Clinical Benefit of Ripretinib Dose Escalation After Disease Progression in Advanced Gastrointestinal Stromal Tumor: An Analysis of the INVICTUS Study.
Dermatopathological review of cutaneous squamous cell carcinoma events in patients with gastrointestinal stromal tumor treated with ripretinib.
Ripretinib and MEK inhibitors synergize to induce apoptosis in preclinical models of GIST and Systemic Mastocytosis.
Population pharmacokinetics of ripretinib in patients with advanced malignancies.
Discovery of vimseltinib (DCC -3014), a highly selective switch -control inhibitor of CSF1R kinase.
Discovery of ULK1/2 inhibitor DCC 3116 for treatment of RAS driven cancers.
A phase 1 study of rebastinib and carboplatin in patients with metastatic solid tumors.
A phase 1b/2 study of rebastinib and paclitaxel in advanced or metastatic platinum-resistant ovarian cancer.
Switch Control Inhibition of KIT and PDGFRA in Patients With Advanced Gastrointestinal Stromal Tumor: A Phase I Study of Ripretinib.
Ripretinib in patients with advanced gastrointestinal stromal tumours (INVICTUS): a double-blind, randomised, placebo-controlled, phase 3 trial.
Preclinical studies with DCC-3116, an ULK kinase inhibitor designed to inhibit autophagy as a potential strategy to address mutant RAS cancers.
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 Stromal TUmorS (GIST) Who Have Received Treatment with Prior Anticancer Therapies (NCT03353753).
The INVICTUS Trial: Ripretinib As ≥4th-Line Therapy In Patients With Advanced Gastrointestinal Stromal Tumors (GIST)
DCC-3116: A Selective ULK Kinase Inhibitor; Potential First-in-Class Autophagy Inhibitor to Treat Mutant RAS Cancers
Ripretinib (DCC-2618) Is a Switch Control Kinase Inhibitor of a Broad Spectrum of Oncogenic and Drug-Resistant KIT and PDGFRA Variants.
DCC-2618, a broad-spectrum inhibitor of KIT and PDGFRA mutants,synergizes with inhibitors of the MAPK pathway.
Mutation Profile of Drug Resistant GIST Patients Enrolled in the Phase 1 Study of DCC-2618
Inhibition of oncogenic and drug-resistant PDGFRA and KIT alterations by DCC-2618.
The KIT and PDGFRA switch-control inhibitor DCC-2618 blocks growth and survival of multiple neoplastic cell types in advanced mastocytosis.
DCC-2618, a novel pan-KIT and PDGFRα kinase switch control inhibitor, shows encouraging signal in a patient with glioblastoma (GBM).
The selective TIE2 inhibitor rebastinib blocks recruitment and function of TIE2Hi macrophages in breast cancer and pancreatic neuroendocrine tumors.
Encouraging activity of novel pan-KIT and PDGFRα inhibitor DCC-2618 in patients (pts) with gastrointestinal stromal tumor. (GIST)
Neoadjuvant chemotherapy induces breast cancer metastasis through a TMEM-mediated mechanism.
Translational research in a phase I proof-of-concept study supports that DCC-2618 is a pan-KIT inhibitor.
Phase 1 dose-finding study of rebastinib (DCC-2036) in patients with relapsed chronic myeloid leukemia and acute myeloid leukemia.
DCC-2618, a pan-KIT and PDGFRA switch control inhibitor, achieves proof-of-concept in a first-in-human study.
The highly specific CSF1R inhibitor DCC-3014 exhibits Immunomodulatory and anti-invasive activities in cancer models.
DCC-2618 is a potent inhibitor of wild type and mutant KIT, including refractory Exon 17 D816 KIT mutations.
Rebastinib potently inhibits function of perivascular TIE2 expressing macrophages in vitro and in vivo.
Mechanisms of transendothelial migration by invasive breast carcinoma cells from patients.
Inhibiting endothelium directed tumor cell streaming by targeting the HGF/c-MET and EGF/CSF-1 signaling pathways.
The specific FMS kinase inhibitor, DCC-3014, durably inhibits FMS kinase in vivo and blocks cancer bone invasiveness.
Rebastinib in combination with paclitaxel ablates TIE2-expressing macrophages, reduces metastasis, and increases survival in the PyMT metastatic breast cancer model.
Rebastinib in combination with eribulin ablates TIE2-expressing macrophages, reduces metastasis, and increases survival in the PyMT metastatic breast cancer model.
Targeting the KIT activating switch control pocket: a novel mechanism to inhibit neoplastic mast cell proliferation and mast cell activation.
The ABL Switch Control Inhibitor DCC-2036 Is Active against the Chronic Myeloid Leukemia Mutant BCR-ABLT315I and Exhibits a Narrow Resistance Profile.
Conformational Control Inhibition of the BCR-ABL1 Tyrosine Kinase, Including the Gatekeeper T315I Mutant, by the Switch-Control Inhibitor DCC-2036.
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