Sermorelin is een van een handvol groeihormoon die hormoon vrijgeven (Schuld) Analogen die de afgelopen jaren zijn ontwikkeld in een poging om enkele van de positieve effecten van natuurlijke GHRH te behouden en tegelijkertijd ongewenste effecten te vermijden. Sermorelin (GEREF) wordt momenteel klinisch gebruikt om de secretie van de groeihormoon te beoordelen, maar het peptide is van extra interesse voor zijn vaardigheden om:

• Verminder littekens na hartaanval,
• de botdichtheid verhogen,
• Verbetering van de voeding bij chronische ziekte,
• Verbetering van de nierfunctie,
• vecht tegen de effecten van dementie, en
• Verminder de activiteiten van de aanval.

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Moleculaire formule:C₁₄₉H₂₄₆N₄₄O₄₂S
Molecuulgewicht:3357.933 g/mol
PubChem CID: 16129620

1. Sermorelin en hartgezondheid

Hartaanval, hoewel acuut levensbedreigend, kan ook leiden tot langdurige handicaps als gevolg van hartfalen, hartgeleidingsafwijkingen (aritmieën), verminderde trainingscapaciteit, pijn en meer. Een aantal van deze problemen is het gevolg van cardiale remodellering die na schade aan myocyten (hartspiercellen) volgt. Vaak leidt de remodellering van het hart niet alleen naar littekens in het gebied van schade na een hartaanval, maar ook in de omliggende, onbeschadigde gebieden. Deze remodellering veroorzaakt een aantal problemen op lange termijn en onderzoek heeft aangetoond dat het voorkomen van het gebeuren de resultaten zowel onmiddellijk na hartaanval als jaren later aanzienlijk kan verbeteren.

In 2016 onthulde een onderzoek bij varkens dat de toediening van sermoreline effectief is bij het verminderen van de remodellering die volgt op een hartaanval. Het onderzoek toonde aan dat Sermorelin:

• Vermindert de celdood in cardiomyocyten,
• Verhoogt de productie van extracellulaire matrixcomponenten die nodig zijn voor voldoende genezing,
• verhoogt de groei van bloedvaten tot beschadigd weefsel, en
• Vermindert de productie van stoffen die schadelijke ontsteking veroorzaken.

Klinisch worden de effecten van Sermorelin gezien in verbeterde diastolische functie, verminderde littekengrootte en verhoogde capillaire groei^[1], ^[2]. There is current research exploring the benefits of sermorelin in other forms of heart disease, such as heart failure and even valve disorders.

GHRH treatment reduces scar mass. A. Shows graph of percent change in scar mass over time on top and the relationship between the percent change in scar mass as a percentage of left ventricular mass. B. Shows images of the heart before and after 4 weeks of sermorlin treatment or placebo.

2. Sermorelin and Epilepsy

Gamma-aminobutyric acid (GABA) is a central nervous system signaling molecule known to reduce electrical activity in the spinal cord and reduce overall electrical excitability in the central nervous system. A number of anti-seizure medications work either by increasing levels of GABA in the central nervous system or by binding to GABA receptors and mimicking the effects of GABA. In a recent study of mice with epilepsy, scientists administered GHRH analogues, like sermorelin, to test the effect of these peptides on seizure activity. It turns out that GHRH analogues are effective in suppressing seizures by activating GABA receptors_[3]. This is a very new finding and an active area of research as medications for treating seizure conditions, while effective, have a range of detrimental side effects that reduce their clinical use.

3. Sermorelin and Sleep

There is good evidence that sleep cycles are regulated by orexin, a potent neurochemical produced by certain neurons in the brain. It is also well understood that growth and healing, which are strongly associated with growth hormone secretion, primarily take place during sleep. Research in rainbow trout suggests that this is no coincidence, with an intact GHRH axis being a necessary component for proper orexin secretion and function. In addition, the research reveals that exogenous administration of sermorelin and other GHRH agonists can boost orexin secretion ^[4]. There is ongoing research into the benefits of using sermorelin in sleep disorders.

4. Sermorelin Preferred to Growth Hormone

Sermorelin is a growth hormone releasing hormone derivative and, as such, produces all of the same effects that GH produces, including increasing muscle mass, boosting long bone growth, and reducing adipose tissue. Even though the effects are the same, the side effects are not. In fact, sermorelin is the preferred way to increase GH levels in humans, even over the exogenous administration of growth hormone itself. The primary reason for this preference is that sermorelin is subject to physiological feedback mechanisms that help to prevent common problems encountered with GH administration. These problems include overdose, improper dosing, and unintended side effects like edema, joint pain, and dysregulation of normal physiology^[5].

A second reason to prefer sermorelin is that research shows it is not subject to tachyphylaxis, the process by which the body becomes accustomed to a medication and requires higher and higher doses to achieve desired effects. In some cases, tachyphylaxis is so severe that a drug holiday (complete cessation of use of a medication) is required to regain the effects of a medication. Long-term use of sermorelin in certain clinical settings as well as animal studies of the peptide indicate that the body has a unique response to the peptide. Rather than down-regulate the production of GHRH receptors with administration of sermorelin, the body instead increases their production. This ensures that sermorelin’s effects are unchanged, that tachyphylaxis does not develop to a substantial degree, and that dose escalation is generally not required^[6].

Sermorelin exhibits moderate side effects, low oral and excellent subcutaneous bioavailability in mice. Per kg dosage in mice does not scale to humans. Sermorelin for sale at

The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.

Richard F. Walker, Ph.D, R.Ph, lead author of A better approach to management of adult-onset growth hormone insufficiency?”, received a BS in pharmacy from Rutgers University, a MS in Biochemistry from New Mexico State University and a PhD in a physiology from Rutgers University. He holds postdoctoral fellowships in neuroendocrinology and neuropharmacology at Duke University College of Medicine (Center for the Study of Aging and Human Development) and the University of California, Berkeley, respectively.

Richard F. Walker, Ph.D, R.Ph is being referenced as one of the leading scientists involved in the research and development of Sermorelin. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between

1. L. L. Bagno et al., “Growth Hormone–Releasing Hormone Agonists Reduce Myocardial Infarct Scar in Swine With Subacute Ischemic Cardiomyopathy,” J. Am. Heart Assoc. Cardiovasc. Cerebrovasc. Dis., vol. 4, no. 4, Mar. 2015.
2. R. M. Kanashiro-Takeuchi et al., “New therapeutic approach to heart failure due to myocardial infarction based on targeting growth hormone-releasing hormone receptor,” Oncotarget, vol. 6, no. 12, pp. 9728–9739, Mar. 2015.
3. S. Tang et al., “Interactions between GHRH and GABAARs in the brains of patients with epilepsy and in animal models of epilepsy,” Sci. Rep., vol. 7, Dec. 2017.
4. B. S. Shepherd et al., “Endocrine and orexigenic actions of growth hormone secretagogues in rainbow trout (Oncorhynchus mykiss),” Comp. Biochem. Physiol. A. Mol. Integr. Physiol., vol. 146, no. 3, pp. 390–399, Mar. 2007.
5. R. F. Walker, “Sermorelin: A better approach to management of adult-onset growth hormone insufficiency?,” Clin. Interv. Aging, vol. 1, no. 4, pp. 307–308, Dec. 2006.
6. S. T. Wahid, P. Marbach, B. Stolz, M. Miller, R. A. James, and S. G. Ball, “Partial tachyphylaxis to somatostatin (SST) analogues in a patient with acromegaly: the role of SST receptor desensitisation and circulating antibodies to SST analogues,” Eur. J. Endocrinol., vol. 146, no. 3, pp. 295–302, Mar. 2002.

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