Side-by-side · Research reference
CrystagenvsPE 22-28
Side-by-side comparison across mechanism, dosage, evidence, side effects, administration, and stack synergies. Citations on every claim where available.
AAnimal-MechanisticHUMAN-REVIEWED12/40 cited
BAnimal-StrongHUMAN-REVIEWED16/47 cited
Crystagen
Khavinson Bioregulator · Immune-Thymic
SQ · Protocol variable
PE 22-28
TREK-1 Antagonist · Pre-Clinical
IP · SQ · Once Daily (animal models)Djillani 2017Pietri 2019
01Mechanism of Action
Parameter
Crystagen
PE 22-28
Primary target
B-lymphocytes in splenic tissueСhervyakova 2014
TREK-1 two-pore-domain potassium channelDjillani 2017Ma 2020
Pathway
B-cell activation → Immune modulation during agingСhervyakova 2014
TREK-1 channel blockade → Neuronal membrane depolarisation → Enhanced hippocampal excitability → Increased neuroplasticity
Downstream effect
B-cell activation via apoptosis reduction; no observed increase in splenic cell renewalСhervyakova 2014
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
Feedback intact?
Unknown — bioregulator mechanism not fully characterized
N/A — direct ion channel blockade; not receptor-mediated endocrine axis
Origin
Synthetic Lys-Glu-Asp-Gly tetrapeptide — Khavinson bioregulator series
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
Antibody development
—
Not reported in animal studies
02Dosage Protocols
Parameter
Crystagen
PE 22-28
Standard dose
Not standardized — variable protocols
Russian bioregulator literature does not specify unified human dosing.
—
Evidence basis
Animal / mechanistic
Multiple rodent RCTs; behavioral + electrophysiology endpointsDjillani 2017Qi 2018Wu 2021
Route
Subcutaneous (presumed from bioregulator class)
—
Frequency
Unknown — bioregulator protocols variable
Once daily
Sustained antidepressant effect over 7+ days.
Duration
Unknown — chronic administration presumed in animal models
—
Half-life
Not reported
—
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.
Onset (animal)
—
Within hours (acute); full effect 4–7 days
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.
04Side Effects & Safety
Parameter
Crystagen
PE 22-28
Published adverse events
None reported in available animal literature
—
Human safety data
Absent — no controlled human trials identified
—
Autoimmune considerations
Theoretical concern with B-cell modulators in predisposed individuals
—
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
Absolute Contraindications
Crystagen
- ·Active autoimmune disease (theoretical)
PE 22-28
- ·Human use — no clinical safety data available
Relative Contraindications
Crystagen
- ·Pregnancy / lactation (no data)
- ·Active B-cell malignancies
PE 22-28
- ·Cardiac arrhythmia or channelopathy (theoretical TREK-1 cardiac role)
05Administration Protocol
Parameter
Crystagen
PE 22-28
1. Route
Subcutaneous injection — presumed from bioregulator class convention. Specific anatomical sites not standardized.
Dissolved in sterile saline or vehicle. Intraperitoneal injection, 0.3–3 µg/kg body weight. Once daily administration in rodent behavioral studies.
2. Reconstitution
Protocol not standardized. If lyophilized, sterile water or bacteriostatic saline typical for peptide bioregulators.
Shorter peptide length (7 AA) confers improved plasma stability vs 17-AA spadin. Exact storage conditions not detailed in published protocols.Djillani 2017
3. Timing
Not specified. Bioregulator protocols vary — some practitioners advocate evening dosing, others morning.
Enhanced CNS bioavailability vs full spadin, likely due to smaller size. Mechanism (passive diffusion vs active transport) not fully characterized.
4. Storage
Lyophilized: room temperature, light-protected. Reconstituted: refrigerate, use within days to weeks depending on preservative.
Not established — peptide synthesis methods for research use only. No pharmaceutical-grade formulation available.
06Stack Synergy
Crystagen
+ Vilon
Multi-pathwayVilon (Lys-Glu) activates T-helper cells via apoptosis reduction, while Crystagen activates B-cells. Dual T/B immune modulation in aging models may provide complementary thymic-immune support within the Khavinson bioregulator framework. Both target splenic immune aging through distinct lymphocyte subsets.
- Crystagen
- Dose unknown · SQ
- Vilon
- Dose unknown · SQ
- Frequency
- Protocol variable
- Primary benefit
- Broader thymic-immune coverage (T-cell + B-cell)
PE 22-28
— no documented stacks