Next-generation Bruton's tyrosine kinase inhibitor BIIB091 selectively and potently inhibits B cell and Fc receptor signaling and downstream functions in B cells and myeloid cells
- Clin Transl Immunology. 2021 Jun 14;10(6):e1295. doi: 10.1002/cti2.1295.
- 1. Clinical Sciences Biogen Cambridge MA USA.
- 2. Biogen Research Biogen Cambridge MA USA.
- 3. Biotherapeutics and Medicinal Sciences Biogen Cambridge MA USA.
- 4. Present address: Relay Therapeutics Cambridge MA USA.
- 5. Present address: Gilead Sciences Seattle WA USA.
- 6. Present address: Pandion Therapeutics Watertown MA USA.
- 7. Present address: Giner Labs Newton MA USA.
- 8. Present address: Takeda Cambridge MA USA.
- 9. Global Safety and Regulatory Sciences Biogen Cambridge MA USA.
- 10. Clinical Operations Biogen Maidenhead UK.
- 11. Personalized Health Research Biogen Baar Switzerland.
- 12. Present address: Immunologix Laboratories Cambridge MA USA.
- 13. MS Development Unit Biogen Cambridge MA USA.
Objectives: Bruton's tyrosine kinase (Btk) plays a non-redundant signaling role downstream of the B-cell receptor (BCR) in B cells and the receptors for the Fc region of immunoglobulins (FcR) in myeloid cells. Here, we characterise BIIB091, a novel, potent, selective and reversible small-molecule inhibitor of Btk.
Methods: BIIB091 was evaluated in vitro and in vivo in preclinical models and in phase 1 clinical trial.
Results: In vitro, BIIB091 potently inhibited BTK-dependent proximal signaling and distal functional responses in both B cells and myeloid cells with IC50s ranging from 3 to 106 nm, including antigen presentation to T cells, a key mechanism of action thought to be underlying the efficacy of B cell-targeted therapeutics in Multiple Sclerosis. BIIB091 effectively sequestered tyrosine 551 in the kinase pocket by forming long-lived complexes with Btk with t 1/2 of more than 40 min, thereby preventing its phosphorylation by upstream Kinases. As a key differentiating feature of BIIB091, this property explains the very potent whole blood IC50s of 87 and 106 nm observed with stimulated B cells and myeloid cells, respectively. In vivo, BIIB091 blocked B-cell activation, antibody production and germinal center differentiation. In phase 1 healthy volunteer trial, BIIB091 inhibited naïve and unswitched memory B-cell activation, with an in vivo IC50 of 55 nm and without significant impact on lymphoid or myeloid cell survival after 14 days of dosing.
Conclusion: Pharmacodynamic results obtained in preclinical and early clinical settings support the advancement of BIIB091 in phase 2 clinical trials.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: Btk