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PE-22-28 is a synthetic protein that has captured the attention of researchers for its potential therapeutic applications, particularly in the realm of neuroscience. This research chemical is part of a group of synthetic Spadin analogs.
Derived from the natural peptide Spadin, PE-22-28 is currently under investigation for its intriguing properties, including its impact on the TREK-1 receptor, post-stroke recovery, and its role in neurogenesis. This synthetic compound holds promise as a subject of interest in ongoing studies exploring its antidepressant activity and other potential therapeutic effects.
PE-22-28 is a synthetic protein that has garnered attention in the field of neuroscience and mental health. Derived from the naturally occurring peptide Spadin, PE-22-28 exhibits properties that make it a promising candidate for therapeutic interventions, particularly in the context of antidepressant treatment.
At its core, PE-22-28 functions as a TREK-1 receptor antagonist. The TREK-1 receptor, a two-pore potassium channel, has been identified as a potential target for depression therapy. Preliminary research suggests that the deletion of TREK-1 receptors in mice renders them immune to depression. Moreover, the manipulation of sortilin, a protein abundant in the central nervous system and the source of Spadin, has been associated with increased resilience to depression and enhanced development of neurons and synaptic linkages between them.
Mice treated with PE-22-28 reportedly exhibit greater resistance to the development of generalized seizures. This particular quality positions PE-22-28 as a potential peptide to treat neurodegenerative diseases.
The origin of PE-22-28 from Spadin underscores its connection to sortilin and the intricate interplay within the body’s central nervous system. Notably, Spadin itself is less effective in treating depression compared to shorter analogous versions, with PE-22-28 being one such derivative. Like its natural precursor, PE-22-28 acts on the TREK-1 receptor to produce its therapeutic effects.
Despite of such promising results, PE-22-28 still requires more in-depth studies to confirm its potential benefits.
Imagine the brain of a subject as a control center that manages mood, memory, and learning. In this control center, there’s a specific part called the TREK-1 receptor, which acts like a gatekeeper regulating excitement or calming brain cells (neurons).
Now, researchers found that removing these TREK-1 receptors from mice made them less prone to feeling down or depressed. So, scientists got curious and started looking into ways to influence these receptors for potential depression treatments.
The TREK-1 receptor hangs out in important areas of the brain, like the prefrontal cortex and hippocampus, which are like command centers for your mood and memory. When you stimulate the TREK-1 receptor, it kind of settles down the excitement of neurons. On the flip side, if you decrease the activity of this receptor, neurons get more excited.
This is where things get interesting. Spadin, a natural substance, was found to calm down the TREK-1 receptor and had antidepressant effects. But, there was a catch – its effects only lasted for about 7 hours.
Now, enter PE-22-28. It’s like a supercharged version of Spadin. Just like Spadin, PE-22-28 binds to the TREK-1 receptor and stops it from being too active. This blocking action results in a more stable state of mind and an improvement in mood, which is great for potential depression treatment.
But here’s the cool part: PE-22-28 takes things to the next level. Its effects last much longer, up to 23 hours compared to the 7-hour limit of Spadin. So, it’s like having a longer-lasting mood booster that helps the brain of a subject in a happier and more stable state.
In a nutshell, PE-22-28 is like a superhero that targets a specific part of the brain to make subjects feel better. It’s all about regulating the excitement levels in the brain to potentially promote a positive and stable mindset.
PE-22-28 shows potential in mitigating the impact of neurodegenerative diseases, particularly in the context of epileptic seizures. Studies have revealed that mice lacking sufficient levels of TREK-1, a key player in maintaining brain stability, are more prone to seizures induced by substances like kainic acid (KA) and pentylenetetrazol (PTZ).
When the TREK-1 antagonist spadin is administered to these mice, it doesn’t exacerbate the seizures induced by KA or PTZ. In fact, mice treated with spadin exhibit enhanced resistance against developing generalized seizures. Essentially, spadin acts as a protective factor against the harmful effects of seizures. [R]
While PE-22-28, a synthetic derivative of spadin, has shown similar protective effects in mice, it’s important to note that PE-22-28 is not currently prescribed as a medical treatment for neurodegenerative diseases. Further research studies are necessary to fully understand the extent of PE-22-28’s potential benefits, safety, and applicability in treating neurodegenerative illnesses. In essence, the scientific community is still in the process of investigating whether PE-22-28 could be a viable solution for these conditions.
PE-22-28’s impact on depression is under investigation, and while it stems from the natural peptide Spadin known for its antidepressant (AD) properties, its efficacy is not yet conclusive.
Spadin, a 17-amino acid peptide, inhibits TREK-1 channels, initially identified as a target in depression. This channel inhibition is associated with rapid antidepressant effects. Unlike traditional antidepressant treatment modalities including traditional drugs such as fluoxetine, spadin demonstrates its potential antidepressant properties within just four days of treatment. This rapid action is attributed to increased neurogenesis (formation of new neurons) and synaptogenesis (formation of synaptic connections between neurons). [R] [R] [R]
However, when it comes to PE-22-28, the derivative of spadin, its efficiency in treating depression is still inconclusive. It hasn’t proven to be as effective as existing antidepressant medications. Further in-depth studies are necessary to determine the full extent of PE-22-28’s potential benefits and its comparative efficacy in addressing depression when compared to currently available antidepressant treatments.
Post-stroke depression (PSD) is a prevalent mood disorder following a stroke, significantly impacting patient outcomes and survival. In the context of PSD, the TREK-1 channel plays a crucial role in both stroke pathogenesis and the development of depression. Spadin and its shorter analog, mini-spadin, have demonstrated potent antidepressant properties. [R]
Mini-spadin’s beneficial effects extend beyond its antidepressant properties. Studies have shown that it contributes to neurogenesis (the formation of new neurons) and synaptogenesis (the formation of synaptic connections between neurons). Notably, clinical trials have provided evidence supporting mini-spadin’s modulation of TREK-1 channels during both the early and chronic phases of a stroke. This modulation, coupled with the stimulation of brain plasticity, is believed to play a pivotal role in mini-spadin’s brain-protective effects against stroke and its detrimental consequences, including the onset of PSD. [R]
While these findings suggest a promising avenue for addressing PSD, it’s crucial to note that research on the effectiveness of PE-22-28, a derivative of spadin, in the context of post-stroke depression is still in the early stages. Additional studies are needed to determine the full potential of PE-22-28 and its ability to provide therapeutic benefits for individuals grappling with post-stroke depression.
Research suggests that TREK-1, a specific type of potassium channel, plays a crucial role in how muscles respond to mechanical stimulation. The blockade of TREK-1 seems to increase muscle contractility, making the muscles contract more, while the activation of the channel appears to promote muscle relaxation. [R]
In this context, molecules like PE-22-28 come into play. Understanding how these molecules influence muscle contraction and relaxation could open up new treatment modalities for patients suffering from conditions like myogenic bladder dysfunction. Additionally, delving into the physiology of muscle performance through these studies may uncover novel avenues for research and potential therapeutic interventions. [R]
It’s important to note, however, that certain aspects of the research on muscle relaxation, particularly concerning the effects of PE-22-28, are still in their early stages. Further research is essential to fully understand the potential of PE-22-28 and its potential to promote muscle relaxation.
Ongoing studies are being conducted to evaluate the safety and effectiveness of PE-22-28. Additional research is required to fully understand its mechanism of action. It is currently not deemed safe for human consumption.
TREK-1 is a potassium channel with two pores, distributed widely in the central nervous system. It is opened by polyunsaturated fatty acids and lysophospholipids. Neurotransmitters that elevate intracellular cAMP and those activating the Gq protein pathway have the effect of reducing its activity.
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In conclusion, PE-22-28, a synthetic protein derived from Spadin, is currently under investigation for its potential antidepressant activity. While initial research suggests its influence on the TREK-1 receptor and its role in neurogenesis, the complete mechanism of action and safety profile is yet to be fully understood. As ongoing studies delve into the antidepressant properties of PE-22-28, it remains categorized within the realm of research chemicals, highlighting the need for further research to determine its efficacy, safety, and potential as a novel antidepressant intervention.
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Strength | 8mg, 10mg |
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Works as expected. I will definitely buy again.
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