
Semax
ACTH fragment analog developed at the Russian Institute of Molecular Genetics. In clinical use in Russia since 1996.
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Research Use Only. This product is intended for laboratory research purposes only. Not for human or veterinary use. Not for sale to minors.
Semax — Key Data
A snapshot of published research on Semax. Each figure links to the literature summarized below.
How Semax Works
Semax is a synthetic ACTH(4-10) analog developed at the Russian Institute of Molecular Genetics. Despite a plasma half-life of only 2-3 minutes, its downstream neurotrophin effects persist 20-24 hours. It crosses the blood-brain barrier with 0.093% of dose reaching brain tissue within 2 minutes, and 80% of brain radioactivity remains intact Semax. For research use only.
Discovered 1982100+ publicationsInstitute of Molecular Genetics, Russian Academy of Sciences
- 01
BDNF / Neurotrophin Pathway
Primary- 1.4-fold BDNF protein increase in hippocampus
- 3-fold BDNF exon III mRNA upregulation
- Peak BDNF upregulation at 3-8 hours post-dose
- 02
NGF Upregulation
Primary- 5-fold NGF mRNA increase in glial cells at 30 minutes
- 1.67x NGF increase in hippocampus at 8 hours
- 1.65x NGF increase in frontal cortex at 8 hours
- 03
Dopamine / Serotonin Modulation
Secondary- 3.36-fold dopamine D3 receptor upregulation
- 180% increase in extracellular serotonin metabolite
- Enhanced amphetamine dopamine response with pre-treatment
What the Studies Show
Peer-reviewed outcomes from published Semax research.
0
Healthy human volunteers showed improvement in attention and short-term memory. 250-1000 mcg/kg intranasal for 10 days.
ADDF Semax ReportAdditional Clinical Outcomes
- 0Gusev et al., 2018
Post-ischemic stroke study. 6,000 mcg/day x 10 days x 2 courses. Sustained BDNF elevation throughout 5-month study. Significant NIHSS decrease at 10-14 and 21 days.
- 0Dolotov et al., 2001
In glial cell cultures after 30 minutes of Semax exposure. Accompanied by 1.6-fold trkB phosphorylation increase.
Neurotrophin Upregulation
Glial cell cultures and rat hippocampus (Dolotov et al., 2001)
Research Applications
Reported areas of investigation across the Semax literature.
- 01NEUROPROTECTION
BDNF and NGF Upregulation
Potent dual neurotrophin activator. 1.4-fold BDNF protein increase in hippocampus and 5-fold NGF mRNA increase in glial cells within 30 minutes.
- BDNF protein increase
- 1.4x
- NGF mRNA increase
- 5x
- trkB phosphorylation
- 1.6x
Study finding. Peak BDNF upregulation occurs 3-8 hours post-dose, persisting well beyond the 2-3 minute plasma half-life.
Dolotov et al., 2001 - 02COGNITIVE ENHANCEMENT
Attention and Memory Improvement
Healthy volunteers showed 15-20% improvement in attention and short-term memory with 10-day intranasal protocol.
- Cognitive improvement
- 15-20%
- Protocol duration
- 10 days
Study finding. 250-1000 mcg/kg intranasal for 10 days in healthy human volunteers.
ADDF Semax Report - 03STROKE RECOVERY
Post-Ischemic Neuroprotection
110-patient stroke study showed sustained BDNF elevation and significant NIHSS decrease through 5-month observation.
- Patients studied
- 110
- NIHSS improvement
- Significant at Day 10-14
- BDNF elevation
- Sustained 5 months
Study finding. 6,000 mcg/day for 10 days, 2 courses. Significant NIHSS decrease at 10-14 and 21 days.
Gusev et al., 2018
Reported Observations
- Registered pharmaceutical in Russia and Ukraine since 1996
- Not FDA-approved in the United States
- Rapid enzymatic degradation with 2-3 minute plasma half-life
- No significant adverse events reported in published clinical studies
This summary reflects observations from published peer-reviewed research. It is not a comprehensive safety assessment. Researchers should review primary literature before designing protocols. For Research Use Only.
Compound Profile
What Is Semax?
Stability Information
- Protect from light
- Avoid repeated freeze-thaw cycles
- Store in original sealed container
Lyophilized (powder)
up to 2 years
Reconstituted
up to 30 days
Working solution
Use within 24 hours
References
Gusev et al., 2018
These references are provided for informational purposes. Kern is not affiliated with the authors or institutions listed above.
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