PE-22-28
C35H55N11O9
Research Use Only. PE-22-28 is a research compound intended strictly for laboratory and scientific research purposes. It is not approved for human consumption, therapeutic use, or veterinary use. Information on this page is provided for educational and research reference purposes only.
Overview
PE-22-28 is a synthetic peptide derived from a shorter fragment of spadin (also known as PE 12-28), a naturally occurring peptide that itself originates from the propeptide of the TREK-1 potassium channel sorting receptor. It belongs to a class of peptides studied for their interactions with TREK-1, a two-pore domain potassium channel that has attracted scientific interest in the context of neurological research. PE-22-28 was developed as part of efforts to create more stable and potent analogs of spadin by isolating and refining a specific sequence within the parent peptide. Researchers have investigated how modifications to spadin's structure, including the shortened fragment represented by PE-22-28, may influence binding efficiency and molecular stability compared to the original compound. This peptide is intended strictly for laboratory research purposes and is not approved for human use or consumption.
Compound Data
| CAS Number |
1801959-12-5 |
| Molecular Formula |
C35H55N11O9 |
| Molecular Weight |
773.90 g/mol |
| IUPAC Name |
(2S)-2-[[(2S)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[(2-aminoacetyl)amino]-3-methylbutanoyl]amino]-3-hydroxypropanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]-5-(diaminomethylideneamino)pentanoic acid |
| PubChem CID |
165437303
|
Research & Bioactivity
PE-22-28 is a shortened analog of spadin (PE-12-28), a naturally derived peptide that has attracted scientific interest for its interaction with TREK-1, a two-pore domain potassium channel implicated in neurological signaling. Researchers have studied PE-22-28 primarily in the context of mood-related biology, examining how TREK-1 inhibition by this compound compares to that of its parent peptide in both in vitro binding assays and animal models. Studies have investigated whether the truncated structure of PE-22-28 confers advantages in terms of molecular stability and channel-blocking potency relative to longer spadin analogs. Research conducted in preclinical animal models has examined behavioral outcomes associated with TREK-1 inhibition, with investigators assessing how PE-22-28 performs across standard experimental paradigms used to study mood and stress-related neurobiology. The available literature suggests that researchers have found shortened spadin analogs like PE-22-28 to exhibit notable activity profiles, making them subjects of continued interest for understanding the role of TREK-1 in neurophysiology.
Also Known As
- PE 22-28
- 1801959-12-5
- PE 22-28 (acetate)
- L-Arginine, glycyl-L-valyl-L-seryl-L-tryptophylglycyl-L-leucyl-
- orb1981134
- EX-A8193F
- HY-P3581
- AT52611
- DA-66537
- CS-0615995
- T76311
- (2S)-2-[[(2S)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[(2-aminoacetyl)amino]-3-methylbutanoyl]amino]-3-hydroxypropanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]-5-(diaminomethylideneamino)pentanoic acid
Published Research
Shortened Spadin Analogs Display Better TREK-1 Inhibition, Stability and Antidepressant Activity.
Djillani A, Pietri M, Moreno S, Heurteaux C, Mazella J, et al. — 2017
Depression is a devastating mental disorder that affects 20% of the population worldwide. Despite their proven efficacy, antidepressants present a delayed onset of action and serious adverse effects. Seven years ago, we described spadin (PE 12-28) as a promising endogenous peptide with antidepressant activity. Spadin specifically blocks the TREK-1 channel. Previously, we showed that, spadin activity disappeared beyond 7 h after administration. In order to improve spadin stability and bioavailability, we screened spadin analogs and derivatives. From the study of spadin blood degradation products, we designed a 7 amino-acid peptide, PE 22-28. studies on hTREK-1/HEK cells by using patch-clamp technique, showed that PE 22-28 displayed a better specificity and affinity for TREK-1 channel compared to spadin, IC of 0.12 nM vs. 40-60 nM for spadin. In the same conditions, we also pointed out that different modifications of its N or C-terminal ends maintained or abolished TREK-1 channel activity without affecting PE 22-28 affinity. , the antidepressant properties of PE 22-28 and its derivatives were demonstrated in behavioral models of depression, such as the forced swimming test. Mice treated with spadin-analogs showed a significant reduction of the immobility time. Moreover, in the novelty suppressed feeding test after a 4-day sub-chronic treatment PE 22-28 reduced significantly the latency to eat the food pellet. PE 22-28 and its analogs were able to induce neurogenesis after only a 4-day treatment with a prominent effect of the G/A-PE 22-28. On mouse cortical neurons, PE 22-28 and its derivatives enhanced synaptogenesis measured by the increase of PSD-95 expression level. Finally, the action duration of PE 22-28 and its analogs was largely improved in comparison with that of spadin, up to 23 h instead of 7 h. Taken together, our results demonstrated that PE 22-28 and its derivatives represent other promising molecules that could be an alternative to spadin in the treatment of depression.