Sermorelin is among the growth hormone-releasing hormone (GHRH) analogs. It is classified as a GHRH as researchers have suggested that the peptide acts to induce the endogenous production and release of growth hormone (hGH). Growth hormone has been associated with numerous physiological activities, making Sermorelin and other GHRH analogs, potentially relevant in growth hormone-related research. Examples of of studies employing GHRH analogs include research in the context of tissue scarring following cardiac disfunction, as well as those examining bone density, renal function, dementia and seizure activity.
MOLECULAR FORMULA: C149H246N44O42S
MOLECULAR WEIGHT: 3357.9 g/mol
SEQUENCE: Tyr-Ala-Asp-Ala-lle-Phe-DL-Thr-Asn-Ser-Tyr-Arg-Lys-Val-Leu-Gly-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Met-Ser-Arg-NH2
SERMORELIN AND CARDIAC FUNCTION
Heart attacks may induce secondary cardiac failure, cardiac conduction abnormalities (arrhythmias), and decreased cardiac capacity. Many of these risks have been associated with cardiac remodeling due to damaged myocytes (heart muscle cells), and may impact surrounding tissues. In 2016, a study in pigs observed that Sermorelin exposure appeared to reduce the instances of cardiac remodeling exhibited following a cardiac attack. Researchers suggested as a result of these findings that the peptide may have acted to decrease cell death in cardiomyocytes, as well as improve production of extracellular matrix components and angiogenesis to damaged tissue. The peptide has also been studied for its potential to assist in diastolic function, decrease scar size, and increase capillary growth.[1] [2] The researchers note that “[Exposure to] GHRH agonists appears to reduce the inflammatory responses post-MI and may consequently improve mechanisms of healing and cardiac remodeling by regulating pathways involved in fibrosis, apoptosis and cardiac repair.” It is being explored for different cardiac diseases like a cardiac failure and valve disorders.
SERMORELIN AND EPILEPSY
Gamma-aminobutyric acid (GABA) is a central nervous system signaling molecule that researchers consider may decrease electrical activity in the spinal cord and reduce overall electrical excitability in the central nervous system. Many anti-seizure compounds act either to: enhance levels of GABA in the central nervous system; or mimic GABA by binding to GABA. In one study using a murine model of epilepsy, scientists introduced Sermorelin to study the impact on the models’ seizure activity. GHRH analogs were observed to activate GABA receptors and inhibit seizures.[3]
SERMORELIN AND SLEEP
Orexin is a powerful neurochemical secreted by certain neurons in the brain. It has been suggested to regulate sleep cycles. Growth hormone secretion, in parallel, is considered to occur maximally during sleep. Studies have suggested that a functional GHRH axis is required for orexin production and function, and that exposure to Sermorelin and other GHRH agonists appears to enhance orexin secretion.[4] Sermorelin is being studied in the context of sleep disorders.
SERMORELIN AND GROWTH HORMONE
Sermorelin is a growth hormone-releasing hormone derivative that was developed to mediate the activity of growth hormone, with limited ancillary effects. Sermorelin has been studied for its potential to increase hormone levels as the peptide appears to be regulated through physiological feedback mechanisms that prevent certain ancillary actions of excess growth hormone. Such actions may include instances of edema, joint pain, and dysregulation of normal physiology.[5] Sermorelin researchers have posited that the peptide may not be subject to tachyphylaxis, the process by which the body becomes acclimatized to a compound and thereby negates its action.[6] Scientists conclude that “that the short time course of resensitisation following acute octreotide withdrawal is suggestive of an effect(s) on receptor function or on the receptor signal transduction cascade at sites further downstream, rather than an immune-mediated phenomenon.” Studies have suggested peptide-induced production of GHRH receptors, rather than a down-regulation of them. This action may prevent the onset of tachyphylaxis.
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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.
