Why TB-4 isn't TB-500, why Thymosin Alpha-1 isn't Thymogen, and how the peptide world ended up with a naming system that nobody actually agreed to.

A patient asks if TB-500 and Thymosin Beta-4 are the same thing. Half the internet says yes. Half the internet says no. The answer matters for dosing, for cost, for what you're actually injecting, and for whether the trial data on one tells you anything about the other.

The answer is no. They are not the same thing. One is a 43-amino-acid endogenous polypeptide. The other is a 7-amino-acid synthetic fragment. They share a sequence motif. They share some biology. They are absolutely not interchangeable, and people calling them interchangeable have been confusing patients for fifteen years.

This is the cleanest example of a much larger problem. The peptide world has a naming system the same way an estate sale has an organizational system. Every lab named their compound whatever made sense to them at the time. Marketing rebranded it. Three continents adopted three different conventions. Decades passed. Nobody fixed it. Now the same molecule has four names and four different molecules share two letters and a hyphen.

Here is what the peptides everyone is asking about actually are.

Thymosin Beta-4 (TB-4)

Identity card

The full polypeptide. A 43-amino-acid endogenous polypeptide encoded by the human TMSB4X gene, present in nearly every cell in the body, with the highest concentrations in platelets and white blood cells.

Residues 43 aa

MW ~4,963 Da

Category Tissue repair

Its primary biological role is binding to monomeric G-actin and regulating cytoskeletal dynamics, which is why it ended up associated with cell migration, wound repair, and angiogenesis.

This is the original molecule. It has been studied for cardiac repair, corneal healing, traumatic brain injury, and ulcer recovery. RegeneRx and other companies have run actual human trials on the full-length peptide, mostly under the development name RGN-259 and similar.

Also called: Tβ4 Timbetasin Thymosin beta 4

TB-500

Identity card

Not the full peptide. A 7-amino-acid synthetic fragment corresponding to residues 17-23 of Thymosin Beta-4.

Sequence Ac-LKKTETQ

Residues 7 aa

MW ~889 Da

Category Tissue repair (fragment)

LKKTETQ is the actin-binding motif of TB-4. The pharmacology argument for using the fragment is that this short sequence captures the "active site" responsible for cytoskeletal effects without needing the full protein. The pharmacology argument against is that the full protein has additional functional regions (notably the Ac-SDKP motif near the N-terminus) that mediate cardiac and anti-fibrotic effects, and the fragment doesn't.

Translation: TB-500 may reproduce some of TB-4's tissue repair activity. It does not reproduce all of it. The internet selling them as identical is selling a half-truth.

Also called: Fequesetide (the international nonproprietary name nobody uses)

Thymosin Alpha-1 (Tα1)

Identity card

Completely different peptide from a completely different precursor. Despite sharing the word "Thymosin" in its name, Tα1 has nothing to do with TB-4 mechanistically.

Residues 28 aa

MW 3,108 Da

Category Immune modulation

The shared word is a historical accident from 1970s thymic extract chemistry, where Allan Goldstein's lab at George Washington University fractionated bovine thymus tissue into "fraction 5" and then sub-fractionated that into alpha and beta peptide groups. The alpha and beta groups turned out to be biologically unrelated.

Sequence (28 aa):

Ac-SDAAVDTSSEITTKDLKEKKEVVEEAEN

Tα1 is derived from prothymosin alpha, a 109-amino-acid precursor. Its biology is immune modulation, not tissue repair. Mechanism: TLR2 and TLR9 activation, dendritic cell maturation, T-cell differentiation toward Th1 phenotypes, NK cell activation.

The synthetic version is called thymalfasin. The brand name is Zadaxin, made originally by SciClone. It is approved in 35-plus countries for chronic hepatitis B, hepatitis C combination therapy, and as an immune adjuvant in certain cancers. The FDA has granted it orphan drug designation for malignant melanoma, chronic active hepatitis B, DiGeorge anomaly, and hepatocellular carcinoma. It is not a fully approved drug in the United States.

11,000+ patients enrolled across 30+ randomized controlled trials of Thymosin Alpha-1

Tα1 is the most clinically validated thymic peptide on the market. Most clinicians using "thymosin" without specifying alpha or beta are talking about Tα1 for immune indications and TB-4 or TB-500 for tissue repair. They are not the same drug. They are not in the same family beyond sharing a thymus origin in the 1970s.

Also called: Thymalfasin Zadaxin Tα1

Thymogen

Identity card

Russian, not American. A synthetic dipeptide of L-glutamic acid and L-tryptophan. The smallest functional peptide on this list by an order of magnitude.

Sequence Glu-Trp (EW)

Residues 2 aa

MW 333 Da

Category Immune modulation

Thymogen was developed by Vladimir Khavinson's group in Russia, isolated as the active component of Thymalin (a crude calf thymus polypeptide extract), and registered as a pharmaceutical in the USSR in 1990. It is approved in Russia in three forms: intramuscular injection, nasal spray, and topical cream. Indications include immunodeficiency states, viral and bacterial respiratory infections, and adjunct treatment after chemotherapy or radiation.

Mechanism: T-cell maturation, normalization of CD4/CD8 ratios, immunoglobulin production stimulation. Functionally similar to Tα1 in some ways. Structurally and historically completely separate.

Also called: Thymagen Oglufanide IM-862

Thymopentin (TP-5)

Identity card

While we're here. Another pentapeptide everyone confuses with TB-500 because "TP-5" and "TB-500" look similar at 2 AM on a forum. They are not the same.

Sequence RKDVY

Residues 5 aa

MW ~680 Da

Category Immune modulation

Thymopentin is Arg-Lys-Asp-Val-Tyr, residues 32-36 of the 49-amino-acid hormone thymopoietin. Its biology is T-cell maturation via cGMP elevation, completely unrelated to TB-4's actin binding. Marketed as Timunox in Italy. Approved in China. Studied for rheumatoid arthritis, immune reconstitution, and chronic hepatitis B with mixed results.

If someone tells you they're using "TP-5" for tendon healing, they have confused two peptides. TP-5 is an immune modulator. TB-500 is a tissue repair fragment. The names look alike. The molecules don't.

Also called: Timunox

What this means

The peptide-by-peptide cheat sheet:

Name	What it is	Residues	Category	INN / Brand
TB-4	Full endogenous polypeptide	43 aa	Tissue repair	Timbetasin
TB-500	Synthetic fragment (residues 17-23 of TB-4)	7 aa	Tissue repair (partial)	Fequesetide
Tα1	Different precursor entirely	28 aa	Immune modulation	Thymalfasin / Zadaxin
Thymogen	Russian dipeptide (Glu-Trp)	2 aa	Immune modulation	Oglufanide / IM-862
TP-5	Thymopoietin fragment (residues 32-36)	5 aa	Immune modulation	Timunox

Five separate molecules. Four different precursor proteins. Three different mechanism categories. At least fifteen different names if you count brand names and INN designations.

This is why prescription literacy matters. A clinician who orders "thymosin" without specifying alpha or beta might get either, depending on the compounding pharmacy. A patient who orders "TB-500" online might receive TB-4 mislabeled, or LKKTETQ short by one amino acid, or something else entirely. The 2023 FDA quality analysis found 40-plus percent of internet-sourced peptides contained inaccurate dosing, contamination, or degraded compound. Naming chaos is part of why the supply chain is so easy to corrupt.

How we got here

A few historical accidents, cumulatively:

In 1966, Allan Goldstein and Abraham White published the first thymic extract activity paper. They named it "thymosin." A lab in 1977 fractionated it into alpha and beta groups. Different groups isolated specific peptides over the following decade. Nobody coordinated naming.

In the 1970s and 1980s, the Khavinson lab in Russia worked on the same biology under a parallel naming convention (Thymogen, Thymalin, Thymulin), without much communication with the American thymosin researchers. Two parallel scientific traditions developed in different languages.

In the 1990s, structure-activity relationship studies began isolating active fragments from full peptides. TB-500 was carved out of TB-4 specifically as a research tool to test which residues mattered. The fragment got its own designation. Then the gray market discovered it was cheaper to synthesize than the full peptide. Then forums started using TB-500 and TB-4 interchangeably to mean "the thymosin beta thing." That conflation is now hardened into common usage.

In the 2010s and 2020s, marketing made it worse. Compounding pharmacies and research-chemical vendors used whichever name was easiest to sell. International nonproprietary names like timbetasin and fequesetide exist on paper but never caught on. Brand names like Zadaxin and Timunox are used in some jurisdictions and unknown in others. The naming system, such as it is, is whatever the loudest voice in your specific corner of the internet uses.

The practical answer

When a clinician or patient asks about one of these compounds, three questions resolve most of the confusion.

1. What is the indication?
Tissue repair points to TB-4 or TB-500. Immune modulation points to Tα1, Thymogen, or TP-5.

2. How many amino acids?
This is the fastest disambiguator. A 43-mer is TB-4. A 28-mer is Tα1. A 7-mer is TB-500. A 5-mer is TP-5. A 2-mer is Thymogen.

3. Who made the trial data?
Goldstein, SciClone, RegeneRx, and the major US/Italian groups worked on the alpha and beta thymosins. Khavinson and the Russian Military Medical Academy worked on Thymogen and Thymalin. Sikiric in Croatia worked on BPC-157, which has nothing to do with any of this but ends up in the same conversations because peptide buyers don't sort their compounds by mechanism.

A peptide is its sequence. The names are inheritance. Treat the names as suspect until you've checked the residues.

The molecules are real. The clinical effects are real. The taxonomy is a forty-year archaeology project, and most of the confusion in the supplement aisle traces back to one fact: the people who named these compounds were not talking to each other, and the people selling them now have no incentive to fix it.

References

Crockford, D., Turjman, N., Allan, C., & Angel, J. (2010). Thymosin beta-4: Structure, function, and biological properties supporting current and future clinical applications. Annals of the New York Academy of Sciences, 1194(1), 179-189. doi:10.1111/j.1749-6632.2010.05492.x
Goldstein, A. L., Hannappel, E., & Kleinman, H. K. (2005). Thymosin beta4: Actin-sequestering protein moonlights to repair injured tissues. Trends in Molecular Medicine, 11(9), 421-429. doi:10.1016/j.molmed.2005.07.004
Goldstein, A. L., & Badamchian, M. (2004). Thymosins: Chemistry and biological properties in health and disease. Expert Opinion on Biological Therapy, 4(4), 559-573. doi:10.1517/14712598.4.4.559
King, R., & Tuthill, C. (2016). Immune modulation with thymosin alpha 1 treatment. Vitamins and Hormones, 102, 151-178. doi:10.1016/bs.vh.2016.04.003
Goldstein, G., Scheid, M. P., Boyse, E. A., Schlesinger, D. H., & Van Wauwe, J. (1979). A synthetic pentapeptide with biological activity characteristic of the thymic hormone thymopoietin. Science, 204(4399), 1309-1310. doi:10.1126/science.451538
Khavinson, V. K. (2002). Peptides and ageing. Neuroendocrinology Letters, 23(Suppl 3), 11-144.
Anisimov, V. N., Khavinson, V. K., & Morozov, V. G. (1994). Twenty years of study on effects of pineal peptide preparation: Epithalamin in experimental gerontology and oncology. Annals of the New York Academy of Sciences, 719(1), 483-493. doi:10.1111/j.1749-6632.1994.tb56853.x
Camerini, R., & Garaci, E. (2015). Historical review of thymosin α 1 in infectious diseases. Expert Opinion on Biological Therapy, 15(Suppl 1), S117-S127. doi:10.1517/14712598.2015.1033393
Bock-Marquette, I., Saxena, A., White, M. D., DiMaio, J. M., & Srivastava, D. (2004). Thymosin β4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair. Nature, 432(7016), 466-472. doi:10.1038/nature03000
Sosne, G., Qiu, P., Christopherson, P. L., & Wheater, M. K. (2007). Thymosin beta 4 suppression of corneal NFκB: A potential anti-inflammatory pathway. Experimental Eye Research, 84(4), 663-669. doi:10.1016/j.exer.2006.12.004

This article is for research and educational purposes only. It is not medical advice. Peptide identification and naming conventions discussed here are intended to improve prescription literacy, not to endorse any specific compound or source. Consult a licensed healthcare provider before making any treatment decisions. IRB PPRN-001-2025.

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