Semax vs Selank
Semax and Selank are synthetic peptides studied in cognition research, but they derive from different parent molecules. Semax is a fragment of ACTH modified to carry no corticotropic activity, while Selank is an analog of the immunomodulatory peptide tuftsin. Research on Semax centers on brain-derived neurotrophic factor expression and dopaminergic and serotonergic systems linked to attention. Selank has been investigated for influence on GABAergic signaling, BDNF expression, and serotonin metabolism. Semax has been studied in animal models of stroke and spinal cord injury and in small human studies, including ischemic stroke patients. Selank has been studied mainly in cell and rodent stress models, with a small randomized controlled trial on anxiety disorders. Human safety data for both are limited.
Key differences
- 01
Semax is derived from ACTH and modified to lack hormonal activity, whereas Selank is an analog of tuftsin, a peptide associated with immune signaling.
- 02
Semax research emphasizes BDNF signaling and dopaminergic and serotonergic attention pathways, while Selank research emphasizes GABAergic signaling and a neuro-immune link to mood regulation.
- 03
Semax has been studied primarily for recovery after ischemic stroke and spinal cord injury, whereas Selank has been studied primarily for anxiety-related behavior and stress modulation.
- 04
The human evidence for Semax includes a clinical trial in ischemic stroke patients and brain network imaging research, while Selank's human evidence consists mainly of a small randomized controlled trial on anxiety disorders.
- 05
A rat study reported that Selank enhanced the anxiety-reducing effect of diazepam, suggesting possible interaction with GABAergic agents, a finding not reported for Semax in the cited studies.
Side by side
BDNF/NGF upregulation, focus, neuroprotection
Anxiolytic, cognitive clarity
Early clinical
Early clinical
Cognition
Cognition
Subcutaneous
Subcutaneous
Research protocols have used 1–2 mg per administration, once daily (morning), in 4-week blocks with 4 weeks off.
Research protocols have used 500–2,000 mcg per administration, once daily (morning), in 4-week blocks with 4 weeks off.
- Recovery after experimental ischemic stroke in rats
- Outcomes in patients at different stages of ischemic stroke
- BDNF and neurotrophic signaling
- Brain network activity, including the default mode network
- Functional recovery after spinal cord injury in mice
- Attention and focus pathways
- Anxiety-related behavior in rodent stress models
- Expression of GABAergic neurotransmission genes in cell and animal models
- Cytokine levels under social stress conditions
- Aversive signs of morphine withdrawal in rats
- Anxiety disorders in a small randomized controlled trial
- Brain functional connectivity alongside Semax
- Human safety data are limited
- Adverse events are not summarized in the cited studies
- Described as an ACTH-derived fragment modified to lack corticotropic activity
- Long-term safety has not been established in large controlled trials
- Human safety data are limited
- Adverse events are not summarized in the cited studies
- A rat study reported that Selank enhanced the anxiety-reducing effect of diazepam, suggesting possible interaction with GABAergic agents
5 cited studies
5 cited studies
Studied ranges describe what published research protocols have used. They are not instructions or recommendations. Products are sold for research purposes only; each order ships with a protocol guide for the specific product.
Mechanism
Semax
Research investigates Semax for its influence on brain-derived neurotrophic factor expression and on the dopaminergic and serotonergic systems associated with attention.
Neurotrophic Support
Studied for a role in BDNF signaling, associated with neural adaptability and resilience.
Attention Pathways
Explored in research on focus and sustained attention, without the hormonal activity of its parent sequence.
Selank
Research investigates Selank for influence on GABAergic signaling and on the expression of brain-derived neurotrophic factor, alongside effects on serotonin metabolism.
Stress Modulation
Studied for anxiolytic-associated signaling that does not carry the sedation profile of conventional agents.
Neuro-Immune Link
Explored at the overlap of mood regulation and immune signaling, reflecting its tuftsin origin.
