Ignyta (RXDX) Will Present RXDX-106 Preclinical Data at Upcoming Conference

November 29, 2016 6:11 AM EST

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Ignyta, Inc. (Nasdaq: RXDX) announced its first disclosed preclinical data on RXDX-106—its potent, selective, type II pseudo-irreversible inhibitor of TYRO3, AXL and MER (or TAM) and c-MET—will be presented at the 2016 EORTC-NCI-AACR (ENA) Molecular Targets and Cancer Therapeutics Symposium in Munich, Germany, highlighting both the immuno-oncology and targeted therapeutic activity of this novel agent. Additionally, the company will present data on multiple compounds in clinical development from its robust pipeline of molecularly targeted oncology therapies, including entrectinib—an orally available, CNS-penetrant tyrosine kinase inhibitor targeting tumors that harbor TRK, ROS1 or ALK fusions—and RXDX-105—a VEGFR-sparing, potent RET inhibitor.

“We are pleased to introduce preclinical data on RXDX-106 at ENA alongside our promising clinical data for entrectinib and RXDX-105,” said Jonathan Lim, M.D., Chairman and CEO of Ignyta. “RXDX-106 is an intriguing, novel agent that may offer a dual mechanism by potentiating the immune system, while also providing selective activity against key molecular targets involved in both primary oncogenesis and resistance.”

In the presented preclinical data on RXDX-106, researchers demonstrated that the agent is a potent and selective inhibitor of TAM and c-MET, and inhibited TAM-mediated and c-MET-mediated tumor growth in vivo. Additionally, researchers demonstrated, via in vitro and in vivo studies, that RXDX-106, as a single agent, appears to release the molecular brakes on immune activation in macrophages, NK cells, and T cells, resulting in the repolarization of the immune response to elicit an anti-tumor effect. Furthermore, emerging in vivo combination data suggest that RXDX-106 potentiates the activity of anti-PD-1 and anti-CTLA-4 agents. These data further support the continued evaluation of RXDX-106 in both a preclinical and clinical setting (Abstract number 73, Poster number P044; Abstract number 65, Poster number P036).

Also presented as part of this poster session were preclinical data on RXDX-105 demonstrating significant anti-tumor activity in models harboring RET fusions (Abstract number 85, Poster number P056), as well as preclinical data on entrectinib showing potent anti-tumor activity in multiple different tumor model systems driven by NTRK1/2/3, ROS1 and ALK fusions, regardless of the fusion partners or the tumor tissue of origin (Abstract number 78, Poster number P049). Additional clinical data on RXDX-105 and entrectinib will be presented later in the week at ENA.



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