PE-22-28: What Research Shows About This Experimental Peptide

PE-22-28 is a synthetic peptide being studied for its effects on the potassium channel TREK-1 in depression research. Laboratory and animal findings explain the scientific interest in the compound. Whether it can become an effective, well-tolerated treatment for people remains an open question.

PE-22-28 is an experimental compound, not an established antidepressant. It has no FDA approval for the uses discussed here. The regulatory information concerns the United States and does not replace individual legal or medical advice.

Key points

• PE-22-28 is not an FDA-approved drug. The October 2026 HHS policy covering conditional compounding of certain peptides does not name PE-22-28.
• The efficacy findings discussed here come from laboratory and rodent studies. These sources provide no published clinical results establishing a benefit or safe dose in people.
• A research label, a clinician’s recommendation, and regulatory approval are different things. An online listing does not establish lawful marketing as a medicine.
• The synthetic peptide contains seven amino acid residues and emerged from the spadin research program. Scientists are investigating antidepressant-like effects through inhibition of the potassium channel TREK-1.
• Positive behavioral and neurogenesis findings provide a research lead. Results for modified analogs should not automatically be attributed to PE-22-28 itself.
• PubChem, CID 165437303, provides chemical reference information. A chemical database entry is not approved prescribing information and does not establish a recommended use. Source 1

Where PE-22-28 comes from and how it works

Origin and discovery: From sortilin to spadin to PE-22-28

Its development traces back to the 2010 paper by Mazella, Pétrault, Lucas, and colleagues in PLoS Biology. As sortilin matures in the Golgi apparatus, a 44-amino-acid propeptide, abbreviated PE, is released. Spadin corresponds to positions 12–28 of that propeptide and contains 17 amino acid residues; PE-22-28 corresponds to positions 22–28. The numbering therefore refers to PE, not to the shorter spadin molecule. Sortilin is a sorting receptor encoded by SORT1 that helps transport proteins within cells.

Spadin selectively blocked TREK-1 and produced rapidly appearing antidepressant-like effects in mouse behavioral tests. These included the forced swim test, a test measuring delayed feeding in an unfamiliar environment, and the learned helplessness model. Source 1

The discovery of spadin drew attention to TREK-1 as a potential pharmacological target for influencing mood. TREK-1 is a two-pore-domain background potassium channel, or K2P channel. Its functional characterization in the brain was the subject of a 2004 paper by Heurteaux and colleagues in The EMBO Journal. Source 1

A study by Moha ou Maati, Veyssière, Labbal, and colleagues, published in Neuropharmacology in 2012, reported no seizure-promoting or cardiac adverse effects of spadin under the preclinical conditions tested, unlike effects observed with less selective TREK-1 modulators. This supported the idea of targeting the channel more selectively. It does not establish general safety in people. Source 1

Spadin’s limited duration of action and stability prompted researchers to look for more stable analogs. A paper by Veyssiere, Moha ou Maati, Mazella, and colleagues in Psychopharmacology reported stronger antidepressant-like effects and increased generation of new neurons in the hippocampus with so-called retro-inverso analogs of spadin. These analogs change the order and spatial configuration of the amino acids. The work was an early optimization step in the program that later produced PE-22-28. Source 1

In 2017, Djillani, Pietri, Moreno, Heurteaux, Mazella, and Borsotto described shortened spadin fragments and additional chemically modified analogs in Frontiers in Pharmacology. They investigated TREK-1 inhibition, behavior, neurogenesis, and markers of synapses. The program included PE-22-28, G/A-PE-22-28, and biotinylated G/A-PE-22-28. These three compounds need to be distinguished when interpreting individual results.

The paper reports a TREK-1 IC50 of approximately 0.10–0.12 nM for PE-22-28, compared with 40–60 nM for spadin. The abstract and a sentence in the results give 0.12 nM, while Figure 3 and the discussion give 0.10 nM; the assignment to G/A-PE-22-28 is also inconsistent within the paper. Inhibitory potency was substantially greater in this assay, but the exact value should not be presented more precisely than the source allows. IC50 is the concentration producing half-maximal inhibition in the particular experimental setup, not a human dose or a direct measurement of binding affinity. A longer behavioral effect is not a measurement of plasma half-life. Source 1

A 2015 review by Borsotto, Veyssiere, Moha ou Maati, and colleagues in the British Journal of Pharmacology placed TREK-1 and the related channel TASK-3 within research on K2P channels as potential targets for new antidepressants. The precursor protein sortilin also remains of interest, particularly its role in moving TREK-1 to the cell membrane. A review by Mazella, Borsotto, and Heurteaux in Frontiers in Pharmacology discusses this relationship. Source 1 Source 2

Proposed mechanisms: TREK-1, serotonin, and hippocampal neurogenesis

TREK-1, also known as KCNK2, is a background potassium channel that maintains a hyperpolarizing resting current in neurons. When the channel opens, potassium can flow out of the cell. This makes the inside of the cell electrically more negative and the neuron less easily excited. Blocking the channel can make the cell more responsive to depolarizing, or excitatory, signals.

Serotonergic neurons in the dorsal raphe nucleus, a region of the brainstem, appear especially relevant to depression research. A study published in Brain Structure and Function in 2016, after first appearing online in 2014, found increased firing of these 5-HT neurons with spadin. The mechanism described by Moha ou Maati, Bourcier-Lucas, Veyssiere, and colleagues involved 5-HT4 receptors in the prefrontal cortex and metabotropic glutamate receptors of the mGluR2 type. 5-HT is the chemical abbreviation for serotonin. A similar mechanism is hypothesized for PE-22-28, but direct neurophysiological data specific to this shorter analog are limited. Source 1

Ma and Lewis refined the mechanism in a 2020 paper in Frontiers in Pharmacology: spadin selectively opposed TREK-1 activation by arachidonic acid. This may help explain why channel inhibition is selective under particular conditions. Source 1

A second proposed mechanism involves brain-derived neurotrophic factor, or BDNF, and the formation of new synapses. A 2015 paper by Devader, Khayachi, Veyssière, and colleagues in the British Journal of Pharmacology found that spadin promoted synapse formation and BDNF expression in hippocampal neurons. The earlier study of retro-inverso spadin analogs also reported increased formation of new neurons in the dentate gyrus, part of the hippocampus. Such neurogenesis has been associated with antidepressant responses across several drug classes. Whether, and to what extent, it causes those responses remains under investigation. Source 1 Source 2

A 2024 paper by Francis-Oliveira, Higa, Viana, and colleagues in Experimental Neurology added to these findings: TREK-1 inhibition promoted synaptic plasticity (the ability of connections between neurons to change) in the prelimbic cortex in the models studied. Separately, Moreno, Devader, Pietri, and colleagues reported in Frontiers in Pharmacology in 2018 that mice lacking sortilin had altered TREK-1 function and less depressive-like behavior. This connected the findings with upstream biological processes involving sortilin. Source 1 Source 2

A genetic basis for studying TREK-1 had already emerged in a 2006 Nature Neuroscience paper by Heurteaux, Lucas, Guy, and colleagues. Mice in which TREK-1 was genetically deleted showed a behavioral phenotype described as “depression-resistant” in several tests, including forced swimming, tail suspension, and learned helplessness. That term describes behavior in an animal model, not a clinical diagnosis. Source 1

Other groups pursued this approach. In 2021, Wu, Sun, Gong, and colleagues reported in CNS Neuroscience & Therapeutics that both genetic and pharmacological inhibition of TREK-1 changed depression-related behavior and hippocampal plasticity in mice. Source 1

Kim, Jung, Kim, and colleagues reported in the International Journal of Molecular Sciences in 2019 that reducing TREK-1 expression in hippocampal neurons attenuated lipopolysaccharide-induced depressive-like behavior. Lipopolysaccharide is used in these models to provoke an inflammatory response. In 2022, Xu, Ding, Qi, and colleagues showed in ACS Chemical Neuroscience that TREK-1 blockade improved neurogenesis deficits in the dentate gyrus of rats with depressive-like behavior. Source 1 Source 2

A 2015 paper by Lin, Zhang, Ye, and colleagues in CNS Neuroscience & Therapeutics linked TREK-1 activity with the antidepressant effects of escitalopram in a rat model of poststroke depression. It therefore explored a connection with a drug already used in clinical care. Source 1

Independent work outside Borsotto’s laboratory includes a 2015 study by Ye, Li, Zhang, and colleagues in European Neuropsychopharmacology. It reported that TREK-1 blockade and signaling through 5-HT1A receptors acted synergistically, involving the CREB–BDNF signaling pathway. Source 1

Developmental and sex-dependent influences have also been investigated. Francis-Oliveira, Shieh, Vilar Higa, and colleagues reported in Behavioural Brain Research in 2021 that maternal separation in an animal model produced sex-dependent changes in TREK-1 and 5-HT1A expression. Source 1

What animal research shows and what it cannot establish

The main behavioral findings come from the 2017 study in male C57BL/6J mice. In the corticosterone model, PE-22-28 was given at 3.0 µg/kg by injection into the abdominal cavity, compared with 100 µg/kg for spadin. The analog program also investigated 1.0 mg/kg delivered by a feeding tube. Some figure captions and pooled analog-dose descriptions are inconsistent; the range of 3.2–4.0 µg/kg therefore should not be presented as a universal dose for unmodified PE-22-28. These amounts describe animal experiments and are not human dosing recommendations.

PE-22-28 reduced immobility in the forced swim test after a single administration and after four days of treatment. In the acute corticosterone model, the paper reports 98.1 ± 8.78 seconds with PE-22-28 versus 164.9 ± 6.03 seconds in the control group, with n = 10 in each group and p < 0.0001. After four days, the delay before eating in an unfamiliar environment also decreased. These tests assess antidepressant-like behavior in an animal model, not clinical depression. A small p-value establishes neither a clinical effect size nor an expected benefit in people.

The frequently cited prolonged effect comes from a different part of the study: Figure 7 examines G/A-PE-22-28 and biotinylated G/A-PE-22-28, not unmodified PE-22-28. Ten mice were tested at each time point. Calculated times to half of the behavioral effect were 14 and 21 hours for G/A-PE-22-28 at 3.2 and 32 µg/kg, respectively, and 17 and 23 hours for the biotinylated analog at 4.0 and 40 µg/kg. The comparison was with an earlier spadin half-effect time of approximately six hours; its behavioral effect disappeared after around seven hours. These are not plasma half-lives. The study also does not establish clinical equivalence to fluoxetine. Source 1 Source 2

Potential neuroprotective effects beyond conventional depression models have also been studied. In 2019, Pietri, Djillani, Mazella, and colleagues described protective effects of sortilin-derived peptides on stroke recovery and poststroke depression in a preclinical model in Neuropharmacology. Source 1

Nonpeptide TREK-1 inhibitors, such as Lig4-4, have also shown neuroprotective effects in rodent models involving occlusion of the middle cerebral artery. A study by Wang, Liu, Xiao, and colleagues appeared in Neuroscience Letters in 2018. It offers a comparison with peptide research but does not establish direct equivalence between the compounds. Source 1

Other studies have examined TREK-1 in blood vessels and inflammation in the nervous system, with differing results. In the Journal of Neuroinflammation in 2019, Fang, Tian, Huang, and colleagues reported that TREK-1 deficiency worsened blood–brain barrier damage and neuroinflammation after intracerebral hemorrhage in mice. By contrast, a 2022 paper by Zheng, Yang, Zhu, and colleagues in Molecular Neurobiology describes TREK-1 as promoting blood–brain barrier breakdown and neuronal death after focal cerebral ischemia, a localized reduction in blood supply to the brain. These opposing directions cannot be merged into one uniform conclusion. Source 1 Source 2

TREK-1’s role appears to depend on brain region, cell type, and the type of injury. Sustained blockade could pose risks in certain neurovascular situations that rodent depression models do not capture. This is a mechanistically plausible possibility, not demonstrated harm from PE-22-28 in people. The underlying review does not identify publicly available, peer-reviewed rodent toxicology data specific to PE-22-28.

There are also general limits to preclinical depression research. Forced swim and tail suspension tests measure behaviors traditionally called “behavioral despair” and used as indirect indicators of antidepressant-like activity. They do not measure human depression. Their ability to predict clinical outcomes in people has historically been limited. Neurophysiology, drug handling in the blood, and properties of the blood–brain barrier also differ substantially between rodents and humans.

What the evidence in people looks like

How many human studies are available?

The sources cited in this article provide no completed clinical efficacy studies of PE-22-28. The original review reported no corresponding PubMed results as of September 2026. That is a limited search finding, not proof that no unpublished investigations or ongoing projects exist anywhere in the world.

The 2019 review by Djillani, Pietri, Mazella, Heurteaux, and Borsotto in Pharmacology & Therapeutics discusses the TREK-1 blocker program, including PE-22-28. Bioavailability, reaching the brain, and translation to people are among the unresolved development questions. The sources available here do not close that gap. This does not claim a current, comprehensive check of every trial registry. Source 1

What does that gap mean for claims online?

Some seller websites and nootropic forums describe PE-22-28 as though an antidepressant effect in people has already been established. The published findings presented here do not support that claim. Behavioral effects in standardized rodent tests can provide a mechanistically plausible starting point for drug development. Whether a compound treats human depression must be investigated in people.

Translating behavioral pharmacology in rodents into antidepressant treatment for humans is difficult.

No studies are identified here that establish PE-22-28’s pharmacokinetic profile in people, whether relevant concentrations reach the brain after systemic administration, or its safety and tolerability. Pharmacokinetics describes how the body absorbs, distributes, breaks down, and eliminates a substance. The 2019 review by Djillani and colleagues identifies bioavailability and translation to human use as unresolved questions for spadin-derived analogs. Source 1

Regulatory and legal status

FDA status

PE-22-28 is not an FDA-approved drug. The HHS policy published in October 2026 on conditional enforcement discretion for certain peptides compounded under Section 503A lists six substances in Appendix A; neither PE-22-28 nor spadin is included. That policy is also not FDA approval. Source 1

The absence of publicly available information about an Investigational New Drug application, or IND, does not establish that no such application exists. Authorization to investigate a drug, marketing approval, and the conditions for compounding are distinct legal questions. The documents reviewed here do not establish a regular approved treatment pathway for PE-22-28; they cannot support a blanket conclusion about every conceivable research or exceptional-access pathway.

What does this mean in practice?

For products sold as PE-22-28 by online research chemical suppliers, oversight comparable to that of approved medicines is not established here. A dose–response relationship validated in humans is also lacking.

The information described here cannot determine how often such products are contaminated, incorrectly dosed, or contain a substance other than the one stated, specifically for PE-22-28.

Offering a product as a research chemical establishes neither pharmaceutical quality nor suitability for human use. The legality of manufacturing, importing, prescribing, or distributing it depends on the product, intended use, and applicable rules. Absence from a single FDA list is not enough for a comprehensive legal assessment.

Safety: What is known and what remains open

Missing clinical safety data

The underlying review identifies no conducted or published phase 1 safety study of PE-22-28. These early clinical studies examine, among other things, tolerability and how a compound behaves in the human body. Without corresponding data, its adverse-effect profile in people remains unknown.

Common unanswered questions at this development stage include immunogenicity (the ability to trigger an immune response), binding to other receptors at higher concentrations, and the safety of breakdown products. Effects in people with multiple or complex medical conditions and interactions with existing medications are also unresolved. The rodent studies described do not report toxicological results in detail. Even extensive rodent safety data would have limited ability to predict human tolerability.

Mechanistic risk signals from TREK-1 biology

TREK-1 has different functions in neurons, astrocytes, and endothelial cells lining blood vessels. Its effects depend on the cell type and brain region involved.

Fang and colleagues’ 2019 study describes worse outcomes with TREK-1 deficiency after brain hemorrhage. Zheng and colleagues’ 2022 study instead describes a harmful role for TREK-1 itself after focal cerebral ischemia, a localized reduction in blood supply to the brain. These findings point in different directions. Source 1 Source 2

It remains unclear whether sustained, widespread TREK-1 blockade could harm people with impaired cerebral circulation, even if it produces favorable behavioral changes in healthy rodents. That is a theoretical risk, not a documented clinical adverse effect of PE-22-28. Controlled rodent depression models cannot answer these questions or define a TREK-1 inhibitor’s entire safety profile.

Risks from unregulated sources

For research chemicals, the product name alone does not reveal whether manufacturing, purity, identity, and dose consistency have been reliably checked. A blanket regulatory assessment of every supplier has not been independently established here.

Injecting unverified substances from outside the pharmaceutical supply chain introduces risks separate from the compound’s mechanism of action. These include inadequate sterility, endotoxin contamination, and incorrect peptide sequences.

Who should not use PE-22-28?

There is no clinical basis for self-directed use of PE-22-28. The data cited here establish neither an effective dose nor safety, pharmacokinetics, or long-term effects in people. Human investigation would require properly regulated clinical research with appropriate manufacturing and monitoring. A product from a research chemical store does not provide those safeguards.

Some mechanistic and practical issues deserve particular attention. The following examples describe unresolved risks. They are not a formal list of contraindications, because there is no approved indication:

• In people with a previous stroke, intracerebral hemorrhage, or another cerebrovascular condition, the neurovascular findings matter. Rodent studies show greater blood–brain barrier damage and neuroinflammation with TREK-1 deficiency in certain injury models. Sustained pharmacological blockade could therefore pose neurovascular risks in especially vulnerable people. The findings nevertheless depend on context and do not consistently point in the same direction.
• Interactions with serotonergic medications are unknown. These include SSRIs, SNRIs, MAO inhibitors, tramadol, meperidine (also called pethidine), linezolid, and other substances. The proposed mechanism of PE-22-28 includes increased activity of serotonergic neurons. Its pharmacodynamic interaction with medications affecting the same signaling system has not been characterized.
• No data on reproduction, embryonic development, or child development during pregnancy or breastfeeding are identified here.
• In competitive sport, the S0 rule for nonapproved pharmacological substances must be considered. It can cover research compounds that are not individually named; classification should be clarified with the relevant antidoping organization.
• For an active psychiatric condition under medical care, independently using an insufficiently characterized research compound could interfere with established treatment.

When symptoms deserve attention

Persistent low mood, anhedonia (loss of pleasure and interest), exhaustion, poor sleep, or cognitive symptoms deserve a careful assessment. Primary or psychiatric care can provide a comprehensive evaluation. Depending on symptoms and the examination, targeted blood tests may help investigate treatable physical contributors.

Evidence-based options include approved medications, including FDA-approved drugs with, in some cases, decades of safety data; structured psychotherapy with good evidence of effectiveness; and scientifically studied lifestyle and daily-life measures. Which options fit depends on the individual situation.

A substantial gap remains between PE-22-28 findings in rodent models and the information needed before use in people. Unresolved questions include pharmacokinetics, an effective dose range, tolerability, and possible interactions. The published data described here do not answer them. Physical contributors can be considered when evaluating mental health symptoms, but objective measurements alone do not provide a complete basis for mental health decisions.

Important safety information

PE-22-28 has no FDA approval for any medical use according to the status described here. Research is largely limited to laboratory and animal studies; the underlying review identifies no robust human clinical trial data. Safety, efficacy, appropriate dosing, and long-term effects in people remain unresolved. This article provides information, not medical advice.

Human clinical safety data for PE-22-28 are also unavailable in the sources presented here. Its adverse-effect profile, tolerability, drug interactions, and pharmacokinetics in people have not been characterized. The efficacy findings described come from preclinical rodent models. They offer clues about potential effects and risks but cannot reliably determine the risk to people.

PE-22-28 should not be used outside a properly authorized clinical trial approved by an appropriate ethics committee or Institutional Review Board (IRB). Particularly relevant unresolved questions concern cerebrovascular disease or previous stroke and brain hemorrhage, concurrent serotonergic medication, pregnancy and breastfeeding, and psychiatric conditions under ongoing treatment. For competitive athletes, the S0 rule for nonapproved substances is an additional consideration. Neurovascular animal findings depend on the model and do not justify a blanket conclusion about every type of brain injury.

For products sold as PE-22-28 through research chemical suppliers, FDA oversight, cGMP manufacturing, and reliable verification of identity and purity have not been established here. Contamination, variable concentrations, and misidentified substances are described as risks of gray-market supply chains. Their frequency specifically for PE-22-28 is not established.

The 2026 WADA Prohibited List does not explicitly name PE-22-28. However, S0 prohibits at all times pharmacological substances not covered by a later section and not approved by any governmental health authority for human therapeutic use. Applying that rule to a particular compound depends on those criteria, not solely on the absence of FDA approval. A missing name therefore does not mean a substance is permitted in sport. Source 1

Depression, persistent low mood, or related symptoms warrant a qualified medical assessment. Approved treatments with clinical safety and efficacy data are available.

Frequently asked questions

Is PE-22-28 FDA-approved?

No. PE-22-28 is not an FDA-approved drug. The October 2026 HHS policy for conditional compounding of certain peptides does not name it. By contrast, the absence of publicly visible information about an IND application does not prove that no application exists. Neither a research label nor an online listing replaces drug approval.

Is PE-22-28 legal in the United States?

Possession, importation, manufacturing, and marketing for human use are different legal questions. This article does not provide a comprehensive assessment under the Controlled Substances Act or applicable state law. Calling a product a research chemical does not establish permission to market it as an unapproved drug for people.

Even the absence of a compound’s name from one list would not resolve every question about distribution or use. A specific legal assessment depends on the product, its actual intended use, the distribution pathway, and the jurisdiction concerned.

Can a clinician prescribe PE-22-28?

There is no regular treatment using an FDA-approved PE-22-28 product. The October 2026 HHS policy does not include PE-22-28. This does not amount to a blanket assessment of every possible clinical research or exceptional-access pathway; those require their own legal and medical evaluation.

The products described outside the approved pharmaceutical supply chain are offered as research chemicals. That label does not make them approved medicines.

How does PE-22-28 differ from spadin?

Spadin contains 17 amino acid residues and corresponds to positions 12–28 of the 44-residue sortilin propeptide PE. Mazella and colleagues described it in 2010 as a TREK-1 blocker with antidepressant-like properties in mice. Source 1

PE-22-28 contains positions 22–28 of the same propeptide, or seven amino acid residues. It was investigated synthetically to develop shorter drug candidates with stronger channel inhibition.

The 2017 paper reports a PE-22-28 IC50 of approximately 0.10–0.12 nM versus 40–60 nM for spadin; the exact assignment of the two lower values is inconsistent within the publication. This describes inhibitory potency in the assay, not clinical superiority. Half-effect times reaching 23 hours concern modified G/A analogs and are not the plasma half-life of unmodified PE-22-28. The sources cited here provide no comparative clinical data in humans. Source 1

What do the rodent behavioral studies actually report?

For PE-22-28, statistically significant reductions are reported in behavioral measures traditionally used as indicators of “behavioral despair.” The main findings are less immobility in the forced swim test and earlier feeding in an unfamiliar environment.

These are preclinical endpoints. The tests cannot reliably predict an antidepressant effect in people. No human studies of PE-22-28 are identified within the search scope described.

What is TREK-1, and why is it an interesting pharmacological research target?

TREK-1, also called KCNK2, is a two-pore-domain background potassium channel. It occurs in many brain regions, including serotonergic neurons in the dorsal raphe nucleus. When open, TREK-1 hyperpolarizes neurons and can reduce their firing rate.

A foundational 2006 paper by Heurteaux, Lucas, Guy, and colleagues in Nature Neuroscience found that mice with genetically deleted TREK-1 showed a phenotype described as depression-resistant across several behavioral tests. These genetic findings provide an important mechanistic foundation for later research on spadin and PE-22-28. Whether the approach can translate into an effective human treatment remains unknown. Source 1

How does PE-22-28 relate to ketamine’s antidepressant mechanism?

A paper listed for 2026 by Song, Song, Du, and colleagues in Neuropharmacology reported that TREK-1 channel blockade mediates the antidepressant-like effects of hydroxynorketamine. Hydroxynorketamine is a ketamine metabolite that contributes to its rapid antidepressant-like effects in rodent models. Source 1

The finding connects TREK-1 biology with research on rapidly acting antidepressant treatments involving clinically used ketamine. It suggests the channel could be a shared target across several signaling pathways. Whether this mechanistic overlap could produce comparable or additional clinical effects in people remains unknown. The study does not establish clinical equivalence between PE-22-28 and ketamine.

Did the FDA’s 2026 changes make peptides legal again?

A change to an FDA list does not grant blanket approval to all peptides. The FDA page distinguishes Category 2 substances from withdrawn nominations. A withdrawn nomination is neither evidence of efficacy nor drug approval. Source 1

The October 2026 HHS policy establishes limited enforcement discretion under specified conditions for BPC-157, epitalon, KPV, MOTS-c, semax, and TB-500. Among other requirements, it specifies compound identities, appropriate quality documentation, patient-specific prescriptions, and reporting of serious adverse events. PE-22-28 is not included in Appendix A. Even for covered substances, the policy is not FDA approval. Source 1

This article is for general information only. According to the status described here, PE-22-28 is not FDA-approved for human use. The text does not replace medical advice, diagnosis, or treatment; health concerns should be discussed with a qualified healthcare professional.

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