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PE 22-28


Stroke Recovery.TREK-1 inhibitor. Assists with mood, memory and learning. Aids muscle function.

SKU: d1e6483e494a-1-2-1-1 Category: Tags: ,

Scientific Name: PE 22-28
Clinical Test Expectation: Stroke Recovery.TREK-1 inhibitor. Assists with mood, memory and learning. Aids muscle function.
MG Strength:  8 mg per vial

Detailed Product Information


Stroke is a major disease associated with high mortality and serious long-term disability. Unfortunately, usual treatments fail to improve long-term recovery and thrombolysis, which is the unique short-term treatment, is efficient only on 10% of patients. Consequently, developing new treatments is necessary. The TREK-1 channel represents an interesting target since its activity has recently been shown to be protective against stroke. We have identified a short molecule (spadin or PE 12-28) derived from a larger endogenous peptide, which is a potent antidepressant and is able to specifically inhibit TREK-1, as a potential new treatment. Using the in vivo model of MCAO in mice, we demonstrated that chronic treatment with spadin or a shorter analog (PE 22-28) improved the post stoke recovery from days to months after the ischemia. The protocol we used was designed thanks to electrophysiology studies and consisted in a two phase treatment, a low dose for one week followed by a high dose treatment for several weeks. Treated mice showed a significant reduction of the immobility time in the Forced Swimming Test. The eat latency in the Novelty Suppressed Feeding test was significantly reduced. The learning capacity was increased in the Morris Water Maze and the motor coordination was improved in both rotarod and pole test. The increase in neurogenesis, measured by BrdU incorporation was still present even at 10 weeks post trauma. Taken together our results suggest that spadin or its analog are very potent candidates for the development of new treatments improving stroke recovery.


Depression is a devastating mood disorder and a leading cause of disability worldwide. Depression affects approximately one in five individuals in the world and represents heavy economic and social burdens. The neurobiological mechanisms of depression are not fully understood, but evidence highlights the role of monoamine neurotransmitter balance. Several antidepressants (ADs) are marketed to treat depression and related mood disorders. However, despite their efficacy, they remain nonspecific and unsafe because they trigger serious adverse effects. Therefore, developing new molecules for new targets in depression has become a real necessity. Eight years ago, spadin was described as a natural peptide with AD properties. This 17-amino acid peptide blocks TREK-1 channels, an original target in depression. Compared to the classical AD drugs such as fluoxetine, which requires 3–4 weeks for the AD effect to manifest, spadin acts rapidly within only 4 days of treatment. The AD properties are associated with increased neurogenesis and synaptogenesis in the brain. Despite the advantages of this fast-acting AD, the in vivo stability is weak and does not last for >7 h. The present review summarizes different strategies such as retro-inverso strategy, cyclization, and shortening the spadin sequence that has led to the development and optimization of spadin as an AD. Shortened spadin analogs present increased inhibition potency for TREK-1, an improved AD activity, and prolonged in vivo bioavailability. Finally, we also discuss about other inhibitors of TREK-1 channels with a proven efficacy in treating depression in the clinic, such as fluoxetine.


There is some research to suggest that TREK-1 plays an important role in the ability of muscle to respond to mechanical stimulation. 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 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 not only provide new treatment modalities for conditions like myogenic bladder dysfunction, but may also open up new pathways for understanding the physiology of muscle performance

Mixing and our recommended dosage

You inject 2ml water into the vial of PE 22-28 from the water vial. 1 full syringe is 1ml. You then wait for the vial powder content to dissolve ON ITS OWN. DO NOT SHAKE THE VIAL TO MIX POWDER. Once dissolved and clear in colour you draw out 0.25 – 0.3 on the syringe each morning before breakfast and inject it into the tummy under the skin into the fatty skin layer. A vial should last 7-8 days.

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