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

Karyotic cell nucleus and endomembrane system as per the chimeric model. The key event in the origin of the eukaryotic cell is postulated to be a symbiotic association between a gram-negative eubacterium (from the proteobacteria-1 group) and likely an "eocyte" archaebacterium. This association led to the loss of the outer membrane from the gram-negative bacterium (not shown). As the membrane of th

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Karyotic cell nucleus and endomembrane system as per the chimeric model. The key event in the origin of the eukaryotic cell is postulated to be a symbiotic association between a gram-negative eubacterium (from the proteobacteria-1 group) and likely an "eocyte" archaebacterium. This association led to the loss of the outer membrane from the gram-negative bacterium (not shown). As the membrane of th

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

Has been described for a number of bacterial species (for a review, see reference 7). In the case of S. pyogenes, the secreted streptococcal cysteine protease SpeB was found to cleave HK directly (8). In addition, the surface-bound M protein, one of the classical virulence determinants of GAS, has been demonstrated to bind HK, followed by bradykinin generation (9, 10). Binding and assembly of cont

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