Pinealon Dosage: Cycle Length & Protocol - Dosage Peptide

Search for Pinealon dosage and you will find confident tables: 200 mcg per day, 10 to 20 day courses, 3 units on an insulin syringe. This article answers a narrower and more useful research question: where do those numbers actually come from, and what level of evidence stands behind them? The short answer, established up front and repeated throughout, is that no published human dose-ranging or pharmacokinetic study of Pinealon exists — the widely circulated figures are a research convention inherited from the Khavinson bioregulator tradition, not a validated protocol.

Pinealon is not approved by the FDA for any indication. It has been marketed in Russia as a Cytogen-class supplement preparation, so “unapproved” does not mean “unsold” — but no regulator anywhere has published dose-ranging data or an approved label for it. It is a research chemical. Nothing below is a recommendation to administer it to a human being.

What Sequence Are You Actually Holding? Pinealon Is EDR, Not KED

Before any arithmetic, a correction that matters more than the arithmetic, because it is the single most common error in the vendor and blog literature on this compound.

Pinealon is the tripeptide Glu-Asp-Arg (EDR). It is not Lys-Glu-Asp (KED). This is not a matter of interpretation. The US National Library of Medicine’s controlled vocabulary maps the term “pinealon” to Glu-Asp-Arg, and PubChem resolves both the name “pinealon” and the sequence “Glu-Asp-Arg” to a single compound record, CID 10273502[1]. Every primary paper on the compound states the sequence explicitly in its abstract: Khavinson and colleagues open their 2011 Rejuvenation Research paper with “the synthetic tripeptide pinealon (Glu-Asp-Arg)”[2], and the 2011 Biochemistry (Moscow) cellular-uptake study lists its test articles as “epithalon, Ala-Glu-Asp-Gly; pinealon, Glu-Asp-Arg; testagen, Lys-Glu-Asp-Gly”[3].

Lys-Glu-Asp (KED) is a different compound with a different name: Vesugen (also transliterated Vezugen). A 2016 Russian comparative geroprotection study makes the pairing unambiguous, describing “complexes lysyl-glutamyl-asparagin and glutamyl-asparagin-arginine (Vezugen and Pinealon)” — KED is Vesugen, EDR is Pinealon[4].

Three peptides that get conflated, side by side

If you are cross-referencing a vendor label against the literature, this table is the reconciliation. The molecular weights are from PubChem compound records.

Pinealon

Glu-Asp-Arg

EDR

C15H26N6O8

418.40

10273502

Vesugen

Lys-Glu-Asp

KED

C15H26N4O8

390.39

87571363

Epithalon

Ala-Glu-Asp-Gly

AEDG

C14H22N4O9

390.35

219042

Note the trap in the last two rows. Vesugen (390.39) and Epithalon (390.35) have nearly identical molecular weights despite being different lengths and different sequences — a mass-spec certificate of analysis reporting “390” does not by itself distinguish them. Pinealon, at 418.40, is the one that separates cleanly on mass alone. If a certificate of analysis for a vial sold as Pinealon reports a parent mass near 390 rather than 418, the label and the contents disagree, and no dosage table in this article applies to it.

Epithalon is a genuinely different molecule with a different research literature — it is a tetrapeptide studied chiefly around telomerase activity, not a synonym or a “stronger version” of Pinealon. Khavinson’s 2003 report of telomerase induction in human fetal fibroblasts is an Epithalon finding and has never been replicated for Pinealon[5]. We cover that compound separately in our overview of Epithalon and the telomerase aging research; do not port numbers between the two.

For the mechanism-level treatment of this compound, see our Pinealon neuroprotective peptide research overview. This article deliberately stays on dose, route, cycle length and arithmetic.

Research Context

Pinealon comes out of a specific and unusually self-contained research program: the short-peptide bioregulator school associated with Vladimir Khavinson and the St. Petersburg Institute of Bioregulation and Gerontology. The founding premise of that school is that very short peptides — di-, tri- and tetrapeptides — act as endogenous regulators of gene expression, penetrating the cell and nucleus and binding DNA in a sequence-specific manner. We treat that framework in general in our guide to peptide bioregulators and the Khavinson short-peptide research.

The size of the literature is the first fact worth knowing

A PubMed query for Pinealon returned 22 records in total as of July 2026[22] — and that figure is not the number of clinical studies, it is the number of publications of any kind that mention the compound. The query is given in the reference so you can re-run it; the count will drift upward as records are indexed, and a count without a date silently rots. Filter that set for relevance and the picture tightens further:

Several are in-vitro or organotypic-culture studies (cerebellar granule cells, PC12 cells, pineal explants).

Several are rat models — hypobaric hypoxia, carotid artery occlusion, Morris water maze learning.

A handful are small human observational or occupational-medicine studies, almost all published in Advances in Gerontology (Uspekhi Gerontologii), in Russian, with English abstracts only.

Several are reviews by the same group, recycling the same primary data.

At least one hit is a false positive: a 2021 Food & Function paper on the tetrapeptide Asp-Arg-Glu-Leu from Jiuzao protein hydrolysates, which matched on peptide chemistry and has nothing to do with Pinealon[26]. Others look like false positives but are not: a rat skin-culture study lists its test article under the code name T-33, which is Glu-Asp-Arg — genuine Pinealon work in disguise.

Two structural features of that corpus deserve emphasis, because they bound everything that follows. First, the authorship is highly concentrated: Khavinson, Linkova, Ryzhak, Mendzheritsky, Karantysh, Kozina and a small number of collaborators account for nearly all of it. Second, independent Western replication is essentially absent. That is not an accusation of error; it is a description of the evidence base. When a compound’s entire literature originates from the institution that developed and commercialises it, the ordinary corrective machinery of science — adversarial replication by parties with no stake in the result — has not yet run.

Zero registered clinical trials

A search of ClinicalTrials.gov for Pinealon, Glu-Asp-Arg or EDR peptide as an intervention returns zero registered trials[6]. There is no Phase 1. There is no first-in-human safety study in the registry. There is no dose-escalation cohort. This is the single most important fact on this page, and it is why every number below is framed as a convention rather than a protocol.

Naming the reviews matters here, because “reviews agree with me” is an appeal to authority unless the reviews are checkable. A January 2026 review of therapeutic peptides in orthopaedics surveys Pinealon alongside Epithalon and delta sleep-inducing peptide, and alongside Selank and Semax, and concludes in its own abstract: “Although preclinical studies are promising, there is a current lack of clinical trials”[19]. That review is written by clinicians who advocate for peptide therapeutics — it is not a sceptical source, and it still says the trials are missing. An earlier Russian-language review of neuroprotective bioregulators from Khavinson’s own group, which groups Pinealon with Semax and Cortagen, likewise rests on clinical application reports rather than controlled trials[20]. When the compound’s advocates and its originators both describe the trial evidence as absent, the absence is not a sceptic’s framing.

What Dose Is Actually Reported in the Research Literature?

Here the article can be unusually concrete, because there is exactly one clearly specified human dosing regimen in the indexed Pinealon literature, and it is worth quoting precisely.

The one specified human regimen: 100 mcg twice daily, orally, for two weeks

A 2012 occupational-medicine study of Russian locomotive-brigade workers — train drivers and assistants — states its regimen in the abstract: participants “used preparation during two weeks (1 capsule containing 100 mkg of Pinealon 2 times a day)”[7]. Translating from the Russian abbreviation, “mkg” is micrograms. So the regimen was:

Amount per dose: 100 mcg

Frequency: twice daily

Total per day: 200 mcg

Route: oral capsule

Course length: 14 days

This is where the ubiquitous “200 mcg per day” figure comes from, and it is where the “10 to 20 day course” convention finds its one concrete anchor: 14 days sits squarely in the middle of that range. The number circulating on vendor sites is not fabricated. It traces to a real, indexed publication.

But note carefully what that study is and is not. Its abstract reports no sample size, no randomisation and no blinding, and PubMed indexes it under case-control studies; on the face of the abstract it is an uncontrolled occupational study, published in Russian, reporting improvements in composite “biological age” indices and adaptation markers — endpoints that are themselves contested constructs. That opacity is itself part of the argument rather than an aside: a reader cannot verify the design, because the abstract does not describe it. It was not designed to find an optimal dose. It tested one dose. A study that administers a single dose level cannot tell you whether that dose is optimal, whether half of it would work identically, or whether double would do more. One dose level is not a dose-response study. It establishes only that somebody once gave 200 mcg per day for 14 days and reported a result.

Other human reports specify the compound but not the milligrams

The remaining human literature is thinner still on numbers. A companion study of professional truck drivers reports psychoemotional improvements from combined Pinealon and Vesugen, with the best effect from the combination rather than either alone[8]. A 32-person study in patients aged 41 to 83 with polymorbidity and organic brain syndrome reported anabolic effects from both peptides — and, notably, found Vesugen more effective than Pinealon, alongside a prooxidant signal on chemiluminescence and a decrease in CD34+ haematopoietic progenitor markers[9]. A further comparison across 110 participants against carbon-dioxide baths, hyperbaric oxygen and massage found the combined oligopeptides most favourable on biological-age indices[4]. Additional work-ability analyses in occupationally exposed workers report similar conclusions without specifying milligram amounts.

Sample sizes across that entire human corpus are in the tens to low hundreds. None are placebo-controlled dose-ranging trials. Several report on the combination rather than Pinealon alone, which means the Pinealon-specific contribution cannot be isolated from them at all.

Where the 20 mg vial and the injectable framing came from

This is the honest gap, and it deserves to be stated plainly rather than papered over. The published human Pinealon studies used oral capsules. The 20 mg lyophilised vial for reconstitution and injection is a research-supply format, not a format that appears in the human literature. The Russian capsule products (marketed as Cytogen-class preparations) delivered 100 mcg per capsule. There is no published human study administering reconstituted Pinealon subcutaneously and reporting the milligrams and the cycle length.

So when a search query asks “Pinealon peptide injection, mg per day, cycle length” — the truthful answer is that the injectable regimen has no published human source at all. The 200 mcg/day figure is imported from an oral study and applied to a parenteral route, which is a substitution nobody has validated. Oral and subcutaneous administration of the same peptide do not deliver the same systemic exposure; assuming they do is an assumption, not a finding.

How Long Is a Pinealon Cycle in the Bioregulator Literature?

The “10 to 20 day course” is the most-repeated cycle-length claim for Pinealon and for Khavinson bioregulators generally. It is worth being precise about its status.

The convention, and its actual basis

Within the bioregulator tradition, short courses followed by long intervals are the standard administration pattern — typically 10 to 20 consecutive days, often repeated once or twice per year. The pattern is doctrinal within that school and is applied across the whole family of peptides, not derived separately for each one.

The concrete anchors that exist in the indexed literature are narrow:

Nazimko et al., 2012[7]

Locomotive-brigade workers

100 mcg oral capsule, 2×/day (200 mcg/day)

14 days

Bashkireva & Artamonova, 2012[8]

Professional truck drivers

Pinealon + Vesugen combination; mg not specified in abstract

Not specified in abstract

Meshchaninov et al., 2015[9]

32 adults, 41–83 y

Pinealon + Vesugen; mg not specified in abstract

That is the load-bearing evidence for cycle length in humans: one study, one course, 14 days, oral. Everything else in the “10–20 days, twice yearly” formulation is extrapolation and tradition. No study has compared a 10-day course against a 20-day course against a 40-day course. No study has tested whether repeating courses annually differs from repeating them quarterly, or from not repeating them. No washout period has been empirically justified.

Why the short-course convention is nonetheless not arbitrary

It would be unfair to describe the convention as pure invention. There is an internal logic to it, even if it has not been tested. The bioregulator hypothesis holds that these peptides act as transcriptional signals rather than as substrates — a nudge to gene expression, not a molecule that needs steady-state plasma levels. Under that hypothesis, a pulse followed by a long interval is the sensible administration pattern, and continuous exposure would be the odd choice. The rodent work does report effects on caspase-3 activity and on Morris-maze learning[10], which at least establishes that measurable effects follow administration at all.

It would be convenient to add that those rodent effects followed short courses, since that would lend the 10–20 day convention a preclinical anchor. This article will not say it, because the abstract does not support it: the rodent paper states no administration duration whatsoever, and the full text is Russian-language and not openly available. The honest position is that the duration is not recoverable from the abstract. So the short-course convention has an internal logic and a mechanism story, but it does not have a dosing-duration citation behind it — not in the human literature, and not in the rodent literature either.

But “consistent with a hypothesis” and “validated” are separated by exactly the studies that have not been done. The convention is a reasonable guess dressed, on most of the internet, in the language of a protocol. Readers deserve to see the seam.

Mechanisms Studied

The mechanistic literature on Pinealon is more substantial than the dosing literature, though it remains overwhelmingly preclinical. It is organised around one central and genuinely interesting claim.

The direct DNA-binding hypothesis

The Khavinson school proposes that short peptides enter the nucleus and bind DNA sequence-specifically, regulating transcription epigenetically. Unusually for a mechanism claim in this space, there is direct experimental work behind the first half of it. Fluorescein-labelled Pinealon, Epithalon and Testagen all produced marked fluorescence in the cytoplasm, nucleus and nucleolus of HeLa cells — reported as evidence that short peptides of this class can physically reach the nucleus[3], though this is a single-laboratory in-vitro result using a fluorescent tag that may itself influence where the molecule ends up. (Note that only Pinealon among those three is a tripeptide; Epithalon and Testagen are tetrapeptides — which is precisely why “short peptides” is the accurate phrase here and “tripeptides” would not be.) The same study used Stern-Volmer fluorescence-quenching constants to argue that different peptides bind different nucleotide sequences preferentially, with Epithalon, Testagen and Pinealon favouring CAG-containing sequences and reportedly discriminating cytosine methylation status.

A 2019 biophysical study from St. Petersburg State University examined the EDR–DNA interaction directly by NMR, viscosimetry, spectroscopy and molecular dynamics, concluding that EDR can partly penetrate the major groove of DNA and interact with guanine N7 and O6 atoms, with magnesium ions promoting the interaction by screening phosphate charge[11]. This is real physical chemistry, and it is one of the few Pinealon-adjacent papers from a group outside the originating institute.

The caveat is the size of the inferential leap. Demonstrating that a tripeptide can enter a nucleus and contact DNA bases in vitro is a long way from demonstrating that this contact regulates specific genes at physiologically achievable concentrations in a living brain. A tripeptide is a small, highly charged molecule; the specificity available to three residues is limited, and the intracellular environment contains an enormous excess of competing polyanions and proteins.

Antioxidant and antiapoptotic signals in cell models

The most-cited primary Pinealon paper reports dose-dependent restriction of reactive oxygen species accumulation in cerebellar granule cells, neutrophils and PC12 cells under oxidative stress, alongside decreased necrotic cell death, delayed ERK 1/2 activation and cell-cycle modification[2]. The authors’ own interpretation is instructive: because ROS restriction saturated at lower concentrations while cell-cycle modulation continued at higher ones, they inferred two distinct mechanisms, one of them genomic.

Interestingly, an earlier in-vitro study from the same circle found that Pinealon, Vesugen, Vilon and Epitalon showed no direct antioxidant activity, and in fact elevated the stationary level of intracellular ROS while simultaneously decreasing the percentage of dead cells in the neuronal population (all except Epitalon)[12]. Pinealon is inside that exception, not outside it, so the tension applies to it directly. That is not a trivial internal tension, and the human study that found a prooxidant chemiluminescence signal echoes it[9]. “Pinealon is an antioxidant” is a claim the literature does not cleanly support; the authors of that 2015 human paper explicitly characterised the peptides as geroprotectors of an anabolic neuroprotective and non-antioxidant type.

Serotonin, caspase-3 and the rodent behavioural work

Beyond DNA binding, the group reports that EDR — and, notably, Vesugen’s KED alongside it — stimulates serotonin expression in ageing brain-cortex cell cultures, using molecular docking to propose that both peptides are complementary to a CCTGCC sequence in the 5-tryptophan hydroxylase gene, which encodes the enzyme controlling serotonin synthesis[17]. That detail cuts against the marketing more than it supports it: the same docking argument is made for the peptide Pinealon is most often confused with. In organotypic pineal culture, EDR did not affect the apoptosis marker AIF, while the related peptides KED and AEDG stimulated the proliferation marker Ki-67[18]. The pattern the group draws from this is tissue-specificity: different short peptides are proposed to act on different genes in different tissues. Note the shape of that claim — it is flexible enough to accommodate almost any result, which makes it difficult to falsify and therefore weak as evidence.

The rodent work clusters around caspase-3 and stress models. In acute hypoxic hypoxia in old rats, Pinealon was studied alongside Cortexin for effects on brain caspase-3 activity and on serum interleukin-6 and tumour necrosis factor; the authors suggested that under brain-hypoxia conditions Pinealon promotes an increase in neurogenesis and a decrease in neuroinflammatory reactions toward a reference level[16]. Read that phrasing carefully — the abstract offers it as the authors’ suggestion, not as a direct demonstration; neurogenesis was inferred rather than measured. In a Morris water maze paradigm, Pinealon was reported to have a more favourable effect on learning than Cortexin in both young and old animals[10]. In a carotid artery occlusion model, short peptides improved survival, though Pinealon also increased behavioural sleep and reduced exploratory and motivational behaviour and motor performance[13] — a result rarely mentioned in summaries that present the compound as a cognitive enhancer.

Three further rodent reports round out that picture, and they are worth stating because two of them complicate the promotional narrative. In a hypobaric-hypoxia model comparing several short peptides, Pinealon was reported to have the most pronounced antihypoxic effect of the group, with the author attributing it less to suppression of ROS than to stimulation of endogenous antioxidant enzymes and possibly to limiting NMDA excitotoxicity[24]. In rat offspring exposed prenatally to methionine-induced hyperhomocysteinemia, administering Pinealon to the pregnant dams was reported to improve the offspring’s spatial orientation and learning and to reduce ROS accumulation and necrotic cell counts in cerebellar neurons[23]. But in an 18-month-old-rat study using acute hypobaric hypoxia and mild hypothermia, Cortexin — not Pinealon — showed the more pronounced effect on free-radical processes and brain caspase-3 activity[25]. The rodent literature does not uniformly favour Pinealon over the comparators it is tested against, and a page that only quoted the Morris-maze result would be selecting the flattering half of the same research group’s output.

A review in Molecules, published online at the very end of 2020 and carried in the 2021 volume, assembles the EDR mechanistic case in the context of Alzheimer’s disease pathogenesis, proposing effects on MAPK/ERK signalling, caspase-3, p53, SOD2, GPX1, PPARA, PPARG, serotonin and calmodulin[14]. It is a useful map of the hypothesis space. It is a review by the originating group, it is not evidence of clinical benefit, and its own framing is explicitly mechanistic and speculative.

How Do You Reconstitute a 20 mg Pinealon Vial?

The arithmetic below is presented so you can check it yourself rather than trust it. It is the same math our peptide dosage calculator performs, and the reconstitution arithmetic — 20 mg in 3 mL, 6.67 mg/mL, 200 mcg as 3 units — matches our Pinealon 20 mg vial dosage protocol reference page. That corroboration is about the arithmetic only. Where any reference page, ours included, presents a dose range or a course length above the single 200 mcg / 14-day oral anchor documented here, it is reproducing the same research-supply convention this article is taking apart — and the evidence assessment on this page is what we would ask you to weigh. For the mechanical handling steps — vial preparation, diluent addition technique, swirling rather than shaking, storage — see the full peptide reconstitution guide.

Step 1: concentration

Concentration is simply peptide mass divided by diluent volume. For the catalog-standard configuration of a 20 mg vial reconstituted with 3 mL of bacteriostatic water:

20 mg ÷ 3 mL = 6.67 mg/mL

Converting to micrograms, since research doses are quoted in mcg: 20 mg = 20,000 mcg

20,000 mcg ÷ 3 mL = 6,666.7 mcg/mL (rounded to 6,667 mcg/mL below)

A note on what reconstitution does and does not change: adding 3 mL of diluent does not create 3.00 mL of solution. The lyophilised powder occupies its own small volume, so the final volume is marginally greater than the diluent added. For 20 mg of a tripeptide the displacement is well under 0.02 mL — below the resolution of any insulin syringe — and every table here follows the standard convention of treating final volume as equal to diluent volume. The error introduced is smaller than the error in reading the syringe.

Step 2: dose volume

Dose volume is dose divided by concentration. For the representative research dose of 200 mcg at 6,667 mcg/mL:

200 mcg ÷ 6,667 mcg/mL = 0.030 mL

Step 3: insulin-syringe units

A U-100 insulin syringe is graduated so that 100 units equals 1 mL. Therefore units = mL × 100:

0.030 mL × 100 = 3 units on a U-100 syringe

That is the complete chain: 20 mg in 3 mL gives 6,667 mcg/mL; a 200 mcg dose is 0.030 mL; 0.030 mL is 3 units. If you want the unit-marking conventions and the U-100 versus U-40 distinction spelled out, our guide to insulin syringe units for peptides covers the failure modes in detail.

A shortcut worth internalising for the 20 mg vial

There is an arithmetic coincidence in this specific configuration that is genuinely useful. For a 20 mg vial and a 200 mcg dose, the number of units on a U-100 syringe is numerically equal to the number of millilitres of diluent you added.

The reason is that 200 mcg is exactly 1/100th of 20 mg. Dose volume is therefore V/100 mL where V is diluent millilitres, and units are (V/100) × 100 = V. At 3 mL, the 200 mcg dose corresponds to 3 units; at 5 mL, to 5 units. This holds only for a 20 mg vial at a 200 mcg dose — it is a mnemonic, not a general rule, and it breaks the moment either number changes.

1 mL

20.00

20,000

0.010 mL

1 unit

2 mL

10.00

10,000

0.020 mL

2 units

3 mL (catalog standard)

6.67

6,667

0.030 mL

3 units

4 mL

5.00

5,000

0.040 mL

4 units

5 mL

4.00

4,000

0.050 mL

5 units

The table makes the trade-off visible. At 1 mL the entire 200 mcg dose is a single unit — the smallest graduation on the syringe, where a half-unit misread is a 50% dose error. At 5 mL the same dose is 5 units, which is far easier to draw accurately, at the cost of a larger vial volume and a lower concentration. Three millilitres is a reasonable middle: 3 units is readable, and the total volume fits comfortably in a standard vial. This is why 3 mL is the catalog convention — it is an ergonomic choice about syringe resolution, not a pharmacological one.

What Does Each Dose Look Like in Syringe Units?

The table below extends the arithmetic across a range of dose sizes at the standard 3 mL / 6,667 mcg/mL concentration. It exists because searchers ask for it, and because seeing the whole range makes the resolution limits obvious. Its inclusion is not an endorsement of any row. Only the 200 mcg/day total has any published human anchor at all, and that anchor is an oral study.

50 mcg

0.0075 mL

0.75 units

No human source; no toxicology at any dose

100 mcg

0.015 mL

1.5 units

Per-capsule amount in the 2012 oral study[7]; no injectable source; no toxicology

150 mcg

0.0225 mL

2.25 units

200 mcg

Daily total in the 2012 oral study[7]; catalog convention; no injectable source; no toxicology

250 mcg

0.0375 mL

3.75 units

No human source; no toxicology at any dose — upper bound unknown

300 mcg

0.045 mL

4.5 units

400 mcg

0.060 mL

6 units

500 mcg

0.075 mL

7.5 units

No toxicology or dose-limiting study exists for Pinealon at any dose or by any route, so the rows above 200 mcg are arithmetic with no safety characterisation behind them. “No human source” in that column is not a statement that a dose is unproven-but-probably-fine; it means nobody has established an upper bound, and there is no evidence base from which one could be inferred. The signals that do exist point the wrong way for casual extrapolation: the human study that reported a prooxidant chemiluminescence effect and reduced CD34+ haematopoietic markers[9], and the rodent occlusion study in which Pinealon increased behavioural sleep and reduced exploratory and motor behaviour[13], were both observed at doses nobody has characterised.

Read the right-hand column before the left. Seven of the eight rows have no human anchor at all — they tell you what a syringe would show, not what anyone has ever studied. The fact that a number can be computed and drawn accurately says nothing whatsoever about whether it is meaningful, and nothing at all about whether it is safe.

The resolution problem at small doses

Notice the fractional units. At 3 mL concentration, a 50 mcg dose is 0.75 units and a 150 mcg dose is 2.25 units. Standard U-100 insulin syringes are graduated in 1-unit or 2-unit increments; half-unit syringes exist but quarter-unit graduations generally do not. A quarter-unit is simply not measurable on the instrument. Anyone attempting these smaller doses at this concentration is estimating between graduation marks, and the estimation error is a large fraction of the dose. If small doses were the goal, a lower concentration — more diluent — would be the arithmetically sound response, spreading the same mass across more measurable volume.

Route: The Injectable Framing Has No Published Human Source

This section restates the point made earlier because it is the specific thing the dose/cycle-length search intent is asking about, and because it is the point most consistently omitted elsewhere.

The compound is sold to researchers as a 20 mg lyophilised vial intended for reconstitution. The search queries ask about injection. The published human studies used oral capsules at 100 mcg[7]. The rodent studies used parenteral routes, including intraperitoneal injection[13] — which is a route not used in humans and not equivalent to subcutaneous administration.

So the chain of inference behind “200 mcg subcutaneously per day for 10–20 days” runs: take a dose from a single uncontrolled human oral study whose abstract reports no blinding, assume the same milligram figure transfers to a different route, assume the 14-day course generalises to a 10–20 day range, and apply it to a vial format that appears in no human study. Each link in that chain is an assumption. None of them is a finding. The result may be perfectly reasonable — but it is reasoning, presented across most of the internet as data.

Why the oral-to-injectable substitution is not trivially safe to assume

The Khavinson school makes a specific and somewhat unusual claim here: that these very short peptides survive gastrointestinal passage sufficiently to be orally active, which is rare for peptides and is part of why the capsule format exists at all. Take that claim at face value and a strange implication follows — if oral 200 mcg was sufficient to produce the reported effects, then injecting 200 mcg bypasses first-pass degradation entirely and delivers a systemic exposure that is plausibly much higher, not equal. Reject the claim, and the oral study’s reported effects become difficult to attribute to the peptide at all. Either way, treating the oral milligram figure as directly portable to a syringe is unsupported. Nobody has measured the bioavailability of either route in humans, because no pharmacokinetic study of Pinealon has been published.

The 20 mg Vial Problem: 100 Doses Against a 14-Day Course

This is a practical arithmetic observation that follows directly from the numbers above and that almost no dosage page addresses.

A 20 mg vial contains 20,000 mcg. At the convention’s 200 mcg per day:

20,000 mcg ÷ 200 mcg/day = 100 days of doses in a single vial

A 14-day course consumes 14 × 200 mcg = 2,800 mcg = 2.8 mg — 14% of the vial

A single 20 mg vial therefore contains roughly seven complete 14-day courses

Now set that against the diluent. Bacteriostatic Water for Injection, USP contains 0.9% (9 mg/mL) or 1.1% (11 mg/mL) benzyl alcohol as a bacteriostatic preservative depending on the presentation — the Hospira label lists 9 mg/mL in 30 mL plastic vials and 11 mg/mL in glass — and is supplied in multiple-dose containers precisely so that repeated withdrawals can be made[15].

The 28-day figure that governs this section needs its provenance stated, because this article would be hypocritical to import a number without saying where it comes from. It is not on the diluent’s label: the Hospira label states no in-use window or discard period after first puncture at all. The 28 days is a compounding standard. USP General Chapter <797> provides that once a conventionally manufactured multiple-dose container has been entered or punctured, it “must not be used for more than 28 days… unless otherwise specified by the manufacturer on the labeling”[21]. That is a beyond-use-dating convention tied to preservative effectiveness — a rule about the container and its preservative, not a stability measurement for any particular peptide dissolved in it.

With that provenance stated, the mismatch is stark. A reconstituted 20 mg Pinealon vial at 200 mcg/day would take 100 days to consume — roughly three and a half times that 28-day window.

The consequence is unavoidable and rarely stated: under the conventional protocol, most of a reconstituted 20 mg vial cannot be used within the diluent’s stability window. The vial size and the protocol are mismatched by design. If the courses are separated by months, as the bioregulator tradition prescribes, a reconstituted vial cannot survive the interval between them either.

This mismatch is itself evidence about the provenance of the 20 mg format. A vial sized for a hundred days of a protocol that runs fourteen is not a vial sized by anyone reasoning from the protocol. It is a vial sized by a supply chain — a convenient manufacturing and shipping unit, priced per milligram. It is one more reason to read the “20 mg vial, 3 mL, 200 mcg” configuration as a commercial artifact rather than a clinical one, and it reinforces the article’s central point: these numbers are conventions, and they were not derived from evidence about Pinealon.

Current Evidence Level

Precision about evidence tier matters more for this compound than for almost any other in the peptide space, because the gap between the confidence of the available dosage tables and the strength of the underlying data is unusually wide.

Regulatory status

Pinealon is not FDA-approved for any indication. It is not an investigational new drug with an active US IND that has produced published dose-ranging data. It is not a compounding-pharmacy preparation with an established monograph. It is a research chemical, sold for laboratory use, and that is the entire extent of its regulatory standing. There is no approved label, which means there is no authoritative dose, no authoritative route, no authoritative course length and no adverse-event reporting system covering it.

The evidence tiers, ranked honestly

Pinealon is Glu-Asp-Arg

PubChem CID 10273502; NLM vocabulary; consistent across all primary papers

Established chemical fact

Short peptides of this class enter the cell nucleus

Fluorescence microscopy in HeLa cells[3]

In vitro, single lab

EDR physically contacts DNA bases

NMR, viscosimetry, molecular dynamics[11]

Biophysical, in vitro

Reduces ROS accumulation and necrotic death under oxidative stress

Cerebellar granule cells, PC12[2] — but contradicted by[12]

In vitro, internally inconsistent

Affects caspase-3 and learning in rats

Morris maze and caspase-3[10]; hypoxia model[16]; occlusion model[13]

Animal only

Improves “biological age” indices in humans

Small Russian occupational studies, no blinding reported[7]

Low-quality human observational

200 mcg/day is an appropriate dose

One oral study using one dose level[7]

Convention — not dose-ranging

10–20 days is an appropriate cycle

One 14-day oral course; tradition

Convention — untested

Any injectable regimen

None

No published human source

Neuroprotective or cognitive benefit in humans

No adequate trial exists

Not established

Pharmacokinetics, bioavailability, half-life

No published study

Unknown

Read the bottom four rows together. The claims that the search intent cares about most — the injectable dose, the cycle length, whether it does anything, and what the body does with it — occupy the tiers where the evidence is a convention, an absence, or an unknown. That is not a rhetorical framing. It is what the literature contains.

What would change this assessment

It is worth naming what evidence would actually move Pinealon up the ladder, because the point is not that the compound is uninteresting — the DNA-interaction biophysics is legitimately interesting — but that specific studies are missing:

A pharmacokinetic study in humans measuring plasma concentration after oral and subcutaneous administration. This would settle the route question in a single experiment and does not exist.

A dose-ranging study testing at least three dose levels against placebo. Without it, “200 mcg” has no more claim on the truth than 100 or 400.

A randomised, blinded, placebo-controlled trial with a prespecified cognitive endpoint. No human study in this set reports blinding in its abstract — which is not the same as proving none was blinded, but it does mean no reader can confirm that any was. Studies of subjective wellbeing endpoints in workers who may know they are receiving a geroprotector are the classic setting for expectancy effects, and an abstract that is silent on blinding cannot rule them out.

Replication by a group with no institutional or commercial connection to the originating institute.

Any formal toxicology and safety data. The prooxidant chemiluminescence signal and the reduced CD34+ marker reported in the 2015 human study[9] are exactly the kind of findings that a proper safety study exists to characterise, and none has been done.

Limitations

Beyond the evidence-tier assessment, several specific limitations constrain what this article — and any Pinealon dosage page — can honestly claim.

The literature is not independently verifiable in its details

Nearly all the human work is published in Advances in Gerontology in Russian, with only English abstracts indexed. That means the regimen details, statistical methods, inclusion criteria and adverse-event reporting for those studies are not accessible to most readers, and in several cases the abstract simply does not state the dose. This article has been careful to cite only what the abstracts explicitly say. Where an abstract does not state a milligram figure, this article says so rather than filling the gap. That is why the cycle-length table above has “not specified in abstract” in it — those cells are honest, not lazy.

The combination problem

Several of the human studies administered Pinealon together with Vesugen and reported the combination’s effect. One of them found Vesugen the more effective agent, stating that “Vesugen has demonstrated more visible geroprophylactic effect than Pinealon”[9]. The other two combination studies did not find Vesugen superior; they found the combination superior — the truck-driver study reports that “the best effect was obtained in case of combined application”[8], and the 110-participant comparison reports the most pronounced effect “during the combined use of these two Oligopeptide complexes”[4]. That distinction matters, and it does not rescue the Pinealon-specific case: a combination study cannot attribute an effect to one component, so a finding that the pair works best is precisely a finding that leaves Pinealon’s individual contribution unmeasured. Between the one study favouring the other peptide and the two favouring only the pair, the Pinealon-specific human evidence base shrinks considerably below what a raw citation count suggests.

Endpoint validity

“Biological age” and “adaptation potential” are composite indices whose construction varies between laboratories and whose relationship to any clinically meaningful outcome is not established. An improvement in a biological-age index is not an improvement in health, longevity or cognition. It is a change in a number that a particular research group computes in a particular way.

The arithmetic is exact; what it describes is not

The reconstitution math on this page is straightforward and correct: 20 mg in 3 mL is 6,667 mcg/mL, and 200 mcg is 0.030 mL is 3 units. This will not vary. But arithmetic precision is seductive, and it is worth being explicit about the trap: the confidence of the calculation says nothing about the validity of the input. You can compute 3 units to arbitrary precision from a dose figure that has no dose-response study behind it. The decimal places are real. The dose is a convention. Do not let the former lend credibility to the latter.

Product identity risk

Because Pinealon is a research chemical and not a regulated pharmaceutical, there is no assurance that a given vial contains what its label says, at the stated mass or purity. The KED/EDR naming confusion documented at the top of this article makes this a live concern rather than a theoretical one: a supplier that believes Pinealon is Lys-Glu-Asp may be shipping Lys-Glu-Asp. Every calculation here assumes the vial contains 20 mg of Glu-Asp-Arg. Third-party mass-spec analysis is the only way to test that assumption, and a parent mass near 418 rather than 390 is the discriminator.

Frequently Asked Questions

What is the standard Pinealon dosage?

The most commonly cited figure is 200 mcg per day, and it traces to a single 2012 Russian occupational study in which participants took 100 mcg orally twice daily for 14 days. That is one study, at one dose level, using oral capsules, with no blinding reported in its abstract. It is a convention, not a validated dose. No dose-ranging trial has ever compared 200 mcg against any other amount, so there is no evidence that this figure is optimal or even distinguishable from alternatives.

How long should a Pinealon cycle be?

The bioregulator literature conventionally describes 10 to 20 day courses, often repeated once or twice yearly. The only concrete anchor in the indexed literature is a single 14-day oral course. No study has compared different course lengths, tested repeat intervals, or justified a washout period. The 10–20 day range is doctrine inherited from the Khavinson school and applied across the whole peptide family, not a finding derived for Pinealon specifically.

Is Pinealon Lys-Glu-Asp or Glu-Asp-Arg?

Pinealon is Glu-Asp-Arg (EDR), molecular weight 418.40, PubChem CID 10273502. Lys-Glu-Asp (KED) is a different peptide called Vesugen, molecular weight 390.39. This error is widespread in vendor listings and blog posts. If a source tells you Pinealon is KED, it has confused it with Vesugen, and you should treat that source’s other claims with corresponding caution.

How do I reconstitute a 20 mg Pinealon vial?

The catalog-standard configuration adds 3 mL of bacteriostatic water to a 20 mg vial, yielding 6.67 mg/mL or 6,667 mcg/mL. At that concentration a 200 mcg dose is 200 ÷ 6,667 = 0.030 mL, which is 3 units on a U-100 insulin syringe. A useful shortcut for this vial size at this dose: the number of units equals the number of millilitres of diluent added, so 3 mL gives 3 units and 5 mL gives 5 units.

How many units of Pinealon is 200 mcg?

Three units on a U-100 insulin syringe, when a 20 mg vial has been reconstituted with 3 mL of bacteriostatic water. The chain is: 20,000 mcg ÷ 3 mL = 6,667 mcg/mL; 200 mcg ÷ 6,667 mcg/mL = 0.030 mL; 0.030 mL × 100 units/mL = 3 units. Change the diluent volume and the unit count changes proportionally — 2 mL would make the same dose 2 units, and 5 mL would make it 5 units.

Is Pinealon injected or taken orally?

This is the most important gap in the popular literature. The published human studies used oral capsules at 100 mcg. The rodent studies used parenteral routes including intraperitoneal injection. The 20 mg lyophilised vial sold for reconstitution and subcutaneous injection appears in no human study. So there is no published human source for any injectable Pinealon regimen — the injectable protocol is an extrapolation from oral data, and oral and subcutaneous routes do not deliver equivalent systemic exposure.

How long does a reconstituted Pinealon vial last?

Arithmetically, a 20 mg vial holds 100 days of doses at 200 mcg/day — roughly seven complete 14-day courses. That creates a real mismatch, because USP General Chapter <797> assigns a 28-day beyond-use date to a multiple-dose container once it has been punctured — a compounding standard tied to preservative effectiveness, not a figure printed on the diluent’s label — and 100 days of use far exceeds it. Under the conventional protocol, most of a reconstituted 20 mg vial cannot be consumed within the diluent’s stability window. The vial size reflects supply-chain convenience rather than the protocol.

Is Pinealon FDA-approved?

No. Pinealon is not approved by the FDA for any indication and is not an investigational drug with published dose-ranging data. It is a research chemical. A ClinicalTrials.gov search for Pinealon, Glu-Asp-Arg or EDR peptide as an intervention returns zero registered trials worldwide — no Phase 1, no first-in-human safety study, no dose escalation.

Does Pinealon improve memory or protect the brain?

This is not established. There are rodent reports of improved Morris water maze learning and altered caspase-3 activity, and small human studies — none reporting blinding — describing improvements in composite “biological age” and psychoemotional indices. None of that constitutes evidence of cognitive or neuroprotective benefit in humans, because no randomised, blinded, placebo-controlled trial with a prespecified cognitive endpoint has been conducted. Notably, one rodent study reported that Pinealon increased behavioural sleep and reduced exploratory and motivational behaviour and motor performance.

References

National Center for Biotechnology Information. PubChem Compound Summary for CID 10273502, Glu-Asp-Arg (Pinealon). https://pubchem.ncbi.nlm.nih.gov/compound/10273502

Khavinson V, Ribakova Y, Kulebiakin K, Vladychenskaya E, Kozina L, Arutjunyan A, Boldyrev A. Pinealon increases cell viability by suppression of free radical levels and activating proliferative processes. Rejuvenation Res. 2011;14(5):535–41. PMID 21978084 · doi:10.1089/rej.2011.1172

Fedoreyeva LI, Kireev II, Khavinson VKh, Vanyushin BF. Penetration of short fluorescence-labeled peptides into the nucleus in HeLa cells and in vitro specific interaction of the peptides with deoxyribooligonucleotides and DNA. Biochemistry (Mosc). 2011;76(11):1210–9. PMID 22117547 · doi:10.1134/S0006297911110022

Myakotnykh VS, Torgashov MN, Egorin KV, Meshchaninov VN, Gavrilov VI, Borovkova TA, Zvezdina EM, Verzhbitskaya TY, Tkachenko EL. [Comparative analysis of different methods of geroprotective]. Adv Gerontol. 2016;29(4):594–601. PMID 28539017

Khavinson VKh, Bondarev IE, Butyugov AA. Epithalon peptide induces telomerase activity and telomere elongation in human somatic cells. Bull Exp Biol Med. 2003;135(6):590–2. PMID 12937682 · doi:10.1023/a:1025493705728

ClinicalTrials.gov. Search results for intervention “Pinealon”. US National Library of Medicine. https://clinicaltrials.gov/search?intr=Pinealon

Nazimko VA, Morgul’ EV, Petrova OA, Sheikhova RG, Kozina LS, Savenko MA, Lysenko DS. [Analysis of some parameters of biological age and adaptation possibilities of workers of locomotive brigades]. Adv Gerontol. 2012;25(1):57–62. PMID 22708445

Bashkireva AS, Artamonova VG. [The peptide correction of neurotic disorders among professional truck-drivers]. Adv Gerontol. 2012;25(4):718–28. PMID 23734521

Meshchaninov VN, Tkachenko EL, Zharkov SV, Gavrilov IV, Katyreva IuE. [Effect of synthetic peptides on aging of patients with chronic polymorbidity and organic brain syndrome of the central nervous system in remission]. Adv Gerontol. 2015;28(1):62–7. PMID 26390612

Mendzheritski AM, Karantysh GV, Abramchuk VA, Ryzhak GA. [Effect of peptide geroprotectors on the navigation system learning and caspase-3 in brain structures in rats of different age]. Adv Gerontol. 2013;26(2):252–257. PMID 28976148

Silanteva IA, Komolkin AV, Morozova EA, Vorontsov-Velyaminov PN, Kasyanenko NA. Role of Mono- and Divalent Ions in Peptide Glu-Asp-Arg–DNA Interaction. J Phys Chem B. 2019;123(9):1896–1902. PMID 30762356 · doi:10.1021/acs.jpcb.8b10359

Kozina LS, Arutiunian AV, Stvolinskii SL, Khavinson VKh. [Biological activity of regulatory peptides in model experiments in vitro]. Adv Gerontol. 2008;21(1):68–73. PMID 18546826

Mendzheritskii AM, Karantysh GV, Ivonina KO. [Effects of introduction of short peptides before carotid artery occlusion on behaviour and caspase-3 activity in the brain of old rats]. Adv Gerontol. 2011;24(1):74–9. PMID 21809624

Khavinson V, Linkova N, Kozhevnikova E, Trofimova S. EDR Peptide: Possible Mechanism of Gene Expression and Protein Synthesis Regulation Involved in the Pathogenesis of Alzheimer’s Disease. Molecules. 2021;26(1):159. Epub 2020 Dec 31. PMID 33396470 · PMC7795577 · doi:10.3390/molecules26010159

Bacteriostatic Water for Injection, USP (Hospira, Inc.) — FDA prescribing information. DailyMed, US National Library of Medicine. DailyMed label

Mendzheritskii AM, Karantysh GV, Ryzhak GA, Dem’ianenko SV. [Regulation of content of cytokines in blood serum and of caspase-3 activity in brains of old rats in model of sharp hypoxic hypoxia with Cortexin and Pinealon]. Adv Gerontol. 2014;27(1):94–7. PMID 25051764

Khavinson VKh, Lin’kova NS, Tarnovskaya SI, Umnov RS, Elashkina EV, Durnova AO. Short peptides stimulate serotonin expression in cells of brain cortex. Bull Exp Biol Med. 2014;157(1):77–80. PMID 24909721 · doi:10.1007/s10517-014-2496-y

Khavinson VKh, Linkova NS, Chalisova NI, Dudkov AV, Koncevaya EA. Effect of short peptides on expression of signaling molecules in organotypic pineal cell culture. Bull Exp Biol Med. 2011;152(1):138–41. PMID 22803060 · doi:10.1007/s10517-011-1473-y

Rahman OF, Lee SJ, Seeds WA. Therapeutic Peptides in Orthopaedics: Applications, Challenges, and Future Directions. J Am Acad Orthop Surg Glob Res Rev. 2026;10(1). PMID 41490200 · doi:10.5435/JAAOSGlobal-D-25-00236

Umnov RS, Lin’kova NS, Khavinson VKh. [Neuroprotective effects of peptides bioregulators in people of various age]. Adv Gerontol. 2013;26(4):671–8. PMID 24738258

United States Pharmacopeia. General Chapter <797> Pharmaceutical Compounding — Sterile Preparations, §13.2 (Use of Conventionally Manufactured Multiple-Dose Containers): the beyond-use date after initially entering or puncturing a multiple-dose container is 28 days unless otherwise specified by the manufacturer. USP <797> chapter text (PDF)

PubMed search, US National Library of Medicine. Query: "pinealon"[Supplementary Concept] OR "pinealon"[All Fields] — 22 records retrieved July 2026. Run this search

Arutjunyan A, Kozina L, Stvolinskiy S, Bulygina Y, Mashkina A, Khavinson V. Pinealon protects the rat offspring from prenatal hyperhomocysteinemia. Int J Clin Exp Med. 2012;5(2):179–85. PMID 22567179 · PMC3342713

Kozina LS. [Investigation of antihypoxic properties of short peptides]. Adv Gerontol. 2008;21(1):61–7. PMID 18546825

Mendzheritsky AM, Karantysh GV, Ryzhak GA, Prokofiev VN. [Pinealon and Cortexin influence on behavior and neurochemical processes in 18-month aged rats within hypoxia and hypothermia]. Adv Gerontol. 2015;28(3):532–539. PMID 28509493

Jiang Y, Wang R, Yin Z, et al. Optimization of protein hydrolysis conditions and antioxidant activity of tetrapeptide Asp-Arg-Glu-Leu… Food Funct. 2021;12(11):4808–4824. (Cited as an example of a PubMed false-positive match, unrelated to Pinealon.) PMID 33876788 · doi:10.1039/d0fo02852e

Terminology used throughout this article — lyophilisation, reconstitution, U-100, bioregulator, organotypic culture — is defined in our peptide research glossary.

Research use only. Pinealon is not approved by the FDA or any comparable regulatory authority for any indication, and no published human dose-ranging, pharmacokinetic or controlled efficacy trial exists for it. The doses, concentrations, cycle lengths and syringe volumes described on this page are reported here solely to document what has appeared in the research literature and in research-supply conventions, and they are presented for reference and educational purposes only. Nothing in this article is medical advice, a recommendation to administer any substance to a human being, or a suggestion that Pinealon treats, cures, prevents or mitigates any disease or condition. Dosagepeptide.com is an independent reference library; we do not sell peptides and we have no commercial interest in any supplier of this compound.