Highlights：

1.Clear MoA.

T cells are activated to eliminate tumor cells by targeting BAFFR. BAFFR×CD3 bsAb treats the CD19-resistant or CD20-resistant B-cell malignancies.

2. Significant clinical efficacy and low toxicity & side effects.

a) 2:1(TAA:CD3) structure, high binding to TAA, relative low affinity to CD3, reduce non-specific T cell activation.

b) Human single domain antibody for TAA, stable as Nano antibody, with low immunogenicity.

c) High efficacy in-vitro and in-vivo.

d) Long PK in-vivo with Fc (t1/2=13.7 days).

3. Global competitiveness.

a) FIC potential. No similar competing drugs, and few study on BAFFR antibody in B lymphocyte carcinoma indications. The guideline for the treatment of B-lymphocyte cancer has great side effects and is easy to be resistant to drugs.

b) Stable enough for downstream development.

Research progress：

1) Complete the anti-BAFFR Screening.

2) BAFFR-CD3 bsAb cytotoxic activity in vitro shows the killing activity against jeko-1-luci cells.

3) BAFFR-CD3 bsAb cytotoxic activity in vivo. In the PBMC transplanted tumor model, showed excellent in vivo efficacy in both high and low dose groups (10 mg/kg;1 mg/kg). After four doses, the tumors of both mice disappeared.