Thymosin Beta 4(TB-500)

[johnjuanb1]

Thymosin Beta 4 was identified as a gene that was up-regulated four-to-six fold during early blood vessel formation and found to promote the growth of new blood cells from the existing vessels. This peptide is present in wound fluid and when administered subcutaneously, it promotes wound healing, muscle building and speeds up recovery time of muscles fibres and their cells.

 

[johnjuanb1]

Research confirms that T4 is a potent, naturally occurring wound repair factor with anti-inflammatory properties. T_¨_4 is different from other repair factors, such as growth factors, in that it promotes endothelial and keratinocyte migration. It also does not bind to the extracellular matrix and has a very low molecular weight meaning it can travel relatively long distances through tissues.

 

[johnjuanb1]

TB-500 reduces stomach acid which helps eliminate ulcers.

 

[chgolatin2]

I just underwent rotator cuff and bicep surgery... My shoulders are not the same anymore, need to truly study this compound out.. Thanks!

 

[johnjuanb1]

I just underwent rotator cuff and bicep surgery... My shoulders are not the same anymore, need to truly study this compound out.. Thanks!

I'll PM you now about your injuries.

 

[johnjuanb1]

Thymosin beta4 increases hair growth by activation of hair follicle stem cells.


AuthorsPhilp D, et al. Show all Journal
FASEB J. 2004 Feb;18(2):385-7. Epub 2003 Dec 4.


Affiliation
Abstract
Thymosin beta4, a 43-amino acid polypeptide that is an important mediator of cell migration and differentiation, also promotes angiogenesis and wound healing. Here, we report that thymosin beta4 stimulates hair growth in normal rats and mice. A specific subset of hair follicular keratinocytes in mouse skin expresses thymosin beta4 in a highly coordinated manner during the hair growth cycle. These keratinocytes originate in the hair follicle bulge region, a niche for skin stem cells. Rat vibrissa follicle clonogenic keratinocytes, closely related, if not identical, to the bulge-residing stem cells, were isolated and their migration and differentiation increased in the presence of nanomolar concentrations of thymosin beta4. Expression and secretion of the extracellular matrix-degrading enzyme matrix metalloproteinase-2 were increased by thymosin beta4. Thus, thymosin beta4 accelerates hair growth, in part, due to its effect on critical events in the active phase of the hair follicle cycle, including promoting the migration of stem cells and their immediate progeny to the base of the follicle, differentiation, and extracellular matrix remodeling.


PMID 14657002 [PubMed - indexed for MEDLINE]

 

[allornothing]

@ JJ

If TB-500 also helps with organ repair could it not also be possible that it would help with liver regeneration and health? Could it be a valuable tool for someone who has done damage to the liver due to high dosing of toxic orals?

Just curious? You've got me thinking about this one and it's multiple uses and possibilities.

 

[johnjuanb1]

@ JJ

If TB-500 also helps with organ repair could it not also be possible that it would help with liver regeneration and health? Could it be a valuable tool for someone who has done damage to the liver due to high dosing of toxic orals?

Just curious? You've got me thinking about this one and it's multiple uses and possibilities.

This study shows that thymosin beta 4 is lower in those with liver issues so it would make sense that the addition of TB4/TB-500 would help:

Serum thymosin beta4 levels in patients with hepatitis B virus-related liver failure.

AuthorsHan T, et al. Show all Journal
World J Gastroenterol. 2010 Feb 7;16(5):625-30.

Affiliation
Abstract
AIM: To investigate whether serum thymosin beta4 can provide diagnostic or prognostic information in liver failure patients caused by chronic hepatitis B virus (HBV) infection.

METHODS: Serum thymosin beta4 levels were measured in 30 patients with acute-on-chronic liver failure (ACLF), 31 patients with chronic liver failure (CLF), 30 patients with compensated liver cirrhosis (CR) and 32 patients with chronic hepatitis B and 30 healthy controls. Serum thymosin beta4 levels were measured by enzyme-linked immunosorbent assay and Child-Pugh and model for end-stage liver disease (MELD) scores were calculated for each patient on admission.

RESULTS: Compared with healthy controls, serum thymosin beta4 levels in ACLF, CLF, CR and chronic hepatitis B patients were significantly lower, 6.5047 (4.7879-10.5314) microg/mL vs 0.4632 (0.2759-0.8768) microg/mL, 0.6981 (0.5209-1.2008) microg/mL, 1.8053 (0.8110-2.3397) microg/mL, 3.7803 (1.8570-6.4722) microg/mL, respectively (P < 0.001). The levels of thymosin beta4 in liver failure (ACLF or CLF) patients were markedly lower than that in CR (P < 0.001), and a difference was also found between CLF and ACLF patients (P = 0.038). In patients with chronic liver disease, there was a positive relationship between thymosin beta4 levels and albumin, choline esterase, and platelet (P < 0.001), and negative relationship with alanine aminotransferase (P = 0.020), aspartate aminotransferase, total bilirubin, international normalized ratio of prothrombin time, and Child-Pugh and MELD scores (P < 0.001). Of the 61 liver failure patients, the thymosin beta4 levels of non-survivors were significantly lower than that of survivors (P = 0.007). Receiver operating characteristics analysis identified a thymosin beta4 cutoff level of 0.5708 microg/mL for predicting poor prognosis in all liver failure patients. The serial thymosin beta4 values were observed in 13 liver failure inpatients. Lower initial values were observed in the death. While greater improvement in thymosin beta4 value was found in those who recovered from the disease.

CONCLUSION: Serum thymosin beta4 can be used as an important potential predictor for liver failure caused by chronic HBV infection.

 

[johnjuanb1]

They're busting race horses for having an unfair advantage now. Hahaha does that mean they have to sit out a certain number of races like in baseball? Hahahaha

Doping control analysis of TB-500, a synthetic version of an active region of thymosin β₄, in equine urine and plasma by liquid chromatography-mass spectrometry.

AuthorsHo EN, et al. Show all Journal
J Chromatogr A. 2012 Nov 23;1265:57-69. doi: 10.1016/j.chroma.2012.09.043. Epub 2012 Sep 23.

Affiliation
Abstract
A veterinary preparation known as TB-500 and containing a synthetic version of the naturally occurring peptide LKKTETQ has emerged. The peptide segment (17)LKKTETQ(23) is the active site within the protein thymosin β(4) responsible for actin binding, cell migration and wound healing. The key ingredient of TB-500 is the peptide LKKTETQ with artificial acetylation of the N-terminus. TB-500 is claimed to promote endothelial cell differentiation, angiogenesis in dermal tissues, keratinocyte migration, collagen deposition and decrease inflammation. In order to control the misuse of TB-500 in equine sports, a method to definitely identify its prior use in horses is required. This study describes a method for the simultaneous detection of N-acetylated LKKTETQ and its metabolites in equine urine and plasma samples. The possible metabolites of N-acetylated LKKTETQ were first identified from in vitro studies. The parent peptide and its metabolites were isolated from equine urine or plasma by solid-phase extraction using ion-exchange cartridges, and analysed by liquid chromatography-mass spectrometry (LC/MS). These analytes were identified according to their LC retention times and relative abundances of the major product ions. The peptide N-acetylated LKKTETQ could be detected and confirmed at 0.02 ng/mL in equine plasma and 0.01 ng/mL in equine urine. This method was successful in confirming the presence of N-acetylated LKKTETQ and its metabolites in equine urine and plasma collected from horses administered with a single dose of TB-500 (containing 10mg of N-acetylated LKKTETQ). To our knowledge, this is the first identification of TB-500 and its metabolites in post-administration samples from horses.

 

[johnjuanb1]

Thymosin β4 increases the potency of transplanted mesenchymal stem cells for myocardial repair.

AuthorsYe L, et al. Show all Journal
Circulation. 2013 Sep 10;128(11 Suppl 1):S32-41. doi: 10.1161/CIRCULATIONAHA.112.000025.

Affiliation
Abstract
BACKGROUND: Thymosin β4 (Tβ4) has been shown to enhance the survival of cultured cardiomyocytes. Here, we investigated whether the cytoprotective effects of Tβ4 can increase the effectiveness of transplanted swine mesenchymal stem cells (sMSCs) for cardiac repair in a rat model of myocardial infarction (MI).

METHODS AND RESULTS: Under hypoxic conditions, cellular damage (lactate dehydrogenase leakage), apoptosis (terminal deoxynucleotidyl transferase dUTP nick end labelingc cells), and caspase-8 activity were significantly lower, whereas B-cell lymphoma-extra large protein expression was significantly higher, in sMSCs cultured with Tβ4 (1 μg/mL) than in sMSCs cultured without Tβ4, and Tβ4 also increased sMSC proliferation. For in vivo experiments, animals were treated with basal medium (MI: n=6), a fibrin patch (Patch: n=6), a patch containing sMSCs (sMSC: n=9), or a patch containing sMSCs and Tβ4 (sMSC/Tβ4: n=11); Tβ4 was encapsulated in gelatin microspheres to extend Tβ4 delivery. Four weeks after treatment, echocardiographic assessments of left-ventricular ejection fraction and fractional shortening were significantly better (P<0.05) in sMSC/Tβ4 animals (left-ventricular ejection fraction=51.7 ± 1.1%; fractional shortening=26.7 ± 0.7%) than in animals from MI (39 ± 3%; 19.5 ± 1.7%) and Patch (43 ± 1.4%; 21.6 ± 0.9%) groups. Histological assessment of infarct wall thickness was significantly higher (P<0.05) in sMSC/Tβ4 animals (50%, [45%, 80%]) than in animals from MI (25%, [20%, 25%]) group. Measurements in sMSC (left-ventricular ejection fraction=45 ± 2.6%; fractional shortening=22.9 ± 1.6%; TH = 43% [25%, 45%]), Patch, and MI animals were similar. Tβ4 administration also significantly increased vascular growth, the retention/survival of the transplanted sMSCs, and the recruitment of endogenous c-Kit(+) progenitor cells to the infarcted region.

CONCLUSIONS: Extended-release Tβ4 administration improves the retention, survival, and regenerative potency of transplanted sMSCs after myocardial injury.

 

[johnjuanb1]

Animal studies with thymosin beta, a multifunctional tissue repair and regeneration peptide.
Review article
Philp D, et al. Ann N Y Acad Sci. 2010.
Show full citation
Abstract
Studies in various animal models of disease and repair with thymosin beta(4) (Tbeta(4)), the major actin-sequestering molecule in mammalian cells, have provided the scientific foundation for the ongoing dermal, corneal, and cardiac wound repair multicenter clinical trials. Tbeta(4) has of multiple biological activities, which include down-regulation of inflammatory chemokines and cytokines, and promotion of cell migration, blood vessel formation, cell survival, and stem cell maturation. All of these activities contribute to the multiple wound healing properties that have been observed in animal studies.

 

[johnjuanb1]

Thymosin Beta-4 Is Elevated in Women With Heart Failure With Preserved Ejection Fraction.
Drum CL, et al. J Am Heart Assoc. 2017.

Abstract

BACKGROUND: Thymosin beta-4 (TB4) is an X-linked gene product with cardioprotective properties. Little is known about plasma concentration of TB4 in heart failure (HF), and its relationship with other cardiovascular biomarkers. We sought to evaluate circulating TB4 in HF patients with preserved (HFpEF) or reduced (HFrEF) ejection fraction compared to non-HF controls.

METHODS AND RESULTS: TB4 was measured using a liquid chromatography and mass spectrometry assay in age- and sex-matched HFpEF (n=219), HFrEF (n=219) patients, and controls (n=219) from a prospective nationwide study. Additionally, a 92-marker multiplex proximity extension assay was measured to identify biomarker covariates. Compared with controls, plasma TB4 was elevated in HFpEF (985 [421-1723] ng/mL versus 1401 [720-2379] ng/mL, P<0.001), but not in HFrEF (1106 [556-1955] ng/mL, P=0.642). Stratifying by sex, only women (1623 [1040-2625] ng/mL versus 942 [386-1891] ng/mL, P<0.001), but not men (1238.5 [586-1967] ng/mL versus 1004 [451-1538] ng/mL, P=1.0), had significantly elevated TB4 in the setting of HFpEF. Adjusted for New York Heart Association class, N-terminal pro B-type natriuretic peptide, age, and myocardial infarction, hazard ratio to all-cause mortality is significantly higher in women with elevated TB4 (1.668, P=0.036), but not in men (0.791, P=0.456) with HF. TB4 is strongly correlated with a cluster of 7 markers from the proximity extension assay panel, which are either X-linked, regulated by sex hormones, or involved with NF-κB signaling.

CONCLUSIONS: We show that plasma TB4 is elevated in women with HFpEF and has prognostic information. Because TB4 can preserve EF in animal studies of cardiac injury, the relation of endogenous, circulating TB4 to X chromosome biology and differential outcomes in female heart disease warrants further study.

 

[johnjuanb1]

Cardioprotection by Thymosin Beta 4.
Review article
Pipes GT, et al. Vitam Horm. 2016.

Abstract

Treatment with thymosin beta 4 (Tβ4) reduces infarct volume and preserves cardiac function in preclinical models of cardiac ischemic injury. These effects stem in part from decreased infarct size, but additional benefits are likely due to specific antifibrotic and proangiogenic activities. Injected or transgenic Tβ4 increase blood vessel growth in large and small animal models, consistent with Tβ4 converting hibernating myocardium to an actively contractile state following ischemia. Tβ4 and its degradation products have antifibrotic effects in in vitro assays and in animal models of fibrosis not related to cardiac injury. This large number of pleiotropic effects results from Tβ4's many interactions with cellular signaling pathways, particularly indirect regulation of cellular motility and movement via the SRF-MRTF-G-actin transcriptional pathway. Variation in effects and effect sizes in animal models may potentially be due to variable distribution of Tβ4. Preclinical studies of PK/PD relationships and a reliable pharmacodynamic biomarker would facilitate clinical development of Tβ4.

 

[opietaylor]

increased red blood cells?? could be a problem for those trying to control H/H

Thymosin Beta 4, also known as TB500 or TB-500, is a synthetic version of the naturally occurring Peptide present in virtually all-human and animal cells, Thymosin Beta 4 (T4). It is a first-in-class candidate that promotes the following*:

WHAT THIS DOES:

1. Increases Red Blood Cells

2. Stops bleeding

3. Increase Endurance

4. Reduces Tie Up

5. Helps breathing

6. Reduces stomach acid which eliminates ulcers

7. Increases lean muscle mass

8. Helps repair tendons and ligaments

 

[johnjuanb1]

I just ordered 3 viais of TB-500. I’m going to try a protocol of 1mg EOD subQ. I’m looking for relief from my daily aches and pains in my wrists, elbows, knees, delts, everything on this old ass body. Hahaha I turn 50 in a few months.

 

[rmtt]

I just ordered 3 viais of TB-500. I’m going to try a protocol of 1mg EOD subQ. I’m looking for relief from my daily aches and pains in my wrists, elbows, knees, delts, everything on this old ass body. Hahaha [emoji23] I turn 50 in a few months.

I will be watching. I'm really liking what I'm seeing so far. Yesterday was #7 or #8 of my 2mg E3D dosage. I think I have maybe 3 more if those left...than I'm going to 2mg weekly.

But I've seen a pretty dramatic difference already. Feels like I went in for an oil change!!

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[johnjuanb1]

I will be watching. I'm really liking what I'm seeing so far. Yesterday was #7 or #8 of my 2mg E3D dosage. I think I have maybe 3 more if those left...than I'm going to 2mg weekly.

But I've seen a pretty dramatic difference already. Feels like I went in for an oil change!!

Sent from my LG-H871 using Tapatalk

That’s very cool! I can’t wait to get started!
I’m trying to be cheap and do a lower dose to see if it works well. With horses they give them 10mg once a week for 6 weeks then maintenance dose which i can’t recall off hand. We’ll see if 1mg EOD is enough.

 

[rmtt]

That’s very cool! I can’t wait to get started!
I’m trying to be cheap and do a lower dose to see if it works well. With horses they give them 10mg once a week for 6 weeks then maintenance dose which i can’t recall off hand. We’ll see if 1mg EOD is enough.

I remember doing the extrapolation between horses and humans from some studies....and it actually came out to about 7mg a week for saturation doses. In another...it was like you said...10mg a week for 6 weeks and the 10mg a month.

Either way....it's like filling a gas tank...eventually you get there and you then just keep it topped off.

So that doesn't seem too bad considering the benefits.

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[galaxy]

My dog has degenerative myopathy. At best she could have survived 6 months to a year. As her condition worsened I felt I had no choice and started her on tb500, which btw is much cheaper through vet suppliers. Anyway, she initially responded quite well but that may have just been the anti inflammatory effects. I also knew I could be exacerbating any cancer in her if I went this route . It was worth it to me as she would have died either way. Long story short, her calcium levels are off the charts and if I don’t get her infection under control she will be dead in a couple days. It’s not worth playing around with unless your situation is dire. For most of you guys it seems to me a low dose of hgh would be better and safer option and if you looking for heart repair I believe hexarelin to be a better option. For that matter hgh still may do the same if studied the same. And this could all be correlation. Not causation. Just my .02

 

[rmtt]

My dog has degenerative myopathy. At best she could have survived 6 months to a year. As her condition worsened I felt I had no choice and started her on tb500, which btw is much cheaper through vet suppliers. Anyway, she initially responded quite well but that may have just been the anti inflammatory effects. I also knew I could be exacerbating any cancer in her if I went this route . It was worth it to me as she would have died either way. Long story short, her calcium levels are off the charts and if I don’t get her infection under control she will be dead in a couple days. It’s not worth playing around with unless your situation is dire. For most of you guys it seems to me a low dose of hgh would be better and safer option and if you looking for heart repair I believe hexarelin to be a better option. For that matter hgh still may do the same if studied the same. And this could all be correlation. Not causation. Just my .02

So sorry to hear about your dog....I've been there.

But keep in mind that TB500 in trials has been shown to dissolve calcium deposits and inhibit tumor growth.

TB 500 doesn't cause cancer, but may cause proliferation of existing cancer of solid tumor cells (doesn't cause but promote the growth/proliferation) while inhibiting the growth/proliferation of other types of non solid cancer cells (multiple myloma, leukemia etc.)...and their are tons of studies showing enhanced cardiac repair.

Also these tests were performed with using Thymosin beta 4 which is the full peptide sequence...while TB500 is just a part of that sequence. But it's supposed to be the part that gives the joint, wound healing abilities that everyone has been experiencing.