Thymogen
Glu-Trp (immune dipeptide)
Thymogen is Glu-Trp — a dipeptide, and the defined-sequence half of the thymus pair. Thymalin is the extract; this is the molecule the extract is claimed to work through. That makes it the cleanest test of the whole 'the extract works because of the short peptides in it' argument, because if the argument is right, the two should behave alike.
Thymogen quick facts
| Reported research dose | 2mg-5mg |
| Route | Subq |
| Frequency | 1x Daily · Daily (course) |
| Half-life | ~20 min |
| Forms | Injectable |
| Evidence level | Russian studies; limited |
Immune bioregulator — short seasonal courses, not year-round. Immune-directed, and close enough to Thymalin that they are alternatives rather than a stack. Course pattern: roughly 10 days on, then off, once or twice a year. To know whether it did anything, CBC with differential, plus how often you actually get ill over a season. Run it as an experiment you measure, not a protocol you trust.
How Thymogen works — what 2 residues can and cannot do
Thymogen is Glu-Trp — a dipeptide, molecular weight 333.4 g/mol, isoelectric point 3.85, net charge about -1.1 at blood pH. Those four numbers are computed from the sequence, not quoted from a vendor.
Two residues. Glu-Trp. This is the smallest molecule in the catalog making a sequence-specific gene-regulation claim, which makes it the cleanest test case for whether the claim can be true at all.
The claim, stated precisely. The mechanism review does not hedge: “molecular modeling showed that the EW dipeptide binds to dsDNA in the classical B-form according to the presence of the GGAG nucleotide sequence,” and it reports that this sequence appears in two promoters of the ATP gene, four promoters of MT-CO1, and in the promoters of HBA1 and HSP90 — genes whose expression the peptide is said to regulate in vitro. That is admirably specific. It also contains its own problem.
Do the counting, because nobody else does. GGAG is four bases long. A given four-base string occurs about once every 44 = 256 base pairs of random sequence. A typical 1,000-base-pair promoter therefore contains roughly four copies by chance, and the human genome — about 3.1 billion base pairs — contains on the order of twelve million. Finding GGAG in the promoter of HSP90 is not a discovery; it would be remarkable to find a promoter of that length without one. So the observation that regulated genes contain the motif carries essentially no information about specificity, and no published analysis has asked whether GGAG is enriched in the regulated genes relative to the unregulated ones. That single control would settle the question, and it has not been done.
What the systematic screen says about dipeptides in general. Khavinson's own group docked all 400 possible dipeptides against 136 tetranucleotide contexts — 108,800 complexes — and concluded that “the vast majority of the dipeptides were found to be unable to bind dsDNA.” Around 30.8% bound any sequence at all, and only 57 complexes were both low-energy and selective. They also noted that most of the selective binders are uncharged and rich in polar and aromatic residues. Glu-Trp is exactly that shape — one acidic residue and one large aromatic — so the argument for EW is at least the argument the screen supports, rather than one invented afterwards. It remains a computed docking preference. No dissociation constant for Glu-Trp against GGAG or anything else has ever been published.
Glu-Trp. The only peptide in this cohort carrying an aromatic residue, which is why it is the one with a genuine spectroscopic handle.
What the primary literature on Thymogen actually says
Peptide Drug Thymalin Regulates Immune Status in Severe COVID-19 Older Patients
Kuznik B, Khavinson V, Shapovalov K, Linkova N, Lukyanov S, Smolyakov Yu, Tereshkov P, Shapovalov Yu, Konnov V, Tsybikov N · Advances in Gerontology 2021;11(4):368–376
Cited here for its identity claim rather than its outcome: the authors state plainly that Thymalin's mechanism 'is due to the effects of the short peptides KE, EW, EDP in its composition.' EW is Thymogen. That sentence is the bridge — and the testable claim — between the extract and this molecule.
Peptide Regulation of Gene Expression: A Systematic Review
Khavinson VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR · Molecules 2021;26(22):7053 · PMID 34834147
EW is reported to bind the GGAG sequence. Note what that gives you: a named four-base target, which is a falsifiable statement rather than a vague one.
Systematic search for structural motifs of peptide binding to double-stranded DNA
Kolchina N, Khavinson V, Linkova N, Yakimov A, Baitin D, Afanasyeva A, Petukhov M · Nucleic Acids Research 2019;47(20):10553–10563 · PMID 31598715
The dipeptide docking study covers all 400 dipeptides, EW included, and is the reason to be cautious about the previous line: most dipeptides cannot bind dsDNA at all, and the ones that can are selected on computed energy, not measured affinity.
What is not here. Nothing clinical is indexed under the trade name Thymogen. The Glu-Trp dipeptide appears in the mechanism literature as a named constituent of the thymus complex. Searched through Europe PMC, PubMed and Google Scholar on 2 September 2026. Naming the gap is more useful than filling it with a paragraph of hedging.
Why the Thymogen evidence is weak — and what it still showed
Almost every human result in this class comes from one school — Vladimir Khavinson's institute in St Petersburg and the groups around it. That means single-center data, collected by the people who developed the compound, rarely blinded, never pre-registered, and reported across enough endpoints that something was always going to move. Read anything below against that.
Specific to Thymogen. The gap on this page is specific and worth naming. Thymogen has a long Russian clinical-use history that is not indexed in PubMed under that trade name, so a Western reader cannot check it. What is indexed is mechanism work. Treat the clinical history as real but unreadable rather than as either proof or fiction — and note that the strongest trial in this family was run on the extract, not on this dipeptide.
What the data does support. The honest count of clinical trials published under the trade name Thymogen is zero — nothing is indexed. What exists is the constituent claim: Kuznik et al. name EW as one of three short peptides responsible for Thymalin's action, and Thymalin does have a randomized placebo-controlled trial. So the evidence for this molecule is entirely inherited, and inherited evidence is exactly the kind that needs saying out loud rather than blurring.
Beyond that: a DNA-microarray study established that EW, KE and AEDG regulate the expression of a wide range of genes, and molecular modeling identified the GGAG binding preference. Both are in- vitro or in-silico. Neither has a human readout.
The specific epistemic position: a dipeptide with a plausible transporter story, an unusually specific computational binding claim, one named target motif, and no trial of its own. That is early — not refuted.
What is actually measured, and what is not. Measured: a computed docking preference for the GGAG motif, and gene-expression changes in vitro for the ATP, MT-CO1, HBA1 and HSP90 promoters. Not measured, by anyone: a dissociation constant for Glu-Trp against GGAG or anything else; plasma half-life; oral bioavailability; whether GGAG is enriched in the regulated genes relative to unregulated ones. And no clinical endpoint of any kind, in any trial, under this name.
Not proven is not the same as disproven. Everything above says the evidence is weak. None of it says the compound does nothing. There is no adequately powered trial that ran and came back null, because outside Russia there is essentially no trial at all — this class is unfunded, not failed. A reader who leaves thinking “disproven” has learned something false, and so has one who leaves thinking “proven”.
Thymogen pharmacokinetics — how much of it actually gets in
What degrades it. One peptide bond. That is the entire molecule's structural defense against proteolysis, and it is not one. Serum aminopeptidases and dipeptidases cleave Glu-Trp directly to two free amino acids, and the quick facts above put the half-life at “~20 min” — a figure that circulates for this class with no traceable human study behind it. A minutes-scale figure is the right order of magnitude for an unprotected dipeptide even if that specific number is unsourced.
The strongest oral argument in the whole catalog, and it belongs here. PEPT1, the proton-coupled oligopeptide transporter on the brush-border membrane of the small intestine, is described in the review from this same research group as covering “basically all di- and tripeptides”, with dipeptides the preferred substrates. Glu-Trp is a dipeptide. Of everything in this family, this molecule has the best mechanistic claim to intestinal absorption — and Thymogen is nonetheless sold here as injectable only, which is the opposite of what the mechanism would predict.
The argument against, which matters more. Crossing the brush border is not reaching the blood. Peptides taken up by PEPT1 land in the enterocyte cytosol, which is dense with peptidases, and that is where most of them are hydrolyzed to free amino acids before ever seeing portal blood. An injection sidesteps the gut wall and hepatic first-pass entirely and is 100% bioavailable by definition; the swallowed fraction that appears intact in the circulation has not been measured for Glu-Trp by anyone. That is the number the whole oral bioregulator market is missing.
The ratio the catalog itself implies. Across this class, the oral products carry a median of roughly 29x more material per day than the injectable ones. Nobody arrived at that by measuring absorption — no oral bioavailability figure has been published for any compound in this family — but the gap is the vendors' own implicit answer to the question: swallowing it is assumed to deliver a small fraction of what an injection delivers, and an injection is fully bioavailable by definition. Treat that as a bound on the plausible exposure, not as a measurement, because a measurement is exactly what is missing.
What would have to be true for Thymogen to work
What would have to be true. Glu-Trp would have to reach lymphoid tissue intact despite a minutes-scale serum half-life; enter cells and then nuclei; bind GGAG-containing promoters preferentially over the twelve million other GGAG sites in the genome; and change transcription enough to shift a cell count. The third step is the weakest and it is the one with an obvious experiment attached: a chromatin immunoprecipitation or a motif-enrichment analysis comparing regulated genes against unregulated ones. Neither has been published.
Because Thymogen is claimed to be the active fragment of an extract with a real trial, its predictions are the extract's predictions — which makes it directly checkable.
- Prediction 1 — Complete Blood Count (CBC) with Differential. should reproduce Thymalin's lymphocyte effect if the extract really works through its short peptides, one course, head to head. This is the experiment that would settle the extract-versus-peptide question for the whole class, and it does not exist. If Glu-Trp cannot reproduce what the extract does, the mechanism story attached to every bioregulator on this site is wrong.
- Prediction 2 — hs-CRP (High-Sensitivity C-Reactive Protein). should fall alongside any lymphocyte change, within a course. Separates an immune effect from a marker artefact.
Run these before and after, not after alone. A single post-course number tells you what your body is doing, not what Thymogen did to it — and that difference is the entire point of testing.
Thymogen versus the alternatives
Thymogen versus Thymalin — the defined peptide against the extract it is supposed to explain. Thymalin has the trial: randomized, placebo-controlled, with lymphocyte subsets as prespecified endpoints. Thymogen has the sequence, a computable mass and a verifiable purity number. Neither has what the other has. If Glu-Trp reproduced Thymalin's lymphocyte response in even a small controlled study, the extract becomes an unnecessarily unverifiable way to buy a known dipeptide. If it did not, the published explanation for how Thymalin works is wrong. Either result would be more informative than anything currently published in this field, and the study has never been done.
And against the credible alternative — thymosin alpha-1. A defined 28-residue peptide with registered clinical use and independent trial data in several countries. On evidence it wins outright. The only coherent reason to be reading about a dipeptide instead is that you have already exhausted the things that are proven.
What you are actually buying when you buy Thymogen
What is verifiable and what is not. Glu-Trp is a defined molecule, so mass spectrometry can confirm its mass outright and HPLC can put a real number on purity. Both claims are falsifiable, which is the only kind worth paying for.
What a certificate cannot tell you is that Thymogen means Glu-Trp. That mapping is vendor consensus, not something any paper establishes: the peer-reviewed literature names EW as a constituent peptide of the thymus complex, and names it repeatedly, but no indexed clinical paper defines the trade name Thymogen as that dipeptide. This repo records the sequence as claimed rather than verified for exactly that reason. A mass spectrum confirms what is in the vial; it cannot confirm that what is in the vial is what the trade name is supposed to mean.
Tryptophan gives this one an advantage nothing else in the cohort has: it absorbs at 280 nm, so a UV trace can say something about content without a mass spectrometer. Expect/mol.
Where to get Thymogen
Buy Thymogen 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 Thymogen
Graded by what exists behind each claim.
✅ Clinically validated
- Registered in Russia as an immunostimulant, with domestic clinical use in infection and post-surgical immune support behind that registration. Available there in injectable and nasal forms.
- 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 as the synthetic, defined-sequence alternative to Thymalin's extract. Long Russian practice record; almost no independent Western use, so there is little to weigh outside the domestic literature.
🧪 Theoretical / extrapolated
- Glu-Trp — a dipeptide, and the shortest thing in this catalog. It is the identified active fragment of Thymalin, which is a genuinely rational piece of drug development: isolate what does the work, drop the extract.
- Being a defined dipeptide instead of a tissue extract is a real advantage — batch identity is verifiable, which is not true of any of the 'natural' bioregulators. The immune mechanism and its autoimmune caution are the same as Thymalin's.
What that tier rests on here. The tier above is inherited. Nothing is indexed under the trade name Thymogen; the evidence belongs to Thymalin, the extract this dipeptide is named as a constituent of.
How to read the Soviet clinical series →
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 →
Cell, rodent, human — and where it stops
Glu-Trp is chemically unlike everything else here, and that is the mechanism story. Two residues, 333.4 g/mol — but one of them is tryptophan, an indole ring, the only large hydrophobic aromatic side chain in this entire catalog. Every other bioregulator on this site is built from small charged residues. A tryptophan gives this dipeptide something the others do not have: a face that can stack, insert into a membrane, and sit in a hydrophobic pocket.
In silico and in cells. Linkova 2023 docked EW against double-stranded DNA and reported GGAG in the B-form as its preferred site, with ACE2 and CYSLTR1 as candidate target genes. In the same paper, EW applied to lipopolysaccharide-stimulated human peripheral blood mononuclear cells — blood from four donors — cut IL-1β, IL-6 and TNF-α by 1.4 to 6.0 times. Earlier work put short peptides of this family on the sphingomyelin pathway in thymocytes Khavinson 2002 and reported effects on interleukin-2 gene expression in splenocytes Kazakova 2002.
And here is the result that makes this the best sequence-to-mechanism argument in the whole cohort. Deigin 2024 sets Thymogen beside Thymodepressin. Thymogen is L-Glu-L-Trp and is an immunostimulant. Thymodepressin is D-Glu-(D-Trp) and is an immunosuppressor. Same two amino acids, same order, same mass, same formula — mirrored at every chiral center, and the biological effect runs in the opposite direction. Both are described as registered peptide pharmaceuticals in Deigin 2022. Nothing else in this catalog has anything like it, and it settles a question the rest of the class only asserts: the structure is doing the work, because a molecule of identical composition and opposite handedness does the opposite thing. A bulk amino-acid effect cannot produce that.
Two independent rat studies, and one word in both titles decides what they are worth. Chulanova 2023 and Chulanova 2025 report reparative, antioxidant and hepatoprotective effects in experimental liver damage and in hydrazine hepatopathy, in Bulletin of Experimental Biology and Medicine in 2023 and 2025. Both are titled as studies of new analogs of the immunomodulator — not of Thymogen itself. They show this chemistry is still being worked on by other hands; they are not evidence about the molecule in the vial. Deigin 2022, from the same group, works on Ile-Glu-Trp — a tripeptide carrying the same Glu-Trp at its C-terminus.
Where it stops. No controlled human trial of Thymogen alone appears in an indexed journal, and a PubTator3 search of the trade name on 6 September 2026 returned 10 records, none of them a clinical trial of the dipeptide. The clinical claims travel with Thymalin, of which EW is described as one of two active components, and the transport work that would explain how either reaches a cell Khavinson 2022 is molecular docking rather than measured flux.
What nobody has tested yet
The tryptophan is a free analytical handle nobody uses. Tryptophan fluoresces. A peptide containing one can be tracked in plasma, in cell lysate and across a membrane without a radiolabel, using equipment most university laboratories already own. Of all the peptides in this class, this is the one whose pharmacokinetics could be measured most cheaply — and it is as uncharacterized as the rest.
The ACE2 claim deserves its own experiment. If EW really engages ACE2, that is a cardiovascular mechanism sitting inside an immune product, and it predicts an effect on blood pressure that nobody has looked for. A cuff costs nothing and is already in every clinic that would ever run this study.
Extrapolation, labeled as such. Free tryptophan is the precursor for serotonin and, downstream, melatonin, and a dipeptide that is hydrolyzed by serum peptidases releases it. That means part of any subjective effect people report could be tryptophan delivery rather than peptide signaling — a boring explanation that has never been controlled for, and one a single arm dosed with free tryptophan at matched molar content would rule in or out. The chirality result gives that control a sharper form: the D-isomer releases D-tryptophan, which the serotonin pathway barely uses, so running the two enantiomers side by side would separate peptide signaling from amino-acid delivery in a single experiment. Nobody has published it.
Sources read for this page
- Deigin V. The First Reciprocal Activities of Chiral Peptide Pharmaceuticals: Thymogen and Thymodepressin, as Examples. International Journal of Molecular Sciences 2024 · PMID 38732260
- Chulanova AA. Hepatoprotective Effects of Thymogen Analogues in Hydrazine Hepatopathy in Rats. Bulletin of Experimental Biology and Medicine 2025 · PMID 40442470
- Chulanova AA. Reparative and Antioxidant Effects of New Analogues of Immunomodulator Thymogen in Experimental Model of Liver Damage. Bulletin of Experimental Biology and Medicine 2023 · PMID 37861903
- Deigin VI. Development of Peptide Biopharmaceuticals in Russia. Pharmaceutics 2022 · PMID 35456550
- Linkova N. The Influence of KE and EW Dipeptides in the Composition of the Thymalin Drug on Gene Expression and Protein Synthesis Involved in the Pathogenesis of COVID-19. International Journal of Molecular Sciences 2023 · PMID 37686182
- Khavinson VKh, Rybakina EG, Malinin VV, Pivanovich IY, Shanin SN, Korneva EA. Effects of short peptides on thymocyte blast transformation and signal transduction along the sphingomyelin pathway. Bulletin of Experimental Biology and Medicine 2002;133(5):497-499 · PMID 12420072
- Kazakova TB, Barabanova SV, Khavinson VKh, Glushikhina MS, Parkhomenko EP, Malinin VV, Korneva EA. In vitro effect of short peptides on expression of interleukin-2 gene in splenocytes. Bulletin of Experimental Biology and Medicine 2002;133(6):614-616 · PMID 12447482
- Deigin V. Peptide ILE-GLU-TRP (Stemokin) Potential Adjuvant Stimulating a Balanced Immune Response. International Journal of Peptide Research and Therapeutics 2022 · PMID 36313476
- 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
Thymogen — 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.
Thymogen — safety specifics for this compound
Specific to Thymogen: this is the smallest molecule in the class and the one whose degradation products are least interesting — cleavage yields glutamate and tryptophan, both ordinary dietary amino acids. The mechanistic risk is therefore not toxicity but the immune direction of travel: an agent proposed to raise T-cell and NK activity is being used in people with no measured deficit, and nothing in the literature examines what that does in autoimmune disease. The honest unknown here is immunological, not toxicological. The safety consequence of that zero is specific rather than rhetorical: with 0 trials indexed under this name, every tolerability statement about Thymogen is borrowed from Thymalin's n=36 arm, and Thymogen is one of three peptides in that preparation rather than the preparation. Nobody has given Ala-Glu alone to a human under observation and written down what happened, so the direction that matters — whether raising T-cell and NK activity is wanted in a body that has an autoimmune process nobody has looked for — has never been measured in anyone.
Thymogen — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Thymogen 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 — Thymogen in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Thymogen
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
Thymogen — frequently asked questions
What is the amino acid sequence of Thymogen?
Thymogen is Glu-Trp — 2 residues, 333.4 g/mol, isoelectric point 3.85. Those figures are computed from the sequence rather than quoted.
Can a peptide that short really bind DNA?
Not the way a transcription factor does. A zinc finger needs about 30 residues to read three base pairs. When Khavinson's group docked all 400 dipeptides against DNA, the vast majority could not bind double-stranded DNA at all. The claim is a computational prediction supported by gene-expression readouts in cells, not a measured binding event.
Is there a human trial of Thymogen?
Nothing clinical is indexed under the trade name Thymogen. The Glu-Trp dipeptide appears in the mechanism literature as a named constituent of the thymus complex.
What should I measure if I run Thymogen?
Before and after, not after alone. The falsifiability section on this page names the specific markers, the direction each should move and the timescale — and says what a null result would rule out.
References & further reading
- Kuznik B, Khavinson V, Shapovalov K, Linkova N, Lukyanov S, Smolyakov Yu, Tereshkov P, Shapovalov Yu, Konnov V, Tsybikov N — Peptide Drug Thymalin Regulates Immune Status in Severe COVID-19 Older Patients · Advances in Gerontology 2021;11(4):368–376
- 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
Thymogen inside a finished plan
One arm of 2 Protocol Blueprints, free to read in full.
What Thymogen is used for
Thymogen appears under 2 goals in the goal router.
Related Longevity & Bioregulators compounds
Where this goes next
Thymogen is the immune 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.