Lenvatinib (Lenvima)
New oral anticancer drug Lenvima (lenvatinib) has recently been approved by Japan for the treatment of unresectable thyroid cancer. This is another important market that the drug has captured since it was approved by the United States in February of this year. Previously, lenvatinib was granted orphan drug status and priority review qualifications in the United States, Japan, and the European Union. The drug, as an innovative drug with significant public health benefits, will help address the severe unmet medical needs in the field of glandulae cancer.
Eisai dixit Lenvima novum vexillum fiet pro curatio clinica cancri thyreoidis irresectabilis. Industria valde optima est de Lenvima, et expectatur medicamentum novum nummi bovis Eisai fiet, cum venditiones annuae plus quam $1 miliardis sescenti.
According to Eisai’s official information, in a large phase III SELECT study, lenvatinib significantly prolonged the progression-free survival of radioiodine-refractory differentiated thyroid cancer compared to placebo (PFS: 18.3 months vs 3.6 months At the same time, a significantly higher proportion of patients in the lenvatinib treatment group achieved tuberculum volume reduction (65% vs 2%). In addition, in another phase II study in Japan, lenvatinib also showed good efficacy and tolerance for medullary thyroid cancer and undifferentiated thyroid cancer.
Based on these results, Lenvima was approved by the Japanese regulatory agency to become the first molecular targeted therapy for unresectable thyroid cancer (including differentiated thyroid cancer, medullary thyroid cancer, and undifferentiated thyroid cancer).
In statu, licet plura genera cancri thyroideae tractari possint, paucae sunt optiones curationis semel ingravescente. Cancer differentialis thyreoideae (DTC) est communis tumor thyreoideae malignae, et eius incidentia in annis constanter aucta est.
Lenvatinib oralis multi-receptor tyrosinum kinase (RTK) inhibitor cum nova ligandi ratione. Praeter inhibendo alias RTKs quae in tumore proliferatione et oncogenico viae significationis implicantur, potest etiam selective inhibere augmentum vascularium endotheliale factoris (VEGF) receptoris kinasi activitatis.
