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Abstract: SA-PO0821

Topologically Engineered, Superdimeric α-CD19 x α-CD20 Bispecific Antibodies with Dual Enhanced Fc Domains: New Class of Natural Killer (NK)/Monocyte Engagers for Deep B Cell Depletion in Lupus Nephritis

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Capon, Daniel J, Hinge Bio, Inc., Burlingame, California, United States
  • Lewis, Gavin M, Hinge Bio, Inc., Burlingame, California, United States
  • Troitskaya, Larisa, Hinge Bio, Inc., Burlingame, California, United States
  • Fomin, Marina E, Hinge Bio, Inc., Burlingame, California, United States
  • Law, Brian, Hinge Bio, Inc., Burlingame, California, United States
  • Frank, Brendon, Hinge Bio, Inc., Burlingame, California, United States
  • Chan, Lap Shun Nelson, Hinge Bio, Inc., Burlingame, California, United States
  • Edman, Ursula, Hinge Bio, Inc., Burlingame, California, United States
  • Chapin, Steven J, Hinge Bio, Inc., Burlingame, California, United States
  • Gefter, Malcolm L, Hinge Bio, Inc., Burlingame, California, United States
  • Punnonen, Juha, Hinge Bio, Inc., Burlingame, California, United States
Background

The dramatic efficacy of anti-CD19 CAR-T in systemic lupus erythematosus (SLE) (N Engl J Med 2024 Feb 22;390(8):687-700) has opened up the possibility that autoimmune responses underlying LN may be reset leading to durable remissions. Given the challenges of CAR-T at large scale there is interest in safe and scalable NK/monocyte engagers capable of deep depletion of autoantibody producing B cells.

Methods

We describe GEM-DIMERTM technology, allowing us to engineer superdimeric, tetrahedral antibodies demonstrating bispecific binding to target cells and cooperative binding to recombinant Fcγ receptors expressed on cells. These include NK/monocyte engagers (i.e., CD16a engagers) comprising two α-CD19 (huFMC63) and two α-CD20 (rituximab) targeting domains, and two Fc domains incorporating S239D/I332E mutations that enhance Fcγ receptor binding.

Results

HB2198 demonstrated robust depletion of human B cells in cultures of whole blood or PBMCs, including PBMCs derived from SLE patients. HB2198 also demonstrated potent antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, direct cell killing activity, and macrophage mediated antibody-dependent cellular phagocytosis in the presence of physiological human IgG levels. Treatment of cynomolgus monkeys with HB2198 resulted in >99% depletion of circulating B cells within 1-3 days and remodeling of the B cell compartment as evidenced by a durable shift in proportions of naïve and memory B cells.

Conclusion

Our findings demonstrate the potential of HB2198 as an improved, off-the shelf treatment for LN, SLE and related diseases via deep and broad depletion of both CD19+ and CD20+ cells. First-in-human trials are anticipated in 2025.

GEM-DIMERTM technology used to create clinical candidate HB2198

Funding

  • Commercial Support – Hinge Bio, Inc.

Digital Object Identifier (DOI)