Ripretinib and MEK inhibitors synergize to induce apoptosis in preclinical models of GIST and Systemic Mastocytosis.
Effect of gastric acid reduction and strong CYP3A induction/inhibition on the pharmacokinetics of ripretinib, a switch control tyrosine kinase inhibitor.
Population pharmacokinetics of ripretinib in patients with advanced malignancies.
Targeting the KIT activating switch control pocket: a novel mechanism to inhibit neoplastic mast cell proliferation and mast cell activation.
DCC-2618 is a potent inhibitor of wild-type and mutant KIT, including refractory Exon 17 D816 KIT mutations, and exhibits efficacy in refractory GIST and AML xenograft models
DCC-2618, a pan-KIT and PDGFRA switch control inhibitor, achieves proof-of-concept in a first-in-human study.
Translational research in a phase I proof-of-concept study supports that DCC-2618 is a pan-KIT inhibitor.
Pharmacokinetic-driven Phase I study of DCC-2618, a pan-KIT and PDGFRα inhibitor, in patients with Gastrointestinal Stromal Tumor (GIST) and other solid tumors.
Thresholds for Meaningful Change for the EQ-5D VAS and EORTC QLQ-C30 Physical and Role Functioning Scale in Gastrointestional-Related Cancers
The INVICTUS Trial: Ripretinib As ≥4th-Line Therapy In Patients With Advanced Gastrointestinal Stromal Tumors (GIST)
