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 skjaldkirtilskrabbamein.
Eisai sagði að Lenvima muni verða nýr staðall fyrir klíníska meðferð á óskurðtæku skjaldkirtilskrabbameini. Iðnaðurinn er mjög bjartsýnn á Lenvima og búist er við að lyfið verði ný sjóðakú fyrir Eisai, með ársvelta sem fer hæst í meira en 1 milljarð dollara.
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 æxli 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).
Eins og er, þó að hægt sé að meðhöndla flestar tegundir skjaldkirtilskrabbameins, þá eru fáir möguleikar til meðferðar þegar það versnar. Mismunandi skjaldkirtilskrabbamein (DTC) er algengasta illkynja skjaldkirtilsæxlið og hefur tíðni þess aukist jafnt og þétt undanfarin ár.
Lenvatinib er fjölviðtaka týrósínkínasa (RTK) hemill til inntöku með nýjan bindingaraðferð. Auk þess að hindra önnur RTK sem taka þátt í æxlisfjölgun og krabbameinsvaldandi boðleiðum, getur það einnig hamlað sértækt æðakirtlavaxtarþáttar (VEGF) viðtaka kínasavirkni.
