TB500

TB-500 is a synthetic 7-amino-acid peptide (Ac-LKKTETQ) corresponding to residues 17–23 of full-length Thymosin Beta-4, with a molecular weight near 0.85 kDa versus ~4.96 kDa for the parent 43-mer [21]. It is the minimal G-actin–sequestering motif of TB-4, which is why research protocols favour the fragment over the full protein — the smaller size permits easier synthesis and higher purity [15]. JCSG.org supplies research-grade TB-500 to the UK with batch-specific HPLC verification.

No peer-reviewed human trial of TB-500 itself has been indexed by 2026. Published clinical work involves full-length thymosin beta-4, and orthopaedic reviews confirm that dosing, frequency, and duration "remain unknown" because no standardised human protocol has been established [9][18].

Key Takeaways

• TB-500 (Ac-LKKTETQ) is a 7-amino-acid fragment of thymosin beta-4, not the full 43-residue parent protein; the distinction matters for mechanism and pharmacokinetics
• No peer-reviewed human clinical trials of TB-500 exist as of 2026; all published dosing and safety data describe animal models or full-length thymosin beta-4
• TB-500 is not a controlled drug in the UK but holds no MHRA authorisation; it is sold for laboratory research purposes only
• The proposed mechanism is G-actin sequestration, which regulates cell migration and cytoskeletal remodelling, but long-term physiological effects and human safety remain unknown
• TB-500 is frequently paired with BPC-157 in lay protocols, but no peer-reviewed study has tested the combination

What this guide covers:

• How TB-500 differs from full-length thymosin beta-4 and why researchers use the fragment
• The cellular mechanisms TB-500 is proposed to activate, based on pre-clinical evidence
• Dose ranges reported in animal literature and why they do not translate to humans
• The legal status of TB-500 across the UK, EU, US, and Australia as of November 2026

What Is TB-500? A Plain-English Definition

TB-500 is a synthetic heptapeptide with the sequence Ac-LKKTETQ, corresponding to amino acids 17–23 of endogenous Thymosin Beta-4 and N-terminally acetylated for stability [1][26]. It is the minimal G-actin–sequestering motif of the parent 43-residue protein, supplied to laboratories as a lyophilised white powder for reconstitution in bacteriostatic or sterile water [1][26].

It is not full-length Thymosin Beta-4. TB-4 is a 43-amino-acid signalling protein (~4,963 Da); TB-500 is the 7-residue active fragment (~0.85 kDa), roughly one-sixth the mass [12][14]. Vendor pages and lay sources frequently conflate the two, but the distinction matters for mechanism, pharmacokinetics, and any extrapolation from TB-4 animal data to TB-500 protocols, because the missing 36 residues carry non-actin binding functions [12].

Quick reference

• Name: TB-500 (also written TB500, Thymosin Beta-4 fragment 17–23)
• Sequence: Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln (Ac-LKKTETQ)
• Length: 7 amino acids
• Approx. molecular weight: ~842–860 Da [13]
• Parent protein: Thymosin Beta-4, 43 aa, ~4,963 Da [14]
• Physical form: lyophilised powder

Readers arriving via the combination-protocol query cluster should also see our entry on BPC-157, which is frequently discussed alongside TB-500 despite the absence of any controlled combination study [18][20]. A wider index of peptides in our UK research library places TB-500 in context with related research compounds.

TB-500 vs Thymosin Beta-4: Why Use the Fragment?

The Ac-LKKTETQ fragment is used in preference to full-length Thymosin Beta-4 for three reasons: it retains the minimal G-actin–sequestering motif of the parent protein, costs far less to synthesise to high purity, and remains stable in aqueous solution [7]. Full-length TB-4 is a 43-residue, ~4,963 Da signalling protein; TB-500 is the 7-residue heptapeptide spanning residues 17–23 [7][9].

Shared activity: actin sequestration

Structural and biochemical work on beta-thymosins identified residues 17–23 as the minimal G-actin–binding domain of TB-4, with Ac-LKKTETQ occupying a defined groove on monomeric actin and stabilising it against polymerisation [5][6]. The 2026 UK mechanistic review translates this directly to TB-500, describing G-actin sequestration as its primary molecular function and the basis for downstream effects on cell migration, cytoskeletal remodelling, and repair signalling [4]. Pharmacology characterisations additionally describe TB-500 as exhibiting anti-fibrotic and wound-healing activity associated with modulation of the Akt pathway, though this sits downstream of the actin-binding event rather than as an independent mechanism.

Why researchers prefer the 7-mer

A 7-residue acetylated peptide can be made by standard solid-phase Fmoc synthesis in a single short run, with HPLC purity routinely above 98% and minimal deletion sequences [7]. A 43-residue protein requires either extended solid-phase peptide synthesis with cumulative coupling losses or recombinant expression [7]. Both longer synthesis routes introduce batch-to-batch variability that complicates dose-response work. The fragment also dissolves cleanly in bacteriostatic water without the aggregation and surface adsorption issues seen with longer beta-thymosins, which matters for reproducible in vitro concentrations [7].

What the fragment cannot do

TB-500 is not a like-for-like substitute for TB-4. The parent protein has nuclear localisation, interactions with Ku80 and other non-actin binding partners, and roles in angiogenesis and cardiac progenitor recruitment that depend on sequence outside residues 17–23 [4]. Extrapolating TB-4 animal data (typically low-mg/kg IP or IV dosing of the full protein) to TB-500 protocols therefore overstates what the fragment has actually been shown to do. The 2025 orthopaedic peptide primer makes this explicit, noting that dosing, frequency, and duration remain unknown for TB-500 specifically [1].

Comparison table

Property	Thymosin Beta-4 (full length)	TB-500 (Ac-LKKTETQ)
Length	43 aa	7 aa
Approx. MW	~4,963 Da [9]	~842–860 Da [8]
Synthesis	Long SPPS or recombinant; higher variability	Single short SPPS run; high purity routine
Solution stability	Aggregation-prone	Stable in bacteriostatic water
Actin sequestration	Yes [5]	Yes (retains minimal motif) [4][5]
Nuclear / non-actin roles	Yes [4]	No (sequence absent)
Human clinical data	Phase 1–2 in dry eye, cardiac [13]	None indexed as of 2026 [1][13]

Readers comparing TB-500 with adjacent repair peptides should see our entry on BPC-157; the wider set of peptides in our UK research library places both in context.

Mechanism of Action: How TB-500 Works at the Cellular Level

TB-500 acts on tissue repair primarily through G-actin sequestration, with secondary effects on Akt signalling, VEGF-mediated angiogenesis, and immune cell trafficking [15]. The heptapeptide Ac-LKKTETQ corresponds to residues 17–23 of thymosin beta-4 and retains the minimal motif needed to bind monomeric actin. Mechanistic studies of TB-4 are partially transferable to the fragment, but never fully so, because the missing residues carry independent functions [15][16].

Actin sequestration and cell migration

The Ac-LKKTETQ motif binds G-actin in a defined groove, stabilising the monomeric pool and modulating the polymerisation–depolymerisation equilibrium that drives lamellipodial extension [15][16]. Actin dynamics directly control the rate of leading-edge protrusion, which in turn governs how rapidly fibroblasts, keratinocytes, and endothelial cells can reorganise their cytoskeleton to migrate into a wound bed [15]. The 2026 UK mechanistic review frames G-actin sequestration as TB-500's primary molecular function, with downstream effects on cell migration and repair signalling following from that single biochemical event rather than from a distinct receptor [15].

Akt pathway modulation and anti-fibrotic signalling

Pre-clinical work on thymosin beta-4 has linked the peptide to attenuated Akt phosphorylation in fibroblast and cardiac models. This is the mechanism most often invoked to explain its anti-fibrotic profile, because Akt inhibition reduces myofibroblast differentiation [12]. Because Ac-LKKTETQ lacks the C-terminal residues that mediate several of TB-4's non-actin interactions, the extent to which TB-500 reproduces Akt-related anti-fibrotic effects in vivo is not settled. The 2025 orthopaedic primer explicitly states that indications, dosing, and duration for the fragment remain unknown [12]. Akt-pathway claims sourced from full-length TB-4 experiments are best treated as hypotheses for TB-500, not established findings.

Angiogenesis and VEGF upregulation

Thymosin beta-4 has been associated with VEGF upregulation and endothelial cell migration in rodent ischaemia and wound models, with capillary sprouting in granulation tissue dependent on endothelial motility [13]. The fragment's contribution to angiogenesis is mechanistically plausible through actin-dependent endothelial motility. Separate VEGF-induction data for Ac-LKKTETQ specifically were not indexed in the sources reviewed for this article as of 2026 [12][13].

Immune cell migration and long-term effects

TB-500 influences leucocyte trafficking, producing short-term anti-inflammatory effects in pre-clinical wound and tendon models through altered immune cell motility [7]. A March 2026 Spectrum Healthcare summary cited in UK-facing peptide reviews states: "TB-500 influences immune cell migration and activity. While short-term anti-inflammatory effects can be helpful, long-term immune regulation effects remain under investigation" [6]. No human immunological safety dataset for TB-500 is indexed in 2026, and the orthopaedic primer confirms that clinical parameters for the fragment are not established [18].

For combination-protocol context, see our entry on BPC-157; note that no peer-reviewed study has tested TB-500 plus BPC-157 as a defined co-therapy [1][2].

TB-500 Research Applications and Studied Effects

TB-500 has been studied almost exclusively in pre-clinical models across five overlapping areas: tissue repair and wound healing, musculoskeletal recovery, cardiac tissue, neurological injury, and anti-fibrotic signalling [10][11]. No approved human clinical trial has been published as of 2026 [10][11]. The 2025 orthopaedic primer states plainly that "human orthopaedic data are lacking" for TB-4 and its TB-500 derivative, and that indications, dosing, frequency, and duration remain unknown [10][4]. Most cited data describe the full-length 43-mer parent rather than Ac-LKKTETQ specifically.

Tissue repair and wound healing

Pre-clinical wound and dermal repair studies between 2020 and 2022 reported low-mg/kg parenteral or topical thymosin beta-4 in rodents with improved closure rates and re-epithelialisation [6]. Fragment versus full-length attribution is rarely specified, because most protocols do not distinguish between the two [6]. A January 2026 summary lists tissue repair, inflammation reduction, and muscle recovery as the principal applications discussed in the lay-research literature, while noting that clinical parameters are unestablished [12].

Musculoskeletal recovery: tendon, muscle, cartilage

The 2025 PubMed-indexed orthopaedic primer reviews TB-4/TB-500 in tendon and ligament healing models and concludes that no standardised dose or duration has emerged from animal work, because published protocols vary widely in dose, route, and outcome measurement [1][4]. Earlier equine tendon-injury studies described intra-lesional thymosin beta-4 at mg-range doses per lesion, repeated over several weeks, with improved histologic healing [2]. Whether the clinical material was TB-500 or full-length TB-4 is generally not stated [2]. Equine racing regulators list TB-4/TB-500 as prohibited performance-enhancing substances, which signals off-label field use rather than controlled dose-finding research [3][14].

Cardiac tissue studies

Rodent myocardial infarction work from 2007–2015 used approximately 6 mg/kg thymosin beta-4 IP or IV, reporting reduced infarct size and improved functional recovery [5]. These protocols predate routine fragment specification and should be read as TB-4 data rather than confirmed TB-500 data [5]. No 2024–2026 cardiac trial of Ac-LKKTETQ is indexed.

Neurological and anti-fibrotic models

Neurological and anti-fibrotic claims for TB-500 are extrapolations from full-length TB-4 organ-protection studies in the 2020–2022 window, which reported mg/kg dosing without fragment specification [6]. Published 2025–2026 research summaries both note that mechanistic plausibility exists but that direct TB-500 evidence for neuroprotection and anti-fibrosis is animal-only and frequently anecdotal in human contexts [11][12].

The BPC-157 pairing

TB-500 is frequently discussed alongside BPC-157 on the rationale that the two peptides act through non-overlapping pathways — BPC-157 via growth-factor and angiogenic signalling, TB-500 via G-actin sequestration and cytoskeletal dynamics [7]. No peer-reviewed pre-clinical study has tested the combination as a defined co-therapy [7][8]. A 2026 lay research guide explicitly frames combined use as "an off-label, user-driven practice rather than an evidence-based protocol" [8]. Stack claims extrapolate from single-agent animal data and are not supported by indexed combination trials [9].

For related compounds, explore the full UK peptides catalogue.

TB-500 Dosage: What Pre-Clinical Research Shows (2026)

No peer-reviewed human clinical trials establishing safe or effective doses of TB-500 (Ac-LKKTETQ) had been published as of 2026 [18]. The figures below are drawn exclusively from pre-clinical or full-length thymosin beta-4 research and must not be read as human dosage recommendations. The 2025 PubMed-indexed orthopaedic peptide primer states plainly that "indications, dosing, frequency and duration remain unknown" for TB-4/TB-500 [6].

Note. Every figure tabulated here describes animal or in-vitro work, most of it using full-length thymosin beta-4 rather than the confirmed Ac-LKKTETQ fragment. Allometric scaling, route-of-administration differences (IP and IV in rodents have no clean human equivalent), and species-specific clearance kinetics make direct mg/kg translation to humans scientifically unreliable. Community-circulated regimens from forums are not peer-reviewed and are not cited below.

Pre-clinical reference table

Study Model	Dose Used	Route	Frequency	Outcome Measured	Source & Year
Rodent myocardial infarction (TB-4, fragment unspecified)	~6 mg/kg	IP or IV	Single or repeated dosing windows	Reduced infarct size, improved functional recovery	[7] 2007–2015
Rodent/veterinary wound and organ protection (TB-4, fragment unspecified)	Low mg/kg range	Systemic or local	Variable	Wound closure, organ protection endpoints	[8] 2020–2022
Equine tendon injury (TB-4, fragment unspecified)	mg-range per lesion	Intralesional injection	Repeated over several weeks	Improved histologic tendon healing	[10] 2000s–2010s
Orthopaedic/sports-medicine summary (TB-4/TB-500)	Not standardised	Not standardised	Not standardised	Tendon and ligament repair signals; no clinical dosing standard	[9] 2025

Why these figures do not translate to humans

Three constraints matter here. First, allometric scaling from a 25 g mouse to a 70 kg human is not a linear mg/kg conversion; surface-area and metabolic-rate corrections routinely shift effective doses by an order of magnitude, because metabolic rate does not scale linearly with body weight [24]. Second, IP and IV rodent routes bypass absorption barriers that subcutaneous human use does not, altering bioavailability and peak concentration [24]. Third, the cited figures almost all describe the 43-residue parent peptide (~4,963 Da), not the ~842–860 Da Ac-LKKTETQ fragment marketed as TB-500 [24]. Pharmacokinetic comparability is unestablished.

Readers comparing protocols with BPC-157 should note that no combination dosing study is indexed [12].

TB-500 Side Effects: What the Evidence Says

No controlled human safety data exist for TB-500 (Ac-LKKTETQ) as of 2026, so any side-effect profile must be assembled from pre-clinical signals, mechanistic inference, and explicitly anecdotal human reports [15][16]. The honest position is that the risk picture is incomplete, not that the peptide is "safe" or "unsafe".

Pre-clinical signals

Rodent and veterinary studies of thymosin beta-4 at low-mg/kg parenteral doses report few overt acute toxicities at the dose ranges tested [13][14]. These studies were powered for efficacy endpoints (infarct size, wound closure, tendon histology) rather than systematic adverse-event capture, because the research question was repair, not toxicology [13][14]. The 2025 orthopaedic peptide primer states plainly that indications, dosing, frequency, and duration remain unknown, which applies equally to any defined safety margin [12]. Pre-clinical work also overwhelmingly used the full-length 43-mer, so adverse-event extrapolation to the ~860 Da Ac-LKKTETQ fragment is unestablished [24].

Theoretical mechanism-based risks

The most discussed theoretical concern is angiogenesis. Because TB-4 promotes endothelial migration and vessel formation, commentators have raised the question of whether existing occult tumour biology could be supported by exogenous peptide exposure, given that angiogenesis is required for tumour growth [15][16]. This is a mechanistic hypothesis, not a documented clinical signal, and no human dataset confirms or refutes it [15][16]. Immune-modulation uncertainty is similarly mechanism-derived rather than trial-derived; the 2025 primer frames TB-4/TB-500 as experimental with unknown long-term physiological consequences [5].

Anecdotal human reports and administration-related issues

Lay and clinic-adjacent sources describe transient lethargy, head-pressure sensations, and injection-site reactions (erythema, transient swelling, sterile abscess risk with poor reconstitution technique) following subcutaneous self-administration [16][17]. These are anecdotal, uncontrolled, and unverifiable against placebo, because no blinded trial has been conducted. Injection-site issues are a function of aseptic technique, bacteriostatic water quality, and needle gauge in research handling, not pharmacology per se [16].

What is absent

There are no published human TB-500 trials, no case series, no pharmacovigilance dataset, and no long-term follow-up cohorts as of 2026 [15][16]. Combination safety with BPC-157 is similarly unstudied [9]. Across the peptides in our UK research library, any "tolerability" claim sourced from marketing copy should be treated as marketing rather than evidence.

Legal and Regulatory Status: UK, EU, US & Australia (2026)

TB-500 has no marketing authorisation in any of the four jurisdictions reviewed here as of November 2026. It is sold lawfully only as a research chemical, and any presentation for therapeutic use brings it within prescription-medicine or unapproved-drug enforcement regimes [19][20][1]. Possession by individuals is not specifically criminalised under controlled-drug legislation in the UK, EU, US, or Australia, but supply for human use is, because the regulatory frameworks treat unlicensed therapeutic claims as violations.

United Kingdom

TB-500 is not listed under the Misuse of Drugs Act 1971 or the Misuse of Drugs Regulations 2001, and the MHRA has issued no marketing authorisation for the Ac-LKKTETQ fragment or full-length thymosin beta-4 [20]. Under the Human Medicines Regulations 2012, any substance presented as treating or preventing disease becomes a medicinal product requiring authorisation. UK research chemical suppliers accordingly restrict sales to laboratory research purposes only [19]. Regulatory status is determined by presentation and intended use, not the retail channel [19].

European Union

The EMA has issued no centralised marketing authorisation, CHMP opinion, or reflection paper on thymosin beta-4, TB-500, or Ac-LKKTETQ as of 2026 [27]. Member states regulate access via national competent authorities under unapproved-medicine and special-access frameworks; no EU-wide product registration exists [27][28].

United States

The FDA has not approved TB-500 for any indication, and 2024–2025 clinical reviews explicitly describe it as an unapproved new drug with unknown dosing, frequency, and duration [1][5]. TB-500 is not named on publicly available 503A/503B "allowed" bulks lists, and FDA enforcement guidance has treated thymosin beta-4-related peptides as unapproved substances unsuitable for routine compounding [2][8]. US compounding pharmacies that dispense it do so under physician direction within a contested regulatory space still subject to Office of Compounding Quality and Compliance updates [2].

Australia

The TGA has not registered TB-500 or thymosin beta-4 on the Australian Register of Therapeutic Goods, and neither is named explicitly in current S2–S9 Poisons Standard schedules [11]. Australian peptide-prescribing advisories from 2024–2025 indicate tightening TGA scrutiny, with access available, if at all, through compounding or Special Access Scheme pathways [12].

Regulatory Accuracy Notice

Last verified: November 2026. Regulatory status changes without notice. Verify directly with the MHRA, EMA, FDA Office of Compounding Quality and Compliance, and TGA before relying on any statement above. Researchers comparing legal frameworks across stacks such as BPC-157 and the wider set of peptides in our UK research library should treat each agent's status as independent.

TB-500 in Research Protocols: Practical Considerations

Research-grade TB-500 is supplied as a lyophilised powder in 5 mg vials at purities above 99%, reconstituted on-bench with bacteriostatic water for in vitro and animal-model work [1]. JCSG.org stocks research-grade TB-500 with batch-specific Certificates of Analysis.

For laboratory research use only — not for human consumption.

Reconstitution and Storage

Standard practice is to reconstitute the vial with 1–2 ml of bacteriostatic water (0.9% benzyl alcohol) to yield a workable stock concentration. Swirl rather than shake to avoid shearing the peptide, because mechanical stress can denature the structure [2]. Lyophilised TB-500 is typically stored at –20 °C protected from light; once reconstituted, refrigerated solutions are generally treated as short-shelf-life reagents on the order of weeks rather than months, because peptide solutions are prone to bacterial overgrowth and oxidation [2]. These are conventional peptide-handling steps and are not specific to any approved clinical protocol, since none exists [2][13].

Purity, Certificate of Analysis and Supplier Selection

A vendor-stated >99% purity figure is not equivalent to independent verification. Researchers should request a batch-specific Certificate of Analysis with HPLC and mass spectrometry traces confirming the Ac-LKKTETQ sequence (~0.85 kDa) rather than full-length thymosin beta-4 (~5.0 kDa), because misidentification is a documented supply-chain risk [23]. Grey-market channels carry documented identity and contamination risks; specialist suppliers issuing per-lot Certificates of Analysis are the minimum threshold for reproducible work [23].

JCSG.org sources TB-500 through Body Pharm (bodypharm.co.uk), a specialist research peptide manufacturer, so purity is backed by per-lot documentation.

Why TB-500 Is Paired with BPC-157

In published reviews, TB-500 and BPC-157 are described as mechanistically complementary: TB-500 acts via G-actin sequestration and cytoskeletal remodelling, whereas BPC-157 is described through growth-factor and angiogenic signalling pathways [7][8]. No peer-reviewed controlled study has tested the combination as a defined co-therapy as of 2026; stack protocols circulating online extrapolate from single-agent animal data [7][8][9]. For context across adjacent compounds, see the peptides in our UK research library.

Frequently Asked Questions About TB-500