TY - JOUR
T1 - Combining the Allosteric Inhibitor Asciminib with Ponatinib Suppresses Emergence of and Restores Efficacy against Highly Resistant BCR-ABL1 Mutants
AU - Eide, Christopher A.
AU - Zabriskie, Matthew S.
AU - Savage Stevens, Samantha L.
AU - Antelope, Orlando
AU - Vellore, Nadeem A.
AU - Than, Hein
AU - Schultz, Anna Reister
AU - Clair, Phillip
AU - Bowler, Amber D.
AU - Pomicter, Anthony D.
AU - Yan, Dongqing
AU - Senina, Anna V.
AU - Qiang, Wang
AU - Kelley, Todd W.
AU - Szankasi, Philippe
AU - Heinrich, Michael C.
AU - Tyner, Jeffrey W.
AU - Rea, Delphine
AU - Cayuela, Jean Michel
AU - Kim, Dong Wook
AU - Tognon, Cristina E.
AU - O'Hare, Thomas
AU - Druker, Brian J.
AU - Deininger, Michael W.
N1 - Publisher Copyright:
© 2019 Elsevier Inc.
PY - 2019/10/14
Y1 - 2019/10/14
N2 - Most clinical BCR-ABL1 compound mutants are insensitive to current clinical tyrosine kinase inhibitors. Eide et al. show that adding asciminib, an allosteric inhibitor, to ponatinib, an ATP site inhibitor, effectively targets compound mutants and provides a potential mechanism for the collaborative effect.
AB - Most clinical BCR-ABL1 compound mutants are insensitive to current clinical tyrosine kinase inhibitors. Eide et al. show that adding asciminib, an allosteric inhibitor, to ponatinib, an ATP site inhibitor, effectively targets compound mutants and provides a potential mechanism for the collaborative effect.
KW - ABL001
KW - allosteric inhibitors
KW - asciminib
KW - chronic myeloid leukemia
KW - compound mutation
KW - ponatinib
KW - targeted therapy
UR - http://www.scopus.com/inward/record.url?scp=85072922152&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85072922152&partnerID=8YFLogxK
U2 - 10.1016/j.ccell.2019.08.004
DO - 10.1016/j.ccell.2019.08.004
M3 - Article
C2 - 31543464
AN - SCOPUS:85072922152
SN - 1535-6108
VL - 36
SP - 431-443.e5
JO - Cancer Cell
JF - Cancer Cell
IS - 4
ER -