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Its binding constant (pKa 16.44) is similar to albumin's copper transport site (log = 16.2), allowing GHK to exchange copper with albumin for intracellular delivery.[3] Discovery and design rationale GHK was first identified in 1973 in fractions of human plasma that promoted survival of liver cells in culture

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Actin Sequestration and Cytoskeletal Remodeling TB-500 functions as the primary actin-sequestering molecule in the blend, binding globular actin (G-actin) and regulating actin polymerization[2]

The compound appears to maintain NO homeostasis under conditions of both excess and deficiency upregulating eNOS-derived NO in ischemic models while attenuating iNOS-driven overproduction in inflammatory contexts (Sikiric et al., 2014, Current Pharmaceutical Design 2014

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