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The cAC10-L4-MMAF in which cAC10 (anti-CD30) linked to the antimitotic auristatin derivative MMAF via a non-cleavable maleimidocaproyl linker was approximately as potent as cAC10-L1-MMAF with a dipeptide linker in vitro against a large panel of cell lines and was equally potent in vivo (Figure 5) [48,49]

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Aryl hydrocarbon receptor activation in chronic kidney disease: role of uremic toxins

Nature of nonfunctional envelope proteins on the surface of human immunodeficiency virus type 1

Of note, the decrease in homoeostatic capacity of astrocytes seems to be the prevailing mechanism across various neuropathologies