Publications

Extensive Research Supports Clinical Development of
Entinostat and SNDX-6352

Entinostat / Immunomodulation

Johnson M. et al. (2017, June). “ENCORE 601: A Phase 2 study of entinostat (ENT) in combination with pembrolizumab (PEMBRO) in patients with melanoma.” Poster presented at the American Society of Clinical Oncology Annual Meeting, Chicago, IL.

Johnson M., A. Adjei, et al. (2016, November). “Dose-escalation/confirmation results of ENCORE 601, a Phase 1b/2, open-label study of entinostat (ENT) in combination with pembrolizumab (PEMBRO) in patients with non–small cell lung cancer (NSCLC).” Poster presented at the Society for the Immunotherapy of Cancer Annual Meeting, National Harbor, MD.

Gameiro SR, AS Malamas, et al. (2016). “Inhibitors of histone deacetylase 1 reverse the immune evasion phenotype to enhance T-cell mediated lysis of prostate and breast carcinoma cells.” Oncotarget. 7(7):7390-402.

Shen, L., A. Orillion, R. Pili. (2016). “Histone deacetylase inhibitors as immunomodulators in cancer therapeutics.” Epigenomics. 8(3):415-28.

Park J., S. Thomas, and P. Munster. (2015). “Epigenetic modulation with histone deacetylase inhibitors in combination with immunotherapy”. Epigenomics. 7(4):641-52.

Kim, K., A. Skora, et al. (2014). “Eradication of metastatic mouse cancers resistant to immune checkpoint blockade by suppression of myeloid-derived cells.” PNAS. 111(32):11774-9.

Youn JI, V. Kumar, et al. (2013). “Epigenetic silencing of retinoblastoma gene regulates pathologic differentiation of myeloid cells in cancer.” Nat. Immunol. 14(3): 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(3): 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): e30815.

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(7): 598–607.
Entinostat / Breast Cancer

Merino, VF., N. Nguyen, et al. (2016). “Combined Treatment with Epigenetic, Differentiating, and Chemotherapeutic Agents Cooperatively Targets Tumor-Initiating Cells in Triple-Negative Breast Cancer.” Cancer Res. 76(7):2013-24.

Tomita, Y., M. Lee, et al. (2016). “The interplay of epigenetic therapy and immunity in locally recurrent or metastatic estrogen receptor-positive breast cancer: Correlative analysis of ENCORE 301, a randomized, placebo controlled phase II trial of exemestane with or without entinostat.” OncoImmunology. DOI: 10.1080/2162402X.2016.1219008

Schech A, A. Kazi, et al. (2015). “Histone Deacetylase Inhibitor Entinostat Inhibits Tumor-Initiating Cells in Triple-Negative Breast Cancer Cells.” Mol Cancer Ther. 14(8): 1848–1857.

Connolly R. et al. (2014, December). “E2112: A randomized phase III trial of endocrine therapy plus entinostat or placebo in patients with hormone receptor-positive advanced breast cancer.” Poster presented at the San Antonio Breast Cancer Symposium, San Antonio, TX.

Sabnis, G., O. Goloubeva, et al. (2013). “HDAC inhibitor entinostat restores responsiveness of letrozole resistant MCF-7Ca xenografts to AIs through modulation of Her-2.” Mol Cancer Ther. 12(12):2804-16.

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. 143(1):99-111.

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.” J Clin Oncol. 31(17):2128-35.

Connolly, R., and V. Stearns (2012). “Epigenetics as a therapeutic target in breast cancer.” J Mammary Gland Biol Neoplasia. 17(3-4):191-204.

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.
Entinostat / Other

Batlevi CL, Y. Kasamon, et al. (2016). “ENGAGE- 501: phase II study of entinostat (SNDX-275) in relapsed and refractory Hodgkin lymphoma.” Haematologica. 101(8):968-75.

Wang S., L. Zhu, et al. (2016). “MicroRNA-mediated epigenetic targeting of Survivin significantly enhances the antitumor activity of paclitaxel against non-small cell lung cancer.” Oncotarget. doi: 10.18632/oncotarget.9264.

Frys S., Z. Simons, et al. (2015). “Entinostat, a novel histone deacetylase inhibitor is active in B-cell lymphoma and enhances the anti-tumour activity of rituximab and chemotherapy agents.” Br J Haematol. 169(4):506-19.
SNDX-6352 / Targeting CSF-1R

Ordentlich P., P. Vajjah, et. al. (2016, November). “Targeting colony stimulating factor- 1 receptor (CSF-1R) with SNDX-6352, a novel anti-CSF-1R targeted antibody.” Poster presented at the Society for the Immunotherapy of Cancer Annual Meeting, National Harbor, MD.

Ruffell B., and L. Coussens (2015). “Macrophages and Therapeutic Resistance in Cancer.” Cancer Cell. 27(4):462-72.