Surovatamig (AZD0486; TNB-486) is a fully human anti- CD19 / CD3 IgG4 bispecific antibody. Surovatamig triggers T cell activation, releases cytotoxic granules, and induces T cell-dependent cellular cytotoxicity and tumor cell lysis. Surovatamig can reduces release of pro-inflammatory cytokines including IL-2, IFNγ, TNF. Surovatamig can be used for the research of cancer, such as B cell non-Hodgkin lymphoma [1] [2].
In Vivo, Surovatamig (10 ng-10 μg/mouse; i.v.; every 5 days; 3 doses) induces dose-dependent tumor reduction and clearance in a disseminated Burkitt lymphoma xenograft model[1]. Surovatamig (1-100 μg/mouse; i.v.; every 4 days; 6 doses) induces dose-dependent tumor growth inhibition in a subcutaneous diffuse large B-cell lymphoma xenograft model, with the 100 μg/mouse dose achieving 88.52% tumor growth inhibition by day 40 post-implantation[1]. Surovatamig (0.4 mg/kg) delivers potent anti-tumor activity while inducing significantly reduced CRS-associated systemic cytokine release in a humanized disseminated DLBCL xenograft model[2].
In Vitro, Surovatamig specifically binds to CD19+ human B cell lines with an EC50 range of 1.2-5.2 nM and a cell surface Kd of 1.8 nM on Nalm6 cells[1]. Surovatamig (24 h) activates human CD4+ and CD8+ T cells in the presence of CD19+ RI-1 tumor cells, with EC50 values of 103.6 pM and 121.8 pM, respectively[1]. Surovatamig (5 day) induces proliferation of human CD4+ and CD8+ T cells in the presence of CD19+ RI-1 tumor cells, with EC50 values of 62.9 pM and 46.9 pM, respectively[1]. Surovatamig (0.0001-100 nM；48 h) triggers the release of cytotoxic granules (perforin and granzyme B) from human T cells in the presence of CD19+ RI-1 tumor cells[1]. Surovatamig (24-96 h) induces time-dependent lysis of primary human B cells via T cell redirection, with >90% lysis by 96 h and an EC50 range of 0.93-1.35 nM[1]. Surovatamig (48 h) induces concentration-dependent, CD19-specific lysis of multiple human B-NHL/ALL cell lines via both CD4+ and CD8+ T cell redirection, with EC50 values of 23.5 ± 11.5 pM (Raji) and 0.9 ± 0.2 nM (RI-1)[1]. Surovatamig (48 h) induces potent CD19-specific tumor cell lysis with significantly lower levels of proinflammatory cytokines (IL-2, IFNγ, TNF) and higher cytokine release EC50 values[1].
References:
[1]. Malik-Chaudhry HK, et al. TNB-486 induces potent tumor cell cytotoxicity coupled with low cytokine release in preclinical models of B-NHL. MAbs. 2021;13(1):1890411.
[2]. Lin W, et al. Pre-clinical evaluation of surovatamig (AZD0486) in comparison to CD20xCD3 bispecific antibodies[J]. 2025.
In Vivo, Surovatamig (10 ng-10 μg/mouse; i.v.; every 5 days; 3 doses) induces dose-dependent tumor reduction and clearance in a disseminated Burkitt lymphoma xenograft model[1]. Surovatamig (1-100 μg/mouse; i.v.; every 4 days; 6 doses) induces dose-dependent tumor growth inhibition in a subcutaneous diffuse large B-cell lymphoma xenograft model, with the 100 μg/mouse dose achieving 88.52% tumor growth inhibition by day 40 post-implantation[1]. Surovatamig (0.4 mg/kg) delivers potent anti-tumor activity while inducing significantly reduced CRS-associated systemic cytokine release in a humanized disseminated DLBCL xenograft model[2].
In Vitro, Surovatamig specifically binds to CD19+ human B cell lines with an EC50 range of 1.2-5.2 nM and a cell surface Kd of 1.8 nM on Nalm6 cells[1]. Surovatamig (24 h) activates human CD4+ and CD8+ T cells in the presence of CD19+ RI-1 tumor cells, with EC50 values of 103.6 pM and 121.8 pM, respectively[1]. Surovatamig (5 day) induces proliferation of human CD4+ and CD8+ T cells in the presence of CD19+ RI-1 tumor cells, with EC50 values of 62.9 pM and 46.9 pM, respectively[1]. Surovatamig (0.0001-100 nM；48 h) triggers the release of cytotoxic granules (perforin and granzyme B) from human T cells in the presence of CD19+ RI-1 tumor cells[1]. Surovatamig (24-96 h) induces time-dependent lysis of primary human B cells via T cell redirection, with >90% lysis by 96 h and an EC50 range of 0.93-1.35 nM[1]. Surovatamig (48 h) induces concentration-dependent, CD19-specific lysis of multiple human B-NHL/ALL cell lines via both CD4+ and CD8+ T cell redirection, with EC50 values of 23.5 ± 11.5 pM (Raji) and 0.9 ± 0.2 nM (RI-1)[1]. Surovatamig (48 h) induces potent CD19-specific tumor cell lysis with significantly lower levels of proinflammatory cytokines (IL-2, IFNγ, TNF) and higher cytokine release EC50 values[1].
References:
[1]. Malik-Chaudhry HK, et al. TNB-486 induces potent tumor cell cytotoxicity coupled with low cytokine release in preclinical models of B-NHL. MAbs. 2021;13(1):1890411.
[2]. Lin W, et al. Pre-clinical evaluation of surovatamig (AZD0486) in comparison to CD20xCD3 bispecific antibodies[J]. 2025.