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    Thread: PEPTIDES: descriptions, theories & some good articles

    1. #11
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      It's come to my attention that there are some new peptides on the market. One of which is MYO-029 aka Stamulumab, originally made by Wyeth Pharmaceuticals in NJ. It was designed to block myostatin, the gene that inhibits muscle growth.

      Some sources are selling this for over $100 per 1mg

      Save your hard earned money, this is nothing but crap. Let me show you why....

      ** MYO-029 **

      Description:
      MYO-029) is an experimental myostatin inhibiting research chemical. The product appears to block the actions of a protein- GDF8- that decreases muscle mass, increases fat accumilation, and increases blood glucose. As an anti-GDF8 antibody, MYO-029 has the potential to decrease the high glucose levels that characterize Type 2 diabetes. MYO-029 also may have the potential to treat muscle-waisting diseases such as age related frailty and muscular dystrophy.



      Wyeth won't develop MYO-029 for MD
      , taken from http://www.mda.org/research/080311md_myo-029.html,
      originally posted March 11th, 2008.



      Wyeth Pharmaceuticals of Madison, N.J., has announced it will not continue development of its experimental compound MYO-029 for muscular dystrophy.

      MYO-029 is an antibody (immune-system protein) designed to stick to and interfere with the actions of myostatin, a protein that limits muscle growth. By blocking myostatin, it was hoped that muscles affected by muscular dystrophy would become larger and stronger. Development of MYO-029 was based in part on preclinical research funded by MDA.

      “We're disappointed that MYO-029 will not be moving forward," said Sharon Hesterlee, MDA vice president of translational research. "But I doubt this is the end of the line for myostatin inhibition. MDA is looking at other ways to block myostatin and, of course, other strategies to improve muscle health.”

      Beginning in 2005, with supplemental funding to trial sites from MDA, Wyeth began a phase 1-2 clinical trial to test the safety and tolerability of MYO-029 in 116 adults with Becker, facioscapulohumeral and limb-girdle types of muscular dystrophy.

      The compound was found to be safe and well tolerated at three dosage levels, reports a paper published online todayin Annals of Neurology by Kathryn Wagner at Johns Hopkins University School of Medicine in Baltimore, and colleagues.

      However, the investigators found no improvements in muscle strength or function, and no statistically significant muscle growth in trial participants.
      (The authors note that the study was not designed to measure efficacy.)

      Investigators say the MYO-029 clinical trial supports the hypothesis that systemic administration of agents that block myostatin is safe enough for future studies and that further evaluation of more potent myostatin inhibitors than MYO-029 should be considered.

      Wyeth Executive Vice President and Chief Medical Officer Gary Stiles says the company “remains committed to discovering and developing treatments for muscle diseases and continues to explore myostatin inhibition along with other strategies,” despite its discontinuation of the MYO-029 program.

    2. #12
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      Can one of the mods or Admin ban this spamming, scamming, fraudulent advertising Piece Of Sh...??!?!?


      DAMN this guy ticks me off!
      !! Go FUCK Yourself EdHardy!!

    3. #13
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      ** IPAMORELIN **



      Description:
      Ipamorelin or NNC 26-0161, a polypeptide hormone, is a growth hormone secretagogue and ghrelin mimetic and analog developed by Novo Nordisk[3]. Ipamorelin belongs to the most recent generation of GHRPs from the mid 1990s and causes significant release of growth hormone by itself, due both to its suppression of somatostatin (an antagonist to GHRH) and stimulation of release of GH from the anterior pituitary, similar to GHRP-2 and GHRP-6 which are compounds from the same class (growth hormone releasing peptides).[1] The cells that produce and release GH are known as somatotropes.[2] Like GHRP-2 and GHRP-6, ipamorelin does not have ghrelin’s lipogenic properties. Like GHRP-2 and unlike GHRP-6 ipamorelin never induces hunger in mammals. Ipamorelin acts synergistically when applied during a native GHRH (growth-hormone releasing hormone) pulse or when coadministered with GHRH or a GHRH analog such as Sermorelin or GRF 1-29 (growth releasing factor, aminos 1-29).[1] The synergy comes both due to the suppression of somatostatin and the fact that ipamorelin increases GH release per-somatotrope, while GHRH increases the number of somatotropes releasing GH.[1,2]


      There is also a secondary effect of neuronal excitation in the hypothalamus caused by ipamorelin, which lasts for approximately 3 hours after application, similar to GHRP-2 and GHRP-6

      Ipamorelin has a unique property among the GHRP class of peptides. That property is known as selectiveness. Raun et al demonstrated the selectiveness of ipamorelin for GH release only in a study:

      The development and pharmacology of a new potent growth hormone (GH) secretagogue, ipamorelin, is described. Ipamorelin is a pentapeptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2), which displays high GH releasing potency and efficacy in vitro and in vivo. As an outcome of a major chemistry programme, ipamorelin was identified within a series of compounds lacking the central dipeptide Ala-Trp of growth hormone-releasing peptide (GHRP)-1. In vitro, ipamorelin released GH from primary rat pituitary cells with a potency and efficacy similar to GHRP-6 (ECs) = 1.3+/-0.4nmol/l and Emax = 85+/-5% vs 2.2+/-0.3nmol/l and 100%). A pharmacological profiling using GHRP and growth hormone-releasing hormone (GHRH) antagonists clearly demonstrated that ipamorelin, like GHRP-6, stimulates GH release via a GHRP-like receptor. In pentobarbital anaesthetised rats, ipamorelin released GH with a potency and efficacy comparable to GHRP-6 (ED50 = 80+/-42nmol/kg and Emax = 1545+/-250ng GH/ml vs 115+/-36nmol/kg and 1167+/-120ng GH/ml). In conscious swine, ipamorelin released GH with an ED50 = 2.3+/-0.03 nmol/kg and an Emax = 65+/-0.2 ng GH/ml plasma. Again, this was very similar to GHRP-6 (ED50 = 3.9+/-1.4 nmol/kg and Emax = 74+/-7ng GH/ml plasma). GHRP-2 displayed higher potency but lower efficacy (ED50 = 0.6 nmol/kg and Emax = 56+/-6 ng GH/ml plasma). The specificity for GH release was studied in swine. None of the GH secretagogues tested affected FSH, LH, PRL or TSH plasma levels. Administration of both GHRP-6 and GHRP-2 resulted in increased plasma levels of ACTH and cortisol. Very surprisingly, ipamorelin did not release ACTH or cortisol in levels significantly different from those observed following GHRH stimulation. This lack of effect on ACTH and cortisol plasma levels was evident even at doses more than 200-fold higher than the ED50 for GH release. In conclusion, ipamorelin is the first GHRP-receptor agonist with a selectivity for GH release similar to that displayed by GHRH. The specificity of ipamorelin makes this compound a very interesting candidate for future clinical development.[3]


      Whereas GHRP-6 and GHRP-2 cause a release and increase in cortisol and prolactin levels, ipamorelin only selectively releases GH at any dose. Further, a mega-dose of ipamorelin results in a concomitant mega-release of GH (up to the entire amount present in the pituitary), whereas GHRP-2 and GHRP-6 have limits of approximately 1mcg/kg in humans for their maximal GH release.[4,5]



      Cititations:

      [1] Bowers CY, Momany F, Reynolds GA. In vitro and in vivo activity of a small synthetic peptide with potent GH releasing activity. 64th Annual Meeting of the Endocrine Society, San Francisco, 1982, p. 205.
      [2]Bowers CY, Momany F, Reynolds GA, Sartor O. Multiple receptors mediate GH release. 7th International Congress of Endocrinology, Quebec, Canada, 1984, p. 464.

      [3] Raun K, Hansen BS, Johansen NL, Thøgersen H, Madsen K, Ankersen M, Andersen PH. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998 Nov;139(5):552-61.

      [4] Brosnan-Cook, M. et al. (1998) Iontophoretic delivery of ipamorelin, a growth hormone secretagogue. Proceedings of 80th Annual Meeting Endocrine Society, New Orleans, USA. Abstract Pp1-186.

      [5] Jogarao V S Gobburu; Henrik Agerso; William J Jusko . Pharmacokinetic-Pharmacodynamic Modeling of Ipamorelin, a Growth Hormone Releasing Peptide in Human Volunteers. Lars Ynddal Pharmaceutical Research: Sep 1999; 16, 9; ProQuest Nursing & Allied Health Source p. 1412.
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    4. #14
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      ** Hexarelin **

      Hexarelin belongs to a class of growth hormone secretagogues specifically known and referred to as Ghrelin mimetics or GHRPs. As opposed to GHRHs (growth hormone releasing hormones such as Sermorelin, Modified GRF 1-29, and CJC-1295), which are a separate class of growth hormone secretagogues, Ghrelin mimetics primarily increase growth hormone release in the somatotrophs within the pituitary. GHRHs, on the other hand, slighty increase somatotroph output while concurrently causing more somatrophs overall to release growth hormone.


      Ghrelin mimetics have been demonstrated in clinical environments to release more growth hormone than GHRHs in comparison studies. [2] Ghrelin mimetics are less susceptible to environmental, hormonal, and physiological factors that inhibit GHRH-induced GH release, such as somatostatin, fatty acids circulating in plasma, and timing of the natural rhythmic growth hormone pulse in the human body. [1]


      The most-studied Ghrelin mimetic peptides are GHRP-2, GHRP-6, hexarelin, and ipamorelin. Of these, ipamorelin is the least potent GH releasing compound but the compound that also has the least effect on cortisol and prolactin release. GHRP-6 is more potent with slightly more cortisol and prolactin release; GHRP-2 is more potent still; and hexarelin is the most potent of the four, with the most release of cortisol and prolactin as well. [3]


      Each of the Ghrelin mimetics has unique properties largely unrelated, in most cases, to effecting the release of growth hormone from the pituitary. Hexarelin "reduces injury of cerebral cortex and hippocampus after brain hypoxia-ischemia in neonatal rats" according to one study; this effect may possibly be achieved with ghrelin, as well. [4] The ghrelin mimetics (GHRPs) are believed, as a whole, to potentially exert an antioxidant benefit on the testis by action involving the GHS-R type 1a present in Sertoli and Leydig cells; it may have antioxidant and anti-inflammatory effect through reduction of lipid peroxidation as well as increasing the activity of the body's three main antioxidant systems (superoxidate dismutase, glutathione peroxidase, and catalase), and may additionally protect spermatozoa from free radicals. [5]


      Pang et al found, regarding hexarelin's potential cardioprotective effects, that:

      GHS-R mRNA was abundantly expressed in cardiomyocytes and was unregulated after administration of hexarelin. These results suggest that hexarelin abates cardiomyocytes from ANG II-induced apoptosis possibly via inhibiting the increased caspase-3 activity and Bax expression induced by ANG II and by increasing the expression of Bcl-2, which is depressed by ANG II. [6]


      In a separate study, Pang et al found data leading them to believe that hexarelin may have potential benefits in humans for treating atherosclerosis:

      Hexarelin suppressed the formation of atherosclerotic plaques and neointima, partially reversed serum HDL-c/LDL-c ratio and increased the levels of serum NO and aortic mRNAs of eNOS, GHSR and CD36 in As rats. Hexarelin also decreased [(3)H]-TdR incorporation in cultured vascular smooth muscle cell (VSMC) and calcium sedimentation in aortic wall. Furthermore, foam cell formation induced by ox-LDL was decreased by hexarelin. In conclusion, hexarelin suppresses high lipid diet and vitamin D3-induced atherosclerosis in rats, possibly through up regulating HDL-c/LDL-c ratio, vascular NO production and downregulating the VSMC proliferation, aortic calcium sedimentation and foam cell formation. These novel anti-atherosclerotic actions of hexarelin suggest that the peptide might have a clinical potential in treating atherosclerosis. [7]


      Bresciani et al concluded, due to findings that hexarelin induces hunger in rats even with chronic use, that "hexarelin is endowed with long-lasting orexigenic activity and might represent a potential therapeutic approach for pathological conditions characterized by a decline in food intake." [8]




      Citations:


      [1]Penalva, A., Carballo, A., Pombo, M., Casanueva, F.F. and Dieguez, C. (1993) Effect of growth hormone (GH)-releasing hormone (GHRH), atropine, pyridostigmine or hypoglycemia on GHRP- 6-induced GH secretion in man. J. Clin. Endocrinol. Metab. 76, 168–171

      [2]Bowers CY, Reynolds GA, Chang D, Hong A, Chang K, Momany F. A study on the regulation of GH release from the pituitary of rats, in vitro. Endocrinology 1981;108(3):1070–1079.

      [3]Ghigo, E., Arvat, E., Muccioli, G. and Camanni, F. (1997) Growth hormone releasing peptides. Eur. J. Endocrinol. 136, 445–460

      [4]Liu Y, Wang PS, Xie D, Liu K, Chen L. Ghrelin reduces injury of hippocampal neurons in a rat model of cerebral ischemia/reperfusion. Chin J Physiol. 2006 Oct 31;49(5):244-50.

      [5]Kheradmand. Antioxidant enzyme activity and MDA level in the rat testis following chronic administration of ghrelin. Andrologia, Nov 2008, Volume 41, Issue 6, Pages 335-340

      [6]Pang JJ, Xu RK, Xu XB, Cao JM, Ni C, Zhu WL, Asotra K, Chen MC, Chen C. Hexarelin protects rat cardiomyocytes from angiotensin II-induced apoptosis in vitro. Am J Physiol Heart Circ Physiol. 2004 Mar;286(3):H1063-9. Epub 2003 Nov 13.

      [7]Pang J, Xu Q, Xu X, Yin H, Xu R, Guo S, Hao W, Wang L, Chen C, Cao JM. Hexarelin suppresses high lipid diet and vitamin D3-induced atherosclerosis in the rat. Peptides. 2010 Apr;31(4):630-8. Epub 2009 Nov 30.

      [8] Bresciani E, Pitsikas N, Tamiazzo L, Luoni M, Bulgarelli I, Cocchi D, Locatelli V, Torsello A. Feeding behavior during long-term hexarelin administration in young and old rats. J Endocrinol Invest. 2008 Jul;31(7):647-52.
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