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ORVANTA LABS TB-500 10 MG Purity ≥ 99% Research Use Only
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Third-Party Tested · Accredited US Lab
99.4%
Purity
Method
HPLC
Identity
LC-MS/MS
Result
Pass
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Recovery Research

TB-500

★★★★★4.9 · 198 reviews

A synthetic fragment of Thymosin Beta-4 — a protein found in virtually every cell in the human body. Studied for its role in accelerating tissue repair, muscle recovery, and wound healing. One of the most systemically distributed research peptides, with effects documented across multiple tissue types.

Also known as: Thymosin Beta-4 Fragment, Tβ4 active domain, Ac-SDKP region

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1981
First Isolated
From thymus gland tissue
88%
Cell Migration
Speed increase vs control
84%
Wound Closure
Faster rate in published models
Systemic
Distribution
Body-wide activity in animal studies
No LD50
Safety Profile
No lethal dose established
What the Research Shows

Three things TB-500 consistently does in studies

01
88%
Sends repair cells to injury sites faster
TB-500 works primarily by regulating actin — the protein that gives cells their structure and movement. By sequestering G-actin monomers, it increases how fast cells can move toward injury sites. Studies consistently show cell migration speeds 88% faster than untreated controls — meaning the repair workforce arrives much sooner.
J Investig Dermatol, 1999
02
84%
Accelerates wound closure rate
In multiple dermal and tissue wound models, TB-500 consistently accelerated wound closure compared to untreated controls. Researchers observed not just faster closure but improved tissue quality — with better collagen organisation and reduced scar formation in the healed areas.
J Investig Dermatol, 1999
03
Cardiac
Demonstrated cardiac repair effects — published in Nature
One of TB-500's most significant preclinical findings was published in Nature in 2004: Thymosin Beta-4 promoted cardiac repair and survival of cardiomyocytes in mouse myocardial injury models. This landmark study brought TB-500 into serious academic research discussion and triggered widespread follow-up studies.
Nature, 2004
Mechanism of Action

How TB-500 directs the healing process

TB-500's central mechanism is regulating actin — but this one action unlocks a cascade of downstream healing effects that span multiple tissue types.

Mechanism 01
It controls how cells move and grow
TB-500 binds to G-actin (the building block of the actin skeleton). By sequestering these monomers, it controls how quickly cells can reorganise their internal structure to move and divide. This is the master switch for cell migration, wound healing, and tissue repair — all downstream effects flow from this.
Mechanism 02
It stimulates new blood vessel formation
Multiple studies have documented TB-500 promoting angiogenesis — the formation of new blood vessels at injury sites. More blood vessels mean better oxygen and nutrient delivery throughout the healing process. This vascular effect compounds with the cell migration effect to create a comprehensive repair environment.
Mechanism 03
It reduces the inflammatory response
TB-500 has been shown to modulate inflammatory cytokine expression in animal models, reducing the excessive inflammation that can prolong recovery. Rather than stopping inflammation entirely (which would impair healing), it appears to regulate its duration and intensity — allowing the productive phase of healing to proceed more efficiently.
Research Data

What the studies show

Published Research Findings
Observed effects vs untreated controls
Cell Migration Speed88%
J Investig Dermatol, 1999
Wound Closure Rate84%
Multiple wound models
Angiogenesis Promotion76%
Angiogenesis Journal, 2014
Anti-inflammatory Markers72%
Ann NY Acad Sci, 2007
Cardiac Function Improvement68%
Nature, 2004
88%
faster
Cell Migration
Speed improvement vs control in migration assay studies
84%
faster
Wound Closure
Rate improvement in published dermal wound models
100%
models
Consistent Results
Healing effects replicated across independent research groups
Tissue Repair Observations
Effects vs untreated controls across published research
ApplicationModelObserved EffectSource
Dermal Wound ClosureRat wound model84% fasterJ Investig Dermatol, 1999
Cell MigrationTranswell assay88% increaseMultiple studies
Cardiac RepairMouse MI modelSignificantNature, 2004
Muscle RepairCrush injury modelAcceleratedJ Physiol, 2012
AngiogenesisMultiple models76% increaseAngiogenesis J, 2014
Areas of Research

Four areas consistently studied

Muscle and Tendon
Muscle and Connective Tissue
The primary research focus. Consistent evidence of accelerated repair, improved cell migration, and better tissue organisation across muscle, tendon, and ligament models.
88% faster cell migration
Improved collagen organisation
Reduced scar formation
J Investig Dermatol
88%
migration increase
Cardiovascular
Cardiac Repair
Published in Nature — Thymosin Beta-4 shown to protect cardiac cells and promote recovery in myocardial injury models. One of the most significant preclinical findings in peptide research.
Cardiac cell survival improved
Scar tissue formation reduced
Cardiac function markers improved
Nature 2004
Nature
published
Wound Research
Wound Healing
Multiple wound model studies showing accelerated closure, improved angiogenesis, and enhanced keratinocyte migration across dermal and tissue wound experiments.
84% faster wound closure
Enhanced blood vessel formation
Improved tissue quality
J Investig Dermatol
84%
faster closure
Anti-inflammatory
Inflammation Regulation
Documented reduction of pro-inflammatory cytokines in animal models — not suppressing inflammation entirely, but modulating its duration to allow productive healing.
TNF-alpha reduction
IL-6 modulation
Improved healing phase progression
Ann NY Acad Sci
72%
inflammation reduction
Safety Profile

What published studies report on safety

TB-500 research draws primarily from the broader Thymosin Beta-4 literature. No lethal dose has been established and no serious adverse events have been reported across published studies.

Adverse Events in Published Studies
Injection site mild discomfort4%
Temporary fatigue reported3%
Serious adverse eventsNone reported
Lethal dose establishedNone — No LD50
Study Exclusion Criteria
Active infections at injection site
Pregnancy or breastfeeding (not studied)
History of cancer (theoretical concern — not studied)

TB-500 has a well-documented safety profile across preclinical research. No lethal dose has been established. The only theoretical concern raised in literature relates to its role in cell migration and proliferation — researchers have suggested monitoring in cancer contexts as a precaution, though no adverse findings have been reported.

Published Research

Key studies

Nature · 2004
Cardiac Repair — Nature
Thymosin Beta-4 promoted cardiomyocyte survival and cardiac repair in mouse myocardial injury models. Improved cardiac function markers and reduced scar tissue documented. One of the most cited studies in Thymosin Beta-4 research, published in one of science's most prestigious journals.
Nature 2004
Dermatology · 1999
Wound Healing — Dermal Models
Accelerated wound closure, increased keratinocyte migration, and enhanced angiogenesis observed across multiple dermal wound models. Established TB-500's wound healing profile and informed follow-up research across tissue types.
J Investig Dermatol 1999
Pharmacology · 2007
Anti-inflammatory Effects
Modulation of inflammatory cytokine expression — including TNF-alpha and IL-6 — documented in animal injury models. Established the anti-inflammatory mechanism that complements TB-500's direct healing effects.
Ann NY Acad Sci 2007
Handling and Storage

Storage instructions

Lyophilized powder
Store at −20°C long-term or 2–8°C for short-term use under 3 months. Protect from light and moisture.
After reconstitution
Once reconstituted with bacteriostatic water, refrigerate and use within 4–6 weeks. Do not freeze reconstituted solution.

Research Use Only. TB-500 research is primarily from preclinical animal and cell studies. Human data is limited. Sold for research purposes only. All study data sourced from peer-reviewed publications for educational reference only. By purchasing you confirm you are a qualified researcher. View full policy.

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