Pinealon (20mg vials)

Pinealon – 20mg Vials

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Peptide Partners Manufacturer Id: WF03

Batch Id: PN202603

Research Studies

(for educational purposes only)

Pinealon Increases Cell Viability by Suppression of Free Radical Levels and Activating Proliferative Processes

Authors: V. Khavinson, Y. Ribakova, K. Kulebiakin, E. Vladychenskaya, L. Kozina, A. Arutjunyan, A. Boldyrev

Publication: Rejuvenation Research, Volume 14, Issue 5, October 2011

URL: https://pubmed.ncbi.nlm.nih.gov/21978084/

Scientific Summary

This study investigated the effects of the synthetic tripeptide Pinealon (Glu-Asp-Arg) on cell metabolism under oxidative stress conditions in vitro. The researchers utilized three cell models: dissociated rat cerebellar granule cells, rat peripheral blood neutrophils, and pheochromocytoma (PC12) cell cultures. Oxidative stress was induced using receptor-dependent agents (ouabain and homocysteine) and a non-receptor agent (hydrogen peroxide, H2O2). Flow cytometry and chemiluminescence assays demonstrated that Pinealon dose-dependently restricted the accumulation of reactive oxygen species (ROS) in all three cell types. In PC12 cells exposed to 1 mM H2O2, Pinealon significantly decreased necrotic cell death as measured by propidium iodide staining. Furthermore, Western blot analysis revealed that Pinealon delayed the activation of ERK 1/2 kinase induced by homocysteine. Cell cycle analysis showed that Pinealon modulated proliferative activity, decreasing the number of cells in the G1 phase while increasing those in the G2 and S phases. The researchers concluded that because ROS restriction saturated at lower concentrations (100 nM) while cell cycle modulation continued at higher concentrations (up to 500 nM), Pinealon likely interacts directly with the cell genome or gene expression factors in addition to its antioxidant activity.

Plain English Interpretation

This laboratory study tested how well the Pinealon peptide protects different types of nerve and immune cells from damage caused by “oxidative stress”—a harmful process where unstable molecules called free radicals build up and damage cells. The researchers exposed the cells to toxic chemicals that trigger this stress. They found that adding Pinealon significantly reduced the buildup of these harmful free radicals in all the cell types tested. When nerve-like cells were exposed to a strong toxin (hydrogen peroxide), Pinealon successfully kept more of the cells alive and prevented them from dying. Interestingly, the researchers also discovered that Pinealon does more than just act as an antioxidant; it actually influences the cells’ internal clock (the cell cycle), encouraging them to grow and divide. This suggests that Pinealon works by interacting directly with the cells’ genetic machinery to promote survival and repair.

Neuroprotective Effects of Tripeptides—Epigenetic Regulators in Mouse Model of Alzheimer’s Disease

Authors: Vladimir Khavinson, Anastasiia Ilina, Nina Kraskovskaya, Natalia Linkova, Nina Kolchina, Ekaterina Mironova, Alexander Erofeev, Michael Petukhov

Publication: Pharmaceuticals (Basel), Volume 14, Issue 6, May 2021

URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC8227791/

Scientific Summary

This research explored the epigenetic mechanisms underlying the neuroprotective effects of the EDR peptide (Pinealon) and KED peptide in a 5xFAD mouse model of Alzheimer’s disease (AD). While the study included in vivo components, it heavily relied on in vitro molecular modeling and docking of the peptides to double-stranded DNA (dsDNA) to elucidate their mechanism of action. The researchers found that the EDR peptide binds specifically to the promoter regions of several genes critically involved in AD pathogenesis, including CASP3 (caspase-3, involved in apoptosis), NES (nestin, a neurogenesis marker), GAP43 (growth associated protein 43, involved in neuroplasticity), and APOE (apolipoprotein E). In the associated ex vivo/in vitro morphological analyses of hippocampal CA1 neurons, the EDR peptide was shown to prevent the elimination of dendritic spines—the small protrusions on neurons essential for synaptic transmission and memory. Specifically, EDR peptide administration restored overall dendritic spine density to control levels and reduced the pathological increase in “thin” spines associated with AD progression. The study concluded that the neuroprotective effect of the EDR peptide is mediated at the molecular epigenetic level through direct interaction with DNA, thereby regulating the expression of genes responsible for neuroplasticity and preventing dendritic spine loss.

Plain English Interpretation

This study investigated exactly how the Pinealon (EDR) peptide protects the brain in Alzheimer’s disease. The researchers used advanced computer modeling to see how the peptide interacts with DNA, and they examined brain cells under a microscope. They discovered that Pinealon works as an “epigenetic regulator”—meaning it attaches directly to specific sections of DNA to turn certain genes on or off. Specifically, it targets genes that control cell death, nerve growth, and brain plasticity. When they looked at the actual nerve cells, they found that Alzheimer’s disease normally causes neurons to lose their “dendritic spines,” which are tiny connection points crucial for memory and learning. Treatment with the Pinealon peptide prevented this loss, keeping the nerve connections intact and healthy. In simple terms, Pinealon protects memory by going straight to the DNA to activate repair genes, which physically preserves the communication bridges between brain cells.

Short Peptides Protect Fibroblast-Derived Induced Neurons from Age-Related Changes

Authors: Nina Kraskovskaya, Natalia Linkova, Elena Sakhenberg, Daria Krieger, Victoria Polyakova, Dmitrii Medvedev, Alexander Krasichkov, Mikhail Khotin, Galina Ryzhak

Publication: International Journal of Molecular Sciences, Volume 25, Issue 21, October 2024

URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC11546785/

Scientific Summary

This recent in vitro study evaluated the neuroprotective effects of short peptides, including EDR (Pinealon), using a novel cellular model of human neuronal aging. The researchers utilized direct reprogramming (transdifferentiation) to convert aged dermal fibroblasts from elderly human donors (aged 61-68) directly into induced cortical neurons (iNs). This advanced model preserves the age-related epigenetic and metabolic signatures of the donors. The induced neurons were treated with the EDR peptide (10 µg/mL) for 10 days. Immunofluorescent analysis revealed that the EDR peptide significantly reduced oxidative DNA damage in the aged neurons, as evidenced by a 23% decrease in 8-OHdG (8-hydroxydeoxyguanosine) levels compared to untreated controls. Furthermore, morphological analysis of the dendritic tree demonstrated that the EDR peptide strongly stimulated dendritogenesis; it significantly increased the number of primary neuronal processes by 28%, branching points by 65%, and the total length of dendrites by 46%. While the peptide did not significantly alter mitochondrial or lysosomal activity, or the expression of senescence markers p16 and laminB1, its profound effects on reducing DNA damage and enhancing dendritic arborization led the authors to conclude that the EDR peptide partially protects human neurons from age-related deterioration and stimulates structural neuroplasticity.

Plain English Interpretation

In this cutting-edge 2024 study, scientists created a unique laboratory model of human brain aging. Instead of using animal cells, they took skin cells from elderly human donors and genetically transformed them directly into brain cells (neurons). Because the original cells were old, the resulting neurons also showed signs of natural aging. The researchers then treated these aged human neurons with the Pinealon (EDR) peptide. They found two major benefits. First, Pinealon significantly reduced oxidative damage to the cells’ DNA, acting as a protective shield for the genetic material. Second, and most impressively, Pinealon caused the neurons to grow significantly more branches (dendrites). The treated neurons grew 28% more main branches and the total length of their connection networks increased by 46%. This means that Pinealon not only protects aging human brain cells from genetic damage but also actively stimulates them to grow new connections, which is vital for maintaining a healthy, functioning brain as we age.