Frequently Asked Questions About TB-500

TB-500 is a synthetic heptapeptide (Ac-LKKTETQ) corresponding to amino acids 17–23 of Thymosin Beta-4 (Tβ4), an endogenous 43-amino-acid actin-sequestering protein. It weighs 796.9 daltons and carries the central actin-binding domain responsible for Tβ4's wound-healing and cell-migration activity.^[1] It is studied primarily in rodent and equine wound-healing, angiogenesis, and tissue-repair models. It is not approved for human use.

TB-500 is proposed to bind free G-actin monomers, regulate cell migration, promote angiogenesis via VEGFR2/VEGF signaling, and suppress NF-κB-driven inflammation.^[1][15] These effects have been observed in preclinical muscle, tendon, cardiac, and neural tissue models. No validated human mechanism data exists for the TB-500 fragment specifically.

The most commonly reported side effect is mild injection site redness and discomfort. Transient fatigue, nausea, and dizziness have been reported anecdotally. No controlled human safety trial has characterized the side effect profile for injectable TB-500. The full-length Tβ4 protein IV Phase I study found no serious adverse events in 54 healthy volunteers,^[16] but that data applies to the parent protein, not this fragment.

No human clinical trials have evaluated injectable TB-500 safety. Animal studies show a generally favorable short-term profile. The FDA classifies TB-500 as a Category 2 bulk drug substance of safety concern, prohibiting pharmaceutical compounding for humans. All injected human use exists outside a regulated clinical framework; safety for humans is undemonstrated.^[16][20]

TB-500 promotes angiogenesis via VEGF upregulation — the same pathway used by tumors. In mouse melanoma models, Tβ4 overexpression produced 4.3x more lung metastases and 4.4x greater tumor vascularization.^[12] In human colon cancer tissue, Tβ4 stabilizes HIF-1alpha → VEGF pathway components.^[13] No human study confirms or rules out cancer promotion from exogenous TB-500; researchers flag this as an unresolved concern.

Long-term human safety is undocumented. The longest preclinical data point is a 6-month dystrophic mouse study showing no overt toxicity.^[11] No multi-year human cohort data exists. Absence of reported harms in uncontrolled settings is not equivalent to demonstrated safety in a controlled trial.^[20]

Yes. TB-500 and Thymosin Beta-4 are prohibited by WADA under the Prohibited List category for peptide hormones, growth factors, and related substances — banned both in- and out-of-competition.^[18] A Canadian athlete received a 4-year ineligibility period in connection with a non-analytical positive for combined use with another peptide. The US Department of Defense has adopted aligned prohibitions. Competitive athletes — in any sanctioned sport — should treat TB-500 as a prohibited substance.

As of 2026, no completed Phase I/II human clinical trial on TB-500 (Ac-LKKTETQ) has been published. NCT07487363 is registered on ClinicalTrials.gov but its completion status was unconfirmed at time of research. All published human safety data covers the full Tβ4 protein (IV Phase I trial;^[16] topical ophthalmic Phase II trial^[23]) — the parent protein, not the heptapeptide fragment.

No validated human half-life exists for injectable TB-500 fragment. Rat metabolite data shows the primary metabolite Ac-LK peaks at 0–6 hours; Ac-LKK is detectable up to 72 hours.^[19] Full-length Tβ4 IV in humans has a half-life of 0.5–2.08 hours^[16] — not directly applicable to the fragment. Dosing frequency from this data cannot be determined.

Thymosin Beta-4 (Tβ4) is a 43-amino-acid endogenous protein. TB-500 is a synthetic 7-amino-acid fragment (positions 17–23) corresponding to the active actin-binding domain.^[1] Most mechanistic and human safety literature covers the full protein; TB-500-specific studies are primarily doping-control and metabolite detection work.^[18][19] Effects attributed to TB-500 are often extrapolated from Tβ4 research.

BPC-157 is a 15-amino-acid gastric-peptide fragment studied primarily in gut and tendon models via localized injection, with proposed NO-synthase mechanisms. TB-500 is a 7-amino-acid Tβ4 fragment with systemic angiogenic and cell-migration effects via G-actin sequestration and VEGF signaling. Different mechanisms, different tissue systems, different evidence bases. No peer-reviewed head-to-head study exists.

In rodent models, local Tβ4 delivery (1 µg in fibrin sealant) produced superior biomechanical properties and collagen organization in surgically transected rat MCL at 4 weeks.^[9] Multiple equine studies supported musculoskeletal use in horses. Human tendon trial data is entirely absent.

Tβ4 promotes hair growth in rat and mouse models via activation, migration, and differentiation of hair follicle stem cells, including in transgenic Tβ4-overexpressing mice.^[4] TB-500 shares the actin-binding properties underlying this effect. Human evidence specifically for hair growth is sparse.

In rat coronary artery occlusion models, Tβ4 at 5.37 mg/kg IP reduced infarct size by 43% at 28 days.^[6] In mouse coronary artery ligation models, Tβ4 promoted cardiomyocyte survival and upregulated Akt/ILK survival signaling.^[5] These are rodent models; whether these effects translate to humans is unknown.

In rat TBI models, Tβ4 at 30 mg/kg IP (initiated 6 hours post-injury) improved sensorimotor recovery, reduced cortical lesion volume, and enhanced hippocampal neurogenesis.^[7] In a rat embolic stroke model, the optimal dose for day-56 neurological recovery was calculated at 3.75 mg/kg.^[8] Human neurological data for TB-500 is absent.

Mild redness, swelling, and discomfort at the injection site are the most consistently reported effects. Severity appears low in documented reports; systemic reactions are uncommon. No controlled study has systematically characterized injection site reaction incidence for TB-500 in any species.

Not reliably. A 2023 analytical study found that commercially available TB500/TB1000 products are "not systematically consistent with their descriptions."^[17] Contamination risks — endotoxins, incorrect sequences, undisclosed excipients — are independent of the compound's pharmacology and represent a distinct safety hazard in the unregulated supply chain.

Yes on both counts. TB-500 promotes new blood vessel formation via VEGF/HIF-1alpha upregulation^[13] — the proposed mechanism of tissue repair benefit and the same pathway exploited by tumors. Mouse melanoma overexpression studies showed 4.3x more lung metastases and 4.4x greater tumor vascularization.^[12] Researchers flag this as an unresolved safety concern. No human study resolves it.