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The critical dependence of Li + inhibition of NMDAR currents on extracellular Ca 2+ forced us to the conclusion that Li + inhibits NMDARs indirectly breaking the Ca 2+ extrusion from neurons by NCXs, which are involved in regulation of pre-membrane Ca 2+ concentration in the close proximity to the NMDAR intracellular domains during Ca 2+ entry through the channels of activated NMDARs

Clinical and experimental rheumatology 19 , 321324 (2001)

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Studies suggest that the combination targets distinct but overlapping pathways: BPC-157 through vascular and growth factor signaling, and TB-500 through cytoskeletal dynamics and extracellular matrix remodeling

A: Yes, ~95% vs ~100% bioavailability

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