Preloaded Autoinjector | Chonluten | 3ml Pen | 20mg

The chonluten pen is a preloaded 3ml research autoinjector holding the tripeptide Glu-Asp-Gly in solution at [STRENGTH]/3 mg/ml, giving [STRENGTH]mg per device. Three separate non-enzymatic degradation routes run in this molecule at once, and their pH optima point in different directions, so no formulation pH switches all three off.

Specification Table

What Changes When Chonluten Ships in Solution?

Three non-enzymatic reactions open at once in a molecule of only three residues: the N-terminal glutamate cyclises to pyroglutamate, the aspartate-glycine pair forms a succinimide, and the whole tripeptide can collapse into a diketopiperazine with the loss of glycine.

Take them in order of what they do to the mass. Pyroglutamate formation is the visible one. A free N-terminal glutamic acid can close onto its own side chain to give 5-oxoproline with loss of water, a route documented in antibodies and peptides by Chelius and colleagues (2006), slower than the same reaction from N-terminal glutamine but accelerated by heat and mildly acidic conditions. The product, pGlu-Asp-Gly, is C₁₁H₁₅N₃O₇ at 301.26 daltons, 18.01 lighter than the parent and eluting at a different retention time. This route does not exist in Ala-Glu-Asp-Gly, which has alanine at the N-terminus, and it is the first chemical consequence of removing that alanine.

The second reaction is the invisible one. The backbone nitrogen of Gly3 attacks the side-chain carbonyl of Asp2, closes a five-membered ring and reopens as either alpha-linked aspartate or beta-linked isoaspartate, roughly one to three in favour of the isomer, with some D-aspartate from racemisation at the ring stage. Every product of that succinimide route has the parent formula and the parent mass. Glycine is the worst possible neighbour for it: Stephenson and Clarke (1989) measured ring closure 6.5 to 17.6-fold faster with glycine after aspartate than with alanine, because glycine has no side chain to obstruct the approach. Oliyai and Borchardt (1993) added the pH map for the same bond: above pH 6 the isomer is the only product, at pH 4 to 5 isomerisation runs alongside direct hydrolysis, and below pH 3 hydrolysis dominates, cutting off glycine to leave Glu-Asp at 262.2 daltons.

The third reaction is the one specific to how short this molecule is. A tripeptide with a free N-terminal amine is the classic length for diketopiperazine formation: the amine attacks the second peptide carbonyl, a six-membered ring closes and the C-terminal residue leaves. Here that gives cyclo(Glu-Asp) at about 244.2 daltons and free glycine at 75.1. Goolcharran and Borchardt (1998) showed the rate rises with pH, because the nucleophile is the unprotonated amine. It has never been measured for this sequence, which makes it the least quantified of the three and not the least likely.

What the molecule does not have is short. No methionine, tryptophan, cysteine, histidine or tyrosine, so oxidation has no target and nothing absorbs above about 220 nanometres. Aggregation is neither expected nor reported for a three-residue anion with a calculated XLogP3 of -5.3, though it has never been measured. Nothing has been published on this compound’s stability in solution, and the Khavinson group’s own patent, EP 2667887 B1, claims a composition whose dosage form could not be read for this page.

Three Routes, Three pH Optima: Why No Fill Is Ideal

The pH that slows one of these reactions accelerates another, which is unusual: most peptides have a single dominant route and therefore a single best pH, and this one does not.

Mildly acidic conditions suppress diketopiperazine formation, because the N-terminal amine spends more time protonated and cannot act as a nucleophile. The same conditions accelerate pyroglutamate formation and push the aspartate-glycine pair toward direct hydrolysis. Near-neutral conditions do the reverse: pyroglutamate slows, hydrolysis slows, and both the succinimide route and diketopiperazine formation stay fully open, with the isomer becoming the only aspartyl product above pH 6.

A formulator choosing a pH for this tripeptide is therefore choosing which degradant to accumulate rather than whether to accumulate one. Around pH 6 to 7 is the least-bad compromise, since it removes two of the three mass-visible routes and leaves the isomer, which is chemically the most conservative change. That is a judgement from model-peptide kinetics rather than a measurement, because no stability study of this compound exists in any form. The product record does not state the pH.

How Concentrated Is the Chonluten Pen?

At [STRENGTH]mg in 3 ml the concentration is [STRENGTH]/3 mg/ml, the molar concentration is [STRENGTH] x 1.044 mM, and each 0.01 ml increment carries [STRENGTH]/300 mg, which for a 10 mg fill is 33.3 micrograms.

Working the 10 mg example: 3.333 mg/ml divided by 319.27 g/mol and multiplied by 1000 gives 10.44 mM, or 10,440 micromolar. That is the highest molarity per milligram in this range of products, because 319.27 g/mol is the smallest molecular weight in it: one milligram is 3.13 micromoles, so the same mass of this tripeptide is about 20 percent more concentrated in molar terms than the same mass of the pineal tetrapeptide. One 0.01 ml increment holds 33.3 ug, which is 104 nanomoles, and ten increments deliver 333 ug.

Against the published assay range the fill is very large. The Khavinson group’s working range for this family is 2 to 200 nanograms per millilitre, which for a 319.27 g/mol peptide is 6.3 to 626 nanomolar. Reaching 100 nanomolar from 10.44 mM requires a serial dilution of roughly 104,000-fold, and a single 0.01 ml increment would bring 330 millilitres of medium to 100 nanograms per millilitre. No water solubility figure has been published for the compound, so nothing in the literature caps the fill strength.

Chonluten vs Bronchogen: What Is the Difference?

Chonluten is the tripeptide Glu-Asp-Gly and Bronchogen is the tetrapeptide Ala-Glu-Asp-Leu, and the difference that matters for a solution product is that Bronchogen has neither of this molecule’s two fast routes.

Bronchogen begins with alanine, so pyroglutamate formation is not available to it, and its aspartate is followed by leucine, whose bulky side chain slows succinimide formation by the same factor that glycine accelerates it. Written as a stability comparison rather than a marketing one, the edg vs aedl peptide contrast favours the tetrapeptide in water. The sequence itself is not entirely settled in the literature: the Khavinson group writes AEDL in its 2012 and 2021 papers and ADEL in the 2011 and 2014 work.

The evidence contrast runs the other way from what the marketing suggests. The bronchial epithelium gene-expression work, which reports changes in NKX2-1, SCGB1A1, SCGB3A2, FOXA1, FOXA2, MUC4 and MUC5AC in human embryonic bronchial epithelial cells at passages 1, 7 and 14, is a study of Bronchogen published in Lung in 2014. It is not a study of this compound, though it is frequently attached to it. The only peer-reviewed in-vivo abstract for T-34, the code this tripeptide carries in the primary literature, concerns gastric ulcer. Anyone comparing chonluten vs bronchogen on published data is comparing a lung dataset with a gastric one, and the shared lung positioning is a description of how both are sold. The bioregulator research overview covers the family.

Chonluten Pen vs Vial: What Does the Format Suit?

The chonluten pen vs vial question is sharper here than for most compounds, because a dry cake stops all three degradation routes at once and a solution starts all three at once.

The Chonluten lyophilized vial keeps the molecule chemically quiet until diluent goes in, so material reconstituted on the morning of an experiment has an age known to the hour. The device removes diluent-volume, dissolution and transfer error and fixes concentration at manufacture, which is the general trade the pen versus vial article works through.

The tilt for this molecule follows from the mass balance. Two of the three routes are mass-visible, at 301.26 and 244.2 daltons, so an aged fill can be assessed by chromatography, and only the isomer hides. Repeated equivalent draws over a few weeks are defensible on that basis. Work running for months, or work where the intact fraction has to be known at the moment of use, is better served by a vial opened fresh. The preloaded autoinjector category page covers graduation resolution and cold-chain history, and a nasal spray presentation is listed as well.

What the Chonluten Pen Product Record Does Not State

Four values are absent and each one affects how a result should be read: the formulation pH, the excipient system, the salt form and the fill date.

The pH is the one that decides which of three degradants accumulates, as set out above, and no default can be assumed because the compound has no approved formulation anywhere to borrow one from. The excipient system follows the solution into any assay, and buffer species and ionic strength are not neutral background for a three-residue anion carrying a net charge near minus two.

The salt form changes how much peptide a weighed milligram holds, and it matters more here than for larger molecules: one trifluoroacetate counterion is 114 daltons against a 319.27 dalton peptide, so a substantial fraction of a weighed milligram could be counterion. Vendor sheets say acetate without verification. The fill date sets the solution’s age, which with the pH is what an estimate of intact material would be built from. Confirm all four against certificate of analysis.

Chonluten Pen Storage and Verifying the Device

Correct chonluten pen storage is 2 to 8°C, protected from light and never frozen, and the temperature is doing real work here because all three degradation routes are thermally accelerated.

Inspect the solution against a white background before each draw: clear, colourless, free of particulate. Let the cartridge reach ambient temperature before actuating, since cold solution is more viscous and viscosity shifts delivered volume in a spring-driven mechanism, and verify delivered volume gravimetrically once per device.

Verification of contents needs one method that sees mass and one that does not. Liquid chromatography with mass detection resolves the parent at 319.27 from pyroglutamate at 301.26, from cyclo(Glu-Asp) at 244.2 with free glycine at 75.1, and from Glu-Asp at 262.2 if the fill has been acidic. Those four peaks are a readable degradation profile. The isoaspartyl isomer will not appear among them, because it carries the parent mass, so separating it needs a shallow reversed-phase gradient run against a same-day reference reconstituted from lyophilized material, or an isoaspartate-specific enzymatic assay. Ultraviolet detection has to run at 210 to 220 nanometres, since there is no aromatic residue and nothing absorbs at 280, which puts excipient carbonyls in the same window and makes a matched blank necessary for any concentration estimate.

What Does the Chonluten Literature Actually Report?

The peer-reviewed record for Glu-Asp-Gly is one 2012 animal abstract on gastric ulcer and gene expression, one 2022 cell-line paper on monocytes and macrophages, and a granted European patent. There is no human study, no pharmacokinetic study and no lung model.

Khavinson and colleagues (2012) reported that the peptide, coded T-34, regulates messenger RNA expression of genes encoding antioxidant and anti-inflammatory proteins in a gastric-ulcer context, with the abstract stating that it normalises synthesis of those proteins by regulating expression of the corresponding genes. Species, quantity and route are not given in the abstract. Patent EP 2667887 B1, granted to the same group, claims a pharmaceutical composition containing Glu-Asp-Gly for Helicobacter pylori induced gastroduodenal disease. A granted patent is a claim examined for novelty, not for efficacy.

Avolio and colleagues (2022) tested the peptide in THP-1 monocytes and in PMA-differentiated macrophages alongside Epitalon, Vilon, Thymogen and Thymalin. All the peptides reduced lipopolysaccharide-induced release of tumour necrosis factor and interleukin 6. This one increased STAT1 phosphorylation, produced a moderate apoptotic fraction, contributed to reduced monocyte adhesion to endothelium, and was less effective than Thymogen at reducing interleukin 17. The working concentrations were described only as known to be effective, which is not a number. Khavinson is a co-author, so the paper does not count as independent replication.

The mechanism on offer is the group’s general model, set out in its 2021 systematic review: that peptides of two to seven residues enter nuclei and interact with DNA and histones to modulate transcription. No receptor has been identified for this molecule. Unstudied: any human exposure, pharmacokinetics in any species, in-vivo concentration-response, toxicology, immunogenicity, solution stability, and any lung or bronchial model using this tripeptide itself. The site’s overview article on this compound covers the background.

What Is the Safety and Regulatory Position?

No regulator anywhere has approved this tripeptide, and unlike several compounds sold beside it, it has never been nominated for US pharmacy compounding, so it holds no FDA category and appears in no advisory committee record.

Nothing appears in Drugs@FDA, the EMA register, PMDA, TGA or Health Canada. The compound is absent from the FDA interim 503A bulk drug substances list of 29 September 2023, from the significant-safety-risk page as updated on 22 April 2026, and from every Pharmacy Compounding Advisory Committee docket between 2024 and 2026. That absence means no regulator has examined the substance, which is neither an endorsement nor a warning. Its Russian status could not be verified, and EP 2667887 B1 is a granted patent rather than a marketing authorisation. The compound was not found by name on the WADA Prohibited List, which should be confirmed against the current document.

No adverse findings have been reported, and the size of the literature is the reason. The moderate apoptotic fraction Avolio and colleagues observed in THP-1 cells is a cell-culture observation and not a safety finding. There is no toxicology, no immunogenicity work and no pharmacokinetic study in any species. The device is a laboratory research item, and nothing on this page describes administration to a person or an animal.

Published Literature

Each entry was checked against the publisher record or a primary index; none concerns the pen format, on which nothing has been published.

1. Khavinson VKh, Lin’kova NS, Dudkov AV, et al. Bull Exp Biol Med. 2012;152(5):615-618. DOI: 10.1007/s10517-012-1590-2
2. Avolio F, Martinotti S, Khavinson VKh, et al. Int J Mol Sci. 2022;23(7):3607. DOI: 10.3390/ijms23073607
3. Khavinson VKh, Tendler SM, Vanyushin BF, et al. Lung. 2014;192(5):781-791. DOI: 10.1007/s00408-014-9620-7
4. Khavinson VKh, Popovich IG, Linkova NS, et al. Molecules. 2021;26(22):7053. DOI: 10.3390/molecules26227053
5. Stephenson RC, Clarke S. J Biol Chem. 1989;264(11):6164-6170. DOI: 10.1016/S0021-9258(18)83327-0 PMID: 2703484
6. Oliyai C, Borchardt RT. Pharm Res. 1993;10(1):95-102. DOI: 10.1023/A:1018981231468
7. Chelius D, Jing K, Lueras A, et al. Anal Chem. 2006;78(7):2370-2376. DOI: 10.1021/ac051827k
8. Goolcharran C, Borchardt RT. J Pharm Sci. 1998;87(3):283-288. DOI: 10.1021/js970325m

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