To mediate ADCC in vitro [9, 17, 23]. Although the contribution of ADCC activity to clinical efficacy is unclear, it is important to characterize all activities of the candidate mAb, especially those that can be affected by differences in post-translational modifications, such as glycosylation. The ability of ABP 501 to induce ADCC was assessed using MT-3 cells as target cells, and NK-92M1 cells s
To mediate ADCC in vitro [9, 17, 23]. Although the contribution of ADCC activity to clinical efficacy is unclear, it is important to characterize all activities of the candidate mAb, especially those that can be affected by differences in post-translational modifications, such as glycosylation. The ability of ABP 501 to induce ADCC was assessed using MT-3 cells as target cells, and NK-92M1 cells s
Assessment of the bioactivity of adalimumab should include assessment of multiple in vitro endpoints (NFjB-dependent and NFjB-independent) and should include binding to both soluble and transmembrane TNFa. ABP 501 has been shown to be similar to adalimumab in its ability to neutralize TNFa-induced caspase activation, chemokine production, and cytotoxicity, functions inclusive of both NFjB-dependen
Alimumab (US) (black), and adalimumab (EU) (blue). Each point represents results from testing a unique lot. The dotted lines represent the quality range established based on the adalimumab (US) lots tested (mean ?3 standard deviations). Adalimumab (EU) EU-authorized adalimumab, adalimumab (US) FDA-licensed adalimumab, CDC complementdependent cytotoxicityFunctional Characterization of ABP 501, Bios
Alimumab (US) (black), and adalimumab (EU) (blue). Each point represents results from testing a unique lot. The dotted lines represent the quality range established based on the adalimumab (US) lots tested (mean ?3 standard deviations). Adalimumab (EU) EU-authorized adalimumab, adalimumab (US) FDA-licensed adalimumab, CDC complementdependent cytotoxicityFunctional Characterization of ABP 501, Bios
To mediate ADCC in vitro [9, 17, 23]. Although the contribution of ADCC activity to clinical efficacy is unclear, it is important to characterize all activities of the candidate mAb, especially those that can be affected by differences in post-translational modifications, such as glycosylation. The ability of ABP 501 to induce ADCC was assessed using MT-3 cells as target cells, and NK-92M1 cells s
Functions in order to finely control the immune response in vivo. Among its cellular functions, TNFa is able to induce cytokines, chemokines, proliferation, and also cell death. The induction of pro-inflammatory versus death signals depends upon the molecular context of the responding cell, and specifically whether NFjB is involved [8]. Adding to the complexity of signaling, it is also reported th
Functions in order to finely control the immune response in vivo. Among its cellular functions, TNFa is able to induce cytokines, chemokines, proliferation, and also cell death. The induction of pro-inflammatory versus death signals depends upon the molecular context of the responding cell, and specifically whether NFjB is involved [8]. Adding to the complexity of signaling, it is also reported th