TRANSECT 04 · FAQ
TB-500 FAQ — direct answers from the literature
Twenty-four questions, each surfaced as a single specimen against the dark. Quantitative claims cite the source.
What is TB-500?
A synthetic heptapeptide (Ac-LKKTETQ) corresponding to amino acids 17-23 of the endogenous protein thymosin beta-4. Investigated in preclinical models for tissue repair, angiogenesis, and cell migration. Molecular weight 889.0 Da [1][18]. It is not approved by the FDA for any human therapeutic indication and is restricted by major sports-governance bodies [16].
What does TB-500 do?
In animal studies it binds G-actin and modulates the actin cytoskeleton, promotes cell migration, supports angiogenesis through HIF-1α-driven VEGF upregulation [18], and downregulates inflammatory mediators implicated in tissue repair [9][20]. The downstream observables include accelerated dermal re-epithelialization [2] and improved collagen organization in repaired ligament [4].
What is TB-500 used for in research?
Investigated in preclinical models of tendon, ligament, muscle, cardiac, and corneal repair [1][2][4][6][12]. Not FDA-approved for any human indication. The clinical-trial program that has progressed furthest is the ophthalmic application of full-length Tβ4 (RGN-259) in dry eye and neurotrophic keratopathy [12][13][15].
TB-500 Peptide Overview
A short synthetic peptide derived from the N-acetylated active region of thymosin beta-4, used as a research tool to probe tissue-repair pathways. Sequence Ac-LKKTETQ. Molecular weight 889.0 Da. The LKKTETQ motif retains the actin-binding activity of the parent peptide [3][18].
Is TB-500 safe?
Long-term human safety has not been established. No completed Phase 3 trials of the LKKTETQ fragment. Banned by WADA and the Association of Racing Commissioners International for performance use [16]. Human safety data for full-length Tβ4 come from short-duration Phase 1 IV [14] and topical ophthalmic Phase 2 and Phase 3 trials [12][13][15]; these do not extrapolate to long-term systemic exposure to the fragment.
How long does it take for TB-500 to work?
Preclinical tendon- and dermal-healing studies report measurable histological changes within 2 to 4 weeks. The Malinda 1999 dermal study measured a 42% re-epithelialization increase by day 4 and 61% by day 7 in rats [2]. No validated human onset data exist.
Can I take TB-500 every day?
Most preclinical protocols use 1 to 3 doses per week, not daily. The Xu 2013 MCL study used 150 µg intraperitoneal every other day [4]. Daily dosing has not been studied in controlled trials. No validated daily human protocol exists in the peer-reviewed record.
Reported TB-500 side effects
Animal-study and anecdotal reports include injection-site reactions, lethargy, and theoretical concerns about angiogenesis-related effects on existing tumors grounded in the Cha 2003 preclinical findings [11]. Human side-effect data for the fragment are limited. See the TB-500 side effects page for the full adverse-event log.
TB-500 and cardiac repair research
Thymosin beta-4 has been investigated in murine post-MI models for myocardial repair — the Bock-Marquette 2004 Nature paper is the landmark specimen [6], replicated by Wei 2022 [recent2]. Phase 2 clinical trials of full-length Tβ4 (RGN-352) in acute MI did not complete due to manufacturing-quality issues.
Tendon-repair findings
Rat MCL-transection studies show improved collagen organization and significantly larger fibril diameters after Tβ4 administration at 150 µg intraperitoneal every other day [4]. Human tendon data are absent; no completed clinical trial has measured tendon outcomes with TB-500 in humans.
TB-500 and hair growth
Thymosin beta-4 is implicated in hair-follicle bulge stem-cell migration in mice, with MMP-2 upregulation as a mechanistic correlate [8][recent5]. No clinical hair-growth trials of TB-500 or full-length Tβ4 have been published. The hair-growth claim is preclinical and mechanistic, not clinically validated.
What is the difference between TB-500 and BPC-157?
TB-500 is a Tβ4 fragment acting via actin-sequestration and cell migration through the LKKTETQ motif [18]. BPC-157 is a gastric-pentadecapeptide derivative thought to act via VEGFR2 and nitric oxide pathways. Different molecules, different proposed mechanisms. Both are preclinical research peptides; neither is FDA-approved.
What is TB-500 half-life?
Reported plasma half-life for full-length Tβ4 in healthy human IV dosing is in the 0.95-2.1 hour range, dose-dependent [14]. Validated human pharmacokinetics for the LKKTETQ heptapeptide fragment have not been published. The short circulating half-life of native peptide motivated 2025 engineered tandem-Tβ4 work [recent1].
How long does TB-500 stay in your system?
Anti-doping laboratories report LC-MS detection windows in days to weeks depending on sample matrix [16][19]. Pharmacological clearance is substantially faster than the analytical detection window — Tβ4 plasma half-life is 1-2 hours [14], while detection persists for days. Detection sensitivity has been validated to 0.02 ng/mL in plasma and 0.01 ng/mL in urine [19].
How to reconstitute TB-500?
Lyophilized TB-500 is typically reconstituted with sterile or bacteriostatic water in laboratory protocols, with aqueous solutions refrigerated for stability. These notes describe laboratory handling for research use and are not dosing guidance.
Is TB-500 FDA approved?
No. TB-500 is not approved by the FDA for any human therapeutic use. The most advanced clinical program in the thymosin-beta-4 family is the ophthalmic application of full-length Tβ4 (RGN-259) in neurotrophic keratopathy and dry eye — that program has produced positive Phase 3 results in neurotrophic keratopathy [13] and mixed results in dry eye [15], but no FDA approval exists as of 2026.
Is TB-500 a steroid?
No. TB-500 is a peptide — a chain of seven amino acids (Ac-LKKTETQ), molecular weight 889.0 Da. It is not a steroid hormone. Peptides and steroid hormones are structurally and pharmacologically distinct molecule classes.
How does TB-500 work in research models?
Proposed mechanism centers on G-actin sequestration via the LKKTETQ motif [18], modulating cytoskeletal dynamics, cell migration, angiogenesis (HIF-1α stabilization and VEGF upregulation) [18], and downregulation of pro-inflammatory cytokines through NF-κB suppression [9][20]. ILK-Akt activation has been implicated in the cardiac-repair mechanism [6].
What does TB-500 stand for?
TB-500 is a research-compound code derived from the original supplier nomenclature for a thymosin-beta-4 active-fragment analog. It is not an FDA-recognized drug name. The molecule it labels is Ac-LKKTETQ — the N-acetylated 17-23 fragment of Tβ4.
Reported TB-500 dose ranges
Preclinical and equine protocols describe weekly doses in the 2-5 mg range divided across the week rather than daily administration [16]. Rodent preclinical doses are smaller per administration — 5 µg topical per wound [2][3], 60 µg/kg IP for dermal models [2], 150 µg IP every other day for MCL [4]. See TB-500 dosage for the full register.
Relationship to Thymosin Beta-4 (Tβ4)
TB-500 (Ac-LKKTETQ) is a synthetic peptide corresponding to amino acids 17-23 of the 43-residue endogenous protein thymosin beta-4 — it is the active region, not the full protein [18]. The seven-residue fragment retains the actin-binding activity of the parent peptide [3].
Routes of administration in studies
Preclinical studies report subcutaneous, intramuscular, intraperitoneal, and intravenous administration depending on the model and endpoint. Intraperitoneal is the most common rodent route [2][4][6]. Topical and ophthalmic application were used in the RGN-259 corneal trials [12][13].
Is TB-500 banned by WADA?
Yes. TB-500 (and thymosin beta-4) is prohibited at all times under WADA's S2 class as well as by the Association of Racing Commissioners International. Listed since 1 January 2012. Analytical detection by LC-MS is in active anti-doping use [16][19].
TB-500 Cycling Patterns in Reports
Anecdotal protocols describe a 4-6 week loading phase followed by a maintenance or off-cycle period. No validated cycle length exists in peer-reviewed human research. Preclinical study durations are dictated by tissue-repair endpoints rather than by cycling logic — see TB-500 dosage for the by-model protocol durations.