Pinealon (EDR): Complete Research Guide — Neuroprotective Tripeptide, Proposed DNA Interaction & Circadian Biology (2026)
- Pinealon (also designated EDR; CAS: 110590-60-8; Glu-Asp-Arg; MW: ~390 Da) is a synthetic tripeptide belonging to the Khavinson peptide bioregulator class developed at the St. Petersburg Institute of Bioregulation and Gerontology. Despite its name suggesting pineal gland origin, Pinealon (EDR) was actually isolated from Cortexin, a bovine brain cortex polypeptide extract; its “pineal” designation refers to its proposed neuroendocrine target effects on pineal gland function, not its tissue source.
- Unlike receptor-mediated peptides, Pinealon is proposed to act by penetrating the blood-brain barrier and interacting directly with neuronal chromatin (DNA), modulating gene expression in neurons involved in circadian regulation, neuroprotection, and antioxidant defense. This proposed epigenetic/nuclear mechanism is not receptor-dependent and has not been confirmed by X-ray crystallography or biochemical receptor binding studies — it remains a working mechanistic hypothesis in published Russian research.
- Published data documents: suppression of reactive oxygen species (ROS) in cerebellar granule cells, upregulation of antioxidant enzymes SOD2 and GPX1 in neural tissue, ERK 1/2 MAPK pathway modulation, improved cell viability under hypoxic conditions, and neuroprotective effects in prenatal hyperhomocysteinemia models (Khavinson et al., Rejuvenation Research, 2012 — PMID: 22567179).
- Important evidence caveat: as of April 2026, virtually all published Pinealon research originates from a single institute (Khavinson group, St. Petersburg). No independent replication has been published in international peer-reviewed journals, and no ClinicalTrials.gov registered trials for Pinealon are listed. Researchers should treat available data as preliminary and single-center.
- Research-grade Pinealon is available as YPB.273 20mg (Research Use Only) through the YPB catalog.
- ~3,000 monthly US searches; positioned as the neuroprotective complement to Epitalon in the Khavinson tripeptide series — addressing neural aging and circadian biology from the neuron level rather than the pineal gland level. Updated April 2026.
What Is Pinealon and How Does It Fit the Khavinson Peptide Framework?
Khavinson Peptide Bioregulator
Proposed DNA/Chromatin Interaction
Pinealon (EDR; Glu-Asp-Arg; CAS: 110590-60-8; MW: ~390 Da) is a synthetic tripeptide developed by Vladimir Khavinson and colleagues at the St. Petersburg Institute of Bioregulation and Gerontology — the same research group responsible for Epitalon (AEDG), Thymalin (TKDQ), Vilon (KE), and the broader class of “peptide bioregulators” that form a distinctive body of Russian longevity and neuroendocrine research literature. Updated April 2026. Pinealon is part of a systematic research program in which short peptides (2–4 amino acids) are derived from tissue-specific polypeptide extracts and characterized for tissue-targeted effects on gene expression, aging biology, and organ function.
A clarification important for research accuracy: despite its name suggesting pineal gland derivation, Pinealon (EDR) was isolated from Cortexin — a bovine brain cortex polypeptide extract — not from pineal tissue. The “Pinealon” name refers to the compound’s proposed effects on pineal gland function and circadian regulation, not its anatomical origin. Researchers citing tissue-source information should note this distinction. Separately, the Khavinson group has also studied Epithalamin (a different pineal peptide complex) and Epitalon (AEDG tetrapeptide derived from the pineal gland fraction), which are distinct from Pinealon despite topical overlap in circadian biology research.
Key Characteristics
| Parameter | Value |
|---|---|
| Sequence | Glu-Asp-Arg (glutamic acid — aspartic acid — arginine) |
| Designation | Pinealon; EDR peptide; Glu-Asp-Arg tripeptide |
| CAS Number | 110590-60-8 |
| Molecular Weight | ~390.38 Da (tripeptide free acid) |
| Amino Acids | 3 (tripeptide; EDR one-letter code: Glu-Asp-Arg) |
| Tissue Source | Isolated from Cortexin (bovine brain cortex polypeptide extract); not from pineal gland tissue |
| Research Group | Khavinson group, St. Petersburg Institute of Bioregulation and Gerontology, Russia |
| Proposed Mechanism | Direct DNA/chromatin interaction in neurons (proposed gene expression modulation without receptor binding); BBB penetration; SOD2/GPX1 upregulation; ERK 1/2 MAPK modulation; ROS suppression |
| Receptor | No specific receptor identified; proposed mechanism is nuclear/chromatin-level rather than cell-surface receptor-mediated |
| Half-Life | Short (unprotected tripeptide; susceptible to peptidase cleavage in plasma); small size may facilitate oral and BBB penetration despite short systemic half-life |
| FDA Status | Not FDA-approved for human use. Investigational/research compound (RUO). Research Use Only (RUO). |
| WADA Status | Not listed on WADA Prohibited List 2025 |
| Storage | Lyophilized: −20°C. Reconstituted: 2–8°C, use within 14 days |
| Evidence Caveat | All published research from a single institute (Khavinson group); no independent replication; no ClinicalTrials.gov entries as of April 2026 |
How Does Pinealon Work? The Proposed Nuclear/Chromatin Mechanism
Pinealon’s proposed mechanism is pharmacologically unusual: it is hypothesized to act not through a membrane receptor but by penetrating cell membranes and the blood-brain barrier to interact directly with neuronal chromatin (DNA), modulating gene expression in a tissue-specific manner. This mechanism places Pinealon in the same general framework as the other Khavinson bioregulator peptides, which are collectively proposed to function as sequence-specific DNA-binding peptides that regulate promoter activity for specific genes.
Proposed DNA Interaction Framework
The Khavinson group has proposed that short tripeptides like EDR interact with specific DNA sequence elements in gene promoter regions, modulating transcription of neuroprotective genes including those encoding antioxidant enzymes (SOD2, GPX1), neurotrophic factors, and circadian rhythm regulators. Published molecular modeling and fluorescence studies from the Khavinson group provide the primary evidence for this mechanism. The proposed binding involves the positively charged arginine residue interacting with the anionic DNA backbone, with sequence-specific contacts from the glutamic acid and aspartic acid residues. This mechanism has not been confirmed by independent X-ray crystallography, ChIP-seq, or CRISPR-based functional genomics, and should be treated as a working hypothesis.
Documented Downstream Effects
Regardless of the upstream mechanism, published cell biology data documents reproducible downstream effects in neural research models:
- ROS suppression: Dose-dependent reduction of reactive oxygen species in cerebellar granule cells under oxidative stress conditions (Khavinson et al., Rejuvenation Research, 2012 — PMID: 22567179)
- Cell viability enhancement: Improved survival of neurons under hypoxic conditions; suppression of apoptotic signaling
- ERK 1/2 MAPK modulation: Activation of ERK 1/2 signaling, which promotes neuronal survival and proliferative pathways
- SOD2 and GPX1 upregulation: Increased expression of mitochondrial superoxide dismutase 2 and glutathione peroxidase 1 — two primary antioxidant enzymes in neural tissue
- Circadian regulation: Proposed modulation of circadian clock gene expression in pineal gland and hypothalamic neurons; studies in animal models document improved circadian rhythm parameters under disrupted conditions
What Systems Has Pinealon Been Investigated For?
Neuroprotection and Neural Aging Research
The primary published research application for Pinealon is neuroprotection in neural aging and hypoxic stress models. Published cell culture studies document improved neuron viability under oxidative stress and hypoxic conditions. Animal studies have examined Pinealon’s effects on age-related neurodegeneration markers and cognitive function in older age groups. Meshchaninov et al. (2015, PMID: 26390612) characterized Pinealon within the broader context of pineal brain peptide research on neural aging and brain homeostasis.
Circadian Rhythm Disruption Research
Pinealon has been studied in published animal models of circadian disruption, where its proposed modulation of pineal gland gene expression may influence melatonin synthesis pathways and circadian clock gene regulation. Research has examined Pinealon in contexts of shift-work-simulated circadian disruption in rodents, documenting improved circadian rhythm metrics under disrupted lighting conditions in published Khavinson group studies.
Prenatal Hyperhomocysteinemia Models
Arutjunyan et al. published data on Pinealon’s neuroprotective effects in prenatal hyperhomocysteinemia models — an experimental context in which elevated homocysteine during gestation produces neurological damage in offspring. Pinealon administration reduced markers of neural oxidative stress and improved functional neurological outcomes in these models.
Retinal Research
Retinal cells are among the highest-oxygen-demand tissues in the body and are vulnerable to oxidative stress-driven degeneration. Published Khavinson group data has examined Pinealon in retinal cell models, where its antioxidant enzyme upregulation and ROS suppression properties have been characterized in photoreceptor cell biology contexts.
What Does the Human Research Data Show?
| Evidence Type | Model / N | Key Finding & Adverse Events | Year |
|---|---|---|---|
| Cell culture (cerebellar granule cells) | In vitro neural cell models | Dose-dependent ROS suppression; improved cell viability under oxidative/hypoxic conditions; ERK 1/2 activation; SOD2/GPX1 upregulation. No cytotoxicity at research concentrations. (Khavinson et al. 2012, PMID: 22567179) | 2012 |
| Animal models (rodent neural aging) | Preclinical rodent studies | Improved cognitive and behavioral metrics in aging rodents; circadian rhythm normalization under disrupted conditions; reduced neurodegeneration markers in prenatal hyperhomocysteinemia offspring models. Well tolerated; no serious adverse events in published animal studies. | Various |
| Human observational data (Russian clinical context) | Small-N Russian clinical observations | Limited human observational data from Russian medical contexts; cognitive improvement reports in age-related cognitive decline (TBI consequences study: 72 research subjects, 0.2 mg oral twice daily). Not published as rigorous controlled trial in international peer-reviewed format. | Various |
| Large-scale human RCT | No ClinicalTrials.gov entries as of April 2026 | No published large-scale placebo-controlled RCT for Pinealon. No registered trials in international clinical trial databases as of April 2026. All evidence is cell culture, animal model, or small-N observational from a single institute. | N/A |
How Does Pinealon Compare to Epitalon and Other Neuroendocrine Research Peptides?
Pinealon and Epitalon are commonly discussed together because both belong to the Khavinson peptide bioregulator series and both address brain aging and circadian biology. Understanding their mechanistic distinction is important for research protocol design.
| Parameter | Pinealon (EDR) | Epitalon (AEDG) | DSIP | Selank |
|---|---|---|---|---|
| Sequence | Glu-Asp-Arg (3 AA) | Ala-Glu-Asp-Gly (4 AA) | Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu (9 AA) | Thr-Lys-Pro-Arg-Pro-Gly-Pro + Gly-Pro sequence (7 AA) |
| Origin | Cortexin (brain cortex extract); name refers to proposed pineal effects, not tissue source | Pineal gland fraction (Epithalamin); truly from pineal tissue | Isolated from rabbit cerebral venous blood 1977 | Synthetic analog of tuftsin; developed in Moscow |
| Primary Research Target | Neuroprotection at the neuronal level: antioxidant enzymes (SOD2/GPX1), hypoxia protection, ERK 1/2 | Pineal gland/upstream circadian: telomerase activation (hTERT/AANAT), melatonin synthesis pathway, cell cycle | Slow-wave sleep (SWS/delta); HPA axis; SRIF inhibition; GH release | Anxiolytic; cognitive; IL-6/IL-10; enkephalin analog |
| Proposed Mechanism | DNA/chromatin direct interaction in neurons (proposed, not receptor-confirmed) | DNA/chromatin direct interaction in pinealocytes (same framework as Pinealon) | No receptor identified (45+ years); empirically documented effects | Angiotensin IV receptor analog; enkephalin catabolism inhibition |
| Published Human Data | Small-N Russian observational; no registered RCT | Small-N Russian studies; longer history (Epithalamin animal longevity studies 1970s–present) | Small-N early phase human data (1981–1984 Eur Neurol) | Human anxiety trials (Russian literature) |
| Independent Replication | None as of April 2026 | Limited; primarily from same research group | Some international EEG replication; primarily Russian | Some international anxiety data |
| YPB SKU | YPB.273 — 20mg | YPB.253/.254 — see guide | YPB.230/.252 — see guide | YPB.228 — see guide |
Pinealon and Epitalon address the neuroendocrine aging axis from different cellular perspectives: Epitalon (see the Epitalon Research Guide) works upstream at the pineal gland level, modulating melatonin synthesis and telomerase activation; Pinealon works downstream at the individual neuron level, upregulating antioxidant enzymes and protecting against oxidative damage in neural tissue. Researchers studying circadian-neurological aging can study both compounds with complementary research protocols addressing different cellular levels of the same biological process.
What Should Researchers Know About Pinealon Stability and Handling?
Pinealon at ~390 Da is the smallest tripeptide in the YPB catalog. Its small size is a pharmacological double-edge: it may facilitate BBB penetration and oral bioavailability (as proposed in published Khavinson research), while also making it susceptible to rapid peptidase degradation in plasma and GI tract.
Storage and Reconstitution
Lyophilized Pinealon is stable at −20°C for up to 24 months. Reconstitute with bacteriostatic water; the compound is highly water-soluble due to its charged amino acid composition (two acidic residues: Glu, Asp; one basic: Arg; net charge is approximately −1 at physiological pH). Once reconstituted, hold at 2–8°C and use within 14 days.
COA Verification
HPLC purity (≥98%) and MS confirmation at ~390.38 Da is the standard quality protocol. The sequence Glu-Asp-Arg should be confirmed; isomeric sequences (e.g., Asp-Glu-Arg) would have identical MW but different biological activity. Amino acid analysis confirming the correct Glu-Asp-Arg order provides additional quality assurance. All YPB Pinealon batches include lot-traceable COA documentation through the COA Library.
Key Research Findings: Pinealon in 2026
Key Research Findings
- Khavinson peptide bioregulator series: Pinealon (EDR) is part of the systematic Russian peptide bioregulator research program; the same framework that produced Epitalon (AEDG), studied across neural aging, circadian biology, and longevity research.
- NOT derived from pineal tissue: Isolated from Cortexin (bovine brain cortex extract); the “Pinealon” name refers to proposed pineal-axis effects, not tissue origin — a common source of confusion in competitor articles.
- Proposed DNA/chromatin mechanism (not receptor-confirmed): The Khavinson group hypothesizes sequence-specific DNA promoter binding that modulates neuroprotective gene expression; this mechanism has not been independently confirmed by X-ray crystallography or international biochemical methods.
- ROS suppression in cerebellar granule cells (Khavinson 2012, PMID: 22567179): Dose-dependent ROS reduction; improved cell viability under hypoxic conditions; the most reproducibly documented in vitro effect.
- SOD2 and GPX1 upregulation in neural tissue: Increased expression of the two primary mitochondrial and cytoplasmic antioxidant enzymes in neurons — downstream effects consistent with the proposed epigenetic regulatory mechanism.
- ERK 1/2 MAPK activation: Published data documents ERK 1/2 pathway modulation promoting neuronal survival and proliferative signaling.
- All research from a single institute; no independent replication: The critical evidence limitation — all Pinealon publications originate from the Khavinson group; no international independent replication and no ClinicalTrials.gov entries as of April 2026.
- Neuroprotective complement to Epitalon: Pinealon (neuronal antioxidant/survival) + Epitalon (pineal gland/telomerase/circadian) address the neuro-circadian aging axis from complementary cellular perspectives within the same research framework.
Browse the Full Research Catalog
Market Demand and Research Interest
| Demand Indicator | Pinealon Data Point |
|---|---|
| Monthly US searches | ~3,000/mo |
| PubMed publications | 40+ (Pinealon / EDR / Glu-Asp-Arg; primarily Khavinson group) |
| Key published paper | Khavinson et al. (2012) Rejuvenation Research (PMID: 22567179): cell viability via ROS suppression |
| Evidence caveat | Single-institute research; no independent replication; no international RCT |
| Research appeal | Novel DNA/epigenetic interaction hypothesis; neuroprotective antioxidant data; circadian biology overlap with Epitalon |
| Unique catalog position | Only neural antioxidant enzyme (SOD2/GPX1) upregulating peptide in YPB catalog; neuroprotective complement to Epitalon |
| Keyword difficulty range | Very low (KD <5) |
How Can Researchers Offer Pinealon Under Their Own Brand?
Pinealon Wholesale Pricing & Margin Analysis
| SKU | Compound | Premier ($497/mo) | Core ($297/mo) | Suggested MSRP | Premier Margin |
|---|---|---|---|---|---|
| YPB.273 (RUO) | Pinealon (EDR) 20mg | TBC Premier | TBC Core | $120.00 | Strong margin at Premier tier |
Contact the YPB team for confirmed Premier and Core tier pricing. Use the YPB Profit Calculator to model projected revenue. White-label brands offering Pinealon alongside Epitalon create the most complete Khavinson peptide bioregulator pair available: Pinealon (neuronal antioxidant/survival) + Epitalon (pineal/telomerase/circadian) covers two complementary levels of the neuroendocrine aging axis from a single Russian bioregulator research buyer audience. Download the full catalog for all longevity category SKU pricing.
Methodology & Data Sources
Methodology & Data Sources
Scientific literature: PubMed searched for “Pinealon,” “EDR peptide,” “Glu-Asp-Arg neuroprotection,” “Khavinson tripeptide brain,” and CAS 110590-60-8. Search conducted through April 2026.
Key sources: Khavinson et al. (2012) Rejuvenation Research (PMID: 22567179, cell viability via ROS suppression); Meshchaninov et al. (2015, PMID: 26390612) (neural aging and brain homeostasis context); Arutjunyan et al. (prenatal hyperhomocysteinemia model); Wikipedia (EDR/Pinealon characterization confirmed against primary sources).
Limitations: All published research originates from the Khavinson group (St. Petersburg Institute of Bioregulation). No independent international replication exists. No ClinicalTrials.gov registered trials as of April 2026. The proposed DNA/chromatin mechanism has not been confirmed by independent biochemical methods (X-ray crystallography, ChIP-seq, CRISPR functional genomics). Researchers should treat available data as preliminary single-center observations. This article is for educational purposes only.
References
- Khavinson, V., Ribakova, Y., Kulebiakin, K., Vladychenskaya, E., Kozina, L., Arutjunyan, A., & Boldyrev, A. (2012). Pinealon increases cell viability by suppression of free radical levels and activating proliferative processes. Rejuvenation Research, 15(3), 313–316. PMID: 22567179
- Meshchaninov, V. N., Menshchikova, E. B., Zanin, S. A., & Kirilyuk, I. A. (2015). Short peptides and pineal gland regulation in aging and brain homeostasis. Bull Exp Biol Med, 159(4), 547–551. PMID: 26390612
- Khavinson, V., Linkova, N., Diatlova, A., & Trofimova, S. (2021). EDR Peptide: Possible mechanism of gene expression and protein synthesis regulation involved in the pathogenesis of Alzheimer’s disease. Molecules, 26(1), 159.
- Arutjunyan, A. V., Kozina, L. S., Milyutina, Y. P., Korenevsky, A. V., Stepanov, M. G., & Khavinson, V. K. (2012). Peptide-dependent suppression of oxidative and nitrosative stress in prenatal hyperhomocysteinemia. Peptides, 37(1), 1–9.
- Khavinson, V. K., & Morozov, V. G. (2003). Peptides of pineal gland and thymus prolong human life. Neuro Endocrinol Lett, 24(3–4), 233–240.
- Linkova, N. S., Medvedev, D. S., Khavinson, V. K., et al. (2012). Peptide regulation of neuronal differentiation. Bull Exp Biol Med, 153(2), 295–299.
- Khavinson, V. K., Kuznik, B. I., Tarnovskaya, S. I., & Lin’kova, N. S. (2016). Short peptides and telomere length regulator hormone irisin. Bull Exp Biol Med, 160(3), 347–349. PMID: 26742748
- Umnov, R. S., Linkova, N. S., & Khavinson, V. K. (various years). Studies on the epigenetic bioregulatory activity of short peptides in the Glu-Asp-Arg class. St. Petersburg Institute of Bioregulation publications.
- Khavinson, V. K. (2001). Peptide regulation of aging. Neuroendocrinology Letters, 22(4), 251–254. (Khavinson bioregulator peptide framework context.)
Frequently Asked Questions
Pinealon (EDR; CAS: 110590-60-8; Glu-Asp-Arg; MW: ~390 Da) is a synthetic tripeptide from the Khavinson peptide bioregulator series, isolated from Cortexin (bovine brain cortex extract). Despite the name, it was not isolated from pineal tissue. In research models, published data from the Khavinson group documents: dose-dependent ROS suppression in cerebellar granule cells (Khavinson et al. 2012, PMID: 22567179), improved cell viability under hypoxic conditions, ERK 1/2 MAPK activation, and upregulation of antioxidant enzymes SOD2 and GPX1 in neural tissue. The proposed mechanism is direct DNA/chromatin interaction in neurons (proposed, not receptor-confirmed). Important: all research from a single institute with no independent replication as of April 2026. Research Use Only (RUO). Updated April 2026.
This is one of the most common sources of confusion in Pinealon research content. Pinealon (EDR) was isolated from Cortexin — a polypeptide extract prepared from bovine brain cortex tissue — not from pineal gland tissue. The Khavinson group named it “Pinealon” based on its proposed target effects: modulation of pineal gland function, circadian regulation, and melatonin synthesis pathways — not its anatomical origin. The related compound Epitalon (AEDG tetrapeptide) was derived from the pineal fraction of bovine brain (Epithalamin), making Epitalon the true pineal-derived peptide in the Khavinson series. Pinealon is the cortex-derived neuroprotective complement that targets the downstream neuronal level, while Epitalon targets the upstream pineal gland level. Researchers citing tissue origins should note this distinction to avoid mischaracterizing either compound’s source.
The Khavinson group proposes that Pinealon (EDR), like other short bioregulator peptides in their series, penetrates cell membranes and the blood-brain barrier and binds directly to specific DNA sequence elements in gene promoter regions, modulating transcription of neuroprotective genes (SOD2, GPX1, neurotrophic factors, circadian regulators). This mechanism does not involve a cell-surface receptor. The evidence for this mechanism is primarily from molecular modeling studies, fluorescence binding assays, and downstream gene expression measurements published by the Khavinson group. What is less well established — and should be flagged in research protocols — is independent confirmation by X-ray crystallography, ChIP-seq (chromatin immunoprecipitation sequencing), CRISPR-based functional genomics, or other modern epigenomics methods. The downstream effects (ROS suppression, SOD2/GPX1 upregulation, ERK activation) are documented regardless of whether the proposed upstream mechanism is precisely correct, but the mechanistic model itself should be treated as a working hypothesis requiring further validation.
Both Pinealon (EDR, Glu-Asp-Arg) and Epitalon (AEDG, Ala-Glu-Asp-Gly) belong to the Khavinson peptide bioregulator series and address brain aging and circadian biology. Their published research targets differ by cellular level. Epitalon is derived from the pineal gland fraction (Epithalamin) and is proposed to work at the pineal gland level: activating telomerase (hTERT), modulating melatonin synthesis pathway enzymes (AANAT), and regulating upstream circadian clock gene expression. Pinealon is derived from brain cortex (Cortexin) and is proposed to work at the individual neuron level: upregulating SOD2/GPX1 antioxidant enzymes, suppressing ROS, activating ERK 1/2 survival signaling, and protecting neurons from hypoxic and oxidative damage. In the Khavinson framework: Epitalon = upstream circadian gland regulator; Pinealon = downstream neuronal antioxidant protector. Both share the proposed DNA/chromatin mechanism and the single-institute evidence limitation.
Several important limitations should be documented in any Pinealon research protocol as of April 2026: (1) All published Pinealon research originates from a single institute (Khavinson group, St. Petersburg Institute of Bioregulation). No independent international laboratory replication of key findings has been published. (2) No Pinealon clinical trial is registered on ClinicalTrials.gov or the EU Clinical Trials Register. (3) The proposed DNA/chromatin mechanism has not been confirmed by independent biochemical methods (X-ray crystallography, ChIP-seq). (4) The claimed human observational data is not published as a rigorous randomized controlled trial. (5) Researchers should not cite Pinealon as “derived from the pineal gland” — it was derived from brain cortex extract (Cortexin). These limitations do not invalidate the documented in vitro antioxidant enzyme and cell viability data, but they establish the current evidence as preliminary and single-source, requiring independent validation before broader research conclusions can be drawn.
Yes. YourPeptideBrand.com provides white-label dropship for Pinealon in a 20mg configuration (Research Use Only). White-label storefronts include pre-built RUO-compliant product pages with molecular data tables, EDR mechanism descriptions, evidence caveats, and COA library links. Contact the YPB team for confirmed Premier and Core tier pricing, and use the profit calculator to model projected revenue at your pricing.
Every Pinealon batch includes a lot-specific COA: HPLC purity (≥98%), MS confirmation at ~390.38 Da (Glu-Asp-Arg), amino acid analysis confirming the correct Glu-Asp-Arg sequence order (not an isomeric sequence), endotoxin (<1 EU/mg), TAMC, and TYMC. Sequence-order confirmation by amino acid analysis is recommended because isomeric tripeptides (e.g., Asp-Glu-Arg or Glu-Arg-Asp) would have identical molecular weight but different biological activity profiles. Documentation is accessible through the batch-specific COA library.
Pinealon and Epitalon are the neuroprotective and pineal-regulatory complements of the Khavinson bioregulator series — two distinct research tools addressing the same overall neuroendocrine aging space from different cellular levels. Positioning: Epitalon = upstream circadian/telomere/pineal gland research; Pinealon = downstream neuronal antioxidant/neuroprotective research. Buyers already interested in the Khavinson research program and longevity biology are the natural audience for both. A catalog offering both creates a complete Khavinson series entry point: researchers interested in Epitalon’s longevity/circadian data will frequently be interested in Pinealon’s neuroprotective complement for comprehensive neural aging protocols. Both share the same evidence limitation (single-institute; should be disclosed) and the same RUO classification, and both attract the same longevity/anti-aging research buyer from the same catalog category.
Key Takeaways
Research Takeaways
- EDR tripeptide from Cortexin (brain cortex), not pineal gland: Common nomenclature confusion — the name refers to proposed effects, not tissue source. Distinguish clearly from Epitalon (true pineal-derived peptide).
- Proposed DNA/chromatin interaction mechanism (not receptor-confirmed): Working hypothesis; downstream effects (ROS suppression, SOD2/GPX1 upregulation, ERK activation) documented regardless of mechanism confirmation status.
- ROS suppression in cerebellar granule cells confirmed (Khavinson 2012, PMID: 22567179): Primary published in vitro evidence; dose-dependent; cell viability improved under hypoxic conditions.
- SOD2 and GPX1 upregulation in neural tissue: Key antioxidant enzyme upregulation addressing the brain’s high-oxygen, limited-antioxidant vulnerability.
- Single-institute research; no independent replication; no ClinicalTrials.gov entries as of April 2026: The most important evidence caveat for researchers. Should be documented in all protocols using Pinealon.
- Neuroprotective complement to Epitalon in the Khavinson series: neuronal-level antioxidant protection (Pinealon) + pineal/telomerase/circadian upstream regulation (Epitalon).
Business Takeaways
- $120 MSRP — contact YPB for confirmed wholesale pricing at Premier tier.
- ~3,000 monthly searches at very low KD — niche but dedicated longevity/Khavinson peptide buyer audience with high purchase intent.
- Pinealon + Epitalon longevity pair captures the complete Khavinson bioregulator research audience; natural cross-sell for any brand already offering Epitalon.
- Evidence transparency as a differentiator — clearly stating the single-institute limitation and no-independent-replication caveat builds research credibility vs. competitor guides that overstate the evidence base.
Ready to add Pinealon to your research catalog? Book a consultation with the YPB team.
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