Tag Archive for IGF1

Understand the Various IGFs bodybuilding peptides


IGF-1 LR3 is the most common, popular and prevalent form available right now. But, there is a big question of whether it works and by what mechanism. Originally we had a bio-identical version of igf-1, rigf-1, that was very short acting. Though it was in and out of your system very quickly it had a reputation for inducing hyperplasia (activation and maturation of muscle satellite cells). LR3 was developed for use in the lab in tissue cultures because the bio-identical igf-1 was not lasting in experiments. rigf-1= 70 amino acids, LR3= 83 amino acid sequence. As a result LR3 works very differently. Most in the know say that it is not going to activate satellite cells/induce hyperplasia because of it’s amino acid structure. It just doesn’t bind to the cells and cannot be broken down properly in the body for that purpose. It does, however, have insulin-like effects (duh, right?). I’ve experienced this first hand. So, used on a steroid cycle it’ll boost gains just as humalog would. Do you get pumps and greater vascularity from insulin? Well, you’ll get it from IGF-1 LR3 as well. And, imo, that’s about it. It’s all of the “insulin like” with non of the (for our purposes/hyperplasia) special “growth factor.”


The second most common/popular igf-1 drug is MGF/PEG-MGF- Mechano Growth Factor. Another name for it is IGF-1Ec. It is different than IGF-1 LR3 in structure and effect. The PEG form is simply a longer acting form of MGF, not an entirely different structure like we see in rigf-1 vs igf-1 lr3. Most people will say that PEG-MGF’s effects are systemic and MGF’s effects are local. i.e. PEG is for the whole body and regular MGF is for “site-enhancement.” Personally, I don’t buy this. Like I said, it’s not two entirely different structures like the two igf-1s. MGF is so short acting that I doubt its effects can fully be seen even when used for site enhancement. It’s simply broken down too fast. So the question is: Is PEG MGF so resistant to being metabolized that it can’t work at the local level in the muscle?

For local/site-enhancement to work the product has to basically be used while it is in said location. I.e. you shoot it in your biceps and before it can move out into the rest of your body it is broken down in the muscle and “put to work” stimulating the satellite cells and helping them become new muscle. How long does PEG-MGF stay in that “site”? How effective is MGF at this to begin with?

I don’t know. That’s the short answer. But, I do know that it has more potential for site-enhancement than IGF-1LR3 because it is still a usable form when it comes to effecting satellite cells. It’s up to you whether you want to use the PEG form or not. I honestly couldn’t tell you which is best and you’ll see people swearing each one is better than the other.

The main thing I want to get across is that it isn’t like LR3 where they totally changed the structure to make it “longer acting”. With MGF they simply PEGylated it so that it would hold up longer in the system. You still have the original drug, just a longer-acting version of it. To me, since PEG MGF is longer-acting and also an original, bio-available form of IGF-1, I give it better chances at working overall than IGF-1 LR3. I know some will say I’m comparing apples to oranges here. But, I feel more like I’m comparing IGF-1 to insulin. PEG-MGF is still going to have unique effects other than nutrient shuttling, IGF-1 LR3 is not!

DES (1-3) IGF-1

DES (1-3) IGF-1 is the latest and, to me, the most promising of all the igf-1 drugs. It is basically bio-available igf-1 (like the original) but with the last 3 amino acids taken off. Some would ask, why does this make it better? Well, that makes it the most bio-available form.

See, here’s what happens in our bodies naturally. When we lift weights we produce lactic acid. We also increase hormone output, insulin, GH, test, igf-1 etc. One of the ways that our bodies grow is this: when igf-1 comes in contact with lactic acid some of it is destroyed, but some of it is resilient and only the last 3 amino acids are “cleaved” off of it. This is the form that really goes to work inducing growth! That’s why it has been recommended that igf-1 and MGF are injected into the muscles worked post-workout- to take advantage of this phenomena.

With DES (1-2) IGF-1, the work is already done for us. And, since it’s a larger dose (especially considering what would survive in the end naturally) than our bodies puts out naturally, it is theoretically many times more effective than original rIGF-1 and the other forms.

Here’s a bit longer post from a couple years ago when this stuff was super expensive and hard to find. It’s still hard to find, but it’s out there….


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 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 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? 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 work out sessions. Unfortunately, lactic acid destroys some of the IGF-1 present in muscles being trained…. But wait, this is also positive!

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.


This one is kind of obscure. But, from what I can gather about it it is a hormone that is present during gestation. It has a 67 amino acid sequence (like DES (1-3) IGF-1). It is said to do the same thing as IGF-1 LR3, but faster. Well, if that refers to hyperplasia then I’d agree that, at least on paper, this should be much faster! I mean, it actually is a substance produced in the body whereas 1-LR3 isn’t even bio-available for what we want it for (83 amino acid chain remember, doesn’t “fit” in the receptor!).

It is said to have a synergistic effect when combined with 1-LR3. But, my instincts would say to combine it with DES for better results. The idea being that, just like a lot of GH peptides, combining a good IGF-1 with a good IGF-2 has a synergistic effect where the whole is greater than the sum of its parts. i.e. if you took igf-1 alone it’d do x amount of what you want, same with igf-2, but combine them and the results are multiplied supposedly. Again, I’d (and will) go with DES (1-3) IGF-1 when combining with IGF-2 Lr3 rather than combining it with IGF-1 LR3 for reasons stated before.

Putting it all together, what’s the best protocol?
Obviously I’m taking a bit of a stab in the dark at what the optimal igf protocol might be at this time. But, it is an educated guess.

First of all, I want to clarify a few myths:
1) It’s the fact that IGF-1 LR3 is “long acting” that makes it not as good for site-enhancement/hyperplasia. That’s what makes it a “systemic” igf hormones vs a “local” site-enhancement drug.

Wrong. While it is longer acting than original rIGF-1, it is the fact that it is an 83 amino acid sequence that causes it not to work for our purposes. It basically (and yes, I’m waaay over-simplifying it, that’s what I do!) doesn’t “fit” in the receptor site! It still has insulin-like properties. And, for those that have used it and other variants you’ll see that it actually has the most insulin-like properties of any of them. My theory is specifically because it doesn’t get used any other way! It isn’t metabolised/broken down like normal igf-1 and it can be used by the muscle the same way. What’s left? Yep, systemic, insulin-like effects similar to low-moderately dosed humalog or humalin-r. That doesn’t make it worthless, just over-priced for it’s actually benefits.

2) PEG-MGF will not have localized effects because it is too long-acting
Wrong. This one doesn’t make sense when you think about it: In one bicep you have a shot of regular MGF suspended in water. In the other bicep you have PEG-MGF and you’ve just finished an arm workout. The drugs and water are both going to “pass through” the muscle where it was injected at the same rate. Why would one get used and the other not just because one has a longer “half-life”?

Here’s the real question: Does the PEGylation make the MGF molecule too large to fit into the receptor as it passes through? (they are both -peg and non peg- exiting the muscle at the same basic rate remember) If the PEGylation is too heavy making the molecule too large, then yes, PEG-MGF will not be as effective locally/in said muscle. But, it has nothing to do with how long it lasts in and of itself.

Does PEGylation make MGF too large to work? It depends on how its done and how heavy the formula is.
The other thing to consider is: how stable is MGf without PEGylation? The answer is: Not very! It is said that to keep it totally undamaged you must freeze it several degrees below zero! It’s a very fragile drug, that’s why PEG was added to it to begin with. So, it’s a bit of a trade off. If you want to get full, hyperplasia inducing benefits from regular MGF then you better mix it and use it all pretty quick!! If you are willing to put up with somewhat reduced benefits (i.e. not all of the MGF being used in the muscle because of the PEGylation, but still some of it getting in) while having a more stable drug that will last much longer, then go with PEG-MGF. Money wise I’d go the second route. I’m guessing a percentage of it is still going to be effective even with PEGylation. Though the same could be said about regular MGF’s degradation over time- some of it will still be useful. Just how much either way is getting to the muscle is hard to say!

3) Since IGF-2 LR3 is an LR3 drug, then it must be similar to IGF-1 LR3.
Wrong. It’s not even close. 1-LR3 is 83 amino acids and 2-LR3 is 67. One is ideal and one is almost useless.

So, what’s the best overall protocol?
Again, this is my best educated guess. But, based on the science, I would proceed like this: DES (1-3) IGF-1 + IGF-2 LR3 immediately pre workout with PEG (or non PEG, your call) MGF immediately post workout. The reasoning behind this is because the first two drugs are what I’d call “stimulators” in that they tell the satellite cells to “wake-up”! During the workout satellite cells are going to be stimulated and it is a natural environment to have igf-1 in your system. These two drugs can shuttle nutrients most effectively at this time (have your carbs, creatine and amino acids during your workout) and the muscles are active and receptive to igf hormones!

MGF is a gene spliced version of IGF-1 and it is more of a “defining” drug. I don’t mean fat loss, I mean that it tells the now-active satellite cells what to become. Immediately post workout is when your body has the greatest amount of trauma to the muscle and the satellite cells are most active in the muscles you’ve just worked. Taking MGF at this time helps define those cells as muscle, puts them to work and tells them what to do! Have another carb/amino/creatine etc. shake after your MGF shot. Shoot the MGF into the muscles worked that you want to see more site growth from.

How much should you take? Where should you buy it? I don’t know. Go with a supplier you trust and read up on dosages. Most DES and Igf-2 users take somewhere around 10-20mcg ea. which sounds about right to me. If you are having trouble getting/finding these, talk to your supplier and let them know you are interested in these. They respond to demand not necessarily science. So, speak up! Give this a shot if you are curious.

I’m not guaranteeing results from exogenous IGF-I analog protein peptide administrations… But I thought it’d be nice to air theory – define what works and why and hear other people’s thought on it – Do you have experience with these polypeptides? What do you think of the new best-seller, deer antler velvet? I want to hear others experiences and thoughts on it, at your leisure please.

Share with your friendsEmail this to someoneTweet about this on TwitterShare on Google+Share on FacebookPin on PinterestDigg thisShare on StumbleUponShare on TumblrShare on Reddit

Insulin like growth factor-1 (IGF-1)


Insulin like growth factor-1 (IGF-1)

Pharmaceutical Name: Insulin-Like Growth Factor 1
Drug Classification: Polypeptide Hormone
Active Life: huIGF-1: approximately 10 minutes, Long R3 IGF-1: 2-5 hours

Insulin-Like Growth Factor-1 (IGF-1) is a polypeptide protein hormone that is one of the primary substances that is responsible for tissue growth in humans, including muscle growth (1). IGF-1 is primarily secreted by the liver, with a small minority of the circulating amount of the hormone being produced and delivered by other tissues. The basic function of the hormone is to induce cellular activities. For bodybuilders and strength athletes this compound could produce good results when used due to the ability of the compound to potentially enhance muscle hyperplasia, the actual increase in number of muscle cells in the body or particular muscle.

This effect of muscle hyperplasia that IGF-1 can help promote is the primary reason why it has become so popular among bodybuilders. It is believed that IGF-1 may be able to produce localized growth in the muscles that the IGF1 is administered into post-workout. However this effect of the hormone remains more theoretical in nature because of the lack of research available on the subject using human subjects. Despite this many users still claim that they have seen results from IGF1 when using it for this explicit purpose and it remains within the realm of possibilities. However simply because science can not discount the result as implausible does not mean that it is a given either.

Among the other anabolic effects that IGF-1 can produce in the body are things such as increasing protein synthesis, increasing nitrogen retention, as well as inducing the growth of more muscle fibers. When an appropriate amount of amino acids (protein) is available, all of these actions within the body are able to be completed. It has been demonstrated that IGF1 can help to improve collagen production as well as the reproduction of cartilage in joints (2). The hormone has also been shown to exhibit the ability to act as a neuro-protector and promoter (3) mainly because IGF1 receptors are located in the tissue of the brain (4). It has been demonstrated that there is a potential for when supplemented with IGF1 a decrease in the progress of some brain diseases can be brought about as well as slowing the deterioration of brain function in some elderly subjects. However similar findings or any evidence of improved brain function or capacity has not been demonstrated in young, healthy individuals.

Obviously by helping to promote these anabolic mechanisms for growth IGF-1 also acts as an anti-catabolic. This would be beneficial to those users in a calorie deficit or in other circumstances that place them at risk of losing muscle mass. IGF1 also has the ability to positively affect lipolysis in users if other necessary conditions are met, namely proper diet and training protocols. When combined with the ability to preserve muscle mass, IGF1 appears to be an attractive choice for those that are attempting to decrease their body fat while maintaining as much of their muscle mass as possible.

IGF1 is composed of seventy amino acids, the same number as insulin. As stated earlier, it is primarily secreted by the liver. The stimulus that is responsible for this secretion is the presence of growth hormone. In fact IGF1 is primarily the causal connection between growth hormone and its anabolic and anti-catabolic capabilities. This is not to say that effects caused by growth hormone could be produced with only IGF1, but rather that the two compounds are very much related to one another and both are needed for optimal tissue growth.

In some animal studies there have been significant findings that support the idea that IGF1 administration can help to induce large increases in both strength and muscle size. While these results have not been reproduced in humans they do suggest that the gains experienced by users are connected to the administration of IGF1 and related to the anabolic mechanisms that are caused by the hormone. However to say that the findings of some of these studies could be replicated in humans would be incorrect. For example, a twenty-seven percent increase in muscle strength was produced in mice advanced in age when administered moderate dosages of IGF1 (5). Of course it would be dubious to claim that similar gains could be made by a trained athlete that chose to use IGF1 but it does suggest that the hormone will promote at least some of the mechanisms responsible for muscle growth.

As stated, the IGF-1 produced by the human body is seventy amino acids in length. However a different IGF1 composition is available. Called Long R3 Insulin-Like Growth Factor-1 (LR3 IGF1), it has the original seventy amino acids of regular IGF1 with a substitution of Arginine in place of Glutamic Acid at position three in the sequence. Additionally thirteen more amino acids have been added to the sequence. This extension peptide is located at the N-terminus in the sequence. These alterations were made so that the hormone would be more likely to remain active and potent when it encounters Insulin-Like Growth Factor-1 binding proteins in the body (6). All of this adds up to LR3 IGF1 being potentially three times as potent as the regular version of IGF1, or human IGF1 (huIGF1). Obviously this makes LR3 IGF1 more attractive for strength athletes and bodybuilders. For this reason it is now the most widely available version for purchase due to the compound having all of the benefits of regular IGF1, and being potentially three times as potent, while having no additional risks or side effects to that of regular IGF1.


Depending upon which form of IGF1 which a person is administering, the dosing will differ slightly. For huIGF1 dosing users will want to inject the drug post-workout, most likely in the muscle(s) that was worked out to help produce any potential local site growth if any is indeed possible. Due to the extremely short active life of the drug users will likely want to inject the drug several times to help and prolong the effects of the drug. Splitting the dose into two to four injections should be sufficient. When administering the compound on days where the user does not work out a similar dosing protocol could be used in any of the muscles that the user desires.

For LR3 IGF1, because of the longer active life of the drug in comparison to huIGF1, users will not have to administer the drug as frequently. Twice daily injections should be sufficient, although a single injection daily should also be able to produce significant results for the majority of users. Again, users will want to inject the drug post-workout in the muscle(s) that were worked. However, a second injection should be done elsewhere in the day. If not, a single injection time post-workout should be used. On off days from the gym, as with huIGF1, an injection can be made and may best be administered in the morning as to best fight off muscle catabolism. Barring this, any convenient time in the day can be used. However there are those users who simply opt not to administer any IGF1 on non-training days. It is at the discretion of the user.

Due to the possible local site growth that IGF1 may induce in users, many will split their doses and inject bilaterally. That is to say inject half of the dose into the muscle on the left side of their body and the other half of the dose in the right side of their body. Alternatively the user can simply inject the entire dose of IGF1 in one muscle on one day while making sure to inject the other muscle with the entire dose the next time that that muscle group falls in the injection rotation of the user.

The duration that a user will want to run IGF1 for is determined by the fact that IGF1 receptors in the body become saturated as large amounts of the hormone are introduced into the body. As the use of IGF1 continues, these receptors will begin to downgrade and the effects of the hormone will begin to lessen. For this reason consistent breaks from use of IGF1 need to be taken by users. Anecdotally the majority of users report seeing their gains from IGF1 begin to diminish after using the drug for about four to six weeks. This would seemingly indicate that receptor downgrade would be happening around this mark. However there is little to no information regarding IGF1 receptor downgrade and exactly how long it takes to occur and how long it takes for these receptors to recover. We are left to decipher these personal experiences with the drug and extrapolate the most efficient way to use it. As stated, it seems that cycles of about four to six weeks are ideal for many users although longer cycles are certainly possible. When coming off of the compound an equal amount of time spent off of it as was spent using it seems to allow for the IGF1 receptors to “upgrade” and once again be able to produce the results the user experienced initially. However despite these assumptions there are countless theories and protocols that users may administer IGF1 with and if they find it beneficial then there is no reason not to use these alternative protocols. There is simply not enough research to make definitive statements about how best or how long to run this drug.

In terms of dosing for huIGF1, users have reported seen good results when administering dosing ranging from 100 to 160 mcg per day. This total dose would be split into several injections, most of which would likely be administered post-workout. For LR3 IGF1, the generally excepted or reported range for dosing is seemingly between 40 to 120 mcg per day. Again however due to the lack of research concerning IGF1 and its use in athletes these dosages are composed of through the collection of anecdotal evidence from users and not scientific research.

Risks/Side Effects

Beyond the natural downgrading of the IGF1 receptors when using exogenous IGF1, there are appears to be little in the way of significant risks to the health of the user associated with its use. Caution has to be used when saying this however again due to the lack of empirical research conducted using this drug on human subjects.

One major risk that could potentially become problematic for some users is the ability of IGF1 to promote or enhance the growth of pre-existing tumors and cancers (1). Similarly to growth hormone, IGF1 can
accelerate the growth of tumors which is not to be unexpected due to the very nature of IGF1 as a growth factor within the body and the effect it has on cells. For this reason it is advisable that prior to undertaking use of IGF1 a user gets medically cleared by a doctor and ensures that no tumors or other diseases that could be exasperated by use of the drug are present.

A far less potentially severe side effect of IGF1 use is the suppression of the endogenous human growth hormone production in users. Endogenous IGF1 creates a negative feedback loop for growth hormone in humans. Exogenous IGF1 will have the same effect and therefore will likely cause growth hormone production to be temporarily suppressed in users. This is another reason why users will want to cycle their use of IGF1 and not attempt to stay on the drug for extended periods of time. By limiting the use of IGF1 to only a few weeks, this should ensure the general health of the user as well as the mechanism responsible for the production of both IGF1 as well as human growth hormone.

While not being significant, IGF1 also has the ability to lower blood glucose levels. For the most part the compound will not lower the blood glucose in users to dangerous levels unless a pre-existing condition is evident. However this lowering of blood glucose will often cause the user to feel lethargic. This sometimes lasts the duration of use of the drug but should subside once the administration of the compound ceases.

A trait that again is shared with human growth hormone is the fact that use of IGF1 sometimes results in users having aches and pains form most notably in their wrists, fingers and hands. This is a common side effect but if it becomes unbearable a lowering of the dosage should reduce the severity of the symptoms. They will cease once administration of the drug is discontinued.

In addition, while it is possible that IGF1 could cause abnormal organ growth and/or acromegaly it would simply take overly large doses used for long durations of time for this to occur in users. With normal use of the drug these side effects should not be a concern for the vast majority of users however.


1. Smith GD, Gunnell D, Holly J. Cancer and insulin-like growth factor-I. A potential mechanism linking the environment with cancer risk. BMJ. 2000 Oct 7;321(7265):847-8.

2. Sienkiewicz P, Palka M, Palka J. Oxidative stress induces IGF-I receptor signaling disturbances in cultured human dermal fibroblasts. A possible mechanism for collagen biosynthesis inhibition. Cell Mol Biol Lett. 2004;9(4A):643-50.

3. Mendez P, Azcoitia I, Garcia-Segura LM. Interdependence of oestrogen and insulin-like growth factor-I in the brain: potential for analysing neuroprotective mechanisms. J Endocrinol. 2005 Apr;185(1):11-7.

4. Creyghton WM, van Dam PS, Koppeschaar HP. The role of the somatotropic system in cognition and other cerebral functions. Semin Vasc Med. 2004 May;4(2):167-72.

5. Barton-Davis ER, Shoturma DI, Musaro A, Rosenthal N, Sweeney HL. Viral mediated expression of insulin-like growth factor I blocks the aging-related loss of skeletal muscle function. Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15603-7.

6. Walton PE, Dunshea FR, Ballard FJ. In vivo actions of IGF analogues with poor affinities for IGFBPs: metabolic and growth effects in pigs of different ages and GH responsiveness. Prog Growth Factor Res. 1995;6(2-4):385-95.

Share with your friendsEmail this to someoneTweet about this on TwitterShare on Google+Share on FacebookPin on PinterestDigg thisShare on StumbleUponShare on TumblrShare on Reddit
eXTReMe Tracker