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Semax, often hailed as a ‘miracle peptide,’ may enhance neurological function, reduce cortisol levels, help reverse neural dysfunction and aid in mitigating heavy metal-induced neurotoxicity.
In this thread, I will give you background on the drug, its biological predecessors and the evidence behind its multifunctional purpose.
History
Semax was developed in Russia during the late 1980s to early 1990s.
It was first developed for a wide range of conditions stemming from Traumatic brain injuries (from external mechanical force) to acquired brain injuries (strokes, tumours, lack of oxygen, etc).
pubmed.ncbi.nlm.nih.gov
Semax is effectively employed currently in ischemic stroke therapy (In experimental studies, it showed angioprotective, antihypoxic and neurotrophic activity in doses of 100-150 micrograms/kg) and is used in cases of Dementia and other degenerative neurological disorders. However, especially in recent years, it has been vouched for its nootropic function.
It was first developed for a wide range of conditions stemming from Traumatic brain injuries (from external mechanical force) to acquired brain injuries (strokes, tumours, lack of oxygen, etc).
[The efficacy of semax in the tretament of patients at different stages of ischemic stroke] - PubMed
Early rehabilitation and administration of semax increase BDNF plasma level, speed functional recovery, and improve motor performance.
pubmed.ncbi.nlm.nih.gov
Semax is effectively employed currently in ischemic stroke therapy (In experimental studies, it showed angioprotective, antihypoxic and neurotrophic activity in doses of 100-150 micrograms/kg) and is used in cases of Dementia and other degenerative neurological disorders. However, especially in recent years, it has been vouched for its nootropic function.
Semax is a synthetic analogue of a fragment of adrenocorticotropic hormone (ACTH). ACTH, also known as corticotropin, is produced to combat biological stress through the hypothalamic pituitary adrenal axis.
Proopiomelanocortin
ACTH is secreted from corticotropic cells in the anterior lobe of the pituitary gland. ACTH acts by binding to cell surface ACTH receptors, which are located primarily on adrenocortical cells of the adrenal cortex.
ACTH Receptors Signalling Cascade
ACTH binds melanocortin 2 receptors (MC2R) on adrenal cortex cells, activating G protein–coupled cAMP/PKA signalling, which phosphorylates steroidogenic proteins, ultimately stimulating cortisol synthesis and coordinating the body’s hormonal response to stress.
Signal pathway depicting activation of G protein-coupled receptors
I've kind of got sidetracked, so I'll move back onto Semax.
Proopiomelanocortin
ACTH is secreted from corticotropic cells in the anterior lobe of the pituitary gland. ACTH acts by binding to cell surface ACTH receptors, which are located primarily on adrenocortical cells of the adrenal cortex.
ACTH Receptors Signalling Cascade
ACTH binds melanocortin 2 receptors (MC2R) on adrenal cortex cells, activating G protein–coupled cAMP/PKA signalling, which phosphorylates steroidogenic proteins, ultimately stimulating cortisol synthesis and coordinating the body’s hormonal response to stress.
Signal pathway depicting activation of G protein-coupled receptors
I've kind of got sidetracked, so I'll move back onto Semax.
Biological Function
The molecular mechanisms of Semax aren't fully elucidated yet. However, current research highlights several key pathways worth examining.
Semax has been proven to activate the transcription of neurotrophins and their receptors in the cortex in rats. Semax treatment enhanced the expression of Bdnf and Ngf mRNA in the cortex of ischemic rats after occlusion. This is the key understanding as to why Semax is so effective in treating stroke patients, due to its neuroprotective effect, which could also be related to the neurotrophic factors and their receptors.
Ischemic and normal regions in rat brains
Semax's positive effect on hypoxia has led researchers to believe may modulate the body's stress response through interactions with the hypothalamic-pituitary-adrenal (HPA) axis, which is responsible for regulating stress hormones like cortisol. Semax may help mitigate the negative effects of chronic stress on brain function by normalising HPA axis activity.
HPA Axis Function and Stress Response
Now for the interesting part, the nootropic effect. Semax appears to stimulate neurogenesis (new neurons formed in the brain). Semax peptide may upregulate BDNF protein by approximately 140%, coupled with a 160% increase in trkB tyrosine phosphorylation. There is an additional 300% increase in exon III BDNF and a 200% increase in trkB mRNA levels.
Rats subjected to this peptide exhibit a notable increase in the number of conditioned avoidance reactions, indicating the peptide’s potential influence on enhancing cognitive brain functions through the hippocampal BDNF/trkB system.
Alertness of rats on Semax to visual stimuli compared to the control group
Semax may potentially exert a protective effect against metal-induced cell toxicity, potentially inducing reduced copper-induced cytotoxicity. This suggests that Semax may help protect the brain against heavy metal toxicity. This is massive, as heavy metal toxicity is the under-reported killer in our modern society. It has been linked to Autism, ADHD, Lower IQ, and motor skills delay in developing children. Additionally, heavy metal toxicity leads to oxidative stress, which quite literally alters DNA.
Heavy metal toxicity symptoms
Semax has been proven to activate the transcription of neurotrophins and their receptors in the cortex in rats. Semax treatment enhanced the expression of Bdnf and Ngf mRNA in the cortex of ischemic rats after occlusion. This is the key understanding as to why Semax is so effective in treating stroke patients, due to its neuroprotective effect, which could also be related to the neurotrophic factors and their receptors.
Ischemic and normal regions in rat brains
Semax's positive effect on hypoxia has led researchers to believe may modulate the body's stress response through interactions with the hypothalamic-pituitary-adrenal (HPA) axis, which is responsible for regulating stress hormones like cortisol. Semax may help mitigate the negative effects of chronic stress on brain function by normalising HPA axis activity.
HPA Axis Function and Stress Response
Now for the interesting part, the nootropic effect. Semax appears to stimulate neurogenesis (new neurons formed in the brain). Semax peptide may upregulate BDNF protein by approximately 140%, coupled with a 160% increase in trkB tyrosine phosphorylation. There is an additional 300% increase in exon III BDNF and a 200% increase in trkB mRNA levels.
Rats subjected to this peptide exhibit a notable increase in the number of conditioned avoidance reactions, indicating the peptide’s potential influence on enhancing cognitive brain functions through the hippocampal BDNF/trkB system.
Alertness of rats on Semax to visual stimuli compared to the control group
Semax may potentially exert a protective effect against metal-induced cell toxicity, potentially inducing reduced copper-induced cytotoxicity. This suggests that Semax may help protect the brain against heavy metal toxicity. This is massive, as heavy metal toxicity is the under-reported killer in our modern society. It has been linked to Autism, ADHD, Lower IQ, and motor skills delay in developing children. Additionally, heavy metal toxicity leads to oxidative stress, which quite literally alters DNA.
Heavy metal toxicity symptoms
Disclaimer
All of this is still theoretical and not 100% correct. Please DYOR and read with caution. Please rep, this took a while. 
Feel free to correct me or ask any questions!
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Feel free to correct me or ask any questions!
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