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Discovery of Mcl-1-specific inhibitor AZD5991 and preclinical activity in multiple myeloma and acute myeloid leukemia

Title: Discovery of Mcl-1-specific inhibitor AZD5991 and preclinical activity in multiple myeloma and acute myeloid leukemia
Authors: Tron, AE; Belmonte, MA; Adam, A; Aquila, BM; Boise, LH; Chiarparin, E; Cidado, J; Embrey, KJ; Gangl, E; Gibbons, FD; Gregory, GP; Hargreaves, D; Hendricks, JA; Johannes, JW; Johnstone, RW; Kazmirski, SL; Kettle, JG; Lamb, ML; Matulis, SM; Nooka, AK; Packer, MJ; Peng, B; Rawlins, PB; Robbins, DW; Schuller, AG; Su, N; Yang, W; Ye, Q; Zheng, X; Secrist, JP; Clark, EA; Wilson, DM; Fawell, SE; Hird, AW
Publisher Information: NATURE PUBLISHING GROUP
Publication Year: 2018
Collection: The University of Melbourne: Digital Repository
Description: Mcl-1 is a member of the Bcl-2 family of proteins that promotes cell survival by preventing induction of apoptosis in many cancers. High expression of Mcl-1 causes tumorigenesis and resistance to anticancer therapies highlighting the potential of Mcl-1 inhibitors as anticancer drugs. Here, we describe AZD5991, a rationally designed macrocyclic molecule with high selectivity and affinity for Mcl-1 currently in clinical development. Our studies demonstrate that AZD5991 binds directly to Mcl-1 and induces rapid apoptosis in cancer cells, most notably myeloma and acute myeloid leukemia, by activating the Bak-dependent mitochondrial apoptotic pathway. AZD5991 shows potent antitumor activity in vivo with complete tumor regression in several models of multiple myeloma and acute myeloid leukemia after a single tolerated dose as monotherapy or in combination with bortezomib or venetoclax. Based on these promising data, a Phase I clinical trial has been launched for evaluation of AZD5991 in patients with hematological malignancies (NCT03218683).
Document Type: article in journal/newspaper
Language: English
ISSN: 2041-1723
Relation: https://hdl.handle.net/11343/253625
Availability: https://hdl.handle.net/11343/253625
Rights: https://creativecommons.org/licenses/by/4.0 ; CC BY
Accession Number: edsbas.F2E4CD68
Database: BASE