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Of particular note, the researchers reported that lower levels of CD320 or dietary B 12 restriction worsened the disease course in an animal model of MS and reduced the therapeutic efficacy of fingolimod, which occurred through a mechanism in which fingolimod hitchhikes by binding to the TCN2-B12 complex, allowing delivery of all to the astrocytes via interactions with CD320, with component losses disrupting the process and worsening disease

It interacts with the nitric oxide pathway, providing benefits like improved oxygen transport

The primary biomarkers traditionally employed are total serum vitamin B12 and holotranscobalamin (also known as Active B12), which represents the metabolically active fraction of B12 bound to its transport protein

Published literature describes GHK and GHK-Cu as being involved in tissue repair, fibroblast activity, angiogenesis, and collagen/elastin-related biological processes