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 skjoldbruskkreft.
Eisai sa at Lenvima vil bli den nye standarden for klinisk behandling av ikke-opererbar kreft i skjoldbruskkjertelen. Bransjen er veldig optimistisk med tanke på Lenvima, og det er forventet at stoffet vil bli en ny kontantku for Eisai, med en årlig omsetning på over 1 milliard dollar.
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 svulst 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).
For øyeblikket, selv om de fleste typer kreft i skjoldbruskkjertelen kan behandles, er det få alternativer for behandling når det blir verre. Differensiell skjoldbruskkjertelkreft (DTC) er den vanligste maligne skjoldbruskkjertelsvulsten, og forekomsten har økt jevnt de siste årene.
Lenvatinib er en oral multi-reseptor tyrosinkinase (RTK) hemmer med en ny bindingsmodus. I tillegg til å hemme andre RTK-er involvert i tumorproliferasjon og onkogene signalveier, kan det også selektivt hemme vaskulær endotelial vekstfaktor (VEGF) reseptorkinaseaktivitet.
