The chemical synthesis of huperzine A has been optimized, while an in vitro technique hasprovided a renewable plant source. Pharmacological studies showed that the drug inhibits the enzymeacetylcholinesterase reversibly and selectively.
Huperzine A also displayed good pharmacokinetics witha rapid absorption and a widedistribution in the body at a low to moderate rate of elimination.
Presently,inadequate toxicity data in human have been reported, yet animal studies demonstrated mild to moderate cholinergic side effects at therapeutic doses.
Previous clinical trials have shown improvement inmemory function using MMSE, MQ, ADAS-COG, and ADL tests. In an unpublished phase II clinical trial, the ADAS-COG and MMSE tests indicated cognitive enhancement at a dose of 0.4 mg, yet no improvement was observed at a dose of 0.2 mg.
The MMSE scores indicated cognitive enhancement at 0.4 mg. Promising data suggested that huperzine A is well tolerated at doses up to 0.4 mg for 24 weeks. Therefore, huperzine A seems to be a potential treatment option for AD
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