Deciphera Pharmaceut?icals Announces Initiation of Phase 1 Cancer Trial of Kinase Inhibitor for Solid Tumours

Deciphera Pharmaceuticals, a clinical stage biotechnology company focused on improved kinase inhibitor treatments for cancer, has announced the initiation of a Phase I clinical trial of its MET/TIE2/VEGFR2/TRK inhibitor altiratinib (DCC-2701). The Phase I trial will evaluate the safety, tolerability and initial efficacy of altiratinib in cancer patients with solid tumours. Altiratinib has been shown to exhibit high potency and selectivity for inhibiting MET, TIE2, VEGFR2, and TRK kinases in preclinical studies. Companion diagnostic assays have also been developed to support clinical study.

In preclinical cancer models, altiratinib has shown impressive activity against multiple tumors including breast, melanoma, colorectal, ovarian, glioblastoma and gastric cancers.

“We are pleased to advance altiratinib into clinical development based on the encouraging preclinical data demonstrated to date,” says Michael D. Taylor, PhD, Deciphera’s President and Chief Executive Officer. “With its balanced inhibition of key kinase mechanisms, including MET, TIE2, VEGFR2 and TRK, altiratinib was designed to address both tumour cells and the tumour microenvironment by providing high potency and inhibition against cancer cells, metastases and invasiveness. We look forward to reporting on our progress with altiratinib, which has the potential to provide an important new option for cancer patients with solid tumours.”

Altiratinib is an oral, small molecule shown to exhibit high potency and selectivity for inhibiting MET, TIE2, VEGFR2 and TRK kinases in cellular and in vivo cancer studies. Inhibition of MET kinase blocks a key mechanism in tumour cells that causes cancer invasiveness and metastasis. Altiratinib also inhibits activation loop oncogenic MET mutants known to drive certain cancers. Inhibition of these key kinases also blocks major mechanisms of tumour microenvironment invasiveness and metastasis. By inhibiting these kinases we block the mechanisms that tumours use to build new blood vessels required for tumour growth offering the potential to more durably inhibit tumour blood vessel formation than approaches that only impact one of these pathways. In addition, inhibition of TRK signaling has been shown to be an important mechanism for treatment of a wide range of tumours.