Anti-PCSK9 (Bococizumab)-MC-MMAF ADC (ADC-W-2230)

 ADC Target

  • Name
  • PCSK9
  • Alternative Names
  • PCSK9; proprotein convertase subtilisin/kexin type 9; HCHOLA3, hypercholesterolemia, autosomal dominant 3; FH3; NARC 1; NARC1; NARC-1; HCHOLA3;
  • Target Entrez Gene ID
  • 255738
  • Overview
  • This gene encodes a member of the subtilisin-like proprotein convertase family, which includes proteases that process protein and peptide precursors trafficking through regulated or constitutive branches of the secretory pathway. The encoded protein undergoes an autocatalytic processing event with its prosegment in the ER and is constitutively secreted as an inactive protease into the extracellular matrix and trans-Golgi network. It is expressed in liver, intestine and kidney tissues and escorts specific receptors for lysosomal degradation. It plays a role in cholesterol and fatty acid metabolism. Mutations in this gene have been associated with autosomal dominant familial hypercholesterolemia. Alternative splicing results in multiple transcript variants.

 ADC Antibody

  • Overview
  • Humanized Anti-PCSK9 IgG2-kappa antibody, Bococizumab
  • Generic name
  • Bococizumab
  • Host animal
  • Mouse

 ADC Linker

  • Name
  • MC (maleimidocaproyl)
  • Description
  • Noncleavable linkers, is considered noncleavable-meaning linker cleavage, and payload release does not depend on the differential properties between the plasma and some cytoplasmic compartments. Instead, the release of the cytotoxic drug is postulated to occur after internalization of the ADC via antigen-mediated endocytosis and delivery to lysosomal compartment, where the antibody is degraded to the level of amino acids through intracellular proteolytic degradation.

 ADC payload drug

  • Name
  • MMAF
  • Description
  • Derived from Auristatin,are water-soluble dolastatin analogs of dolastatin 10. Dolastatin 10 belongs to dolastatin family and it can powerfully bind to tubulin, thus inhibiting polymerization mediated through the binding to the vinca alkaloid binding domain, and causes cell to accumulate in metaphase arrest.

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