TB-500: the monograph

TB-500 is a synthetic 7-amino-acid peptide: the sequence Leu-Lys-Lys-Thr-Glu-Thr-Gln with an acetyl group on the front end, written Ac-LKKTETQ, molecular weight 889 Da³⁴. That sequence is residues 17 to 23 of a much larger natural protein called thymosin beta-4, which is 43 amino acids and 4963 Da³⁵. Residues 17 to 23 are the part of the protein that binds actin, which is why a fragment was cut out and sold in the first place⁶.

When doping-control chemists bought a TB-500 product and put it through high-resolution mass spectrometry in 2012, what they found in the vial was exactly that: the N-terminally acetylated 17-23 fragment of human thymosin beta-4¹. FDA lists the same substance on its compounding safety-risks page under the name "Thymosin beta-4, fragment (LKKTETQ), also known as TB-500"³⁰.

This distinction is the whole story of this site, and it is the reason the page exists. The impressive human trial record that appears in TB-500 marketing belongs to the full 43-amino-acid protein, not to the fragment in the vial. This monograph labels every study row with the molecule that was actually administered, alongside the species, so you can see which is which without taking anyone's word for it.

Every chip below carries an evidence grade and, where a study is involved, the molecule that was actually tested. Animal means rat, mouse or horse data; in vitro means cell or tissue experiments; regulatory means an FDA, WADA or registry record. None of these facts rests on a completed human trial of the fragment, because none exists.

No, and the gap is not a technicality. Thymosin beta-4 is a 43-amino-acid protein of 4963 Da³⁵. TB-500 is a 7-amino-acid fragment of 889 Da with an acetyl cap that the natural protein does not have³⁴¹. One is roughly a sixth of the mass of the other and carries a chemical modification that does not occur in the body.

The consequence is what matters. Thymosin beta-4, the full protein, has a real clinical trial history: eye drops (RGN-259) taken through phase 3 in dry eye and neurotrophic keratopathy, topical gels (RGN-137) taken through phase 2 in venous stasis ulcers, pressure ulcers and epidermolysis bullosa, and recombinant human thymosin beta-4 taken through phase 1 and phase 2 in China. Adding up actual enrolment across the 15 completed or terminated registered trials of the full protein listed below gives 2,143 participants. The number of people who have completed a registered trial of the LKKTETQ fragment sold as TB-500 is zero.

There is now one registry record for the fragment itself: a phase 1/2 randomized, placebo-controlled dose-escalation study in adults with stable atherosclerotic cardiovascular disease, target 80 participants, sponsored by Hudson Biotech, first posted in March 2026, with treatment-emergent and serious adverse events as its primary endpoints. It is recruiting in Shenzhen and has posted no results³⁷. A recruiting safety study is not evidence of benefit; it is the field admitting the safety question is still open.

So when a vendor page cites "clinical trials" for TB-500, the honest reading is almost always: those trials tested a different molecule, usually by a different route, often into an eye or onto a wound rather than into a muscle. The table below is the full-protein trial ledger, published so the 2,143 figure can be recomputed by anyone who wants to add it up.

TB-500 (a thymosin beta-4 fragment) is not FDA approved. FDA reports no human exposure data for it, and it is sold only for research use with no established human efficacy. A Drugs@FDA search returns no approved product containing thymosin beta-4 in any form³³.

FDA has said more than that. Its compounding safety-risks list carries an entry headed "Thymosin beta-4, fragment (LKKTETQ), also known as TB-500", which states that compounded drugs containing the fragment "may pose risk for immunogenicity for certain routes of administration due to the potential for aggregation as well as peptide-related impurities", that "FDA has not identified any human exposure data" for drug products containing it, and that the agency "lacks important information regarding any safety issues raised by this drug, including whether it would cause harm if administered to humans"³⁰. That page was current as of April 22, 2026.

On July 23, 2026, FDA's Pharmacy Compounding Advisory Committee took up TB-500-related bulk drug substances³¹. The nomination (from Wells Pharmacy Network) had been withdrawn by the nominator, but FDA elected to proceed with the presentation anyway, and its briefing document states plainly: "FDA is proposing that TB-500 (free base) NOT be included on the 503A Bulks List" and "FDA is proposing that TB-500 acetate NOT be included on the 503A Bulks List"³². Committee advice is non-binding and rulemaking is pending. Being added to that list would not make a substance FDA approved in any case; it would only make it legal for pharmacies to compound.

In sport, the 2026 WADA Prohibited List names "Thymosin-beta4 and its derivatives e.g. TB-500" under section S2.3, growth factors and growth factor modulators³⁶. S2 is prohibited at all times, in and out of competition, and the list states that all prohibited substances in the S2 class are non-Specified Substances. That last detail matters and is often missed: our sister site covers BPC-157, which sits in S0 where every substance is a Specified Substance. TB-500 sits in S2, where they are not. Specified status is what gives an athlete room to argue that a substance was more likely taken for a reason other than performance; TB-500 does not have it.

The mechanistic case for the fragment is a structural argument, not a clinical one. Thymosin beta-4 is the major actin-sequestering molecule in eukaryotic cells, and its actin-binding site is the LKKTETQ sequence at residues 17 to 23. A 2010 review by the group that mapped these sites reports that a short sequence containing LKKTETQ promotes angiogenesis, wound repair and cell migration, while a different fragment at the other end of the protein (Ac-SDKP) blocks inflammation and reduces fibrosis⁶. Different fragments, different jobs, and neither one is the whole protein.

Direct fragment work exists and is worth reading precisely. In human hepatic stellate cells, the 17-23 peptide but not the 1-15 peptide blocked PDGF-BB-driven upregulation of the PDGF receptor, alpha-SMA and collagen 1, and inhibited proliferation and migration; the authors concluded the anti-fibrogenic action of thymosin beta-4 is exerted via 17-23⁷. In wounded skin, the LKKTETQ peptide significantly enhanced repair in vitro and in vivo, with the effect suggested to run through purinergic receptors⁵.

The full protein's mechanism literature is broader and better known, which is exactly why it gets borrowed. Thymosin beta-4 forms a complex with PINCH and integrin-linked kinase, activates Akt, and improved early myocyte survival and cardiac function after coronary artery ligation in mice¹⁶. That is a mouse result about a 43-amino-acid protein. It is not a TB-500 result.

One 2024 finding complicates the fragment story from the inside. When TB-500 was given to rats and its metabolites profiled, the parent peptide was not the most active thing present: only the metabolite Ac-LKKTE showed significant wound-repair activity in the fibroblast assay, and the authors wrote that "the previously reported wound-repair activity of TB-500 in literature may be due to its metabolite Ac-LKKTE rather than the parent form"². Nobody has resolved that.

The table below is the core of this monograph: 26 primary research and registry entries, each labelled with the species, the route, and the molecule that was actually administered. The species census is 14 human rows and 12 nonhuman or laboratory rows. The molecule census is what makes this compound unusual: 11 rows tested the TB-500 fragment, 13 tested the full 43-amino-acid protein, 1 tested both side by side, and 1 human row records a peptide the source calls "TB4" without saying which molecule it was.

Cross that census with the species column and the honest summary falls out. Of the 11 fragment rows, 10 are animal, in vitro or analytical, and the single human one is a registry record with no results³⁷. Of the 13 full-protein rows, 12 are human. The human evidence and the fragment do not overlap anywhere in this table.

Independent reviewers describe the field the same way. A 2026 scoping review in the American Journal of Sports Medicine covering six popular peptides including TB-500 found that 67% of identified publications used preclinical animal models, that human clinical studies were "limited to a handful of investigations, most lacking robust controls or rigorous study designs", and concluded that the claimed benefits "remain unsubstantiated by current human trials"²⁵. A 2026 narrative review in Sports Medicine covering the same gray market notes that many unapproved peptides show favourable outcomes in animal models "but rigorous human safety data are scarce, and there is potential for serious harm"²⁶. A 2026 primer for orthopaedic surgeons states that thymosin beta-4 and its derivative TB-500 "promoted angiogenesis and tissue repair in preclinical models, but human orthopaedic data are lacking, and both remain banned substances in sports"²⁷. A 2026 review of therapeutic peptides in orthopaedics lists TB-500 among the wound-repair peptides and states plainly that despite promising preclinical studies "there is a current lack of clinical trials"²⁸.

Strip away everything that tested the full protein and this is what is left for the molecule in the vial.

One rat tendon study, from 2026. An independent Turkish orthopaedic group transected and repaired the Achilles tendon in 32 rats and randomised them to control, BPC-157 at 10 ug/kg/day, TB-500 at 60 ug/kg/day, or both, given intraperitoneally for four weeks. Maximum load to failure was higher in both peptide groups than in controls, reaching statistical significance in the TB-500 group (p < 0.05). Total Bonar scores were significantly lower with TB-500 (p = 0.016) and total Movin scores were significantly lower with TB-500 and with the combination (p = 0.017 and p = 0.040). BPC-157 alone was numerically better without reaching significance on total scores, and the combination added nothing over either agent alone³.

We report that result at the grade it actually holds, and the grade is low. This is one exploratory study, 8 rats per group, four weeks, in an animal whose Achilles tendon is not a human one, published by authors who themselves describe the findings as preliminary and call for dose optimisation and longer-term work. Our sister site on BPC-157 presented the same study against its own compound's interest, and we are not going to spend it as a marketing point here just because the arrow points our way this time. A single rat study is a single rat study in both directions.

Fragment wound-repair work in mice and cells. The 7-amino-acid peptide promoted repair in 26-month-old aged mice comparably to the parent molecule in a 2003 study that tested both⁴, and LKKTETQ significantly enhanced skin wound repair in vitro and in vivo in 2006⁵. A 2025 paper built TB500 into an enzyme-triggered hydrogel and reported accelerated epithelial regeneration in an alkali burn model plus migration and proliferation of human corneal epithelial cells, calling it the first ocular application of TB500; the abstract does not state the animal species⁸. A 2026 study reported that TB500 and Ac-SDKP improved Morris water maze and novel object recognition performance in 5xFAD mice while leaving hippocampal amyloid burden unchanged⁹.

Metabolism, in rats. After TB-500 was administered to rats, Ac-LK was the primary metabolite in the 0 to 6 hour window and Ac-LKK was detectable to 72 hours; no cytotoxicity was found for parent or metabolites; and only Ac-LKKTE showed significant wound-repair activity in the assay².

That is the complete fragment efficacy literature relevant to what people buy TB-500 for: one rat tendon study, a handful of mouse and cell wound experiments, one hydrogel formulation study, and one rat metabolism study that questions whether the parent peptide is the active molecule at all. There is no human efficacy study of any kind.

Because the full protein's trials get cited on TB-500 pages, it is worth reporting what they found, in full, including the parts that do not flatter the molecule.

Dry eye. A phase 2 trial randomised 72 subjects to 0.1% thymosin beta-4 eye drops or placebo in a controlled adverse environment model. Neither primary endpoint, ocular discomfort or inferior corneal staining, showed a significant difference. Several secondary endpoints did: discomfort during the environmental challenge was reduced 27% (P = 0.0244), and central and superior corneal staining improved (P = 0.0075 and P = 0.0210)¹⁷. A separate 9-patient phase 2 trial in severe dry eye reported 35.1% less ocular discomfort and 59.1% less total corneal fluorescein staining versus vehicle at day 56¹⁸. The program then went to phase 3 three times: ARISE-1 (317 participants), ARISE-2 (601) and ARISE-3 (700)⁴⁰³⁹³⁸. In the results posted for ARISE-2, mean change from baseline at day 29 was 0.07 for RGN-259 versus -0.04 for placebo on ocular discomfort, and 0.07 versus -0.01 on corneal fluorescein staining: neither co-primary endpoint favoured the drug³⁹.

Neurotrophic keratopathy. The phase 3 SEER-1 trial was terminated after 18 participants for a business decision⁴¹. The 2025 Cochrane review of interventions for neurotrophic keratopathy included it and found that 0.1% RGN-259 may not increase the proportion of participants achieving corneal re-epithelialization (RR 9.00, 95% CI 0.57 to 141.88; 18 participants; low-certainty evidence)²³. A confidence interval running from 0.57 to 141.88 is a statement that nobody knows. SEER-2 is recruiting⁴².

Chronic wounds. Phase 2 trials of topical thymosin beta-4 gel ran in venous stasis ulcers and pressure ulcers, 72 participants each, both with results posted⁴⁶⁴⁷. The venous ulcer study, run at eight European sites and randomising 73 patients, reported that the safety profile at all doses was acceptable and comparable to placebo, and that efficacy findings "suggest that a Tbeta4 dose of 0.03% may have potential to speed wound closure, with complete closure within three months in about 25% of patients²¹. A 2012 review by the investigators summarised both trials as shortening time to closure by almost a month in those patients whose ulcers closed²⁰. Both epidermolysis bullosa trials were terminated early, one for lack of patient availability and expired study drug, the other after four participants for a business decision⁴⁸⁴⁹.

Systemic dosing. Intravenous thymosin beta-4 has been given to healthy volunteers: a published phase 1 study dosed four cohorts of 10 subjects at 42, 140, 420 or 1260 mg, single dose and then daily for 14 days, and reported infrequent mild-to-moderate adverse events with no dose-limiting toxicity¹⁹. Recombinant human thymosin beta-4 has since been through phase 1a (54 subjects, single IV doses of 0.5 to 25 ug/kg) and phase 1b (30 subjects, 0.5 to 5.0 ug/kg daily for 10 days) in Chinese healthy volunteers, and phase 2a and 2b trials in acute myocardial infarction with 62 and 90 participants^50515253. None of those four records has posted results. The one US injectable program, RGN-352 for ST-elevation myocardial infarction, was withdrawn with the note "Trial never initiated", and a companion phase 1 intravenous study was withdrawn as "never initiated due to contract manufacturing issues"⁵⁴⁵⁵.

The summary for the molecule that does have trials: no regulator has approved it. A 2025 paper from an independent ophthalmology group describes RGN-259 as having reached clinical trials "with full US Food and Drug Administration approval still pending"²⁴, and Drugs@FDA returns nothing for thymosin beta-4 in any form³³. Borrowing this record for the fragment therefore borrows a record that has not itself produced an approved product.

The best-documented in vivo administrations of TB-500 in the published literature are not in humans or rodents. They are in horses, and they were done by racing laboratories trying to catch it.

In 2012 the Hong Kong Jockey Club racing laboratory published a detection method for TB-500 in equine urine and plasma, describing it as "a veterinary preparation known as TB-500 and containing a synthetic version of the naturally occurring peptide LKKTETQ". The method confirmed the parent peptide at 0.02 ng/mL in plasma and 0.01 ng/mL in urine, and was validated on samples from horses given a single dose of TB-500 containing 10 mg of N-acetylated LKKTETQ. The authors describe it as the first identification of TB-500 and its metabolites in post-administration samples from horses¹⁰. A companion 2013 paper extended the method to seven peptides and reported detection of N-acetylated LKKTETQ and its metabolite after subcutaneous administration of TB-500 (10 mg) to two thoroughbred geldings¹¹.

The French racing laboratory published a 2025 population study establishing baseline endogenous thymosin beta-4 concentrations in racing horses, noting that its use is "forbidden by the IFHA, the FEI, and the WADA" while "numerous products available online" claim to contain either a synthetic acetylated fragment of the protein or the protein itself. They also showed that a non-natural synthesis impurity is detectable in equine plasma after a single administration of a TB4-containing product¹².

Two things follow. First, the dose scale that has actually been administered and measured in a large mammal is 10 mg subcutaneously, in a horse, for the purpose of building a test. Second, an impurity signature specific to synthesis is one of the ways these products are identified, which tells you something about what is in them.

We looked for individual racing-authority disciplinary actions naming TB-500 and did not verify any against a primary regulator source within this build, so none is cited here. The peer-reviewed racing-laboratory literature above is the documentable part of the horse-doping story, and it is enough.

No human study of the LKKTETQ fragment has ever been published, for any indication, of any design. FDA's own position, stated on its compounding safety-risks page, is that it "has not identified any human exposure data" for drug products containing the thymosin beta-4 fragment³⁰. That is a regulator saying it could not find evidence that people have taken this and been followed.

Two things sit adjacent to that emptiness and get mistaken for filling it.

The first is the registry record: the phase 1/2 dose-escalation safety study in stable atherosclerotic cardiovascular disease, 80 participants planned, three sequential dose cohorts randomised 3:1 against placebo, primary endpoints treatment-emergent and serious adverse events, recruiting since February 2026, no results posted³⁷. When it reports, it will be the first human safety data on this molecule. Until then it is a plan, not a finding.

The second is a retrospective knee-pain chart review from a Florida clinic, which is the only published human report anywhere that involves a peptide the authors call TB4. Of 16 patients reached by telephone, 12 had received BPC-157 alone and 4 had received BPC-157 combined with TB4; of those 4, three reported significant improvement and one reported no relief. There was no control group, no imaging, and "no specific tools were used to measure their improvement"²⁹. The abstract names "thymosin-beta-4 (TB4)" and never states whether the injected material was the full protein or the fragment, so it cannot be attributed to TB-500 at all. Four uncontrolled patients on a combination of two peptides, with the molecule unidentified, is not a basis for anything.

Everything else offered as human evidence for TB-500 is evidence about thymosin beta-4, the full protein, and belongs to the section above.

There is no human pharmacokinetic study of TB-500. No half-life, no bioavailability, no exposure curve, no clearance route has been measured in a person for this molecule, which follows directly from FDA having identified no human exposure data at all³⁰.

What exists is animal and analytical. In rats given TB-500, Ac-LK was the metabolite present at highest concentration in the 0 to 6 hour interval and Ac-LKK persisted as a long-term metabolite detectable to 72 hours². In horses, the parent peptide and the Ac-LK metabolite were confirmed in plasma and urine after a single subcutaneous 10 mg dose, at detection limits around 0.01 to 0.02 ng/mL¹⁰¹¹. Separate rat work on the full protein identified Ac-Tb1-14 as a urinary metabolite quantifiable to 48 hours after a 20 mg/kg intraperitoneal dose, with peak concentrations between 0 and 6 hours¹⁴.

A practical laboratory note that also matters for anyone handling this compound: TB-500 is one of four model peptides used in a published study of adsorption to glassware and plasticware, precisely because peptides at low concentration stick to surfaces and disappear from solution¹⁵. Concentration in a vial is not a fixed property of the vial.

By contrast, the full protein does have published human pharmacokinetics: single intravenous doses of 42 to 1260 mg in healthy volunteers showed a dose-proportional response and a half-life that increased with dose¹⁹. Those doses are between roughly 4 and 140 times the entire contents of a typical gray-market TB-500 vial, of a molecule six times larger. The two are not interchangeable in any direction.

TB-500 is sold as a lyophilised powder in sealed vials, commonly labelled 2 mg, 5 mg or 10 mg, to be reconstituted with bacteriostatic water and injected. FDA's compounding entry addresses exactly this class of product and flags immunogenicity risk "for certain routes of administration"³⁰.

The research routes are a different map. The fragment's animal efficacy work used intraperitoneal injection (the rat tendon study, 60 ug/kg/day)³, topical application (the mouse wound studies)⁴⁵, and an ocular hydrogel⁸. The documented large-animal route is subcutaneous, in horses, at 10 mg¹⁰. The full protein's human work is overwhelmingly topical or ocular: eye drops in every dry eye and keratopathy trial, gel in every wound trial. The only systemic human route studied is intravenous, and only for the full protein¹⁹.

Nobody has published a study of subcutaneous or intramuscular TB-500 in a human being. That is the route almost everyone buying it uses. See the fragment-versus-full-protein comparison table for the route-by-route breakdown.

There is no established human dose of TB-500. No human dose-finding study has been published, and the one registered dose-escalation study has not reported its dose levels publicly or posted any results³⁷.

The doses that do exist, labelled by molecule and species: the fragment was given at 60 ug/kg/day intraperitoneally for four weeks to rats in the 2026 tendon study³, and as a single subcutaneous dose containing 10 mg of N-acetylated LKKTETQ to horses in the racing-laboratory administration studies¹⁰¹¹. The full protein was given intravenously to healthy human volunteers at 42, 140, 420 and 1260 mg¹⁹, and recombinant human thymosin beta-4 at 0.5 to 25 ug/kg intravenously in phase 1 and 0.25 to 2.0 ug/kg in the myocardial infarction trials⁵⁰⁵². Topical human trials used concentrations, not masses: 0.01%, 0.03% and 0.1% gels and 0.1% eye drops⁴⁶⁴⁰.

Those numbers sit in four different unit systems across two different molecules and four species. There is no validated method for converting any of them into a dose for a person injecting the fragment, and this site does not attempt one. Our study-dose explorer displays every published dose with its molecule and species attached, and our reconstitution calculator does arithmetic on numbers you enter. Neither recommends a dose, because no source supports one.

Nobody knows, and that is not a hedge. FDA states it "lacks important information regarding any safety issues raised by this drug, including whether it would cause harm if administered to humans", having identified no human exposure data for it at all³⁰. There is no human safety dataset to summarise.

What is reported: in the rat metabolism study, neither the parent peptide nor its metabolites showed cytotoxicity in the assays used², and no adverse effects were reported in the small animal efficacy studies. Absence of observed harm in rats and in cell assays is not human safety evidence, and no animal toxicology program for this fragment has been published.

What is specifically flagged as unassessed is immunogenicity: FDA's stated concern is that compounded drugs containing the fragment "may pose risk for immunogenicity for certain routes of administration due to the potential for aggregation as well as peptide-related impurities"³⁰. Aggregation is a specific property of peptides in solution, and the aggregation behaviour of this peptide in the vials being sold has not been characterised in any published work we could find.

Two further considerations belong here honestly. The proposed mechanism is pro-angiogenic and pro-migratory: the same actin-binding and cell-migration biology that is offered as the benefit is biology that people with a cancer history should want a clinician's view on before going near it, and no study has examined that population⁶. And the practical risk sits upstream of pharmacology entirely: the contents of the vial. See the sourcing section.

No side-effect profile exists for TB-500 in humans, because no human study of the fragment has reported one. Any list of TB-500 side effects circulating online is either invented, copied from the full protein, or extrapolated from other peptides.

The nearest real data are for the different molecule. In the published phase 1 study of intravenous thymosin beta-4 in 40 healthy volunteers at 42 to 1260 mg, adverse events were "infrequent, and mild or moderate in intensity", with no dose-limiting toxicities and no serious adverse events¹⁹. In the topical wound trials the safety profile at all doses was described as acceptable and comparable to placebo²¹, and the small dry eye trials reported no adverse events¹⁷. Those are tolerability findings for a 43-amino-acid protein given intravenously, in an eye or onto a wound. They say nothing about a 7-amino-acid acetylated fragment injected under the skin from an unregulated vial.

The registered phase 1/2 study of the fragment has treatment-emergent adverse events and serious adverse events as its two primary endpoints³⁷. That is the study designed to answer this question, and it has not answered it yet.

For the fragment, the honest answer is everyone. No human population has been studied, so every group below is an absence rather than a documented risk.

Groups with zero data and specific reasons for caution: pregnant or breastfeeding people; children; people with a current or past cancer, given that the proposed mechanism is pro-angiogenic and pro-migratory⁶¹⁶; people with cardiovascular disease, who are precisely the population the first registered human study is now enrolling under close safety monitoring³⁷; and people with immune conditions, since immunogenicity is the specific risk FDA names as unassessed³⁰.

No drug interaction study of TB-500 exists in any species. None of the published animal work co-administered other drugs and measured an interaction.

Tested athletes are a separate case with a definite answer. Thymosin beta-4 and its derivatives including TB-500 are prohibited at all times under WADA S2, and S2 substances are non-Specified, which removes the mitigation route that Specified status can provide³⁶. In horse racing the same applies through IFHA and FEI rules, with validated detection methods in routine use¹².

This is the question with the best published answer on the whole page, and the answer is not reassuring.

A French racing laboratory bought products sold as TB500, TB1000 and SGF1000 over the internet and analysed them. Their conclusion: "the content of TB500/TB1000 products is not systematically consistent with it's former descriptions", and the third product, SGF1000, was mainly sheep extracellular matrix and blood proteins with the purported active ingredient "excessively diluted"¹³. Independently, the 2012 Ghent doping-control work that first characterised a TB-500 product had to synthesise Ac-LKKTETQ themselves to have a reference standard to compare against¹, and the 2024 Korean metabolism work noted that TB-500 and its metabolites had never been simultaneously quantified or structurally identified using synthesised authentic standards until they did it².

Racing laboratories also report detecting non-natural synthesis impurities in equine plasma after administration of a TB4-containing product, which is a direct measurement that these products carry manufacturing residues¹². FDA names peptide-related impurities and aggregation potential as the specific reasons compounded versions concern it³⁰.

There is no USP monograph for this peptide, no pharmaceutical-grade formulation, and no validated quality standard for the vials being sold. A certificate of analysis supplied by the seller of a product is a document produced by the seller. The published record shows the contents of these products have not consistently matched their labels.

No validated storage or reconstitution standard exists for TB-500, because no pharmaceutical-grade formulation of it exists. Handling practices circulating on forums are laboratory convention, not tested product science, and this site will not present them as data.

Two documented properties are worth knowing. First, adsorption: TB-500 was selected as one of four model doping-relevant peptides in a published study of peptide loss to glassware and plasticware, which found that the best choice of consumable depends on the specific peptide's physicochemical properties rather than on price¹⁵. Peptide solutions lose material to container surfaces, and a stated concentration is not automatically the delivered concentration. Second, degradation to metabolites is rapid in vivo: in rats, the parent peptide gave way to Ac-LK within hours, with Ac-LKK still detectable at 72 hours².

The comparison molecule shows what a real formulation program looks like: the recombinant human thymosin beta-4 injection under study in China is described in its registry record as a sterile solution supplied in 1.5 mg vials stored at 2 to 8 degrees Celsius, with defined dilution to a 5 mL administration volume⁵³. Nothing equivalent exists for the fragment.

This block renders limits_text.

Twelve questions, each answered in 320 characters or fewer for the answer-ready layer, with a longer answer beneath. Every answer is consistent with the graded evidence table above and names the molecule where the molecule is the point.

Every reference below was fetched and verified against its source on 2026-08-14: PubMed records via the NCBI E-utilities API, FDA pages and the July 2026 PCAC briefing document retrieved directly from fda.gov with a browser user agent, the 2026 WADA Prohibited List PDF text-extracted from the archived file, trial records from the ClinicalTrials.gov v2 API, chemical identity from PubChem, and approval-status absence from the openFDA Drugs@FDA API. Study and document titles are reproduced verbatim. A machine-readable version of this list ships as the citation manifest for this page.