Biochemical characterization of tirabrutinib and other irreversible inhibitors of Bruton's tyrosine kinase reveals differences in on - and off - target inhibition.


Journal

Biochimica et biophysica acta. General subjects
ISSN: 1872-8006
Titre abrégé: Biochim Biophys Acta Gen Subj
Pays: Netherlands
ID NLM: 101731726

Informations de publication

Date de publication:
04 2020
Historique:
received: 27 08 2019
revised: 23 12 2019
accepted: 13 01 2020
pubmed: 19 1 2020
medline: 15 9 2020
entrez: 19 1 2020
Statut: ppublish

Résumé

Bruton's tyrosine kinase (BTK) is a key component of the B-cell receptor (BCR) pathway and a clinically validated target for small molecule inhibitors such as ibrutinib in the treatment of B-cell malignancies. Tirabrutinib (GS-4059/ONO-4059) is a selective, once daily, oral BTK inhibitor with clinical activity against many relapsed/refractory B-cell malignancies. Covalent binding of tirabrutinib to BTK Cys-481 was assessed by LC-MSMS analysis of BTK using compound as a variable modification search parameter. Inhibition potency of tirabrutinib, ibrutinib, acalabrutinib, and spebrutinib against BTK and related kinases was studied in a dose-dependent manner either after a fixed incubation time (as used in conventional IC Tirabrutinib irreversibly and covalently binds to BTK Cys-481. The inactivation efficiency k For the BTK inhibitors tested in this study, analysis of the inactivation kinetics yielded a more accurate measurement of potency and selectivity than conventional single-time point inhibition measurements. Subtle but clear differences were identified between clinically tested BTK inhibitors which may translate into differentiated clinical efficacy and safety. This is the first study that offers a detailed side-by-side comparison of four clinically-relevant BTK inhibitors with respect to their inactivation of BTK and related kinases.

Sections du résumé

BACKGROUND
Bruton's tyrosine kinase (BTK) is a key component of the B-cell receptor (BCR) pathway and a clinically validated target for small molecule inhibitors such as ibrutinib in the treatment of B-cell malignancies. Tirabrutinib (GS-4059/ONO-4059) is a selective, once daily, oral BTK inhibitor with clinical activity against many relapsed/refractory B-cell malignancies.
METHODS
Covalent binding of tirabrutinib to BTK Cys-481 was assessed by LC-MSMS analysis of BTK using compound as a variable modification search parameter. Inhibition potency of tirabrutinib, ibrutinib, acalabrutinib, and spebrutinib against BTK and related kinases was studied in a dose-dependent manner either after a fixed incubation time (as used in conventional IC
RESULTS
Tirabrutinib irreversibly and covalently binds to BTK Cys-481. The inactivation efficiency k
CONCLUSIONS
For the BTK inhibitors tested in this study, analysis of the inactivation kinetics yielded a more accurate measurement of potency and selectivity than conventional single-time point inhibition measurements. Subtle but clear differences were identified between clinically tested BTK inhibitors which may translate into differentiated clinical efficacy and safety.
GENERAL SIGNIFICANCE
This is the first study that offers a detailed side-by-side comparison of four clinically-relevant BTK inhibitors with respect to their inactivation of BTK and related kinases.

Identifiants

pubmed: 31953125
pii: S0304-4165(20)30021-0
doi: 10.1016/j.bbagen.2020.129531
pii:
doi:

Substances chimiques

Imidazoles 0
Protein Kinase Inhibitors 0
Pyrimidines 0
Agammaglobulinaemia Tyrosine Kinase EC 2.7.10.2
BTK protein, human EC 2.7.10.2
tirabrutinib LXG44NDL2T

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

129531

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest All authors are current or former employees and shareholders of Gilead Sciences, Inc.

Auteurs

Albert Liclican (A)

Gilead Sciences Inc, 333 Lakeside Drive, Foster City, CA 94404, United States of America.

Loredana Serafini (L)

Gilead Sciences Inc, 333 Lakeside Drive, Foster City, CA 94404, United States of America.

Weimei Xing (W)

Gilead Sciences Inc, 333 Lakeside Drive, Foster City, CA 94404, United States of America.

Gregg Czerwieniec (G)

Gilead Sciences Inc, 333 Lakeside Drive, Foster City, CA 94404, United States of America.

Bart Steiner (B)

Gilead Sciences Inc, 333 Lakeside Drive, Foster City, CA 94404, United States of America.

Ting Wang (T)

Gilead Sciences Inc, 333 Lakeside Drive, Foster City, CA 94404, United States of America.

Katherine M Brendza (KM)

Gilead Sciences Inc, 333 Lakeside Drive, Foster City, CA 94404, United States of America.

Justin D Lutz (JD)

Gilead Sciences Inc, 333 Lakeside Drive, Foster City, CA 94404, United States of America.

Kathleen S Keegan (KS)

Gilead Sciences Inc, 333 Lakeside Drive, Foster City, CA 94404, United States of America.

Adrian S Ray (AS)

Gilead Sciences Inc, 333 Lakeside Drive, Foster City, CA 94404, United States of America.

Brian E Schultz (BE)

Gilead Sciences Inc, 333 Lakeside Drive, Foster City, CA 94404, United States of America.

Roman Sakowicz (R)

Gilead Sciences Inc, 333 Lakeside Drive, Foster City, CA 94404, United States of America.

Joy Y Feng (JY)

Gilead Sciences Inc, 333 Lakeside Drive, Foster City, CA 94404, United States of America. Electronic address: joy.feng@gilead.com.

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Classifications MeSH