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Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). DSIP is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
DSIP, also called delta sleep-inducing peptide, is described as a well-known neuropeptide with the sequence WAGGDASGE. The source states that DSIP possesses numerous beneficial properties, including its abilities in burn treatment and neuronal protection. In an animal study, DSIP was compared with the closely related peptide KND (WKGGNASGE) in in vivo assays of physiological activity.
The amino acid sequence of DSIP is given as WAGGDASGE. In an animal study, DSIP (WAGGDASGE) was described as a well-known neuropeptide and was compared with the closely related peptide KND (WKGGNASGE) in in vivo assays.
The cited source describes DSIP as having numerous beneficial properties, including its abilities in burn treatment and neuronal protection. Sixteen DSIP analogues, each with substitutions of 1-2 amino acid residues, were synthesized to investigate their potential use in medicine.
In a human clinical trial, DSIP was delivered intranasally 30 min before photostress in diabetic patients. In diabetic patients with retinopathy, treatment with deltalicin (daily dose of 0.0003 g of delta sleep-inducing peptide intranasally for two months) decreased the latent period of the visual evoked potential and reduced the period of restoration of VEP characteristics to 95.1 ± 6.8 s. Under combined use of deltalycyn and transcranial magnetic stimulation, the period of VEP restoration was shortened to 82.5 ± 6.5 s in the same human study. In diabetic patients with retinopathy, VEP restoration after photostress took 137.2 ± 11.3 s, versus 73.5 ± 3.3 s in the control group.
In rats after focal stroke, intranasal administration of DSIP over 8 days was found to accelerate recovery of motor functions. In the same rat studies, DSIP-treated animals showed a significant recovery of motor performance in the rotarod test.
In one animal study of rats under chronic stress, DSIP given at all doses increased catalase and superoxide dismutase activity. In another animal study of rats under chronic stress, DSIP at 120 μg/kg decreased SOD activity and MDA concentration. In the same chronic-stress rat setting, DSIP at 40 μg/kg decreased catalase and SOD activities and MDA concentration, and this dose was described as causing the most pronounced effect. The reports therefore disagree on whether DSIP raised or lowered catalase and SOD activity, and all of these findings come from rat studies.
In rats, p-DSIP treatment lowered monoamine levels and tyrosine hydroxylase (TH) expression. The same rat study found that p-DSIP increased expression of monoamine oxidase A (MAO A), glutamic acid decarboxylase (GAD) and choline acetyltransferase (ChAT).
In a preliminary pilot study in animals, DSIP given during coronary occlusion in a myocardial infarction model resulted in 100% mortality. In other words, all of the animals in that pilot study died.
In postnatal rats of different ages, administration of DSIP (emideltide) was found to decrease serum total lipid level, total cholesterol level, and atherogenicity index. The same rat study also found that DSIP increased the level of high-density lipoprotein cholesterol.
In a PCPA-induced insomnia mouse model, the DSIP-CBBBP fusion peptide showed a better restorative effect than DSIP (emideltide) on neurotransmitter imbalance. The same mouse study found that the DSIP-CBBBP fusion peptide had a greater potential to enhance sleep than DSIP. These comparisons were observed in mice.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.