Has anyone tried these compounds before?

[11rdc11]

I was reading Chemical Muscle Enhanchment and came across these other compounds. Has anyone tried them before or know any more info on them?

DES (1-3) IGF-1
Interleukin-15 (IL-15)
Prostaglandins (PG's)
TGF ( Transforming Growth Factor)
TNF (Tumor Necrosis Factor)
Adequan

[Alin]

Try doing some google searches on items in question.

[Tyree33]

Way too complicated for me. And to be honest w/ u I would just stick to what works. Just curious what's your motive for trying out all of these mostly unheard of compounds?

[11rdc11]

I was just really curious about these products. I don't plan to use them to expensive and no need to. I was just curious because I think I heard that Interleukin-15 (IL-15) could possibly be used to treat fibromalygia.

[Milky87]

Apparently, Adequan at 500mg every 4 ays gives a 13.5% mass increase after 12 weeks. Or so Hooker says

[Mr.Huge]

& anti-gdf8 is what is said to have made the frreaks of today. This is what is said to have given them the next level beyond that or the norm.

The PGF2/prostoglandins benefits are not worth the pain and suffering from injections is what has been said by most.

IGF-1 you will get more cost effective gains using Growth Hormone -vs- IGF-1


Mr.Huge

[rAJJIN]

all new to me.
Ill stick to the stuff I know :D

[hooker]

TUMOR NECROSIS FACTOR is catabolic, man...

[GIO]

good luck finding TGF,TNF & DES.
I have use PGF-2 but it upsets your stomich bad.
IL-15 I would like to use if I can find it.I found a lab that has but for mice. I don't know if I can use that one & I would have to see if they would sale it to me.

[11rdc11]

TNF (TUMOR NECROSIS FACTOR)
Reported Characteristics

Drug Class: Adipocyte Necrosis Stimulator
HPTA Suppression: None
TNF should not be confused with TGF. Though similar in reaction, their action is through a different mechanism. Endogenous TNF production is normally a response to infections. Once released TNF kills fat cells through necrosis. Let me explain that. Every cell in genetic material contains specific DNA for cellular death. The exception is cancer cells. When the body has either the need for energy or factors contained within a cell the DNA is triggered through one or more chemical messengers to give up the factor. In the case of TNF, the message is “commit cellular suicide�. When applied to fat cells (adipocyte) the result is a reduction in adipose tissue. It sounds cool, but the same signal can kill muscle cells as well.


TGF (TRANSFORMING GROWTH FACTOR)
Reported Characteristics

Drug Class: Adipocyte apoptosis stimulator
Water Retention: None
High Blood Pressure: Rare
DHT Conversion: None
HPTA Suppression: None


TGF is an endogenously produced hormone-like substance that plays a role in fat cell apoptosis (cell death). In times of starvation, such as long term carbohydrate depletion, adipose tissue produces TGF as a means of blocking fat cell anabolism, this means insulin in unable to trigger fat cell growth yet still possesses its powerful anabolic signal for muscle. This in turn facilitates the process of fatty acid mobilization (release from adipocytes/fat cells) and subsequent utilization as an energy source for the body. The result is fat cell starvation and eventual apoptosis. This is synergistic with natural PGF-2 elevation since localized increases in PGF-2 also result in an increase in TGF production. There also appears to be correlation between endogenous /exogenous GH levels and TGF. The higher the GH level, the more TGF produced in/by adipose tissue. This somewhat explains the extreme fat loss that occurs during GH administration even without a change in dietary habits.

Bodybuilders utilized exogenous forms of TGF as a means of fat cell eradication. Picture the number of fat cells in an athlete's body decreased by 20-50 %! During administration, fatty acids provide food for hard training muscle. Post administration, the athletes possessed a much lower potential for gaining fat tissue while creating a superior ability to utilize calories to build muscle. Simply stated, this means less mouths (cells) to feed = more calories for muscular repair and growth. Obviously there was a synergistic chemistry possibility utilized by athletes. TGF alone would be catabolic to lean mass tissue so an increase in the anabolic signal from GH, insulin, PGF-2, and/or IGF-1 was reported to be utilized by the few who had personally experimented with the drug. This was mostly done through TGF use to create an Absolute Anabolic Phase (See "Building The Perfect Beast" featuring "Frank N. Steroid" for more info on Absolute Anabolic Phases and Max Androgen Phases).There was a few report of pro bodybuilders who layered TGF into a Max Androgen Phase as a means of decreasing fat accumulation during mass weight gain protocols.

[11rdc11]

Interlukin-15 (IL-15)

Interlukin-15 (IL-15) is an anabolic cytokine that is produced in skeletal
muscle tissue and has a highly active roll in muscle growth.(1) Evidence suggests it has both anti-catabolic and anti- adipocyte(fat cell) activity.(2 3) Studies show that Interlukin-15 overexpression caused a 2-5 fold increase in the muscle contractile protein myosin(2)and significantly reduces muscle wasting(4) this will surely result in a net anabolic effect. Since the proteins that are responsible for muscle contractions are increased an improvement of muscle strength or power may be seen from IL-15 administration.

Fat loss.

Studies also show it to be a potent fat loss agent(3)IL-15 acts directly on the fat cells (adipocytes) to control fat accretion by enhancing fat breakdown or suppressing fat formation(3) and may be an important factor in mobilizing fat and shuttling it to other cells in the body(3) The fat loss effect of IL-15 also seems to be dose-dependent(3).

Interlukin-15 and insulin-like growth factor-I.


IL-15 seems to be far superior to insulin-like growth factor-I (IGF-1) when it comes to improving body composition. IL-15 induces muscle growth via mechanisms that IGF-1 does not(2), while IGF-1 promoted protein build-up only, IL-15 stimulated protein buildup and inhibited protein breakdown.(2) This also suggests that IL-15 promotes anabolism in a different manner than IGF-1(2). One other study showed that IL-15 was as effective as IGF-1 but at a tenth of the dosage(5).

IL-15, IGF-1 combo.

Interesting thing about anabolic steroids is stacking compounds that induce muscle growth via different pathways independent of each other, trenbolone and stanozolol are good examples. IL-15 and IGF-1 are no exception with the combo increasing the muscle protein myosin chain accumulation close to five-fold(5).

As good as IL-15 sounds on paper in regard to muscle growth it also has a vital role to play in the immune system(2). So the drugs side effects in humans using it for muscle mass and fat burning are unknown.


Des (1-3) Igf-1 (not The Same As Igf-1)

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Ok so we know what IGF-1 (Insulin like growth factor-1) is,Des (1-3) IGF-1 is over 10 times (1000%) more anabolic than IGF-1.

IGF-1 is actually produced from both Insulin and growth hormone in the liver and other tissues. IGF-1 is made up of 70 amino acids in a chain. Well, when a clever chemist removes the last 3 amino acids in the IGF-1 chain (the N-terminal tri-peptide) it becomes Des (1-3) IGF-1 and 1000% plus more anabolic.

IGF-1 circulates through our blood stream and tissue 24 hours a day, 7 days a week. Unfortunately, most of the IGF-1 is inactive because it is bound by another protein called (get this) IGF-1 Binding Protein-3, or IGF-1-BP-3 for short. Since bound hormones can not fit into and trigger a receptor-site, the majority of circulating and muscle IGF-1 can not trigger an anabolic stimulus. Like tons of cellulite in a porno movie (who watches those?) there is little good stuff happening. However, when IGF-1 is altered and becomes Des (1-3) IGF-1 the binding protein IGF-1-BP-3 can not bind to it and it is totally active. Another reason Des (1-3) IGF-1 is so potent is its unique ability to fit into lactic acid altered IGF-1 receptor sites. (YUP) When we train we burn carbohydrates as a fuel to make cellular ATP. When cells switch to this ATP pathway, the by-product is Lactic Acid. This is of course the cause of most of the burn we feel during intense or higher rep sets. Well, the lactic acid build-up is called acidosis, and it destroys the shape of some receptor-sites for period of time. Therefore some anabolic/anti-catabolic hormones have difficulty merging with their respective receptorsite and triggering a response (such as even unbound IGF-1). Not so with Des (1-3) IGF- 1, the super growth factor. It fits into the IGF-1 receptor-site even after acidosis. Des (1- 3) IGF-1 is unbound, over 10 times more potent than IGF-1, and it picks receptor-site locks. Too bad it has only a few minute active-life.

Did you know that our body's make Des (1-3) IGF-1 naturally? Most un-informed individuals claim other wise, but it is true. When an athlete trains lactic acid builds up in muscle tissue. As we know, there is always IGF-1 / GH present in the blood stream and tissues (including muscle) from prior work-outs and other metabolic factors. That lactic acid burn triggers IGF-1/GH secretion from both prior and present work-outs. Unfortunately, lactic acid destroys some of the IGF-1 present in muscles being trained. But wait, this is good too!

Lactic acid also cuts (truncates) the last 3 amino acids off the 70 amino acid chain of "some" of the surviving IGF-1 and creates Des (I-3) IGF-1. So acidosis increases GH/IGF-1 production in the liver, "unbinds" IGF-1 locally in the muscle being trained (burned), destroys some of the IGF-1, and converts some IGF-1 into Des (I-3) IGF-1.

[11rdc11]

I got all that from AR and give credit to goose4 and big k.l.g

[thepopo]

TGF sounds pretty interesting.