BDNF and TrkB
Rat studies found increased hippocampal BDNF expression and TrkB activation following Semax administration, supporting continued research into neuronal plasticity, learning, and cellular resilience.
P—14 • Investigational profile
Semax
A concise educational overview of an investigational ACTH-derived regulatory peptide studied across neurotrophic signaling, learning, memory, cerebral ischemia, and neurological recovery.
Name
Semax
Also known as ACTH(4-7)-Pro-Gly-Pro or ACTH(4-7)PGP; amino-acid sequence: Met-Glu-His-Phe-Pro-Gly-Pro
- Scientific classification
- Synthetic nonhormonal ACTH-derived regulatory heptapeptide combining the ACTH(4-7) fragment with a C-terminal Pro-Gly-Pro sequence
- Library family
- Neuroactive
- Research status
- Investigational, with limited human clinical research and a larger body of animal, molecular, and cerebral-ischemia studies
- Regulatory status
- Not FDA approved in the United States; FDA identifies compounded Semax as presenting potential immunogenicity concerns and notes that available safety information is insufficient
Compound overview
A neuroactive regulatory peptide developed from a short fragment of adrenocorticotropic hormone.
Semax was designed to retain neuroactive properties associated with the ACTH fragment without functioning as a conventional corticosteroid hormone.
Research primarily explores its relationship with neurotrophic signaling, learning, memory, cerebral ischemia, inflammation, and neurological recovery.
Mechanism under study
Coordinated neurotrophic and cellular-response signaling
Semax appears to influence multiple neurotrophic, inflammatory, neurotransmitter, and cellular-recovery pathways rather than acting through one fully established receptor mechanism.
Neuroimmune regulation
Cerebral-ischemia models indicate that Semax changes the expression of genes associated with inflammatory signaling, immune activity, stress response, and neurotransmission.
Recovery-related pathways
Preclinical research reports effects involving CREB, JNK, MMP-9, neurotrophins, and vascular-response genes relevant to neuronal survival and recovery after experimental injury.
These interconnected mechanisms remain under investigation and have not been fully established in humans.
Current research areas
Questions under investigation
- BDNF, TrkB, and neuroplasticity
- Cerebral ischemia and neurological recovery
- Learning and memory
- Neuroinflammatory signaling
- Neurotransmitter and cellular-stress responses
Evidence summary
Reported neuroactive research findings
- Post-stroke rehabilitation: A 110-participant clinical study associated Semax treatment with increased plasma BDNF and improved recovery measured through the Barthel Index.
- Neurotrophic activation: Animal studies report changes in BDNF, NGF, and their associated receptor pathways.
- Learning and memory: Rat research reported increased conditioned-learning responses alongside activation of hippocampal BDNF and TrkB signaling.
- Ischemic-response regulation: Experimental stroke models found that Semax moderated gene-expression disturbances involving inflammation and neurotransmission.
- Cellular recovery potential: Preclinical findings report changes in regulation of proteins involved in cell survival, inflammatory control, vascular response, and neurological recovery.
These findings warrant continued investigation. Most mechanistic evidence remains preclinical, and available human studies do not establish broad clinical effectiveness or long-term safety.
Educational notice
Education, not usage guidance.
This profile is provided for scientific education only. It is not medical advice, prescribing guidance, dosing information, or instructions for Semax use. Semax is not FDA approved in the United States. FDA reports that compounded Semax may present immunogenicity concerns related to peptide aggregation and impurities and states that available safety information is insufficient to determine whether it could cause harm. Compounded or commercially marketed products should not be assumed to match the identity, purity, safety, or evidence associated with materials used in published research.
Key scientific referencesComing soon
A curated primary-source reference list will be added during the next educational expansion.