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How BMS-986489 Works in SCLC

BMS-986012: Binding: BMS-986012 (atigotatug) binds to the fuc-GM1 receptor, which is expressed in 50% to 90% of Small Cell Lung Cancer (SCLC) tumors. Immune Activation: The Fc portion of BMS-986012 engages natural killer cells, macrophages, and complement, leading to Antibody-Dependent Cellular Cytotoxicity (ADCC), Antibody-Dependent Cellular Phagocytosis (ADCP), and Complement-Dependent Cytotoxicity (CDC). Nivolumab: PD-1 Blockade: Nivolumab binds to the PD-1 receptor on CD8+ T cells, preventing the interaction with PD-L1 expressed by cancer cells. This blockade reactivates the T cells. Antitumor Immunity: The activated T cells then target and kill the tumor cells, enhancing antitumor immunity and leading to cancer cell death.
  • Fucosyl GM1 (Fuc-GM1) is a glycosphingolipid expressed predominately on lung cancers and limited on normal tissue. Tumor expression estimates: 50-90% of SCLC. Normal tissue expression limited to peripheral nerve.
  • BMS-986012 (atigotatug) is a non-fucosylated human IgG1 antibody that binds selectively to Fuc-GM1.
  • Pre-clinically, binding of atigotatug to tumor cells results in tumor cell death via: antibody-dependent cellular cytotoxicity (ADCC); antibody-dependent cellular phagocytosis (ADCP); complement-dependent cytotoxicity (CDC).
    Both atigotatug and nivolumab can individually lead to tumor cell death, through distinct but complementary mechanisms of action.

Reference: Ponath P et al. Clin Cancer Res. 2018 Oct 15; 24(20):5178-89

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This website is for US physicians to provide general information about ongoing BMS clinical trials and as an exchange of scientific information related to BMS investigational product BMS-986489. BMS-986489 is not currently approved in any market and has not been approved by the FDA as safe or effective for Extensive-Stage Small Cell Lung Cancer.

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