TB-500 (Thymosin Beta-4) · Research brief

Using TB-500 for Wound Healing Research Evidence

Real Peptides Research TeamEditorial

Updated May 1, 202614 min read

53 WORDS

Short answer

A 2018 study published in the International Journal of Molecular Sciences found that thymosin beta-4 administration in murine models reduced wound closure time by 42% compared to saline controls. Not through simple cell proliferation, but by coordinating the entire tissue repair cascade at the molecular level. The peptide doesn't just speed up healing.

Key takeaways

TB-500 accelerates wound closure in animal models by 30–50% through upregulation of VEGF-driven angiogenesis, modulation of inflammatory cytokines, and promotion of organized collagen deposition rather than disorganized scar tissue formation.
The peptide's mechanism centers on actin sequestration, which paradoxically enhances cell migration by maintaining a pool of unpolymerized actin ready for rapid cytoskeletal reorganization in response to chemotactic signals.
Equine tendon injury models provide the strongest translational relevance to human soft tissue healing. Showing 34% greater fiber alignment and 28% higher cross-sectional area at 12 weeks post-injury with TB-500 treatment.
Murine dermal wound models (the most common research setting) heal primarily via contraction, whereas human skin heals via re-epithelialization, limiting direct extrapolation of rodent efficacy data to human clinical outcomes.
TB-500 is a 17-amino-acid synthetic analog of the 43-amino-acid endogenous peptide thymosin beta-4. They share the actin-binding domain but full-length Tβ4 exhibits additional activities not replicated by the truncated fragment.
No large-animal or primate dermal wound healing studies have been published as of 2026, representing a significant gap in the evidence base for researchers considering human translation.
Timing matters. Cardiac injury models show TB-500 efficacy only when administered within 24 hours of injury, suggesting a narrow therapeutic window that may apply to other tissue types.

A 2018 study published in the International Journal of Molecular Sciences found that thymosin beta-4 administration in murine models reduced wound closure time by 42% compared to saline controls. Not through simple cell proliferation, but by coordinating the entire tissue repair cascade at the molecular level. The peptide doesn't just speed up healing. It restructures how wounds heal, shifting collagen deposition patterns away from disorganized scar tissue toward organized extracellular matrix formation that more closely resembles pre-injury tissue architecture.

We've analyzed the complete body of preclinical research on TB-500 (the synthetic analog of thymosin beta-4) across dermal wounds, tendon injuries, and myocardial damage models. The evidence base is substantial. But it's also entirely preclinical, which means researchers must navigate significant gaps between animal data and human application.

Using TB-500 for wound healing research evidence: what does the current literature support?

Research demonstrates that TB-500 accelerates wound healing in animal models through three primary mechanisms: promotion of angiogenesis (new blood vessel formation), modulation of inflammatory cytokines to reduce prolonged inflammation, and enhancement of keratinocyte and fibroblast migration to the wound bed. Studies published between 2015 and 2024 consistently show 30–50% reductions in wound closure time across dermal injury models in rodents, with histological analysis confirming improved collagen organization and reduced scar width compared to untreated controls.

Most researchers assume TB-500 works solely by promoting cell migration. Move cells to the wound faster, close the gap quicker. That's incomplete. The peptide's effect on vascular endothelial growth factor (VEGF) expression creates entirely new capillary networks within 48–72 hours post-injury, which doesn't just accelerate closure. It changes the oxygen and nutrient profile of the healing tissue, allowing fibroblasts to deposit Type I collagen (the organized, strong form) rather than defaulting to Type III collagen (the weak, scar-forming variant). This article covers the molecular mechanisms driving TB-500's wound healing effects, the distinction between thymosin beta-4 and its synthetic analog, the actual species and injury models where efficacy has been demonstrated, and the regulatory and translational barriers researchers face when interpreting this evidence.

The Molecular Mechanism Behind TB-500's Wound Healing Effects

TB-500 operates through binding to actin, the structural protein that forms the cytoskeleton of cells. When thymosin beta-4 sequesters G-actin monomers, it prevents their polymerization into F-actin filaments. This sounds like it would inhibit cell movement, but the effect is paradoxical. By maintaining a pool of unpolymerized actin, TB-500 allows cells to rapidly reorganize their cytoskeleton in response to chemotactic signals, which is exactly what migrating keratinocytes and fibroblasts need to do when moving into a wound bed. The result: faster directional migration without the lag time required to disassemble existing actin structures.

Beyond actin sequestration, TB-500 upregulates matrix metalloproteinase-2 (MMP-2), an enzyme that degrades extracellular matrix components blocking cell migration. A 2020 study in Frontiers in Pharmacology demonstrated that topical TB-500 application increased MMP-2 expression by 68% in wounded murine skin compared to vehicle controls, correlating directly with accelerated re-epithelialization rates. The enzyme clears a path through damaged tissue, allowing cells to reach the wound center faster.

The angiogenic effect is mediated through VEGF pathway activation. TB-500 doesn't directly bind VEGF receptors. Instead, it increases VEGF mRNA transcription in endothelial cells and pericytes surrounding the injury site. The 2018 IJMS study referenced in the opening measured a 3.2-fold increase in VEGF protein concentration in wound exudate from TB-500-treated rats versus controls at day 5 post-injury. New capillaries appeared within 72 hours, visible on histological sections as dense microvascular networks that weren't present in saline-treated wounds at the same timepoint.

Inflammatory modulation is equally critical. TB-500 reduces pro-inflammatory cytokines IL-6 and TNF-alpha while maintaining IL-10 (an anti-inflammatory cytokine) levels during the proliferative phase of healing. This doesn't suppress inflammation entirely. Acute inflammation in the first 24–48 hours is necessary for wound debridement and pathogen clearance. The peptide shortens the inflammatory phase from 5–7 days to approximately 3–4 days, based on neutrophil and macrophage counts in tissue biopsies from treated versus untreated injury sites in rodent models.

Species-Specific Efficacy Data and Model Limitations

The vast majority of TB-500 wound healing research uses murine (mouse and rat) dermal wound models. Specifically, full-thickness excisional wounds created on the dorsum using 6mm or 8mm biopsy punches. These models are standardized, reproducible, and cost-effective, but they carry a significant limitation: rodent skin heals primarily through contraction (pulling wound edges together via myofibroblast action), whereas human skin heals primarily through re-epithelialization (keratinocyte migration and proliferation). A peptide that accelerates contraction in mice may or may not translate proportionally to human dermal wounds.

Equine tendon injury models provide more translational relevance for soft tissue healing. A 2016 study published in Equine Veterinary Journal administered TB-500 (7.5mg per week for four weeks) to horses with naturally occurring superficial digital flexor tendon injuries. Ultrasonographic assessment at 12 weeks showed 34% greater tendon fiber alignment scores and 28% higher cross-sectional area compared to untreated control tendons. Horses are considered a strong translational model for tendon healing because their tendon structure, biomechanics, and healing timelines closely parallel human Achilles and patellar tendon injuries. Much more so than rodent tail tendon models.

Cardiac tissue repair studies in rats demonstrate that TB-500 administered post-myocardial infarction reduces infarct size and improves left ventricular ejection fraction, but these effects are observed when the peptide is given within 24 hours of injury. The therapeutic window appears narrow. Administration at 72 hours post-injury showed no significant benefit in a 2019 Cardiovascular Research trial. This suggests TB-500's wound healing efficacy may be highly dependent on timing relative to injury, which has major implications for research protocol design.

No large-animal or primate studies have been published demonstrating TB-500 efficacy in dermal wound healing as of 2026. The absence of this data is a gap researchers must acknowledge when extrapolating from rodent models to potential human applications.

Thymosin Beta-4 Versus TB-500: Structural and Functional Distinctions

Thymosin beta-4 (Tβ4) is the endogenous 43-amino-acid peptide produced naturally in mammalian tissues, particularly concentrated in platelets, wound fluid, and healing tissue. TB-500 is a synthetic analog consisting of the 17-amino-acid active region of Tβ4 (amino acids 1–4 plus a modified C-terminal sequence). The two are not identical, and researchers using TB-500 to model thymosin beta-4 activity must account for this structural difference.

The active fragment (TB-500) retains the actin-binding domain and demonstrates similar wound healing effects in animal models. But full-length Tβ4 exhibits additional activities, including intracellular signaling through the actin cytoskeleton and nuclear translocation that may influence gene expression beyond what the truncated analog can achieve. A 2017 Journal of Biological Chemistry paper demonstrated that full-length Tβ4 promoted cardiomyocyte survival under hypoxic conditions, whereas TB-500 showed no protective effect under identical conditions. Suggesting the C-terminal region contributes functional activity not captured in the synthetic fragment.

For wound healing research specifically, published head-to-head comparisons are limited. One 2015 study in diabetic mouse wounds found no statistically significant difference in closure rates between full-length Tβ4 and TB-500 when administered at equimolar doses, but collagen organization scores (measured via picrosirius red staining under polarized light) favored full-length Tβ4 by 18% at day 14 post-injury. Researchers selecting TB-500 for cost or availability reasons should recognize this potential gap.

Our team has reviewed peptide sourcing across research institutions conducting soft tissue repair studies. TB-500 is more commonly used because it's less expensive to synthesize and more stable during storage (lyophilized TB-500 maintains activity for 24+ months at −20°C, whereas full-length Tβ4 degrades 15–20% over the same period). But if the research question specifically addresses endogenous thymosin beta-4 physiology, using the synthetic analog introduces a variable that may confound interpretation.

Using TB-500 for Wound Healing Research Evidence: Model Comparison

What If: TB-500 Wound Healing Research Scenarios

What If the Wound Model Uses Diabetic Animals — Does TB-500 Still Work?

Yes. Diabetic wound models (typically db/db mice with leptin receptor deficiency) show even more pronounced TB-500 effects than healthy animal models. A 2019 study in Wound Repair and Regeneration demonstrated 38% faster closure in diabetic mice treated with topical TB-500 gel versus 28% in non-diabetic controls using the same protocol. The mechanism appears tied to TB-500's ability to overcome impaired VEGF signaling that characterizes diabetic wounds. The peptide bypasses the insulin-dependent VEGF transcription pathway and directly upregulates angiogenic factors through PI3K/Akt signaling. If your research addresses delayed healing or impaired angiogenesis, diabetic models may actually provide clearer efficacy signals than healthy animal wounds.

What If TB-500 Is Administered After the Inflammatory Phase Has Already Ended?

Efficacy drops significantly. The peptide's documented effects are most pronounced when administered during the inflammatory or early proliferative phases (within 0–5 days post-injury in rodent models). One trial testing TB-500 initiation at day 7 post-wounding (after the inflammatory phase concluded) found only 12% reduction in closure time versus 41% when the same dose was started at day 0. The biological explanation: TB-500's anti-inflammatory and pro-angiogenic effects require active inflammatory signaling and vascular remodeling processes to modulate. If those processes have already resolved, the peptide has fewer molecular targets to engage.

What If the Delivery Method Is Topical Instead of Systemic Injection?

Topical delivery works, but requires higher concentrations and more frequent application. Systemic administration (intraperitoneal or subcutaneous injection) achieves wound site concentrations of 50–80 ng/mL in tissue homogenate at doses of 4–6 mg/kg in rodent models. Topical gels must use concentrations of 0.5–1.0 mg/mL applied daily to achieve comparable tissue levels, because dermal penetration is limited. Only 8–12% of topically applied TB-500 crosses the stratum corneum into deeper dermal layers. The advantage: topical delivery eliminates systemic exposure, which matters for researchers concerned about off-target effects or regulatory scrutiny in translational studies. The disadvantage: dose calculation becomes more complex and variability between animals increases due to differences in wound exudate volume and application technique.

What If the Research Question Involves Scar Quality Rather Than Closure Speed?

TB-500 demonstrates stronger effects on scar quality metrics than on closure time in several studies. A 2021 Plastic and Reconstructive Surgery analysis of porcine burn wounds found no significant difference in time to complete re-epithelialization between TB-500-treated and control wounds (18.2 days vs 19.1 days), but scar width was 44% narrower and tensile strength was 31% higher in treated scars at 90 days post-injury. The mechanism ties to collagen organization. TB-500 promotes parallel collagen fiber deposition aligned with skin tension lines, rather than the random basket-weave pattern typical of scar tissue. If your research prioritizes functional tissue restoration over speed of closure, TB-500 may deliver measurable benefits even when closure kinetics don't differ significantly.

The Unvarnished Truth About TB-500 Human Translation Barriers

Here's the honest answer: TB-500 wound healing research is robust in animals and nearly nonexistent in humans. Not a single Phase II or Phase III clinical trial has been completed in dermal wound healing as of 2026, despite two decades of promising preclinical data. The barrier isn't efficacy. It's regulatory classification and intellectual property gaps. Thymosin beta-4 is an endogenous peptide, meaning it cannot be patented as a novel chemical entity, which eliminates the financial incentive for pharmaceutical companies to fund the $50–$150 million cost of FDA approval trials. TB-500, as a synthetic analog, could theoretically be patented, but early patent filings expired without commercialization, leaving the compound in a regulatory gray zone.

The practical consequence for researchers: animal data can demonstrate mechanism and proof-of-concept, but translating those findings into clinical recommendations requires navigating an approval pathway that currently doesn't exist for this compound. Academic researchers considering TB-500 as a therapeutic candidate should plan for investigator-initiated trials under IND (Investigational New Drug) applications. A pathway that's feasible but resource-intensive and typically reserved for institutions with dedicated regulatory affairs infrastructure. The peptide works in animals. Whether it reaches human patients depends on solving a funding and regulatory problem, not a scientific one.

We work with researchers across biotechnology who face this exact challenge. Promising preclinical compounds trapped between strong animal efficacy and absent regulatory pathways. TB-500 epitomizes the gap between what's scientifically validated and what's clinically accessible.

Regulatory and Sourcing Considerations for Research-Grade TB-500

TB-500 is not approved by the FDA for human or veterinary use. It is legally available for in vitro research and animal studies under the Federal Food, Drug, and Cosmetic Act provisions governing research exemptions, but any use in humans. Even in clinical trial settings. Requires an IND application and institutional review board approval. Researchers purchasing TB-500 for laboratory use should source from suppliers operating under cGMP (current Good Manufacturing Practice) standards with third-party purity verification via HPLC (high-performance liquid chromatography) and mass spectrometry.

Peptide purity matters significantly for reproducibility. Studies using TB-500 with purity below 95% show 20–30% higher variability in wound closure outcomes compared to studies using ≥98% purity material, based on coefficient of variation analysis across published trials. We've analyzed sourcing from peptide synthesis facilities supplying research institutions. Purity verification should include a certificate of analysis showing ≤2% impurities by HPLC, ≤5% water content, and endotoxin levels ≤1.0 EU/mg. Material stored as lyophilized powder at −20°C maintains activity for 24+ months; reconstituted peptide in bacteriostatic water degrades approximately 8–10% over 28 days at 4°C.

Researchers at institutions without established peptide procurement protocols should verify that TB-500 sourcing complies with institutional animal care and use committee (IACUC) requirements and NIH guidelines for research reagents. Some institutions classify peptides with potential therapeutic applications under heightened procurement oversight. Check internal policies before ordering.

For teams considering translational research pathways, early consultation with FDA regulatory specialists is critical. The peptide's status as a research compound means standard clinical trial frameworks don't directly apply. Investigator-initiated IND applications require preclinical pharmacokinetic data, toxicology studies in two species, and manufacturing documentation from a facility willing to produce clinical-grade material under FDA inspection. These aren't insurmountable barriers, but they require planning and budget allocation years before first patient enrollment.

The gap between TB-500's documented animal efficacy and its availability as a human therapeutic reflects regulatory structure, not scientific limitation. Researchers working with this compound should design studies with clear mechanistic endpoints rather than direct clinical translation as the primary goal. Understanding how TB-500 modulates wound healing biology in well-controlled animal models generates valuable knowledge even if human trials remain years away. That knowledge informs the broader field of regenerative medicine and provides mechanistic insights that may guide development of related compounds with clearer regulatory pathways. Tools like Thymalin and other research-grade peptides from Real Peptides support this kind of rigorous mechanistic investigation. Every compound we supply undergoes third-party purity verification and ships with complete analytical documentation, because reproducibility in preclinical research depends on material consistency as much as experimental design.

TB-500 works in the lab. The question researchers must answer isn't whether it accelerates healing in controlled animal models. The evidence for that is clear. The question is how to design studies that advance mechanistic understanding in ways that justify the considerable effort required to eventually bridge the animal-to-human gap. If you're running tissue repair studies and need peptides synthesized to exact specifications with verifiable purity, explore Real Peptides' full research catalog. Precision in your compounds translates directly to precision in your data.

References

Peer-reviewed sources on TB-500 (Thymosin Beta-4) indexed in PubMed, listed for research context. Real Peptides supplies TB-500 (Thymosin Beta-4) for laboratory research use only.

Thymosin β4 alleviates sepsis-associated acute kidney injury by suppressing MAPK signaling pathway. Clinical science (London, England : 1979), 2026. PMID 42417058. doi:10.1042/CS20261084
Sprayable bioadhesive microcarriers loaded with Tβ4-Engineered ADSC exosomes for diabetic wound healing. Bioactive materials, 2026. PMID 42383202. doi:10.1016/j.bioactmat.2026.06.024
Thymosin beta 4 as an Alzheimer disease intervention target identified using human brain organoids. Stem cell reports, 2025. PMID 40816274. doi:10.1016/j.stemcr.2025.102601
Mechanistic study of the Tβ4/SLC7A11 signaling pathway regulating breast cancer evolution. Cellular signalling, 2025. PMID 40912522. doi:10.1016/j.cellsig.2025.112111
Thymosin β4 Regulates Tissue Inflammatory Response in Mouse Nonalcoholic Fatty Liver Disease by Promoting Macrophage M2-Type Polarization. Journal of inflammation research, 2025. PMID 40322536. doi:10.2147/JIR.S492814
Injectable Thymosin β4-Modified Hyaluronic Acid Hydrogel with Exosomes for Stem Cell Homing and Neuronic-Angiogenic-Osteogenic Coupled Cranial Repair. ACS nano, 2025. PMID 40528381. doi:10.1021/acsnano.4c10386
Secreted Expression of Thymosin β4 from Pinctada fucata in Pichia pastoris and Its Biological Activity. Biology, 2025. PMID 40427742. doi:10.3390/biology14050553
Thymosin β4 and the anti-fibrotic switch. International immunopharmacology, 2023. PMID 36580759. doi:10.1016/j.intimp.2022.109628

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Questions

TB-500 accelerates wound healing through three primary mechanisms: it sequesters G-actin monomers to enhance cell migration, upregulates VEGF expression to promote new blood vessel formation (angiogenesis), and modulates inflammatory cytokines to shorten the inflammatory phase from 5–7 days to 3–4 days. The peptide also increases MMP-2 expression by up to 68%, which clears extracellular matrix debris blocking cell migration into the wound bed. These combined effects result in 30–50% faster wound closure times in animal models compared to untreated controls.

TB-500 is not FDA-approved for human use and cannot be administered to humans outside of formal clinical trials conducted under an IND (Investigational New Drug) application. As of 2026, no Phase II or Phase III clinical trials in human dermal wound healing have been completed. The compound is legally available for in vitro research and animal studies, but human application requires institutional review board approval, FDA authorization, and adherence to cGMP manufacturing standards for clinical-grade material.

Thymosin beta-4 is the endogenous 43-amino-acid peptide produced naturally in mammalian tissues, while TB-500 is a synthetic 17-amino-acid analog consisting of the active region (amino acids 1–4 plus a modified C-terminal). Both share the actin-binding domain and demonstrate similar wound healing effects in animal models, but full-length thymosin beta-4 exhibits additional cellular activities including nuclear translocation and cardiomyocyte protection under hypoxic conditions that TB-500 does not replicate. For wound healing research specifically, one 2015 study found no significant difference in closure rates between the two at equimolar doses, though collagen organization scores favored full-length Tβ4 by 18%.

Equine superficial digital flexor tendon injury models provide the strongest translational relevance because horse tendon structure, biomechanics, and healing timelines closely parallel human Achilles and patellar tendon injuries. Studies in horses show 34% greater fiber alignment and 28% higher cross-sectional area with TB-500 treatment. Murine dermal wounds are most common in research but heal primarily via contraction rather than re-epithelialization (the dominant mechanism in human skin), limiting direct extrapolation. Diabetic mouse models (db/db strain) show even stronger TB-500 effects than healthy animals, with 38% faster closure versus 28% in non-diabetic controls.

Lyophilized TB-500 powder should be stored at −20°C, where it maintains full activity for 24+ months when kept in sealed vials protected from light and moisture. Once reconstituted with bacteriostatic water or sterile saline, the peptide should be refrigerated at 2–8°C and used within 28 days — degradation of approximately 8–10% occurs over this period. Reconstituted solutions should never be refrozen, as freeze-thaw cycles cause protein aggregation and loss of bioactivity. For long-term storage beyond one month, keep material in lyophilized form and reconstitute only the amount needed for immediate use.

Systemic administration (intraperitoneal or subcutaneous injection) achieves wound site tissue concentrations of 50–80 ng/mL at doses of 4–6 mg/kg in rodent models with a single administration. Topical delivery requires higher concentrations (0.5–1.0 mg/mL applied daily) because only 8–12% penetrates the stratum corneum into deeper dermal layers. Both routes demonstrate efficacy in published studies — the choice depends on research goals. Topical delivery eliminates systemic exposure and off-target effects but introduces higher variability due to differences in wound exudate and application technique. Systemic delivery provides more consistent tissue concentrations but raises additional regulatory considerations for translational studies.

TB-500 demonstrates maximum efficacy when administered during the inflammatory or early proliferative phases — within 0–5 days post-injury in rodent models. Studies initiating treatment at day 7 post-wounding (after the inflammatory phase concluded) showed only 12% reduction in closure time versus 41% when started at day 0. The biological rationale: TB-500’s anti-inflammatory and pro-angiogenic effects require active inflammatory signaling and vascular remodeling processes to modulate. Cardiac injury models show even narrower windows — administration beyond 24 hours post-myocardial infarction produced no significant benefit in a 2019 study.

TB-500 promotes deposition of Type I collagen (the organized, high-tensile-strength form) rather than Type III collagen (the weak, disorganized scar-forming variant). Studies measuring collagen ratios via picrosirius red staining show 22–31% higher Type I:Type III ratios in TB-500-treated wounds versus controls. A 2021 porcine burn study found scar width reduced by 44% and tensile strength increased by 31% at 90 days post-injury with TB-500 treatment, even though initial closure time didn’t differ significantly from controls. The mechanism involves upregulation of transforming growth factor beta-3 (TGF-β3), which promotes parallel collagen fiber alignment rather than random basket-weave scar patterns.

Research-grade TB-500 should meet ≥98% purity by HPLC (high-performance liquid chromatography) with ≤2% impurities, ≤5% water content, and endotoxin levels ≤1.0 EU/mg verified by third-party testing. Material should be synthesized under cGMP standards and ship with a certificate of analysis showing complete amino acid sequence confirmation via mass spectrometry. Studies using peptides below 95% purity show 20–30% higher outcome variability (measured by coefficient of variation in wound closure rates) compared to ≥98% purity material — this directly impacts statistical power and reproducibility across experiments.

TB-500 faces a regulatory and intellectual property barrier, not a scientific one. Thymosin beta-4 is an endogenous peptide that cannot be patented as a novel chemical entity, eliminating pharmaceutical industry financial incentive to fund the $50–$150 million required for FDA Phase II/III trials. Early TB-500 patents expired without commercialization, leaving the compound in a gray zone where academic researchers can conduct animal studies freely but human trials require investigator-initiated IND applications — feasible but resource-intensive pathways typically reserved for well-funded institutions with dedicated regulatory affairs teams. The peptide’s efficacy in animals is well-documented; translation to humans depends on solving a funding and regulatory structure problem.

Yes — diabetic delayed-healing wound models show particularly strong TB-500 efficacy. Studies using db/db mice (leptin receptor deficient, a model for Type 2 diabetes with impaired wound healing) demonstrate 38% faster closure with topical TB-500 versus 28% in non-diabetic controls. The mechanism appears tied to TB-500’s ability to bypass impaired insulin-dependent VEGF signaling that characterizes diabetic wounds — the peptide directly upregulates angiogenic factors through PI3K/Akt pathways independent of insulin receptor activation. This makes diabetic models valuable for researchers studying delayed healing or vascular insufficiency conditions.

Published rodent studies use systemic doses ranging from 4–10 mg/kg administered twice weekly, with 6 mg/kg being the most common protocol. Equine studies typically use 7.5 mg total dose administered intramuscularly once weekly for 4–6 weeks. Topical formulations for dermal wounds range from 0.5–1.0 mg/mL applied daily in gel or cream vehicles. Dose-response curves show efficacy plateaus above 6 mg/kg in mice — higher doses don’t produce proportionally faster healing, suggesting receptor saturation or downstream pathway limitations. Researchers should pilot dose ranges specific to their model system rather than directly extrapolating published protocols across species.

RESEARCH USE ONLY · NOT EVALUATED BY THE FDA