Anti-CCR8 mAb BCG005

Our CCR8 antibodies demonstrated potent anti-tumor activity compared to all three benchmarks. Thus, our fully human CCR8 antibodies may be good preclinical candidates suitable for drug development.

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  • Highlights of anti-CCR8 mAb
  • About CCR8

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    Highlights of anti-CCR8 mAb
    • Bind specifically to human CCR8, and not to other related proteins.
    • Bind to both human and mouse CCR8 expressing cells with similar EC50.
    • Demonstrate good ADCC potential that is further enhanced by FC engineering.
    • Efficiently inhibit CCL1 induced calcium flux in human CCR8 overexpressed 293T cells.
    • Demonstrate potent in vivo anti-tumor effect in CCR8 humanized mouse models with similar or superior efficacy than all 3 benchmark antibodies.
    CCR8 antibodies that can recognize both human, mouse and monkey CCR8.
    EC50(ug/ml) Clone A Clone B Clone C Company A Company B Company C
    293T-hCCR8 0.287 0.104 0.194 0.058 0.035 0.039
    293T-mCCR8 0.400 0.127 0.177 >10 >10 >10
    293T-cyCCR8 >10 >10 0.226 >10 >10 >10

    293T cells were transfected with humanCCR8 (hCCR8), mouse CCR8 (mCCR8) or cynomolgusCCR8 (cyCCR8), antibody binding to these cells were measured by FACS. Company A: Shionogi 10A11 analog; Company B: BMS 4A19 analog; Company C: Gilead 7B16 analog.

    Good in vivo anti-tumor activity in humanized mouse model

    Anti-CCR8 antibodies were tested for their effects on tumor growth in vivo in a colon cancer model. About 5 × 105 MC38 cells (murine colon cancer cells) were injected subcutaneously in each B-hCCR8 mouse or B-hPD-1/hPD-L1/hCCR8 mice . When the tumors in the mice reached a volume of about 100 mm3, the mice were randomly placed into different groups based on tumor volumes. The mice were then injected with phosphate buffer saline (PBS) or anti-human CCR8 antibodies by intraperitoneal (i.p.) administration, tumor volume was monitored. Company A: Shionogi 10A11 analog; Company B: BMS 4A19 analog; Company C: Gilead 7B16 analog.

    Potent in vivo anti-tumor activity when combined to PD-1 antibody in humanized mouse model

    5 × 105 MC38 cells (murine colon cancer cells) were injected subcutaneously in B-hPD-1/hPD-L1/hCCR8 mice. When the tumors in the mice reached a volume of about 100-150 mm3, the mice were randomly placed into different groups based on tumor volumes (6 mice in each group). The mice were then injected with PBS, 0.3 mg/kg Pembrolizumab analog, 3 mg/kg Clone A, or a combination of 0.3 mg/kg Pembrolizumab analog and 3 mg/kg clone A by intraperitoneal injection. The antibody was administered on the first day and the fourth day of each week for 3 weeks (6 injections in total). The tumor volume was monitored.

    About CCR8

    Immune checkpoint blockade therapy (ICT) has demonstrated significant benefits in treating various types of tumors. However, a considerable number of patients respond poorly to ICT. One proposed mechanism for resistance to ICT is the infiltration of large numbers of regulatory T cells (Tregs) into tumors, which hinder the development of effective antitumor immunity and result in poor prognosis. CCR8 is a G-protein-coupled receptor (GPCR), which is predominantly expressed on tumor Tregs.

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