Everything below concerns prohibited list. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-01-26. Where a claim depends on a specific study, the study is described rather than over-claimed.
Thymosin beta-4 is a 43-residue actin-binding protein found in most mammalian cell types, where it participates in cytoskeletal regulation and cell migration. TB-500 represents only a short fragment of that protein and does not include the remaining residues. Whether the isolated fragment reproduces the full range of activities reported for the intact protein remains an open question. Researchers commonly treat the two as related but distinct entities when comparing results.
Published work involving this sequence spans actin-binding assays, cell-migration studies, wound-healing models, and cardiovascular or musculoskeletal experiments. Much of the biological rationale derives from in vitro systems and animal models, and the number of controlled human studies is small. Reported outcomes vary across preparations, doses, and routes, which complicates comparison between studies. Reviews generally describe the evidence base as preliminary rather than settled. Mechanistic explanations are often proposed by analogy to the parent protein rather than demonstrated directly.
TB-500 is a synthetic seven-amino-acid peptide with the sequence LKKTETQ, corresponding to residues 17 through 23 of the protein thymosin beta-4. The N-terminus is typically acetylated in the described form, giving a monoisotopic mass near 888.5 Da and an average mass of about 889 Da. The designation TB-500 is a catalogue label rather than a formal chemical name, and the same sequence appears in the literature under several alternative abbreviations. It is handled as a research reagent rather than a pharmaceutical product.
Regulatory status differs by country, but TB-500 is not an approved pharmaceutical in major jurisdictions. It is commonly sold as a research chemical for laboratory use, which places responsibility for identity and purity on the supplier and the laboratory. Published human data are limited, and most reports involve preclinical models or cell culture. Questions about whether the fragment mimics all actions of thymosin beta-4, and under which conditions, remain open. Independent verification of any material is therefore a practical requirement in research settings.
TB-500 is a synthetic heptapeptide with the sequence Ac-LKKTETQ. It corresponds to a short N-terminal region of thymosin beta-4, a 43-amino-acid protein found in many cell types. The fragment contains an actin-binding motif, which is one reason it appears in laboratory studies of cell migration and cytoskeletal dynamics. TB-500 is not the full-length protein and is produced as a research chemical rather than an approved therapeutic agent. Its molecular weight is approximately 889 Da.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C38H68N10O14 | Acetylated heptapeptide form |
| Monoisotopic mass | 888.5 Da | Average mass about 889 Da |
| Appearance | White to off-white solid | Usually supplied as lyophilised powder |
| Solubility class | Highly water soluble | Also dissolves in aqueous buffers |
| Common synonyms | Tbeta4 fragment, thymosin beta-4 (17-23) | Refer to the same sequence |
Thymosin beta-4 itself is a natural peptide of 43 residues found in many cell types and body fluids. Its best-characterised function is binding and sequestering actin monomers, which influences cytoskeletal dynamics. The sequence most often associated with TB-500, LKKTETQ, corresponds to part of that actin-binding region. A different fragment, Ac-SDKP, is also derived from the same parent peptide and is studied in its own right, which is one reason discussions of thymosin fragments can become confusing. The two are structurally distinct and are not interchangeable.
Interest in the fragment grew during the 1990s and 2000s, when it moved from laboratory work into sports and supplement markets. Anti-doping bodies added thymosin beta-4 fragments to prohibited lists, and a small number of adverse analytical findings have been reported in competition testing. Published controlled human trials remain scarce. Most mechanistic evidence comes from cell culture and animal models, and those studies examine endpoints such as cell migration, wound closure and inflammation markers. That evidence supports research interest but does not establish clinical benefit, and broad regenerative claims should be read as unverified.
Research interest in thymosin beta-4 fragments centres on actin sequestration, cell migration and tissue repair models. Most published work uses cultured cells or animal wound and cardiac preparations, and findings are generally described as preliminary. No fragment of this protein has been approved as a therapeutic product by major regulators. Reviews of the field note inconsistent dosing, delivery routes and outcome measures across studies, which complicates direct comparison. The material is best understood as a laboratory reagent with an active but unresolved research literature.
TB-500 is a catalogue name applied to a synthetic peptide related to thymosin beta-4, an actin-binding protein found in most mammalian cells. Suppliers do not use the label consistently: some describe it as the full 43-residue protein, others as a short fragment from the actin-binding region, and others as a related tetrapeptide. Because the name is commercial rather than chemical, two products sold under it may not contain the same molecule. This naming ambiguity is the first point to check in any description of the material.
No major regulatory agency has approved TB-500 for therapeutic use, and it holds no pharmacopoeial monograph. The name appears on the World Anti-Doping Agency prohibited list within the class covering peptide hormones, growth factors, and related substances. Detection in doping control relies on mass spectrometric methods applied to urine, often after preparation steps that concentrate the analyte. Discussion of TB-500 therefore clusters in biochemistry, sports medicine, and anti-doping literature rather than in registered clinical trials.
TB-500 is a synthetic peptide preparation marketed under a name derived from thymosin beta-4, a 43-residue actin-binding protein first isolated from thymus tissue. The full-length protein has a reported molecular mass near 4963 Da, while material sold as TB-500 is often described as a fragment containing the actin-binding motif LKKTETQ. Because suppliers use the name inconsistently, published sources sometimes refer to the same label as a fragment, a synthetic copy, or a related analog. This naming ambiguity complicates direct comparison of reports across studies.
The seven-residue chain carries several polar and charged side chains, so it dissolves readily in water and in aqueous buffers near neutral pH. No cysteine is present, so disulphide formation is not a concern and reducing agents are unnecessary. Dilute ammonium hydroxide or acetonitrile-water mixtures are sometimes used for stock solutions when initial dissolution is slow. Strongly alkaline conditions and prolonged contact with oxidising agents are avoided because they can modify lysine-containing stretches, and haze in solution usually signals incomplete dissolution or aggregated material.
Identity and purity are checked with reversed-phase high-performance liquid chromatography, which separates the target sequence from truncated or deletion analogues, and with mass spectrometry, which confirms the expected molecular mass. Amino acid analysis and peptide mapping give orthogonal confirmation but are used less often outside specialist laboratories. Counter-ion content varies: material purified on trifluoroacetic acid gradients retains trifluoroacetate, and ion exchange can convert the salt form. Residual water and solvent are measured by Karl Fischer titration or thermogravimetric analysis, and any purity figure should be read together with the method used to obtain it.
Lyophilised peptide powders are hygroscopic, and the fragment absorbs atmospheric moisture when a vial is opened at room temperature. Weighing and aliquoting are normally done quickly in a dry environment, and stock solutions are divided into single-use portions before freezing. Repeated freeze-thaw cycles are avoided because they promote aggregation and can shift the measured content of a vial. These practices are general to synthetic peptides rather than unique to this sequence, but they matter more for short chains kept for long periods.
== Ketosis prone diabetes == The entity of ketosis-prone type 2 diabetes was first fully described in 1987 after several preceding case reports. It was initially thought to be a form of maturity onset diabetes of the young, and went through several other descriptive names (such as "idiopathic type 1 diabetes", "Flatbush diabetes", "atypical diabetes" and "type 1.5 diabetes") before the current terminology of "ketosis-prone type 2 diabetes" was adopted. It has been reported predominantly in non-white ethnicity in African–Americans, Hispanics, Black Africans and Black Caribbeans. There is a link with G6PD deficiency.
However, NMDA-mediated receptor signaling is probably necessary to trigger the upregulation of BDNF exon IV expression because normally CREB interaction with CRE and the subsequent translation of the BDNF transcript is blocked by of the basic helix–loop–helix transcription factor protein 2 (BHLHB2). NMDA receptor activation triggers the release of the regulatory inhibitor, allowing for BDNF exon IV upregulation to take place in response to the activity-initiated calcium influx. Activation of dopamine receptor D5 also promotes expression of BDNF in prefrontal cortex neurons.
=== Discontinued === Acolbifene/prasterone (dehydroepiandrosterone/acolbifene; DHEA/acolbifene; prasterone/acolbifene; Femivia) – combination of acolbifene (selective estrogen receptor modulator (SERM)) and prasterone (dehydroepiandrosterone; DHEA) (androgen, other actions) – decreased libido [68] Alprostadil SEPA (prostaglandin E1 SEPA; alprostadil/soft enhancement of percutaneous absorption; Topiglan) – prostaglandin E1 (PGE1) agonist – erectile dysfunction [69] Alprostadil/lidocaine (NM02216; NM100061) – combination of alprostadil (prostaglandin E1 (PGE1) agonist) and lidocaine (sodium channel blocker, local anesthetic) – premature ejaculation [70] Amesergide (LY-237733; LY237733; LY-237,733) – serotonin 5-HT2A, 5-HT2B, and 5-HT2C receptor antagonist, other actions – erectile dysfunction, premature ejaculation [71] Apomorphine inhalation (VR-004; VR-040; VR-400) – non-selective dopamine receptor agonist, other actions – erectile dysfunction, female sexual dysfunction [72] Apomorphine intranasal – non-selective dopamine receptor agonist, other actions – erectile dysfunction [73] Avanafil (Razatus; Spedra; Stendra; TA-1790; Zepeed) – phosphodiesterase PDE5 inhibitor – female sexual dysfunction, premature ejaculation [74] BAY-604552 (BAY98-7081; sGC activator) – guanylate cyclase stimulant – erectile dysfunction [75] Bremelanotide (Rekynda; Vyleesi; PT-141) – melanocortin MC4 receptor agonist – erectile dysfunction [76] CP-866087 (CP-866,087) – μ-opioid receptor antagonist – female sexual dysfunction [77] DA-8031 (DA8031) – selective serotonin reuptake inhibitor (SSRI) – premature ejaculation [78] Dapoxetine (IMD dapoxetine; YHD-1044) – selective serotonin reuptake inhibitor (SSRI) – premature ejaculation [79] Delequamine (RS-15385; RS-15385197) – α2-adrenergic receptor antagonist – erectile dysfunction [80] Estradiol/testosterone transdermal (testosterone/estradiol transdermal) – combination of estradiol (estrogen) and testosterone (androgen) – female sexual dysfunction [81] GM-1485 (GPI-1485; NIL-A) – immunophilin modulator – erectile dysfunction [82] Heparin/lidocaine/sodium bicarbonate (alkalised lidocaine and heparin formulation; Hep-Lido-A compounded formulation; U-101; URG-101) – combination of heparin (Factor Xa inhibitor, thrombin inhibitor), lidocaine (sodium channel blocker, local anesthetic), and sodium bicarbonate (absorption enhancer) – dyspareunia [83] hMaxi-K gene therapy (pVAX/hSlo; URO-902) – gene transference – erectile dysfunction [84] INO-1001 (INO1001; Pardex) – poly(ADP-ribose) polymerase inhibitor – erectile dysfunction [85] LGD-2941 (LGD2941; LGD122941; LGD-122941) – selective androgen receptor modulator (SARM) – female sexual dysfunction, male sexual dysfunction [86] Melanotan II (MT-II; PT-14) – melanocortin receptor agonist – erectile dysfunction, male sexual dysfunction [87] Milnacipran (Dalcipran; F-2207; Impulsor; Ixel; Joncia; Midacipran; Midalcipran; Savella; TN-912; Toledomin) – serotonin–norepinephrine reuptake inhibitor (SNRI) – vulvodynia [88] Nitroglycerin topical (Anogesic; Cellegesic; Rectiv; Rectogesic) – nitric oxide donor – dyspareunia, vulvodynia [89] NMI-870 – α2-adrenergic receptor antagonist, nitric oxide donor – erectile dysfunction, female sexual dysfunction [90] Oxytocin (oxytocin gel; oxytocin topical; Vagitocin) – oxytocin receptor agonist – atrophic vaginitis [91] Pagoclone (IP-456; Panex; RP-62955) – GABAA receptor positive allosteric modulator and nonbenzodiazepine/cyclopyrrolone – premature ejaculation [92] PF-446687 (PF-00446687; PF-446,687) – melanocortin MC4 receptor agonist – sexual function disorders [93] PF-592379 (PF-000592379; PF-592,379) – dopamine D3 receptor agonist – erectile dysfunction [94] Research programme: therapeutics - Re-Pharm (RP-0217; RP0217) – protein phosphatase 2A (PP2A) inhibitor – sexual function disorders [95] [96] RO-0282425 (RO0282425) – melanocortin MC4 receptor agonist – erectile dysfunction [97] RTN-001 (KD-027; SLX-2101; SLx-2101) – phosphodiesterase PDE5 inhibitor – erectile dysfunction [98] SAR-407899 (SAR407899; SAR407899A) – Rho-associated kinase inhibitor – erectile dysfunction [99] Sertraline (Aremis; Besitran; CP-51974; CP-51974-01; Gladem; J Zoloft; Lustral; Serad; Serlain; Tatig; Zoloft) – selective serotonin reuptake inhibitor (SSRI) – premature ejaculation [100] Sildenafil (Revatio; Revatio IV; UK-92480; Viagra) – phosphodiesterase PDE5 inhibitor – female sexual dysfunction [101] Tadalafil (Adcirca; Cialis; GF-196960; IC-351; LY-450190; Zalutia) – phosphodiesterase PDE5 inhibitor – female sexual dysfunction [102] Tadalafil sublingual (APC-8000) – phosphodiesterase PDE5 inhibitor – erectile dysfunction [103] Tadalafil/tamsulosin (CKD-397; tamsulosin/tadalafil) – combination of tadalafil (phosphodiesterase PDE5 inhibitor) and tamsulosin (α1-adrenergic receptor antagonist) – erectile dysfunction [104] Tadalafil/tamsulosin (YBH-1603) – phosphodiesterase PDE5 inhibitor – erectile dysfunction [105] Testosterone topical (ESP-210) – androgen (androgen receptor agonist) – female sexual dysfunction [106] Testosterone transdermal (FemTestosterone TDS) – androgen (androgen receptor agonist) – female sexual dysfunction [107] Testosterone transdermal (Luramist; testosterone MDTS; testosterone transdermal spray) – androgen (androgen receptor agonist) – female sexual dysfunction [108] TEMPE (Topical Eutectic Mixture for Premature Ejaculation) – undefined mechanism of action – premature ejaculation [109] UK-357903 (UK-357,903) – phosphodiesterase PDE5 inhibitor – erectile dysfunction [110] UK-390957 (UK-390,957) – serotonin reuptake inhibitor (SRI) – premature ejaculation [111] UK-447841 (UK-447,841) – neprilysin inhibitor – female sexual dysfunction [112] VML-670 (VML670; CEB-1555) – serotonin 5-HT1A receptor agonist – female sexual dysfunction, male sexual dysfunction [113]
== Disease relevance == Homozygous or compound heterozygous mutations in 3-phosphoglycerate dehydrogenase cause Neu–Laxova syndrome and phosphoglycerate dehydrogenase deficiency. In addition significantly shortening lifespan, PHGDH deficiencies are known to cause congenital microcephaly, psychomotor retardation, and intractable seizures in both humans and rats, presumably due to the essential signaling within the nervous system that serine, glycine, and other downstream molecules are intimately involved with. Treatment typically involves oral supplementation of serine and glycine and has been shown most effective when started in utero via oral ingestion by the mother. Mutations that result in increased PHGDH activity are also associated with increased risk of oncogenesis, including certain breast cancers. This finding suggests that pathways providing an outlet for diverting carbon out of glycolysis may be beneficial for rapid cell growth. It has been reported that PHGDH can also catalyze the conversion of alpha-ketoglutarate to 2-Hydroxyglutaric acid in certain variants. Thus, a mutation in the enzyme is hypothesized to contribute to 2-Hydroxyglutaric aciduria in humans, although there is debate as to whether or not this catalysis is shared by human PHGDH. Research results suggest that PHGDH could serve as a blood biomarker of Alzheimer's disease.
The basic process, patented in 1922, is called the Bosch–Meiser urea process after its discoverers Carl Bosch and Wilhelm Meiser. The process consists of two main equilibrium reactions, with incomplete conversion of the reactants. The first is carbamate formation: the fast exothermic reaction of liquid ammonia with gaseous carbon dioxide (CO2) at high temperature and pressure to form ammonium carbamate ([NH4]+[NH2COO]−):
Sources: en.wikipedia.org
== Further reading == National Academies of Sciences, Engineering, and Medicine (2019). A Research Agenda for Transforming Separation Science (Report). Washington, DC: The National Academies Press. doi:10.17226/25421. ISBN 978-0-309-49170-9.{{cite report}}: CS1 maint: multiple names: authors list (link)
Where the concentration of the enzyme is much less than the concentration of the substrate, the rate of reaction is directly proportional to the total enzyme concentration. The hydrolysis of a peptide bond however is an energetically favourable reaction. Recent experiments with both crude caricain and purified caricain indicated that the reaction which controls detoxification of a wheat gliadin digest at pH7.5 and 37 °C was indeed a 1st order reaction with a rate constant of 1.7 x 10 −4 sec.−1. The rate of reaction was followed by the disappearance of gliadin peptides which were toxic to rat liver lysosomes.
=== Methodology === A sample of water is collected in the field in a vial without headspace and capped with a Teflon septum or crimp top to minimize the escape of volatile gases. It is beneficial to store the bottles upside down to further minimize loss of analytes. Before analysis begins, the sample is brought to room temperature and temperature is recorded. In the laboratory, a headspace is created by displacing water with high purity helium. The bottle is then shaken upside down for a minimum of five minutes in order to equilibrate the dissolved gases into the headspace. It's important to note that the bottle must be kept upside down for the remainder of analysis if manually injected. A known volume of headspace gas is then injected onto a gas chromatographic column. An automated process can also be utilized. Individual components (gases) are separated and detected by either a thermal conductivity detector (TCD), a flame ionization detector (FID), or an electron capture detector (ECD). Using the known temperature of the sample, the bottle volume, the concentrations of gas in the headspace (as determined by GC), and Henry's law constant, the concentration of the original water sample is calculated.
=== Sevilla === 777 Partners' first investment in soccer was to purchase a minority stake in Spanish La Liga club Sevilla FC in 2018. In 2020, it elevated its share to 7.5%. 777 does not legally own shares in Sevilla as its involvement is as the owner of a group called Sevillistas Unidos S.L.. The latter organization has denounced 777 for listing Sevilla as one of "Our Portfolio Brands" on its website. Sevilla had been identified by 777 Partners as an opportunity for investment due to their focus on buying and selling players under sporting director Monchi. Their investment had been greeted with suspicion due to the club's history of being owned by local dynasties. 777 Partners' investment around Sevilla was allegedly funded in part by a loan from Oleg Boyko, a Russian businessman sanctioned by several countries for reported connections to the Russian state. In 2024, Boyko allegedly demanded 777's shares in Sevilla as collateral for his loan.
Sources: en.wikipedia.org
No. TB-500 is a short synthetic peptide matching residues 17 to 23 of thymosin beta-4, while the parent protein contains 43 residues. The fragment lacks the rest of the protein sequence, so the two are related but not identical.
It consists of leucine, lysine, lysine, threonine, glutamic acid, threonine, and glutamine in that order. The N-terminal leucine is usually acetylated in the forms described in catalogues.
Controlled human data is limited, and most published findings come from cell culture or animal work. This makes it difficult to state clinical effects with confidence.
TB-500 is a synthetic heptapeptide corresponding to a fragment of thymosin beta-4. It is used in laboratory research and is not an approved drug.