セルモレリンは、一握りの成長ホルモンを放出するホルモンの1つです（罪悪感）望ましくない効果を避けながら、自然GHRHのプラスの効果のいくつかを維持するために近年開発された類似体。セルモレリン（geref）は現在、成長ホルモン分泌を評価するために臨床的に使用されていますが、ペプチドは次の能力にさらに興味があります。

• 心臓発作後の瘢痕を減らし、
• 骨密度を上げる、
• 慢性疾患の栄養を改善し、
• 腎機能を改善し、
• 認知症の影響と戦う
• 発作活動を減らします。

順序：tyr-dl-ala-dl-asp-dl-ala-dl-xiile-dl-dl-xithr-dl-asn-ser-dl-dl-arg-dl-lys-dl-val-dl-leu-gl y-dl-gln-dl-dl-dl-ser-dl-dl-ala-dl-arg-dl-lys-leu-dl-leu-dl-gln-dl-dl-xiile-dl-met-dl-ser-dl-arg
分子式：c₁₄₉h₂₄₆n₄₄o₄₂s
分子量：3357.933 g/mol
Pubchem cid： 16129620

1。セルモレリンと心臓の健康

心臓発作は、急激に生命を脅かすものの、心不全、心臓の伝導異常（不整脈）、運動能力の低下、痛みなどに続発する長期障害にもつながる可能性があります。これらの問題の多くは、筋細胞（心筋細胞）への損傷に続く心臓リモデリングに起因します。多くの場合、心臓のリモデリングは、心臓発作後の損傷領域での瘢痕だけでなく、周囲の損傷のない領域にも瘢痕化されます。この改造により、多くの長期的な問題が発生し、研究により、それが起こらないようにすることで、心臓発作の直後と数年後の両方の結果が大幅に改善できることが示されています。

2016年、ブタでの研究により、セルモレリン投与は心臓発作に続くリモデリングを減らすのに効果的であることが明らかになりました。この研究は、セルモレリンが次のことを示しました。

• 心筋細胞の細胞死を減らす、
• 適切な治癒に必要な細胞外マトリックス成分の生成を増やし、
• 損傷した組織に血管の成長を増加させ、
• 炎症の損傷を引き起こす物質の産生を減らします。

臨床的には、セルモレリンの影響は、拡張機能の改善、瘢痕サイズの減少、毛細血管の成長の増加に見られます^[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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