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

ARA 290vsCrystagen

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

APhase 2HUMAN-REVIEWED17/59 cited
BAnimal-MechanisticHUMAN-REVIEWED12/40 cited
ARA 290
EPO-Derived Peptide · Innate Repair Receptor Agonist
28 daysPhase 2 durationCulver 2017
Non-erythropoieticSafety profileBrines 2015Liu 2014
Crystagen
Khavinson Bioregulator · Immune-Thymic
B-cellPrimary targetСhervyakova 2014
SpleenTissue specificityСhervyakova 2014
AnimalEvidence level
SQ · Protocol variable

01Mechanism of Action

Parameter
ARA 290
Crystagen
Primary target
Innate repair receptor (EPO receptor / CD131 heterodimer)
B-lymphocytes in splenic tissueСhervyakova 2014
Pathway
EPO/CD131 → JAK2 activation → PI3K/AKT, MAPK signaling → anti-inflammatory, anti-apoptotic cascades
B-cell activation → Immune modulation during agingСhervyakova 2014
Downstream effect
Tissue protection, nerve fiber regeneration, suppression of inflammatory macrophage activation, altered T-cell differentiation (↑Treg, ↑Th2, ↓Th1)Liu 2014Culver 2017
B-cell activation via apoptosis reduction; no observed increase in splenic cell renewalСhervyakova 2014
Feedback intact?
N/A — does not interact with hematopoietic EPO receptorLiu 2014
Unknown — bioregulator mechanism not fully characterized
Origin
11-amino-acid sequence from EPO helix B, engineered to eliminate hematopoietic activity while retaining tissue-protective properties
Synthetic Lys-Glu-Asp-Gly tetrapeptide — Khavinson bioregulator series
Antibody development
Not reported in clinical trials

02Dosage Protocols

Parameter
ARA 290
Crystagen
Standard dose (Phase 2)
4 mg / dayBrines 2015Culver 2017
Sarcoidosis SFN and diabetic neuropathy trials.
Frequency
Once daily
Self-administered subcutaneously.
Unknown — bioregulator protocols variable
Duration
28 days (Phase 2)Culver 2017
Corneal nerve improvements observed by day 28.
Unknown — chronic administration presumed in animal models
Evidence basis
Phase 2 RCTsCulver 2017Brines 2015
64-subject sarcoidosis trial, type 2 diabetes trial.
Animal / mechanistic
Route
SubcutaneousBrines 2015
Subcutaneous (presumed from bioregulator class)
Timing
Any time of day
No circadian dependence reported.
Standard dose
Not standardized — variable protocols
Russian bioregulator literature does not specify unified human dosing.
Half-life
Not reported

03Metabolic / Fat Loss Evidence

Parameter
ARA 290
Crystagen
Primary effect
Improved metabolic control (HbA1c, fasting glucose)Brines 2015
Secondary to neuropathy treatment; direct lipolytic effects not established.
HbA1c
Significant reduction vs placebo
Observed in type 2 diabetes + neuropathy trial.
Fasting glucose
Improved in ARA 290 group
Body composition
Not directly quantified
Fat loss not a primary endpoint; metabolic improvements may reflect insulin sensitivity.

04Side Effects & Safety

Parameter
ARA 290
Crystagen
Injection site reaction
Mild, transient
Hematopoiesis
None — non-erythropoietic
Distinguishes ARA 290 from native EPO.
Cardiovascular
No thrombotic events or hypertension reported
Immunogenicity
No antibody formation reported
Tolerability
Well-tolerated in Phase 2 trialsCulver 2017Brines 2015
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
Absolute Contraindications
ARA 290
  • ·Hypersensitivity to ARA 290
Crystagen
  • ·Active autoimmune disease (theoretical)
Relative Contraindications
ARA 290
  • ·Active malignancy (theoretical EPO-axis concern; not observed in trials)
Crystagen
  • ·Pregnancy / lactation (no data)
  • ·Active B-cell malignancies

05Administration Protocol

Parameter
ARA 290
Crystagen
1. Preparation
Reconstitute lyophilised powder per manufacturer instructions. Use sterile technique.
Subcutaneous injection — presumed from bioregulator class convention. Specific anatomical sites not standardized.
2. Injection site
Subcutaneous — abdomen, thigh, or upper arm. Rotate sites to avoid lipohypertrophy.
Protocol not standardized. If lyophilized, sterile water or bacteriostatic saline typical for peptide bioregulators.
3. Timing
Once daily, any time of day. Self-administered in Phase 2 trials.Brines 2015
Not specified. Bioregulator protocols vary — some practitioners advocate evening dosing, others morning.
4. Dosing
4 mg daily for 28 days (Phase 2 protocol). Duration for chronic use not established.Culver 2017
Lyophilized: room temperature, light-protected. Reconstituted: refrigerate, use within days to weeks depending on preservative.
5. Storage
Lyophilised: store at controlled room temperature. Reconstituted: refrigerate, use within specified timeframe.

06Stack Synergy

ARA 290
+ BPC-157
Moderate
View BPC-157

ARA 290 targets the innate repair receptor (EPO/CD131) for nerve regeneration and anti-inflammatory signaling, while BPC-157 promotes angiogenesis and tissue repair through distinct mechanisms (likely involving VEGF, growth hormone receptor pathways). Combined, they may address both neuroinflammation and structural tissue repair in neuropathy or injury models. No direct clinical data; mechanistic overlap in tissue protection.

ARA 290
4 mg SQ · daily
BPC-157
250–500 mcg SQ · daily
Frequency
Once daily, same or separate injections
Primary benefit
Nerve regeneration, pain reduction, tissue healing
Crystagen
+ Vilon
Multi-pathway
View Vilon

Vilon (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)