Plitidepsin: a potential new treatment for relapsed/refractory multiple myeloma

被引：39

作者：

Leisch, Michael ^{[1
,2
]}

Egle, Alexander ^{[1
,2
]}

Greil, Richard ^{[1
,2
]}

机构：

[1] Paracelsus Med Univ, Dept Internal Med Haematol Med Oncol Haemostaseol, Ctr Oncol, SCRI,LIMCR, Salzburg, Austria

[2] Canc Cluster Salzburg, Salzburg, Austria

来源：

FUTURE ONCOLOGY | 2019年 / 15卷 / 02期

关键词：

Aplidin; eukaryotic translation elongation factor 1 2; multiple myeloma; plitidepsin; I DOSE-ESCALATION; EVERY; 2; WEEKS; PHASE-II; 2ND-LINE THERAPY; HEMATOPOIETIC PROGENITORS; BIWEEKLY PLITIDEPSIN; LEUKEMIC-CELLS; VITRO TOXICITY; CANCER-CELLS; SOLID TUMORS;

D O I：

10.2217/fon-2018-0492

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Plitidepsin is a marine-derived anticancer compound isolated from the Mediterranean tunicate Applidium albicans. It exerts pleiotropic effects on cancer cells, most likely by binding to the eukaryotic translation eEF1A2. This ultimately leads to cell-cycle arrest, growth inhibition and induction of apoptosis via multiple pathway alterations. Recently, a Phase III randomized trial in patients with relapsed/refractory multiple myeloma reported outcomes for plitidepsin plus dexamethasone compared with dexamethasone. Median progression-free survival was 3.8 months in the plitidepsin arm and 1.9 months in the dexamethasone arm (HR: 0.611; p=0.0048). Here, we review preclinical data regarding plitidepsins mechanism of action, give an overview of clinical trial results across different tumor types as well as the latest results in multiple myeloma.

引用

页码：109 / 120

页数：12

共 63 条

[1] In vitro toxicity of ET-743 and aplidine, two marine-derived antineoplastics, on human bone marrow haematopoietic progenitors:: comparison with the clinical results [J].