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BND-67

BND-67

First-in-Class Therapy Targeting CD28 Shedding

BND-67 is a first-in-class, VHH-based antibody designed to inhibit pathological CD28 shedding, a novel immune regulatory mechanism discovered and validated by Biond in cancer patients.

CD28 is a central co-stimulatory receptor required for effective T-cell activation, proliferation, and persistence. In cancer, protease-mediated shedding of CD28 from the surface of T cells impairs anti-tumor immunity and may contribute to resistance to immune checkpoint inhibitors.

By selectively blocking CD28 shedding, BND-67 restores CD28 expression and delivers a differentiated dual mechanism of action: enhancing effector T-cell activation and expansion while reducing the suppressive activity of regulatory T cells (Tregs). This results in a potent and sustained anti-tumor immune response.

Preclinical studies have demonstrated robust anti-tumor activity for BND-67 both as monotherapy and in combination with anti–PD-1 agents and T-cell engagers. In non-human primate toxicology studies, BND-67 showed a favorable safety profile and confirmed its pharmacodynamic activity.

BND-67 is currently being evaluated in a Phase 1, open-label, dose-escalation study designed to assess safety, tolerability, pharmacokinetics, pharmacodynamics, and preliminary anti-tumor activity. The clinical trial focuses on patients who relapsed following prior checkpoint inhibitor treatment.

See Clinical Trials

BND-67 represents a novel approach to restoring T-cell function by targeting a central regulatory mechanism of immune escape, with the potential to work as monotherapy and enhance the efficacy of both existing and emerging cancer immunotherapies.

Restoring T Cell Activation