Hey guys,
I will be running a log of Superior peptides MK-677, t3, and cjc1295. I ordered myself the t3 and cjc1295 tonight and will let you guys know when I receive them so you can see how fast shipping is and I will let you know about packaging and appearance. I wanted to just get this little log and info thread ready. On payday I will be ordering up the mk677. I will not be changing any other "supplements" in my arsenal during this time frame as I am using Uncle Z's test e, deca, and m1t.
Im looking to lean up a tad for beach season :eek: I cant look like a beached whale next to my girlfriend when we go out on the boat and hit the beach! Just excited to get this started, so here it goes!!!!
*Just a little info on MK-677:
MK-677, or Ibutamoren, is a drug which acts as a potent, orally active growth hormone secretagogue,[1][2] mimicking the GH stimulating action of the endogenous hormone ghrelin.[3][4] It has been demonstrated to increase the release of, and produces sustained increases in plasma levels of several hormones including growth hormone and IGF-1, but without affecting cortisol levels.[5] It is currently under development as a potential treatment for reduced levels of these hormones, such as in growth hormone deficient children or elderly adults,[6][7][8] and human studies have shown it to increase both muscle mass and bone mineral density,[9][10] making it a promising therapy for the treatment of frailty in the elderly.[11][12] It also alters metabolism of body fat and so may have application in the treatment of obesity.[13][14]
*References according to Wikipedia:
^ Patchett AA, Nargund RP, Tata JR, Chen MH, Barakat KJ, Johnston DB, Cheng K, Chan WW, Butler B, Hickey G, et al. Design and biological activities of L-163,191 (MK-0677): a potent, orally active growth hormone secretagogue. Proceedings of the National Academy of Sciences USA. 1995 Jul 18;92(15):7001-5. PMID 7624358
2.Jump up ^ Pong SS, Chaung LY, Dean DC, Nargund RP, Patchett AA, Smith RG. Identification of a new G-protein-linked receptor for growth hormone secretagogues. Molecular Endocrinology. 1996 Jan;10(1):57–61. PMID 8838145
3.Jump up ^ Cassoni P, Papotti M, Ghè C, Catapano F, Sapino A, Graziani A, Deghenghi R, Reissmann T, Ghigo E, Muccioli G. Identification, characterization, and biological activity of specific receptors for natural (ghrelin) and synthetic growth hormone secretagogues and analogs in human breast carcinomas and cell lines. Journal of Clinical Endocrinology and Metabolism. 2001 Apr;86(4):1738–45. PMID 11297611
4.Jump up ^ Holst B, Frimurer TM, Mokrosinski J, Halkjaer T, Cullberg KB, Underwood CR, Schwartz TW. Overlapping Binding Site for the Endogenous Agonist, Small Molecule Agonists and Ago-allosteric Modulators on the Ghrelin Receptor. Molecular Pharmacology. 2008 Oct 15. PMID 18923064
5.Jump up ^ Copinschi G, Van Onderbergen A, L'Hermite-Balériaux M, Mendel CM, Caufriez A, Leproult R, Bolognese JA, De Smet M, Thorner MO, Van Cauter E. Effects of a 7-day treatment with a novel, orally active, growth hormone (GH) secretagogue, MK-677, on 24-hour GH profiles, insulin-like growth factor I, and adrenocortical function in normal young men. Journal of Clinical Endocrinology and Metabolism. 1996 Aug;81(8):2776-82. PMID 8768828
6.Jump up ^ Chapman IM, Bach MA, Van Cauter E, Farmer M, Krupa D, Taylor AM, Schilling LM, Cole KY, Skiles EH, Pezzoli SS, Hartman ML, Veldhuis JD, Gormley GJ, Thorner MO. Stimulation of the growth hormone (GH)-insulin-like growth factor I axis by daily oral administration of a GH secretogogue (MK-677) in healthy elderly subjects. Journal of Clinical Endocrinology and Metabolism. 1996 Dec;81(12):4249-57. PMID 8954023
7.Jump up ^ Thorner MO, Chapman IM, Gaylinn BD, Pezzoli SS, Hartman ML. Growth hormone-releasing hormone and growth hormone-releasing peptide as therapeutic agents to enhance growth hormone secretion in disease and aging. Recent Progress in Hormone Research. 1997;52:215-46. PMID 9238854
8.Jump up ^ Chapman IM, Pescovitz OH, Murphy G, Treep T, Cerchio KA, Krupa D, Gertz B, Polvino WJ, Skiles EH, Pezzoli SS, Thorner MO. Oral administration of growth hormone (GH) releasing peptide-mimetic MK-677 stimulates the GH/insulin-like growth factor-I axis in selected GH-deficient adults. Journal of Clinical Endocrinology and Metabolism. 1997 Oct;82(10):3455-63. PMID 9329386
9.Jump up ^ Murphy MG, Bach MA, Plotkin D, Bolognese J, Ng J, Krupa D, Cerchio K, Gertz BJ. Oral administration of the growth hormone secretagogue MK-677 increases markers of bone turnover in healthy and functionally impaired elderly adults. The MK-677 Study Group. Journal of Bone and Mineral Research. 1999 Jul;14(7):1182-8. PMID 10404019
10.Jump up ^ Murphy MG, Weiss S, McClung M, Schnitzer T, Cerchio K, Connor J, Krupa D, Gertz BJ; MK-677/Alendronate Study Group. Effect of alendronate and MK-677 (a growth hormone secretagogue), individually and in combination, on markers of bone turnover and bone mineral density in postmenopausal osteoporotic women. Journal of Clinical Endocrinology and Metabolism. 2001 Mar;86(3):1116–25. PMID 11238495
11.Jump up ^ Smith RG, Sun Y, Jiang H, Albarran-Zeckler R, Timchenko N. Ghrelin receptor (GHS-R1A) agonists show potential as interventive agents during aging. Annals of the New York Academy of Sciences. 2007 Nov;1119:147-64. PMID 18056963
12.Jump up ^ An Anti-frailty Pill For Seniors? New Drug Increases Muscle Mass In Arms And Legs Of Older Adults. ScienceDaily November 5th, 2008
13.Jump up ^ Svensson J, Lönn L, Jansson JO, Murphy G, Wyss D, Krupa D, Cerchio K, Polvino W, Gertz B, Boseaus I, Sjöström L, Bengtsson BA. Two-month treatment of obese subjects with the oral growth hormone (GH) secretagogue MK-677 increases GH secretion, fat-free mass, and energy expenditure. Journal of Clinical Endocrinology and Metabolism. 1998 Feb;83(2):362-9. PMID 9467542
14.Jump up ^ Svensson J, Jansson JO, Ottosson M, Johannsson G, Taskinen MR, Wiklund O, Bengtsson BA. Treatment of obese subjects with the oral growth hormone secretagogue MK-677 affects serum concentrations of several lipoproteins, but not lipoprotein(a). Journal of Clinical Endocrinology and Metabolism. 1999 Jun;84(6):2028–33. PMID 10372705
*A few interesting studies:
!.)
Subjects-
Eight healthy male volunteers were recruited. They were 24–39 yr old (mean age, 32.3 yr), within 20% of ideal body weight (Metropolitan Life Insurance tables), and ranged from 64–83.5 kg (mean, 73.2 kg). All subjects were in general good health on the basis of medical history, physical exam, electrocardiogram, and routine laboratory safety studies. All subjects were nonsmokers. Total testosterone and thyroid function tests (T4 and T3 by RIA, and sensitive TSH by immunoradiometric assay) were normal at screening for all subjects. The study was approved by the University of North Carolina Institutional Committee for the Protection of the Rights of Human Subjects and written informed consent was obtained from each subject.
Study design-
This was a double-blind, placebo-controlled, randomized, two-period, cross-over study. Moderate catabolism was produced in eight healthy young adult volunteers by restricting their dietary intake. During the first 7 days of each 14-day treatment period, subjects received a hypocaloric diet and were administered a single-blind placebo tablet each night at bedtime. During the last 7 days of each 14-day study period, subjects continued the same caloric-restricted diet and received either 25 mg MK-677 or placebo orally once daily at bedtime. The sequence of MK-677 and placebo treatments during the last 7 days of caloric restriction was randomized among the subjects according to a computer-generated allocation schedule. There was a 14- to 21-day washout interval between periods, during which time the subjects consumed their normal diet. Previously, this period of time has been shown to restore nitrogen balance and IGF-I to values that are comparable with those that were present before dietary restriction (21).
RESULTS-
Nitrogen balance
Nitrogen balance calculated daily for MK-677 and placebo treatments is shown in Fig. 1. During the first week of caloric restriction (i.e. diet alone), daily nitrogen losses were similar for both treatment groups (mean ± se values were −2.67 ± 0.40 g/day and −2.83 ± 0.26 g/day for the MK-677 and placebo groups, respectively). During the second week (diet and study drug), MK-677 improved average daily nitrogen balance to 0.31 ± 0.21 g/day compared with −1.48± 0.21 g/day in the placebo group. Nitrogen losses clearly reversed after the first dose in the MK-677 treatment group (day 8). In the MK-677 treatment group, daily nitrogen balance increased to approximately +1 and approximately +0.3 g/day after 2 and 7 days treatment, respectively [vs. ∼ −2 and ∼ −1 g/day on the same days for placebo (Fig. 1)]. MK-677 improved overall nitrogen balance integrated over the subsequent 7 days of treatment; AUCdays 8–14 nitrogen balance was +2.69 ± 5 (se) vs. −8.97 ± 5.26 g/day for MK-677 and placebo treatments, respectively (P = 0.001). Further, when the mean AUCdays 8–14 was compared with 0, the 25-mg MK-677 treatment was associated with a nearly significant increase (P = 0.09), whereas placebo treatment was associated with a significant decrease (P = 0.001). Analysis of AUCdays 8–14 based on nitrogen balance corrected for creatinine excretion yielded similar results. Changes in serum urea nitrogen were consistent with the nitrogen balance results. Serum urea nitrogen decreased from a mean of 14.6 ± 2.4 to 12.9 ± 2.1 mg/dL over the last 4 days of each interval of placebo treatment. In contrast, the subjects remaining on MK-677 had a mean serum urea nitrogen that decreased from 13.8 ± 2.3 to 9.55± 1.9 mg/dL. This change was significantly greater than the change that occurred with placebo P < 0.01.
Dietary restriction during the first week (days 1–7) caused all subjects to lose an average approximately 2.5 kg. During the study treatment week (days 8–14), there was less weight loss in the MK-677 treatment group compared with the placebo group (day 14/day 8 mean weight ratio = 0.99 for MK-677 compared with 0.98 for placebo; P < 0.05).
GH response
The peak and integrated (AUC0–8 h) GH response for days 8 and 14 are shown in Table 1. MK-677 produced a peak GH response of 55.9 ± 31.7 μg/L after the first dose (day 8) and 22.6 ± 9.3 μg/L after a week of dosing (day 14) compared with peak GH responses of approximately 9μ g/L (day 8) and approximately 7 μg/L (day 14) with placebo (P < 0.05 for both comparisons).
IGF-I and IGFBPs
The changes in nitrogen balance were accompanied by changes in IGF-I levels (Fig. 2). Following the initial 7 days of caloric restriction, IGF-I declined for each group from a mean of 236 ± 56 ng/mL to 174 ± 64 ng/mL in the placebo group and from 232 ± 69 ng/mL to 185 ± 53 ng/ml in the group that subsequently received MK-677 [P = not significant (NS)]. IGF-I increased progressively to 256 ± 84 ng/mL by day 3 of MK-677 treatment, then remained elevated through the last treatment day. The placebo group showed no change. When the mean value for the last 5 days of MK-677 treatment (264 ± 31 ng/mL) was compared with the mean value for placebo subjects (188 ± 19 ng/mL), the difference was significant (P < 0.01). When the individual daily values from days 10–14 were compared, the individual values for days 10–14 on MK-677 treatment were significantly greater than the placebo treatment values (P < 0.05). No significant difference in IGFBP-2 was found between the MK-677 and placebo treatments (data not shown). IGFBP-3 also increased significantly during treatment (Fig. 3). Dietary restriction resulted in a decline from 2974 ± 578 ng/mL to 2752 ± 514 ng/mL in the placebo group after 7 days of restriction. The decrease in the MK-677 group was similar from 2871 ± 659 ng/mL to 2747 ± 623 ng/mL (P = NS). Following MK-677, IGFBP-3 increased progressively to a mean day-12 (fifth treatment day) value of 3374± 917 ng/mL (P < 0.05 compared with day 8). In contrast, the placebo group showed no change (day-12 value = 2673 ± 636 ng/mL; P = NS compared with day 8). When the average IGFBP-3 value for the last 5 treatment days on MK-677 (3273 ± 330 ng/mL) was compared with placebo (2604 ± 253 ng/mL), the difference was significant (P < 0.01).
Cortisol and PRL
Cortisol and PRL concentrations are known to be increased by single doses of GHRP-6 and its nonpeptide mimetics (13, 14). The changes in these hormones during MK-677 treatment are shown in Table 2. Although there was an effect of MK-677 on serum cortisol AUC0–8 h on day 8 (120.3 ± 28.0μ g·h/dL vs. 54.8 ± 15.1 μg·h/dL for placebo, P = 0.001), the comparison of the mean cortisol response on day 14 showed no difference between treatment groups (cortisol AUC0–8 h: MK-677 71.2 ± 18.4 μg·h/dL vs. placebo 60.2 ± 14.1 μg·h/dL, P> 0.2). MK-677 also increased urinary cortisol on day 8 (first dose) but not on day 14 (seventh dose) as shown in Table 2.
There was also a small effect of MK-677 on serum PRL concentrations on day 8 (first dose) that was substantially attenuated by day 14 (seventh dose) (peak PRL = 26.6 ± 12.8 μg/L vs. 17.4 ± 6.3 μg/L for MK-677 and placebo on day 8, respectively, compared with peak PRL = 18.4 ± 8.1 μg/L and 15.2 ± 11.9 μg/L for MK-677 and placebo, respectively, on day 14).
Full study can be seen at: An Error Occurred Setting Your User Cookie <--- I don't know why its coming up as this but link is correct and works.
2.)
Oral administration of growth hormone (GH) releasing peptide-mimetic MK-677 stimulates the GH/insulin-like growth factor-I axis in selected GH-deficient adults.
Abstract
To determine the effect of the GH releasing peptide (GHRP)-mimetic, MK-677, on the GH/insulin-like growth factor-I (IGF-I) axis in selected GH-deficient adults, we studied nine severely GH-deficient men [peak serum GH concentration in response to insulin-induced hypoglycemia of 1.2 +/- 1.5 micrograms/L, mean +/- SD (range 0.02-4.79)], age 17-34 yr, height 168 +/- 1.5 cm, body mass index 22.6 +/- 3.3 kg/m2, who had been treated for GH deficiency with GH during childhood. In a double-blind rising-dose design, subjects received once daily oral doses of 10 or 50 mg MK-677 or placebo for 4 days over two treatment periods separated by at least 28 days. Four subjects received placebo and 10 mg/day MK-677 in a cross-over fashion in periods 1 and 2. Five subjects received 10 mg and then 50 mg/day MK-677 in a sequential, rising-dose fashion in periods 1 and 2, respectively. Blood was collected every 20 min for 24 h before treatment and at the end of each period for GH measurement using an ultrasensitive assay. The drug was generally well tolerated, with no significant changes from baseline in circulating concentrations of cortisol, PRL, and thyroid hormones. Serum IGF-i and 24-H mean GH concentrations increased in all subjects after treatment with both 10 and 50 mg/day MK-677 vs. baseline. After treatment with 10 mg MK-677, IGF-I concentrations increased 52 +/- 20% (65 +/- 6 to 99 +/- 9 micrograms/L, geometric mean +/- intrasubject SE, P < or = 0.05 vs. baseline), and 24 h mean GH concentrations increased 79 +/- 19% (0.14 +/- 0.01 to 0.26 +/- 0.02 microgram/L, P < or = 0.05 vs. baseline). Following treatment with 50 mg MK-677, IGF-I concentrations increased 79 +/- 9% (84 +/- 3 to 150 +/- 6 micrograms/L, P < or = 0.05 vs. baseline) and 24-h mean GH concentrations increased 82 +/- 29% (0.21 +/- 0.02 to 0.39 +/- 0.04 microgram/L, P < or = 0.05 vs. baseline), respectively. Serum IGF binding protein-3 concentrations increased with both 10 mg (1.2 +/- 0.1 to 1.7 +/- 0.1 micrograms/L, P < or = 0.05) and 50 mg MK-677 (1.7 +/- 0.1 to 2.2 +/- 0.2 micrograms/L, P < or = 0.05). The GH response to MK-677 was greater in subjects who were the least GH/IGF-I deficient at baseline; by linear regression analysis the increase in 24-h mean GH concentration was positively related to both baseline 24-h mean GH concentration (r = 0.81, P = 0.009) and baseline IGF-I (r = 0.79, P = 0.01) for 10 mg MK-677. IGF-I responses were not significantly related to any baseline measurement. Fasting and postprandial insulin and postprandial glucose increased significantly after MK-677 treatment, and the clinical significance of these changes will need to be assessed in longer term studies. Oral administration of such GHRP-mimetic compounds may have a role in the treatment of GH deficiency of childhood onset.
Full study can be seen here: Oral administration of growth hormon... [J Clin Endocrinol Metab. 1997] - PubMed - NCBI