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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

Nhibitor TSA on the mRNA expression of MAGE-A1 gene and the other family members (MAGE-A2, -A3 and -A12) in different cell lines. Moreover, we assessed the methylation status of the MAGE-A promoters by sodium bisulfite mappingbefore and after stimulation with the demethylating agent 5-aza-CdR and/or TSA. While the methylation patterns clearly correlated with the basal MAGE RNA transcript levels, u

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

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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

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