A 9-amino-acid zinc-dependent thymic nonapeptide (pGlu-Ala-Lys-Ser-Gln-Gly-Gly-Ser-Asn), originally isolated as Facteur Thymique Sérique (FTS) from porcine serum by the Bach group at Hôpital Necker (Paris) in 1977. Never approved as a drug anywhere. Substantial preclinical literature; limited dated human data.
Thymulin is a synthetic nonapeptide with sequence pGlu-Ala-Lys-Ser-Gln-Gly-Gly-Ser-Asn — nine amino acids, with N-terminal pyroglutamate (cyclized glutamine) and C-terminal asparagine. One-letter: <Q-A-K-S-Q-G-G-S-N. Free peptide MW (apo form) is ~857.9 Da; molecular formula (apo) C33H55N13O15.
It was isolated from porcine serum at Hôpital Necker (Paris) by the Bach group in 1977 under the original name Facteur Thymique Sérique (FTS) — French for "serum thymic factor." Renamed thymulin around 1981–1985 as the broader thymic-hormone field consolidated nomenclature. Foundational papers: Dardenne et al. J Biol Chem 1977 (PMID 303241, isolation/purification); Pleau et al. J Biol Chem 1977 (PMID 914862, sequence); Pleau et al. Mol Cell Biochem 1981 (PMID 6276717); Pleau et al. Methods Enzymol 1985 (PMID 3878920, the chapter that effectively renamed FTS to "thymulin"); Auger et al. Biol Chem Hoppe-Seyler 1987 (PMID 3497643, eight thymulin analogs / SAR work).
The 1:1 zinc-thymulin complex is the bioactive form. Apo-thymulin (the zinc-free peptide) is biologically inactive in standard rosette-formation assays. Zinc-binding stoichiometry is characterized in Bach & Dardenne Med Oncol Tumor Pharmacother 1989 (PMID 2657247) and Dardenne et al. 1993 (PMID 7681212).
It's endogenous to humans and other mammals; secreted by thymic epithelial cells (subcapsular and medullary TEC subsets) into systemic circulation. Production declines with age — an aspect of immunosenescence. Thymulin levels are sensitively reduced in zinc deficiency and partially restored with zinc repletion (Prasad et al. 1988, PMID 3262625, J Clin Invest).
Thymulin's mechanism has been worked on for nearly five decades and is partially characterized but not fully resolved at the receptor level.
Zinc-dependent biological activity. The 1:1 Zn2+-thymulin complex is the bioactive form; apo-thymulin shows little to no activity in T-cell rosette assays. Zinc binding involves coordination through residues clustered near the C-terminal half of the peptide (Auger 1987 PMID 3497643; Bach & Dardenne 1989 PMID 2657247; Dardenne 1993 PMID 7681212).
T-cell maturation. Thymulin promotes the differentiation of bone-marrow-derived precursors into T lymphocytes, including the appearance of T-cell-specific surface markers — demonstrated in the original Bach-group rosette assays (1977–1980) and confirmed in subsequent groups. It influences the CD4/CD8 balance and the maturation of regulatory T-cell subsets, though specific receptor identification has been elusive.
Cytokine modulation (anti-inflammatory at physiological doses). Thymulin modulates release of multiple cytokines from peripheral blood mononuclear cells (IL-1, IL-2, IL-6, IFN-γ, TNF-α). The pattern is generally anti-inflammatory at physiological doses — suppressing overproduction of pro-inflammatory cytokines in inflammation-bearing animals (Safieh-Garabedian 1993 PMID 8508050; Lunin 2008 PMID 18991101).
HPA-axis / neuroendocrine interactions. Thymulin both influences and is influenced by the HPA axis. Glucocorticoids upregulate thymulin secretion at physiological levels but suppress it at supraphysiological levels (U-shaped). Thyroid hormone and growth hormone both stimulate thymulin secretion (Mocchegiani & Fabris 1992, PMID 1605502). Conversely, intra-pituitary thymulin gene therapy in aged rodents partially restores corticotrope and gonadotrope function (Goya/Reggiani group, PMIDs 21360440, 22700775, 21952687). Goya 2004 (PMID 15003367) is the canonical review.
Anti-inflammatory / analgesic activity. The Safieh-Garabedian/Saádé group at AUB Beirut has produced a substantial series demonstrating thymulin and a thymulin-related peptide analog (PAT) attenuate inflammatory hyperalgesia in rodent models, apparently through cytokine modulation locally and centrally (PMIDs 9876233, 14580936, 17192563, 21059360, 22861065, 30503917, 30851702).
The "thymulin receptor" on T-cells has been studied since the 1980s but a single, definitive G-protein-coupled or single-pass-transmembrane receptor hasn't been cleanly cloned and characterized in the way the GLP-1 receptor or melanocortin receptors have. Modern proposals include direct interaction with a TCR-adjacent surface complex on T-cells, but no published high-resolution structure of a thymulin-receptor complex exists.
No modern Phase 2/3 RCT exists for thymulin in any indication. The clinical record is dated 1980s/1990s biomarker observations and small open-label treatment studies.
Biomarker / observational anchors: zinc deficiency / immune function (Prasad 1988, PMID 3262625, J Clin Invest) — in zinc-deficient subjects, serum thymulin activity is reduced and is restored with zinc supplementation, establishing thymulin as a sensitive biomarker of zinc status; anorexia nervosa (Wade 1985, PMID 3927699, Am J Clin Nutr) — patients show reduced Zn-FTS activity, partially restored with refeeding and zinc repletion; thyroid/GH-axis interactions in elderly (Mocchegiani & Fabris 1992, PMID 1605502) — bidirectional dependence with the GH/thyroid axes in aging-related immunosenescence.
Small open-label treatment trials (1980s/1990s): several small open-label studies in rheumatoid arthritis and SLE (PMIDs 1418292, 8508050); small-cohort Italian/EU work on synthetic thymulin in children with primary immune deficiencies (PMIDs 1427431, 27634199). Outcomes were mixed; no controlled Phase 2/3 was conducted; none led to regulatory approval.
Modern preclinical work is substantial and multi-group: allergic asthma via DNA-nanoparticle-delivered thymulin gene therapy (da Silva 2014 PMID 24556417, J Control Release; da Silva 2020 PMID 32577505, Sci Adv — Morales/Rocco UFRJ); septic inflammation (Novoselova 2018 PMID 29795607); pulmonary hypertension (Henriques-Coelho 2008 PMID 18511508); pituitary aging via intra-pituitary gene therapy (Goya/Reggiani group, La Plata — PMIDs 21952687, 22700775, 21360440, 24588820 review, 28501652); inflammatory/neuropathic pain (Safieh-Garabedian/Saádé multi-paper series above); lung diseases review (Santos 2010 PMID 20055713).
Honest framing: demonstrated mechanistic and preclinical activity, with limited dated human data and no modern controlled trial. Any claim of "demonstrated efficacy in humans" is overreach.
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Start Tracking FreeThymulin's plasma half-life is on the order of 5–15 minutes for IV administration in animal models. The molecule is small (~858 Da apo), unprotected by terminal modifications other than the natural N-terminal pGlu cyclization, and is rapidly cleared by glomerular filtration and proteolytic degradation.
The very short half-life is the design driver for the modern preclinical work: the Goya/Reggiani gene-therapy program and the Morales/Rocco DNA-nanoparticle program both exist explicitly to circumvent it. Direct subcutaneous or intravenous dosing of free thymulin requires either continuous infusion or frequent boluses to maintain biologically meaningful plasma concentrations. Vendor claims of "long-acting thymulin" or "extended-release thymulin" without specific delivery-system citation should be treated as unsupported.
Bioavailability and route: not characterized in published controlled studies for SC or oral routes in humans. Oral bioavailability is presumed near-zero (proteolytic degradation). Intranasal isn't quantified in published studies. Thymulin-related peptide analogs cross the BBB (the basis for the analgesia work in CNS endotoxin models).
Limited human safety data exist; no Western pharmacovigilance database (FAERS, EudraVigilance) data, since thymulin has never been an approved drug. 1980s/1990s open-label trials in immunodeficiency and autoimmune populations didn't surface a distinctive thymulin-attributable adverse event signal beyond local injection-site reactions (sample sizes small, tens of patients).
Theoretical immune-modulation concerns: provoking or worsening autoimmune flares in susceptible individuals; interfering with vaccine response; interfering with concurrent immunosuppressive therapy; possible effect on tumor immunosurveillance in patients with active or recent malignancy; concurrent zinc supplementation interaction (not formally studied for safety).
No published carcinogenicity, reproductive toxicity, or chronic-toxicity studies meeting modern regulatory standards. The 1970s–1990s preclinical work predates standardized ICH safety-pharmacology requirements. Vendor / community reports (anecdotal): mild injection-site soreness, occasional fatigue or headache, no consistent serious adverse event reports.
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Multiple peptides in the immune / thymic-hormone space have similar names, similar marketing positioning, or both. Vendor product naming is inconsistent.
| Compound | What it actually is | Difference from Thymulin |
|---|---|---|
| Thymalin (Тималин) | Polypeptide complex (multi-component extract from calf/bovine thymus). Khavinson group, St. Petersburg. | Different molecule. Russian-registered, undefined exact composition. Highest confusion-risk pair. |
| Thymosin Alpha-1 (Tα1, thymalfasin, Zadaxin) | 28-amino-acid acetylated peptide; approved internationally for Hep B/C / immune indications (not US). | Different molecule. 28-mer, not 9-mer. Approved in 35+ countries; thymulin has no regulatory dossier. |
| Thymopoietin | 49-amino-acid full-length thymic protein (Goldstein 1970s) | Different molecule. Originally a 49-mer; gene encodes nuclear-envelope protein. |
| Thymopentin (TP-5) | Pentapeptide RKDVY, the minimal-active fragment of thymopoietin | Different molecule. 5-mer not 9-mer. Some Italian/EU registration but not FDA. |
| Thymogen (Тимоген) | Dipeptide Glu-Trp (EW). Khavinson 1980s | Different molecule. Dipeptide, not nonapeptide. Russian-registered. |
| TB-500 / Thymosin Beta-4 | 43-amino-acid actin-binding protein; cell migration / wound healing / angiogenesis | Completely different mechanism. Despite the "thymosin" naming, Tβ4 is in the actin-sequestering / wound-healing space. |
| Vilon (KE) | Khavinson dipeptide (Lys-Glu) | Different molecule. Khavinson framework, not Bach. |
| Thymostimulin (TP-1) | Calf-thymus polypeptide extract | Different molecule. Italian registration; never FDA. |
The two disambiguations to memorize: thymulin ≠ thymalin (Bach 9-mer synthetic vs Khavinson polypeptide-complex extract — different lineages, different molecular categories, different regulatory status); and thymulin ≠ thymosin alpha-1 (9-mer never approved vs 28-mer approved in 35+ countries — the "thymosin" naming is historical and refers to a heterogeneous family; thymulin isn't part of the thymosin family in the modern molecular-biology sense).
Vendor product identity: research-chem vendors selling "Thymulin" 5 mg or 10 mg vials may be supplying the synthetic 9-mer (most common), or may be mislabeling another thymic peptide. There's no industry-standard verification — no analytical certificate verified to a USP or EP monograph (because thymulin has no monograph). Buyer-beware.
Thymulin is a research peptide not approved by the FDA for human use. It is sold only as a research chemical, and StackTrax does not endorse or facilitate personal use.
Quality varies enormously among research-chemical suppliers. At minimum, look for:
StackTrax’s preferred partner NextGen Peptides does not currently carry Thymulinin their catalog, which is why you don’t see a direct purchase link here. Other major research-chemical suppliers carry it; we don’t specifically recommend one for this compound.
Build your protocol, log every dose, monitor your body's response, and get reminders so you never miss a dose.
Start Tracking FreeThymulin is a synthetic 9-amino-acid zinc-dependent thymic nonapeptide with sequence pGlu-Ala-Lys-Ser-Gln-Gly-Gly-Ser-Asn (one-letter: <Q-A-K-S-Q-G-G-S-N), with N-terminal pyroglutamate and C-terminal asparagine. Free peptide MW is about 858 Da. It was isolated from porcine serum by the Bach group at Hopital Necker in Paris in 1977 under the original name Facteur Thymique Serique (FTS), and renamed thymulin around 1981 to 1985. It is endogenous to humans and other mammals, secreted by thymic epithelial cells.
Thymulin and Thymalin are different molecules. Thymulin is a single defined 9-amino-acid synthetic nonapeptide from the Bach lineage (Hopital Necker, Paris, 1977). Thymalin is a Russian-registered multi-component polypeptide complex extracted from calf or bovine thymus from the Khavinson lineage (St. Petersburg) with undefined exact composition. They are the highest confusion-risk pair in the thymic-peptide space. Thymulin is also distinct from Thymosin Alpha-1 (a 28-amino-acid peptide approved in 35+ countries) and from Thymopentin / Thymopoietin / Thymogen / Vilon, which are all different molecules.
The 1:1 zinc-thymulin complex is the bioactive form. Apo-thymulin (the zinc-free peptide) is biologically inactive in standard T-cell rosette-formation assays. Zinc binding involves coordination through residues clustered near the C-terminal half of the peptide. Thymulin activity is also a sensitive biomarker of zinc status in humans: Prasad 1988 (PMID 3262625, J Clin Invest) showed reduced thymulin activity in zinc-deficient subjects with restoration on zinc supplementation, and similar findings were reported in anorexia nervosa (Wade 1985, PMID 3927699).
Thymulin secretion by thymic epithelial cells declines with age as part of immunosenescence, paralleling the broader involution of the thymus. The peptide also has bidirectional interactions with the HPA axis and the GH/thyroid axes: glucocorticoids upregulate thymulin secretion at physiological levels but suppress it at supraphysiological levels (U-shaped), and thyroid hormone and growth hormone both stimulate thymulin secretion (Mocchegiani and Fabris 1992, PMID 1605502). Intra-pituitary thymulin gene therapy in aged rodents partially restores corticotrope and gonadotrope function (Goya/Reggiani group).
No. Thymulin has never been approved as a drug anywhere, including France (the origin country, despite the foundational work at Hopital Necker). No NDA or IND is on file with the FDA, and it is not on the 503A bulks list. It is sold as a research chemical. Synthetic thymulin (the 9-mer) is not in the Russian State Register either; confusable Russian-market products like Thymalin, Thymogen, and Vilon are different molecules. Regarding WADA 2026, thymulin is not on the prohibited list by name, but the S0 catch-all for unapproved investigational substances may apply. (The existing StackTrax encyclopedia line saying "WADA Banned: Yes" is overstated.)
No modern Phase 2 or 3 RCT exists for thymulin in any indication. The clinical record is dated 1980s and 1990s biomarker observations (zinc deficiency, anorexia nervosa, immunosenescence) plus small open-label treatment studies in rheumatoid arthritis, SLE, and pediatric primary immune deficiencies (PMIDs 1418292, 8508050, 1427431, 27634199), with mixed outcomes and no controlled trial. Modern work is substantial preclinical: gene-therapy / DNA-nanoparticle delivery for asthma and pituitary aging, septic inflammation, pulmonary hypertension, and inflammatory/neuropathic pain models. Honest framing: demonstrated mechanistic and preclinical activity, limited dated human data, no modern controlled trial. Any claim of demonstrated efficacy in humans is overreach.
Thymulin's plasma half-life is on the order of 5 to 15 minutes for IV administration in animal models because the molecule is small and unprotected, so direct injection requires frequent dosing to maintain meaningful plasma concentrations. Vendor claims of long-acting or extended-release thymulin without specific delivery-system citation should be treated as unsupported. Oral bioavailability is presumed near-zero. Limited human safety data exist; 1980s/1990s open-label trials did not surface a distinctive thymulin-attributable adverse event signal beyond local injection-site reactions (small sample sizes, tens of patients). Theoretical concerns include autoimmune flare, altered vaccine response, tumor immunosurveillance, and uncharacterized interactions with concurrent immunosuppressive therapy. Default contraindications: pregnancy or breastfeeding, active or prior cancer, active autoimmune flare, immunosuppressive therapy, recent vaccination, and pediatric routine use.
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