Source comparison
TB-500 Popular in Research: Comparison Across Study Models
Wound Healing (Dermal) Fibroblast migration, keratinocyte proliferation, angiogenesis 2–5 mg/kg subcutaneous in rodents; topical application in some studies 20–30% faster wound closure, increased collagen deposition, reduced scar width 7–14 days TB-500 consist
This comparison does not assign a generated winner or score.
- Wound Healing (Dermal)
- Fibroblast migration, keratinocyte proliferation, angiogenesis
- 2–5 mg/kg subcutaneous in rodents; topical application in some studies
- 20–30% faster wound closure, increased collagen deposition, reduced scar width
- 7–14 days
- TB-500 consistently accelerates closure in acute wound models but shows variable effects in chronic diabetic wounds where underlying vascular impairment limits angiogenesis.
- Myocardial Infarction (Cardiac)
- Cardiac progenitor cell differentiation, angiogenesis in ischemic tissue, anti-inflammatory signaling
- 6–10 mg/kg intraperitoneal in rodent MI models
- 18–25% reduction in infarct size, improved ejection fraction, reduced fibrosis
- 14–28 days
- Most robust evidence exists for TB-500 in cardiac repair. Multiple studies confirm functional improvement beyond scar reduction alone, suggesting genuine cardiomyocyte salvage rather than passive fibrosis attenuation.
- Spinal Cord Injury (Neurological)
- Axonal sprouting, neural progenitor proliferation, neuroinflammation suppression
- 6–12 mg/kg intraperitoneal in rodent contusion models
- 25–35% improvement in motor function scores, increased axonal density in lesion periphery
- 21–42 days
- Effects are delayed compared to cardiac models. Neural regeneration timelines are inherently slower. TB-500 shows consistent motor recovery improvements but doesn't reverse complete transection injuries.
- Stroke (Cerebrovascular)
- Angiogenesis in peri-infarct zones, blood-brain barrier stabilization, anti-apoptotic signaling
- 6–10 mg/kg intraperitoneal initiated 24–72 hours post-stroke
- 22–30% lesion volume reduction, improved sensorimotor function at 28 days
- TB-500's delayed administration window (up to 72 hours post-injury) makes it more practical than acute neuroprotectants that require immediate dosing. Persistent effects at 28 days suggest structural repair rather than transient neuroprotection.
- TB-500 popular in research across these models because it targets rate-limiting steps. Cell migration, vascular formation, inflammation resolution. That govern repair speed regardless of tissue type. The peptide doesn't fix everything, but it removes structural bottlenecks that otherwise slow endogenous repair mechanisms.