Presentations and Publications

Ripretinib and MEK inhibitors synergize to induce apoptosis in preclinical models of GIST and Systemic Mastocytosis. Molecular Cancer Therapeutics, 2021.

Effect of gastric acid reduction and strong CYP3A induction/inhibition on the pharmacokinetics of ripretinib, a switch control tyrosine kinase inhibitor, AACR 2021

Discovery of ULK1/2 inhibitor DCC 3116 for treatment of RAS driven cancers. Autophagy Summit

Ripretinib demonstrated activity across all KIT/PDGFRA mutations in patients with fourth-line advanced gastrointestinal stromal tumor: Analysis from the phase 3 INVICTUS study. CTOS Annual Meeting.

Ripretinib Intra-Patient Dose Escalation Following Disease Progression Provides Clinically Meaningful Progression-Free Survival in Gastrointestinal Stromal Tumor in Phase 1 Study. CTOS Annual Meeting.

Ripretinib Intra-patient Dose Escalation (IPDE) Following Disease Progression Provides Clinically Meaningful Progression Free Survival (PFS) in Gastrointestinal Stromal Tumor (GIST) in Phase 1 Study. ESMO 2020 Virtual Meeting.

A phase 1 study of rebastinib and carboplatin in patients with metastatic solid tumors. ESMO 2020 Virtual Meeting.

Switch Control Inhibition of KIT and PDGFRA in Patients With Advanced Gastrointestinal Stromal Tumor: A Phase I Study of Ripretinib.  Journal of Clinical Oncology 38, 2020

Ripretinib in patients with advanced gastrointestinal stromal tumours (INVICTUS): a double-blind, randomised, placebo-controlled, phase 3 trial. The Lancet Oncology, S1470-2045(20) 30168-6.

Quality of life (QoL) and self reported function with ripretinib in ≥4th line therapy for patients with gastrointestinal stromal tumors (GIST): Analyses from INVICTUS. Abstract: 11535, Poster: 423, ASCO.

INVICTUS, A Phase 3, interventional, double blind, placebo controlled study to assess the safety and efficacy of ripretinib (DCC 2618) in patients with advanced gastrointestinal stromal tumors (GIST) who have received treatment with prior anticancer therapies. Connective Tissue Oncology Society (CTOS) Annual Meeting; Tokyo, Japan.

Updated results of phase 1 study of ripretinib (DCC-2618), a broad spectrum KIT and PDGFRA inhibitor, in patients with gastrointestinal stromal tumor (GIST) by line of therapy (NCT02571036). AACR-NCI-EORTC Conference on Molecular Targets and Cancer Therapeutics. Boston, 2019.

Phase 1b/2 study of rebastinib (DCC-2036) in combination with paclitaxel: Preliminary safety, efficacy, pharmacokinetics, and pharmacodynamics in patients with advanced or metastatic solid tumors. 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.

Ripretinib (DCC-2618) Pharmacokinetics (PK) in a Phase 1 Study in Patients with Gastrointestinal Stromal Tumors (GIST) and other Advanced Malignancies: A Retrospective Evaluation of the PK Effects of Proton Pump Inhibitors (PPIs). AACR 2019 Annual Meeting, Atlanta, GA.
Abstract CT058

Initial Results of Phase 1 Study of DCC-2618, a Broad-Spectrum KIT and PDGFR⍺ Inhibitor, in Patients (PTS) with Gastrointestinal Stromal Tumor (GIST) by Number of Prior Regimens.  ESMO Congress 2018, Munich, Germany.

Inhibition of oncogenic and drug-resistant PDGFRA and KIT alterations by DCC-2618. 2018 American Association for Cancer Research (AACR) Annual Meeting. Chicago, IL.

“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 demonstrates encouraging activity in patients (pts) with Gastrointestinal Stromal Tumors (GIST).” CTOS 2017 Annual Meeting, Maui, HI.

“Discovery and Development of DCC-3014, a Highly Specific Inhibitor of CSF1R Kinase.” CHI Discovery on Target: Targeting Tumor Myeloid Cells. Boston, MA.

“Neoadjuvant chemotherapy induces breast cancer metastasis through a TMEM-mediated mechanism.” Sci. Transl. Med. 9, eaan0026 (2017)

“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.

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.

“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.

“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.

“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

“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.

“Mechanisms of transendothelial migration by invasive breast carcinoma cells from patients.” AACR 106th Annual Meeting, Philadelphia, PA. Cancer Res 75(15 Suppl): Abstract 4112.

“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.

“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.

“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.

“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 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

“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

“Rebastinib and DCC-2701: Targeting of resistance mechanisms in cancer treatment.” 245th National American Chemical Society Symposium, New Orleans, LA 2013

“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

“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

“Targeted Inhibition of Multiple Receptor Tyrosine Kinases in Mesothelioma.” Neoplasia, Volume 13, Number 1 , 12-22, January 2011