This material is supplied exclusively as a laboratory research chemical for in vitro scientific study. All descriptions and are provided for informational and educational purposes only.
This compound is not approved for human or animal consumption, injection, ingestion, inhalation, topical use, or any other biological application. It must be handled only by qualified, trained personnel in a properly equipped laboratory.
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(Delta SleepâInducing Peptide â Nonapeptide Neuromodulator)
DSIP is an endogenous nonapeptide neuromodulator investigated for its influence on neuroendocrine signaling, stress-axis regulation, and sleep-associated neuronal pathways. Although its primary receptor has not been conclusively identified, research models indicate indirect modulation of GABAergic, glutamatergic, noradrenergic, and CRH-related pathways.
Studies report DSIPâs interaction with inhibitory/excitatory neurotransmission:
Upstream modulation of GABA-A receptorâlinked chloride channels
Potential regulatory effects on NMDA receptor pathways and Ca²⺠influx
Altered intracellular ion channel signaling influencing neuronal excitability
Downstream effects studied:
Changes in intracellular Ca²âş-dependent enzymes
Modulation of CaMKII and PKC signaling
CREB phosphorylation in sleep-associated neuronal nuclei
DSIP is examined for influence on neuroendocrine gene transcription:
Indirect suppression models of CRH release
Interaction with ACTH and corticosteroid feedback pathways
Associated impact on POMC-derived peptide regulation
Genes often monitored in research:
CRH (Corticotropin-Releasing Hormone)
POMC (Proopiomelanocortin)
NR3C1 (Glucocorticoid Receptor)
DSIP appears to modulate monoamine turnover and enzyme activity:
Tryptophan hydroxylase (serotonin synthesis)
Tyrosine hydroxylase (catecholamine synthesis)
Altered degradation via MAO-A/B (monoamine oxidases)
These changes are studied in relation to neuronal firing patterns, REM/NREM cycling, and circadian neurochemistry.
In vitro, DSIP exposure has been associated with:
PKA and PKC pathway modulation
MAPK / ERK phosphorylation in neuronal cells
Changes in cAMP and phosphoinositide signaling
Reduced oxidative-stressâinduced caspase activation models
Although no single DSIP receptor is confirmed, evidence points to:
GABA-A receptor-linked chloride channel modulation
Possible regulatory interaction with NMDA receptor complex
Indirect effects on adenylate cyclase â cAMP â CREB pathway
Crosstalk with neurosteroid and neuropeptide systems
| Category | Targets Studied |
|---|---|
| Neurotransmitter Enzymes | MAO-A/B, Tyrosine Hydroxylase, Tryptophan Hydroxylase |
| Kinase Systems | PKA, PKC, ERK1/2 |
| Receptors | GABA-A, NMDA receptor regulation (indirect models) |
| Gene Programs | CRH, POMC, NR3C1, CREB-mediated transcription |
| Cellular Markers | Caspase-3 (in stress-related neuron models) |
DSIP is used to study:
Neuroendocrine stress-axis signaling
Sleep/wake cycle neurochemistry
GABAergic / glutamatergic balance
Monoaminergic enzymatic turnover
cAMP/CREB-driven neuronal gene expression
This compound is provided strictly for in-vitro laboratory research.
Not for human or animal use, medical application, or diagnostic purposes.
| Size | 15 Mg |
|---|
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