Best IGF out. It has a fast half life so less potential to go systemic. This is my IGF of choice!


Took this writeup from another forum~
DES (1-3) IGF-1 (NOT THE SAME AS IGF-1)
Most athletes have heard of IGF-1 (Insulin-like growth factor-1) and the amazing anabolic effects it has been reported to have upon protein based tissue such as muscle.
Des (1-3) IGF-1 is over 10 times (1000%) more anabolic than IGF-1. Now that is amazing!!
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. Why? 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 o 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 receptor- site 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. Huh, good deal. And the synthetic form of this super anabolic stuff is beginning to show up on the black market more frequently.
Referance: Ballard FJ Des(1-3)IGF-I: a truncated form of insulin-like growth factor-I. International Journal of Biochemistry and Cell Biology 28(10): 1085-1087 (1996)
DES(1-3) IGF-1 is now available at PurchasePeptides
PM me for possible discounts!
-T
Last edited by TwisT; 05-23-2012 at 11:02 PM.
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Best IGF out. It has a fast half life so less potential to go systemic. This is my IGF of choice!


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i like DES post workout 50mcg total bilaterally. Since DES fits into the IGFr when it is mis-shaped from lactic acid I think it is best to use right after working out.
Although there might be some good effects if used 24 hours post workout to let MGF do its thing. Maybe using a tourniquet to induce lactic acid......


I think the optimal use would be directly P/wo because of the acidosis, as you stated, and use it in conjunction with lr3 for the 24h block. At the price of this stuff, and the incredibly short active life, we should best save it for post w/o where it will be most effective.
-T
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Prototype Nutrition
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I'm curious as to how to take it and at what dose.
Do you just pick a lagging body part and do it bilaterally? I've never used a slin pin.


What we really have to look at is the active life. Obviously, lr3 is going to be in out body for quite a while, while the new des is only active for up to about 20 minutes. With that said, the amount we inject would be roughly the same, I think the optimal amount would be about 33.3mcg in each side, intra-muscular, and immediately post w/o. This will let DES do exactly what its designed to do, fit into the igf receptors weather they are misshapen or not, giving you the best saturation possible. Now we obviously dont want 24/h saturation, but there would be other benefits to maybe have a small dose of lr3 in us aswell. My theory would include a small injection of around 20mcg lr3 sub-q in the morning, while DES post workout. Obviously, I've never seen anyone do this but I'm pretty confident it would yield some great results. But then again the DES alone will yield great results itself.
-T
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Sub Q is verrrrry easy. You pinch the skin next to your belly button and stick the inslun needle in. The needle is only a half inch long, then you just inject! Its painless, unlike normal IM pinning.
Eh its slow, doing my best to educate people on the benefits of peps so hopefully it will pick up soon. Adding DES is helping, not many companies are able to produce it yet
-T
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I thought by Bi-laterally you meant you hit each body part with it. Like if I worked bi's I'd pin each bi post W/O. I'm not the skinniest person ever but still that'd be hard to get it under the skin I think.
I'm glad it's working out for you man.
I'm kinda wondering if it's sooo expensive why I got it thrown into my order for free. That has me a little worried.![]()


If you are doing IM bilat then yes, you do each outter or inner head of the bicep for example. If doing sub-q bilat, its not hard to get under the skin at all, you're injecting into the fat, your skin layer is actually quite thin. I would definitely do IM for DES. As long as the needle is all the way in, you're g2g. Hmm, that is odd, maybe someone was feeling quite generous haha.
-T
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Or it's bunk and/or just reggie IGF.
So the perfered method for DES is IM bi-lat? Or Sub-q?
I know the difference in technique but what is the difference in results? Obviously the sub-q in the stomach would absorb into the entire body correct? And the IM would be more of a localized deal?
Thanks for all of the info and not talking down like I'm a noob btw. I'm sure other people have the same questions I do.


There are many theories, but what we have to look at is a) how long it takes for sub-q absorption and b) active life. Now with DES, the active life only being up to 20 minutes, Sub-q may be inferior because of how long it takes for the amino to be released into the bloodstream. So, your best bet would be to pin DES IM Bilat post W/O
-T
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Awesome info! Thanks man.
Do you sell bac water and/or slin pins?


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Prototype Nutrition
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Yes IM is the best way to go and a good idea would be to do multiple micro injections, i.e. 4mcg injections IM 8x bi-laterally. The thinking is that only pinning a small amount 8x covering the entire area of the muscle will keep IGF more localized instead of Injecting 40mcg 1x bi-laterally. When you do one mass injection you have more of a chance for the IGF to "over fill" the receptors and go systemic which is not what we want. This of course is just an idea.
Now the dilema with IGF and timing......After we workout our body creates MGF that causes In response to mechanical strain, satellite cells to become activated. Activated satellite cells initially proliferate as skeletal myoblasts before undergoing myogenic differentiation. when we inject IGF we blunt proliferation and cause myoblast cell differentiation (The process whereby a relatively unspecialized cell acquires specialized features of a myoblast. A myoblast is a mononucleate cell type that, by fusion with other myoblasts, gives rise to the myotubes that eventually develop into striated muscle fibers)
I have always thought that people not getting good results from IGF where because the timing of the injects were off. We want MGF to do its thing for at least 24 hours before we inject IGF and cause differentiation. I have suggested the use of MGF post workout and injections every few hours of MGF to keep a pulse going for 24 hours to create the most proliferation before we inject IGF and cause differentiation. After 24 hours inject IGF-1LR3 (again multiple micro injections around the entire area of the muscle bi-laterally)
Now I have read a cool study about IGF and muscle in a state of hypoxia (oxygen deficiency) like after working out, proliferation will occur. When IGF is administered to a muscle in a normal state of O2 differentiation will occur. We know that IGF-1 DES 1,3 works best in a state of hypoxia because lactic acid is present. This brings me to thinking that DES should be administerd immediately post workout and then 12-24 hours IGF-1 LR3 or IGF-2 LR3 should be administered (of course multiple micro injections bi-laterally).

(Science Daily)
Researchers Solve a Molecular Mystery in Muscle
ScienceDaily (Mar. 15, 2010) — The muscle-building abilities of hormones known as insulin-like growth factors (IGFs) are legendary. Just do an online search and you'll find not only scientific papers discussing the effects of IGFs on the cells that give rise to muscle tissue, but also scores of ads touting the purported benefits of IGF supplements for bodybuilding.
But in spite of widespread interest in these potent molecules, key details about how IGFs work on muscle cells have been lacking.
A research by a team led by University of Michigan molecular biologist Cunming Duan has cleared up a longstanding mystery about the workings of IGFs. The team's findings, scheduled to be published online in the Proceedings of the National Academy of Sciences, could lead to new treatments for muscle-wasting diseases and new ways of preventing the muscle loss that accompanies aging.
And because IGFs also are implicated in the growth and spread of malignant tumors, the new insights may have implications in cancer biology.
Like other peptide and protein hormones, IGFs work by binding to receptors on the cells they target. The binding then sets off a cascade of reactions that ultimately direct the cell to do something. You might think that a given hormone, binding to a particular receptor, would always elicit the same response from the cell, but that's not what happens in the case of IGF and myoblasts (immature cells that develop into muscle tissue).
During muscle formation, the binding of IGF to its receptor can prompt either of two very different responses in myoblasts, said Duan, a professor in the Department of Molecular, Cellular and Developmental Biology. Some of the cells are stimulated to divide, while others interpret the very same signal as an order to differentiate (become specialized).
"These are opposite and mutually exclusive cellular events -- once a muscle cell divides, it can't differentiate, and once it differentiates, it can never divide again," Duan said. How activation of the same receptor by the same hormone can elicit two such distinctly different responses has been one of the most puzzling questions about IGF, but Duan and colleagues have found the answer.
"The myoblasts' response is controlled by oxygen availability," said Duan. When oxygen levels are normal, IGF promotes muscle cell differentiation; when oxygen levels are below normal, IGF promotes muscle cell division. Teasing out the molecular details, the researchers discovered that low oxygen activates an intermediary called the HIF-1 complex, which reprograms the cascade of steps that ultimately controls the cell's response.
The findings not only reveal how muscle cells respond to varying oxygen levels during normal development, but also have implications for human disease, Duan said. "For example, a major reason that muscle atrophy occurs as people get older is that the IGF signal gets weaker. If we can find a way to affect IGF signaling, we may be able to stop or reverse the loss." Although manipulating the oxygen levels in living cells could be difficult, it may be possible to manipulate HIF-1 in ways that would mimic changing oxygen levels.
The work also could help scientists better understand the processes involved in cancer progression and spread. It's known that IGF can promote tumor cell division and survival and also that oxygen levels are often lower in tumor tissue than in normal tissue. Finding the link between IGF activity and oxygen levels may lead to new strategies for cancer treatment.
Duan's coauthors on the paper are former graduate student Hongxia Ren, now a postdoctoral fellow at Columbia University, and Domenico Accili, professor of medicine at Columbia .
The research was funded by the National Institutes of Health, the National Science Foundation and the University of Michigan.


Good info Myosin.
DES (1-3) IGF-1 is extreamly expensive to synthesize in the US at the moment... so please be aware of this when looking for a DES source. I am offering it at the best price that I can right now. Remember, in the world of anabolics and peps... cheaper is not always better...especially when you don't know exactly what in in those vials. There is a certain cost to synthesize this peptide... and seeing it in places being sold at a lower price really makes you wonder
/end rant
-T
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