Healing Peptide Thymosin Beta 4 – TB500

Explanation and common uses of TB-500:

Thymosin Beta 4 is the thymosin peptide shown to promote protection, growth, repair, remodeling and healing. Studies have shown that it can promote migration of cells, formation of blood vessels, maturation of stem cells, activation of progenitor cells, survival of various cell types and lowering of the production of pro-inflammatory cytokines. Thymosin Beta 4 is the form that is naturally produced within the human body and obviously cant be bought. The synthetic form of Thymosin Beta 4 that is synthesized and manufactured is called TB-500 ie this is what can be bought, injected etc. There is no difference in efficacy between the two

Buy your tb-500 here

Thymosin Beta 4 Dose:

Dosage depends on the purpose and severity of the injury / damage you are treating. People generally use between 4 to 8 mg of TB500 per week during the initial (loading) period of 4 to 6 weeks. Afterwards some opt to maintain the effects with a low 2 to 6 mg dose once every 2 weeks. The effects of TB-500 wear off within 2 – 3 weeks of injection.

How to take Thymosin Beta 4:

1. Get the tops of your vial and bacteriostatic/sterile water vial off.
2. Using an alcohol pad, clean the top of both vials (tb-500 and water)
3. Using a new sterile insulin syringe, draw syringe full of air(1ml) and inject it into the bacteriostatic vial then withdraw 1ml of bacteriostatic water.
4. Inject this 1ml of bacteriostatic water into the side of the tb-500 vial. Don’t force it and don’t spray it onto the lyophilized powder but rather into side of the vial so that the powder merely dissolves into it.
5. You can repeat step 3 and 4 if you are going to dilute the powder using more than 1ml eg 2ml
6. Check to see that all powder has dissolved and gently roll vial to ensure it has all dissolved well. DO NOT SHAKE.
7. If you want to equalize the pressure inside the vial you can pierce it with your insulin syringe but with no plunger in it
8. Withdraw appropriate amount of the now dissolved tb-500 into your syringe, try and avoid any major bubbles by tapping side of syringe and adjusting plunger. Ready for injection. (You can use a brand new syringe if you want the needle to be sharp and use the one that you pierced the rubber tops of your vials with to simply fill/load the new syringe with)


Duration:
1. Thymosin Beta 4 loading phase:

• duration: between 4 – 6 weeks
• dosage: between 4 – 8 mg of TB-500 per week
• frequency of injection:2 mg per injection, between 2 – 4 times per week (depending on the total weekly dosage)

TB-500 maintainance phase:

• duration: as long as needed
• dosage: between 2 – 6 mg of TB-500 per 2 weeks
• frequency of injection:2 mg per injection, between 2 – 3 times per 2 weeks (depending on the total bi-weekly dosage)

Dilution:
BA water

Side effects of Thymosin Beta 4 :

There have been no reported side effects during the past few years since TB-500 became popular by athletes. For some reason people expect the TB-500 to produce flu-like symptoms. After thorough research through every Thymosin beta-4 related usage log on bodybuilding forums, there are simply no reports to confirm any side effects.

HOW TO USE TB-500 Thymosin beta 4 for healing benefits

Research has shown that the best results are achieved when using sterile saline solution (Sodium Chloride Injection BP 0.9%) to mix TB-500 (thymosin beta4).


Important:
Only prepare the vials that will be used immediately. If using doses that are lower than the recommended dose, prepared vials must be stored in the fridge and be used within 8 days.


TB-500 preparation:
Remove the plastic protective cap of the sealed vial containing the powder of peptides.
Insert the filled syringe of 2ml of sodium chloride solution into the rubber top of the vial and release the 2ml of sodium chloride into the vial.
Remove the syringe and gently rotate the vial until the powder is completely dissolved.
Ensure that the solution is well mixed with all powder thoroughly dissolved for maximum safety and effectiveness.


TB-500 Administration:
A Subcutaneous (S/C) inj.


TB-500 Frequency:
Research studies have further shown that one (2ml. vial) Sub-Q Inj. each week for six consecutive weeks provides the best results.  There after, use only one (2ml. vial) per month.  It’s best to give the Sub-Q Inj. 6 days before intense work outs. Therefore for best results, one vial per Sub-Q injection per week for 6 consecutive weeks, then 1 vial per month (the glass vial is 2ml, with 10mg TB-500 per vial), so it is 10mg/2ml).


Contraindications:
No known contraindication with tb4 peptide products, however tb500 has not been thoroughly tested to know its full effects.
The product should not be used if the subject is pregnant or breast feeding.


TB500 Storage:
Store the product at room temperature in a non humid environment. An opened vile can be kept for up to 8 days in refrigerated storage.

What is TB-500?TB-500 is a synthetic version of the naturally occurring peptide present in virtually all human and animal cells, Thymosin Beta 4 (TB-500). It is a first-in-class drug candidate that promotes the following*:
•  Endothelial (blood vessels) cell differentiation
•  Angiogenesis (growth of new blood cells from pre-existing vessels) in dermal tissues
•  Keratinocyte migration
•  Collagen deposition; and
•  Decreases inflammation.
One of TB500 key mechanisms of action is its ability to regulate the cell-building protein, Actin, a vital component of cell structure and movement. Of the thousands of proteins present in cells, actin represents up to 10% of the total proteins which therefore plays a major role in the genetic makeup of the cell.


This potent peptide is a member of a ubiquitous family of 16 related molecules with a high conservation of sequence and localization in most tissues and circulating cells in the body. Thymosin beta-4 not only binds to actin, but also blocks actin polymerization and is the actin-sequestering molecule.


Tß4 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.
An additional key factor of TB500 is that it promotes cell migration through a specific interaction with actin in the cell cytoskeleton. It has been demonstrated that a central small amino acid long-actin binding domain has both blood cell reproduction and wound healing characteristics. These characteristics are uncovered by accelerating the migration of endothelial cells and keratinocytes. It also increases the production of extracellular matrix-degrading enzymes.
Research confirms that TB500 is a potent, naturally occurring wound repair factor with anti-inflammatory properties. TB-500 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.

DAC CJC 1295

DAC CJC 1295

DAC conjugated CJC 1295 (Receptor Grade) is an hGH secretogue that is unique by way of an additional lysine molecule that is added to facilitate the DAC complex. This conjugation makes for a much longer half-life. DAC CJC 1295 tends to have a very limited availability everywhere due to expense and difficulty to manufacture. CJC 1295 DAC is a exceptionally designed peptide and is known for being the finest of the hGH secretogues. Receptor grade: 98%+ pure 2000mcg / 2ml glass vial. THIS PRODUCT IS INTENDED FOR RESEARCH PURPOSES ONLY. CAN BE HARMFUL IF USED INAPPROPRIATELY.

In the healthy human body, large amounts of growth hormone are stored in the pituitary. The cells within the pituitary release growth hormone in response to signaling by GHRH (Growth Hormone Releasing Hormone), Ghrelin (of which GHRPs - Growth Hormone Releasing Peptides - are mimetics), and are inhibited from releasing these stores by Somatostatin. GHRH and Ghrelin act on different populations of somatotropes (GH releasing cells). GHRP/Ghrelin increases the number of somatotropes releasing GH but not the amount released by each cell;
GHRH affects both the number of secreting cells and - moreso - the amount they each secrete. [1] GHRH and Ghrelin are released in specific patterns that vary depending on event and environment: post-exercise, in response to slow wave sleep, in certain stages of life and physical development, and so on.

Most people (even the diseased) continue to possess the ability to make GH in the pituitary. The problem is in the signaling of the pituitary to release it (and make more). So yes CJC is meant to replace the external administration of GH in some (but not all) cases. Even most people with diseases that affect growth hormone secretion retain the ability to continue to make GH in their pituitaries. The disease states and symptoms result, most typically, in altered (dysfunctional) GH release signaling and this also affects the ability of the pituitary to continue to make more GH. [2]

GHRH, which has a forty-four amino acid long chain (and a specific shape - thus making it a peptide as well as a hormone), has been marketed for the longest as Sermorelin. However, Sermorelin has been demonstrated to be degraded rapidly in the body and is cost-inefficient. But because most patients in need of GH therapy doretain the ability to produce and secrete their own GH, treatment with a GHRH-type analog remained hypothetically preferable to exogenous GH treatment. GH itself when administered exogenously results not only in "unnatural" release patterns, it results universally in down regulation of endogenous GH production - as do many hormones when applied exogenously. [2]

Sermorelin's limitations naturally resulted in a variety of formulations of GHRH analogs for therapeutic. The most effective (in terms of minimal degradation in the body - which is different from half-life) analogs with the longest half-lives were those created with an attached 3-maleimidopropionic acid (MPA) unit, which results in binding to albumin after exogenous injection into blood plasma.
The research chemicals CJC-1293 and CJC-1295 are GHRH (the 44-amino acid long version) with 15 aminos removed, thus a total of 29 amino acids, and bound to MPA. [2] MPA is also called Drug Affinity Complex, and CJC-1295 is often referred to as GHRH with Drug Affinity Complex (DAC).

Based on measured GH release in rats over a two hour period, CJC-1295 released twice as much GH as CJC-1293, thus rendering it preferable based on immediate effectiveness; however, CJC-1293 has a 9% edge in stability (meaning less degradation) with in vitro stability tests.
CJC-1293, over a two-hour period, results in a rise-fall-rise-fall type pattern whereas CJC-1295 results in more of an inverted-U shape with a more gentle and longer peak. [2]

In a CJC-1295 pulsatility study performed on normal non-GH deficient people reported plasma levels were between 1 and 2 ng/ml or 1000-2000ng/L one week after injection of between 60 or 90 mcg/kg of CJC-1295. In a 100kg man that is a 6mg or 9mg per week dose.

"Knockout rats" are mice with genetically removed M3 muscarinic acetylcholine receptors. The scientists conducting the study [4] inhibited these genes and the mice became dwarves.. Those mice, labeled Br-M3-KO mice experienced short stature and a shrunken pituitary. Scientists treated Br-M3-KO mice and normal control mice with CJC-1295 for eight weeks, resulting in complete growth restoration in the knockout mice as well as - notably - a restored pituitary size. More specific data regarding CJC-1295 can be extrapolated by examining some of the control mice, which were not "knockout rats" but still received CJC-1295. The controls, male and female, experienced both accelerated & increased overall growth over the non-CJC-1295-dosed controls. Referring back to the notable finding that pituitary size was restored in knockout specimens dosed with CJC-1295, it is equally notable that the controls who did receive CJC-1295 did not have any pituitary hyperplasia or growth of the pituitary whatsoever. This supports the conclusion that CJC-1295 is a substantially less risky treatment for non-diseased subjects, and a substantially more beneficial therapy for subjects with pituitary disease, than conventional (synthetic) GH treatment. [4]

In conclusion, CJC-1295 is an exciting treatment from the standpoint of cost efficiency, safety, and ease of administration when compared with regular GHRH or synthetic Growth Hormone treatment. It has been demonstrated to be as effective as GH for most uses, and vastly preferable for safety reasons where feasible. GH will not be fully supplanted by GHRH analogs such as CJC-1295 for reasons alluded to above, but the vast majority of treatments in the types of applications mentioned in this article will probably begin to use CJC-1295 for safety, cost-efficiency, and the need to administer only one or two times per week instead of multiple times per day

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Raloxifen

Raloxifen

Raloxifen belongs to the class of compounds known as SERMs or selective estrogen receptor modulators. SERMs decrease activity of estrogen and are therefore considered an “anti-estrogen” treatment. However, SERMs do not act by decreasing serum estrogen or aromatase-mediated conversion, but rather through a blocking activity at the estrogen receptor on a cellular level. In other words, raloxifen and its metabolites are active at the estrogen receptor but not as an estrogen-like stimulus (agonist). Instead, they prevent estrogen from exerting its effects at the cellular level. This (as well as other means of blocking estrogenic activity or reducing estrogen levels) creates a rise in testosterone in men because testosterone production is modulated partially via serum estrogen levels.



Raloxifen and its sister drug tamoxifen are typically used in treating estrogen-receptor dependent breast cancer in women[1]. Raloxifen may prove to have more diverse uses than tamoxifen for several reasons:



Selective estrogen receptor modulators (SERMs) or estrogen agonists/antagonists have shown promise in osteoporosis in that they have the potential to reduce the risk of fracture, and also reduce the risk of breast cancer. SERMs maybe classified according to their core structure, which is typically a variation of the 17 beta-estradiol template and sub-classified according to the side chain at the helix 12 affector region. The best known are the triphenylethylenes such as tamoxifen, used in the management of breast cancer. However, the clinical application of this class of SERMs has been limited due to endometrial stimulation. A second class is the benzothiophenes such as raloxifene and arzoxifene, which have skeletal benefit with little, if any, uterine stimulation.[1]



In a study conducted by Christodoulakis et al, “raloxifene users did not exhibit any difference with respect to sex steroids and HOMA-IR levels.”[2]



Raloxifen increased serum testosterone but reduced serum IGF-1 in a study performed by Duschek et al:



In aging men serum levels of testosterone and insulin-like growth factor-1 (IGF-1) decline, potential factors in the reduced muscle strength, abdominal obesity, sexual dysfunction and impaired general well being of aging. The partial estrogen agonist and antagonist raloxifene increase serum testosterone levels in aging men, but the effect of raloxifene on serum IGF-1 levels in men is unknown. In this study the effects of raloxifene on IGF-1 levels and the associated increase in serum testosterone were compared to the effects of oral testosterone supplementation…. RESULTS: Compared to placebo raloxifene increased serum testosterone by 20% but it decreased serum IGF-1 levels by 24.5% (95% confidence interval (CI): -13.0 to -36.1%). No significant change in serum IGFBP-3 levels was found. The effect of raloxifene on serum IGF-1 has been observed with other oral estrogens, and, therefore, is likely to be ascribed to the partial estrogen agonist activity of raloxifene.[3]



According to Nordt et al, raloxifen may hold potential as an intervention in adolescent gynecomastia: “Newer treatment strategies, such as the antiestrogen raloxifene, have shown promising results; however, further studies are needed to determine long-term efficacy. As a result of the limited pharmaceutical treatment options, many more adolescents are seeking surgical intervention.[4]”



As the title of the study suggests, raloxifen is also a promising treatment for male osteoporosis:



Raloxifene has been shown to increase bone mineral density of the hip in men receiving androgen deprivation therapy for prostate cancer. Moreover, experimental data demonstrated dramatic increase in cell death in human prostate cancer cell lines after the treatment with raloxifene. All these observations suggest that SERMs may be useful for the prevention and treatment of osteoporosis not only in postmenopausal women but also in elderly men. However, our hypothesis should be tested in a proper designed clinical trial.[5]



Kastelan goes on to write that there are still issues of dose and duration to be assessed by further clinical study, as well as more markers of health and physical balance to be weighed against the benefits of raloxifen treatment.

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