SR-17018 is a drug that acts as a biased agonist at the μ-opioid receptor, meaning it preferentially activates the G-protein signaling pathway over β-arrestin 2 recruitment. In animal studies, it has shown analgesic effects with less respiratory depression and tolerance development compared to traditional opioids, according to ScienceDirect.com and the National Institutes of Health (NIH). It's also been identified as a highly G protein-biased mu opioid peptide (MOP) receptor agonist.
From https://pmc.ncbi.nlm.nih.gov/articles/PMC8348759/ : "Opioid-associated overdoses and deaths due to respiratory depression are a major public health problem in the US and other Western countries. In the past decade, much research effort has been directed towards the development of G-protein-biased µ-opioid receptor (MOP) agonists as a possible means to circumvent this problem. The bias hypothesis proposes that G-protein signaling mediates analgesia, whereas ß-arrestin signaling mediates respiratory depression. SR-17018 was initially reported as a highly biased µ-opioid with an extremely wide therapeutic window. It was later shown that SR-17018 can also reverse morphine tolerance and prevent withdrawal via a hitherto unknown mechanism of action. Here, we examined the temporal dynamics of SR-17018-induced MOP phosphorylation and dephosphorylation. Exposure of MOP to saturating concentrations of SR-17018 for extended periods of time stimulated a MOP phosphorylation pattern that was indistinguishable from that induced by the full agonist DAMGO. Unlike DAMGO-induced MOP phosphorylation, which is reversible within minutes after agonist washout, SR-17018-induced MOP phosphorylation persisted for hours under otherwise identical conditions. Such delayed MOP dephosphorylation kinetics were also found for the partial agonist buprenorphine. However, buprenorphine, SR-17018-induced MOP phosphorylation was fully reversible when naloxone was included in the washout solution. SR-17018 exhibits a qualitative and temporal MOP phosphorylation profile that is strikingly different from any other known biased, partial, or full MOP agonist. We conclude that detailed analysis of receptor phosphorylation may provide novel insights into previously unappreciated pharmacological properties of newly synthesized MOP ligands. "
Peptides we carry:
NAD+ (nicotinamide adenine dinucleotide) is a vital coenzyme present in all living cells, crucial for metabolic processes and cellular function. It helps mediate redox reactions, shifting between its oxidized (NAD+) and reduced (NADH) forms to facilitate electron transfer. This process is essential for energy production and sustaining life. Involved in over 500 enzymatic reactions, NAD+ is central to maintaining cellular homeostasis, the state of equilibrium in an organism's internal environment.
Research indicates that NAD+ may be beneficial for improving muscle function, protecting the nervous system, and generally reducing the effects of aging.
Beyond its role in energy metabolism, NAD+ supports DNA repair and gene regulation through key enzymes like sirtuins and PARPs. Sirtuins utilize NAD+ to regulate various cellular functions, including DNA repair, gene expression, and aging. Similarly, PARPs use NAD+ to repair DNA damage and maintain genomic stability. These functions highlight NAD+'s importance in preserving cellular integrity and helping to combat the aging process.
BPC-157 is a synthetic peptide derived from a protein found in human gastric juice. It has been studied for its potential to promote healing and reduce inflammation, particularly in musculoskeletal injuries and gastrointestinal issues. While preclinical research suggests various beneficial effects, it's important to note that BPC-157 is not currently approved for human use as a drug by regulatory bodies like the FDA.
Epithalon
**Epithalon is a synthetic peptide based on the naturally occurring peptide Epithalamin from the pineal gland, known for its potential anti-aging and health benefits.
Key features and potential benefits:
Potential side effects