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Free U.S. shipping on orders over $150Semax is a synthetic peptide derived from the adrenocorticotropic hormone (ACTH) fragment Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP) [1].
It was originally developed in Russia in the 1980s as part of a government initiative to create neuroprotective agents with both cognitive-enhancing and therapeutic potential [1].
Unlike the parent ACTH peptide, Semax does not exhibit hormonal activity, which reduces concerns about systemic endocrine effects while preserving its neuromodulatory properties [1].
Research has focused on Semax primarily as a nootropic and neuroprotective compound.
It has been investigated in both preclinical and clinical contexts for conditions such as:
Because of its stability and ability to cross the blood-brain barrier, Semax has drawn attention as a candidate for regulating processes tied to neuroinflammation, oxidative stress, and neurotransmitter balance.
One of the most widely studied effects of Semax is its role in neuroprotection and cognitive function.
Preclinical studies have demonstrated that Semax influences neurotrophic factors, particularly brain-derived neurotrophic factor (BDNF), which is essential for [2]:
In an animal study with six Wistar rats, a single intranasal spray of Semax at 50 μg/kg resulted in a 1.4 fold increase of BDNF protein levels in the hippocampus, a memory forming area of the brain. Rats were subsequently able to learn significantly more conditioned avoidance reactions (p < 0.05) [3].
An animal study of ~70 rats investigated whether Semax could counteract the negative effects of acute restraint stress on cognitive function and anxiety-related behavior. Semax was administered intraperitoneally at 0.1 mg/kg 30 minutes prior to stress exposure (electric bell sounds) [4].
Pretreatment with Semax significantly prevented stress-induced deficits in reaction time and latency, maintaining performance similar to controls (p < 0.01). Semax exposure also significantly decreased anxiety-like behavior (p < 0.04).
These effects appear to result from enhanced synaptic signaling and reduced neuronal apoptosis in regions such as the hippocampus.
In a randomized controlled trial, 110 patients who recently suffered from ischemic stroke received 6 mg of Semax twice daily for 10 days. Semax significantly increased plasma BDNF levels and was highly correlated with early rehabilitation and faster improvement of motor outcomes [5].
Overactive stress responses can induce pathogenic immune changes, which contribute to the mechanisms of diseases that may be exacerbated by stress, such as cardiovascular disease, digestive disorders, autoimmune diseases, and skin conditions. Semax has been studied for its ability to modulate stress responses and mood-related pathways.
Semax helps balance monoamine neurotransmitters, dopamine, and serotonin, which play central roles in emotional regulation and resilience to psychological stress [6]. By stabilizing these systems, Semax may mitigate the negative cognitive and behavioral consequences of chronic stress.
A rat study investigated the immunomodulatory effects of Semax during chronic social stress. After 20 days of social stress (sensory contact and daily intermale confrontations), rats were treated intranasally with Semax (150 μg/kg/day) [7].
After Semax administration, investigators observed:
Semax demonstrated immunocorrective and immunomodulatory properties in this rat model by restoring both cellular and humoral immune responses.
The findings suggest that Semax may be useful for counteracting stress-induced immune imbalance.
Semax also exerts antioxidant and anti-inflammatory effects.
Studies in PC12 cells and in rats suggest that semax may reduce markers of oxidative damage, including lipid peroxidation products, while enhancing the activity of endogenous antioxidant enzymes such as superoxide dismutase and catalase [8, 9].
These findings suggest that the peptide helps maintain redox balance during cellular stress and injuries.
Semax also modulates cytokine activity, reducing the release of pro-inflammatory mediators like TNF-α and IL-6 [10].
These actions not only limit secondary damage in ischemic injury but also contribute to preserving neuronal integrity under chronic inflammatory conditions.
Taken together, the antioxidant and anti-inflammatory properties of Semax highlight its potential relevance in research on cerebrovascular and neurodegenerative conditions.
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). Semax is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
Semax is a synthetic heptapeptide, meaning a peptide of seven units, that comprises the ACTH(4-7) fragment and a C-terminal Pro-Gly-Pro tripeptide. It is also described as a synthetic analog of the ACTH(4-10) fragment, specifically ACTH(4-7)-Pro-Gly-Pro, and as noncorticotropic. Its structure includes the Met-Glu-His-Phe (MEHF) fragment of adrenocorticotropic hormone together with the C-terminal tripeptide PGP. In the source describing it, Semax is characterized as exhibiting neuroprotective properties and improving cognitive function.
Semax is the synthetic ACTH(4-7)PGP peptide, a derivative of adrenocorticotropic hormone studied as a drug candidate for preventing consequences of cerebral ischemia. It is a synthetic peptide created on the basis of ACTH and studied as a neuroprotective agent for stroke therapy. Semax is described as actively used as a neuroprotective drug.
Semax, also known as ACTH 4-10, has been described as a neuroprotective compound with neuroprotective and anti-inflammatory properties. A review lists Semax among bioactive peptides that modulate mechanisms such as reduction of oxidative stress, inhibition of neuroinflammation, preservation of mitochondria, and enhancement of synaptic plasticity. In an animal study, Semax was used as a neuroprotector, described as stimulating the secretion of endogenous neurotrophic factors or acting as an antioxidant.
In animal studies, Semax promoted functional recovery after spinal cord injury by targeting μ-opioid receptors. According to that work, the receptor targeting regulated USP18, which in turn led to deubiquitination of the fat mass and obesity-associated protein (FTO). In an in vitro study using network pharmacology and molecular docking, the μ-opioid receptor was identified as a Semax target.
Semax, a synthetic regulatory peptide, is described as having a high affinity for Cu(II) ions. In laboratory experiments in vitro, Semax was able to extract Cu(II) from Cu(II)-amyloid-beta species and influence the redox cycling of the Cu(II)-Aβ complex, which decreased the level of associated reactive oxygen species (ROS) production. In vitro, Semax inhibited fiber formation by interfering with the fibrillogenesis of Aβ:Cu2+ complexes.
In a human clinical trial, Semax was studied for vision recovery after endovitreal surgery for rhegmatogenous retinal detachment. The comparison group of 19 patients received nasal instillations of 0.1% Semax drops starting on day 5 after surgery. By month 6 of follow-up, patients receiving the heliox plus Semax electrophoresis combined treatment showed a higher level of recovery of functional BCVA and fundus microperimetry parameters than patients receiving Semax nasal drops alone. The authors concluded that the combined approach including Semax promotes more effective recovery of visual function and reduces the risk of complications after this surgery.
In a human clinical trial, patients with vascular optic neuropathy in the main group received complex neurostimulation that included endonasal electrophoresis with the neuroprotector drug Semax 0.1%, alongside transcranial magnetic electrical stimulation, an oxybaric chamber and acupuncture. The authors concluded that the neurostimulating complex, of which Semax electrophoresis was a part, objectively increased nerve cell activity, with a significant increase in the boundaries of the field of view and light sensitivity and a decrease in global retinal ganglion complex and optic nerve losses. In the main group receiving this complex, therapeutic efficacy was reported as 94% one week after the end of treatment, 88% at 12 weeks and 83% at 24 weeks.
In spinal cord injury mice and neuroinflammation models, Semax improved functional recovery and inhibited lysosomal membrane permeabilization-related pyroptosis, by decreasing oxidative stress. In an animal study, Semax promoted spinal cord injury functional recovery by targeting μ-opioid receptors, which regulated USP18 and subsequently deubiquitination of the fat mass and obesity-associated protein (FTO).
In mice given MPTP to produce a model of Parkinson-like damage, Semax administered before MPTP treatment was tested for its effect on striatal dopamine. In this mouse model, Semax slightly but reliably increased striatal dopamine. The authors interpreted this as indicating that Semax is more effective as an inducer of endogenous neurotrophic factor secretion than as an antioxidant.
Semax is a synthetic heptapeptide made of the ACTH (4-7) fragment joined to a C-terminal Pro-Gly-Pro tripeptide. The Pro-Gly-Pro (PGP) tripeptide is described as an active factor of resistance to the biodegradation of peptide drugs.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.