PE-22-28 — Research Overview
Chemical Name: PE 22-28 (7-amino acid fragment corresponding to residues 22-28 of the sortilin/NTSR3 propeptide sequence) Also Known As: PE-22-28, Mini-Spadin, spadin analog Parent Compound: Spadin (PE 12-28) — a 17-amino acid secreted peptide derived from the propeptide of the neurotensin receptor 3 / sortilin (NTSR3/sortilin) Origin of PE-22-28: Identified through systematic HPLC analysis of spadin blood degradation products. When spadin (PE 12-28) was incubated with mouse serum at 37°C, HPLC profiling of the resulting fragments revealed a series of shortened peptides. Screening of these natural degradation products and truncated analogs on hTREK-1/HEK cells identified the 7-amino acid sequence PE 22-28 as the shortest fragment capable of potently inhibiting TREK-1 — with dramatically superior affinity compared to the parent spadin molecule. Structure: 7 amino acid linear peptide Primary Target: TREK-1 (TWIK-Related K+ channel 1) — a member of the two-pore domain (K2P) potassium channel family IC50 for TREK-1: 0.12 nM (compared to 40-60 nM for parent spadin — approximately 333-fold to 500-fold more potent) Selectivity: Does not inhibit TREK-2, TRAAK, TRESK, TASK-1, or hERG — establishing high selectivity for TREK-1 within the K2P family and beyond Regulatory Status: No FDA approval, no EMA approval. No human clinical trials published. Preclinical research compound. WADA Status: Not specifically listed on the WADA prohibited list as of the research compilation for this post. Category: TREK-1 K2P potassium channel inhibitor / sortilin propeptide-derived analog / antidepressant research peptide / serotonergic system modulator / hippocampal neurogenesis research tool
Research Use Only — Disclaimer
The scientific literature on this page is provided strictly for educational and informational purposes. All Rogue Compounds products are intended for in-vitro laboratory research use only and are not approved by the FDA for human or animal consumption. The studies referenced below are independent third-party peer-reviewed publications. Rogue Compounds makes no claims that any product diagnoses, treats, cures, or prevents any disease or condition. Researchers are responsible for compliance with all applicable local, state, and federal regulations.
What Is PE-22-28?
PE-22-28 is a 7-amino acid synthetic peptide derived from the systematic optimization of spadin — itself a naturally occurring peptide released from the propeptide of the neurotensin receptor 3 / sortilin protein during its maturation in the trans-Golgi network. PE-22-28 represents the shortest and most potent of a series of spadin-derived analogs developed to improve upon spadin’s TREK-1 inhibitory potency, in vivo stability, and bioavailability profile, and was identified through HPLC-guided analysis of spadin’s natural serum degradation products — a rational drug design approach that used the body’s own enzymatic processing as a guide to pharmacophore identification.
Its scientific significance is rooted in the broader story of TREK-1 as a target in depression biology, and in the larger question of whether the gap left by conventional antidepressants — their delayed onset, their high non-response rates, and their burden of side effects — can be addressed through a fundamentally different neurobiological mechanism. PE-22-28 engages that question through a target class — the two-pore domain K2P potassium channels — that has no representation among any currently approved antidepressant medication.
Understanding PE-22-28 requires understanding three connected layers of biology: the TREK-1 channel itself and its role in neuronal physiology, the sortilin/spadin endogenous system from which PE-22-28 was derived, and the serotonergic mechanism through which TREK-1 inhibition produces antidepressant-like effects. Each layer is independently significant and together they constitute a mechanistically coherent hypothesis for antidepressant action that is genuinely distinct from every approved approach.
The TREK-1 Channel — Biology and Depression Relevance
TREK-1 (TWIK-Related K+ channel 1) is a member of the two-pore domain (K2P) potassium channel family — a structurally and functionally distinct class of background potassium channels that set and regulate neuronal resting membrane potential rather than producing the rapid gated currents associated with voltage-gated channels. K2P channels are “leak” channels — they allow a continuous small outward potassium current that keeps neurons in a hyperpolarized resting state, maintaining the electrochemical gradient that determines how readily a neuron fires in response to excitatory input.
TREK-1 is abundantly expressed throughout the central nervous system, with particularly high expression in the prefrontal cortex, hippocampus, and the serotonergic neurons of the dorsal raphe nucleus — a brainstem structure that is the primary source of serotonin projections to the forebrain. TREK-1 is also expressed in the spinal cord, amygdala, and hypothalamus. The prominence of TREK-1 expression in precisely the brain regions most implicated in mood regulation is one foundational observation supporting its relevance to depression biology.
TREK-1 is a polymodal channel regulated by multiple physiological signals including membrane stretch, temperature, pH, lipids (including arachidonic acid and lysophosphatidylcholine), and a variety of neurotransmitter receptor pathways. The diversity of signals that regulate TREK-1 activity makes it a convergence point for multiple modulatory inputs relevant to mood regulation.
The definitive experimental link between TREK-1 and depression was established by Heurteaux and colleagues in a landmark 2006 Nature Neuroscience paper: mice with homozygous deletion of the TREK-1 gene displayed a complete depression-resistant phenotype in multiple behavioral paradigms — forced swim test, tail suspension test, novelty suppressed feeding, and learned helplessness — while simultaneously showing enhanced serotonergic neuron firing in the dorsal raphe nucleus compared to wild-type controls. This TREK-1 knockout phenotype faithfully recapitulates the behavioral and neurobiological effects of chronic antidepressant treatment — without any drug administration. The convergence of behavioral depression resistance with enhanced serotonergic firing established the mechanistic link between TREK-1 activity, serotonergic tone, and mood state.
The Sortilin-Spadin Endogenous System
Sortilin (also designated NTSR3, neurotensin receptor 3) is a type I transmembrane protein of the vacuolar protein sorting 10 protein (VPS10p) family — a sorting receptor predominantly expressed in brain, liver, and muscle. During its biosynthesis and trafficking through the trans-Golgi network, sortilin’s pro-domain is proteolytically cleaved to generate the mature receptor and release a secreted propeptide called PE (propeptide of sortilin). This propeptide, PE 1-44, is further processed to produce the active peptide spadin, corresponding to residues 12-28 of PE and designated PE 12-28.
The connection between sortilin/NTSR3 and TREK-1 was established when co-immunoprecipitation experiments demonstrated direct physical interaction between NTSR3/sortilin and TREK-1 channels in COS-7 cells and cortical neurons co-expressing both proteins. This interaction appeared to mediate TREK-1 internalization — providing a molecular mechanism by which endogenous sortilin signaling could regulate surface TREK-1 availability.
Spadin’s antidepressant activity was validated in five behavioral tests predicting antidepressant response in mice, and was accompanied by increased 5-HT neuron firing rate in the dorsal raphe nucleus — the same neurobiological signature observed in TREK-1 knockout mice. A 4-day intravenous spadin treatment also induced hippocampal phosphorylation of CREB protein and neurogenesis, representing the neuroplastic changes considered key markers of successful antidepressant treatment. These findings established spadin as the first identified natural antidepressant peptide acting through TREK-1 inhibition.
The limitation of spadin that drove the development of PE-22-28 was pharmacokinetic rather than pharmacodynamic: in vivo, spadin activity disappeared beyond 7 hours after administration due to rapid enzymatic degradation. For a therapeutic or research tool intended to model sustained antidepressant effects, this half-life was insufficient. Improving stability while maintaining or enhancing TREK-1 inhibitory potency became the design objective.
From Spadin to PE-22-28 — Rational Drug Design Through Serum Degradation Analysis
The identification of PE-22-28 from spadin blood degradation products represents an unusually elegant approach to rational drug design. Rather than synthesizing arbitrary truncations or modifications of spadin, the Djillani et al. group systematically analyzed what the body’s own enzymatic machinery produced when spadin was metabolized — using HPLC analysis of spadin incubated with mouse serum at 37°C to identify the natural degradation products. This approach is based on the rational hypothesis that metabolic fragments identified in serum may represent pharmacophoric core sequences capable of engaging the target receptor.
Two primary degradation products were initially identified: PE 14-28 and PE 12-27. Systematic testing of these and additional truncations on hTREK-1/HEK cells using patch-clamp electrophysiology revealed a structure-activity relationship across the shortened sequences. PE 22-28 emerged as the shortest sequence that retained potent TREK-1 inhibitory activity — and dramatically exceeded the parent spadin’s potency with an IC50 of 0.12 nM compared to 40-60 nM for spadin.
The selectivity profile was as important as the potency: PE 22-28 tested against a panel of related K2P channels — TREK-2, TRAAK, TRESK, and TASK-1 — showed no significant inhibition, establishing high selectivity for TREK-1. PE 22-28 was also tested against hERG, the cardiac potassium channel whose inhibition causes QT prolongation and arrhythmia risk — one of the most common drug safety concerns for channel-targeting compounds. PE 22-28 showed no significant hERG inhibition, a critically important safety distinction that sets it apart from many channel-modulating compounds.
Mechanism of Action
TREK-1 inhibition and neuronal membrane potential: PE-22-28 binds to and inhibits the TREK-1 two-pore domain potassium channel, blocking the outward leak potassium current that TREK-1 maintains under resting conditions. By reducing this background potassium conductance, PE-22-28 increases neuronal membrane potential — depolarizing neurons toward threshold — making them more excitable and more responsive to synaptic inputs.
Serotonergic neuron disinhibition in the dorsal raphe nucleus: TREK-1 is expressed in the serotonergic neurons of the dorsal raphe nucleus. Under normal physiological conditions, TREK-1 activity contributes to maintaining the hyperpolarized resting state of these neurons, constraining their firing rate. When TREK-1 is inhibited by PE-22-28, the serotonergic neurons of the dorsal raphe are disinhibited — their firing rate increases, augmenting the release of serotonin into forebrain projection targets including the prefrontal cortex, hippocampus, and limbic structures. This mechanism is upstream of SSRI action: rather than blocking serotonin reuptake after release (the SSRI mechanism), PE-22-28 acts earlier in the signaling chain by increasing the rate of serotonin neuron firing.
This upstream-of-SSRI positioning has a potentially important pharmacological implication: the antidepressant effect does not depend on restoring serotonin signaling within the synaptic cleft after reuptake — it depends on increasing the activity of the neurons producing the serotonin in the first place. This distinction may explain the rapid onset of behavioral antidepressant effects observed with PE-22-28 in rodent models, in contrast to the 2 to 4 week delay characteristic of SSRIs, which require secondary adaptive changes downstream of the reuptake blockade to produce their antidepressant effect.
Hippocampal neurogenesis: Treatment with PE-22-28 and its parent compound spadin promotes hippocampal neurogenesis — measurable by BrdU (5-Bromo-2′-Deoxyuridine) incorporation labeling of newly proliferating cells in the dentate gyrus of the hippocampus. Hippocampal neurogenesis is considered a key marker of antidepressant action after chronic treatment, and its occurrence with PE-22-28 within a short treatment window further distinguishes this approach from conventional antidepressants, which typically require weeks of chronic treatment to produce measurable neurogenesis increases.
Synaptogenesis — PSD-95 upregulation: PE-22-28 treatment increased expression of PSD-95, a postsynaptic density protein that is a key structural and functional marker of excitatory synapses. PSD-95 upregulation indicates promotion of synaptogenesis — the formation of new synaptic connections — which alongside neurogenesis represents the structural neuroplastic changes associated with antidepressant efficacy. The combination of enhanced neurogenesis and synaptogenesis in response to a short treatment course positions PE-22-28 as an agent that promotes the structural brain remodeling that conventional antidepressants require weeks to weeks to induce.
Neuroprotective effects against seizures: In contrast to the theoretical concern that TREK-1 channel deletion (in knockout studies) might increase seizure susceptibility — given TREK-1’s role in constraining neuronal excitability — PE-22-28 treatment did not exacerbate seizure activity in treated mice. Spadin-treated animals actually exhibited heightened resistance to generalized seizures, and PE-22-28 appeared to produce even more pronounced protective effects. This apparently paradoxical neuroprotective effect in the context of TREK-1 inhibition may reflect the difference between complete genetic channel elimination throughout development and acute pharmacological inhibition in adults, and warrants further investigation.
Post-stroke depression research direction: TREK-1 overexpression has been documented following cerebral ischemia, and this overexpression may contribute to the post-stroke depression that occurs in a substantial proportion of stroke survivors and is particularly resistant to conventional antidepressant treatment. The potential for TREK-1 inhibition by PE-22-28 to address a mechanism specifically activated by stroke injury represents a research direction with significant clinical unmet need.
In Vivo Stability — The Core Improvement Over Spadin
One of the most significant practical advances PE-22-28 represents over spadin is in vivo stability. Spadin (PE 12-28) disappears from circulation beyond 7 hours after administration — a half-life that limits its utility as a sustained pharmacological agent and that correlates with the loss of behavioral antidepressant activity beyond this window in forced swim test studies.
G/A-PE 22-28 (the glycine-to-alanine substituted analog of PE-22-28) extended the behavioral activity window to 21 hours, and biotinylated G/A-PE 22-28 to 23 hours — representing a 3-fold improvement in duration of effect compared to spadin, achieved through minor structural modifications while retaining TREK-1 inhibitory potency. The native PE-22-28 sequence shows significantly improved stability compared to spadin.
The behavioral antidepressant effects of PE-22-28 and its analogs are active across multiple routes of administration — intraperitoneal (ip), intravenous (iv), and oral gavage — an important practical finding demonstrating that the antidepressant activity of these compounds is not limited to a single route of delivery.
Published Research
Study 1 — TREK-1 Knockout Establishes the Foundational Depression-Resistance Phenotype
Authors: Heurteaux C, Lucas G, Guy N, El Yacoubi M, Thümmler S et al. Year: 2006 Journal: Nature Neuroscience Referenced via: Nat Neurosci. 2006;9:1134-1141. PMID: 16936722
This landmark Nature Neuroscience paper established TREK-1 as a validated target in depression biology — the foundational observation without which the entire spadin and PE-22-28 research program would not exist.
Mice with homozygous deletion of the TREK-1 gene displayed a complete depression-resistant phenotype across multiple validated behavioral paradigms including the forced swim test, tail suspension test, novelty suppressed feeding, and learned helplessness — all behavioral tests with predictive validity for antidepressant drug response in humans.
The TREK-1 knockout phenotype was accompanied by a significant increase in 5-HT neuron firing rate in the dorsal raphe nucleus — the primary source of serotonin projections to the forebrain — directly establishing the neurobiological mechanism linking TREK-1 activity to serotonergic tone and mood regulation.
The behavioral depression resistance of TREK-1 knockout mice faithfully mimicked the phenotype produced by chronic antidepressant treatment without any pharmacological intervention — establishing that silencing TREK-1 alone is sufficient to produce antidepressant-like effects and validating TREK-1 inhibition as an antidepressant mechanism.
Study 2 — Spadin Discovery: First Natural Antidepressant Peptide Acting Through TREK-1
Authors: 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 Year: 2010 Journal: PLOS Biology PMID: 20405001 Full text: https://pmc.ncbi.nlm.nih.gov/articles/PMC2854129/
This PLOS Biology paper reported the discovery and validation of spadin (PE 12-28) as the first natural antidepressant peptide acting through TREK-1 inhibition — establishing the sortilin propeptide as the source of endogenous TREK-1 regulation and demonstrating in vivo antidepressant efficacy.
Spadin was identified as a peptide secreted from the propeptide generated during maturation of NTSR3/sortilin, and was shown to physically interact with TREK-1 channels in COS-7 cells and cortical neurons co-expressing both proteins — establishing the molecular basis for endogenous TREK-1 regulation through the sortilin system.
In five behavioral tests predicting antidepressant response, spadin-treated mice showed depression resistance equivalent to the TREK-1 knockout phenotype — validating that pharmacological inhibition of TREK-1 by a peptide produces the same behavioral outcome as genetic elimination of the channel.
A 4-day intravenous spadin treatment induced hippocampal phosphorylation of CREB and measurable neurogenesis — neuroplastic markers typically associated with weeks of chronic SSRI treatment, here produced by a short spadin treatment course, supporting the rapid-onset hypothesis.
Spadin also significantly increased 5-HT neuron firing rate in the dorsal raphe nucleus in vivo — directly confirming the serotonergic mechanism connecting TREK-1 inhibition to enhanced serotonergic transmission.
The paper identified spadin as the first natural antidepressant peptide and established the sortilin-TREK-1 axis as a novel pharmacological system for antidepressant drug development.
Study 3 — PE-22-28 Development: Shortened Spadin Analogs Display Better TREK-1 Inhibition, In Vivo Stability and Antidepressant Activity
Authors: Djillani A, Pietri M, Moreno S, Heurteaux C, Mazella J, Borsotto M (Université Côte d’Azur, CNRS, IPMC, France) Year: 2017 Journal: Frontiers in Pharmacology PMID: 28955242 Full text: https://pmc.ncbi.nlm.nih.gov/articles/PMC5601071/
This is the primary discovery and characterization publication for PE-22-28 specifically — reporting its identification from spadin serum degradation analysis, its exceptional TREK-1 inhibitory potency, its selectivity profile, its in vivo antidepressant activity, and its neurogenesis/synaptogenesis effects.
Systematic HPLC analysis of spadin incubated with mouse serum at 37°C identified natural blood degradation products including PE 14-28 and PE 12-27. Screening of these and additional synthetic truncations on hTREK-1/HEK cells using patch-clamp electrophysiology identified PE 22-28 as the shortest effective TREK-1 inhibitor.
In vitro patch-clamp studies on hTREK-1/HEK cells established PE-22-28’s IC50 at 0.12 nM for TREK-1 inhibition — compared to 40-60 nM for spadin, representing a 333-fold to 500-fold potency improvement in a fragment less than half the length of the parent compound.
Selectivity testing confirmed PE-22-28 does not inhibit TREK-2, TRAAK, TRESK, or TASK-1 channels, and does not affect hERG channel activity at tested concentrations — establishing the favorable selectivity and cardiac safety profile at the in vitro level.
In the forced swim test, PE-22-28 and analogs showed antidepressant activity after acute injection at approximately 3-4 micrograms per kilogram — compared to 100 micrograms per kilogram required for spadin — consistent with the dramatically improved potency observed in patch-clamp studies.
In sub-chronic 4-day treatment, PE-22-28 analogs produced antidepressant effects in forced swim test, novelty suppressed feeding, and learned helplessness models. Antidepressant effects were obtained regardless of route of administration (ip, iv, gavage), confirming route-independent activity.
Hippocampal neurogenesis was increased as measured by BrdU labeling, with synaptogenesis confirmed by increased PSD-95 expression — structural neuroplastic effects consistent with antidepressant action produced within the short treatment window.
G/A-PE 22-28 (glycine to alanine substitution at position 22) extended behavioral activity duration from spadin’s 7-hour window to 21 hours, and biotinylated G/A-PE 22-28 to 23 hours — demonstrating that the stability limitation of the parent spadin can be substantially overcome through simple structural modifications of the PE-22-28 core.
Study 4 — Comprehensive Review: Fighting Against Depression with TREK-1 Blockers — Past and Future
Authors: Djillani A, Mazella J, Heurteaux C, Borsotto M (CNRS / Université Côte d’Azur) Year: 2019 Journal: Pharmacology and Therapeutics Full text: https://www.sciencedirect.com/science/article/am/pii/S0163725818301785
This comprehensive review synthesized the complete TREK-1 antidepressant research program — from the foundational TREK-1 knockout phenotype through spadin discovery and PE-22-28 development — and articulated the research roadmap toward clinical application.
PE 22-28 was characterized as the shortest, most efficient sequence capable of blocking the TREK-1 channel, with TREK-1 current blockade specific to TREK-1 and not extending to TREK-2, TRAAK, TRESK, or TASK-1.
The review documented the complete structure-activity relationship for PE-22-28 and its analogs, identifying the N- and C-terminal modifications that abolish or maintain TREK-1 inhibition, providing the pharmacophore understanding needed for further analog development.
G/A-PE 22-28 and biotinylated G/A-PE 22-28 were identified alongside PE-22-28 as the most promising candidates for preclinical development, with the goal articulated of completing full preclinical development before launching clinical trials.
The review placed the TREK-1 inhibitor antidepressant strategy in the context of the broader depression treatment landscape — acknowledging the inadequacy of current treatments (delayed onset, 30-40% non-response rate, significant side effect burdens) and positioning TREK-1 inhibition as a mechanism with both distinct neurobiological rationale and demonstrated behavioral efficacy in multiple validated rodent models.
The TREK-1 inhibitor mechanism was explicitly compared to established and emerging antidepressant mechanisms — noting its distinction from all current approved drugs (no monoamine reuptake inhibition, no direct serotonin receptor agonism, no NMDA receptor antagonism) and its potential relevance to treatment-resistant depression through a completely independent mechanistic pathway.
PE-22-28 in the Context of Depression Treatment Research
Depression affects an estimated 20% of the population worldwide across a lifetime and represents the leading cause of disability globally by years lived with disability. Despite decades of pharmacological development, the treatment landscape has fundamental limitations: SSRIs and SNRIs require 2 to 4 weeks to produce therapeutic response during which symptom burden continues, have non-response rates approaching 30-40% in first-line treatment, and produce common side effects including sexual dysfunction, weight gain, and emotional blunting. The atypical antidepressant ketamine/esketamine produces more rapid onset through NMDA receptor antagonism but carries dissociative side effects and concerns about abuse potential.
PE-22-28 and the broader spadin/TREK-1 research program offer a mechanistically independent approach that addresses several of these limitations by design. The rapid behavioral antidepressant effects observed in rodent models with acute PE-22-28 treatment — without the weeks-long delay of SSRIs — emerge directly from the upstream position of TREK-1 inhibition relative to serotonergic transmission. By increasing serotonergic neuron firing rate rather than blocking reuptake within the synapse, PE-22-28 may produce effects that don’t depend on the secondary adaptive receptor changes that underlie the delayed response of SSRIs.
The neurogenesis and synaptogenesis data are equally significant: the production of measurable hippocampal neurogenesis and PSD-95 upregulation within a 4-day treatment window contrasts sharply with conventional antidepressants, which require weeks of chronic treatment to produce comparable structural neuroplastic changes. The mechanism by which short TREK-1 inhibitor treatment produces rapid neuroplasticity in the hippocampus remains an active research question — but the observation itself distinguishes PE-22-28 from all existing approved antidepressants in terms of the timeline of neurobiological action.
Current Research Status and Honest Limitations
PE-22-28 and the spadin analog research program are fully preclinical as of the current date. All published evidence derives from in vitro electrophysiology studies on hTREK-1/HEK cells and rodent behavioral models of depression. No human pharmacokinetic data, human pharmacodynamic data, or human clinical trials for PE-22-28 have been published.
The translational challenges that remain are meaningful. Rodent models of depression have historically poor predictive validity for human clinical antidepressant efficacy — the forced swim test, tail suspension test, and other behavioral assays used to characterize PE-22-28 were the same assays that predicted efficacy for many compounds that subsequently failed in human trials. The TREK-1 knockout phenotype in mice is a genetic manipulation that may not accurately model the pharmacological situation of adult humans with clinical depression receiving an acute or subchronic TREK-1 inhibitor treatment.
The blood-brain barrier penetration of PE-22-28 in humans, and its distribution to the dorsal raphe nucleus and other relevant CNS structures at pharmacologically meaningful concentrations, has not been established in human subjects. While route-independence in rodents (ip, iv, gavage) is encouraging, oral bioavailability and CNS penetration of a 7-amino acid peptide in humans are not predictable from rodent data alone.
The research group explicitly states the goal of completing preclinical development before launching clinical trials, indicating the program has not yet reached that clinical threshold as of the primary publications reviewed. PE-22-28 and G/A-PE 22-28 are the lead candidates described as promising antidepressants of a new generation in the foundational Djillani et al. review — with the clinical trial ambition clearly stated but not yet realized.
Reconstitution Note
PE-22-28 is a synthetic 7-amino acid linear peptide. Bacteriostatic water is the standard reconstitution solvent. PE-22-28 dissolves readily in aqueous solution. Always confirm the recommended solvent against the specific lot datasheet before reconstitution.
In-Use Period and Storage
Before Reconstitution — Lyophilized Powder
Rogue Compounds stores all products refrigerated prior to shipping to maintain compound integrity from production through to delivery. Upon receipt researchers should store vials at 2 to 8 degrees Celsius immediately. Keep vials sealed, dry, and away from direct light until ready for use. Do not freeze. Repeated freeze-thaw cycling has been documented in peer-reviewed pharmaceutical formulation literature to accelerate structural degradation even in dry powder form, potentially compromising molecular integrity and experimental reproducibility.
Why We Refrigerate Instead of Freeze
Freezing and thawing introduces mechanical and osmotic stress at the molecular level. Published pharmaceutical research identifies freeze-thaw cycling as a significant risk factor for loss of structural integrity in peptides and protein-based compounds. To protect compound quality at every stage of handling and fulfillment, Rogue Compounds maintains refrigerated rather than frozen cold chain storage throughout the entire process.
After Reconstitution — Liquid Solution
Store reconstituted solutions refrigerated at 2 to 8 degrees Celsius immediately after preparation. Protect from light. Avoid repeated freeze-thaw cycles. Use within the timeframe recommended for the individual compound. Label each aliquot with the compound name, concentration, date of reconstitution, and diluent used. Discard any solution that shows visible particulate matter, discoloration, or signs of contamination.
Note: Storage and in-use recommendations on this page are provided as general laboratory guidance based on standard peptide handling practices documented in peer-reviewed pharmaceutical literature. Researchers should always refer to the individual compound’s published research literature and datasheet for any specific requirements. All products sold by Rogue Compounds are intended strictly for in-vitro laboratory research use only.
Available from Rogue Compounds
View the PE-22-28 product page: https://roguecompounds.com/product/pe-22-28/