Is TB-500 the same molecule as Thymosin Beta-4?

Not necessarily, it depends on the vendor. TB-500 is a research-market brand name, not a fixed chemical entity: the veterinary and anti-doping literature that coined the name meant a short synthetic fragment (Ac-LKKTETQ), while many vendors, including this one, use the same name for the full 43-amino-acid Thymosin Beta-4 protein. Only a CoA with mass and sequence data tells you which molecule is actually in a given vial.

Is TB-500 a fragment or the full-length peptide?

Both usages exist in the market, so the name alone will not tell you. Our TB-500 is the full-length, 43-amino-acid Thymosin Beta-4 (CAS 77591-33-4, approximately 4,963 Da), confirmed by third-party Janoshik CoA on mass and identity, not the short Ac-LKKTETQ fragment used in veterinary doping-control testing.

What is the actin-binding domain of Thymosin Beta-4?

It is an internal seven-residue stretch, positions 17 to 23 of the 43-amino-acid sequence (LKKTETQ), which promoted endothelial cell migration and vessel sprouting on its own when synthesized as an isolated fragment. That segment is only one functional region of the full protein though, other parts of the sequence contribute separate, non-redundant activities such as anti-inflammatory effects.

What form of TB-500 do you supply?

The full-length, 43-amino-acid Thymosin Beta-4 protein, the same molecule used in the Goldstein, Kleinman and Sosne wound-healing and angiogenesis literature and in the RGN-259 ophthalmic clinical program, not the short synthetic fragment. Every batch carries a published third-party CoA at /coa confirming mass and sequence.

What does the research show for Thymosin Beta-4 overall?

Preclinically, full-length Tb4 accelerated reepithelialization in rodent dermal wound models, supported angiogenesis and endothelial cell migration, and reduced inflammation and matrix metalloproteinase activity in corneal injury models. In humans the strongest dataset is a small Phase III trial (18 patients) of a topical ophthalmic formulation in neurotrophic keratopathy, with a positive but statistically borderline result. None of this establishes approval for any indication, and it describes the full-length molecule specifically, not the short fragment sometimes sold under the same name.

Why does the fragment-versus-full-length distinction matter for research citations?

Because the two forms are not functionally interchangeable: studies comparing them found that short fragments do not reproduce the full protein's actin-sequestering activity, and that different bioactivities map to different internal regions of the sequence. A citation only transfers to a product if the molecule tested in the study matches the molecule in the vial, so identity should be confirmed by CoA rather than assumed from the product name.

What are Thymosin Beta-4's molecular weight, CAS number and basic identifiers?

Full-length Thymosin Beta-4 is a 43-amino-acid, N-terminally acetylated peptide with CAS number 77591-33-4, a molecular weight of approximately 4,963 Da (4,982 Da in the original 1981 sequencing paper), and an isoelectric point around 5.1. These are the identifiers a CoA's mass-spectrometry result should match if a vial genuinely contains the full-length protein rather than a short fragment.

Where did the name TB-500 originate as a fragment name?

The name originated outside the mainstream Tb4 research literature, in veterinary anti-doping chemistry. A 2012 paper described a liquid chromatography-mass spectrometry method to detect TB-500, the short synthetic Ac-LKKTETQ heptapeptide, in equine urine and plasma for doping control, and a 2025 follow-up paper still treats full-length-versus-fragment identification as analytically relevant in horse racing. That usage spread into the retail research-peptide market, where the same name is now applied inconsistently to both the fragment and the full protein.

What is Ac-SDKP, and is it the same as the TB-500 fragment?

Ac-SDKP is a separate, unrelated fragment, the N-acetylated tetrapeptide corresponding to residues 1 to 4 of Thymosin Beta-4, released by enzymatic cleavage of the intact protein's N-terminus. It has its own literature on regulating hematopoietic stem cell proliferation and on antifibrotic effects, and studies comparing it directly to full-length Tb4 found overlapping but non-identical effects. It is not the actin-binding LKKTETQ fragment and not what most vendors mean by TB-500, but it makes the same point: this protein has multiple distinct sub-regions, and a fragment study should specify which fragment.

What doses of Thymosin Beta-4 have been used in published animal research?

Published animal studies used a range of doses depending on species, route and model, this is research data describing what was tested in a study, not a human dosing guideline. Examples include 1.6 mg/kg/day by continuous intraperitoneal infusion in a mouse cardiac model, 5 mg/kg by intradermal injection twice weekly in a diabetic mouse burn-wound model, and 6 mg/kg intravenously in a pig cardioprotection study that found no benefit. Topical ocular and wound applications instead used absolute microgram amounts that cannot be converted to a body-weight dose.

What side effects or adverse findings has research reported for Thymosin Beta-4?

Reported adverse findings are limited and route-dependent. At a high 6 mg/kg intravenous dose in a pig study, Tb4 caused vasoconstriction in mesenteric arteries, vasodilation in coronary arteries, and reduced blood clot firmness when combined with antiplatelet drugs, while several lower-dose animal wound and eye studies reported no adverse events at all. The human dry-eye and neurotrophic keratopathy trials described it as generally safe and well tolerated, with adverse events mostly mild and ocular, but the overall human safety dataset remains small.

Has full-length Thymosin Beta-4 been tested in human clinical trials?

Yes, but only in ophthalmic formulations (RGN-259) so far. A 9-patient Phase 2 trial in severe dry eye showed statistically significant reductions in discomfort and corneal staining, and an 18-patient Phase III trial (SEER-1) in neurotrophic keratopathy showed a positive but borderline-significant healing signal by day 29. A later Phase III trial in the same program is reported to have missed its primary endpoint, and a first-in-human systemic trial for heart attack was overall negative on infarct size, so the human evidence base is real but still mixed and unresolved.

Is TB-500 approved by the FDA or EMA, and is it legal to buy for research in the EU?

No, neither RGN-259 nor any other Thymosin Beta-4 based product is approved by the FDA or the EMA for any indication, RGN-259 holds FDA Orphan Drug Designation for neurotrophic keratopathy, which is a development incentive, not marketing approval. TB-500 is sold across the EU as an unapproved research chemical for laboratory and in-vitro use only, not for human or veterinary administration, and buyers are responsible for checking their own country's rules on importing and handling research chemicals. The fragment form also shows up in anti-doping testing in competitive and equine sport, which is a separate context from an ordinary research purchase.

How does TB-500 compare to BPC-157?

They are different peptides studied for overlapping but distinct research goals. BPC-157 is a synthetic pentadecapeptide derived from a gastric protective protein, while TB-500 (our full-length Thymosin Beta-4) works through actin sequestration and cell migration. Both are frequently studied together in tissue-repair contexts, which is why they are also sold combined in a single vial as the BPC-157/TB-500 Mix, informally the Wolverine pairing, for researchers who prefer one reconstitution instead of two.

What are GLOW and KLOW, and do they contain full-length TB-500?

GLOW combines full-length TB-500 with GHK-Cu and BPC-157 in a single vial, and KLOW adds KPV to that same three-peptide base, both aimed at broader multi-peptide regenerative research panels. The TB-500 component in both blends is the same full-length, CoA-verified molecule described in this article, not the short fragment.

How should TB-500 be reconstituted and stored?

Like most peptides in our catalogue, TB-500 does not have its own official reconstitution-pH spec since it is not an approved drug, the only officially sourced anchor is the diluent itself, bacteriostatic water, which carries an FDA label pH of about 5.7. As a lyophilized powder it is refrigerator-stable (around +4 C), once reconstituted it should stay refrigerated and be treated as time-limited rather than indefinitely stable, consistent with general peptide-handling practice.

How can I verify the CoA for a specific TB-500 batch?

Every batch we sell has a third-party CoA, most commonly from Janoshik, published at /coa, showing mass-spectrometry and identity data that should match the full-length 43-amino-acid sequence, CAS 77591-33-4, approximately 4,963 Da. We do not operate our own laboratory and do not independently re-verify these certificates ourselves, so check that the batch number printed on your vial matches the batch number on the published CoA before treating the results as applicable to your specific product.

Where can I buy full-length, CoA-verified TB-500 for research in the EU?

We sell full-length, CoA-verified TB-500 for research and laboratory use from within the EU at peptidesdirect.io, with each batch's certificate published at /coa and a purity summary at /purity. Given how inconsistently the TB-500 name is used across the market, when buying from any vendor check that they publish a batch-specific CoA with mass and sequence data rather than relying on a product name and photo alone.

TB-500 vs Thymosin Beta-4: Why the Fragment vs Full-Length Distinction Matters for Research

"TB-500" is not a molecule. It is a name, and the research-peptide market uses that name for two different things: sometimes the full 43-amino-acid Thymosin Beta-4 protein, sometimes a short seven-amino-acid synthetic fragment of it. Both are real, both show up in the literature, and they are not interchangeable. If you are citing a study, comparing a CoA, or just trying to understand what is in the vial in front of you, the distinction is the whole ballgame.

TL;DR: What TB-500 actually is

Thymosin Beta-4 (Tβ4) is a naturally occurring 43-amino-acid, N-terminally acetylated peptide, molecular weight approximately 4,963 Da, CAS 77591-33-4. The doping-control and veterinary literature coined "TB-500" specifically for a short synthetic fragment, the N-acetylated heptapeptide Ac-LKKTETQ (residues 17-23), which contains the actin-binding motif. Many research-peptide vendors (including this one) sell and CoA-verify the full 43-aa protein under the same "TB-500" label. The name alone does not tell you which molecule you are holding. Our TB-500 is the full-length 43-amino-acid Thymosin Beta-4, confirmed by third-party Janoshik CoA on mass and sequence, not the short fragment. This is research material for laboratory use only. Nothing here is a human dosing recommendation.

For research purposes only

This article discusses research peptides for laboratory and in-vitro use. It is not medical advice, not a treatment recommendation, and not an instruction for human or animal administration. Any figures cited from the literature describe what was measured in a study, not a usage guideline.

The founding sequence: what Thymosin Beta-4 actually is

Thymosin Beta-4 (Tβ4) was first sequenced in 1981 by Low, Hu and Goldstein, who isolated it from bovine thymus and published the complete 43-amino-acid sequence [PMID 6940133]. That paper is the reference point for what "full-length Tβ4" means: 43 residues, N-terminally acetylated (Ac-Ser-Asp-Lys-Pro...), molecular weight 4,982 Da in the founding paper (later literature commonly cites approximately 4,963 Da for the free acid), isoelectric point around 5.1, CAS number 77591-33-4.

Tβ4 turned out to be the founding member of the beta-thymosin family. Its core, defining biochemical function was worked out over the following decade: Tβ4 binds monomeric G-actin in a 1:1 complex, buffering the cytoplasmic actin pool and regulating how fast actin polymerizes into filaments (F-actin). Sanders, Goldstein and Wang confirmed Tβ4 as the principal G-actin-sequestering peptide operating in living cells, directly tying it to actin polymerization dynamics [PMID 1584803]. That single mechanism, actin sequestration, sits upstream of almost everything else studied about Tβ4: cell shape, cell migration, and by extension wound repair and vessel formation.

This is the molecule this article calls "full-length Thymosin Beta-4." It is also, per our CoA, what we sell as TB-500.

Where "TB-500" as a fragment name comes from

The name "TB-500" did not originate in the Goldstein/Kleinman/Sosne academic lineage that built the Tβ4 mechanistic case. It originated in veterinary and anti-doping chemistry. Ho and colleagues published a doping-control analytical method in 2012 for detecting "TB-500, a synthetic version of an active region of thymosin beta 4," in equine urine and plasma by liquid chromatography-mass spectrometry [PMID 23084823]. Their target analyte was not the 43-aa protein. It was the short, N-acetylated heptapeptide Ac-LKKTETQ, corresponding to residues 17-23 of the parent sequence, the internal segment that carries the actin-binding activity. Their method could detect this fragment down to 0.02 ng/mL in plasma and 0.01 ng/mL in urine.

That paper is, as far as the indexed literature shows, the historical origin of "TB-500" as shorthand for the short synthetic fragment rather than the full protein. It spread from racing and veterinary contexts into the retail research-peptide market, where it is now used inconsistently: some vendors mean the fragment, others mean the full-length protein, and the product label alone does not tell you which. A more recent 2025 doping-control paper continues to treat this distinction as analytically live, differentiating full-length Tβ4 misuse from fragment or synthetic-impurity signatures in equine plasma [PMID 39314109], which tells you regulators still find the fragment-versus-full-length question relevant today, not just as a historical footnote.

Why does the fragment matter biologically in the first place? Because the actin-binding activity really does localize to a short internal region. Philp, Huff, Gho, Hannappel and Kleinman mapped the actin-binding site to the internal heptapeptide 17LKKTETQ23 and showed that this short synthetic peptide alone, isolated from the rest of the molecule, can promote endothelial cell migration in vitro and vessel sprouting in an ex vivo chick aortic-arch assay [PMID 14500546]. So the fragment is not a fabrication, it is a real, independently active piece of the parent protein. That is exactly why it got its own name and its own doping-control assay.

Fragment or full-length: they are not interchangeable

Here is the part that gets lost when "TB-500" is treated as a single fixed thing: fragments and the intact 43-aa protein do not reproduce the same activity profile.

Hannappel and Wartenberg directly compared full-length Tβ4 against various Tβ4 fragments and Tβ4-like peptides. Short fragments did not reproduce full actin-sequestering function to the same degree as the intact molecule [PMID 8471179]. Sosne, Qiu, Goldstein and Wheater went further, mapping which specific short internal sequences of Tβ4 reproduce which specific bioactivities: actin binding and angiogenesis map largely to the LKKTETQ region, while anti-inflammatory and other effects map to other internal motifs [PMID 20179146]. Their conclusion is the important one for anyone reading Tβ4 literature critically: Tβ4's overall biological profile is distributed across multiple regions of the full sequence. No single fragment reproduces the whole activity picture of the intact peptide, it is not simply "LKKTETQ plus inert padding."

There is also a second, unrelated fragment worth knowing about, because it is easy to confuse with the LKKTETQ region: Ac-SDKP. This is the N-acetylated tetrapeptide corresponding to residues 1-4 of Tβ4 (Ac-Ser-Asp-Lys-Pro), released by enzymatic cleavage of the N-terminus by prolyl oligopeptidase. Pradelles and colleagues characterized Ac-SDKP as a negative regulator of hematopoietic stem cell proliferation, distributed across mouse tissues [PMID 1915845], and it has its own separate literature on antifibrotic effects. Leeanansaksiri and colleagues directly compared full-length Tβ4 against its Ac-SDKP fragment on mast cells and found overlapping but non-identical effects [PMID 17191900]. Ac-SDKP is not the same fragment as the actin-binding LKKTETQ heptapeptide, and it is not what most vendors mean when they say "TB-500," but it illustrates the same underlying point: this 43-aa protein has multiple biologically distinct sub-regions, and citing "a Tβ4 fragment study" without specifying which fragment is imprecise.

A citation only transfers if the molecule matches

If a study used the full 43-aa protein, its findings describe the full protein, not a short fragment sold under the same brand name, and vice versa. Dosing, safety data, and outcome percentages from one form do not automatically apply to the other. The only way to know which molecule a given research product actually is, is a CoA with mass and sequence data, not the product name on its own.

What the full-length protein literature actually shows

Because our product is the full-length 43-aa protein, the relevant evidence base is the Goldstein/Kleinman/Sosne body of work built around the intact molecule, not the doping-control fragment literature.

In rodent dermal wound models, full-length Tβ4 (applied topically and intraperitoneally) increased reepithelialization by 42 percent over saline controls at day four, and up to 61 percent by day seven, along with increased collagen deposition and greater keratinocyte migration in a companion in vitro assay [PMID 10469335]. A later review by Kleinman and Sosne consolidated the mechanistic picture behind that result: keratinocyte and fibroblast migration, angiogenesis, reduced local inflammation, and reduced scarring [PMID 27450738].

Angiogenesis is a recurring theme independent of skin. Smart, Rossdeutsch and Riley reviewed Tβ4's role in endothelial migration, adhesion, tubule formation and aortic ring sprouting, with translational interest in cardiac repair after myocardial injury through activation of epicardial progenitor cells and support for neovascularization [PMID 17632766]. That cardiac-repair interest is not uniformly supported: a separate large-animal pig ischemia-reperfusion study found no cardioprotective effect at 6 mg/kg IV, a negative result that runs counter to the positive cardiac-repair signal described above [PMID 27199757].

The eye is where the full-length molecule has gone furthest into human testing. Sosne, Qiu and Kurpakus-Wheater reviewed Tβ4's corneal actions: promoting corneal epithelial cell migration, decreasing inflammation, reducing apoptosis, and upregulating laminin-5, a subepithelial adhesion protein [PMID 19668473]. In a mouse alkali-injury corneal model, topical full-length Tβ4 reduced matrix metalloproteinase activity (MMP-2 and MMP-9) and neutrophil infiltration compared with a PBS control [PMID 15980226]. Philp and Kleinman's broader animal-data review extends this same molecule across tissue types: dermal wounds, cornea, cardiac tissue, hair follicles and nerve regeneration models [PMID 20536453].

That translational path led to RGN-259, a 0.1 percent topical ophthalmic solution of full-length Tβ4, developed for dry eye and neurotrophic keratopathy, and reviewed by Sosne and colleagues as the field moved toward human ophthalmic trials [PMID 20536468]. The strongest human dataset that exists anywhere for this molecule is the Phase III SEER-1 trial of RGN-259 in neurotrophic keratopathy, published in 2022: 18 patients (10 treated, 8 placebo), dosed five times daily. Complete corneal healing by day 29 occurred in 60 percent of treated patients (6 of 10) versus 12.5 percent of placebo patients (1 of 8). Fisher's exact test on that comparison was not significant (p=0.0656), but an ad hoc chi-square test was (p=0.0400), with a 95 percent confidence interval on the difference of 9.5 to 85.5 percent; healing maintenance at day 43 reached significance (p=0.0359). Adverse events were mostly ocular and mild, with only one treatment-related event and no serious treatment-related events [PMID 36613994].

Read the trial statistics honestly

An 18-patient trial with a borderline primary-endpoint result by one statistical test and a significant result by a different, ad hoc test is a real but fragile signal, not a settled finding. RGN-259 carries FDA Orphan Drug Designation for neurotrophic keratopathy, which is a development incentive, not marketing approval. Neither RGN-259 nor any Tβ4-based product is approved by the FDA or the EMA for any indication. A subsequent Phase III trial in the same program is reported to have missed its primary corneal-healing endpoint. This is genuinely still an open research question, not a resolved one.

What our TB-500 is, and what it is not

Identity

Full-length, 43-amino-acid Thymosin Beta-4, N-terminally acetylated, molecular weight approximately 4,963 Da, CAS 77591-33-4. This matches the molecule used in the Goldstein, Kleinman and Sosne wound-healing, angiogenesis and corneal literature cited above, and in the RGN-259 clinical program.

Not the fragment

It is not the short Ac-LKKTETQ heptapeptide that the veterinary doping-control literature specifically named "TB-500" [PMID 23084823]. It is also not the separate Ac-SDKP N-terminal tetrapeptide fragment [PMID 1915845]. Findings specific to those shorter fragments do not automatically describe our product, and findings specific to our product do not automatically describe those fragments.

Verification

Every batch is tested by an independent third-party laboratory (Janoshik), with the certificate of analysis published per batch at /coa and summarized at /purity. We do not run in-house testing and do not claim to; the CoA is the supplier-sourced, third-party record that confirms mass and identity match the full-length sequence, not a vendor's word for it.

Scope

Sold and shipped as a research chemical for laboratory and in-vitro use only, not licensed as a medicine or approved for human or veterinary therapeutic use in the US or the EU.

EU research framing vs the fragment-driven doping narrative

The "TB-500" name, in its fragment sense, originates in the veterinary and anti-doping corner of the literature, which is a different molecule with a different, thinner evidence base than the full-length protein. Our positioning is deliberately the opposite: full-length, CoA-verified, cited against the mechanistic and clinical literature that actually used the intact 43-aa molecule.

BPC-157 is sold on its own and also pre-combined with TB-500 in a single vial, informally known as the "Wolverine" pairing, for researchers who want to reconstitute one vial instead of two. The related products below cover single-vial combinations and broader multi-peptide panels that include TB-500.

TB-500regeneration

Full-length 43-amino-acid Thymosin Beta-4, a naturally occurring repair protein, independently confirmed by a third-party CoA from Janoshik. Promotes cell migration and new blood vessel formation for systemic tissue healing. Especially researched for muscle, tendon, and cardiac repair.

BPC-157regeneration

Gastric pentadecapeptide (15 amino acids) known for exceptional tissue repair properties. Promotes wound healing, angiogenesis, and cytoprotection across tendons, muscles, gut, and nerves. Over 30 years of preclinical research.

WOLVERINE (BPC-157 + TB-500)regeneration

The Wolverine Stack: BPC-157 + TB-500 in equal parts in one vial (50/50: 10mg = 5mg each, 20mg = 10mg each). The most researched healing peptide duo for tissue repair, tendon recovery, and systemic regeneration. Batch-specific Janoshik COA.

GLOWregeneration

3-in-1 skin peptide blend: GHK-Cu 50mg + BPC-157 10mg + TB-500 10mg. Targets collagen synthesis, tissue regeneration, and skin repair for comprehensive dermatological research.

KLOWregeneration

4-in-1 anti-aging peptide blend: GHK-Cu 50mg + BPC-157 10mg + TB-500 10mg + KPV 10mg. Targets collagen synthesis, tissue regeneration, skin repair, and anti-inflammatory pathways.

Healing & Regenerationregeneration

Tissue repair, wound healing, and recovery peptides

Choosing by research goal

Actin-cytoskeleton and cell-migration mechanism research