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

Adriana E. Tron(AstraZeneca (United States)), Matthew A. Belmonte(Sage Therapeutics (United States)), Ammar Adam(Cambridge Scientific (United States)), Brian Aquila(Alkermes (United States)), Lawrence Boise(Emory University), Elisabetta Chiarparin(AstraZeneca (United Kingdom)), Justin Cidado(AstraZeneca (United States)), Kevin J. Embrey(AstraZeneca (United Kingdom)), Eric T. Gangl(AstraZeneca (United States)), Francis D. Gibbons(AstraZeneca (United States)), Gareth P. Gregory(Peter MacCallum Cancer Centre), David Hargreaves(AstraZeneca (United Kingdom)), J. Adam Hendricks(AstraZeneca (United States)), Jeffrey W. Johannes(AstraZeneca (United States)), Ricky W. Johnstone(Peter MacCallum Cancer Centre), Steven L. Kazmirski(Fulcrum Therapeutics (United States)), Jason G. Kettle(AstraZeneca (United Kingdom)), Michelle L. Lamb(AstraZeneca (United States)), Shannon M. Matulis(Emory University), Ajay K. Nooka(Emory University), Martin J. Packer(AstraZeneca (United Kingdom)), Bo Peng(AstraZeneca (United States)), Philip B. Rawlins(AstraZeneca (United Kingdom)), Daniel Robbins(AstraZeneca (United States)), Alwin G. Schuller(AstraZeneca (United States)), Nancy Su(AstraZeneca (United States)), Wenzhan Yang(AstraZeneca (United States)), Qing Ye(AstraZeneca (United States)), Xiaolan Zheng(AstraZeneca (United States)), J. Paul Secrist(Sage Therapeutics (United States)), Edwin Clark(AstraZeneca (United States)), David M. Wilson(AstraZeneca (United Kingdom)), Stephen E. Fawell(AstraZeneca (United States)), Alexander W. Hird(AstraZeneca (South Korea))
Nature Communications
December 11, 2018
Cited by 485Open Access
Full Text

Abstract

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).


Related Papers