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The potency reported in those assays was described as roughly 7 to 10 orders of magnitude more potent than BDNF on a molar basis for some specific synaptogenic endpoints, which sounds extraordinary because it is, and that is precisely why independent human replication is essential before drawing conclusions

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In peer-reviewed animal work the concrete numbers are oral doses of roughly 1.44–2.88 mg/kg given daily to APP/PS1 Alzheimer-model mice over about three months [3] , and low-mg/kg dosing that reversed scopolamine-induced deficits in rodents [1]