Mod GRF 1-29 & Ipamorelin Blend (10mg)

Description

Modified GRF (1-29) & Ipamorelin Peptide Blend

Modified GRF 1-29 and Ipamorelin are separate peptides, which research indicates may work synergistically to induce potential growth hormone release and growth hormone pulses. This increase may result in several downstream physiological activities associated with increased growth hormone release. Modified GRF 1-29 peptide is an analog of growth hormone-releasing hormone (GHRH).[1] It is also known as tetra-substituted GRF (1-29), and is composed of a sequence thought to be the smallest necessary to interact with GHRH receptors, specifically the first 29 amino acids of GHRH. On the other hand, Ipamorelin is suggested to act via binding to growth hormone secretagogue (GHS) receptors.[2] These receptors are also known as the ghrelin receptors, and Ipamorelin appears to be a highly selective pentapeptide that binds and activates them.

Generally, GRF (1-29) has a short half-life that limits its research potential. However, the structurally modified version of the tetra-substituted peptide, Modified GRF 1-29, is considered to boast a longer half-life and has, therefore, been considered by researchers as a more viable compound for use during experimental research. There are significant structural differences between Modified GRF 1-29 and its unmodified counterpart, mainly due to the substitution of four specific amino acids within the sequence. These changes occur at the 2nd, 8th, 15th, and 27th positions and are believed to possibly enhance the peptide’s stability against enzymatic degradation, particularly from enzymes like dipeptidyl peptidase-4 (DPP-4). For example, the substitution of L-alanine with D-alanine at the 2nd position might improve resistance to molecular breakdown. Replacing asparagine with glutamine at the 8th position might potentially reduce the risk of asparagine rearrangement and amide hydrolysis. The replacement of glycine with alanine at the 15th position is thought to possibly increase bioactivity. Lastly, the change from methionine to leucine at the 27th position is believed to help prevent methionine oxidation.

Likewise, Ipamorelin appears to have a high sensitivity to growth hormone secretagogue receptors, potentially leading to superior viability under research conditions. Combination of these peptides may lead to an increase in growth hormone response compared to control levels.

Mod GRF 1-29 Specifications

Molecular Formula: C152H252N44O42

Molecular Weight: 3367.95 g/mol

Sequence: H-Tyr-D-Ala-Asp-Ala-Ile-Phe-Thr-Gln-Ser-Tyr-Arg-Lys-Val-Leu-Ala-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Leu-Ser-Arg-NH2

Ipamorelin Specifications

Molecular Formula: C38H49N9O5

Molecular Weight: 711.86 g/mol

Sequence: Aib-His-D-2Nal-D-Phe-Lys-NH2

Modified GRF 1-29 & Ipamorelin Research

Modified GRF 1-29 & Ipamorelin and Gastrointestinal Tract

Research suggests that high circulation of growth hormone may induce a positive impact within the gastrointestinal tract, and thereby on inflammatory bowel disease and short bowel syndrome.[3] Researchers report that “65% of [research models] receiving GH achieved … remission, compared to 20% [given] CTX alone.” Growth hormone appears to act via Vasoactive Intestinal Peptide (VIP) receptor VIPC1. This interaction may allow the hormone to improve bowel motility.

Further, it is suggested that Ipamorelin may directly interact with the ghrelin receptor in the gastrointestinal (GI) tract. It is thought to bind to these receptors and potentially trigger several responses, such as enhancing gut motility and improving nutrient absorption. Additionally, Ipamorelin has exhibited some potential in reducing inflammation and aiding in tissue repair in various GI injury models. In one model, researchers investigated the effects of Ipamorelin on gastric functions, comparing them with those of a placebo. They were particularly focused on its potential to accelerate gastric emptying. To evaluate this, researchers evaluated both a peptide-exposed experimental group and a control group in a method involving the measurement of residual radioactivity in the stomach 15 minutes after intestinal intervention to hinder gastric emptying. The researchers observed that abdominal interventions may delay gastric emptying, a phenomenon clearly observable in the control group. Conversely, Ipamorelin appeared to hasten this process. These observations suggest that Ipamorelin may potentially enhance the rate of gastric emptying. Moreover, the researchers sought to explore how Ipamorelin may affect the contractile activity of gastric smooth muscles in response to acetylcholine and electrical field stimulation. The findings indicated that intestinal interventions might significantly diminish the contractile responses to these stimuli. However, this reduction appeared mitigated when Ipamorelin was introduced alongside ghrelin. This suggests that Ipamorelin might not only enhance gastric muscle contractility but also potentially counteract the inhibitory actions associated with certain interventions.[4]

Modified GRF 1-29 & Ipamorelin and Cardiovascular Function

Myocardial Infarction (MI) is considered to lead to scarring of cardiac tissues and may reduce heart function (such as ejection fraction). Studies in animal models have suggested that growth hormone secretagogues similar to Ipamorelin may accelerate heart tissue repair post-MI, reduce infarct size, improve cardiac ejection fraction, and improve overall cardiac function.[5] The scientists reveal that “Through activation of GHS-R1a, secretagogues produced a positive inotropic effect on ischemic cardiomyocytes and protected them from I/R injury probably by protecting or recovering p-PLB (and therefore SR Ca2+ content) to allow the maintenance or recovery of normal cardiac contractility.”

Modified GRF 1-29 & Ipamorelin and Bone

Research in growth hormone stimulating peptides such as Modified GRF 1-29 and Ipamorelin suggests that these peptides, particularly Ipamorelin, when observed in murine models, may potentially completely halt bone loss associated with exogenous factors, such as anabolic steroids.[6] The researchers suggested that Ipamorelin might potentially influence osteoblasts (the cells responsible for bone formation) through mechanisms mediated by growth hormone, which might enhance their proliferation, growth, and specialization. The actions of Ipamorelin on the bone mineral density of these murine models were closely observed using real-time dual X-ray absorptiometry (DEXA) at key sites, including the femur and L6 vertebra. Following the experiment, the femur bones underwent further analysis with mid-diaphyseal peripheral quantitative computed tomography (pQCT) scans. Initial results suggested that the peptide may have increased body mass and raised bone mineral content (BMC) in the tibia and vertebrae, as measured by DEXA, compared to the control group. Additionally, the pQCT data hinted that the observed increase in cortical BMC might have originated from an increase in the cross-sectional area of the bone. Therefore, researchers suggest it may potentially trigger new bone formation and increase the BMC by up to four-fold.

Modified GRF 1-29 & Ipamorelin and Muscle Cells

Research suggests that growth hormone-secretagogues, of which Ipamorelin is classified, may inhibit the catabolic activity of glucocorticoids on muscles (such as muscle wasting).[7] Modified GRF 1-29 & Ipamorelin peptide combination may have a high growth hormone-receptor sensitivity and act via mechanisms including increased Insulin-Like Growth Factor 1 (IGF-1) levels, leading to muscle cell proliferation. [7]

Modified GRF 1-29 & Ipamorelin and Blood Sugar Regulation

Some research suggests that growth hormone secretagogues like Ipamorelin may increase the number of beta-pancreatic cells, leading to an increased insulin secretion. Calcium-driven channels are considered to mediate insulin secretion from pancreatic cells. Growth hormone-secretagogues such as Ipamorelin may trigger insulin release from pancreatic cells via pancreatic cells’ calcium channels.[8]

Modified GRF 1-29 & Ipamorelin and the Thyroid

Thyroid dysfunction may occur concomitantly with growth hormone disturbances. This is often considered the case in conditions involving the pituitary gland, where thyroid dysfunction may be associated with growth hormone deficiency. Researchers have noticed that research models of thyroid insufficiency, when exposed to GRF, appear to exhibit an increase in thyroid support.[9]

Modified GRF 1-29 & Ipamorelin and Appetite Regulation

It is possible that Ipamorelin’s interaction with ghrelin receptors may increase hunger signals and thereby potentially lead to increased body mass. Studies involving experimental models have reported that exposure to Ipamorelin appeared to have resulted in an approximate 15% increase in body weight. It is hypothesized that this increase may correspond to a rise in fat pad weight relative to overall body mass, as suggested by DEXA scans, which appear to show a rise in body fat percentage.[10]

Modified GRF 1-29 & Ipamorelin and Growth Hormone Pulsatility

While no studies specifically target Modified GRF 1-29 actions, investigations have examined structurally similar variants. One particular study assessed the potential impacts of a Modified GRF 1-29 analog on various biological processes such as growth hormone and insulin-like growth factor 1 (IGF-1) production, skin cell proliferation, and muscle tissue growth. This research suggested that the Modified GRF 1-29 analog might influence the growth hormone IGF-1 pathway. More tentatively, the findings indicated that the peptide may lead to a significant increase—potentially between 70% and 107%—in the 12-hour release of growth hormone from the somatotroph cells of the anterior pituitary gland. Additionally, IGF-1 levels were reported to rise by about 28%, hinting at an improved functionality of the growth hormone-IGF-1 axis.[11]

Further studies also propose that Ipamorelin might have the potential to elevate growth hormone levels, possibly reaching up to 80mIU/l (approximately 26.6ng/ml). When compared to control thresholds, which have a baseline of 1.31mIU/l or 0.4ng/ml, this increase might represent more than a 60-fold enhancement. However, these results are preliminary and suggest a need for further exploration.[12]

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing. Bodily introduction of any sort is strictly prohibited by law. All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

References

1. Waelbroeck M, Robberecht P, Coy DH, Camus JC, De Neef P, Christophe J. Interaction of growth hormone-releasing factor (GRF) and 14 GRF analogs with vasoactive intestinal peptide (VIP) receptors of rat pancreas. Discovery of (N-Ac-Tyr1,D-Phe2)-GRF(1-29)-NH2 as a VIP antagonist. Endocrinology. 1985 Jun;116(6):2643-9. doi: 10.1210/endo-116-6-2643. PMID: 2859987.
2. 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. doi: 10.1530/eje.0.1390552. PMID: 9849822.
3. Denson LA, Kim MO, Bezold R, Carey R, Osuntokun B, Nylund C, Willson T, Bonkowski E, Li D, Ballard E, Collins M, Moyer MS, Klein DJ. A randomized controlled trial of growth hormone in active pediatric Crohn disease. J Pediatr Gastroenterol Nutr. 2010 Aug;51(2):130-9. doi: 10.1097/MPG.0b013e3181c992d6. PMID: 20453679; PMCID: PMC2910806.
4. Greenwood-Van Meerveld, B., Tyler, K., Mohammadi, E., & Pietra, C. (2012). Efficacy of ipamorelin, a ghrelin mimetic, on gastric dysmotility in a rodent model of postoperative ileus. Journal of experimental pharmacology, 4, 149–155. https://doi.org/10.2147/JEP.S35396
5. Ma Y, Zhang L, Edwards JN, Launikonis BS, Chen C. Growth hormone secretagogues protect mouse cardiomyocytes from in vitro ischemia/reperfusion injury through regulation of intracellular calcium. PLoS One. 2012;7(4):e35265. doi: 10.1371/journal.pone.0035265. Epub 2012 Apr 6. PMID: 22493744; PMCID: PMC3320867.
6. Svensson J, Lall S, Dickson SL, Bengtsson BA, Rømer J, Ahnfelt-Rønne I, Ohlsson C, Jansson JO. The GH secretagogues ipamorelin and GH-releasing peptide-6 increase bone mineral content in adult female rats. J Endocrinol. 2000 Jun;165(3):569-77. doi: 10.1677/joe.0.1650569. PMID: 10828840.
7. Sinha DK, Balasubramanian A, Tatem AJ, Rivera-Mirabal J, Yu J, Kovac J, Pastuszak AW, Lipshultz LI. Beyond the androgen receptor: the role of growth hormone secretagogues in the modern management of body composition in hypogonadal males. Transl Androl Urol. 2020 Mar;9(Suppl 2):S149-S159. doi: 10.21037/tau.2019.11.30. PMID: 32257855; PMCID: PMC7108996.
8. Adeghate E, Ponery AS. Mechanism of ipamorelin-evoked insulin release from the pancreas of normal and diabetic rats. Neuro Endocrinol Lett. 2004 Dec;25(6):403-6. PMID: 15665799.
9. Valcavi R, Jordan V, Dieguez C, John R, Manicardi E, Portioli I, Rodriguez-Arnao MD, Gomez-Pan A, Hall R, Scanlon MF. Growth hormone responses to GRF 1-29 in patients with primary hypothyroidism before and during replacement therapy with thyroxine. Clin Endocrinol (Oxf). 1986 Jun;24(6):693-8. doi: 10.1111/j.1365-2265.1986.tb01666.x. PMID: 3098458.
10. Lall, S., Tung, L. Y., Ohlsson, C., Jansson, J. O., & Dickson, S. L. (2001). Growth hormone (GH)-independent stimulation of adiposity by GH secretagogues. Biochemical and biophysical research communications, 280(1), 132–138. https://doi.org/10.1006/bbrc.2000.4065
11. Khorram, O., Laughlin, G. A., & Yen, S. S. (1997). Endocrine and metabolic effects of long-term administration of [Nle27]growth hormone-releasing hormone-(1-29)-NH2 in age-advanced men and women. The Journal of clinical endocrinology and metabolism, 82(5), 1472–1479. https://doi.org/10.1210/jcem.82.5.3943
12. Gobburu, J.V.S., Agersø, H., Jusko, W.J. et al. Pharmacokinetic-Pharmacodynamic Modeling of Ipamorelin, a Growth Hormone Releasing Peptide, in Human Volunteers. Pharm Res 16, 1412–1416 (1999).

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Dr. Usman

Dr. Usman (BSc, MBBS, MaRCP) completed his studies in medicine at the Royal College of Physicians, London. He is an avid researcher with more than 30 publications in internationally recognized peer-reviewed journals. Dr. Usman has worked as a researcher and a medical consultant for reputable pharmaceutical companies such as Johnson & Johnson and Sanofi.