Preloaded Autoinjector | Bronchogen | 3ml Pen | 20mg

The bronchogen pen is a preloaded 3ml research autoinjector holding the tetrapeptide L-alanyl-L-glutamyl-L-aspartyl-L-leucine (Ala-Glu-Asp-Leu, AEDL) in solution at 20/3 mg/ml, giving 20mg in the device. Its principal ageing route converts the Asp3-Leu4 bond into an isomer of identical mass that co-elutes closely with the parent, so neither a mass check nor a single chromatographic peak rules it out.

Specification Table

What Changes When Bronchogen Ships in Solution?

Dissolving Ala-Glu-Asp-Leu opens two hydrolytic routes and one rearrangement, and the rearrangement is the one that defeats the usual quality checks because its product weighs the same as the parent and comes off a reversed-phase column at almost the same time.

What is absent first. No asparagine or glutamine, so no deamidation. No methionine, cysteine, tryptophan, histidine or tyrosine, so nothing to oxidise, no disulfide, no chromophore. Nothing fibrillates: three carboxylates keep a 446 Da tetrapeptide fully solvated at neutral pH, and although the leucine adds a small hydrophobic patch, weak self-association is conceivable only near the isoelectric point at high concentration and has never been reported.

The rearrangement is aspartate isomerisation at position 3. The backbone nitrogen of Leu4 closes a five-membered succinimide onto the Asp3 side chain, shedding water, and that ring reopens either to the original alpha-linked peptide or to the beta-linked isoaspartyl form in which the chain now runs through the aspartate side chain. Part of the material racemises to D-aspartate along the way. Because the ring closure loses a water and the reopening restores it, the isoaspartyl product has the same 446.46 g/mol as the parent. That much is shared with Cardiogen. What is specific to AEDL is that the leucine isomers co-elute closely on many gradients, so a single symmetrical HPLC peak is not evidence of an unchanged molecule either. Only the transient succinimide, 18 Da lighter, shows up as a distinct mass.

The bulk of that leucine is also what slows the reaction. Succinimide closure requires the backbone nitrogen to swing onto the side-chain carbonyl, and an isobutyl group hinders the approach, so Asp-Leu isomerises far more slowly than Asp-Gly or Asp-Ser, where nothing obstructs it. Slow is not zero, and no rate has been measured for this sequence at any pH.

The second route runs from the other terminus. The free amine of Ala1 attacks the Glu2 carbonyl, cutting the chain to release cyclo(Ala-Glu) near 200 Da and the dipeptide Asp-Leu near 247 Da. Diketopiperazine cleavage is fastest when residue 2 is proline or glycine and comparatively slow when it is glutamic acid, as here, and unlike the isomerisation it is fully visible: the parent signal falls and two new ones appear.

Charge and hydrophobicity set the handling. Four ionisable groups give a net charge of about -2 at pH 7.4 with an estimated isoelectric point near 3.2, unpublished. An anionic molecule is repelled by glass silanols, so glass adsorption is low. The leucine terminus is the difference: AEDL is the most hydrophobic of the AED-core peptides, more so than Ala-Glu-Asp or Ala-Glu-Asp-Arg, which makes uptake onto polypropylene, plunger elastomer and filter membranes more plausible. At milligram-per-millilitre fill concentrations the fraction lost is negligible. In a working dilution at tens of nanomolar it is not, and low-binding plasticware is a reasonable precaution.

Acid is the last variable. Bonds flanking an aspartate are the most acid-labile in any peptide, and the free acid in unbuffered water sits near pH 3 at tens of millimolar. No approved product containing AEDL exists anywhere to borrow a formulation from; the compounds of this class are sold in Russia as oral capsules classed as dietary supplements, which says nothing about an injectable solution.

What Is Known About Bronchogen Solution Stability?

Nothing measured has been published on bronchogen solution stability: a Crossref search in September 2026 found no forced-degradation, shelf-life or formulation study of AEDL as a pharmaceutical solution.

The physical-chemistry literature that does exist concerns the peptide in water with DNA rather than the peptide on a shelf. Monaselidze and colleagues (2011) ran differential scanning microcalorimetry and reported that AEDL at a peptide-to-base-pair molar ratio of 0.01 to 0.055 raised the melting temperature of calf thymus and mouse liver DNA by 3.1°C with melting enthalpy unchanged at 11.4 and 12.7 cal/g, which they read as non-sequence-specific binding to both strands. That is a binding measurement, not a stability measurement.

So the prediction stands without numbers behind it: slower loss cold and near neutral pH, faster loss warm or acidic, with bronchogen degradation in solution never followed across the weeks a multi-dose device stays in use. One further risk sits outside chemistry entirely. Every approved multi-dose peptide pen contains phenol or metacresol, because a solution punctured repeatedly faces microbial growth whatever its chemical stability, and whether this fill is preserved is not stated.

Concentration and Increment Arithmetic for the Bronchogen Pen

At 20mg in 3 ml the concentration is 20/3 mg/ml, which at 446.46 g/mol is (20/3) divided by 446.46 moles per litre: a 20 mg fill gives 6.667 mg/ml and 14.9 mM, a 1 mg fill gives 0.333 mg/ml and 0.747 mM.

One 0.01 ml graduation holds 20/300 mg and 0.1 ml holds 20/30 mg. At a 20 mg fill that is 66.7 micrograms per 0.01 ml, which is 149 nanomoles, and 667 micrograms per 0.1 ml.

The published concentrations are far below that. Fedoreyeva and colleagues (2020) worked at 10^-7 M, which for this molecule is 44.6 ng/ml, and the Khavinson group’s review gives 2-200 ng/ml as the effective culture window, or 4.5 to 448 nM for AEDL. Reaching 100 nM from a 14.9 mM fill needs a 149,000-fold dilution; from 0.747 mM, 7,470-fold. The DNA calorimetry sits at the other extreme, using peptide-to-base-pair ratios well above anything a cell would meet.

Does Bronchogen Come in a Pen?

Bronchogen does come in a pen: this preloaded 3 ml autoinjector holds AEDL in solution and sits in the catalogue beside the lyophilized Bronchogen vial and the nasal spray presentation.

People searching “does bronchogen come in a pen” have usually seen the vial and want to skip weighing and reconstitution. The general case for the format is covered on the preloaded autoinjector category page. What is specific to bronchogen in pen form is that the solution’s age and its unpublished pH together determine how much of the contents has quietly become the beta-linked isomer, and no routine certificate reports that.

Bronchogen Pen vs Vial: Which Presentation Suits AEDL?

The bronchogen pen vs vial decision turns on isoaspartate, because a dry cake in a freezer is not isomerising and a filled cartridge is, from the moment the solution is made.

The pen suits repeated equivalent draws from one lot across weeks, where weighing a milligram of hygroscopic salt is the largest error in the procedure. It removes the balance, the diluent measurement and the dissolution step together, and it fixes one concentration determined at manufacture.

The vial suits work where the isomer ratio matters or the conditions must be chosen. Reconstituted powder gives a solution of known age, in a buffer and at a pH selected rather than inherited, and provides the same-day comparator an older device has to be judged against. Bronchogen solution vs lyophilized is, for this sequence, a question about time spent in water. The peptide pen versus vial article covers what the two formats share; the bronchogen autoinjector vs vial version is distinctive because the change at stake escapes both mass and a single-peak purity check.

What the Product Record Does Not State

Four values are missing, and the first governs the chemistry above.

Solution pH is not stated. Succinimide formation accelerates as a solution moves toward neutral and alkaline, acid attacks the bonds flanking the aspartate instead, and the unbuffered free acid would sit near pH 3. There is no pH at which nothing happens, only one at which the least happens, and 50 microlitres with a calibrated meter answers the question on receipt.

The excipient system is not stated, so buffer, tonicity agent and any preservative arrive in the assay with the peptide. The salt form is not stated; trifluoroacetate carried through purification is not inert in culture at the concentrations a millimolar stock delivers. The fill date is not stated. Ask for it; the real-time stability data that would make it meaningful does not exist for AEDL in any format.

Verifying the Bronchogen Pen and Detecting a Mass-Silent Change

Inspect the solution against a dark background before each draw: it should be clear, colourless and free of particulate, and because this tetrapeptide does not aggregate, anything visible points to contamination or precipitated excipient rather than to the peptide itself.

Absorbance at 280 nm is useless here. With no tryptophan and no tyrosine there is nothing to absorb, so quantification works through the peptide bond at 205-215 nm, in practice reversed-phase HPLC at 214 nm against a standard prepared the same day from the vial.

Mass spectrometry covers half the problem. It shows the parent at 447 Da protonated (446.201 Da monoisotopic), cyclo(Ala-Glu) near 201 Da and the Asp-Leu dipeptide near 248 Da from diketopiperazine cleavage, and the succinimide intermediate 18 Da below the parent. It cannot show the isoaspartyl product, which has the parent’s mass.

That leaves the isomer, and for AEDL a chromatographic answer is harder than usual because the alpha and beta forms elute close together. Three approaches work. A long shallow gradient on a column with adequate efficiency can resolve them as a shoulder. Protein isoaspartyl methyltransferase methylates isoaspartate specifically and converts the invisible isomer into a countable signal. Chiral or ion-pair separation catches the D-aspartate that accompanies the rearrangement. A same-day solution from a lyophilized vial run on the same method is the reference; the ratio of the two peak areas is the result.

Bronchogen Pen Storage and Handling

Bronchogen pen storage is 2-8°C, protected from light and never frozen, with the device returned to the refrigerator between sessions, because temperature drives both the succinimide route and the diketopiperazine route and nothing else in the handling regime matters as much.

Light protection is the weakest instruction on the label for this compound. AEDL has no chromophore above roughly 220 nm, so photodegradation is not a route available to it; the instruction guards against lamp heat and against photochemistry in whatever excipients are present.

Freezing is prohibited to protect the hardware rather than the peptide. A small, highly soluble tetrapeptide survives freeze-thaw, but 3 ml of solution expanding inside a sealed glass cartridge cracks glass and displaces elastomer plungers, and a damaged cartridge delivers the wrong volume without any visible sign. Record the fill date, the date of first actuation, the volume drawn each session and every excursion outside 2-8°C, because no in-use period has been established by anyone and that log is the only substitute for stability data. The peptide storage and stability guide covers the general principles.

What Does the AEDL Literature Actually Report?

The published record for this tetrapeptide is biophysical rather than physiological: two studies of how it binds DNA and histones, one study of differentiation markers in cultured human bronchial epithelium, and two docking papers.

Monaselidze and colleagues (2011) measured DNA thermostability by microcalorimetry and reported a 3.1°C rise in melting temperature for calf thymus and mouse liver DNA at peptide-to-base-pair ratios of 0.01 to 0.055, with melting enthalpy unchanged at 11.4 and 12.7 cal/g. Their interpretation is non-sequence-specific binding to both strands. That paper is also the source of a naming quirk worth knowing: its title and abstract write the sequence as Ala-Asp-Glu-Leu, while every later paper from the same group writes Ala-Glu-Asp-Leu. AEDL is the form to use, and the discrepancy is unexplained.

Fedoreyeva and colleagues (2020) reported 1:1 binding of AEDL to linker histone H1, at its N-terminal lysine, and to Lys36 of histone H3, measured by fluorescence quenching, and found condensed chromatin domains falling from 45% to 25% at 10^-7 M. Those chromatin measurements were made in tobacco cells, which is a long way from a bronchus.

Khavinson and colleagues (2012) reported that AEDL raised expression of differentiation markers in cultured human bronchial epithelial cells, with a larger effect in late-passage cultures than in early ones; the concentration used is not in the abstract. Docking work assigns AEDL to a “ctcc” DNA tetranucleotide (2016) and scores it against transporters at -25.11 kcal/mol for LAT1, -18.88 for LAT2 and -25.35 for PEPT1 (2023). Those are computed values, and no binding to any transporter has been measured.

The gaps are wide. No asthma, chronic obstructive pulmonary disease, fibrosis, infection or lung-injury model appears in the peer-reviewed literature; no inhaled or injected route has been studied in any species; there is no pharmacokinetics, no toxicology, no dose-response in human cells, and no replication independent of the Khavinson institute. The institute’s own 2014 review of clinical results for peptide bioregulators covers seven other preparations and does not mention this one. The background article on this compound and the bioregulator research overview set that record beside the rest of the family; structurally AEDL is the Cartalax core AED plus a leucine.

What Is the Safety and Regulatory Position?

No safety study of AEDL exists in any species, and no regulator has approved a product containing it: not the FDA, EMA, PMDA, TGA or Health Canada, and it does not appear in the FDA Orange Book.

Russian marketing is as a dietary supplement rather than a medicine, a status not verified against the Russian register during this research. The compound is not on the FDA section 503A bulk-substance list and not in Category 1 or Category 2 of the interim lists (FDA page updated 22 April 2026), is not a component of any approved drug and has no USP monograph, so no lawful basis exists for compounding it from bulk in the United States. It is not named on the WADA Prohibited List as far as this dossier could establish; the 2026 list was not retrievable, so treat that as unverified.

No adverse finding has been reported because no study capable of finding one has been run. Respiratory claims of any kind rest on one differentiation-marker paper in cultured cells, and nothing in the published record describes what this reagent does after injection into any organism.

Published Literature

The entries below concern the tetrapeptide AEDL and the peptide family it belongs to; nothing has been published on this delivery format.

1. Khavinson VK, Linkova NS, Polyakova VO, et al. Peptides Tissue-Specifically Stimulate Cell Differentiation during Their Aging. Bulletin of Experimental Biology and Medicine. 2012;153(1):148-151. DOI: 10.1007/s10517-012-1664-1
2. Monaselidze JR, Khavinson VK, Gorgoshidze MZ, et al. Effect of the Peptide Bronchogen (Ala-Asp-Glu-Leu) on DNA Thermostability. Bulletin of Experimental Biology and Medicine. 2011;150(3):375-377. DOI: 10.1007/s10517-011-1146-x. PMID: 21240358
3. Fedoreyeva LI, Vanyushin BF, Baranova EN. Peptide AEDL alters chromatin conformation via histone binding. AIMS Biophysics. 2020;7(1):1-16. DOI: 10.3934/biophy.2020001
4. Khavinson VK, Lin’kova NS, Tarnovskaya SI. Short Peptides Regulate Gene Expression. Bulletin of Experimental Biology and Medicine. 2016;162(2):288-292. DOI: 10.1007/s10517-016-3596-7
5. Khavinson VK, Linkova NS, Rudskoy AI, et al. Feasibility of Transport of 26 Biologically Active Ultrashort Peptides via LAT and PEPT Family Transporters. Biomolecules. 2023;13(3):552. DOI: 10.3390/biom13030552. PMID: 36979488
6. Khavinson VK, Popovich IG, Linkova NS, et al. Peptide Regulation of Gene Expression: A Systematic Review. Molecules. 2021;26(22):7053. DOI: 10.3390/molecules26227053. PMID: 34834147
7. Khavinson VK, Kuznik BI, Ryzhak GA. Peptide bioregulators: A new class of geroprotectors, report 2. The results of clinical trials. Advances in Gerontology. 2014;4(4):346-361. DOI: 10.1134/S2079057014040122

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