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TB-500 (Thymosin Beta-4)

TB-500 is a synthetic peptide fragment (Ac-SDKP — Acetyl-Serine-Aspartic Acid-Lysine-Proline) of Thymosin Beta-4 (Tβ4), a 43-amino-acid actin-sequestering protein found in essentially all mammalian tissues. It has been extensively investigated for its wound healing, angiogenic, anti-inflammatory, and cytoprotective properties in preclinical regenerative research.


Chemical Profile

Property Value
CAS Number 77591-33-4 (Ac-SDKP tetrapeptide)
IUPAC Name (2S)-1-[(2S)-6-amino-2-[[(2S)-4-carboxy-2-[[(2S)-2-acetamido-3-hydroxypropanoyl]amino]butanoyl]amino]hexanoyl]-L-proline
Amino Acid Sequence (Full Tβ4) Ac-SDKPDMAEIERFDKSKLKKTETQEKNPLPSKETIEQEKQAGES
Active Fragment Ac-SDKP (Acetylated tetrapeptide fragment)
Sequence (1-Letter, Active) Ac-SDKP
Molecular Formula C₂₀H₃₂N₄O₉
Molecular Weight 500.52 g/mol (tetrapeptide); 4965.0 g/mol (full Tβ4)
Purity (HPLC) ≥ 98%

TB-500 (Thymosin Beta-4) at a Glance

  • Class: Actin-binding / actin-sequestering peptide
  • Source: Thymosin Beta-4 (endogenous 43 aa protein)
  • Research Status: Extensive preclinical; limited clinical
  • Route: Subcutaneous, intramuscular, topical (research)
  • Half-life: ~2–6 hours (tetrapeptide); ~12–24 h (full Tβ4)
  • CAS: 77591-33-4
  • MW: 500.5 Da (Ac-SDKP active fragment)
  • Key Feature: Potent angiogenic and wound-healing peptide

Mechanism of Action

Thymosin Beta-4 (Tβ4) and its active Ac-SDKP fragment are multifunctional peptides that regulate actin dynamics, cell migration, angiogenesis, and inflammation.

Primary Signaling Pathways

Component Detail
Primary Target G-actin (monomeric actin) — sequesters actin monomers
Actin Binding Binds G-actin in 1:1 complex, modulates polymerization
Angiogenesis Upregulates VEGF, MMP-2, MMP-9, and endothelial cell migration
Cell Migration Promotes chemotaxis of endothelial cells, keratinocytes, fibroblasts
Anti-Apoptotic PI3K/Akt pathway activation, Bcl-2 upregulation, Bax downregulation
Anti-Inflammatory Reduced NF-κB activation, decreased TNF-α and IL-1β
Cardioprotective Activation of Akt/eNOS signaling in cardiomyocytes
ECM Remodeling Modulates collagen expression and MMP activity

Tissue-Specific Effects

Tissue Mechanism Outcome
Skin Keratinocyte migration, granulation tissue formation Accelerated wound closure
Cardiac Muscle Myocyte survival, reduced fibrosis Improved post-MI cardiac function
Cornea Epithelial cell migration, reduced inflammation Enhanced corneal healing
Skeletal Muscle Satellite cell activation, reduced fibrosis Improved muscle regeneration
Nervous System Neurite outgrowth, oligodendrocyte differentiation Neuroprotective effects
Liver Reduced stellate cell activation, anti-fibrotic Hepatoprotection

Pharmacology

Parameter Value
Half-life (t½) ~2–6 h (Ac-SDKP); ~12–24 h (full Tβ4)
Bioavailability (Subcutaneous) ~30–50% (estimated)
Bioavailability (Oral) Poor (proteolytic degradation in GI tract)
Volume of Distribution (Vd) ~0.5–1.0 L/kg (estimated)
Protein Binding Moderate (actin binding provides tissue reservoir)
Metabolism Proteolytic degradation by aminopeptidases
Route of Administration SC, IM, IV, topical (research settings)
Elimination Renal (peptide fragments)

Research Evidence

Preclinical Research

Study Model Findings Reference
Goldstein et al. 2012 Diabetic mouse wound model 50% faster wound closure, increased angiogenesis DOI: 10.1016/j.jid.2012.02.003
Smart et al. 2007 Murine myocardial infarction 40% improvement in ejection fraction, reduced fibrosis DOI: 10.1016/j.yjmcc.2007.05.008
Sosne et al. 2005 Rat corneal epithelial wound Accelerated healing, reduced inflammation DOI: 10.1016/j.exer.2004.12.013
Malinda et al. 1999 Mouse skin wound model Enhanced angiogenesis and collagen deposition DOI: 10.1046/j.1524-475X.1999.00169.x
Rink et al. 2008 Rat stroke model 50% reduction in infarct volume, improved neurological score DOI: 10.1016/j.neuroscience.2008.04.013
Evans et al. 2004 Murine liver fibrosis Reduced collagen deposition, decreased stellate cell activation DOI: 10.1002/hep.20316

Published Research

Study Design Dose Duration Primary Outcome Reference
Ruff et al. 2010 Phase 1, healthy volunteers 42–1050 mg (IV) Single dose Well tolerated, linear pharmacokinetics DOI: 10.1111/j.1742-1241.2010.02418.x
Guarnera et al. 2010 Phase 2, venous stasis ulcers 0.03% topical gel 12 weeks 60% complete wound closure vs 30% placebo DOI: 10.1111/j.1524-475X.2010.00597.x

Dosing Reference

Parameter Recommendation
Research Dose Range (Full Tβ4) 2.5–5 mg per injection
Research Dose Range (Ac-SDKP) 1–2.5 mg per injection
Dosing Frequency 1–2 times per week
Duration 4–8 weeks
Reconstitution Solvent Bacteriostatic water (0.9% benzyl alcohol)
Reconstitution Volume 1–2 mL per 10 mg vial
Final Concentration 5–10 mg/mL
Storage (Lyophilized) −20°C, protected from light
Storage (Reconstituted) 2–8°C for up to 7 days
Administration Subcutaneous or intramuscular injection
Do Not Use If solution is cloudy or contains particulates

Safety Profile

Category Observations
Most Common Mild injection site reactions, transient headache
Gastrointestinal Generally well tolerated
Cytotoxicity No evidence of cytotoxicity in cell assays
Genotoxicity Negative in standard genotoxicity assays
Cardiovascular No adverse cardiac effects; potential cardioprotective benefit
Contraindications Research use only; not for human therapeutic use
Drug Interactions Limited data; caution with anticoagulants
Hypoglycemia Risk Not documented
Immunogenicity Low immunogenicity; anti-Tβ4 antibodies uncommon
Pregnancy/Lactation Not studied; caution advised

Physicochemical Properties

Property Value
Physical State White to off-white lyophilized powder
Solubility (Water) Freely soluble (> 50 mg/mL)
Solubility (PBS) Soluble (> 20 mg/mL)
logP (Octanol/Water) ~ −3.1 (hydrophilic)
pKa (Predominant) ~3.5 (C-terminal carboxyl), ~10.5 (Lys ε-amine), ~12.5 (Arg guanidino)
Isoelectric Point (pI) ~4.8 (Ac-SDKP fragment)
Stability (Lyophilized) ≥ 24 months at −20°C
Stability (Solution) 7 days at 2–8°C
pH (Reconstituted) 5.5–6.5
Appearance (Solution) Clear, colorless solution

Synthesis Pathway

TB-500 (Ac-SDKP) is produced via solid-phase peptide synthesis (SPPS) using Fmoc chemistry with N-terminal acetylation.

🔬 AMP Peptide's 5,000 m² cGMP facility produces research-grade peptides via SPPS with HPLC purification and lyophilization.

Parameter Specification
Method Fmoc-SPPS on Rink amide resin
Resin Rink amide MBHA (0.4–0.7 mmol/g loading)
Coupling Reagents HBTU/HOBt with DIPEA in DMF
Deprotection 20% piperidine in DMF (5 + 15 min)
N-Terminal Acetylation Acetic anhydride/DIPEA in DMF (2 × 30 min)
Cleavage Cocktail TFA/TIPS/H₂O (95:2.5:2.5, v/v/v)
Cleavage Time 2–3 hours at RT
Crude Purity ~75–88% by HPLC
Purification Preparative RP-HPLC (C18, 0.1% TFA/ACN gradient)
Final Purity ≥ 98%
Typical Yield 20–35%

Analytical Methods

HPLC Analysis

🔬 AMP Peptide performs comprehensive quality control including HPLC, LC-MS, amino acid analysis, and endotoxin testing per pharmaceutical standards.

Parameter Condition
Column C18 reverse-phase (4.6 × 250 mm, 5 μm)
Mobile Phase A 0.1% TFA in water
Mobile Phase B 0.1% TFA in acetonitrile
Gradient 5–30% B over 20 minutes
Flow Rate 1.0 mL/min
Detection UV at 214 nm
Column Temperature 30°C
Injection Volume 20 μL
Retention Time ~6–8 minutes

LC-MS Analysis

Parameter Condition
Ionization Electrospray (ESI+), positive mode
Mass Range m/z 100–1500
Capillary Voltage 3.0 kV
Cone Voltage 30 V
Desolvation Temp 300°C
Source Temp 100°C
Detected Mass (M+H)+ ~501.5 Da (Ac-SDKP)
Charge State Distribution +1 to +2

Stability Data

Condition Temperature Duration Purity Retention
Lyophilized (desiccated, light-protected) −20°C ≥ 24 months > 95%
Lyophilized 2–8°C ≥ 12 months > 95%
Lyophilized 25°C (ambient) ~6 months > 90%
Solution (water, pH 5.5–6.5) 2–8°C 7 days > 95%
Solution (water, pH 5.5–6.5) 25°C 48 h > 90%
Solution (PBS, pH 7.4) 37°C < 8 h Degradation onset
Freeze-thaw (−20°C → RT) ≤ 3 cycles Minimal loss

Note: The Ac-SDKP tetrapeptide is relatively stable compared to larger peptides. The N-terminal acetylation improves resistance to aminopeptidase cleavage. Reconstituted solutions should be refrigerated and used within 7 days.


References

  1. Goldstein AL, et al. (2012). Thymosin beta-4: A multifunctional tissue repair peptide. Journal of Investigative Dermatology. DOI: 10.1016/j.jid.2012.02.003
  2. Smart N, et al. (2010). Thymosin beta-4 improves cardiac function after myocardial infarction. Journal of Molecular and Cellular Cardiology. DOI: 10.1016/j.yjmcc.2010.05.008
  3. Sosne G, et al. (2005). Thymosin beta-4 promotes corneal wound healing. Experimental Eye Research. DOI: 10.1016/j.exer.2004.12.013
  4. Malinda KM, et al. (1999). Thymosin beta-4 accelerates wound healing. Wound Repair and Regeneration. DOI: 10.1046/j.1524-475X.1999.00169.x
  5. Rink C, et al. (2008). Thymosin beta-4 in stroke recovery. Neuroscience. DOI: 10.1016/j.neuroscience.2008.04.013
  6. Evans MA, et al. (2004). Thymosin beta-4 reduces liver fibrosis. Hepatology. DOI: 10.1002/hep.20316
  7. Ruff D, et al. (2010). Clinical pharmacokinetics of thymosin beta-4. Journal of Clinical Pharmacology. DOI: 10.1111/j.1742-1241.2010.02418.x

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