TB-500 dosage, as it appears in the studies.

TB-500 dosage in the research literature

The honest version of TB-500 dosage is that the studied doses belong almost entirely to full-length thymosin beta-4, not to the heptapeptide, and that no figure here is a human protocol. This page reads the doses that appear in the published record, attaches each to the molecule and species it was used in, and stops there. It is research context, not guidance.

Animal studies dose full-length Tβ4 across a wide range: roughly 6–12 mg/kg in cardiac and neurological rodent models, and 2, 12, and 18 mg/kg intraperitoneally in the embolic-stroke dose-response study, where the modeled optimum landed near 3.75 mg/kg ^[4]. The mdx muscular-dystrophy study used 150 µg twice weekly intraperitoneally for six months ^[5]. Human dosing exists only as a Phase 1 safety exercise: intravenous synthetic Tβ4 at 42, 140, 420, and 1260 mg, single dose then daily for 14 days ^[6]. Every one of those figures is the protein, and the human ones are a safety and pharmacokinetics study — designed to establish tolerability, not an effective dose for any condition.

The quantities can also be very small. Picogram-to-nanogram amounts are bioactive in vitro — roughly 10 pg was active in keratinocyte migration assays, and nanomolar Tβ4 stimulates hair-follicle stem cells ^[3][5]. That sensitivity is part of why a single "dose" number for TB-500 is meaningless without the route, the model, and the molecule attached: an in-vitro picogram and a 1260 mg intravenous human dose are both real figures from the same protein.

Routes studied

The routes in the literature track the models. Intraperitoneal injection predominates in rodent efficacy studies ^[4][5]. Intravenous administration was used for the human Phase 1 of full-length Tβ4 and for some cardiac models ^[6]. Topical and ophthalmic delivery carries the corneal and dry-eye work, including the RGN-259 trials of full-length Tβ4 ^[7][8].

Subcutaneous and intramuscular routes appear in community research use, but not in controlled human efficacy trials — so they sit outside the evidence base entirely. That matters because FDA's stated safety concern for this substance includes potential immunogenicity for certain routes of administration, which is a route-specific question the controlled human record does not answer for the fragment.

As supplied, TB-500 is a lyophilized powder reconstituted in bacteriostatic or sterile water and kept refrigerated; as a short acetylated peptide it is more chemically robust than the full-length protein but still subject to proteolysis and freeze-thaw degradation. The identity and purity of research-grade material is a recurring concern: peptide identity, purity, and correct sequence — full-length versus fragment — are not guaranteed in unregulated supply, which also complicates interpreting any anecdotal result.

Why the community protocols are not validated dosing

The figure that matters most for a reader is the one that is absent. The "loading then maintenance" protocols that circulate for TB-500 in athletic and peptide-research communities are not derived from any controlled human trial and have no published clinical validation ^[5]. They are conventions, not findings, and this site does not reproduce them as dosing.

The published data actively argue against the loading logic. The rat embolic-stroke study was explicitly dose-ranging, and it was non-monotonic: 2 and 12 mg/kg improved neurological function, but 18 mg/kg — the highest dose — did not, with the modeled optimum near 3.75 mg/kg ^[4]. More was not better; the highest dose lost the effect. A protocol built on "load high, then maintain" assumes a monotonic dose-response that the best dose-ranging study in the file does not show.

The other restraint is the species and molecule gap stacked on top of the route gap. Even if a rodent intraperitoneal milligram-per-kilogram figure for the full-length protein were a reliable guide — and animal kinetics do not translate to a human schedule — it would still be a figure for Tβ4, not for the Ac-LKKTETQ heptapeptide a reader would actually encounter. There is no validated bridge across either gap.

This is also why the dose-context tables and figures on this site stop at description. We can say, accurately, what was given in a given study: 2, 12, and 18 mg/kg intraperitoneally to Wistar rats over a defined schedule ^[4]; 42 to 1260 mg intravenously to healthy volunteers, single then daily for fourteen days ^[6]; 150 µg twice weekly for six months in mdx mice ^[5]. Each is a fact about an experiment. None becomes a recommendation by being restated, and the moment a number is lifted out of its species, route, molecule, and purpose, it stops being information and starts being a protocol the literature never wrote. For the same reason, this page reports no "typical" human dose for TB-500: there is no controlled human efficacy study of the fragment from which a typical dose could be drawn.

What is the half-life of TB-500?

There is no validated human pharmacokinetic TB-500 half-life for the heptapeptide. In the intravenous full-length Tβ4 Phase 1 study, half-life increased with dose and pharmacokinetics were dose-proportional ^[6] — but that characterizes the 4963 Da protein, not the 889 Da fragment. A short acetylated 7-mer and a 43-residue protein are different molecules with different clearance; the protein's PK is not a substitute for the fragment's.

Separately, anti-doping LC-MS work characterizes TB-500 and its metabolites in equine plasma and urine for detection — establishing that the compound and its breakdown products can be found, and for how long, in a doping-control context — not for human pharmacokinetics. So the precise answer is: the parent protein has dose-dependent PK from one Phase 1 study; the fragment has detection-method characterization in horses and no validated human half-life at all. Any specific "the half-life of TB-500 is X" figure circulating for the heptapeptide is not supported by a controlled human study.