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It binds to cells in the pituitary gland, prompting the release of additional HGH into the bloodstream [11]

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This is the mechanism that makes TB-500 relevant to injuries that involve slow or stalled healing: when the local repair response has exhausted its resources, TB-500 recruits fresh cells from the surrounding tissue and circulatory system into the damage zone

Similarly, the in vivo administration of an equimolar dose of DTT (40 mm) instead of NAC to TNBS+ethanol rats failed to either increase GSH levels and protect against injury, suggesting that the beneficial effect of NAC was due to its role as a GSH precursor

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protection against arrhythmias