Platform
Bispecific antibodies (BsAbs) integrate two antigen-binding specificities into a single molecule, enabling dual-target modulation, pathway blockade, or immune-cell engagement with unprecedented precision.
At Alfa Cytology, we have established a comprehensive bsAb development platform that unifies structure-guided molecular design, developability engineering, and target-driven validation to accelerate next-generation antibody discovery across oncology and immunotherapy.
Our bispecific antibody (bsAb) platform enables the rational design and engineering of antibodies that bind two distinct targets within one molecule—allowing simultaneous pathway blockade, immune-cell engagement, or dual-signal modulation. Through structure-guided modeling, modular construct assembly, and systematic developability screening, Alfa Cytology delivers bsAbs with optimized geometry, valency, and manufacturability, transforming complex biological mechanisms into precise, drug-like molecules.
Some examples showcasing the various formats of Alfa Cytology's previous bispecific antibody productions.
Building on this foundation, we have further advanced the field with the prodrug-based bispecific antibody (p-bsAb)—an evolution that combines dual-target precision with conditional activation. These p-bsAbs are designed to remain pharmacologically inert in circulation and become activated only within the tumor microenvironment (TME) through biochemical triggers such as:
Comprehensive Structural Diversity
Over 30 optimized scaffold types for flexible molecular engineering.
AI-Guided Design Simulation
Predictive modeling of antigen spacing, rotation angles, and immune-synapse topology.
Developability Assurance
Early elimination of instability risks ensures efficient scale-up.
Production-Ready Architecture
CHO-optimized expression with validated purification routes.
Immune-Cell Engagers
Redirect T cells or NK cells toward tumor cells through dual-target recognition (e.g., CD3×tumor antigen or CD16×tumor antigen), enabling potent immune-mediated cytotoxicity with controlled activation.
Dual Pathway Blockade
Simultaneously inhibit parallel or compensatory signaling axes such as EGFR×MET, HER2×HER3, or DLL4×VEGF to overcome resistance mechanisms in solid tumors.
Tumor Microenvironment Modulation
Target tumor-stroma or angiogenesis-related pathways (e.g., VEGF×Ang-2, FAP×DR5) to reprogram the tumor microenvironment and enhance therapeutic penetration.
Cytokine or Receptor Agonism
Engineer bsAbs that co-engage immune receptors (e.g., CD28×tumor antigen or CD137×ligand) to promote localized immune activation while minimizing systemic cytokine release.
Targeted Drug and Payload Delivery
Use internalizing bsAbs as carriers for cytotoxic payloads, radioisotopes, or nanoparticles, forming bispecific antibody–drug conjugates (bsADCs) for enhanced tumor selectivity.
Half-Life and Exposure Optimization
Integrate FcRn-binding or albumin-binding modules into bsAb scaffolds to extend circulation time and improve therapeutic exposure.
| Projects | Target | Indication | Discovery | Preclinical | IND Phase I | Phase II | Phase III |
|---|---|---|---|---|---|---|---|
| BSA001 | To be disclosed | Solid Tumor | |||||
| BSA004 | To be disclosed | Breast & Gastric Cancer | |||||
| BSA007 | To be disclosed | Anti-Angiogenic Therapy | |||||
| BSA010 | To be disclosed | Tumor Microenvironment Remodeling | |||||
| BSA012 | To be disclosed | Solid Tumor (Prodrug-type) | |||||
Q1. What sets bsAbs apart from monoclonal antibodies?
Q2. Why are multiple bsAb formats necessary?
Q3. How do prodrug-type bsAbs improve safety?
Q4. Can bsAbs serve as ADC or radioconjugate scaffolds?