Understanding Peptide Reconstitution Guide

Understanding Peptide Reconstitution

It seems to be increasingly common that users are introducing themselves to the idea of pinning through the use of peptides (although, arguably, hcg usage is also increasing in usage for those running non-injectable cycles). While I personally find these to be a great way to get yourself comfortable with the idea of injecting, it seems many become confused nearly immediately with how to at the first step, reconstitution. So I decided to just create a quick reference for those of you out there, and show you how the simple math required is not intimidating in the least. This guide will be a bit long, as I am hoping to avoid the common questions, but I think it will be a very good guide for some, and maybe too "simple" for others.

A short disclaimer:
This guide is purely hypothetical, and I do not encourage the use of any PED without the close guidance of a physician. This guide takes no consideration to the laws of your country. I do not condone any illegal activity. It is merely designed to be an educational resource.

Alright, so this guide will follow under the assumption that you have aquired your peptide of choice (or hCG), and are ready to reconstitute it.

You will need the following items:
•Your Peptide Vial
•Bacteriostatic Water
•Alcohol Wipes (available at your local pharmacy, usually near diabetic supplies)
•Insulin Syringe (more on this in a moment)

A quick discussion on syringes:

Syringe availability will vary largely depending on the laws of your state/country. In many states, such as mine, low quantity purchases of insulin syringes are available at the pharmacy without the need for a prescription. Laws such as these are in place as a counter measure to help avoid the increase of HIV transmission through unsafe needle usage, by allowing addicts to purchase clean syringes.

Size will depend on your source. An insulin syringe will typically range from 29g to 31g. For those unaware, the smaller the gauge (the "g"), the larger the number. So a 31g will be smaller needle width than a 29g. Generally, smaller gauge needles can provide less soreness through injection, but they are also much more fragile. Having used a 31g, I do prefer them for the ease of injection (minimal "pinch" feel), but they do become increasingly fragile, so proper care is required.

Now that you have your supplies gathered, it is time to reconstitute your peptides. Please make sure that you do this in a clean environment to reduce the risk of contamination.

For this example, I will be using a typical 5mg product, as is typical of the GHRPs provided by many companies. Although your particular product may not contain 5mg, the same idea will hold through to other products, just with a different amount of actives. I will also be under the assumption that you will want 100mcg doses (although again, this will vary by product/your required dosing).

Before you begin, you must do the math to understand how much bacteriostatic water you will need for your reconstitution.

If you are looking for the said 100mcg doses, from a 5mg vial, then you will have 50 doses from this vial. 100mcg x 50 = 5,000mcg, or 5mg. You can apply this to any amount of product. For example, Ipamorelin is usually available in 2mg vials. In that case, you would have 2,000mcg of Ipamorelin, which divided by 100mcg would give you 20 doses. The amount of dosages is important here, as it will dictate how to utilize your reconstituted product.

So back to the original 5mg product, we know we are going to have 50 doses. The idea here then, is to add enough bac water to the peptide in order to allow you to dose those individual dosage. Personally, I like to use as little Bac water as needed, but also attempt to keep it easy enough to dose. The key point here is to know that no matter how much bac water you add to your vial, 1/50 of that will always be 100mcg.

With that said, if you add 1ml of bac water to the vial, your 100mcg dosage will be 2iu on the syringe.
(1ml = 1cc on your syringe = 100iu, so 100iu/50 doses = 2iu).
If you add 2ml of bac water to the vial, your 100mcg dosage will be 4iu (200iu/50 doses = 4iu).
If you add 3ml of bac water to the vial, your 100mcg dosage will be 6iu (300iu/50 doses =6iu).
It is up to you how much bac water you will like to use, and utilizing the option of keeping this guide non-opinionated, I won't give a recommendation on this, however, it will be dictated by how large your vial is and how accurate your pins are (a 50iu *sold as 1/2 cc* syring will make it easier to measure smaller amounts, where a 1cc *100iu* syringe will make it more difficult to measure smaller amounts).

Once you have an amount chosen, we can move on the the actual reconstitution. In this example, I will reconstitute with 2ml of bac water.

1. Snap of off the plastic cover of your peptide vial and your bac water.

2. Take an alcohol wipe, and wipe down the rubber top of both the peptide vial and your bac water, and then discard the wipe and allow vials to dry for a second or two.

3. Take a syringe and remove the safety cap (most will have one cap over the needle, and one over the plunger). Set these caps aside, while taking precaution not to expose your needle to any other object (it is sterile!). Pull the plunger on your syringe to the maximum reading (will usually be either 1/2cc or 1cc) to allow the syringe to fill with air. (It is also common practice to draw this air from the peptide vial. You can do this by inserting the needle into the peptide vial, keeping it right side up, and drawing the air that way. Then pull the syringe from the bottle, and on to step 4).

4. Insert the needle into the rubber portion of your bacteriostatic water. With the syringe inserted, turn the vial of bacteriostatic water upside down, and push the plunger into the syringe (this will cause the air to enter the vial). Then, slowly, draw back on the syringe back to that maximum reading, as it will allow the syringe to fill with bac water.
Quick Note: The reason you fill your syringe with air, and then insert the air into the vial, is to keep the pressure within the vial, which will allow you to draw with much greater ease.

5. You may now turn the vial of back water back to right side up, and remove your syringe, again taking caution to avoid the needle from coming into contact with anything else.

6. We are now ready to insert the bac water into the peptide vial. I recommend reconstituting slowly, and avoiding adding the bac water directly onto the peptide, and rather down the sides of the vial. Take your peptide vial, and insert the syringe through the rubber stopper on an angle, enough so that once the needle penetrates the rubber, it is angled towards the side of the vial.

7. Slowly push down on the plunger allowing the bac water to enter down the sides of the vial. Take your time doing this, as there is no rush.

8. Once all of the bac water is into the vial, remove the syringe and gently (GENTLY!) swirl the vial allowing the peptide to dissolve into the bac water.

9. Depending on the target amount of bac water to be added, and the size of your pin, you must now repeat steps 3-8 until you have added the correct amount of bacteriostatic water. If you are aiming for 2ml of bacteriostatic water, and are using a 1/2cc syringe, this process must be done a total of 4 times, and if using a 1cc syringe, this process must be done a total of twice.

10. Once the proper amount is added, place the caps back on both ends of your syringe and properly discard of it. Do not reuse this syringe for injection.
Depending on your product, refridgeration might be necessary. If so, store reconstituted product in fridge.

That should be it. Happy research. If you have any questions, feel free to ask, but only do so after having completely read through this guide.
If you guys like this guide, I might do some later on some common peptides, when I can get to it.
-h2s

IGF-1 Reverses Aging and Heals damaged brain cells

Growth Hormone Production and IGF-1The production of growth hormone is at its peak during the adolescence period. Most of the HGH is secreted into the bloodstream in brief-bursts manner. It also occurs during the early hours of deep sleep or REM. Once HGH is in the bloodstream, it stays there for a short period, perhaps in a few minutes or longer enough in stimulating its uptake into the liver, wherein conversion to growth factors happen. The Insulin Growth Factors (IGF-1) are the most important of all these growth factors, also called the Somatomedin C.

Furthermore, the growth hormone acts either indirectly or directly through the intermediary insulin growth factors to each organ system in the body. Hence, almost nothing is able to escape from its magic touch. Growth hormone is also capable of increasing the size of several organs and tissues, including the brain. Based on recent studies, involving animals as test subjects, HG has manifested the regeneration of damaged brain tissue.

IGF-1Rather than the growth hormone itself, it is the IGF-1 that varies widely throughout the day and is used in measuring how much GH has been secreted by the body. Thus, the IGF-1 is responsible for the actions and benefits associated with HGH and is 10 times more potent than HGH. To date, HG is under investigation as a separate medication for its many indications similar to HGH. Phil Micans from the London-based International Aging Systems, believes that the IGF-1 will become the top choice among the hormones in just a few years.

HGH and IGF-1 for Anti-aging Doctor Vincent Giampapa, the Clinical Research director of the Longevity Institute International, based in Montclair, New Jersey, said that the blueprint of aging is under the DNA’s hood of telomere, and considered as the “clock” at the end of each chromosome, which is shortened with every cell division.

Hence, reversing the aging at the cellular level is possible through a substance, which will restore the length of telomere. However, that substance is still unavailable. Giampapa strongly believes that the substance will be available in not more than a decade though. Until then, the growth hormone, along with its IGF-1 attendant hormone is able to perform the next best thing, assisting in keeping the cell as healthy as possible.

Overall, the ability and function of the cell largely depend on the DNA, the genetic material in the nucleus that codes for all the enzymes, proteins, and hormones that make it run. Thus, DNA is similar to an army under a consistent attack from ultraviolet light, body heat, oxygen free-radicals, and many other damaging factors. While the DNA has the ability in repairing itself, it still falls short with age, which is the same aging process that largely affects the cell. Simultaneously, damage accumulates in the cell’s mitochondria, the energy center, which has its separate DNA. Among the things to limit the DNA damage is the intake of antioxidant supplements like vitamins E and C in bolstering the body’s defenses.
According to Giampapa and a hormone replacement therapy specialist Thierry Hertoghe, the latest research in Europe indicates that human growth hormone and the IGF-1 could go farther than antioxidants, going beyond what antioxidants can do. All the more, HGH and IGF-1 can transport raw materials to the cells for repair and renovation.
IGF-1 can instigate the delivery of RNA, DNA and nucleic acids directly into the cell nucleus. Meanwhile nucleic acids are helpful in repairing the damage in the DNA, while stimulating cell division. Growth hormone, on the other hand, launches the transport of nucleic acids and amino acids into the cell’s cytoplasm, just outside the nucleus. In this process, the HGH and IGF-1 are not only able to minimize the DNA and cell stellar damage, but also treating the DNA and the cell. In all, both hormones can treat the blueprints of the aging process.

Primarily, the IGF-1 is the GH chain’s other end, the downstream player, which actually exerts the effects associated with the HGH. It is able to cause a great deal of excitement in two groups, including the researchers and the group of bodybuilders, who are both using the substance for individual purposes.
Meanwhile, the IGF-1 is said to be more potent than the HGH, as it latter exerts its effects through the former substance. Without a surprise, IGF-1 injections can do what HGH does, plus other effects in accordance with its proponents. IGF-1 can increase the lean body mass, while reducing fats, building bone, nerves, and muscle all at the same time. Through a direct intake, the pituitary gland is avoided, which could be burnt out throughout the aging process.

Anti-Aging Action – When it comes to the anti-aging efforts, the iGF-1 is said to be more potent than the HGH. Doctor Keith Kelly conducted a research work, indicating that growth hormone was able to reverse the shrinking of the thymus. According to Kelly, only the IGF-1 worked, and not the GH that worked in his experiment on cells in culture. However, both GH and the IGF-1 worked on living animals, saying that both substances are significantly elevated in the older test subjects as they were treated with growth hormone. He predicted that IGF-1 would be the main player though.

Disease and Brain Aging Prevention – Among the other spectacular uses of GH and IGF-1 is their ability to prevent the effects of brain aging, not to mention their capacity to treat such condition. Based on an experiment, the substances manifested momentous implications for stroke, brain injury, neurodegenerative disease, and aging. A team of scientist based in New Zealand said that IGF-1 can halt the death of cells in the brain.
Peter Gluckman, Barabara Johnston, along with their colleagues at the University of Auckland discovered that IGF-1 injections administered in two hours, following brain injury in baby lambs were able to rescue the damaged neurons, salvaging cells that would have died during apoptosis, the programmed cell death. Apoptosis is the brain cell loss that occurs for up to three days upon the initial injury.
In all, the treatment was very effective in stopping the death of brain cells in areas such as the cortex, hippocampus, and other areas linked with the memory and thinking. Results also manifested in the striatum, the brain area that is associated with the Parkinson’s disease in human. Hence, IGF-1 replacement reduced seizures in animals suffering from brain damage.
The researchers further suggest that IGF-1 could be used in preventing the effects of neonatal hypoxia lack of oxygen in the brain that occurs during birth. This condition could leave a baby suffering from permanent brain damage. This ability of the IGF-1 only opens doors for more possibilities, such as the reversal of the programmed cardiac cell death, following a heart attack, which can cause a victim with a heart full of dead tissues.
Keep in mind that the stroke can destroy the brain tissue, and as the cells die, the victim of a stroke is left unable to talk, walk, or think clearly. This also plays a significant role in many other neurodegenerative diseases like muscular dystrophy, Alzheimer’s disease, and multiple sclerosis (MS). For the very first time, there is a considered weapon or treatment against death at the cellular level.

Improvement of Glucose Metabolism – Similar to insulin, the IGF-1 has the same properties with the former as it can also improve the blood sugar profiles of patients with Type 2 diabetes. An increase in insulin resistance is manifested through high doses of GH, but the administration of IGF-1 can actually regulate the insulin resistance.
Researchers Bernard Beaufrere and Nelly Mauras from Jacksonville, Florida’s Nemours Children's Clinic studied several things, including the effect of IGF-1 on protein metabolism as the substance has the ability to halt protein-wasting brought about by glucocorticosteroid drugs such as prednisone, as well as its effects on glucose and insulin metabolism. The researchers divided the group of volunteers into three: IGF-1 alone, Prednisone alone, and IGF-1 plus prednisone.
The study discovered that 100 micrograms of IGF-1 per kilogram of body weight that was administered twice a day, was able to enhance the protein metabolism of the body, in the same manner as growth hormone. IGF-1 decreased the protein breakdown among the subjects who took prednisone, whereas, GH in an earlier research resulted in insulin resistance and carbohydrate intolerance when administered with prednisone did not cause diabetes-like effects. Rather, the volunteers who received IGF-1 with prednisone had a regular glucose metabolism.
The researchers said the discovery was remarkable in line with the glucocorticoids as they are known to curb insulin circulation and decrease insulin sensitivity as well. Due to this discovery and other researches, the experts now believe that IGF-1 promises treatment for protein catabolic states, such as in patients who need IV feedings after a surgery.

Helping Diabetic Patients – Two double-blinded clinical researches in 1997 also showed that recombinant IGF-1 injections could reduce the need for insulin remarkably, up to 45% in people suffering from diabetes mellitus, and who are insulin-dependent. One particular study involved eight adults aged 24 to 49, the other group was 43 children and adolescents aged 8 to 17. IGF-1 resulted in an overall lower cholesterol and triglyceride levels in the adult trial, after four days of IGF-1 treatment.
The clinical trials were only short-term, which lasted for 19 days and four weeks respectively. The insulin requirement that dropped remarkably, without serious side effects indicated that IGF-1 is a promising drug for diabetes treatment. Although it does not do away with insulin requirement, IGF-1 improved the blood sugar control, preventing further complications brought about by the disease, like blindness, peripheral nerve damage, and heart disease.

Nerve Regeneration – Furthermore, IGF-1’s potentials also include its ability in repairing the peripheral nerve tissue, which have been damaged by illness or injury. A torn nerve means that a connection to the muscle is damaged, resulting in loss of movement, along with muscle deterioration. To some extent, peripheral nerves could regenerate, but severe tears of over a few millimeters can lead to permanent injury. IGF-1, however, can repair and reconnect severely injured nerves up to six millimeters, a truly remarkable ability.
Hans-Arne Hansson, a Swedish scientist and works at the Institute of Neurobiology at the University of Goteborg, discovered that IGF-1 combined with other growth factors can stimulate a more drastic regeneration. Hansson added that IGF-1 itself, and when combined with further growth factors is likely to promote further repair and healing process.
In addition, IGF-1 has also shown significant effects on the spinal cord motor neurons, involving studies of cells in animals and culture. The motor neuron activity in the spinal cord cultures had increased by 150% up to 270%. The programmed death of cells in developing chick embryos also decreased in a relative manner. The substance also enhanced the emergence of axons of the spinal cord motor neurons in animal studies, while increasing intramuscular nerve sprouting in normal adult rats. A team of researchers at the Cephalon, Inc., West Chester, Pennsylvania said IGF-1 could be the “long-sought endogenous motor neuron sprouting factor."
In all, the implications of IGF-1 are not mind-boggling at all as it is highly capable of regenerating the spinal cord motor neurons, which is helpful in the treatment of amyotrophic lateral sclerosis (ALS), a health condition that results in the loss of cortical motor neurons and spinal cord neurons that lead to paralysis, and even death. It could likewise help in treating Charcot-Marie-Tooth syndrome, among the peripheral neuropathies conditions.
Apparently, Doctor John Wittig of the UCLA has been using the substance in preventing AIDS wasting among HIV-infected patients. The substance allows more aggressive chemotherapy in certain patients because drugs like Crisplatin and Vincristine at higher doses could lead to peripheral neuropathies.

Network of Growth Factors
Among the body’s growth factor army, the IGF-1 is now identified, isolated, and cloned through a genetic engineering technology for drug use. Doctor Eric Dupont, a growth factor researcher said, GH is equivalent to the general, while the growth factors are the foot soldiers in the army. Growth factors act as hormones, hooking onto the cell receptors, while sending biochemical signal throughout the cell’s interior. On the other hand, hormones generally send a long distance message. Most of the growth factors make the local calls.

IGF-1 as Every Bodybuilder's Dream
To date, many world-class bodybuilders are making use of IGF-1. They have reported massive muscle magnification, up by 20 pounds. Muscle Mass 2000 is an article, trumpeting IGF-1 as the most possible and most potent bodybuilding drug ever. T.C. Luoma, the author of the article said that IGF-1 is widely available in America at the moment, while sold in Venice out of the trunks of cars. In Southern California gyms alone, IGF-1 is discreetly sold in brown paper bags. There are still no supporting evidences of the bodybuilders’ claims, but the anecdotal evidence is certainly building up.
Luoma added that bodybuilders have been testifying their IGF-1 experiences, indicating 5% drop in their body fat, in only a month. The users also testified that their lean body mass increased, and their strength became more incredible. In a particular statement, it indicated that the IGF-1 is the most wonderful thing in the world. On the contrary, there are skeptics like Doctor Mauro Di Pasquale, a performance-enhancing compound expert, although there is a basis for the belief on the capacity of IGF-1 taken with HGH.
Over and above, there is a feedback mechanism between the HGH in the pituitary gland and the IGF-1 in the liver. HGH stimulates the IGF-1 release; however, there could be a rise of IGF-1 levels at a certain period in the circulation. This signals the shutdown of GH. Thus, there is a lag time throughout this process, and indication that growth hormone levels rise at night time, while IGF-1 levels rise in the daytime. Now, bodybuilders are hoping that through growth hormone and IGF-1, the effect on protein synthesis may be doubled as well.

Bottom Line
Growth hormone, most especially its army of growth factors such as the IGF-1 is widely used by bodybuilders, optimizing its bodybuilding effects, including the remarkable anti-aging reversal ability of the substance. Clinical trials have also shown IGF-1’s capability in treating various ailments like cancer and diabetes.

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 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 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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Clomiphene

Clomiphene citrate (USA trade name Clomid) is a selective estrogen receptor modulator (SERM) that increases production of the body's gonadotropins via disruption of the natural negative feedback system in the hypothalamus. Clomiphene consists of two bioactive isomers, zuclomifene and enclomiphene. Zuclomifene is responsible for the primary effects of clomiphene, which consists of binding to estrogen receptors for long periods of time. Because the receptors cease recycling (and cannot be reused) for the duration, the hypothalamic estrogen number decreases, meaning the body's feedback system tells it that there is low estrogen. Estrogen modulation is the body's primary method of initiating and controlling negative hypothalamic feedback; with perceived low estrogen, GnRH pulsatility is increased and the pituitary releases more luteinizing hormone (LH) and follicle stimulating hormone (FSH).[1]

Clomiphene is primarily used to treat female fertility issues via its ability to increase the body's gonadotropin release.[1] It is also useful for reasons related to the same mechanisms, as well as novel and newly discovered mechanisms, in treating various forms of male infertility.[1]

Schellen writes and highlights well the diverse uses and progressive versatility shown with clomiphene as a potential treatment for an array of issues:

After the discovery that Clomiphene-citrate (Clomid) increased the secretion of gonadotropins, it was first used to induce ovulation and later on it was also used in males in certain cases of infertility. The effects of Clomid on the hypothalamic-pituitary level made it also possible to use it for a dynamic evaluation of the hypothalamic-pituitary gonadal axis in both females and males. [2]

Clomiphene is often used by bodybuilders who self-administer anabolic-androgenic steroids (AAS) to control undesirable estrogenic side-effects such as gynecomastia, acne, and mood-swings, similar to the way drug tamoxifen and the aromatase inhibitors letrozole, exemestane, and anastrozole are used. Users of AAS also frequently use clomid to exploit its gonadotropin-stimulating effect, in order to increase testosterone levels from a suppressed baseline after a "cycle" of steroids via release of gonadotropin releasing-hormone, follicle stimulating hormone, and luteinizing hormone.

In some cases clomiphene may be preferable over other options such as testosterone therapy for hypogonadism because, as the researches quoted below note, testosterone administration actually causes infertility in many cases; further, as many cases of hypogonadism may be steroid-abuse-induced, testosterone would be ruled out in those cases:

Hypogonadism has a number of important clinical consequences related to androgen deficiency and impaired spermatogenesis. The cause of this condition is multifactorial and can result from hypothalamic, pituitary or gonadal dysfunction as well as factors that affect hormonal signaling along the hypothalamic-pituitary-gonadal axis. While testosterone replacement is the most common treatment, it can paradoxically lead to infertility, and may be a less physiologic therapy for patients with secondary hypogonadism due to pituitary dysfunction. Clomiphene citrate, and its derivatives, may allow for restoration of gonadal function by restoring physiologic pituitary function in a subset of patients with hypogonadism.[3]

Tan and Vasudevan document a case study in which clomiphene successfully treated (by standards of testosterone levels, LH pulsatility, and restoration of pituitary-gonadal axis and feedback system) premature andropause induced by long-term steroid abuse:

Clomiphene citrate is used typically in helping to restore fertility in females. This represents the first case report of the successful use of clomiphene to restore T levels and the pituitary-gonadal axis in a male patient. The axis was previously shut off with multiple anabolic steroid abuse.[4]

Taylor and Levine find clomiphene citrate suitable for long-term use in place of testosterone gel replacement therapy for treating sexual dysfunction and the set of symptoms generally associated with hypogonadism or andropause:

CC represents a treatment option for men with hypogonadism, demonstrating biochemical and clinical efficacy with few side effects and lower cost as compared with TGRT.[5]

Kanayama et al recommend clomiphene as part of a comprehensive treatment program for AAS abusers:

...AAS suppress the male hypothalamic-pituitary-gonadal axis via their androgenic effects, potentially causing hypogonadism during AAS withdrawal. Men experiencing prolonged dysphoric effects or frank major depression from hypogonadism may desire to resume AAS, thus contributing to AAS dependence. AAS-induced hypogonadism may require treatment with human chorionic gonadotropin or clomiphene to reactivate neuroendocrine function, and may necessitate antidepressant treatments in cases of depression inadequately responsive to endocrine therapies alone.[6]

Citations:

[1]Rossi S, editor. Australian Medicines Handbook 2006. Adelaide: Australian Medicines Handbook; 2006.

[2]Schellen TM. Clomiphene treatment in male infertility. Int J Fertil. 1982;27(3):136-45.

[3]Kaminetsky J, Hemani ML. Clomiphene citrate and enclomiphene for the treatment of hypogonadal androgen deficiency. Expert Opin Investig Drugs. 2009 Dec;18(12):1947-55.

[4]Tan RS, Vasudevan D. Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse. Fertil Steril. 2003 Jan;79(1):203-5.

[5]Taylor F, Levine L. Clomiphene citrate and testosterone gel replacement therapy for male hypogonadism: efficacy and treatment cost. J Sex Med. 2010 Jan;7(1 Pt 1):269-76.

[6]Kanayama G, Brower KJ, Wood RI, Hudson JI, Pope HG Jr. Treatment of anabolic-androgenic steroid dependence: Emerging evidence and its implications. Drug Alcohol Depend. 2010 Jun 1;109(1-3):6-13.

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CJC-1295 DAC 5mg

CJC-1295 DAC has shown some amazing results as a growth hormone releasing hormone (GHRH) analog. Not only has CJC-1295 shown the ability to increase growth hormone and IGF-I secretion and its benefits, but it has been able to do so in very large amounts. Recent research studies have shown that CJC - 1295 stimulates GH and IGF-1 Secretion, and will keep a steady increase of HGH and IGF-1 with no increase in prolactin, leading to intense fat loss, and increases protein synthesis.

is a long acting Growth Hormone Releasing Hormone, which causes the anterior pituitary to release more growth hormone. GHRH is released in pulses in the body, which alternate with corresponding pulses of somatostatin (growth-hormone inhibiting-hormone). Clinical Research was first conducted for CJC-1295 during the mid-2000s. The objective of the peptide was to treat visceral fat deposits in obese AIDS patients, as increased levels of exogenous hgH are presumed to increase lipolysis (fat loss). The clinical research was ultimately successful for most research subjects. Ghrelin, released from the gut, which circulates and acts as a hunger hormone, has synergistic activity in the body with GHRH and also suppresses somatostatin to make way for the GHRH pulse. Studies shows that combining a GHRP-6 with CJC 1295 DAC, significantly increase the release of GH and IGF-1 production without an increase in prolactin. An example of a GHRP (GH Releasing Peptide) is Hexarelin or GHRP-2. CJC 1295 DAC is a exceptionally designed peptide and is known for being the finest of the hGH secretogues. The DAC (Drug Affinity Complex) portion increases the half-life by binding with serum albumin and protects the CJC-1295 DAC peptide from degradation. This was formed when a lysine link was bounded to DACs to a reactive chemical called maleimidoproprionic acid (MPA).

CJC-1295 DAC vs. CJC-1295 No DAC

CJC-1295 DAC and CJC-1295 (also known as Modified GRF 1-29) are both Growth Hormone Releasing Hormones (GHRH). Their action in the human body is identical but the difference between the two peptides are the span of the half-life. Modified GRF 1-29 and Sermorelin have a very short acting half-life of about 30 minutes, while CJC-1295 DAC has a half-life that can last up to approximately 8 days. Many a scientist have reported that the short half-life of Sermorelin and Modified GRF 1-29 is considered to be much more natural as they produce a short pulse of Human Growth Hormone.

ConjuChem and The Development of CJC-1295 DAC

CJC-1295 DAC is a tetrasubstituted peptide analogue of Growth Hormone Releasing Hormones with D-Ala, Gln, Ala, and Leu substitutions at positions 2, 8, 15, and 27 respectively. A Canadian biotechnology company called ConjuChem had invented CJC-1295. Clinical Research on CJC-1295 first began during the mid-2000s. The goal of the peptide, acting to raise hgh like Ipamorelin, was to treat visceral fat deposits in obese AIDS patients because it is presumed that increased levels of exogenous hgH increase fat loss, or lipolysis. In one study, results showed that the measured GH release in rats over a two hour period showed that CJC-1295 released twice as much GH as CJC-1293 DAC. This result makes it preferable for immediate effectiveness as a result of the longer peak. With the use of a Growth Hormone Releasing Peptide (GHRP), such as Growth Hormone Releasing Hexapeptide (GHRP-6) in conjuction with CJC-1295 DAC, a study has shown that the GHRP’s create a Growth Hormone pulse which helps the CJC-1295 work effectively. Clinical research's involving CJC-1295 have shown that it had been successful for most research subjects..

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SARMs S4

SARMs, Selective Androgen Receptor Modulators, are a relatively new class of research chemicals that have selective androgenic activity in a given area of the body.[1] The specific activity is determined by which androgen receptors are activated and in what tissue.[1] The clinical capability of SARMs is expected to be more broad and diverse than anabolic/androgenic steroids like testosterone, which are almost never a first choice for treatment.[1] Testosterone and its ilk are considered unsuitable because their androgenic activity is systemic, meaning that undesirable side effects such as virilization in women, left ventricular hypertrophy in patients receiving doses exceeding a certain level, and various other effects that are difficult to prevent are commonplace

In addition to the specific targeted nature of the first-generation SARMs, they offer a major advantage in practical applied treatment over the androgens: they can be dosed orally without liver toxicity, which means that applied treatments require less training of subjects and in the future, use of the research chemicals may be possible for a larger group where injection or oral toxicity of anabolic steroids previously prevented indication by practitioners.[1]

Ke and Wang speculate that in elderly men with osteoporosis, or at risk of osteoporosis, could benefit from SARM therapy that (unlike testosterone and its derivatives) does not have any activity on the testes or prostate.[2]

While future SARMs may be developed with zero androgenic effect in target tissue at all, which would provide benefits such as (for example) anabolism of bone or muscle tissue with zero side effects, current SARMs all have some degree of androgenic effect in tissue, though still less than testosterone. The anabolic/androgenic ratio of SARMs currently available is between 3:1 and 10:1, whereas testosterone is 1:1.[3]

S-4 is an experimental or investigation-stage proprietary SARM research chemical developed by GTx Inc for treatment of benign prostatic hypertrophy, muscle wasting, and osteoporosis.[4] S-4 is considered a partial agonist of the androgen receptors in target tissue.[3] S-4 has less pronounced anabolic and androgenic compared to other SARMs. In trials treating BPH induced in animal models, S-4 reduced prostate weight as effectively as finasteride and without producing any reduction in muscle mass or other side effects common with androgen receptor binding compounds.[5] Gao et al suggest that by binding to androgen receptors, S-4 prevents DHT from binding and activating, but bypasses the expected anti-androgenic effects that would occur from occupying androgen receptors due to the fact that S-4 itself is a partial agonist of androgen receptors.[6] S-4 has also been shown to prevent bone loss, reduce body fat, and improve muscle strength and body composition in orchidectomized and ovariectomized rats.[7,8]

1] Mohler ML, Bohl CE, Jones A, Coss CC, Narayanan R, He Y, Hwang DJ, Dalton JT, Miller DD. Nonsteroidal selective androgen receptor modulators (SARMs): dissociating the anabolic and androgenic activities of the androgen receptor for therapeutic benefit. Journal of Medicinal Chemistry 52 (12): 3597–617. 2009.

[2] Ke HZ, Wang XN, O'Malley J, Lefker B, Thompson DD. Selective androgen receptor modulators--prospects for emerging therapy in osteoporosis? J Musculoskelet Neuronal Interact 5 (4): 355. 2005.

[3]Yin D, Gao W, Kearbey JD, Xu H, Chung K, He Y, Marhefka CA, Veverka KA, Miller DD, Dalton JT. Pharmacodynamics of selective androgen receptor modulators. Journal of Pharmacology and Experimental Therapeutics. 2003 Mar;304(3):1334-40.

[4]Hanada K, Furuya K, Yamamoto N, Nejishima H, Ichikawa K, Nakamura T, Miyakawa M, Amano S, Sumita Y, Oguro N. Bone anabolic effects of S-40503, a novel nonsteroidal selective androgen receptor modulator (SARM), in rat models of osteoporosis. Biol. Pharm. Bull. 26 (11): 1563–9. 2003.

[5] Gao W, Kearbey JD, Nair VA, Chung K, Parlow AF, Miller DD, Dalton JT. Comparison of the pharmacological effects of a novel selective androgen receptor modulator, the 5alpha-reductase inhibitor finasteride, and the antiandrogen hydroxyflutamide in intact rats: new approach for benign prostate hyperplasia. Endocrinology. 2004 Dec;145(12):5420-8.

[6] Gao W, Kim J, Dalton JT. Pharmacokinetics and pharmacodynamics of nonsteroidal androgen receptor ligands. Pharmaceutical Research. 2006 Aug;23(8):1641-58.

[7] Kearbey JD, Gao W, Narayanan R, Fisher SJ, Wu D, Miller DD, Dalton JT. Selective Androgen Receptor Modulator (SARM) treatment prevents bone loss and reduces body fat in ovariectomized rats. Pharm Res. 2007 Feb;24(2):328-35.

[8] Gao W, Reiser PJ, Coss CC, Phelps MA, Kearbey JD, Miller DD, Dalton JT. Selective androgen receptor modulator treatment improves muscle strength and body composition and prevents bone loss in orchidectomized rats. Endocrinology. 2005 Nov;146(11):4887-97.

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Ostarine / MK-2866

Ostarine / MK-2866
Ostarine or MK-2866 (CAS# 1235370-13-4) is a research chemical developed originally by Merck Inc. and now owned by GTx Inc. It is undergoing trials for Phase II (human) research. MK-2688 belongs to a class of chemicals known as SARMs or selective androgen receptor modulators. SARMs create selective anabolic activity at certain androgen receptors and not others, hence their name. Compared to testosterone, the sex hormone, the advantage of SARMs such as MK-2688 is that they do not have androgenic activity in non-skeletal-muscle tissues. MK-2866 is undergoing clinical trials for and may eventually be medically indicated and approved for prevention of cachexia, atrophy, and sarcopenia primarily in the elderly and sick population.

Testosterone and other androgenic anabolic steroids (AAS) are very effective at preventing muscle-wasting as well as increasing appetite and physical strength in humans and animal test subjects. However, AAS have a specific set of side-effects related to their non-specific androgen receptor activity that makes them contraindicated in many cases where they would otherwise be useful. Additionally, testosterone is subject to enzymatic conversion to a number of other bioactive hormones such as estrogen via the aromatase enzyme and DHT via the 5-alpha-reductase enzyme. While additional drugs may be prescribed to lower aromatase and 5-AR, or to minimize the side effects of AAS in some other fashion, testosterone is primarily only indicated for male hormone replacement therapy due to the fact that it is a problematic and complicated compound to use for its androgenic properties and the side-effects can vary greatly from individual to individual. Even primarily-anabolic AAS such as oxandrolone (Anavar), which are often used in terminally ill patients, do not entirely circumvent androgenic and other problematic side-effects.

Ostarine exerts its anabolic effects on skeletal muscle tissue almost exclusively, and therefore represents a new potential treatment option for a wide spectrum of conditions from age-related muscular atrophy (sarcopenia), AIDS or cancer-related wasting/cachexia, and even an agent to minimize atrophy during recovery periods from serious surgery or similar situations. It is effective in not only maintaining lean body mass (LBM) but actually increases it:
In the study, Ostarine met the primary endpoint of LBM, measured by a dual energy X-ray absorptiometry (DEXA) scan, by demonstrating statistically significant increases in LBM compared to baseline in both the Ostarine 1 mg and 3 mg treatment cohorts. Specifically, the change from baseline in LBM for the placebo, 1 mg and 3 mg treatment groups was 0.1 kg (p=0.874 compared to baseline), 1.5 kg (p=0.001) and 1.3 kg (p=0.045), respectively, at the end of the 16-week trial.[1]

Dr. Adrian Dobs, MD, MHS, an investigator in the Phase II trial for treatment of cancer cachexia, had the following to say about MK-2688:
Approximately half of all cancer patients suffer from the devastating effects of cancer induced muscle loss. Increasing lean body mass may improve patients' quality of life and even their response to cancer treatment. These Phase II results demonstrate the potential of a SARM to fill an important unmet need as there are currently no FDA-approved therapies available for cancer cachexia.[1]

As mentioned above as well as by Dobs, there exist few treatments for cachexia, no FDA-approved indicated treatments, and certainly no ideal treatments; the same is true of the majority of muscle-wasting conditions. Muscle-wasting related to cancer is the cause of a full 20% of cancer-related deaths, and it is likely that in related and similar conditions the instance of morbidity is equally high.[1]

As mentioned by Furuya, the effects of MK-2688 translate to anabolism in bone as well as skeletal muscle tissue, which means it could be indicated in an extremely wide variety of uses such as osteoporosis and as a concurrent treatment with drugs that reduce bone density, such as the class of cancer-treatment drugs known as selective estrogen receptor modulators:
Many efforts to produce novel drug materials maintaining a desired biological activity with an adequate tissue selectivity, which is so-called selective androgen receptor modulators (SARMs) , are being performed. As one of such efforts, studies on SARMs against bone tissues which possess a significant potential to stimulate a bone formation with reducing undesirable androgenic virilizing activities are in progress all over the world.[2]

Maddedu and Mantovani suggest in a review of candidate-drugs for cachexia that a tailored combination regimen may be more effective than any one currently-researched drug:
There are no published conclusive phase III controlled clinical trials nor general consensus about treatment approaches despite several years of coordinated efforts in basic and clinical research. Consequently, practice guidelines for the prevention and treatment of cancer-related muscle wasting are lacking. The purpose of this review is to supply an update on the promising agents and/or combined approaches for the treatment of cancer cachexia. RECENT FINDINGS: The choice for cancer cachexia treatment in clinical practice is very limited: the only approved drugs in Europe are progestagens. Several drugs with a strong rationale have failed or have not shown univocal results in clinical trials: they include eicosapentaenoic acid, cannabinoids, bortezomib and anti-tumor necrosis factor (TNF)-alpha monoclonal antibody. Several emerging drugs have shown promising results but are still under clinical investigation [thalidomide, selective cyclooxygenase (COX)-2 inhibitors, ghrelin mimetics, oxandrolone, olanzapine]. Moreover, increasing knowledge of cachexia pathophysiology and preliminary clinical findings seem to suggest that a combined treatment approach may be the most effective option. SUMMARY: A number of promising new agents are currently being developed but are not as yet regarded as standard of care. They include: selective COX-2 inhibitors, ghrelin mimetics, oxandrolone, selective androgen receptor modulators (ostarine), olanzapine, anti-IL-6 antibody and an innovative approach of multitargeted combined treatment. The data reported seem to suggest that the most effective treatment for cancer cachexia may be a combination regimen rather than single-agent treatments. This is in keeping with the general consensus that cancer cachexia is a multifactorial process and, hence, a potentially effective approach should be multimodal.[3]

Cititations:
[1] “GTx Presents Phase II Ostarine (MK-2866) Cancer Cachexia Clinical Trial Results At Endocrine Society Annual Meeting.” Medical News TODAY. 6-14-2009. http://www.medicalnewstoday.com/articles/153779.php; Accessed 9-21-2010.
[2] Furuya K. [Translated title from Japanese: Bone and Men's Health. Bone selective androgen receptor modulators]. Clin Calcium. 2010 Feb;20(2):225-33.
[3] Madeddu C, Mantovani G. An update on promising agents for the treatment of cancer cachexia. Curr Opin Support Palliat Care. 2009 Dec;3(4):258-62.

*The latter article is intended for educational / informational purposes only. THIS PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. Bodily introduction of any kind into humans or animals is strictly forbidden by law.

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DAC CJC 1295

DAC CJC 1295

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 signalling 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 signalling 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 signalling 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 downregulation 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. [3]

Citations:
[1] Lewis UJ. Growth hormone: what is it and what does it do? Trends Endocrinol Metab 1992;3:117-121
[2] Synthesis and Biological Evaluation of Superactive Agonists of Growth Hormone-Releasing Hormone, J Izdebski, J Pinski, JE Horvath, G Halmos, K Groot and AV Schally, Proceedings of the National Academy of Sciences, Vol 92, 4872-4876
[3] Pulsatile Secretion of Growth Hormone (GH) Persists during Continuous Stimulation by CJC-1295, a Long- Acting GH-Releasing Hormone Analog, Madalina Ionescu and Lawrence A. Frohman, The Journal of Clinical Endocrinology & Metabolism 2006 91(12):4792-4797
[4] Neuronal M3 muscarinic acetylcholine receptors are essential for somatotroph proliferation and normal somatic growth, Dinesh Gautam, PNAS April 14, 2009 vol. 106 no. 15

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Melanotan 2 (MT2) Tanning Injections

Research shows it can prevent cancer causing skin damage by increasing the natural UV sun protective pigment melanin. Melanin can be found in the skin cells in varying quantities naturally based on ethnicity: African, Hispanic, Middle East, Indian, Asian, and European etc. Researchers know that melanin is produced in the skin to protect from sun exposure, but until now personal genetics limited melanin production, especially for the fairest skin types such as redheads, blondes, and those with blue eyes. MT2 gradually increases the amount of melanin your skin can produce, and with minimal sun exposure even the palest individuals can develop an attractive and beneficial tan. Many researchers also noticed reduced wrinkles and improved skin texture, possibly also related to the skins protective response to the sun. MT2 is the second generation of melanotan, and has reduced side effects compared to MT1. Additionally, redheads naturally produce a different shade of melanin, and will benefit from the improved melanotan 2 formula to create a darker and more even tan

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Benefits of IGF 1

IGF 1 Supplements

The growth hormone IGF 1 or insulin-like growth factor is similar to insulin in its molecular structure. It is made up of 70 single-chained amino acids with three intramolecular disulfide bridges. This hormone plays a major part in every person’s bodily functions and growth.

Mechanism of Action

Insulin-like growth factor 1 receptor binds to particular receptors to activate cell proliferation and growth. Once the anterior pituitary gland produces the growth hormone, it is released in the blood stream. This growth hormone then signals the liver to produce insulin-like growth hormones. The body’s growth and development relies on the process involved with these hormones. The hormone also has effects on the body’s cellular DNA synthesis.

Benefits of IGF 1

The IGF hormone plays an active role in adult body anabolism and in children’s body development and growth. It is one of the hormones responsible for cell growth and repair that is vital to body tissues such as the muscles, liver, bones, kidneys, nerves, lungs and skin. Studies have also shown that the insulin-like growth hormone’s positively affects athletes’ or bodybuilders’ tissue repair and regeneration.

Insufficiency in the insulin-like growth hormone leads to growth defects such as stunted growth. People with an IGF deficiency often experience dwarfism and increased body aging. IGF 1 supplements can be taken along with Ipamorelin to increase growth. These supplements result in rapid cell growth and repair.

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CJC-1295 with DAC

CJC-1295 with DAC is a long acting version of GHRH (Growth Hormone releasing hormone) modified form (GRF 1-29) with drug affinity complex)

CJC-1295 w/o DAC Mod 1-29
CJC-1295 is a tetrasubstituted peptide of 29 amino acid length, primarily functioning as a growth hormone releasing hormone (GHRH) analog. CJC 1295 without dac (synonym CJC 1295 w/o dac-complex, modified form GRF 1-29 without DAC-complex) belongs to peptides hormones and contains 29 amino acids; as well it is quite stable analog of growth hormone releasing hormone with D-Ala, Gln, Ala and Leu substitutions in certain positions – 2,8,18, 27, and in a such way it is enhance this protein’s biological activity. Its molecular formula is C152H252N44O42 and its molecular mass is 3367.97.

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AICAR, an amide-conjugated nucleoside

AICAR

Introduction

AICAR, an amide-conjugated nucleoside, is an analog of adenosine. The international nonproprietary name (INN) of AICAR is acadesine; the full unabbreviated name is 5-Amino-1-(5-O-phosphono-ß-D-ribofuranosyl)-1H-imidazole-4-carboxamide (Chemspider aicar entry. (n.d.), and it is variously referred to as AICA riboside, AICA ribonucleotide, Z-nucleotide, and ZMP (however, it should be noted that ZMP specifically refers to the phosphorylated form – AICA riboside monophosphate – that is converted within cells after administration of AICAR). Its actions are primarily mediated by selective AMPK activation as well as conversion into factors that also act on AMPK.

AMPK: The key to understanding AICAR

In seeking to understand AICAR, researchers are well-served by first understanding AMPK. AMPK, long known to play a role in cellular energy-switching from use of ATP to ADP and AMP as an energy-transfer substrate, has recently (within the past decade) been shown to act as a cellular as well as whole-body energy “sensor” that plays an active and intriguing role in many systemic processes, and of which dysregulation contributes to many disease states.
Because AICAR induces AMPK signaling through a relatively direct pathway, is used in many studies to study and better understand AMPK itself. At the time of writing (2012), however, there are vastly more published inquiries into AMPK than of AICAR specifically; since AICAR’s effects are similar (or identical to) AMPK, it is possible to better AICAR by closely reviewing AMPK studies to infer AICAR’s effects.

AICAR therapeutic uses

The actions of AICAR vary greatly by method of administration, duration of application, and dosage. Administration of exogenous AICAR orally or by injection shows promise for a plethora of medical problems and disease states: ischemia, hypertension, diabetes, obesity, cancer, Alzheimer’s disease, and even aging may be addressed to varying degrees by use of AICAR as a drug (Salminen et al).

Lifestyle factors such as overeating or under-exercising appear to initiate a cascade of pathological events that are mediated by altered AMPK signaling; AMPK expression is associated with exercise and periods of not eating. Other genetic factors also predispose individuals to AMPK dysregulation. Eventual effects of AMPK dysregulation – such as obesity, diabetes, even Alzheimer’s disease – can be treated or even partially reversed by AICAR-induced AMPK expression, whereas diet or exercise may not exert a major effect past an early or undetectable point in the pathology.
Currently, AICAR (under the INN acadesine) is in use as a myoprotective agent: when applied, it protects the heart against myocardial reperfusion (re-introduction of blood-flow) after ischemia (restriction of blood-flow, either acutely or chronically. It is also being researched for treatment of lymphoma.
AMPK acts in nearly all tissues of the body, both as a local cellular energy balance signal and sensor – controlling energy-in versus energy-out pathways in response to changes in other cellular factors and available energy – and as a systemic controller of metabolic state and other non-metabolic processes. AMPK also acts as an important bridge between cellular and peripheral tissue energy regulation and systemic energy regulation. AMPK acts within the master control switch of the body, the hypothalamus, as well as in nearly all types of cells.

Research uses of AICAR peptides

AICAR is useful in researching the purine synthesis pathways and their downstream effects to better interpret biomarkers for different disease states. Most cancer cells rely on the de novo purine synthesis pathway, while normal cells prefer the salvage pathway; many chemotherapeutic drugs inhibit purine synthesis. A better understanding of these differences between cancer cells and normal cells should lead to more-selective less-toxic chemotherapy drugs, as well as better ability to tailor therapies to individuals via improved understanding of biomarkers related to purine synthesis inhibition in various cell types (Boccalatte et al, 2009).

AICAR, AMPK, and purine synthesis pathways

Endogenous AICAR also exists in cells; it is an intermediate in the de novo purine nucleotide synthesis pathway, specifically in the generation of inosine monophosphate (IMP), from which adenosine monophosphate and adenosine triphosphate are generated (Berg et al, 2002). However, as an exogenous AMPK-activator, AICAR does not disrupt AMP-to-ATP ratios within cells. A few of the effects of AICAR administration such as induction of apoptosis in cultured immortalized T-cell lymphocytes, do not involve activation of AMPK (López et al, 2003).
ATP (adenosine triphosphate) acts within the human body as an energy transfer molecule within cells. It is an unstable molecule with high-energy phosphate bonds; when the bonds are “broken” via hydrolysis, the released energy is utilized within cells to do work. ATP breaks down into ADP (adenosine diphosphate) and phosphate. ADP can be further hydrolyzed into AMP (adenosine monophosphate) to release more energy. Shifts in the ratio of ATP to AMP correlate with energy balance; a lower ratio means that less energy is available and/or ATP demand is high due to exercise demand. AMPK inhibits energy- consuming pathways such as protein synthesis and fatty acid synthesis, and upregulates energy-generating pathways such as fatty acid oxidation and glucose transport.
AMPK expression changes according to ATP-to-AMP (and ADP) ratios, which fluctuate according to energy availability. AMPK expression or absence then exerts an appropriate effect according to energy availability: energy storage in times of surplus, energy usage in times of scarcity.

Roles of AMPK signaling in various physiological systems and states

In 2008 AICAR research at the Salk institute in San Diego, California generated headlines like the LA Times article “’Exercise Pill could take the work out of workouts.” The portrayal as a pill can mimic exercise has intrigued the public, despite some factual errors (Bamford et al write “AICAR treatment did not alter the MHC-based fibre type composition in fast- or slow-twitch muscles” (2003) and the 2008 article merely discussed specific gene-expression related to the structural adaptation found in endurance athletes (Narkar et al, 2008)):

"Doping,” the use of pharmacological agents to improve athletic performance for competition, is controversial and intrigues the public mind. AICAR improved treadmill performance in untrained mice by 45% (Narkar et al, 2008), leading to speculation that it may work as a performance-enhancing drug (PED) in humans. Tests have been developed for AICAR use in professional athletes, but since the 2008 articles the medical community has focused on AICAR as a way to better understand the profound role of AMPK in health and disease states and on AICAR as a treatment for a variety of pathologies."

AMPK and mTOR in resistance and endurance exercise

In humans, AMPK is increased in response to both endurance and resistance training, but mTOR response is thought to be specific to resistance training (Vissing et al, 2007). Basal concentrations of mTOR and AMPK were not permanently affected in a study of three groups (control, endurance, resistance training) undertaking ten weeks of training (Vissing et all, 2007). Although Nader speculates (2006) that concurrent endurance and strength training may be counterproductive due to the potential of AMPK (expressed with endurance training) to limit mTOR’s effect, Medeiros et al found that in the rat swimming increases transduction activity of proteins involved in insulin-dependent protein synthesis and the mTOR pathway (2011).
The likely explanation is that presence or absence of factors such as insulin and amino acids is as important an influence on the ultimate physiological outcome of exercise as the nature of the exercise; AMPK expression occurs in a fasted state regardless of nature of exercise, as well as in response to any exercise; mTOR proteins are expressed primarily in a fed state, and in response to resistance exercise – but are unlikely to be expressed in significant quantities if the exercise is performed fasted.
The increased potential for mTOR protein transduction after endurance exercise may be explained by the cross-talk between AMPK and mTOR; AMPK acts as an mTOR control and regulates plasticity of muscle tissue (Lantier et al, 2010). As a therapeutic agent, this suggests that ongoing AICAR use should not significantly disrupt signaling cascades relevant to anabolism provided that insulin and amino acids are present during and after resistance exercise.
In an animal model of obesity, Williamson and Drake (2011) found that two weeks of AICAR administration paradoxically promoted muscle-growth. The authors of the study hypothesize that lower fasting AMPK levels, which relate to insulin-resistance found in obese, aging, or otherwise insulin-resistant muscle tissue, results in an overall lower metabolic capacity of the tissues and therefore a reduction in mTOR effect; normalizing AMPK levels results in a net reduction of mTOR with a surprising effect:

Our recent data show that short-term (2-week), daily treatment of obese (ob/ob) mice with AICAR normalized their hyperactive, fasted-state mTOR signaling. Along with the expected reductions in circulating blood glucose and insulin concentrations, and muscle lipid and glycogen content after AICAR treatment, translational capacity and mass (including muscle fiber areas) of the plantar flexor muscle complex were significantly increased in the obese treated mice. It is our view that the oxidative metabolism/capacity of the muscle and the regulatory processes of muscle growth (i.e. mTOR and translational control) need to be normalized to elicit growth in insulin resistant (e.g. obese, aged) muscle.

Paradoxically, mTOR reduction in certain physiological states by AMPK/AICAR can result in improved protein synthesis and muscle-cross section.
Lantier et al, 2010). AMPK directly inhibits mTORC1, the mTOR complex involved in overloading-induced hypertrophy of muscle cells (Lantier et al, 2010).
Lantier et al tested the effect of total AMPK inhibition in myotubes and found that it resulted in myotubes 1.5 times bigger than AMPK-expressing myotubes. However, the AMPK-deficient myotubes failed to respond to mTOR pathway activation: while they started with an initial greater size, they did not increase in size whatsoever when stimulated with mTOR pathway effectors (Lantier et al, 2010).
One possible explanation is that protein synthesis could not be increased any further and so the mTOR effector had no effect, but another – echoing Drake and Williamson’s 2011 paper – is that AMPK deletion limits muscle growth due to limiting energy-generating capabilities necessary for muscle growth (Lantier et al, 2010).
AMPK also limits cardiac hypertrophy, and AMPK deletion results in cardiac hypertrophy (Lantier et al, 2010), a state probably caused in part by mTOR overexpression.
Fatty acid synthesis and oxidation
AMPK is a master lipid metabolism regulator (Lim et al, 2009): high levels of AMPK inhibit cholesterol and fatty acid synthesis. AMPK also acts as a cellular signal to increase fatty acid oxidation by indirectly increasing levels of carnitine palmitoyltransferase-1 (CPT-1), which is the rate-limiting factor in mitochondrial uptake of free fatty acids (FFAs). In other words, AICAR and AMPK increase the upper limit of the body’s ability to burn stored fat for energy.
Yin finds that AMPK is upregulated in fat cells during beta-adrenergic agonist-induced lipolysis due to intracellular fat level via cAMP increases and greater phosphorylation of AMPK, and AMPK is necessary for optimal beta-induced lipolysis (2005).
AMPK dysregulation is implicated in obesity: lipolysis is inhibited and constant low-grade fatty acid synthesis may take place. A steady caloric surplus (energy surplus) suppresses AMPK, resulting in reduced release of fat for fuel usage, and instead resulting in constant low-grade fat storage.
Direct application of AICAR is likely to result in improved lipolysis and fat oxidation, as well as decreased levels of fatty acid synthesis. This is a revelation for development of future obesity treatment strategies.

Conclusion

AICAR has yet to be realized as a mainstream treatment, likely because wide-range systemically acting drugs with profound cellular and systemic effects are difficult to press into medical use under current the regulatory climate in the United States, Canada, and EU countries; the wide range of effects raises hard-to-answer questions about the safety and appropriateness of AICAR for any given disease, particularly “lifestyle” conditions such as obesity and insulin resistance, which have accepted “lifestyle” remedies of diet and exercise and accepted medical remedies as they reach a certain point in pathology.
In the case of Type 2 diabetes, further animal and human safety and efficacy studies could prove AICAR to be a viable candidate, but the current drug metformin is a viable AMPK-targeting agent; AICAR could also be a financially risky choice for investors with a viable (if perhaps less-effective) similar drug on the market. In the case of Alzheimer’s disease, AICAR may also prove to be a next-generation treatment; a better understanding is needed, though, as AMPK appears to play a role in advancing late-stage Alzheimer’s.
For now, AICAR will continue to be used by researchers to better understand the effects of AMPK (and as a treatment for lymphoma and after cardiac ischemia); doubtless, medical advances will continue to be made due to AICAR’s usefulness as a research aid, regardless of when AICAR itself is brought in as a therapeutic agent for the conditions discussed herein.
Note: Researchers who inquire about personal aicar peptide use including, but not limited to bodybuilding, dosing, injections or cycling will be added to our DO NOT SELL LIST.

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