T assays were conducted, and the mean percent relative activity is reported (see text). A dose response from a single assay of the three is presented here as representative data. e Representative nonconstrained dose?response curves of ABP 501 (red), adalimumab (US) (black), and adalimumab (EU) (blue) showing binding to FcRn. Each point is a mean of three replicates ?standard deviation. Adalimumab
T assays were conducted, and the mean percent relative activity is reported (see text). A dose response from a single assay of the three is presented here as representative data. e Representative nonconstrained dose?response curves of ABP 501 (red), adalimumab (US) (black), and adalimumab (EU) (blue) showing binding to FcRn. Each point is a mean of three replicates ?standard deviation. Adalimumab
Onstrated since all of the ABP 501 lots fell within the quality range established based on the adalimumab (US) lots tested. Another mechanism for inducing cell death is the induction of CDC in cells expressing mbTNFa. A comparison of the CDC activity of ABP 501 to that of adalimumab (US) and adalimumab (EU) using MT-3 cells as target cells was conducted. Mean (three independent experiments) percen
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
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
N of the mAb were shown to be able to discriminate a thermally degraded sample (data not shown), demonstrating that the utilized assays are sensitive to detect differences in activity, if they did exist. It is well established that IgG1 mAbs are efficient mediators of effector function, and are able to bind to many of the known FccRs. A sensitive comparison of these Fcdependent activities is impor
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