DSIP benefits those who struggle to sleep. DSIP or delta sleep-inducing peptide is a research peptide that is still being studied. It has many positive results in helping treat insomnia and sleep problems. If you are in the research industry and want to buy DSIP click here now.
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What is DSIP?
DSIP peptide is also called “insomniac peptide” because of its ability to induce sleep in rabbits in the presence of other physiological and pharmacological sedative agents. The sleep-inducing effect of Delta-sleep-inducing peptide is believed to be mediated by a mechanism involving the suprachiasmatic nucleus (SCN) and the medial preoptic nucleus (MPN).
In 1983, using bioassay techniques and mass spectroscopy, Saito et al. isolated and identified Delta-sleep-inducing peptide as a polypeptide having the following amino acid sequence: His-Ser-Gly-Asp-Gly-Lys-Thr-Pro-Phe-Arg-Arg-Arg-Pro-Ile-Ala-Arg-Ile-Leu-Arg-Leu-Arg-Lys-Lys-Leu-Val-Gly-Ser-Phe-Leu-Phe-Lys-Leu-Lys-Leu-Glu-Glu-Asp-Leu-Leu-Ser-Arg (SEQ ID NO: 1).
What is the DSIP experience?
The peptide was found to have a molecular weight of 1161.3 Da. In 1981, using a radioimmunoassay, researchers at Eisai Co., Ltd. confirmed that Delta-sleep-inducing peptide immunoreactivity was present in the plasma of rabbits, rats and sheep. In 1982, Saito et al. determined the primary structure of human Delta-sleep-inducing peptide and, in 1985, Saito et al. synthesized an analog of Delta-sleep-inducing peptide that is active in inducing sleep in rabbits.
What are DSIP Benefits?
As a somatogenic peptide, Delta-sleep-inducing peptide is structurally similar to somatostatin, bombesin, and vasoactive intestinal peptide. The effect of somatostatin on cell proliferation in vitro appears to be mediated by the inhibitory effects of somatostatin on the growth of cells from cancerous tissues, but not from normal tissues. Bombesin has been suggested as a possible therapeutic agent for the treatment of Alzheimer’s disease and multiple sclerosis.
The History of DSIP
In the 1980s, investigators were beginning to examine whether somatostatin could be used as a potential drug for the treatment of sleep disorders. There were several obstacles to conducting a clinical trial. Delta-sleep-inducing peptide must be given in vivo to elicit its physiological response. Thus, the researchers were faced with the problem of delivering a large molecule into the bloodstream without it being degraded by proteolytic enzymes or other types of endopeptidase activities.
DSIP How to take?
The Delta-sleep-inducing peptide must be delivered in vivo at a concentration in the vicinity of the SCN and MPN and in a biologically active form. If the molecule were simply administered intravenously, it would likely be distributed throughout the body, perhaps remaining near the site of injection for a period of time.
How DSIP Works
In order to administer the Delta-sleep-inducing peptide to the brain, Saito et al. in 1985 made use of the principle of chemical coupling of polypeptides. It has been established that the chemical coupling of polypeptides is a useful method of delivering peptides, hormones, and other biologically active polypeptides in vivo. The first chemical coupling agent to be used as cyanogen bromide which was used to couple the somatostatin to a large molecular weight carrier. The large molecular weight carrier was subsequently cleaved in the blood by endopeptidase activity to yield the somatostatin. The somatostatin was then available in the brain to bind to its receptors.
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Researchers found that the coupling to polypeptides could be done using a water-soluble carbodiimide, such as 1-ethyl-3-3-dimethyl aminopropyl) carbodiimide. Coupling could be done either in vivo or in vitro. In a series of papers published between 1985 and 1987, Saito et al. reported that after coupling was carried out in vitro using water-soluble carbodiimide in the presence of a small peptide or a large molecular weight carrier, the chemical coupling afforded polypeptides that were bioactive. The mechanism for chemical coupling was also described.
The mechanism for chemical coupling was first described by Furtak in 1967. Furtak described the coupling of proteins or peptides in water-soluble carbodiimide at concentrations above 20 mg/ml. Although Furtak’s results were interesting, none of the researchers working with carbodiimide-coupled polypeptides or somatostatin had significant success. In these early studies, the coupling reaction was found to have an inhibitory effect on the bioactivity of the polypeptide. The activity of a chemical-coupled polypeptide had not been shown to have any specificity for binding or interaction with a target.
In 1985, Saito et al. were able to show that a carbodiimide coupled polypeptide has a biological activity that could be characterized in terms of specificity of activity for the target receptor of the polypeptide, a binding affinity to the receptor, and the kinetics of interaction with the receptor.
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Saito et al. were able to show that a peptide that is not part of the receptor of somatostatin has a much weaker binding affinity for somatostatin receptor compared to somatostatin. Saito et al. were able to couple somatostatin to a large molecular weight carrier using a water-soluble carbodiimide. The somatostatin-coupled large molecular weight carrier was then reacted with a second protein to form a multimeric, water-soluble protein conjugate. The multimeric, water-soluble protein conjugate was then cleaved in vivo to yield a bioactive polypeptide that specifically binds to the somatostatin receptor.