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.
Eris Bame  1 Hao Tang  2 Jeremy C Burns  2 Million Arefayene  1 Klaus Michelsen  3  4 Bin Ma  3 Isaac Marx  3 Robin Prince  3 Allie M Roach  2  5 Urjana Poreci  1  6 Douglas Donaldson  1  7 Patrick Cullen  2 Fergal Casey  2 Jing Zhu  2 Thomas M Carlile  2 Dipen Sangurdekar  2  8 Baohong Zhang  2 Patrick Trapa  3 Joseph Santoro  3 Param Muragan  3 Alex Pellerin  2 Stephen Rubino  2 Davide Gianni  3 Bekim Bajrami  3 Xiaomei Peng  9 Alex Coppell  10 Katherine Riester  1 Shibeshih Belachew  11 Devangi Mehta  1  12 Mike Palte  13 Brian T Hopkins  3 Matthew Scaramozza  13 Nathalie Franchimont  13 Michael Mingueneau  2
Affiliations
  • 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.
Abstract

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.

Keywords
B cells; BTK inhibitor; B‐cell receptor; Fc receptor; multiple sclerosis; myeloid cells.
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