Please Scroll Down to See Forums Below 
.jpg "Research Chemical Sciences")
.png "Research Chemical Sciences")
needtogetaas
New member
IGF-lr3 along with
Lr3IGF-1 (Long R3 Insulin-like Growth Factor-I or Long R3IGF-I) is an 83 amino acid analog of human IGF-I that comprises the complete human IGF-1 sequence but with the replacement of an Arg for the Glu at position 3, as well as a 13 amino acid chain peptide at the N-terminus. This makes Long R3IGF-I two to three more potent than IGF-I in studies, because it has a lower affinity to be made inactive by IGF binding proteins, and as a result more possible activity in the body. The enhanced potency of Lr3IGF-1 over IGF-1 is due to the decreased binding of Long R3 IGF-1to all known IGF binding proteins. These binding proteins normally inhibit the biological actions of IGF's. This also will allow the peptide to have a longer half life of around 20-30 hours. Increasing the activity of biological IGF results in positive are increased amino acid transport to cells, increased glucose transport, increased Protein synthesis, decreased Protein degradation, and increased RNA synthesis. In another investigation, injection ofLR3-IGF-1 in various amounts to investigate the effects on the somatotropic axis (plasma levels of IGF-1 and 2, IGFBPs) was done. They have reported that plasma Long-R3 increased when administered subcutaneously but with no such activity when administered orally.
Additionally, LR3 lowered the levels of native IGF-1in rbGH-injected in calves, but L-R3 increased the amounts of IGF-II concentrations when administered with L-R3 subcutaneously. The parenteral administration of the Long R3 IGF-1 decreased the growth hormone concentration but did not affect the secretion of GH. It was also reported that the somatotrophic acis is essentially functioning in neonatal calves and can be influenced by nutrition, growth hormone and Long-R3-IGF-1 (IGF1-LR3). (Hammonand Blum 1997). Furthermore, it has been shown that in mycocytes, IGF-1 R3stimulates the cardiomyocyte splitting in vivo (Sundgren et al. 2003).
IGF-1LR3Mechanisms of function First primary action is to bind to the IGF1R,a receptor tyrosine kinase, which initiates intracellular signaling. IGF-1 isone of the most powerful endogenous activators of the AKT signaling pathway, as timulator of cell growth and production, and a strong inhibitor of involuntary cell death. IGF-1 LR3 actions have been blocked by the ERK and P13K which completely abolished the BrdU uptake. This causes IGF-1 to produce GH which is crucial for health of maintenance of bodily organ functions. Even though itdoes bind to insulin receptors, its binding frequency to insulin is not as strong as compared to IGF-1 but noted. IGF-1
IGF-1 also known as somatomedin C is a polypeptide of 70 amino acids (7650 daltons), and is one of the number of associated insulin-like growth factors present in the flow. This polypeptide hormone about the same size as insulin and mimics insulin as well.
So if one decides to stack the two, be careful becauseIGF-1 will make the effects of insulin much more potent. It is produced mostly in the Liver in response to growth hormone (GH) release from the pituitary gland. The molecule shows approximately 50% sequence homology with pro insulin and has a number of biological activities comparable to insulin. IGF-1 is a moderator of longitudinal growth in humans which translates to how tall you are capable of becoming. Total Serum IGF-1concentrations are altered by age, nutritional state, body composition, and of course growth hormone secretion. A single basal IGF-1 level is useful in the assessment of short stature in children and in nutritional support studies of acutely ill patients. For diagnosing the condition acromegaly, a single IGF-1 concentration is much more reliable than a random GH measurement (Oppizi, et al., 1986). IGF-1 can be used for the evaluation of disease activity in acromegaly (Barkan, et al., 198. IGF-1’seffects are not limited to building new muscle, however. It has a strong effect on lipid/ cholesterol metabolism, and helps the body shed fat at a drastically predominate rate. Also to be noted, IGF-1 is both a neuro protector and neuro re generator(nerve reproduction), which improves cognitive functions such as reflexes,memory, and learning ability.IGF is also important for production of connective tissue and insuring proper bone mineral density.
One study displayed rats that were given IGF-1 and did nothing were bigger and stronger than rats that weren’t given IGF-1 but exercised. Logically the group of rats that were given IGF-1 and exercised were the most muscular, and strongest rats in the house. The positive effects of IGF-1 on the rats continued for months even after the rats stopped getting the supply of the peptide hormone, while the exercising rats immediately lost size and strength as soon as they stopped exercising.In another study, the muscle fibers of 27month old rats (considered old age for rats) were given IGF-1 during middle age, exhibited no weakening of muscle fibers that indicate the usual and foreseeable signs of aging. These rats did not lose any fast twitch muscle fibers during or post treatment. These fibers are responsible for power and speed which are found in abundance among athletes. Also interesting to note, they had the same speed and power output that they had when they were six months of age. IGF-1Deficiency and Diseases Lacking the ability to produce sufficient amounts of IGF and GH can result in conditions, diseases and even cancer. One such disorder, termed Laron dwarfism does not respond at all to growth hormone treatment due to a lack of GH receptors. The IGF signaling pathway appears to play a crucial role in cancer. Several studies have shown that increased levels of IGF lead to an increased risk of cancer. Especially in the prevention of lung cancer, here is an abstract from study that shows the potential of IGF-1treatment with patients suffering from lunger cancer in conjunction with their chemo treatment: “Lung cancer is the leading cause of cancer-related death in the United States. Despite the availability of several cytotoxic and a few molecularity targeted agents, the outlook for patients with advance cell lung cancer continues to be dismal. Novel approaches are desperately needed. The insulin-like growth factor (IGF) pathway plays an important role in a number of human malignancies contributing to unregulated cell proliferation. The IGF pathway has several targets for therapeutic intervention. Preclinical studies of IGF inhibitors have demonstrated synergism when combined with chemotherapy agents and radiation. Clinical studies are currently ongoing to investigate the safety and efficacy of IGF inhibitors in combination with chemotherapy agents. In this review, we discuss the biology ofthe IGF pathway and various potential targets for therapy.Transaction of IGFBP-3 into lung cancer cell lines seemed to have profound anti tumor effect to the tumor cells in vitro andin vivo.45,46Similar results have been found using recombinant human IGFBP-3 in lung carcinoma models using 3LL Lewis lung carcinoma allograft, suggesting apotential therapeutic role of IGFBP-3.47,48Thus, IGBP-3 may also represent a potential target.In summary,the IGF pathway seems to play a critical role in human neoplasia in general andin lung cancer in particular. Clinical trials with IGF inhibitors just begun inNSCLC hopefully will show promising results.” (Journal of Thoracic Oncology: September 2006 - Volume 1 - Issue 7- pp 607-610)
Lr3IGF-1 (Long R3 Insulin-like Growth Factor-I or Long R3IGF-I) is an 83 amino acid analog of human IGF-I that comprises the complete human IGF-1 sequence but with the replacement of an Arg for the Glu at position 3, as well as a 13 amino acid chain peptide at the N-terminus. This makes Long R3IGF-I two to three more potent than IGF-I in studies, because it has a lower affinity to be made inactive by IGF binding proteins, and as a result more possible activity in the body. The enhanced potency of Lr3IGF-1 over IGF-1 is due to the decreased binding of Long R3 IGF-1to all known IGF binding proteins. These binding proteins normally inhibit the biological actions of IGF's. This also will allow the peptide to have a longer half life of around 20-30 hours. Increasing the activity of biological IGF results in positive are increased amino acid transport to cells, increased glucose transport, increased Protein synthesis, decreased Protein degradation, and increased RNA synthesis. In another investigation, injection ofLR3-IGF-1 in various amounts to investigate the effects on the somatotropic axis (plasma levels of IGF-1 and 2, IGFBPs) was done. They have reported that plasma Long-R3 increased when administered subcutaneously but with no such activity when administered orally.
Additionally, LR3 lowered the levels of native IGF-1in rbGH-injected in calves, but L-R3 increased the amounts of IGF-II concentrations when administered with L-R3 subcutaneously. The parenteral administration of the Long R3 IGF-1 decreased the growth hormone concentration but did not affect the secretion of GH. It was also reported that the somatotrophic acis is essentially functioning in neonatal calves and can be influenced by nutrition, growth hormone and Long-R3-IGF-1 (IGF1-LR3). (Hammonand Blum 1997). Furthermore, it has been shown that in mycocytes, IGF-1 R3stimulates the cardiomyocyte splitting in vivo (Sundgren et al. 2003).
IGF-1LR3Mechanisms of function First primary action is to bind to the IGF1R,a receptor tyrosine kinase, which initiates intracellular signaling. IGF-1 isone of the most powerful endogenous activators of the AKT signaling pathway, as timulator of cell growth and production, and a strong inhibitor of involuntary cell death. IGF-1 LR3 actions have been blocked by the ERK and P13K which completely abolished the BrdU uptake. This causes IGF-1 to produce GH which is crucial for health of maintenance of bodily organ functions. Even though itdoes bind to insulin receptors, its binding frequency to insulin is not as strong as compared to IGF-1 but noted. IGF-1
IGF-1 also known as somatomedin C is a polypeptide of 70 amino acids (7650 daltons), and is one of the number of associated insulin-like growth factors present in the flow. This polypeptide hormone about the same size as insulin and mimics insulin as well.
So if one decides to stack the two, be careful becauseIGF-1 will make the effects of insulin much more potent. It is produced mostly in the Liver in response to growth hormone (GH) release from the pituitary gland. The molecule shows approximately 50% sequence homology with pro insulin and has a number of biological activities comparable to insulin. IGF-1 is a moderator of longitudinal growth in humans which translates to how tall you are capable of becoming. Total Serum IGF-1concentrations are altered by age, nutritional state, body composition, and of course growth hormone secretion. A single basal IGF-1 level is useful in the assessment of short stature in children and in nutritional support studies of acutely ill patients. For diagnosing the condition acromegaly, a single IGF-1 concentration is much more reliable than a random GH measurement (Oppizi, et al., 1986). IGF-1 can be used for the evaluation of disease activity in acromegaly (Barkan, et al., 198. IGF-1’seffects are not limited to building new muscle, however. It has a strong effect on lipid/ cholesterol metabolism, and helps the body shed fat at a drastically predominate rate. Also to be noted, IGF-1 is both a neuro protector and neuro re generator(nerve reproduction), which improves cognitive functions such as reflexes,memory, and learning ability.IGF is also important for production of connective tissue and insuring proper bone mineral density.
One study displayed rats that were given IGF-1 and did nothing were bigger and stronger than rats that weren’t given IGF-1 but exercised. Logically the group of rats that were given IGF-1 and exercised were the most muscular, and strongest rats in the house. The positive effects of IGF-1 on the rats continued for months even after the rats stopped getting the supply of the peptide hormone, while the exercising rats immediately lost size and strength as soon as they stopped exercising.In another study, the muscle fibers of 27month old rats (considered old age for rats) were given IGF-1 during middle age, exhibited no weakening of muscle fibers that indicate the usual and foreseeable signs of aging. These rats did not lose any fast twitch muscle fibers during or post treatment. These fibers are responsible for power and speed which are found in abundance among athletes. Also interesting to note, they had the same speed and power output that they had when they were six months of age. IGF-1Deficiency and Diseases Lacking the ability to produce sufficient amounts of IGF and GH can result in conditions, diseases and even cancer. One such disorder, termed Laron dwarfism does not respond at all to growth hormone treatment due to a lack of GH receptors. The IGF signaling pathway appears to play a crucial role in cancer. Several studies have shown that increased levels of IGF lead to an increased risk of cancer. Especially in the prevention of lung cancer, here is an abstract from study that shows the potential of IGF-1treatment with patients suffering from lunger cancer in conjunction with their chemo treatment: “Lung cancer is the leading cause of cancer-related death in the United States. Despite the availability of several cytotoxic and a few molecularity targeted agents, the outlook for patients with advance cell lung cancer continues to be dismal. Novel approaches are desperately needed. The insulin-like growth factor (IGF) pathway plays an important role in a number of human malignancies contributing to unregulated cell proliferation. The IGF pathway has several targets for therapeutic intervention. Preclinical studies of IGF inhibitors have demonstrated synergism when combined with chemotherapy agents and radiation. Clinical studies are currently ongoing to investigate the safety and efficacy of IGF inhibitors in combination with chemotherapy agents. In this review, we discuss the biology ofthe IGF pathway and various potential targets for therapy.Transaction of IGFBP-3 into lung cancer cell lines seemed to have profound anti tumor effect to the tumor cells in vitro andin vivo.45,46Similar results have been found using recombinant human IGFBP-3 in lung carcinoma models using 3LL Lewis lung carcinoma allograft, suggesting apotential therapeutic role of IGFBP-3.47,48Thus, IGBP-3 may also represent a potential target.In summary,the IGF pathway seems to play a critical role in human neoplasia in general andin lung cancer in particular. Clinical trials with IGF inhibitors just begun inNSCLC hopefully will show promising results.” (Journal of Thoracic Oncology: September 2006 - Volume 1 - Issue 7- pp 607-610)
