Extensive Research Supports Clinical Development of Entinostat

Shen, L., A. Orillion, R. Pili. (2016) “Histone deacetylase inhibitors as immunomodulators in cancer therapeutics.” Epigenomics. 2016 Mar 7:1-14. doi: 10.2117/epi.15.118.

Park J., S. Thomas, and P. Munster. (2015). “Epigenetic modulation with histone deacetylase inhibitors in combination with immunotherapy”. Epigenomics. 7: 641–652

Butt A., and K. Mills (2014). “Immunosuppressive networks and checkpoints controlling antitumor immunity and their blockade in the development of cancer immunotherapeutics and vaccines.” Oncogene. 33: 4623–4631.

Forde PM, J.R. Brahmer, and R.J. Kelly. (2014). “New strategies in lung cancer: epigenetic therapy for non-small cell lung cancer.” Clin. Cancer Res. 20: 2244–8.

Kim, K., A. Skora, et al. (2014). “Eradication of metastatic mouse cancers resistant to immune checkpoint blockade by suppression of myeloid-derived cells.” PNAS. 2014 July 28. Online.

Brahmer J, and D. Pardoll. (2013). “Immune Checkpoint Inhibitors: Making Immunotherapy a Reality for the Treatment of Lung Cancer.” Cancer Immunol Res. 1: 85–91.

Najjar Y, and J. Finke. (2013). “Clinical Perspectives on Targeting of Myeloid Derived Suppressor Cells in the Treatment of Cancer.” Front. Oncol. 3.

Pili, R., L. Shen, et al. (2013). “Phase I study of high-dose interleukin 2, aldesleukin, in combination with the histone deacetylase inhibitor, entinostat, in patients with metastatic renal cell carcinoma: Safety data.” ASCO Genitourinary poster.

Youn J-I, V. Kumar, et al. (2013). “Epigenetic silencing of retinoblastoma gene regulates pathologic differentiation of myeloid cells in cancer.” Nat. Immunol. 14: 211–220.

Zhu S., C. Denman, et al. (2013). “The narrow-spectrum HDAC inhibitor entinostat enhances NKG2D expression without NK cell toxicity, leading to enhanced recognition of cancer cells.” Pharm. Res. 32: 779–92.

Shen, L., M. Ciesielksi, et al. (2012). “Class I histone deacetylase inhibitor entinostat suppresses regulatory T cells and enhances immunotherapies in renal and prostate cancer models.” PLoSOne. 7(1):1-14.

Buglio, D., N. Kashkhely, et al. (2011). “HDAC11 plays an essential role in regulating OX40 ligand expression in Hodgkin lymphoma.” Blood. 117(10): 2910 – 2917.

Juergens RA, J. Wrangle, et al. (2011). “Combination epigenetic therapy has efficacy in patients with refractory advanced non-small cell lung cancer.” Cancer Discov. 1: 598–607

Schech A, A. Kazi, et al. (2015). “Histone Deacetylase Inhibitor Entinostat Inhibits Tumor-Initiating Cells in Triple-Negative Breast Cancer Cells.” Molecular Cancer Therapeutics 14: 1848–1857.

Shah, P., Gau, Y., Sabnis, G. (2013). ” Histone deacetylase inhibitor entinostat reverses epithelial to mesenchymal transition of breast cancer cells by reversing the repression of E-cadherin.” Breast Canc Res Treat

Yardley, D., R. Ismail-Khan, et al. (2013). “A randomized phase 2, double-blind, placebo-controlled study of exemestane with and without entinostat (SNDX-275) in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a non-steroidal aromatase inhibitor.” JCO

Connolly, R., and V. Stearns (2012). “Epigenetics as a therapeutic target in breast cancer.” J Mammary Gland Biol Neoplasia. Published on-line 27July2012.

Chumsri, S., T. Howes, et al. (2011). “Aromatase, aromatase inhibitors, and breast cancer.” J Steroid Biochem Mol Biol. 125:13-22.

Sabnis, G., O. Goloubeva, et al. (2011). “Functional activation of the estrogen receptor-a and aromatase by the HDAC inhibitor entinostat sensitizes ER-negative tumors to letrozole.” Cancer Res. Mar 1;71(5):1893-903. Epub 2011 Jan 18

Brodie, A., L. Macedo, et al. (2010). “Aromatase resistance mechanisms in model systems in vivo.” J Steroid Biochem Mol Biol. 118:283-87.

Sabnis, G., O. Goloubeva, et al. (2010). “HDAC inhibitor entinostat restores responsiveness of letrozole resistant MCF-7Ca xenografts to AIs through modulation of Her-2.” Mol Cancer Ther. 2013 Oct 3. [Epub ahead of print]

Srivastava, R., R. Kurzrock, et al. (2010). “MS-275 sensitizes TRAIL-resistant breast cancer cells, inhibits angiogenesis and metastasis, and reverses epithelial-mesenchymal transition In vivo.” Mol Cancer Ther. 9(12):3254-66.

Wardley, A.M., R. Stein, et al. (2010). “Phase II data for entinostat, a class 1 selective histone deacetylase inhibitor, in patients whose breast cancer is progressing on aromatase inhibitor therapy.” JCO. 2010 ASCO annual meeting proceedings; 28(15)_suppl; 1052.

Lustberg, M.B. and B. Ramaswamy. (2009). “Epigenetic targeting in breast cancer: therapeutic impact and future direction.” Drug News Perspect. 22(7):369-81.

Thomas, S. and P.N. Munster. (2009). “Histone deacetylase inhibitor induced modulation of anti-estrogen therapy.” Cancer Lett. 280:184-91.

Hodges-Gallagher, L., C.D. Valentine, et al. (2007). “Inhibition of histone deacetylase enhances the anti-proliferative action of antiestrogens on breast cancer cells and blocks tamoxifen-induced proliferation of uterine cells.” Breast Cancer Res Treat. 105(3):297-309.

Arrowsmith, C.H., C. Bountra, et al. (2012) “Epigenetic protein families: a new frontier for drug discovery.” Nature Drug Disc. 11:384-400.

April 7, 2012. “Cancer’s epicentre.” The Economist. Pgs 89-90.

Baylin, S. and P.A. Jones (2010). “Epigenetic drugs take on cancer.” Science. 330:576-578.

Esteller (2008). “Molecular origins of cancer: epigenetics in cancer.” New England J Med 2008; 358:1148-59.

Jones, P.A. and S. Baylin (2007). “The epigenetics of cancer.” Cell. 128:683-92.

Falkenberg K., and R. Johnstone. (2014). “Histone deacetylases and their inhibitors in cancer, neurological diseases and immune disorders.” Nat Rev Drug Disc. 13: 673–691.

Lakshmaiah K.C., L.A. Jacob, et al. (2014). “Epigenetic therapy of cancer with histone deacetylase inhibitors.” J Cancer Res Ther. 10: 469–78.

Bradner, J.E., N. West, et al (2010). “Chemical phylogenetics of histone deacetylases.” Nat Chem Biol. 6(March): 238-43.

Singh, A. and J. Settelman (2010). “EMT, cancer stem cells and drug resistance: an emerging axis of evil in the war on cancer.” Oncogene. 29:4741-51.

Lane, A.A. and B.A. Bradner (2009). “Histone deacetylase inhibitors in cancer therapy.” J Clin Onc. 27(32):5459-68.

Witt, O., H.E. Deubzer, et al (2009). “HDAC family: What are the cancer relevant targets?” Cancer Lett. 277:8-21.

Lee, M.J., Y.S. Kim, et al (2008). “Histone deacetylase inhibitors in cancer therapy.” Curr Opin Oncol. 20(6):639-49.

Kaiser, J. (2010) “Epigenetics drugs take on cancer.” Science. 330:576-78.

Ganesan, A., L. Nolan, et al (2009). ” Epigenetic Therapy: Histone Acetylation, DNA Methylation and Anti-Cancer Drug Discovery.” Curr Cancer Drug Targets. 9:963-81.

Stearns, V., Q. Zhou, et al (2007). “Epigenetic regulation as a new target for breast cancer therapy.” Canc Invest. 25:659–65.

Cameron, E.E., K.E. Bachman, et al. (1999). “Synergy of demethylation and histone deacetylase inhibition in the re-expression of genes silenced in cancer.” Nature Gen. 21:103-07.

 

Juergens, R.A., and C.M. Rudin (2013). “Aberrant Epigenetic Regulation: A Central Contributor to Lung Carcinogenesis and a New Therapeutic Target.” ASCO Educational Book.

Wrangle J, W. Wang, et al. (2013). “Alterations of immune response of non-small cell lung cancer with Azacytidine.” Oncotarget. 4: 2067–2079.

Belinsky, S., M. Grimes, et al. (2011). “Combination therapy with vidaza and entinostat suppresses tumor growth and reprograms the epigenome in an orthotopic lung cancer model.” Cancer Res. 71(2):OF1-9.

Juergens, R., J. Wrangle, et al. (2011). “Combination epigenetic therapy has efficacy in patients with refractory advanced non–small cell lung cancer.” Cancer Discovery. OF1-10.

Rodriquez-Paredes, M. and M. Esteller. (2011). “A Combined epigenetic therapy equals the efficacy of conventional chemotherapy in refractory advanced non-small cell lung cancer.” Cancer Discovery. OF1-3.

Ruiz R, L. Raez, and C. Rolfo. (2015). “Entinostat (SNDX-275) for the treatment of non-small cell lung cancer.” Expert Opin. Investig. Drugs 24: 11011109.

Neal, J.W. and L.V. Sequist (2012). “Complex role of histone deacetylase inhibitors in the treatment of non-small-cell lung cancer.” JCO, ahead of print. 30:1-3.

Witta, S., R.M. Jotte, et al. (2012) “Randomized Phase II Trial of Erlotinib With and Without Entinostat in Patients With Advanced Non–Small-Cell Lung Cancer Who Progressed on Prior Chemotherapy.” JCO 30(18):2248-2255

Suda, K., K.Tomizawa, et al. (2011) “Epithelial to mesenchymal transition in an epidermal growth factor receptor-mutant lung cancer cell line with acquired resistance to erlotinib.” J Thor Onc. 6(7):1-10.

Dannenberg, J-H. and A. Berns (2010). “Drugging drug resistance.” Cell. 141:18-20.

Sharma, S.V., D.Y. Lee, et al. (2010). “A chromatin-mediated reversible drug-tolerant state in cancer cell subpopulations.” Cell. 141:69-80.

Workman, P. and J. Travers. (2010). “Drug-tolerant insurgents.” Nature. 464:844-85.

Kakihana, M., T. Ohira, et al. (2009). “Induction of E-cadherin in lung cancer and interaction with growth suppression by histone deacetylase inhibition.” J Thor Oncology. 4(12):1455-65.

Witta, S.E., R.M. Gemmill, et al. (2006). “Restoring E-cadherin expression increases sensitivity to epidermal growth factor receptor inhibitors in lung cancer cell lines.” Cancer Res 66(2): 944-50.

Ramsey, J. L. M. J. Kettyle, et. al. (2013) “Entinostat Prevents Leukemia Maintenance in a Collaborating Oncogene-Dependent Model of Cytogenetically Normal Acute Myeloid Leukemia.” Stem Cells 2013(31):1434–1445.

Frys, S., M. J. Barth, et al. (2012) “Entinostat, a novel histone deacetylase (HDACi) inhibitor enhances the anti-tumor activity of Bortezomib (BTZ) in rituximab-chemotherapy sensitive and resistant lymphoma cell lines.” ASH 2012 poster.

Younes, A., F. Hernandez, et al. (2011). “The HDAC inhibitor entinostat (SNDX-275) induces clinical responses in patients with relapsed and refractory Hodgkin’s lymphoma: results of ENGAGE-501 multicenter phase 2 study.” ASH 2011 poster.

Younes, A., P.J. Rosen, et al. (2010). “ENGAGE-501: Phase II study investigating the role of epigenetic therapy with entinostat (SNDX-275) in relapsed and refractory Hodgkin’s lymphoma (HL).” ASCO 2010 poster. J Clin Oncol 28: 15s, 210 (suppl; abstr TPS298).

Ashraf, U., M.S. Czuczman, et al. (2009). “Entinostat (SNDX-275), a novel DAC inhibitor, is highly effective in rituximab-[chemotherapy]-sensitive or rituximab-[chemotherapy]-resistant lymphomas and has synergistic anti-tumor activity when combined with bortezomib.” ASH Meeting Poster.

Abraham, J., Nunez-Alvarez, Y., et al. (2014) “Lineage of origin in rhabdomyosarcoma informs pharmacological response.” Genes Dev. 28:1578-1591.

Choudhary, C., C. Kumar, et al. (2009). “Lysine acetylation targets protein complexes and co-regulates major cellular functions.” SciencExpress. 1-16.

Gore, L., M. Rothenberg, et al. (2008). “A phase I and pharmacokinetic study of the oral histone deacetylase inhibitor, MS-275, in patients with refractory solid tumors and lymphomas.” Clin Cancer Res. 14(14):4517-25.

Hauschild, A., U. Trefzer, et al. (2008). “Multicenter phase II trial of the histone deacetylase inhibitor pyridylmethyl-N-{4-[(2-aminophenyl)-carbamoyl]-benzyl}-carbamate in pretreated metastatic melanoma.” Melanoma Res. 18(4):274-78.

Gojo, I., A. Jiemjit, et al. (2007) “Phase 1 and pharmacologic study of MS-275, a histone deacetylase inhibitor, in adults with refractory and relapsed acute leukemias.” Blood. 109(7):2781-90.

Hess-Stumpp, H., T.U. Bracker, et al. (2007). “MS-275, a potent orally available inhibitor of histone deacetylases–the development of an anticancer agent.” Int J Biochem Cell Biol. 39(7-8):1388-405.

Kummar, S., M. Gutierrez, et al. (2007). “Phase I trial of MS-275, a histone deacetylase inhibitor, administered weekly in refractory solid tumors and lymphoid malignancies.” Clin Cancer Res 13(18):5411-17.

Chung, E.J., S. Lee, et al. (2005). “Histone deacetylase inhibitor pharmacodynamic analysis by multiparameter flow cytometry.” Annals Clin Lab Science. 35(4):397-405.

Ryan, Q.C., D. Headlee, et al. (2005). “Phase I and pharmacokinetic study of MS-275, a histone deacetylase inhibitor, in patients with advanced and refractory solid tumors or lymphoma.” J Clin Oncol. 23(17):3912–22.