# TB-500 Dosage in the Research Literature and TB-500 Half-Life

> TB-500 dosage as reported in research: wide animal ranges for thymosin beta-4 (2-18 mg/kg in the stroke study), human Phase 1 IV doses of 42-1260 mg, and the absence of a validated human half-life for the fragment.

Animal ranges are wide, the one human dataset is full-length protein given intravenously, and community loading protocols have no controlled-trial basis.

## TB-500 Dosage Ranges Reported in the Research Literature

**TB-500 dosage** is reported here strictly as what was administered to which species, by which route, at which amount — never as a human recommendation. And almost all of it is full-length thymosin beta-4, not the 7-mer.

Animal studies span a wide range. Cardiac and neurological rodent models have used roughly `6-12 mg/kg`; the rat embolic-stroke dose-response used `2`, `12`, and `18 mg/kg` intraperitoneally, with a modeled optimum near `~3.75 mg/kg` and no benefit at the top dose [4]. A long-running muscular-dystrophy (mdx) mouse study used `150 µg` twice weekly intraperitoneally for six months. In vitro, picogram-to-nanogram amounts are bioactive — `~10 pg` was active in keratinocyte migration assays [3]. The spread is enormous because the route, the model, and the readout all differ; there is no single "research dose" of thymosin beta-4, let alone of TB-500.

## The one human dataset: Phase 1 intravenous

Human dosing data exist only for full-length thymosin beta-4. In a randomized, placebo-controlled Phase 1 study, synthetic thymosin beta-4 was given intravenously to 40 healthy volunteers — four cohorts of ten — as a single dose then daily for 14 days at `42`, `140`, `420`, or `1260 mg`. It was well tolerated to the top dose, with only infrequent mild or moderate adverse events and no dose-limiting toxicities or serious adverse events [6].

Two things to hold onto. The amounts are in *milligrams* by *intravenous* infusion under trial supervision — a different world from the subcutaneous community use TB-500 is associated with. And, again, the molecule was the full-length protein, not the `Ac-LKKTETQ` fragment.

## Routes studied

The routes in the literature are, predominantly, intraperitoneal in rodent efficacy studies; intravenous in the human Phase 1 and some cardiac models [6]; and topical or ophthalmic in corneal and dermal wound work and the dry-eye trials of RGN-259 [9]. Subcutaneous and intramuscular routes appear in community research use, but those are not the routes of controlled human efficacy trials.

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 it remains subject to proteolysis and freeze-thaw degradation — and the identity and purity of research-grade material is a recurring, unresolved concern [10].

## Why community loading protocols have no controlled-trial basis

The "load high for a few weeks, then maintain" protocols that circulate in athletic and peptide-research communities are not derived from controlled human trials and have no published clinical validation [10]. The stroke data argue directly against the premise: more was not better — `18 mg/kg` underperformed `12 mg/kg` in the dose-response [4]. A non-monotonic curve is the worst possible backdrop for an open-ended loading strategy, and there is no human pharmacokinetic anchor to calibrate against.

## TB-500 Half-Life and Pharmacokinetics

There is no validated human pharmacokinetic **half-life** for the TB-500 heptapeptide [10]. In the intravenous full-length thymosin beta-4 Phase 1 study, pharmacokinetics were dose-proportional and the half-life increased with dose [6]. Separately, anti-doping LC-MS work has characterized TB-500 and its metabolites — in equine plasma and urine, and in vitro — for *detection*, not for human PK [10].

So the honest summary is short. Dose-dependent, dose-proportional PK is documented for the full-length protein given intravenously; nothing equivalent is published for the fragment in humans. Detectability has been worked out for anti-doping purposes; a clean human clearance window for TB-500 has not. For where that detection science came from — racehorses — and what it means for sport, see [TB-500 WADA anti-doping status](/legal-status#wada).

## Form, stability, and why material identity complicates every dose

Dose is only as meaningful as the molecule behind it, and that is a live problem for TB-500. Research-grade material is supplied as a lyophilized powder, reconstituted in bacteriostatic or sterile water and kept refrigerated. As a short acetylated peptide, `Ac-LKKTETQ` is more chemically robust than the full-length protein, but it remains subject to proteolysis and freeze-thaw degradation — so handling matters to whatever the label claims.

The deeper issue is identity. In unregulated supply, the peptide's purity and correct sequence are not guaranteed, and a recurring concern across the literature is whether a vial sold as "TB-500" contains the heptapeptide, the full-length protein, a different fragment, or a degraded mixture [10]. That ambiguity does two things at once: it makes any stated research dose hard to interpret, and it muddies the anecdotal reports that circulate alongside the science. A figure like `2 mg/kg` only means something if the substance dosed is actually what it says on the vial — which is exactly the assurance the framework on [TB-500 legal status and FDA 503A category](/legal-status) is built to provide, and which research-grade supply does not.

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The TB-500 record drawn as a comic page — each repair figure, stroke dose and safety signal inked into its own panel and logged to its study, the fragment-versus-full-length caveat stamped on every page, with no clinic behind the gutters and nothing here dispensed or sold.