Dosing in the literature
TB-500 dosing in research: what was administered, to which species, by which route
Research-context doses only — no human protocol exists for the fragment, and the figures below describe experiments, not recommendations.
What doses were actually used
TB-500 dosing figures in the literature come almost entirely from animal studies of full-length thymosin beta-4, and they span a wide range. Cardiac and neurological rodent models commonly used roughly 6 to 12 mg/kg; the embolic-stroke dose-response study tested 2, 12, and 18 mg/kg intraperitoneally and modeled an optimal near 3.75 mg/kg [4]. The muscular-dystrophy (mdx) study used 150 µg twice weekly intraperitoneally for six months [5].
Human dosing exists only for the parent protein in a single Phase 1 study: synthetic thymosin beta-4 given intravenously at 42, 140, 420, or 1260 mg — a single dose, then daily for 14 days — and well tolerated to the top dose [6]. At the other end of the scale, picogram-to-nanogram amounts are bioactive in vitro: roughly 10 pg was active in keratinocyte-migration assays [3].
None of these is a human use instruction, and none is for the TB-500 fragment in people. They are the conditions of specific experiments. The figures are reported here so the TB-500 research findings can be read with their doses attached.
Routes studied
Intraperitoneal injection predominates in the rodent efficacy studies [4][5]. Intravenous administration was used in the human Phase 1 of full-length thymosin beta-4 and in some cardiac models [6]. Topical and ophthalmic routes carry the corneal and dermal wound work, including the RGN-259 dry-eye formulation [7]. Subcutaneous and intramuscular routes circulate in community research use but do not come from controlled human efficacy trials [5].
Route is not a footnote here. The Phase 1 safety data are intravenous; the wound data are topical or intraperitoneal. A safety or efficacy result obtained by one route does not transfer to another, and the regulatory record specifically flags potential immunogenicity for certain routes — a point covered on the TB-500 legal status and 503A compounding page.
TB-500 half-life and dosing frequency in the literature
There is no validated human pharmacokinetic half-life for the TB-500 heptapeptide [5]. This is the direct, honest answer to one of the most-asked questions, and it is worth stating plainly rather than filling the gap with a number lifted from elsewhere.
The nearest human PK data are again for the full-length protein. In the IV Phase 1 study, half-life increased with dose — the pharmacokinetics were dose-proportional rather than fixed [6]. Separately, anti-doping LC-MS work has characterized TB-500 and its metabolites in equine plasma and urine, but that work exists to detect the compound, not to establish a human PK profile [15].
Because no validated human half-life exists, the dosing-frequency schedules that circulate in athletic and peptide-research communities — typically a "loading" phase followed by "maintenance" — have no basis in controlled human trials and no published clinical validation [5]. The non-monotonic stroke result, where 18 mg/kg underperformed 12 mg/kg, is a direct argument against assuming more or more-frequent is better [4].
Reconstitution and stability
TB-500 is supplied as a lyophilized (freeze-dried) powder for research use, reconstituted in bacteriostatic or sterile water and kept refrigerated [5]. As a short acetylated peptide, it is more chemically robust than the full-length protein, but it remains subject to proteolysis and freeze-thaw degradation, so repeated thaw cycles are a known way to lose material.
Identity and purity of research-grade material are a recurring concern. In unregulated supply, the correct sequence — and even whether a sample is the fragment or the full-length protein — is not guaranteed, which complicates interpreting any result obtained with it [5]. That quality question sits underneath every anecdotal report and is one more reason the controlled literature, not user accounts, anchors this digest.