Semax

Human Semax reports include ischemic-stroke rehabilitation research, but FDA’s 2026 review identified only two references addressing Semax for cerebral ischemia, migraine or trigeminal neuralgia, could not determine which salt form (free base or acetate) those references used, found no human pharmacokinetic data for any route, and concluded that the available evidence demonstrated a lack of effectiveness for those indications. This evidence does not establish healthy-person cognitive enhancement or effectiveness of subcutaneous Semax.^[1][2]

• The parent peptide evidence cannot verify N-acetyl Semax amidate or other modified analogues.
• FDA's 'lack of effectiveness' conclusion applied specifically to the cerebral-ischemia/migraine/trigeminal-neuralgia references it reviewed and is not a comprehensive verdict on every published Semax study, including the separate ischemic-stroke rehabilitation biomarker report cited here, or the separate motor-neuron-disease report recorded as a further addition.

A separate open-label 2007 trial gave 1% intranasal Semax to 27 patients with motor neuron disease (ALS) for two 10-day courses. Semax did not change the course of chronic partial denervation on needle electromyography or the disease-progression scales used, but was associated with an improvement in a quality-of-life scale reflecting emotional state and motivation, largest at day 10. This is a different, more severe patient population than the ischemic-stroke study cited elsewhere and does not establish disease-modifying benefit or cognitive enhancement.^[3]

• PubMed's indexing tags this record as a randomized controlled trial, but the abstract itself describes an open-label trial in sequential groups with no described comparator/placebo arm; it is treated here as an uncontrolled observational report.
• A subjective quality-of-life improvement in a small, severely ill population is not evidence of a disease-modifying effect or of cognitive enhancement in other populations.