Presentations and Publications
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Phase 1 study of DCC-3014, an oral inhibitor of CSF1R, to assess the safety, tolerability, pharmacokinetics, and pharmacodynamics in patients with advanced solid tumors, including diffuse-type tenosynovial giant cell tumor. AACR-NCI-EORTC Conference on Molecular Targets and Cancer Therapeutics. Boston, 2019.
INVICTUS, A Phase 3, INterVentional , Double Blind, Placebo Controlled
Study to Assess the Safety and Efficacy of Ripretinib as
≥4th Line Therapy In Patients with AdvanCed Gastrointestinal
StromalTUmorS (GIST) Who Have Received Treatment with
Prior Anticancer Therapies (NCT03353753) Presentation. ESMO Congress 2019, Barcelona, Spain.
DCC-2618, a broad-spectrum inhibitor of KIT and PDGFRA mutants,synergizes with inhibitors of the MAPK pathway. ECRTC-NCI-AACR Annual Meeting, Nov 13-16, 208 Dublin, Ireland
“The KIT and PDGFRA switch-control inhibitor DCC-2618 blocks growth and survival of multiple neoplastic cell types in advanced mastocytosis.” Haematologica 2018.
“DCC-2618, a novel pan-KIT and PDGFRα kinase switch control inhibitor, shows encouraging signal in a patient with glioblastoma (GBM)” Society for NeuroOncology 22nd Annual Scientific Meeting and Education, San Francisco, CA.
“The selective TIE2 inhibitor rebastinib blocks recruitment and function of TIE2Hi macrophages in breast cancer and pancreatic neuroendocrine tumors.” Mol Cancer Thera 16: 2486-2501.
“Discovery and Development of DCC-3014, a Highly Specific Inhibitor of CSF1R Kinase.” CHI Discovery on Target: Targeting Tumor Myeloid Cells. Boston, MA.
“Encouraging activity of novel pan-KIT and PDGFRα inhibitor DCC-2618 in patients (pts) with gastrointestinal stromal tumor. (GIST)” ESMO 2017 Annual Meeting, Madrid, Spain.
“Neoadjuvant chemotherapy induces breast cancer metastasis through a TMEM-mediated mechanism.” Sci. Transl. Med. 9, eaan0026 (2017)
“Pharmacokinetic-driven phase I study of DCC-2618 a pan-KIT and PDGFR inhibitor in patients (pts) with gastrointestinal stromal tumor (GIST) and other solid tumors.” ASCO 2017 Annual Meeting, Chicago, Il. Abstract# 2515
“Translational research in a phase I proof-of-concept study supports that DCC-2618 is a pan-KIT inhibitor.” AACR 2017 Annual Meeting, Washington DC. Abstract# LB-039.
“Phase 1 dose-finding study of rebastinib (DCC-2036) in patients with relapsed chronic myeloid leukemia and acute myeloid leukemia.” Haematologica 102: 519-528.
DCC-2618, a pan-KIT and PDGFRA switch control inhibitor, achieves proof-of-concept in a first-in-human study.” 2016 EORTC-NCI-AACR, Munich, Germany.
“The multi-kinase inhibitor DCC-2618 inhibits proliferation and survival of neoplastic mast cells and other cell types involved in systemic mastocytosis.” 58th ASH Annual Meeting, San Diego, CA.
“Novel MET/TIE2/VEGFR2 inhibitor altiratinib inhibits tumor growth and invasiveness in bevacizumab-resistant glioblastoma mouse models.” Neuro Oncology 18: 1230-1241.
“Oncogenic BRaf Deletions That Function as Homodimers and Are Sensitive to Inhibition by Raf Dimer Inhibitor LY3009120”, Cancer Discovery 2016; Jan. online.
“Altiratinib Inhibits Tumor Growth, Invasion, Angiogenesis, and Microenvironment-Mediated Drug Resistance via Balanced Inhibition of MET, TIE2, and VEGFR2.” Mol Cancer Ther. 2015; 14(9):2023-34.
“Inhibition of RAF Isoforms and Active Dimers by LY3009120 Leads to Anti-tumor Activities in RAS or BRAF Mutant Cancers.” Cancer Cell 2015; 28:384-98.
“Discovery of 1‑(3,3-Dimethylbutyl)-3-(2-fluoro-4-methyl-5-(7-methyl-2-(methylamino)pyrido[2,3‑d]pyrimidin-6-yl)phenyl)urea (LY3009120) as a Pan-RAF Inhibitor with Minimal Paradoxical Activation and Activity against BRAF or RAS Mutant Tumor Cells.” J. Medicinal Chemistry 2015; 58, 4165−79.
“DCC-2618 is a potent inhibitor of wild type and mutant KIT, including refractory Exon 17 D816 KIT mutations.” AACR 106th Annual Meeting, Philadelphia, PA. Cancer Res 75(15 Suppl); Abstract 2690
“Altiratinib is a potent inhibitor of TRK kinases and is efficacious in TRK-fusion driven cancer models.” AACR 106th Annual Meeting, Philadelphia, PA. Cancer Res 75(15 Suppl): Abstract 790.
“Rebastinib potently inhibits function of perivascular TIE2 expressing macrophages in vitro and in vivo.” AACR 106th Annual Meeting, Philadelphia, PA. Cancer Res 75(15 Suppl): Abstract 397.
“Imaging the tumor microenvironment of metastasis reveals the mechanism of transient blood vessel permeability and tumor cell intravasation.” AACR 106th Annual Meeting, Philadelphia, PA. Cancer Res 75(15 Suppl): Abstract 5125.
“Mechanisms of transendothelial migration by invasive breast carcinoma cells from patients.” AACR 106th Annual Meeting, Philadelphia, PA. Cancer Res 75(15 Suppl): Abstract 4112.
“Mouse PDX Trial Suggests Combination Efficacy of Raf and EGFR Inhibition in Colorectal Cancer with BRaf or KRas mutation.” [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr LB-004.
“Novel oncogenic BRaf deletions functioning as BRaf homodimer and sensitive to inhibition by LY3009120, a pan Raf and Raf dimer inhibitor.” [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2142.
“Inhibiting endothelium directed tumor cell streaming by targeting the HGF/c-MET and EGF/CSF-1 signaling pathways.” AACR 106th Annual Meeting, Philadelphia, PA. Cancer Res 75(15 Suppl): Abstract 5091.
“Altiratinib (DCC-2701): a balanced inhibitor of MET, TIE2, and VEGFR2 kinases that exhibits broad anti-tumor and anti-angiogenic activities.” 26th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics, Barcelona, Spain.
“The novel c-MET inhibitor altiratinib (DCC-2701) inhibits tumor growth and invasion in a bevacizumab resistant glioblastoma mouse model.” Society for Neuro-Oncology Annual Meeting, Miami, FL. Neuro Oncol 16(suppl 5): v6.
“Identification of LY3009120 as a pan inhibitor of Raf isoforms and dimer with activity against BRaf or Ras mutant tumor cells and minimal paradoxical activation.” AACR Annual Meeting, San Diego, CA. Cancer Res 74(19 Suppl): Abstract DDT02-02.
“Rebastinib, a selective TIE2 kinase inhibitor, decreases TIE2-expressing macrophages, reduces metastasis, and increases survival in murine cancer models.” AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment Meeting, Cancer Res 75(1 Suppl): Abstract PR01. San Diego, CA.
“Rebastinib, a selective TIE2 kinase inhibitor, decreases TIE2-expressing macrophages, reduces metastasis, and increases survival in murine cancer models.” AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment Meeting, San Diego, CA. Cancer Res 75(1 Suppl): Abstract PR01.
“The specific FMS kinase inhibitor, DCC-3014, durably inhibits FMS kinase in vivo and blocks cancer bone invasiveness.” AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment Meeting, San Diego, CA. Cancer Res 75(1 Suppl): Abstract A53.
“Rebastinib in combination with paclitaxel ablates TIE2-expressing macrophages, reduces metastasis, and increases survival in the PyMT metastatic breast cancer model.” San Antonio Breast Cancer Symposium, San Antonio, TX 2013
“Rebastinib in combination with eribulin ablates TIE2-expressing macrophages, reduces metastasis, and increases survival in the PyMT metastatic breast cancer model.” San Antonio Breast Cancer Symposium, San Antonio, TX 2013
“Effective inhibition of c-MET-mediated signaling, growth and migration of ovarian cancer cells is influenced by the ovarian tissue microenvironment.” Oncogene, December 2013
“Use of μCT imaging in the PyMT breast cancer model to monitor lung metastasis development and determine therapeutic benefit in real time.” AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics, Boston, MA. Mol Cancer Ther November 2013 12; B145
“Selective FMS Kinase inhibitors for Cancer.” 11th Annual CHI Discovery on Target, Boston, MA 2013
“Rebastinib and DCC-2701: Targeting of resistance mechanisms in cancer treatment.” 245th National American Chemical Society Symposium, New Orleans, LA 2013
“Targeting the KIT activating switch control pocket: a novel mechanism to inhibit neoplastic mast cell proliferation and mast cell activation.” Leukemia 2012; 27:278-85.
“Rebastinib, a small molecule TIE2 kinase inhibitor, prevents primary tumor growth and lung metastasis in the PyMT breast cancer model.” AACR Special Conference on Tumor Invasion and Metastasis; San Diego, CA. Cancer Res February 1, 2013 73; B78
“A phase 1 study of DCC-2036, a novel oral inhibitor of BCR-ABL kinase, in adult subjects with Philadelphia chromosome positive (Ph+) leukemias including subjects with T315I mutation.” American Society of Hematology Annual Meeting, San Diego, CA. Blood (ASH Annual Meeting Abstracts) 118: 601.
“The ABL Switch Control Inhibitor DCC-2036 Is Active against the Chronic Myeloid Leukemia Mutant BCR-ABLT315I and Exhibits a Narrow Resistance Profile”, Cancer Research, Volume 71, Issue 9, 3189-95, April 2011
“Conformational Control Inhibition of the BCR-ABL1 Tyrosine Kinase, Including the Gatekeeper T315I Mutant, by the Switch-Control Inhibitor DCC-2036”, Cancer Cell, Volume 19, Issue 4, 556-568, April 2011
“Targeted Inhibition of Multiple Receptor Tyrosine Kinases in Mesothelioma.” Neoplasia, Volume 13, Number 1 , 12-22, January 2011
“Switch Control Pocket Inhibitors of p38-MAP Kinase. Durable Type II Inhibitors that do not Require Binding into the Canonical ATP Hinge Region”, Bioorg. Med. Chem Letters, Vol 20, Issue 19, 5793-5798, October 2010
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