ANB032 — Overview
ANB032 is a novel, non-depleting antibody that binds to the BTLA checkpoint receptor and inhibits activated T cell proliferation, reduces inflammatory cytokine secretion and modulates dendritic cell (DC) function, including inducing Tregs, both in inflamed tissue and the periphery
ANB032 has potential to treat a wide range of systemic inflammatory diseases
ANB032: IgG4 antibody (non-depleting)
- Binds to BTLA on epitope proximal to immune cell
- Fc receptor binding profile contributes to differentiated potency
- Non-blocking of HVEM engagement with optimized antigen binding affinity
ANB032’s agonist signal modulates immune cells
- Inhibits activated T cell proliferation
- Reduces inflammatory cytokine secretion
- Modulates DC function, including inducing Tregs
BTLA is key node of immune regulation
- B and T lymphocyte attenuator (BTLA) is a potent modulator of T cells, B cells and dendritic cells (DC)
- Expressed only on immune cells and preferentially on activated immune cells
- Dysregulation of BTLA pathway accelerates onset and exacerbates disease
Jurkat BTLA SHP2 Recruitment Assay methodology: BTLA and SHP2 are fused with complementary enzyme fragments, when SHP2 is recruited to activated phosphorylated BTLA, the enzyme donor and enzyme acceptor form active β-gal that is detected by chemiluminescence.
ANB032 demonstrated favorable safety and tolerability with rapid and sustained PK/PD activity
96 healthy volunteers in SAD and MAD cohorts in Phase 1 study
- Favorable ~2-week half-life with IV and SQ dosing
- Full receptor occupancy (RO) within hours and maintained for >30 days
Rapid and sustained target engagement on both T and B cells
- Duration of reduced BTLA expression persisted in dose-dependent manner
Well-tolerated with no dose limiting tox
- No SAEs
- Most AEs mild-to-moderate, short duration, dose independent and resolved without sequelae
- No evidence of infection risk or cancer risk to date
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