Details
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Product: |
IGF-1-LR3 |
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Synonyms: |
Long R3 IGF-1 or Insulin-Like Growth Factor-I LR3, somatomedin C |
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CAS RN.: |
946870-92-4 |
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Sequence: |
83 amino chain: MFPAMPLSSL FVNGPRTLCG AELVDALQFV CGDRGFYFNK PTGYGSSSRR APQTGIVDEC CFRSCDLRRL EMYCAPLKPA KSA |
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Molecular Mass: |
9111 Daltons |
IGF-1 LR3 Description
Long R3 IGF-1 (Insulin-like Growth Factor -1) is a polypeptide hormone that structurally and molecularly, shares some properties with insulin, which is where it got “Insulin-like” from in its nomenclature. IGF-1’s primary roles include long bone growth in kids, and in adults it affects the growth and repair of muscle tissue. Regular IGF has a half life of only about 20 minutes, where as the modified version called LR3 is altered some to prevent deactivation by binding proteins in the blood and extends the half life to about 20 hours making it able to be more effective.
IGF-1 LR3 contains the complete IGF-1 sequence, but with the substitution of an Arginine (Arg) for the Glutamic Acid (Glu) at position 3, as well as a 13 amino acid extension peptide is an 83 amino acid analog making the chain 83 aminos in length. This slight change in sequence allows the IGF-1 to avoid binding to proteins and have a much longer half life, around 20-30 hours. This effectively increases the biological activity of the IGF peptide. Effects seen in research are increased glucose transport, increased protein synthesis, decreased protein degradation and increased amino acid transport to cells. Active IGF behaves differently in different tissues. In muscle cells proteins and associated cell components are stimulated. Protein synthesis is increased along with amino acid absorption. IGF mobilizes fat for use as energy in adipose tissue. In lean tissue the cells have to switch to burning off fat as a source of energy, as IGF prevents insulin from transporting glucose across cell membranes. IGF-1 promotes nitrogen retention and protein synthesis. This assists the growth of muscles through both hyperplasia (increased number of muscle cells) and mitogenesis (growth of new muscle fibers).
IGF-1 LR3 Conserves Muscle in Heifers
This study indicates that IGF treated livestock retained muscle mass while in a catabolic state as a result of underfeeding indicating that IGF-1’s importance in controlling muscle growth. On a restricted, low calorie, low quality diet heifers maintained lean mass while being infused with IGF-1 LR3.
IGF-1 LR3 used to help a cancer drug work better
Due to the amount of IGF receptors in cancer cells, physicians and scientists used this to their advantage in placing a cancer drug into cells using IGF as a type of carrier or transport. The result was a significantly higher ability to localize the drug and fight cancer cells:
Study shows IGF-1 to have plaque stabilizing effect in patients with atherosclerosis
Atherosclerosis (also known as ASVD which is arteriosclerotic vascular disease) is a condition where thickening of an arterial wall occurs from the build-up of cholesterol and fatty materials. It is commonly referred to as a hardening of the arteries, caused by the formation of multiple plaques within the arteries.
Atherosclerosis can go unnoticed for decades and not show any symptoms. Atherosclerotic lesions, or plaques can be separated into two categories: Stable and unstable.
Stable atherosclerotic plaques, which tend to be asymptomatic, are rich in extracellular matrix and smooth muscle cells, while, unstable plaques are rich in macrophages and foam cells and the extracellular matrix separating the lesion from the arterial lumen is usually weak and prone to rupture. Ruptures of the fibrous cap expose thrombogenic material, such as collagen to the circulation and eventually induce thrombus formation in the lumen. Upon formation, intraluminal thrombi can occlude arteries outright (i.e. coronary occlusion), but more often they detach, move into the circulation and eventually occlude smaller downstream branches causing thromboembolism (i.e. Stroke is often caused by thrombus formation in the carotid arteries).
These complications of advanced atherosclerosis are chronic, slowly progressive and cumulative. Most commonly, soft plaque suddenly ruptures, causing the formation of a thrombus that will rapidly slow or stop blood flow, leading to death of the tissues fed by the artery in approximately 5 minutes. This catastrophic event is called an infarction. One of the most common recognized scenarios is called coronary thrombosis of a coronary artery, causing myocardial infarction (a heart attack). The same process in an artery to the brain is commonly called stroke. Another common scenario in very advanced disease is claudication from insufficient blood supply to the legs, typically caused by a combination of both stenosis and aneurysmal segments narrowed with clots. [3]
“Insulin-like growth factor-1 (IGF-1) signaling is important for the maintenance of plaque stability in atherosclerosis due to its effects on vascular smooth muscle cell (vSMC) phenotype. To investigate this hypothesis, we studied the effects of the highly inflammatory milieu of the atherosclerotic plaque on IGF-1 signaling and stability-related phenotypic parameters of murine vSMCs in vitro, and the effects of IGF-1 supplementation on plaque phenotype in an atherosclerotic mouse model. M1-polarized, macrophage-conditioned medium inhibited IGF-1 signaling by ablating IGF-1 and increasing IGF-binding protein 3, increased vSMC apoptosis, and decreased proliferation. Expression of α-actin and col3a1 genes was strongly attenuated by macrophage-conditioned medium, whereas expression of matrix-degrading enzymes was increased. Importantly, all of these effects could be corrected by supplementation with IGF-1. In vivo, treatment with the stable IGF-1 analog Long R3 IGF-1 in apolipoprotein E knockout mice reduced stenosis and core size, and doubled cap/core ratio in early atherosclerosis. In advanced plaques, Long R3 IGF-1 increased the vSMC content of the plaque by more than twofold and significantly reduced the rate of intraplaque hemorrhage. We believe that IGF-1 in atherosclerotic plaques may have a role in preventing plaque instability, not only by modulating smooth muscle cell turnover, but also by altering smooth muscle cell phenotype.” [4]By preventing instability in arterial plaque, this study suggests that IGF could help reduce strokes, infarctions and other life threatening complications due to atherosclerosis. With more study this could be a huge medical find for patients suffering with hardened arteries.
Recent study showing IGF-1 having muscle hypertrophy effects
A study completed in October 2012 shows some promise in IGF promoting muscle mass in combination with resistance training in rats.
“The purpose of this study was to test the hypothesis that skeletal muscle adaptations induced by long-term resistance training (RT) are associated with increased myogenic regulatory factors (MRF) and insulin-like growth factor-I (IGF-I) mRNA expression in rats skeletal muscle. Male Wistar rats were divided into 4 groups: 8-week control (C8), 8-week trained (T8), 12-week control (C12) and 12-week trained (T12). Trained rats were submitted to a progressive RT program (4 sets of 10-12 repetitions at 65-75% of the 1RM, 3 day/week), using a squat-training apparatus with electric stimulation. Muscle hypertrophy was determined by measurement of muscle fiber cross-sectional area (CSA) of the muscle fibers, and myogenin, MyoD and IGF-I mRNA expression were measured by RT-qPCR. A hypertrophic stabilization occurred between 8 and 12 weeks of RT (control-relative % area increase, T8: 29% vs. T12: 35%; p>0.05) and was accompanied by the stabilization of myogenin (control-relative % increase, T8: 44.8% vs. T12: 37.7%, p>0.05) and MyoD (control-relative % increase, T8: 22.9% vs. T12: 22.3%, p>0.05) mRNA expression and the return of IGF-I mRNA levels to the baseline (control-relative % increase, T8: 30.1% vs. T12: 1.5%, p<0.05). Moreover, there were significant positive correlations between the muscle fiber CSA and mRNA expression for MyoD (r=0.85, p=0.0001), myogenin (r=0.87, p=0.0001), and IGF-I (r=0.88, p=0.0001). The significant (p<0.05) increase in myogenin, MyoD and IGF-I mRNA expression after 8 weeks was not associated with changes in the fiber-type frequency. In addition, there was a type IIX/D-to-IIA fiber conversion at 12 weeks, even with the stabilization of MyoD and myogenin expression and the return of IGF-I levels to baseline. These results indicate a possible interaction between MRFs and IGF-I in the control of muscle hypertrophy during long-term RT and suggest that these factors are involved more in the regulation of muscle mass than in fiber-type conversion.” [5]
Customers inquiring about personal IGF-1 LR3 use including, but not limited to bodybuilding, dosing, injections or cycling will be added to our DO NOT SELL LIST.
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References
[1] Hill RA, Hunter RA, Lindsay DB, Owens PC. (1999). “Action of long(R3)-insulin-like growth factor-1 on protein metabolism in beef heifers.” Domestic Animal Endocrinology. 16(4):219-29.
[2] McTavish H, Griffin RJ, Terai K, Dudek AZ. (2009). “Novel insulin-like growth factor-methotrexate covalent conjugate inhibits tumor growth in vivo at lower dosage than methotrexate alone.” Translational research: The Journal of Lab and Clinical Medicine. 153(6):275-82.
[3] "Atherosclerosis." Wikipedia, The Free Encyclopedia. Wikimedia Foundation, Inc. 22 July 2004. Web. 10 Aug. 2004.
[4] von der Thüsen JH, Borensztajn KS, Moimas S, van Heiningen S, Teeling P, van Berkel TJ, Biessen EA. (2011). “IGF-1 has plaque-stabilizing effects in atherosclerosis by altering vascular smooth muscle cell phenotype.” American Journal of Pathology.” 178(2):924-34.
[5] Aguiar AF, Vechetti-Júnior IJ, Alves de Souza RW, Castan EP, Milanezi-Aguiar RC, Padovani CR, Carvalho RF, Silva MD. (2012). “Myogenin, MyoD and IGF-I Regulate Muscle Mass but not Fiber-type Conversion during Resistance Training in Rats.” International Journal of Sports Medicine. October 2012 (published before print)
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