# TB-500 Dosage in the Research Literature: Doses, Routes, and Half-Life > TB-500 dosage in the research literature: the doses, routes and half-life data actually published — animal mg/kg ranges, the human Phase 1 IV doses of thymosin beta-4, and why no validated human protocol exists. What was administered, to which species, at which dose, by which route — the published dose context for TB-500 and thymosin beta-4, with the honest note that there is no validated human protocol for the heptapeptide. ## What the research doses actually were TB-500 dosage in the research literature is best read as a record of what was administered in studies, not as a protocol. The doses span a wide range because the molecules and models differ. Animal studies of full-length thymosin beta-4 used roughly 6–12 mg/kg in cardiac and neurological rodent models, and 2–18 mg/kg intraperitoneally in the embolic-stroke dose-response study, where the modeled optimum was near 3.75 mg/kg [4]. The mdx muscular-dystrophy study used 150 µg twice weekly intraperitoneally for six months [5]. Picogram-to-nanogram amounts are bioactive in vitro: roughly 10 pg of thymosin beta-4 was active in keratinocyte migration assays, and nanomolar concentrations stimulated hair-follicle stem cells [3][5]. These are study parameters reported for the species and assay used. This site does not convert any of them into a human dose, and no figure here is a recommendation. ## The human dose data: full-length thymosin beta-4 only The only human dose data are for the full protein, not the seven-mer. In the randomized, placebo-controlled Phase 1 study, synthetic thymosin beta-4 was given intravenously at 42, 140, 420 and 1260 mg — a single dose, then daily for 14 days — and was well tolerated to the top dose with no dose-limiting toxicities [6]. That trial defines the human dose range that has actually been studied: intravenous full-length thymosin beta-4, in a 14-day safety and pharmacokinetics setting. There is no comparable human dose study of the TB-500 heptapeptide. Community "loading then maintenance" protocols that circulate in athletic and peptide-research settings are not derived from controlled human trials and have no published clinical validation [5]. The non-monotonic stroke result — where 18 mg/kg underperformed 12 mg/kg in rats [4] — is a direct argument against assuming that more is better, and undermines the rationale behind such loading schemes. ## Half-life and pharmacokinetics in research No validated human pharmacokinetic half-life exists for the TB-500 heptapeptide. The TB-500 half-life question has no clean numeric answer for the seven-mer; what the literature offers is parent-protein and detection data. In the intravenous full-length thymosin beta-4 Phase 1 study, half-life increased with dose — the pharmacokinetics were dose-proportional rather than fixed [6]. Anti-doping LC-MS work characterizes TB-500 and its metabolites in equine plasma and urine for the purpose of detection, not to establish a human pharmacokinetic profile [13]. The practical reading: anyone citing a precise TB-500 half-life in hours is extrapolating beyond the published evidence. The honest statement is that the heptapeptide's human pharmacokinetics have not been characterized, and the only dose-proportional PK on record is for the full protein given intravenously. ## Why community "loading" protocols are not validated dosing The dose context above is a record of experiments, and it is worth being explicit about why it cannot be turned into a protocol. The species differ, the molecule differs (full-length protein versus the seven-mer), the routes differ, and the endpoints differ — a milligram-per-kilogram figure from an intraperitoneal rat stroke study is not convertible into a human regimen for the heptapeptide. No human dose-finding study of TB-500 has been done [6]. The non-monotonic stroke result makes the point sharply. In rats, 2 and 12 mg/kg improved neurological outcomes but 18 mg/kg did not [4] — a direct demonstration that, for this protein, more is not reliably better. "Loading then maintenance" schemes circulated in athletic and peptide-research communities are built on the opposite assumption and have no published clinical validation [5]. Presenting any such schedule as a dose would be presenting community lore as evidence, which this digest does not do. The accurate statement is that there is no established human dose for TB-500, and the published dose data describe other species, other routes, and mostly the full-length protein. ## Routes studied and material form The routes in the literature are specific to their models. Intraperitoneal injection predominates in rodent efficacy studies; intravenous dosing was used in the human Phase 1 of full-length thymosin beta-4 and in some cardiac models; topical and ophthalmic routes appear in the corneal, dermal-wound and dry-eye work with the clinical-grade RGN-259 formulation [16]. Inhaled administration appears in the recent pulmonary anti-fibrotic study [15]. Subcutaneous and intramuscular routes appear in community research use, but not in controlled human efficacy trials [5]. TB-500 is supplied as a lyophilized (freeze-dried) powder for research use, reconstituted in bacteriostatic or sterile water and kept refrigerated [16]. 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 unregulated research-grade material are a recurring concern [17]. That material-quality issue feeds directly back into the dosing question: when the identity, purity and sequence of the powder are not guaranteed, even a carefully measured amount is an uncertain dose, which is one more reason the published animal figures do not translate into a reliable human protocol [11]. --- A depth-layered reading of the TB-500 and thymosin beta-4 record — the seven-mer kept distinct from its full-length parent, the human-trial gap surfaced first, and no clinic, vendor, or prescription anywhere in the void.