Chonluten
Glu-Asp-Gly (lung/respiratory)
Chonluten (Glu-Asp-Gly (lung/respiratory)) is a longevity & bioregulators research compound. Respiratory/bronchial bioregulator — proposed to support lung and gastric mucosal tissue protein synthesis.
Chonluten quick facts
| Reported research dose | 2mg-5mg |
| Route | Subq |
| Frequency | 1x Daily · Daily (course) |
| Half-life | ~30 min |
| Forms | Injectable |
| Evidence level | Russian studies; limited |
Lung/respiratory bioregulator — the injectable cousin to Bronchogen, run in courses. Lung tissue rather than airway specifically, and the injectable counterpart to Bronchogen. Course pattern: roughly 10 days on, then off, once or twice a year. To know whether it did anything, peak flow, and exercise tolerance measured the same way each time. Run it as an experiment you measure, not a protocol you trust.
How Chonluten works
Respiratory/bronchial bioregulator — proposed to support lung and gastric mucosal tissue protein synthesis.
Proposed benefits
Researched for mitochondrial and cellular-energy support, tissue-specific bioregulation and healthy-aging pathways.
Where to get Chonluten
Buy Chonluten at Biolongevity Labs →Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for Chonluten
Graded by what exists behind each claim.
Human clinical evidence
- The human record is Soviet and post-Soviet clinical work — real patients and real endpoints, published in Russian and rarely replicated to Western standards.
📊 Correlative data
- Used for bronchial and gastric mucosal support — an unusual pairing that comes from the tissue it was isolated alongside rather than from a shared mechanism anyone has demonstrated.
- Beyond that the record is self-reported: community dosing logs are real information about tolerability and almost none about efficacy.
🧪 Theoretical / extrapolated
- Glu-Asp-Gly — a synthetic tripeptide proposed to support mucosal tissue protein synthesis in the airway and stomach lining.
- The shared claim across the Khavinson series: peptides this short are proposed to enter the cell nucleus and bind promoter regions of DNA, shifting tissue-specific gene expression.
- Mucosal epithelium turns over fast, which cuts both ways: rapid renewal is where a gene-expression effect should show up soonest, and also where spontaneous improvement is most likely to be mistaken for one.
What community dosing logs are worth → · How to read the Soviet clinical series → · The Khavinson series, in full →
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Chonluten actually does
Chonluten is Glu-Asp-Gly: 3 residues, formula C11H17N3O8, average mass 319.28 Da. It is the smallest molecule on any Khavinson page on this site, and two things follow from that size which nobody selling it mentions.
It is Epitalon with the first residue removed. Epitalon is Ala-Glu-Asp-Gly. Take the N-terminal alanine off and what is left is Glu-Asp-Gly, exactly 71.08 Da lighter. Those are not similar molecules; one is a truncation of the other. And the two are sold for unrelated purposes — the tetrapeptide as a pineal and telomere-associated compound credited in this group's own systematic review with regulating 98 genes, the tripeptide as a lung and stomach product with no named gene of its own in the same review Khavinson 2021. Whatever else is true, the entire difference in claimed target organ rests on one alanine, and no published experiment has ever compared the two.
The size buys it the one thing the tetrapeptides do not have. The carriers this school proposes as the way in are PEPT1 and PEPT2 on epithelial brush borders and LAT1 and LAT2 for amino-acid transport, and the substrate range described for them is di- and tripeptides Khavinson 2022. At 3 residues this molecule falls inside that range; Bronchogen, Cardiogen, Pancragen and Epitalon all have 4 and fall outside it. That is a genuine mechanistic advantage and it is worth stating clearly before the qualification, which is that the 2023 assessment scoring 26 of these peptides against those transporters was computational docking compared against all 8,400 possible di- and tripeptides, with no transport measured in a living cell Khavinson 2023.
The charge, and what it forbids. Glutamate and aspartate carry side-chain carboxyls; with the C-terminal carboxyl and the protonated N-terminus the computed net charge at blood pH is about −2.06 and the isoelectric point is 3.55. A glycine at the third position contributes nothing at all — no side chain, no charge, no bulk — which means that in electrostatic terms Chonluten is close to being a bare Glu-Asp dipeptide with a spacer. Whatever sequence-specific recognition is being claimed has to be carried by two acidic residues and a hydrogen atom, and the structural difficulty of getting sequence specificity out of a peptide that short is the subject of this group's own motif search Kolchina 2019. This is the page in the catalog where that difficulty is most acute.
Cell, rodent, human — and where it stops
The dual-organ claim is the place to start, because it is a logical problem before it is an evidential one. This product is sold for bronchial tissue and for gastric mucosa. The entire premise of the Khavinson series is tissue specificity — a peptide from one organ acting preferentially on that organ. A molecule that specifically targets 2 unrelated organs is not tissue-specific in the sense the class claims. Either the specificity claim is wrong for this compound, or one of the two indications is. There is no version in which both are true as stated, and no vendor page acknowledges the tension.
In cells, and this compound has more than the gene review suggests. The 2021 systematic review credits named gene sets to Ala-Glu-Asp-Gly, Lys-Glu, Ala-Glu-Asp-Leu and Lys-Glu-Asp-Trp, and Glu-Asp-Gly is not one of the peptides carrying a gene list there Khavinson 2021. But a 2022 paper in International Journal of Molecular Sciences tested 5 named preparations from this family — Epitalon, Vilon, Thymogen, Thymalin and Chonluten — on THP-1, a human monocytic leukemia line differentiated into macrophages with PMA Avolio 2022. All 5 raised tyrosine phosphorylation of mitogen-activated cytoplasmic kinases. Chonluten specifically inhibited TNF production by monocytes exposed to bacterial lipopolysaccharide; all 5 suppressed LPS-stimulated TNF and interleukin-6 in terminally differentiated cells; and peptide-treated monocytes adhered less to LPS-activated endothelial cells. A named line, a named stimulus, named cytokines and an adhesion readout is far more concrete than anything else in this compound's file.
Now read the fine print on it, three times over. First, the effect is on LPS-stimulated cytokine release, not on resting output — the cells had to be provoked before the peptide had anything to suppress. Second, the Saint Petersburg institute that originated these peptides is on the author list alongside the Italian groups, so this is a collaboration and not independent replication. Third, and most awkwardly for the marketing: the paper describes Chonluten as derived from bronchial epithelial cells and then demonstrates its effect in monocytes. That is a third tissue, and a peptide that acts on monocytes is not behaving in a tissue-specific way. The nuclear entry all of this presupposes was itself shown in HeLa cells Fedoreyeva 2011, a cervical carcinoma line that is neither bronchial epithelium nor gastric mucosa.
In rodents, and the animal evidence in this space belongs to a different product. The one solid respiratory animal study in this family used the tetrapeptide Bronchogen: rats, chronic obstructive pulmonary disease induced by 60 days of intermittent nitrogen dioxide exposure, 1 month of peptide, with reported reversal of goblet cell hyperplasia, squamous metaplasia, lymphocytic infiltration and emphysema, restoration of ciliated cells, and increased secretory IgA Kuzubova 2015. That result is Bronchogen's, not this compound's, and the two are different molecules of different lengths. A reader choosing between them on evidence should know that one of them has a rodent lung study and the other does not.
In humans: nothing. No randomized trial, no controlled trial, no published series with a respiratory or endoscopic endpoint. The independent systematic review that covers this general family pooled 24 randomized trials over 2,245 participants on cognitive endpoints, rated risk of bias moderate to high and certainty of evidence low to very low, and includes nothing respiratory or gastric Alsulaimani 2021.
The obstacles. (1) The chain has a cell step and a human step and nothing in between: no animal study exists under this trade name, so the jump is from a leukemia cell line straight to a person. (2) The cell result is anti-inflammatory in macrophages, which is not the same claim as bronchial or gastric repair — the mechanism that was demonstrated and the mechanism that is sold are different mechanisms. (3) The rodent lung evidence people cite when buying this belongs to Bronchogen. (4) The dual-organ positioning contradicts the specificity premise, and the monocyte result makes it a triple-organ problem. (5) Delivery is a docking score. (6) Its nearest structural relative is a different product sold for a different purpose, and the comparison has never been run.
What would have to be true, and how you would know it was not
Four predictions. The last is the one that argues against buying this particular product rather than against the class.
1. TNF-alpha is the marker the cell paper hands you, and it comes with a built-in reason it will probably not move. Chonluten suppressed TNF release from macrophages that had been provoked with bacterial lipopolysaccharide Avolio 2022. A healthy person is not provoked. So the mechanistically honest prediction is that circulating TNF-alpha, which this site retests 3 months after an intervention, stays flat in somebody well — and that if the cell result transfers at all, it transfers in people with an ongoing inflammatory stimulus rather than in the healthy buyer. That is a falsifiable statement in both directions and nobody has drawn the blood. Run it beside hs-CRP and an ESR, which this site also retests at 3 months.
2. If the lung claim carries instead, secretory IgA is where it shows first. That is the marker the rat study moved for the related tetrapeptide Kuzubova 2015, and salivary or sputum secretory IgA is a non-invasive assay a person can obtain. It has never been measured on this compound in any species. Beside it, run a CBC with differential at baseline and after a course and read the eosinophil count, because allergic airway inflammation is the confounder that will otherwise be credited to the peptide.
3. If the gastric claim carries, the readout is not a blood test. Gastric mucosal change is seen on endoscopy and biopsy, and there is no serum marker of mucosal healing. What blood can do is catch the consequences of long-standing gastric problems: ferritin, and vitamin B12, both of which fall when acid production and intrinsic factor fail. Neither is a peptide response — they are the reasons to find out what is actually wrong with a stomach before treating it with an unstudied capsule.
4. The prediction that cuts against the product: this compound should underperform its own sibling on any respiratory endpoint, and nobody has ever checked. Bronchogen has a rodent lung study; Chonluten has none. If the two were run side by side over a 20-day course with morning peak flow logged daily, the mechanistically honest expectation is that neither moves and the second-order expectation is that the one with animal data does better. A person buying both, which the community commonly does, has no way to tell them apart and no published reason to expect them to differ.
What nobody has tested yet
Four experiments, and the first of them would tell you whether this product should exist as a separate item.
1. Nobody has compared Glu-Asp-Gly with Ala-Glu-Asp-Gly. One alanine separates this compound from Epitalon, which is the most studied molecule in the whole family. Put both on the same bronchial epithelial cells and the same pineal or fibroblast line, read the same genes, and you learn whether the alanine does anything at all. If it does not, 2 products are 1 product. If it does, the tissue-specificity claim finally has a piece of evidence under it. Both peptides are commercially available and the experiment has never been published.
2. Nobody has tested it on the transporter it supposedly uses. This is one of the few molecules in the catalog short enough to be a plausible PEPT1 substrate Khavinson 2023. A competition assay against a known PEPT1 substrate in a cell line expressing the transporter is an undergraduate-level experiment that would convert the best theoretical argument on this page into a measurement.
3. Nobody has looked at the stomach at all. The gastric half of the marketing has 0 published experiments behind it in any species — no histology, no gastric pH, no mucus thickness, no healing rate in an induced ulcer model, which is one of the oldest and cheapest assays in pharmacology. The claim is 1 sentence on a vendor page repeated for years.
4. No human has ever blown into a tube on this compound. Peak flow, spirometry, exhaled nitric oxide and a 6-minute walk are all inexpensive and all absent. 20 people logging morning peak flow through a course and for a month afterward would create the first human respiratory dataset for this molecule, and the meter costs less than 1 vial.
Chonluten — its own safety story, not its class's
The class safety block on this page was written for injectable peptides as a group. Three things about this one are its own.
A stomach symptom deserves a cause, and there is a curable one at the top of the list. Helicobacter pylori is found with a urea breath test, a stool antigen test or a biopsy, and eradicated with a defined antibiotic course and a confirmatory retest. Behind it sit peptic ulcer disease, medication effects and, in a minority that matters enormously, gastric cancer. Every one of those has a test with a published performance figure. This compound has 0 published results in any gastric condition, which makes taking it for dyspepsia a decision to treat a symptom instead of finding its cause.
An airway symptom has its own red flags. Coughing blood, unintended weight loss, a cough that has changed in a smoker, or hoarseness lasting more than 3 weeks are reasons for imaging and spirometry, not for a course of anything. Spirometry produces a number this compound has never been measured against.
The identity problem, which is sharper here than usual. At 319.28 Da this is a very small molecule, and small peptides are the easiest things in this market to substitute or dilute without detection. No vendor publishes lot-level tandem mass spectrometry, and the mass alone cannot distinguish Glu-Asp-Gly from any other arrangement of the same 3 residues. There are 0 published adverse events for this compound, and with 0 human trials there has never been an arm in which one could have been recorded — so that zero describes the absence of observation, not the presence of safety.
Sources read for this page
- Avolio F, et al. (co-authors include Khavinson VKh). Peptides Regulating Proliferative Activity and Inflammatory Pathways in the Monocyte/Macrophage THP-1 Cell Line. International Journal of Molecular Sciences 2022;23(7):3607 · PMID 35408963
- Fedoreyeva LI, et al. 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 (Moscow) 2011;76(11):1210–1219 · PMID 22117547
- Khavinson VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR. Peptide Regulation of Gene Expression: A Systematic Review. Molecules 2021;26(22):7053 · PMID 34834147
- Kolchina N, Khavinson V, Linkova N, Yakimov A, Baitin D, Afanasyeva A, Petukhov M. Systematic search for structural motifs of peptide binding to double-stranded DNA. Nucleic Acids Research 2019;47(20):10553–10563 · PMID 31598715
- Khavinson V, Linkova N, Kozhevnikova E, Dyatlova A, Petukhov M. Transport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers. International Journal of Molecular Sciences 2022;23(14):7733 · PMID 35887081
- Khavinson VK, Linkova NS, Rudskoy AI, Petukhov MG. Feasibility of Transport of 26 Biologically Active Ultrashort Peptides via LAT and PEPT Family Transporters. Biomolecules 2023;13(3):552 · PMID 36979488
- Kuzubova NA, Lebedeva ES, Dvorakovskaya IV, Surkova EA, Platonova IS, Titova ON. Modulating Effect of Peptide Therapy on the Morphofunctional State of Bronchial Epithelium in Rats with Obstructive Lung Pathology. Bulletin of Experimental Biology and Medicine 2015;159(5):685–688 · PMID 26468022
- Alsulaimani RA, Quinn TJ (independent — not the Khavinson group). The efficacy and safety of animal-derived nootropics in cognitive disorders: Systematic review and meta-analysis. Cerebral Circulation – Cognition and Behavior 2021;2:100012 · PMID 36324709
Chonluten — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- These are short peptide fragments of organ extracts, and the honest starting point is that the mechanism itself is not established in a way that lets anyone predict harm precisely. The proposal is gene-regulatory — short peptides binding DNA and modulating transcription in a tissue-specific way. If that is what they do, the theoretical concern is influencing transcription in tissue you were not aiming at.
- In practice the doses are tiny, the peptides are short, and they are degraded quickly — which is also the argument that they may do very little at all. Those two possibilities are the same uncertainty viewed from opposite ends, and you should hold both.
What has actually been reported
- Decades of Russian clinical use with a strikingly clean tolerability record — injection-site reactions and little else reported.
- That record comes almost entirely from one research school, is largely unreplicated outside it, and safety data from a group with an interest in the outcome is worth less than the same data from a skeptic. This is not an accusation; it is how evidence weighting works.
How to reduce the risk
Same mechanism as the prediction.
- Follow the course printed on the label rather than running continuously. These are the one class in the Vault where a duration is STATED rather than inferred, and it is typically 10–20 days repeated a few times a year. Read the box.
- Run one at a time. They are cheap and it is tempting to stack six. If something changes, a stack of six tells you nothing about which one did it — and given the evidence base, attribution is the entire value of your own experiment.
- Decide your endpoint before you start, and make it a marker or a measurable symptom rather than a feeling. With a compound class this under-evidenced, an unfalsifiable endpoint means you will conclude it worked no matter what happened.
- Buy from a source that publishes third-party testing. Where the molecule itself is uncertain, identity and purity are the only variables you can actually control.
What it does to your bloodwork
A fact about the assay.
- Test the ORGAN, not the peptide. A thymic peptide is judged on immune markers, a pineal one on sleep and IGF-1, a vascular one on lipids and inflammatory markers. There is no assay for the compound itself.
Don't run this if
- Pregnancy — not because of a specific finding, but because nobody has studied it and the mechanism claim is transcriptional.
- Active malignancy, on the same reasoning as any tissue-growth signal: unproven, mechanistically arguable, and not worth finding out.
The honest unknown
- Essentially everything a skeptic would want: independent replication, pharmacokinetics, and whether the oral forms survive digestion at all. Unproven is not the same as ineffective — but here it is a large unproven.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Chonluten — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Chonluten moves on your bloodwork
Expected direction, not a measured one.
- Comprehensive Metabolic Panel (CMP) — ◆ worth watching
These are short peptide fragments given in microgram amounts and there is no mechanism predicting a specific marker shift. Listing markers here would be padding.
What to do: Test the organ system the bioregulator is aimed at, not a generic panel — that is the only measurement that would tell you anything.
The evidence base here is almost entirely one research group's, largely in Russian, and rarely replicated independently. That is the single most important thing to know before running a course, and it is more useful than any interaction list.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Needle gauge and injection site
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Chonluten in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Chonluten
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| hs-CRP (High-Sensitivity C-Reactive Protein) | Chronic low-grade inflammation is the process most of these target |
| ApoB (Apolipoprotein B) | Counts the particles that actually cause plaque, unlike LDL-C |
| HbA1c (Hemoglobin A1c) | Glycation, which is the other half of the ageing story |
| Comprehensive Metabolic Panel (CMP) | Liver and kidney — the two organs that clear everything you take |
| Complete Blood Count (CBC) with Differential | The cheapest broad screen there is |
The Longevity Baseline panel covers these in one order — 13 markers, $219.10 with the discount applied.
Check results you already have → · All 103 markers A–Z
Chonluten — frequently asked questions
What is Chonluten?
Chonluten (Glu-Asp-Gly (lung/respiratory)) is a longevity & bioregulators research compound. Respiratory/bronchial bioregulator — proposed to support lung and gastric mucosal tissue protein synthesis.
Is the full Chonluten protocol on this page?
The reported research dose is on this page, along with how Chonluten works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of Chonluten?
Chonluten has an approximate half-life of ~30 min, which is part of what determines how often it's dosed.
What's the evidence behind Chonluten?
Current evidence level: Russian studies; limited. Chonluten is offered for research purposes only and is not an approved medicine.
Chonluten inside a finished plan
One arm of 2 Protocol Blueprints, free to read in full.
What Chonluten is used for
Chonluten appears under 1 goal in the goal router.
Related Longevity & Bioregulators compounds
Where this goes next
Chonluten is the liver, kidney & gut arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.