The epidermal growth factor receptor (EGFR) is a transmembrane protein on the cell membrane that is overexpressed in tumor cells such as those found in head and neck cancers and colorectal cancers.

Combining small molecule drugs with the anti-EGFR monoclonal antibody not only reduces the damage of toxic small molecule drugs to normal cells but also significantly enhances the cytotoxic effect of the antibody-drug on cancer cells. In addition to these advantages, Lock-EGFR-ADC has the unique feature of antibody locks that are activated only in diseased areas, significantly improving overall treatment precision and reducing side effects.

Cunning cancer cells, such as melanoma and advanced non-small cell lung cancer, utilize the function of T-cell immune checkpoints (PD-1) to suppress T-cell activation and cytotoxic ability.

Cunning cancer cells, such as melanoma and colorectal cancer, utilize the function of T-cell immune checkpoints (CTLA4) to suppress T-cell activation, thereby evading T-cell recognition and attack. PrecisemAb's Lock-CTLA4, once activated in diseased areas, binds to CTLA4 to maintain T-cell activation, thereby inhibiting cancer tumor growth.

Tumor necrosis factor (TNFα) can induce tumor cell apoptosis and systemic inflammatory responses. However, excessive secretion of TNFα can trigger severe inflammatory reactions and even lead to chronic inflammatory diseases, such as rheumatoid arthritis and inflammatory bowel disease. PrecisemAb's Lock-TNFα can neutralize antigens in diseased areas, effectively reducing the side effects (pneumonia, sepsis, opportunistic infections) associated with commercially available anti-TNFα drugs.