TB-500 ist ein 43 Aminosäuresynthetisches Analogon von Thymosin Beta-4 (TB-4), das in nahezu allen Säugetierzellen auf natürliche Weise vorkommt. TB-500 ist bekannt für seine Auswirkungen auf Aktinprotein, Zellmigration und Wundheilung. TB-500 wurde in Tiermodellen und In-vitro-Studien gezeigt, um das Wachstum des Blutgefäßes zu verbessern, die Wundheilung zu beschleunigen, Entzündungen zu verringern und die extrazelluläre Matrixproduktion zu fördern. Das Peptid wird derzeit untersucht, weil er die Fähigkeit zur Verringerung des oxidativen Stresses bei Rückenmarksverletzungen, die Erholung nach Herzinfarkt und seine vielen Anti-Aging-Effekte verbessert.

TB-500 ist die aktive Domäne von TB-4, die eine primäre Rolle als Aktin-Bindungsprotein spielt. Actin ist eine kritische Komponente der Zellstruktur und macht Mikrofilamente aus. Mikrofilamente sind dafür verantwortlich, Zellen ihre Form zu verleihen, die Integrität von Zellmembranen zu schützen, die Zellen zu bewegen/zu migrieren und bestimmte Schritte in der zellulären Reproduktion. Actin ist auch eine der Hauptkomponenten des Muskelproteins. Ohne Aktin konnten sich die Muskeln nicht zusammenziehen. Aktinbindende Proteine ​​wie TB-4, Sequester Actin-Monomere, die einzelnen Aktineinheiten, so dass sie vor Abbau geschützt sind und bei Bedarf für die Polymerisation in Mikrofilamente verfügbar sind.

Sequenz:Ac-ser-asp-lys-pro-asp-met-ala-glu-iil-glu-lys-thr-thr-thr-gln-lys-lys-lys-lys-thr-thr-glu-lys-asn-pro-leu-ser-ser-lys-glu-glu-glu-glu-glu-glu-gl
Molekülformel:C₂₁₂H₃₅₀N₅₆Ö₇₈S
Molmasse:4963.4408
CAS -Nummer:77591-33-4
Pubchem:CID 16132341

1. TB-500 und neurologische Funktion

Untersuchungen an Ratten haben ergeben, dass TB-500 das zentrale und periphere Gewebe des Nervensystems zum Reparieren und Umbau nach einer Verletzung fördert. Obwohl der genaue Mechanismus noch nicht geklärt werden muss, zeigt die Forschung, dass TB-500 die Zellen aktiviert, die Neuronen unterstützen. Diese Zellen, die als Oligodendrozyten bezeichnet werden, halten Neuronen gesund^[1]. Boosting their activity actually improves blood vessel and neuron growth in brain regions that have been damaged, a significant laboratory result that is reflected in clinically significant improvements in behavior, motor control, and cognitive measurements^[2].

Recent research shows that TB-500 can reduce oxidative stress following spinal cord injury and help transplanted neural stem/progenitor cells (NSPCs) to survive long enough to enhance spinal regeneration^[3]. These findings could make TB-500 and other TB-4 derivatives of great use in treating severe spinal cord injury. TB-550 may offer critical insight into spinal recovery that allows paralyzed individuals to regain use of affected body regions.

2. TB-500 and Blood Vessel Growth

TB-500 and TB-4 are potent stimulators of VEGF expression. VEGF is an important signaling molecule in the growth of capillaries (small blood vessels), which are critical to everything from wound healing to hair growth^[4]. It is thought that the role of TB-500 is more complicated than this, however. Scientists speculate that the peptide likely underpins a number of steps in the process of blood vessel growth include extracellular matrix remodeling, vasculogenesis, angiogenesis, and the transition of more primitive mesenchymal tissue to the specialized endothelial tissue that lines blood vessels. This speculation is valid because loss of TB-4 has been shown to interfere with blood vessel growth and stability while exogenous administration improves capillary formation and the recruitment of pericytes following injury^[4].

3. TB-500 and Hair Growth

The discovery that TB-500 improves hair growth happened by accident. When mice that were genetically deficient in TB-4 were shaved for laboratory experiments, it was observed that their hair grew back much slower than wild-type mice. When these same scientists investigated hair growth in mice that were genetically modified to produce increased levels of TB-4, they found that their hair grew back much faster than normal. Under the microscope, these mice show increased numbers of hair shafts and grouped hair follicles^[5].

4. TB-500 and Antibiotic Synergy

Multi-drug resistance is becoming increasingly common in a number of infections, rendering current therapy ineffective. Unfortunately, there are very few new antibiotics in the pipeline and the process of drug development can take upwards of twenty years on average. A recent study on the effects of TB-4 and its adjuvants, however, provides some hope. Studies of mice suffering from a Pseudomonas aeruginosa infection of the eye have found that TB-4 combined with ciprofloxacin, a standard antibiotic for treating Pseudomonas aeruginosa, increases the effects of the antibiotic, improves healing, reduces inflammation, and promotes faster recovery. The results of just five days of combined therapy showed decreased numbers of colony forming units (CFUs), decreased neutrophil (a type of white blood cell) count, and decreased levels of inflammatory reactive oxygen species^[6]. This is the first study to demonstrate that TB-500 and similar peptides might be used to promote and enhance the effects of antibiotics.

A. Number of colony forming units (CFUs) of bacteria after 5 days of treatment. Note that none are detectable when ciprofloxicin is combined with TB-4.
B. Shows number of neutrophils in the corneas of treated mice, an indication of inflammation.
C. Measure of reactive oxygen species in corneas of mice after 5 days of treatment.
D. Nitrate levels from corneal lysates.
Source: PubMed

5. TB-500 and Cardiovascular Health

Two decades of research have shown that TB-4 and its derivatives have a number of beneficial effects in the cardiovascular and renal systems. The exact mechanisms of these positive contributions are not clearly understood, however. Research suggests that the benefits are actually due to several mechanisms. First, TB-500 promotes the growth of collateral blood vessels, which is useful both as a preventative and in restoring function following disease. Second, TB-500 encourage endothelial cell migration and myocycte survival following a heart attack. Finally, it appears that TB-500 works in concert with other natural signaling molecules to reduce inflammation and reduce fibrosis (scar formation)^[7].

Recently, research into hydrogels containing a combination of collagen and TB-4 has shown the peptide promotes angiogenesis and epicardial heart cell migration, thus boosting rates of recovering following ischemia and helping to prevent long-term complications by reducing scarring^[8].

6. TB-500 and Neurodegenerative Diseases

Progress in finding a treatment for neurodegenerative diseases like Alzheimer’s and prion disease has been slow at best. A recent study into the effects of TB-4 on the ability of the immune system to deal with prion protein has shown that the peptide enhances autophagy^[9]. Autophagy is the central nervous system’s primary protective mechanism against neurodegenerative diseases. The ability of TB-4 to enhance this natural immunity is the first progression toward real treatment of these debilitating diseases in a long time.

7. TB-500 Has Wide Application

TB-500 due to its fundamental role in cell structure and function can affect a number of different body tissues. This has resulted in a wide and varied field of research into the effects of this peptide. From treating heart and neurological disease to enhancing the effects of antibiotics, TB-500 is one of the hottest peptides in research today and will likely remain one of the most heavily investigated peptides for the foreseeable future.

TB-500 exhibits minimal side effects, low oral and excellent subcutaneous bioavailability in mice. Per kg dosage in mice does not scale to humans. TB-500 for sale at

The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.

Allan L. Goldstein, MD, Allan L. Goldstein is professor and Catharine B. & William McCormick Chair of the department of Biochemistry and Molecular Biology at The George Washington University School of Medicine and Health Sciences, where he has served since 1978. Thymosins were discovered in the mid 1960’s, when Allan Goldstein from the Laboratory of Abraham White at the Albert Einstein College of Medicine in New York studied the role of the thymus in development of the vertebrate immune system. He is a world-renowned authority on the thymus gland and the workings of the immune system, and co-discoverer of the thymosins. Dr. Goldstein is the author of over 400 scientific articles in professional journals, the inventor on more than 15 U.S. Patents, and the editor of several books in the fields of biochemistry, biomedicine, immunology and neuro-science. He is on the editorial boards of numerous scientific and medical journals and has been a consultant to many re-search organizations in industry and government; co-founder of The Institute for Advanced Studies in Aging and Geriatric Medicine, a non-profit research and educational institute; a member of the Board of Trustees of the Albert Sabin Vaccine Institute; and serves as the Chairman of the Board of RegeneRx Biopharmaceuticals. Dr. Goldstein received his B.S. from Wagner College in 1959 and his M.S. and Ph.D. from Rutgers University in 1964. He served as a faculty member of the Albert Einstein College of Medicine from 1964 to 1972, and moved to the University of Texas Medical Branch in Galveston in 1972 as professor and director of the division of Biochemistry.

Allan L. Goldstein, MD is being referenced as one of the leading scientists involved in the research and development of TB-500 and other Thymosins. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between

1. P. Cheng, F. Kuang, H. Zhang, G. Ju, and J. Wang, “Beneficial effects of thymosin β4 on spinal cord injury in the rat,” Neuropharmacology, vol. 85, pp. 408–416, Oct. 2014. [PubMed]
2. M. Chopp and Z. G. Zhang, “Thymosin β4 as a restorative/regenerative therapy for neurological injury and neurodegenerative diseases,” Expert Opin. Biol. Ther., vol. 15 Suppl 1, pp. S9-12, 2015. [PubMed]
3. H. Li, Y. Wang, X. Hu, B. Ma, and H. Zhang, “Thymosin beta 4 attenuates oxidative stress-induced injury of spinal cord-derived neural stem/progenitor cells through the TLR4/MyD88 pathway,” Gene, vol. 707, pp. 136–142, May 2019. [PubMed]
4. K. N. Dubé and N. Smart, “Thymosin β4 and the vasculature: multiple roles in development, repair and protection against disease,” Expert Opin. Biol. Ther., vol. 18, no. sup1, pp. 131–139, 2018. [PubMed]
5. D. Philp, S. St-Surin, H.-J. Cha, H.-S. Moon, H. K. Kleinman, and M. Elkin, “Thymosin beta 4 induces hair growth via stem cell migration and differentiation,” Ann. N. Y. Acad. Sci., vol. 1112, pp. 95–103, Sep. 2007. [PubMed]
6. T. W. Carion et al., “Thymosin Beta-4 and Ciprofloxacin Adjunctive Therapy Improves Pseudomonas aeruginosa-Induced Keratitis,” Cells, vol. 7, no. 10, Sep. 2018. [PubMed]
7. K. M. Kassem, S. Vaid, H. Peng, S. Sarkar, and N.-E. Rhaleb, “Tβ4-Ac-SDKP pathway: Any relevance for the cardiovascular system?,” Can. J. Physiol. Pharmacol., pp. 1–11, Mar. 2019. [PubMed]
8. A. D. Shaghiera, P. Widiyanti, and H. Yusuf, “Synthesis and Characterization of Injectable Hydrogels with Varying Collagen–Chitosan–Thymosin β4 Composition for Myocardial Infarction Therapy,” J. Funct. Biomater., vol. 9, no. 2, Mar. 2018. [PubMed]
9. H.-J. Han, S. Kim, and J. Kwon, “Thymosin beta 4-Induced Autophagy Increases Cholinergic Signaling in PrP (106-126)-Treated HT22 Cells,” Neurotox. Res., Dec. 2018. [PubMed]
10.  Song, Ran & Choi, Hyun & Yang, Hyung-In & Yoo, Myung & Park, Yong-Beom & Kim, Kyoung. (2012). Association between serum thymosin β4 levels of rheumatoid arthritis patients and disease activity and response to therapy. Clinical rheumatology. 31. 1253-8. 10.1007/s10067-012-2011-7. [Research Gate]
11.  Philp, D., et al. “Thymosin β4 Promotes Angiogenesis, Wound Healing, and Hair Follicle Development.” Mechanisms of Ageing and Development, vol. 125, no. 2, Feb. 2004, pp. 113–115, 10.1016/j.mad.2003.11.005. [PubMed]

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The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body.  These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease.  Bodily introduction of any kind into humans or animals is strictly forbidden by law.