TB-500
Thymosin Beta-4 · 43-amino-acid tissue-repair peptide
TB-500 is the synthetic form of Thymosin β4 (Tβ4), one of the most extensively studied tissue-repair peptides in the preclinical literature. A naturally occurring 43–amino-acid peptide and the body's principal actin-sequestering molecule, Tβ4 has been investigated across decades of work spanning cell migration, angiogenesis, wound healing, and cardiac repair — including a landmark 2004 Nature study of post-infarction cardiac recovery and a human Phase III ophthalmic trial. Note that “TB-500” is sold both as the full-length 43-AA peptide and as a short Ac-LKKTETQ fragment; Ki Peptides ships the full-length Thymosin β4, which is what nearly all of the research below describes. The systemic evidence base is overwhelmingly preclinical. Regulatory agencies classify it as an unapproved drug, and it is prohibited in sport (WADA).
The short version
TB-500 is a lab-made version of Thymosin β4 — a natural peptide (a short chain of amino acids) that the body uses to organize the internal scaffolding of cells.
In animal studies it has mostly been looked at for tissue repair: helping wounds close, growing new blood vessels, helping cells migrate to where they are needed, and protecting the heart after injury. Most of that work is in rodents; the only human trials that reached late stages used an eye-drop form, not injections.
One important detail: products labeled “TB-500” are not all the same molecule. Some are the full 43-piece peptide and some are just a small fragment of it. Ki Peptides sells the full-length version, which is the one almost all the research is about.
It is not an approved drug, and it is banned in competitive sport.
Molecular identity
Specs
- Molecular weight
- ~4,963 g/mol (average)
- Molecular formula
- C212H350N56O78S
- Monoisotopic mass
- 4960.4863 Da
- CAS / UNII
- 77591-33-4 · 2D5MRE3SSY
- Sequence (43 AA)
- Ac-SDKPDMAEIEKFDKSKLKKTETQEKNPLPSKETIEQEKQAGESUniProt P62328
- Structure / class
- Full-length 43-residue β-thymosin; N-terminally acetylated actin-sequestering peptideUniProt P62328; PubChem CID 16132341
- Molecular target
- Monomeric (G-)actin — 1:1 sequestration; downstream cell migration, angiogenesis, NF-κB modulationUniProt P62328
- WADA status
- Prohibited at all times — S2.3 growth factors (Specified Substance)WADA 2026 Prohibited List
- Regulatory status
- Not approved by FDA or EMA; research-grade. Human trials limited to IV PK/safety + a Phase III ophthalmic programNo drug-approval record; PMID 34346165
Plain English
Mechanism
Thymosin β4 is best understood as the body's main actin-sequestering peptide — meaning it grabs and stores actin, the protein building-block cells use to assemble their internal scaffolding. It binds single actin units one-to-one and holds them in reserve, regulating how quickly a cell can build and take apart the actin filaments (the rope-like fibers) that drive movement — with a markedly stronger grip on the energized (ATP-bound) form than the spent (ADP-bound) form. The LKKTETQ motif (a short stretch, roughly the 17th–23rd amino acids in the chain) is the actin-binding region, and it is this fragment that some vendors isolate and sell separately as “TB-500.”
Research literature proposes that this actin control underlies Tβ4's effects on cell migration (cells crawling to where they are needed) and wound healing, with studies reporting more movement of skin cells (keratinocytes) and blood-vessel-lining cells (endothelial cells) and faster re-epithelialization — the regrowth of the skin's surface layer over a wound. In heart-injury models, a landmark study reported that Tβ4 teams up with two partner proteins (PINCH and integrin-linked kinase, ILK) to switch on Akt — a master pro-survival signal inside the cell — improving heart function and reducing scar after a tied-off coronary artery (an induced heart attack) in mice.
Review literature additionally describes pro-angiogenic activity (promoting the growth of new blood vessels, by raising VEGF — the chief vessel-growth signal — through several signaling chains), anti-inflammatory activity (blocking NF-κB, a master switch for inflammation), and anti-apoptotic activity (tilting the cell's internal balance away from programmed self-destruction). A small fragment the body naturally clips off the end of Tβ4 (Ac-SDKP) carries its own anti-fibrotic activity — reducing the buildup of scar tissue — plus a role in blood-cell regulation.
Across the body of work, the systemic (whole-body) evidence is overwhelmingly preclinical — lab-dish (in-vitro) and rodent models spanning several decades.
Sources:PMID 8506348PMID 25313062PMID 10469335PMID 15565145PMID 34992578UniProt P62328
Why people reach for it
Potential benefits
TB-500 is the recovery peptide people reach for alongside (or instead of) BPC-157 when soft-tissue healing is the goal. Here's what draws them to it.
- Get repair cells to the injury faster — Its headline appeal. As Thymosin β4, TB-500 regulates actin — the cell's internal scaffolding — to speed the migration of fibroblasts, keratinocytes, and vessel-lining cells into a wound, which the research links to faster re-epithelialization.
- Grow new blood supply into healing tissue — In the research it raises VEGF (the chief vessel-growth signal), promoting angiogenesis — the new blood vessels that feed a repair site — so it's reached for when getting circulation into stubborn, poorly-perfused tissue is the aim.
- A whole-body recovery reach, not just one joint — Because it circulates systemically rather than acting only at the injection site, people use it as a broad soft-tissue recovery signal across tendons, ligaments, and muscle.
- Calmer, less-scarred healing — Review literature describes Tβ4 dampening NF-κB inflammation and reducing fibrosis (via the Ac-SDKP fragment it sheds), which is part of the appeal for healing with less scar tissue.
- The classic partner to BPC-157 — It works through cell migration and angiogenesis while BPC-157 adds its own repair pathways — the most common recovery pairing in community use, covering more of the repair biology than either alone.
Sources:PMID 10469335PMID 15565145PMID 34992578PMID 25313062
What people reach for TB-500 for, drawn from what the research reports (systemic evidence is overwhelmingly preclinical) and how it's used — not proven human outcomes or medical claims.
Implied timing
Best time to dose
Implied best time
Evening
Most people take TB-500 in the evening, lining the repair signal up with the body's overnight recovery window — the same logic used for BPC-157.
- Overnight is when the body does most of its repairing — deep sleep brings the natural growth-hormone pulse, peak tissue regeneration, and the least mechanical load on healing tissue. An evening dose puts the migration-and-angiogenesis signal to work as that window opens.
- In the research, TB-500's dosing timing is set relative to the injury, not the time of day — heart and skin-wound studies start it at or near the moment of injury and track repair over the following days. Evening is a sensible human habit, not a studied clock schedule.
- TB-500 runs on a weekly-ish cadence (loading ~2× per week, then once weekly), so which day you dose matters more than the exact hour — and once a week, evening is a clean, consistent anchor.
- Human plasma half-life is short and dose-dependent (≈0.5–2 h IV), so the lasting value is the repair signal it leaves behind; sending that signal just before the long, still, recovery-focused overnight stretch is when it's most useful.
No study establishes an ideal time of day for TB-500 — this is reasoned from its mechanism and how it's actually used. As a rule of thumb most peptide dosing lands in the midday-to-evening window; for TB-500 the lean is evening, on whichever days it's dosed.
How to run it
Dosing & protocol
TB-500 is dosed here as a subcutaneous injection — the form the on-page calculator is built for. The community pattern is a loading phase while a fresh injury is actively healing, then a stepped-down maintenance phase. All numbers below are community and practitioner convention; the human trials of Thymosin β4 are IV pharmacokinetic studies, not recovery-dosing studies.
Community convention, not trial-proven: no validated systemic human dose exists — all human trials used intravenous administration for pharmacokinetics and safety. These figures are extrapolated from preclinical evidence and practitioner convention; TB-500 is not an FDA-approved drug.
Tiered dose ranges
Most protocols tier the weekly dose to injury severity and phase of the cycle.
- Loading — active injury:
- 2–2.5 mg twice per week (4–5 mg/week total) for 4–6 weeks — the front-loaded phase while tissue is actively healing. Run for as long as the injury is acute, then taper.
- Maintenance:
- 2–2.5 mg once per week, held for 4–6 weeks after the loading phase winds down, or as an ongoing low-signal for chronic connective-tissue work.
- General recovery / low dose:
- 500 mcg–1 mg once or twice per week — used by some as a light connective-tissue support dose outside of an acute injury context.
Subcutaneous administration
TB-500 is injected into subcutaneous fat. Proximity to the injured area is a common user preference, not a pharmacokinetic requirement — the peptide circulates systemically.
- Injection site:
- The abdomen (staying 2 inches clear of the navel), the love-handle area, the outer thigh, or near the injury site. Rotate sites between doses to prevent local irritation or lipohypertrophy.
- Measuring the dose:
- Drawn on a U-100 insulin syringe from the reconstituted vial. At the standard mix (10 mg / 2 mL = 5,000 mcg per mL): 500 mcg = 10 IU · 1 mg = 20 IU · 2 mg = 40 IU · 2.5 mg = 50 IU. The on-page calculator adjusts for any vial size.
- Time of day:
- No circadian rule for TB-500 — dosing timing in the research is injury-relative, not clock-relative. Many lean evening to line the repair signal up with overnight recovery (see Best time to dose above); with the weekly cadence the day matters more than the exact hour, so just hold a consistent slot.
- Food window:
- Subcutaneous TB-500 does not compete with food for absorption. Inject independently of meals.
Cycle & washout
TB-500's biology favors a defined block — loading hard while acute injury drives signal demand, then stepping down — rather than continuous indefinite dosing.
- Loading phase:
- 4–6 weeks at 2–2.5 mg twice per week. Begin as close to the acute injury as possible; the research models that showed the strongest signal started Tβ4 at or near the moment of injury.
- Maintenance phase:
- 4–6 weeks at 2–2.5 mg once per week, following the loading block. Re-assess whether to continue based on functional recovery.
- Washout:
- 4 weeks off after a full loading + maintenance block. Track a recovery marker (e.g. pain score, range of motion, hs-CRP) during the break to gauge whether to run another cycle.
- Total cycle:
- A common full run is 8–12 weeks (loading + maintenance), then washout. Acute injuries with clear resolution may warrant stopping maintenance early.
Reconstitution at a glance
The on-page calculator does this live; the quick reference for the default 10 mg vial + 2 mL bacteriostatic water:
- Mixing:
- 10 mg vial + 2 mL bacteriostatic water = 5,000 mcg per mL (5 mcg per µL). On a 100-unit (1 mL) insulin syringe: 500 mcg = 10 IU · 1 mg = 20 IU · 2 mg = 40 IU · 2.5 mg = 50 IU.
- Why 2 mL:
- The 2 mL standard dilution is compact enough for accurate dose measurement across the 500 mcg–2.5 mg range on a standard U-100 syringe without dealing with fractions of a unit at the low end.
Sources:PMID 34346165PMID 20536472PMID 10469335PMID 15565145
Substrate the signal needs
Nutritional cofactor precision
TB-500 signals cells to migrate, promotes new blood vessel growth (angiogenesis), and suppresses NF-κB inflammation around the repair site. The useful cofactors either amplify those signals or supply the structural raw materials the migrating cells need to actually rebuild — without the substrate, the migration signal leads nowhere.
Reasoned from Tβ4's actin-based cell-migration, angiogenic, and NF-κB-inhibiting mechanism plus established connective-tissue nutrition — not a TB-500 cofactor study. Supplement doses are community convention, not TB-500-specific findings.
Supply the tissue-rebuild substrate
Migration and angiogenesis are signals — the body still needs raw material to build new collagen, vessels, and matrix once those cells arrive.
- Hydrolyzed collagen + vitamin C:
- Hydrolyzed collagen 10–15 g daily provides glycine and proline — the dominant amino acids in the new collagen fibers the repair cells lay down. Vitamin C 500 mg alongside it is the cofactor for prolyl and lysyl hydroxylase, the two enzymes that cross-link collagen into its stable triple-helix; deficiency stalls fiber formation even when collagen precursors are plentiful. Take together, away from a heavy meal.
- Adequate total protein:
- 1.6–2.0 g/kg body weight per day — not a supplement but the most common substrate bottleneck in injured people eating below maintenance. Tissue-repair signal without protein supply is limited.
Amplify the angiogenic and perfusion work
TB-500's pro-angiogenic effect (raising VEGF to grow new vessels into the repair zone) depends on adequate nitric oxide in the microvasculature for the new vessels to dilate and perfuse the healing tissue.
- L-arginine or L-citrulline (NO substrate):
- L-arginine 3–6 g or L-citrulline 3 g daily — both raise nitric oxide (NO) production in endothelial cells, supporting perfusion of the repair zone the new vessels are serving. L-citrulline has better oral bioavailability; either form works. Take on an empty stomach or before exercise; skip if blood pressure runs low.
Supply minerals for matrix cross-linking
Zinc and copper are both required for the enzymatic steps that cross-link and harden the new collagen matrix — the final step that turns soft repair tissue into functional tendon, ligament, or skin.
- Zinc + copper (balanced):
- Zinc 15–30 mg daily (picolinate or bisglycinate) supports matrix metalloproteinases (the enzymes that remodel scar tissue) and is broadly required for wound healing. Pair with copper 1–2 mg bisglycinate — long courses of zinc without copper deplete copper, impairing the lysyl oxidase cross-linking step. Take zinc with food; copper can be taken at a different time.
Sources:PMC2589959PMC5793244
Combinations + timing
Stacking notes + timing windows
TB-500 works by promoting cell migration (via actin control) and angiogenesis (new vessel growth) — both structural repair levers. The best pairings bring a different mechanism: anti-inflammatory calming of the repair environment, or a complementary healing signal operating through a separate pathway.
User combinations reasoned from complementary mechanisms — not regimens studied head-to-head, and TB-500 itself has no validated systemic human dose. Doses are community convention; "reached for on" describes where users go, not a proven indication.
TB-500 + BPC-157
The canonical pairing — BPC-157 drives angiogenesis and gut/tendon healing through a different set of pathways; together they cover more of the repair biology than either alone.
- Why it works:
- TB-500's main lever is actin-based cell migration — getting repair cells into the wound — plus a VEGF-driven angiogenic signal. BPC-157 also promotes angiogenesis but through its own mechanism (FAK/paxillin pathway, upregulation of VEGFR2), and adds a strong gut-lining healing signal (EGF receptor activation) that TB-500 does not carry. Two distinct angiogenic pathways + migration + mucosal repair = more repair territory covered.
- The protocol:
- TB-500 on its loading/maintenance schedule (2–2.5 mg SC twice weekly loading, then once weekly maintenance). BPC-157 250–500 mcg SC once daily alongside it. Both can be injected at the same site or nearby, rotated across the abdomen/thigh.
- Outcome:
- The combination users reach for on soft-tissue injuries (tendons, ligaments, muscle tears) and post-surgical recovery. The most common TB-500 stack in community use.
TB-500 + KPV
An anti-inflammatory complement — KPV quiets the NF-κB-driven inflammatory environment around the repair site so TB-500's migration and angiogenesis signals operate in calmer tissue.
- Why it works:
- TB-500 suppresses NF-κB to a degree (one of its reviewed mechanisms), but KPV's entire purpose is intracellular NF-κB inhibition — a dedicated, potent brake on cytokine output. Running both means the pro-repair migration signal (TB-500) and the pro-calm cytokine suppression (KPV) operate simultaneously, rather than repair competing with active inflammation. Different levers, not the same one twice.
- The protocol:
- TB-500 on its standard loading/maintenance schedule. KPV 300–500 mcg SC once daily, run concurrently during the loading phase when local inflammation is highest, then tapered or stopped as the acute phase resolves.
- Outcome:
- Reached for on injuries with significant inflammatory component (acute sprains, tendinopathy, post-surgical swelling) where calming the environment around the repair matters as much as the repair signal itself.
Sources:PMID 34992578
Reconstitution math
Reconstitution calculator
Reconstitution calculator
Calculated for a 1 mL U-100 insulin syringe (100 units/mL).
Units per dose
10
Draw to this mark on a U-100 syringe
- Volume per dose
- 0.1 mL
- Doses per vial
- 20
- Concentration
- 5 mg/mL
One vial lasts
- Daily
- 20 days
- Every other day
- 40 days
- 5×/week
- 28 days
Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.
From the studies
Side effects from research
In human Phase I trials of full-length Thymosin β4 (given intravenously — into a vein — up to 1260 mg), no dose-limiting toxicities (side effects bad enough to cap the dose) or serious adverse events were reported; side effects were mild to moderate and comparable to placebo (an inactive dummy). The Phase III eye-drop (ophthalmic) trial likewise reported mostly mild eye-related side effects.
One genuinely open question deserves emphasis: because Tβ4 promotes both new blood-vessel growth (it is pro-angiogenic) and cell movement (pro-migratory) — the same activities that can feed a tumor — its relationship to cancer growth and metastasis (cancer spreading to new sites) is unresolved in the literature, with both tumor-suppressing and tumor-spreading findings reported across different models. There is no long-term human safety data. This safety picture is from limited human trials and animal studies.
Sources:PMID 34346165PMID 20536472PMID 36613994PMID 34992578
As reported in literature
Research dosing ranges
These are the doses actually reported in the published studies — the evidence the practical figures above lean on, shown separately so research data is never mistaken for a human recovery dose. Most are rodent injury models; the few human studies are intravenous (into a vein) pharmacokinetic and safety trials, not efficacy-dosing studies, and no validated systemic therapeutic dose exists. Doses are reported per kilogram of body weight (1 kg ≈ 2.2 lb) or as fixed amounts. Reported routes include topical (applied to the skin), intraperitoneal (into the abdominal cavity — a lab route), intramyocardial (directly into heart muscle), and intravenous administration.
| Dose | Route | Model | Outcome | Sources: |
|---|---|---|---|---|
| Topical / IP | Topical / IP | Rat (dermal wound) | +42% re-epithelialization (d4), +61% (d7) | PMID 10469335 |
| IP / intramyocardial | IP / intramyocardial | Mouse (myocardial infarction) | Improved ejection fraction, reduced scar | PMID 15565145 |
| 0.05–25 µg/kg | Intravenous | Human (Phase I PK/safety, n=84) | Dose-proportional PK; no dose-limiting toxicity | PMID 34346165 |
| 42–1260 mg | Intravenous | Human (Phase I PK/safety, n=40) | Dose-proportional PK; well tolerated | PMID 20536472 |
Labs before / during / after
Cofactor blood markers to track
Blood tests someone might track around a tissue-repair protocol — general recovery context, not Tβ4-specific:
hsCRP (high-sensitivity C-reactive protein), a blood marker of body-wide inflammation; a complete blood count plus ferritin (the body's stored-iron marker) for iron status and repair raw material — read ferritin alongside CRP, because ferritin also rises with inflammation and can read falsely high; and 25-hydroxy vitamin D (the standard vitamin-D blood test), given vitamin D's role in muscle, bone, and connective-tissue health.
Sources:PMC12782873WHO 2020PMC4530385
Quick answers
Frequently asked
Is TB-500 the same thing as Thymosin β4?
It depends on the product. The full-length TB-500 is the synthetic form of Thymosin β4, a natural 43–amino-acid peptide. Some vendors instead sell only a short fragment of it (Ac-LKKTETQ). Ki Peptides ships the full-length Thymosin β4, which is the form nearly all of the published research describes.
What is TB-500 most studied for?
In the research literature its most-developed areas are cell migration and wound healing, angiogenesis, and cardiac repair after infarction — alongside an ophthalmic formulation that reached a human Phase III trial for corneal healing.
Is TB-500 an approved drug?
No. Regulatory agencies classify it as an unapproved drug, and it is prohibited in sport by WADA at all times. This page presents research literature only and makes no therapeutic claims.
Has TB-500 been studied in humans?
Human studies of full-length Thymosin β4 are limited to intravenous pharmacokinetic and safety trials and an ophthalmic Phase III trial. There is no validated systemic therapeutic dose; systemic efficacy evidence is preclinical.
What is TB-500's half-life?
In human intravenous trials of full-length Thymosin β4, plasma half-life was short and dose-dependent (≈0.5–2 hours). No half-life has been established for the Ac-LKKTETQ fragment or for oral/subcutaneous routes.
Primary sources
References
- PubChem CID 16132341PubChem CID 16132341 (Thymosin β4)
- PubChem CID 62707662PubChem CID 62707662 (Ac-LKKTETQ fragment)
- UniProt P62328UniProt P62328 (human Thymosin β4 / TMSB4X)
- PMID 34346165J Cell Mol Med 2021 (Phase I rhTβ4, IV PK/safety)
- PMID 20536472Phase I synthetic Tβ4, IV PK/safety
- PMID 8506348PNAS 1993 (Tβ4 actin ATP/ADP affinity)
- PMID 25313062PNAS 2014 (structural basis, Tβ4–actin)
- PMID 15565145Nature 2004 (Tβ4, ILK/Akt, cardiac repair)
- PMID 357126782022 (Tβ4 vs cardiac fibrosis, mouse MI)
- PMID 10469335J Invest Dermatol 1999 (Tβ4 wound healing, rat)
- PMID 34992578Front. Endocrinol. 2021 (Tβ4 function & application review)
- PMID 36613994RGN-259 Phase III neurotrophic keratopathy
- WADAWADA Prohibited List (prohibited at all times)
- PMC2589959Ascorbate & collagen (review)
- PMC5793244Zinc in wound healing (review)
- PMC12782873hsCRP review
- WHO 2020WHO 2020 iron guideline
- PMC4530385Vitamin D & muscle (review)
Research use only · Not medical advice · Updated 2026-06-01