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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 works directly on fat cells, breaking down stored triglycerides and blocking new fat from forming

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

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