., Paik, D.S., Czarnik, A.C., Payne, S.G., Spiegel, S., Grant, S. Cancer Res. (2004) [Pubmed]
  19. Cell cycle regulation in the G1 phase: a promising target for the development of new chemotherapeutic anticancer agents. Owa, T., Yoshino, H., Yoshimatsu, K., Nagasu, T. Current medicinal chemistry. (2001) [Pubmed]
  20. Bombesin/gastrin-releasing peptide receptor antagonists increase the ability of histone deacetylase inhibitors to reduce lung cancer proliferation. Moody, T.W., Nakagawa, T., Kang, Y., Jakowlew, S., Chan, D., Jensen, R.T. J. Mol. Neurosci. (2006) [Pubmed]
  21. Transcriptional regulation of the transforming growth factor beta type II receptor gene by histone acetyltransferase and deacetylase is mediated by NF-Y in human breast cancer cells. Park, S.H., Lee, S.R., Kim, B.C., Cho, E.A., Patel, S.P., Kang, H.B., Sausville, E.A., Nakanishi, O., Trepel, J.B., Lee, B.I., Kim, S.J. J. Biol. Chem. (2002) [Pubmed]
WikiGenes - Universities