Message from Gropep

IGF-1 Message from Gropep

I emailed them to ask about selling IGF-1LR3 for human use and I got this response. Many of you know this is used in most IGF's

"Dear Sir/Madam,

Thank you for your interest in GroPep and its products and for your honesty about your intentions. It is refreshing when someone is prepared to be honest on this issue. Appreciated. Seeing as you have been honest with us it is only fair I be honest with you. Simply put, no-one in their right mind would use LONG[TM]R[3]IGF-I in a human. LONG[TM]R[3]IGF-I was specifically formulated for use in Industrial Cell Culture on individual cells. In this application it works brilliantly, being more potent than IGF-I. However isolated cells are not the same as an intact animal as, for example, they do not have kidneys or an immune system. As a result, LONG[TM]R[3]IGF-I should NEVER under ANY circumstances be used in humans as it may prove fatal. This has nothing to do with purity, rather it is the LONG[TM]R[3]IGF-I molecule itself that is the potential problem. Illicit use is therefore a safety issue. Anything anyone tells you to the contrary is rubbish, irrespective of what evidence or experience they CLAIM to have.

The mistaken belief that IGF-I and particularly LONG[TM]R[3]IGF-I are useful as performance enhancing agents has resulted in a high demand for LONG[TM]R[3]IGF-I and a thriving trade in counterfeit GroPep vials, vials that do not contain what is claimed on the label.

Finally, the response I am required to give for all inquiries regarding human use:

We cannot supply or sanction the use of any GroPep Biotechnology Reagent in humans for any purpose. No GroPep Biotechnology Reagent is of Pharmaceutical Grade and are specifically marked "not for human use" for this reason. They are therefore unsafe and may be fatal if used inappropriately.

GroPep therefore accepts no responsibility whatever for any injury caused by the inappropriate use of its products.

GroPep only sells to bona fide Research Institutions or Biotechnology Companies, not to individuals. The same rules also apply to our Distributors.

All our shipments are via Courier and are traced to ensure correct use. No GENUINE GroPep product should therefore be accessible to anyone other than legitimate Researchers.

Yours sincerely,

Dr. Stephen Hardy
Biotechnology Reagents Marketing Manager.
"

anyone have any thoughts on this?

Nice of him to reply like that.

Interesting.

I think he is stating what he has to in order to legally cover his bases (or at least I hope)

Quote:

Originally Posted by mixxin

I think he is stating what he has to in order to legally cover his bases (or at least I hope)

lol. yes i hope he is saying that to cover his ass, but what if he isn't? hmmmmmmmmmmmmmmmmmmmm

i'd like to get some Vets opinions on this please!

Here's what I found awhile ago whilst doing some research.

#1 04-27-2005, 07:55 AM
Syndicate
Senior Member Join Date: Apr 2004
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http://www.ncbi.nlm.nih.gov/entrez/...9&dopt=Citation

Synthesis and characterization of biotinylated forms of insulin-like growth factor-1: topographical evaluation of the IGF-1/IGFBP-2 AND IGFBP-3 interface. Robinson SA, Rosenzweig SA.

Department of Cell and Molecular Pharmacology and Experimental Therapeutics and Hollings Cancer Center, Medical University of South Carolina, 173 Ashley Avenue, Charleston, South Carolina 29425, USA.

Activation of the insulin-like growth factor-1 (IGF)-1 receptor signaling pathways by IGF-1 and IGF-2 results in mitogenic and anabolic effects. The bioavailability of the IGFs is regulated by six soluble binding proteins, the insulin-like growth factor binding proteins (IGFBPs), which bind with approximately 0.1 nM affinity to the IGFs and often serve as endogenous antagonists of IGF action. To identify key domains of IGF-1 involved in the interaction with IGFBP-2 and IGFBP-3, we employed IGF-1 selectively biotinylated on residues Gly 1, Lys 27, Lys 65, and Lys 68. All monobiotinylated species of IGF-1 exhibited high affinity ( approximately 0.1-0.2 nM) for IGFBP-2 and IGFBP-3 in solid-phase-binding assays. However, different labeling intensities were observed in ligand blot analysis of IGFBP-2 and IGFBP-3. The N(epsilon)(Lys65/68)(biotin)-IGF-1 (N(epsilon)(Lys65/68b)-IGF-1) probe exhibited the highest signal intensity, while N(alpha)(Gly1b)-IGF-1 and N(epsilon)(Lys27b)-IGF-1 demonstrated significantly lower signals. When taken together, these results suggest that, once bound to IGFBP-2 or IGFBP-3, the biotin moieties of N(alpha)(Gly1b)-IGF-1 and N(epsilon)(Lys27b)-IGF-1 are inaccessible to NeutrAvidin-peroxidase, the secondary binding component. Ligand blots using IGF-1 derivatized with a long chain form of the N-hydroxysuccinimide biotin (NHS-biotin) to yield N(alpha)(Gly1)(LC-biotin)-IGF-1 and N(epsilon)(Lys27)(LC-biotin)-IGF-1 demonstrated increased signal intensity compared with their NHS-biotin counterparts. In BIAcore analysis, IGFBP-2 and IGFBP-3 bound only to the N(epsilon)(Lys65/68b)-IGF-1-coated flowcell of a biosensor chip, confirming the inaccessibility of Gly 1 and Lys 27 when IGF-1 is bound to IGFBP-2 and IGFBP-3. These data confirm the involvement of the IGFBP-binding domain on IGF-1 in binding to IGFBP-2 and IGFBP-3 and support involvement of the IGF-1R-binding domain in IGFBP binding.

And it seemed to explain why it works, Protein synthesis and insulin pushing more nutrients into the muscle is there anything else I'm missing? I have 2 kits on the way and am reading as much as humanly possible. So I know what to expect and how to deal.

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I think this is answer I was looking for...

http://www.ncbi.nlm.nih.gov/entrez/...t_uids=15302582

IGF-1 induces human myotube hypertrophy by increasing cell recruitment.
Jacquemin V, Furling D, Bigot A, Butler-Browne GS, Mouly V.

Insulin-like growth factor-1 (IGF-1) has been shown in rodents (i) in vivo to induce muscle fiber hypertrophy and to prevent muscle mass decline with age and (ii) in vitro to enhance the proliferative life span of myoblasts and to induce myotube hypertrophy. In this study, performed on human primary cultures, we have shown that IGF-1 has very little effect on the proliferative life span of human myoblasts but does delay replicative senescence. IGF-1 also induces hypertrophy of human myotubes in vitro, as characterized by an increase in the mean number of nuclei per myotube, an increase in the fusion index, and an increase in myosin heavy chain (MyHC) content. In addition, muscle hypertrophy can be triggered in the absence of proliferation by recruiting more mononucleated cells. We propose that IGF-1-induced hypertrophy can involve the recruitment of reserve cells in human skeletal muscle.

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http://www.ncbi.nlm.nih.gov/entrez/...t_uids=14766764

Viral expression of insulin-like growth factor-I enhances muscle hypertrophy in resistance-trained rats. Lee S, Barton ER, Sweeney HL, Farrar RP.

Department of Kinesiology, University of Texas, Austin 78712, USA.

Muscle hypertrophy is the product of increased drive through protein synthetic pathways and the incorporation of newly divided satellite cells. Gains in muscle mass and strength can be achieved through exercise regimens that include resistance training. Increased insulin-like growth factor-I (IGF-I) can also promote hypertrophy through increased protein synthesis and satellite cell proliferation. However, it is not known whether the combined effect of IGF-I and resistance training results in an additive hypertrophic response. Therefore, rats in which viral administration of IGF-I was directed to one limb were subjected to ladder climbing to test the interaction of each intervention on muscle mass and strength. After 8 wk of resistance training, a 23.3% increase in muscle mass and a 14.4% increase in peak tetanic tension (P(o)) were observed in the flexor hallucis longus (FHL). Viral expression of IGF-I without resistance training produced a 14.8% increase in mass and a 16.6% increase in P(o) in the FHL. The combined interventions produced a 31.8% increase in muscle mass and a 28.3% increase in P(o) in the FHL. Therefore, the combination of resistance training and overexpression of IGF-I induced greater hypertrophy than either treatment alone. The effect of increased IGF-I expression on the loss of muscle mass associated with detraining was also addressed. FHL muscles treated with IGF-I lost only 4.8% after detraining, whereas the untreated FHL lost 8.3% muscle mass. These results suggest that a combination of resistance training and overexpression of IGF-I could be an effective measure for attenuating the loss of training-induced adaptations.

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Creatine increases IGF-I and myogenic regulatory factor mRNA in C(2)C(12) cells.

Louis M, Van Beneden R, Dehoux M, Thissen JP, Francaux M.

Departement d'Education Physique et de Readaptation, Universite catholique de Louvain, Place Pierre de Coubertin 1, B-1348 Louvain-la-Neuve, Belgium. [email protected]

Addition of creatine to the differentiation medium of C(2)C(12) cells leads to hypertrophy of the myotubes. To investigate the implication of insulin-like growth factor I (IGF-I) and myogenic regulatory factors (MRFs) in this hypertrophy, their mRNA levels were assessed during the first 72 h of differentiation. Creatine significantly increased the IGF-I mRNA level over the whole investigated period of time, whereas the MRF mRNA levels were only augmented at precise moments, suggesting a general activation mechanism for IGF-I and a specifically regulated mechanism for MRF transcription. Our results suggest therefore that creatine-induced hypertrophy of C(2)C(12) cells is at least partially mediated by overexpression of IGF-I and MRFs.

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Molecular mechanisms modulating muscle mass.

Glass DJ.

Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591-6707, USA. [email protected]

Skeletal muscle atrophy occurs in multiple clinical settings, including cancer, AIDS and sepsis, and is caused in part by an increase in the rate of ATP-dependent ubiquitin-mediated proteolysis. The expression of two recently identified genes encoding ubiquitin-protein ligases, MAFbx/Atrogin-1 and MuRF1, has been shown to increase during muscle atrophy. Mouse knockout studies have demonstrated that MAFbx and MuRF1 are required for muscle atrophy, and thus might be targets for clinical intervention. A second strategy for blocking atrophy involves the stimulation of pathways leading to skeletal muscle hypertrophy. Insulin-like growth factor 1 (IGF-1) is a protein growth factor that can induce skeletal muscle hypertrophy by activating the phosphatidylinositol 3-kinase (PI3K)-Akt pathway. The pathways modulating hypertrophy and atrophy will be further discussed, to highlight potential targets for clinical intervention.
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Persistent IGF-I overexpression in skeletal muscle transiently enhances DNA accretion and growth.

Fiorotto ML, Schwartz RJ, Delaughter MC.

USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030, USA. [email protected]

Adult transgenic mice with muscle-specific overexpression of insulin-like growth factor (IGF)-I have enlarged skeletal muscles. In this study, we; 1) characterized the development of muscle hypertrophy with respect to fiber type, age, and sex; 2) determined the primary anabolic process responsible for development of hypertrophy; and 3) identified secondary effects of muscle hypertrophy on body composition. Transgene expression increased with age and was present only in fibers expressing type IIB fast myosin heavy chain. Muscle masses were greater by 5 wk of age, and by 10 wk of age the differences were maximal despite continued transgene expression. Total DNA and RNA contents of the gastrocnemius muscle were greater for transgenic mice than for nontransgenic littermates. The differences were maximal by 5 wk of age and preceded the increase in protein mass. The accelerated protein deposition ceased when the protein/DNA ratio attained the same value as in nontransgenic controls. Despite localization of IGF-I expression to muscle without changes in plasma IGF-I concentrations, genotype also modified the normal age and sex effects on fat deposition and organ growth. Thus, enhanced DNA accretion by IGF-I was primarily responsible for stimulating muscle growth. In turn, secondary effects on body composition were incurred that likely reflect the impact of muscle mass on whole body metabolism.
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This seems to get into the mechanisms better then what I've found up till now

http://jap.physiology.org/cgi/content/full/93/3/1159

Summary

The continued interest in the role of IGF-I in skeletal muscle adaptation is founded on the extensive body of evidence indicating that 1) IGF-I is both anabolic and mitogenic for skeletal muscle or muscle lineage cells, 2) IGF-I operates in an autocrine/paracrine mode in skeletal muscle, and 3) muscle IGF-I and MGF production are sensitive to increases in loading state. In addition to the effects of IGF-I in promoting skeletal muscle hypertrophy or regeneration, there are a number of other systems that may impact or be impacted by IGF-I signaling that should be considered by muscle researchers. Future challenges in this area include the identification of the cellular level mechanisms that transduce mechanical signals leading to changes in IGF-I signaling and elucidation of the relationships between the various intracellular signaling pathways that allow IGF-I signaling to stimulate the competing processes of cellular differentiation and cellular proliferation.

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Role of IGF-I and IGFBPs in the changes of mass and phenotype induced in rat soleus muscle by clenbuterol. Awede BL, Thissen JP, Lebacq J.

Unite de Physiologie Generale des Muscles, Universite Catholique de Louvain, 1200 Brussels, Belgium.

Clenbuterol induces hypertrophy and a slow-to-fast phenotype change in skeletal muscle, but the signaling mechanisms remain unclear. We hypothesized that clenbuterol could act via local expression of insulin-like growth factor I (IGF-I). Administration of clenbuterol to 3-mo-old female Wistar rats resulted in a 10 and 13% increase of soleus muscle mass after 3 and 9 days, respectively, reaching 16% after 4 wk. When associated with triiodothyronine, clenbuterol induced a dramatic slow-to-fast phenotype change. In parallel, clenbuterol administration induced in soleus muscle a fivefold increase in IGF-I mRNA levels associated with an eightfold increase in IGF-binding protein (IGFBP)-4 and a fivefold increase of IGFBP-5 mRNA levels on day 3. This increased IGF-I gene expression was associated with an increase in muscle IGF-I content, already detected on day 1 and persisting until day 5 without increase in serum IGF-I concentrations. These data show that muscle hypertrophy induced by clenbuterol is associated with a local increase in muscle IGF-I content. They suggest that clenbuterol-induced muscle hypertrophy could be mediated by local production of IGF-I.

I hypothesize that taking clen and IGF-1 would put you in a anabolic like state for hours at a time. Clen has a life of 12-24 hours. Considering that Clen only helps with protien synthesis (building) and IGF-1 with muscle hypertrophy (reconstruction), I conclude the two together would definently improve muscle mass on a massive scale. Any thoughts?
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Heres the series of abstracts I read, I selectivly picked what I thought the board would find interesting. 481 in all... So get comfortable

http://www.ncbi.nlm.nih.gov/entrez/...Pager&DB=pubmed

Enter "IGF-1 hypertrophy" in the search box

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The role of insulin-like growth factor I in clenbuterol-stimulated growth in growing lambs.

We examined the role of IGF-I in muscle growth stimulated by a beta-adrenergic agonist, clenbuterol. Ewe lambs (90 d old, 20.4 kg mean live weight) were allotted to five groups. A pretreatment control group of five lambs was slaughtered immediately (0 d). The other four groups of six ewes ate freely for 38 or 80 d and were then slaughtered. Half those lambs received clenbuterol (400 micrograms.kg live weight-1.d-1) as a dietary supplement. Blood was collected at intervals from 19 d before supplementation began (0 d) until slaughter. Prerigor muscle samples were sectioned for detection of IGF-I receptors and myofibrillar ATPase activity. Carcass weights were slightly increased by treatment, whereas muscle weights (semimembranosus, gastrocnemius, and biceps femoris) were greatly increased (P < .001), up to 48% at 80 d for semimembranosus. Clenbuterol significantly decreased collagen concentration because myofibrillar proteins were preferentially produced. Collagen solubility was unaffected. Total RNA:total DNA in semimembranosus and gastrocnemius showed transcription was still stimulated between 38 and 80 d. Fiber type area analysis indicated a shift toward glycolytic metabolism, confirmed by iron measurements. However, clenbuterol did not change the portion of muscle occupied by each ATPase class, and the data indicated that type I fibers, though smaller, became relatively more numerous. In spite of significant muscle changes, plasma IGF-I was unaffected by clenbuterol. Similarly, there was no difference in the specific binding of [125I]IGF-I at slaughter between treated and control lambs. However, a response in the first few days of treatment, preceding visible hypertrophy, cannot be excluded.
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Insulin and IGF-I induce pronounced hypertrophy of skeletal myofibers in tissue culture.Vandenburgh HH, Karlisch P, Shansky J, Feldstein R.

Department of Pathology, Brown University, Providence, Rhode Island 02906.

Skeletal myofibers differentiated from primary avian myoblasts in tissue culture can be maintained in positive nitrogen balance in a defined serum-free medium for at least 6-7 days when embedded in a three-dimensional collagen gel matrix. Incubation of established myofiber cultures for 3-7 days with insulin (1 microM) or insulin-like growth factor I (IGF-I, 32 nM) stimulates both cell hyperplasia and myofiber hypertrophy. Mean myofiber diameter increases 71-98%. Insulin-like growth factor II stimulates cell hyperplasia but not myofiber hypertrophy. Cell growth results from a 42-62% increase in total protein synthesis and a 28-38% decrease in protein degradation. Myosin heavy-chain content increases 183-258% because of a 55% stimulation of myosin synthesis and 33-61% inhibition of degradation. Associated with myofiber hypertrophy is a 87-148% increase in the number of myofiber nuclei per unit myofiber length. The results indicate that insulin and IGF-I, but not IGF-II, can induce rapid myofiber hypertrophy in vitro, most likely by stimulating myoblast proliferation and/or fusion to established myofibers.
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[email protected]

very interesting. can't understand alot of it though! help vets?

I am sure they know drugs as such are beneficial when it comes to bodybuilding, but they can't say that because LR3 is not spposed to be used for what we use it for. What do you think could happen if they said it was ok for people to use it? They have to say things like that to cover their asses.

-Gear

I'm sure GroPep is making some nice coin selling IGF and I doubt they are that particular who they sell to.

Yes, they do make a lot of "coin" from what they do. They will only sell to one who can provide legitimate documentation stating they are qualified to deal with chemicals as such. They wouldn't take a risk in losing their license or getting a fine just by selling IGF to some BB that wants to gain some muscle. Before you purchase anything from them, you need to prove to them you are "legally" allowed to purchase "x" substance for "research" purposes only. From then on, I am sure they don't care what you do with whatever you purchased. People like biochems can purchase drugs as such, but even they have a limit on how much they can purchase at once. Don't even bother trying to purchase IGF direct from GroPep unless you maybe know someone from "the inside". That's all I can think of.

There was a thread on GroPep quite a while ago, I stated all the information GroPep require to be legible for purchase of GroPep's products.

-Gear

Check out post #29, a reply by me.

http://forums.steroid.com/showthread...ghlight=gropep

-Gear

Yeah I caught that thread a couple weeks ago. I checked out GroPep about a year ago when I first heard about IGF. All of those supply companies require documentation but I'm sure it's not too hard to find someone with the right credentials to purchase supplies for you. You just need to be involved in a lab or research company. What I mean when I say GroPep is not too "particular" is that I doubt they are doing background checks on their customers. After all look at MR, Omega and the other IGF suppliers that buy from them. You think GroPep cares what happens to the IGF once it leaves the factory. They cover their ass with that disclaimer and thats that.

i personally am very glad you posted this, i was considering trying this but not now. the point to me is that yes they have to cover their asses but... why wouldnt he just say the legal jargen that he did at the end? there was no reason to go so in depth if he didnt honestly believe what he was saying. read it again and it may scare you as much as it did me

I would never use IGFLR3 myself.

You guys just don't understand the cascade of effects IGF-1 has.

I guarantee a lot of you IGFLR3 users will regret using it in the years ahead whether or not you have health problems.

yeah i wonder what exactly the side effects are of the IGF? hmmmmmmmmm. maybe 5 years after it is used the person grows a 2nd head. who knows!?!?

Quote:

Originally Posted by jerseyboy

.What I mean when I say GroPep is not too "particular" is that I doubt they are doing background checks on their customers. After all look at MR, Omega and the other IGF suppliers that buy from them. You think GroPep cares what happens to the IGF once it leaves the factory. They cover their ass with that disclaimer and thats that.

As long as one can purchase their products legally, I also believe GroPep don't care about their background. Omega, MR etc all have qualifications that allow them to purchase drugs as such.

-Gear