Next-Generation Bispecific Nanobody Targeting CD86 and CTLA4 for Innovative Autoimmune Disease Therapy
VHH-P573 is a humanized bispecific nanobody simultaneously targeting CD86 molecule (CD86) and cytotoxic T-lymphocyte associated protein 4 (CTLA4). Designed for the treatment of autoimmune disease, this innovative construct is currently advancing through the Biological Testing stage. By engaging both CD86 molecule (CD86) and cytotoxic T-lymphocyte associated protein 4 (CTLA4), VHH-P573 aims to finely tune immune checkpoint pathways implicated in autoimmunity. This program leverages the distinct advantages of nanobody engineering, supporting its therapeutic potential for autoimmune disease where precise immunomodulation is crucial.
| Candidate | VHH-P573 |
| Target | CD86 molecule (CD86) cytotoxic T-lymphocyte associated protein 4 (CTLA4) |
| Modality | humanized bispecific VHH |
| Indication | Autoimmune Disease |
Licensing Opportunity
VHH-P573 is available for out-licensing and collaborative development. We welcome inquiries from industry partners seeking innovative, bispecific nanobody solutions in the autoimmune disease space.
Contact UsDevelopment Phase
| Program | Research | Preclinical | Phase 1 |
|---|---|---|---|
| VHH-P573 |
Modality
VHH-P573 is a bispecific nanobody construct composed of two single-domain antibodies: a humanized anti-CD86 nanobody and a humanized anti-CTLA4 nanobody, linked in series by a flexible (G4S)2 peptide linker. The construct’s small molecular size and single-domain architecture confer superior tissue penetration, increased stability, and reduced immunogenicity compared to conventional antibodies. Expressed in human embryonic kidney Expi293F cells, VHH-P573 benefits from robust expression and scalability. The unique structure allows for simultaneous, high-affinity engagement of CD86 and CTLA4, addressing key immune pathways in autoimmune disease and offering the prospect for enhanced efficacy and safety.
Target
CD86 and CTLA4 are both crucial immune checkpoint molecules regulating T cell activity. CD86 is predominantly expressed on antigen-presenting cells and plays a pivotal role in the co-stimulation of T cells. CTLA4, primarily found on activated T cells and regulatory T cells, acts as an inhibitory receptor counterbalancing immune responses. Both CD86 and CTLA4 are essential in controlling lymphocyte activation and immune tolerance. Dysregulation of CD86 or CTLA4 pathways is strongly linked to the pathogenesis of autoimmune disease. The dual engagement of CD86 and CTLA4 by VHH-P573 addresses the complex immune network involved in autoimmunity, providing strategic value for targeted therapeutic intervention and positioning this program as an attractive asset for treating autoimmune disorders.
Mechanism of Action
VHH-P573 exerts its function through simultaneous blockade of CD86 and CTLA4, two key immune checkpoint regulators. By interfering with the interaction between CD86 and its ligands on T cells, as well as inhibiting CTLA4-mediated inhibitory signaling, VHH-P573 modulates T cell activation and restores immune balance. This dual-acting mechanism supports the re-establishment of immune homeostasis necessary in autoimmune disease. The nanobody platform underlying VHH-P573 offers modular flexibility, supporting future extension into multivalent bispecifics, antibody-drug conjugates, or additional immune-targeting combinations, creating broad therapeutic application opportunities beyond current immune checkpoint inhibitor modalities.
Autoimmune Disease
Autoimmune disease comprises a heterogeneous group of disorders characterized by immune-mediated attacks against self-tissues. These conditions are prevalent worldwide, affecting millions of individuals with varying degrees of severity. Common autoimmune disease entities include rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis. Current therapeutic approaches encompass immunosuppressive agents, corticosteroids, biologics targeting specific immune pathways, and emerging cell therapies. Despite recent advances, many patients experience incomplete response, treatment resistance, or significant adverse effects. Persistent inflammation, organ damage, and reduced quality of life underscore the unmet clinical needs in this field. VHH-P573, by targeting both CD86 and CTLA4 with precision, offers a promising new strategy for immune modulation in autoimmune disease, aiming to improve patient outcomes while minimizing collateral immunosuppression.