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PE-22-28 peptides are Synthesized and Lyophilized in the USA.
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What is the PE-22-28 Peptide?
PE-22-28 is a synthetic variant of the naturally occurring peptide Spadin. Spadin is a secreted peptide obtained from Sortilin. It appears to act as an antagonist of the TREK-1 (TWIK-related-potassium channel) receptor, a two-pore potassium channel identified as a potential target in treating depression and as a possible neurogenic regulator. Studies in mice have shown that TREK-1 receptor deletion makes them resistant to depression. Sortilin treatment also leads to resistance to depression by promoting neuronal growth and intersynaptic connections. PE-22-28 represents the group of synthetic Spadin analogs with potentially higher efficacy and stability than Spadin. Neurogenesis is a long-term consequence of consuming anti-depressant medications (e.g., SSRIs). Neuronal growth indicates the efficacy of anti-depressants. Research studies suggest PE-22-28 has the potential to act faster than any known anti-depressant, inducing neurogenesis after just four days. The peptide may treat neurodegenerative diseases, stroke, and boost memory.
AKA: Spadin Analog, PE2228, TREK-1 Antagonist, PE 22 28, Sortilin Derivative, PE 2228
Molecular Formula: C35H55N11O9
Molecular Weight: 773.8947 g/mol
PE-22-28 and TREK-1 Receptors
TREK-1 is a cognate receptor for Spadin and thus PE-22-28. It is a two-pore potassium channel regulated by several different molecules and regulates neuronal excitability. TREK-1 is abundant in the prefrontal cortex, the amygdala, and the hippocampus. By reducing the neuron’s excitability, TREK-1 may help protect against excitotoxicity.
PE-22-28 Peptide and Depression
Researchers suggest PE-22-28 has the potential to be effective in reversing depression than any currently used treatment and with fewer side effects. It has been suggested to relieve depression in just four days without producing any side effects on other functions that are controlled by the TREK-1 channel. PE-22-28 appears to reverse the loss of hippocampal volume by stimulating neurogenesis and thus may help fight depression. Studies report that the peptide does not exhibit any of the significant side effects which are commonly associated with antidepressant medication. Current treatments for depression have a host of known side effects ranging from suicidal tendencies, to libido changes and cognition problems. PE-22-28 appears to promote neurogenesis without triggering these side effects.
PE-22-28 Peptide and Post-Stroke Depression
Post-stroke depression (PSD) is a common symptom of post-brain ischemia and affects standard treatment caused by TREK-1 overexpression. In mouse model experiments, this upregulation may be suppressed or reversed using both SSRI anti-depressants as well as TREK-1 blockers like Spadin.The researchers reveal that “These findings point out spadin as a putative antidepressant of new generation with a rapid onset of action. Spadin can be regarded as the first natural antidepressant peptide identified. It corresponds to a new concept to address the treatment of depression.”
PE-22-28 Peptide and Neurogenesis
PE-22-28 appears to promote neurogenesis but in a shorter duration of time. Studies in mice suggest that PE-22-28 has the potential to increase neurogenesis and synaptogenesis in as little as four days. CREB (cAMP response element-binding protein) is a transcription factor associated with neuronal plasticity, memory formation, and the development of spatial memory. CREB appears to be a necessary component in not just the growth of neurons but also in their protection. It has been demonstrated in animal models that removing the TREK-1 channel is a recipe for disaster. In previous mouse models, knockout of TREK-1 increased the likelihood of seizure activity significantly and reduced the normal ability of this two-pore potassium channel to protect neurons from excitotoxicity. It came as a bit of surprise then that neither Spadin nor PE-22-28 appeared to enhance seizure activity. Even more interesting is the fact that mice treated with Spadin are reported by researchers to appear more resistant to developing generalized seizures. PE-22-28 may have even more profound protective effects than Spadin.
PE-22-28 Peptide and Muscle Function
There is some research to suggest that TREK-1 plays an important role in the ability of a muscle to respond to mechanical stimulation. Scientists note that “Application of negative pressure to cell-attached patches (-20 mmHg) caused a 19-fold increase in the open probability (NPo) of human TREK-1 channels.” In particular, TREK-1 blockade appears to increase contractility in muscle tissue, while activation of the channel appears to promote muscle relaxation. While this particular aspect of the TREK-1 channel is still in the early stages of the investigation, it is becoming increasingly important. There is hope that understanding the role of molecules like PE-22-28 in muscle contraction and relaxation may provide new treatment modalities for conditions like myogenic bladder dysfunction and may also open up new pathways for understanding the physiology of muscle performance.
PE-22-28 Peptide Summary
Researchers suggest PE-22-28 peptide may be an effective treatment for depression and a potent stimulator of neurogenesis and synaptogenesis in the hippocampus. It appears to have far fewer side effects than existing anti-depressant medications. It also appears to retain much of its ability to antagonize TREK-1 even after modifications that boost half-life or alter the route of administration. In short, PE-22-28 may provide a strong target for guiding the development of a new generation of antidepressants and may help to shed light on the burgeoning field of nootropics. Research on this peptide is also helping to expand the arsenal of medications used to treat neurodegenerative diseases like Alzheimer’s disease.
- Djillani A, Pietri M, Moreno S, Heurteaux C, Mazella J, Borsotto M. Shortened Spadin Analogs Display Better TREK-1 Inhibition, In Vivo Stability and Antidepressant Activity. Front Pharmacol. 2017 Sep 12;8:643. doi: 10.3389/fphar.2017.00643. PMID: 28955242; PMCID: PMC5601071.
- A. Djillani, J. Mazella, C. Heurteaux, and M. Borsotto, “Role of TREK-1 in Health and Disease, Focus on the Central Nervous System,” Front. Pharmacol., vol. 10, Apr. 2019, doi: 10.3389/fphar.2019.00379.
- R. S. Duman, S. Nakagawa, and J. Malberg, “Regulation of adult neurogenesis by antidepressant treatment,”Neuropsychopharmacol. Off. Publ. Am. Coll. Neuropsychopharmacol., vol. 25, no. 6, pp. 836–844, Dec. 2001, doi: 10.1016/S0893-133X(01)00358-X.
- H. Moha Ou Maati et al., “Spadin as a new antidepressant: absence of TREK-1-related side effects,” Neuropharmacology, vol. 62, no. 1, pp. 278–288, Jan. 2012, doi: 10.1016/j.neuropharm.2011.07.019.
- Mazella J, Pétrault O, Lucas G, Deval E, Béraud-Dufour S, Gandin C, El-Yacoubi M, Widmann C, Guyon A, Chevet E, Taouji S, Conductier G, Corinus A, Coppola T, Gobbi G, Nahon JL, Heurteaux C, Borsotto M. Spadin, a sortilin-derived peptide, targeting rodent TREK-1 channels: a new concept in the antidepressant drug design. PLoS Biol. 2010 Apr 13;8(4):e1000355. doi: 10.1371/journal.pbio.1000355. PMID: 20405001; PMCID: PMC2854129.
- C. Devader et al., “In vitro and in vivo regulation of synaptogenesis by the novel antidepressant spadin,” Br. J. Pharmacol., vol. 172, no. 10, pp. 2604–2617, May 2015, doi: 10.1111/bph.13083.
- A. J. Silva, J. H. Kogan, P. W. Frankland, and S. Kida, “CREB and memory,” Annu. Rev. Neurosci., vol. 21, pp. 127–148,1998, doi: 10.1146/annurev.neuro.21.1.127.
- Q. Lei, X.-Q. Pan, S. Chang, S. B. Malkowicz, T. J. Guzzo, and A. P. Malykhina, “Response of the human detrusor to stretch is regulated by TREK-1, a two-pore-domain (K2P) mechano-gated potassium channel,” J. Physiol., vol. 592, no. 14, pp. 3013–3030, Jul. 2014, doi: 10.1113/jphysiol.2014.271718.
Dr. Usman (BSc, MBBS, MaRCP) completed his studies in medicine at the Royal College of Physicians, London. He is an avid researcher with more than 30 publications in internationally recognized peer-reviewed journals. Dr. Usman has worked as a researcher and a medical consultant for reputable pharmaceutical companies such as Johnson & Johnson and Sanofi.
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This is the most effective peptide I have found for my projects!
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I have been researching depression for years now and the results I get from testing this peptide are very promising. Will definitely consider keeping BP as my top 3 peptide suppliers