Semax Study Index
Semax (Met-Glu-His-Phe-Pro-Gly-Pro) is a synthetic heptapeptide analog of the adrenocorticotropic hormone fragment ACTH(4-7), developed in Soviet and Russian neuroscience research in the 1980s. Its primary documented mechanisms involve upregulation of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in CNS preclinical models, along with interactions with dopaminergic and serotonergic neurotransmitter systems that contribute to its documented effects on attention, memory, and cognitive performance in rodents. Semax has also been studied for neuroprotective properties in ischemic injury models where BDNF elevation is associated with reduced neuronal loss.
Studies Listed
6
Curated Study References
Click column headers to sort. PubMed links open in a new tab where available.
| Authors ↕ | Year ↓ | Journal ↕ | Key Finding | PubMed |
|---|---|---|---|---|
| Kolomin et al. | 2013 | Journal of Molecular Neuroscience | Review documenting Semax alongside other synthetic neuropeptide analogs, summarizing evidence for BDNF induction, dopaminergic modulation, and cognitive performance effects across multiple preclinical and limited clinical contexts. | 24337817 ↗ |
| Lebedeva et al. | 2008 | Human Physiology | Semax treatment in human patients with mild cognitive impairment produced measurable neurophysiological improvements including enhanced memory-related EEG parameters, providing one of the limited human-relevant data points for its cognitive effects. | N/A |
| Agapova et al. | 2007 | Bulletin of Experimental Biology and Medicine | Semax demonstrated antidepressant-like effects in rodent forced swim and tail suspension models, with dopaminergic pathway modulation proposed as the mechanism, extending its research profile beyond cognition into mood-relevant preclinical models. | 18493644 ↗ |
| Dolotov et al. | 2006 | Journal of Neurochemistry | Semax administration significantly increased BDNF and NGF expression in rat cortex and hippocampus, establishing neurotrophic factor upregulation as a primary mechanism for its neuroprotective and cognitive effects. | 16483274 ↗ |
| Meyerson et al. | 1997 | Zhurnal Vysshei Nervnoi Deyatelnosti | Semax demonstrated dose-dependent improvements in learning and memory task performance in rodent models, providing early preclinical evidence for cognitive enhancement effects relevant to its ACTH analog mechanism. | N/A |
| Gusev et al. | 1997 | Cerebrovascular Diseases | Semax administration in acute ischemic stroke patients was associated with improved neurological outcome scores compared to controls, providing clinical context data for its documented neuroprotective effects in ischemia models. | 9299958 ↗ |
Kolomin et al.
2013, Journal of Molecular Neuroscience
Review documenting Semax alongside other synthetic neuropeptide analogs, summarizing evidence for BDNF induction, dopaminergic modulation, and cognitive performance effects across multiple preclinical and limited clinical contexts.
Lebedeva et al.
2008, Human Physiology
Semax treatment in human patients with mild cognitive impairment produced measurable neurophysiological improvements including enhanced memory-related EEG parameters, providing one of the limited human-relevant data points for its cognitive effects.
Agapova et al.
2007, Bulletin of Experimental Biology and Medicine
Semax demonstrated antidepressant-like effects in rodent forced swim and tail suspension models, with dopaminergic pathway modulation proposed as the mechanism, extending its research profile beyond cognition into mood-relevant preclinical models.
Dolotov et al.
2006, Journal of Neurochemistry
Semax administration significantly increased BDNF and NGF expression in rat cortex and hippocampus, establishing neurotrophic factor upregulation as a primary mechanism for its neuroprotective and cognitive effects.
Meyerson et al.
1997, Zhurnal Vysshei Nervnoi Deyatelnosti
Semax demonstrated dose-dependent improvements in learning and memory task performance in rodent models, providing early preclinical evidence for cognitive enhancement effects relevant to its ACTH analog mechanism.
Gusev et al.
1997, Cerebrovascular Diseases
Semax administration in acute ischemic stroke patients was associated with improved neurological outcome scores compared to controls, providing clinical context data for its documented neuroprotective effects in ischemia models.
All citations are for informational research reference purposes. Always verify directly via PubMed for current status.
Research Questions
Common questions about Semax research context, mechanism, and procurement.
What is Semax and what is its research origin?+
What does Semax research show about BDNF upregulation?+
Has Semax been studied in ischemic injury research?+
What dopaminergic research has been conducted on Semax?+
Related Compound Comparisons
Explore how Semax compares to other research compounds.
Source Semax
Semax is available from Spartan Peptides at least 98% HPLC-verified purity. Domestic US supply with same-day dispatch before 2 PM. For in-vitro research use only.
Order Semax ($159)For in-vitro research use only. Not intended for human consumption.