Abstract
Entrectinib is a selective inhibitor of tyrosine kinases , tropomyosin receptor kinases that targets oncogenic rearrangements in Neurotropic Tyrosine Receptor kinase, c-ros oncogene 1 and Anaplastic lymphoma kinase used for the treatment of various solid tumors. Entrectinib gained its first worldwide approval in Japan in June 2019 for the treatment of NTRK fusion-positive, advanced or recurring solid tumours in adults and children. In august 15, 2019 drug got FDA approval for the treatment of solid tumors in adult and children aged 12 and above. This article summarizes current status of Entrectinib from ongoing clinical trails and ideal place for drug in therapy.
Highlights
Entrectinib gained its first worldwide approval in Japan in June 2019 for the treatment of neurotrophic tyrosine receptor kinase (NTRK) fusion-positive, advanced or recurring solid tumours in adults and children [3]
[20] Patients with advanced solid tumours and molecular changes in TrkA, ROS1 or anaplastic lymphoma kinase (ALK) were treated in fed state as either once daily in continuous 28-day cycles or in a 4 day-on 3 day-off schedule without rest
Patients with CNS and solid tumours harbouring target aberrations in NTRK1/2/3, ROS1 or ALK as well as neuroblastoma, independent of mutant spectrum were enrolled in the expansion cohorts
Summary
Highly effective and safe oral targeted therapy for advanced solid tumours with molecular altrations. The Food and Drug Administration (FDA) authorised the drug Entrectinib on August 15, 2019 for the treatment of solid tumours that have a neurotrophic tyrosine receptor kinase (NTRK) gene fusion without acquired resistance mutation in adults and children aged 12 and above [4]. Into 20 subfamilies [9] It inhibits tropomyosin receptor tyrosine kinases (TRK) TRKA, TRKB, and TRKC as well as the proto-oncogene tyrosine-protein kinase ROS1 and anaplastic lymphoma kinase (ALK) by the activation of mitogen-activated protein kinase, phosphoinositide 3-kinase, and phospholipase C-. With the addition of downstream JAK/STAT activation, ALK creates comparable signalling [11] Inhibition of these mechanisms inhibits cancer cell growth and changes the balance toward apoptosis, resulting in tumour volume reduction. Inhibition of these mechanisms inhibits cancer cell growth and changes the balance toward apoptosis, resulting in tumour volume reduction. (Fig. 2)
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