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The principle of using mAbs to increase IgG catabolism was also demonstrated in NHPs, when Nixon and colleagues at Dyax Corp used phage-display selected human IgG1 mAbs with high pH-independent affinity towards FcRn to reduce circulatory IgG without affecting albumin levels in NHPs [122]

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Furthermore, both the canonical and non-canonical signaling pathways require the dimerization and autophosphorylation of c-Met

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