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Specimen Atlas of Research Peptides81 plates · MIT
Side-by-side · Research reference

PE 22-28vsProstamax

Side-by-side comparison across mechanism, dosage, evidence, side effects, administration, and stack synergies. Citations on every claim where available.

AAnimal-StrongHUMAN-REVIEWED16/47 cited
BAnimal-MechanisticHUMAN-REVIEWED11/38 cited
PE 22-28
TREK-1 Antagonist · Pre-Clinical
0.12 nMTREK-1 IC50Djillani 2017
7 AAPeptide lengthDjillani 2017
AnimalEvidence stage
IP · SQ · Once Daily (animal models)Djillani 2017Pietri 2019
Prostamax
Khavinson Bioregulator · Tissue-Specific Peptide
0.05 ng/mLActive concentrationZakutskiĭ 2006
2.5×SCE frequency increaseDzhokhadze 2012
4 AAPeptide length
SQ · Protocol per Khavinson tradition

01Mechanism of Action

Parameter
PE 22-28
Prostamax
Primary target
TREK-1 two-pore-domain potassium channelDjillani 2017Ma 2020
Chromatin in prostatic cells — pericentromeric heterochromatin regions
Pathway
TREK-1 channel blockade → Neuronal membrane depolarisation → Enhanced hippocampal excitability → Increased neuroplasticity
Epigenetic modulation → heterochromatin decondensation → transcriptional derepressionDzhokhadze 2012
Downstream effect
Antidepressant-like activity in forced swim test and tail suspension test; reduced A1-like reactive astrocyte activation; neuroprotection via NF-κB pathway modulationDjillani 2017Cong 2023Wu 2021
Increased sister chromatid exchange, Ag-NOR activation, reduced C-heterochromatin condensation; tissue-specific regenerative stimulation in prostate organotypic culturesDzhokhadze 2012Zakutskiĭ 2006
Feedback intact?
N/A — direct ion channel blockade; not receptor-mediated endocrine axis
Origin
Synthetic truncation of spadin (PE 12-28), itself derived from the sortilin propeptide C-terminus. Residues 22-28: Val-Val-Arg-Gly-Trp-Leu-Arg.Djillani 2017Mazella 2018
Synthetic tetrapeptide modeled on naturally occurring protein-derived bioregulators isolated between lysine-arginine motifs in long-lived speciesKhavinson 2017
Antibody development
Not reported in animal studies

02Dosage Protocols

Parameter
PE 22-28
Prostamax
Animal dose (antidepressant)
0.3–3 µg/kg IP
Effective in forced swim test, tail suspension test, CUMS models.
Animal dose (neuroprotection)
0.03 µg/kg IPPietri 2019
Low-dose TREK-1 activation post-stroke for 7 days, then high-dose blockade.
Frequency
Once daily
Sustained antidepressant effect over 7+ days.
Onset (animal)
Within hours (acute); full effect 4–7 days
Duration (animal)
7–28 days testedQi 2018Pietri 2019
Comparison to fluoxetine
PE 22-28 outperforms fluoxetine in CUMS-sensitive rats by day 7
Chronic administration shows superior long-term efficacy.
Human equivalent (extrapolated)
Not established — no clinical trials
Allometric scaling from rodent data unavailable.
Evidence basis
Multiple rodent RCTs; behavioral + electrophysiology endpointsDjillani 2017Qi 2018Wu 2021
Animal / organotypic cultureZakutskiĭ 2006Dzhokhadze 2012
No randomized controlled trials in humans.
Effective concentration (in vitro)
0.05 ng/mLZakutskiĭ 2006
Organotypic culture model; demonstrated tissue-specific stimulation.
Human clinical dose
Not established
No published human trials; dosing extrapolated from Russian clinical tradition (not peer-reviewed).
Age groups studied
Young (3-week) and aged (18-month) rats; elderly humans (75–86 years) in vitroZakutskiĭ 2006Dzhokhadze 2012
Duration
Not specified
Khavinson protocols typically 10–20 days per cycle; no long-term safety data.

04Side Effects & Safety

Parameter
PE 22-28
Prostamax
Toxicity (animal)
No adverse effects reported at therapeutic doses
Cardiovascular (theoretical)
TREK-1 expressed in cardiac tissue; arrhythmia risk unclear
Weight change
Not reported in animal studies
Neurological
No seizures or behavioral abnormalities noted
Long-term safety
Unknown — longest animal study 28 days
Published adverse events
None reported in available literature
Genotoxicity signals
Increased sister chromatid exchange (SCE) — marker of DNA recombination/repair; unclear long-term implications
Metal ion interactions
Modulates Cu(II) and Cd(II) chromatin effects; unknown clinical relevance
Human safety data
Absent — no published Phase 1/2/3 trials
Absolute Contraindications
PE 22-28
  • ·Human use — no clinical safety data available
Prostamax
  • ·Active prostate malignancy — epigenetic modulation effects unknown in cancer
Relative Contraindications
PE 22-28
  • ·Cardiac arrhythmia or channelopathy (theoretical TREK-1 cardiac role)
Prostamax
  • ·History of prostate cancer — theoretical concern re: transcriptional activation
  • ·Undiagnosed prostatic nodules or elevated PSA

05Administration Protocol

Parameter
PE 22-28
Prostamax
1. Animal protocol (IP)
Dissolved in sterile saline or vehicle. Intraperitoneal injection, 0.3–3 µg/kg body weight. Once daily administration in rodent behavioral studies.
Subcutaneous or intramuscular — per Khavinson bioregulator tradition. No published human pharmacokinetic data.
2. Stability
Shorter peptide length (7 AA) confers improved plasma stability vs 17-AA spadin. Exact storage conditions not detailed in published protocols.Djillani 2017
If lyophilised: reconstitute with sterile water per manufacturer protocol (not standardized in literature).
3. BBB penetration
Enhanced CNS bioavailability vs full spadin, likely due to smaller size. Mechanism (passive diffusion vs active transport) not fully characterized.
Typically daily or every-other-day in Russian clinical tradition; duration 10–20 days per cycle.
4. Human formulation
Not established — peptide synthesis methods for research use only. No pharmaceutical-grade formulation available.
No established biomarkers. Theoretical: PSA, prostate imaging, symptom scores (IPSS for BPH).
5. Note
All protocols derived from non-peer-reviewed Russian clinical practice; Western regulatory approval absent.