Tesamorelin is a peptide that researchers suggest holds importance in addressing cardiovascular disease in research models of HIV. Findings from studies propose that Tesamorelin peptide may be associated with a reduction in excess fat cell accumulation in models of HIV and lipodystrophy.

What is Tesamorelin Peptide?

Tesamorelin peptide, also known as (TH9507), is a synthetic growth hormone-releasing factor agonist that researchers suggest stimulates the production and release of endogenous growth hormone. Speculative information indicates that it consists of the 44 amino acids of Growth Hormone Releasing Hormone (GHRH) with the addition of a trans-3-hexenoic acid group. It is also speculated to be more potent and stable than GHRH and resistant to cleavage by the enzyme dipeptidyl aminopeptidase.

In animal experiments, it is suggested to have significantly reduced visceral adipose tissue (VAT). Researchers propose that Tesamorelin peptide was found to reduce triglycerides and total cholesterol in research models of lipodystrophy when introduced combinatorily with antiretroviral therapy in research models of HIV.

Structure of Tesamorelin Peptide

Sequence: Unk-Tyr-Ala-Asp-Ala-Ile-Phe-Thr-Asn-Ser-Tyr-Arg-Lys-Val-Leu-Gly-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Met-Ser-Arg-Gln-Gln-Gly-Glu-Ser-Asn-Gln-Glu-Arg-Gly-Ala-Arg-Ala-Arg-Leu-NH2

Molecular Formula: C₂₂₁H₃₆₆N₇₂O₆₇S

Molecular weight: 5136 g/molS

Tesamorelin Peptide Mechanism of Action

Research daata suggests that Tesamorelin peptide binds and stimulates GHRF receptors with similar efficacy to endogenous GHRF. Growth hormone-releasing factor is a hypothalamic peptide speculated to act on the somatotropic cells of the pituitary gland to stimulate the synthesis and pulsatile release of endogenous growth hormone. This growth hormone is speculated to be both anabolic and lipolytic, exerting effects on various target cells.

Studies propose that the main mechanism of action of Tesamorelin is lipolysis, the breakdown of lipids and triglycerides. Generally stored in the  for later energy use, high values for either may increase the risk of heart disease.

Case Study

A study involved Antiretroviral Therapy (ART) HIV research models with excess fat accumulation. These research models were given Tesamorelin  or placebo each day. After 26 weeks, the group of research subjects receiving placebo were switched to Tesamorelin peptide for the next 26 weeks. The exposure to Tesamorelin in the experimental group was continued for another 26 weeks. Observations from the study suggest that exposure to Tesamorelin may decrease Visceral Adipose Tissue (VAT) and maintain the reduction for up to 52 weeks, possibly maintaining abdominal adipose tissue, improving lipids and body image, and without any significant changes in glucose parameters.

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

References

Falutz J, Mamputu JC, Potvin D, Moyle G, Soulban G, Loughrey H, Marsolais C, Turner R, Grinspoon S. Effects of tesamorelin (TH9507), a growth hormone-releasing factor analog, in human immunodeficiency virus-infected patients with excess abdominal fat: a pooled analysis of two multicenter, double-blind placebo-controlled phase 3 trials with safety extension data. J Clin Endocrinol Metab. 2010 Sep;95(9):4291-304

PEG-MGF, or Pegylated Mechano Growth Factor, is a variant of IGF-1. PEG-ylation modifies MGF by fusing polyethylene glycol (PEG) into it, potentially extending its half-life from a few minutes to days, allowing it to travel through the bloodstream for an extended period before breaking down and being excreted by the kidneys. Researchers suggest this process is essential for animal muscle regeneration after physical exertion or injury by promoting nitrogen retention and increasing protein synthesis.

Mechanism of Action

Research data from animal studies suggests that PEG-MGF supports the regeneration process of muscle, positively regulates protein synthesis, and activates satellite cells. In experiments where the PEG-MGF cDNA has been inserted into a plasmid vector and introduced into muscle cells, it appears to be a potent inducer of muscle hypertrophy. The addition of PEG-MGF to muscle myoblasts appeared to have increased proliferation and delayed differentiation, even in the presence of anti – IGF 1 receptor antibodies, potentially by activating fibrinolysis of matrix and metalloproteinase systems. Additionally, researchers propose that intense physical exertion may stimulate the release of growth hormone in the muscles to release MGF, especially as levels of this hormone decrease over time. Furthermore, a recent study of PEG-MGF suggests that the activity of protein kinase C is speculated to be necessary for the activation of this peptide (translocation to the nucleus) of factor 2 related to NFE 2 (Nrf2). This, in turn, is suggested to increase the expression of heme oxygenase 1, an event speculated to mediate neuroprotection of neurons from oxidative stress-induced apoptosis in the brain.

Research into PEG-MGF

In addition to its potential effects on muscle, PEG-MGF is speculated to have other impacts in the bodies of animal research models. Researchers suggest that PEG-MGF may enhance the proliferation and migration of bone marrow-derived mesenchymal stem cells, which are suggested to be a source of autologous stem cells for transplantation to the heart. There is speculative evidence of transient regulation of PEG b MGF expression in response to myocardial infarction associated with ischemia in the heart. Intracoronary exposure to this peptide is suggested to induce myocardial protection and improve hemodynamic function more than mature IGF – 1 after myocardial infarction in sheep. The speculated cellular protection conferred by PEG-MGF is suggested to be based on the inhibition of apoptosis in the border area of the infarct. PEG-MGF has been suggested to stimulate proangiogenic activities in vascular endothelial cells. Therefore, it may confer potentially beneficial action at the level of vascular regeneration and collateralization to restore blood flow to the heart after myocardial infarction. IGF – 1, considered to play an essential role in the interface between neurons in injured or damaged muscles, has shown potential effectiveness in slowing the progression of amyotrophic lateral sclerosis (ALS), a disease characterized by the loss of motor neurons and progressive muscle weakness. Exposure to PEG-MGF has been reported to produce improvements, with more motor neurons surviving in PEG-MGF-treated mice. MGF may be expressed in excess in regenerating regions after global cerebral ischemia. Its transcripts, thought to be expressed during brain development, are suggested to exhibit particular time distributions. Additionally, neonatal hypoxia and insults of hypoxic ischemia are suggested to lead to increased and prolonged expression of only the MGF isoform.

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

What is Epithalon?

Epithalon, also known as Epithalon or Epithalamine, is a synthetic pineal tetrapeptide comprising four amino acids (Alanine, Glutamic acid, Aspartic acid, Glycine). It is considered identical to the natural peptide called Epithalamin, a hormone produced by the pineal gland. The peptide molecule appears to interact with and induce sensitivity in the hypothalamus towards the natural hormone, monitoring the circadian rhythm and controlling melatonin production. Researchers suggest that this peptide may exert positive influences in the realms of cell aging, as well as potentially inhibiting the proliferation of cancer cells, including those in the breast, prostate, and colon. Epithalon is suggested to impact metabolism by increasing the sensitivity of the hypothalamus to its natural hormone influences. This is said to regulate the level of melatonin in the bodies of animal test subjects, thereby regulating the circadian rhythm.

What is Meant by “Aging”?

Aging is a natural physiological phenomenon wherein cells undergoing repeated division cycles, which ultimately shorten their telomere length beyond the Hayflick limit. Such aged cells may undergo self-degradation or, in some instances, adversely affect tissues of various organs, leading to open pathways for diseases to develop.

Epithalon Mechanism of Action

Epithalon, researchers suggest, increases the production of telomerase, a natural enzyme that aids in the reproduction of telomeres—protective components of DNA that prevent the loss of genetic information. Researchers speculate that this results in the prevention of chromosome shortening, which is closely linked to age-related diseases. By activating telomerase, cells may potentially exceed their predetermined time limit and reverse the mechanism of cell aging, as cells with longer telomere strands are believed to provide better function and replication.

Cell Aging and Epithalon

The cell life extension and anti-aging potential of the synthetic tetrapeptide Epithalon is considered to be strong, according to data from various experimental studies. Researchers suggest that Epithalon may achieve this by elongating telomeres and activating telomerase, supporting data that it may prolong the life of cells. Additionally, Epithalon is speculated to stimulate the endogenous secretion of melatonin, an antioxidant that may decrease age-related alterations in the immune and neuroendocrine systems, potentially reducing the incidence of chronic diseases and infections.

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

In this article, we will compare BPC-157 and TB-500, two peptides that have been widely researched for their potential in tissue repair processes, in terms of their chemistry, mechanism of action, and physiological influence.

Chemistry of BPC-157 and TB-500

Both BPC-157 and TB-500 are synthetic in origin, implying that they may not be found in nature and might not have common sequence homology with natural peptides. BPC-157 is a pentadecapeptide of BPC or Body Protection Compound, identified and isolated from the gastric juice. BPC-157 is a partial sequence of BPC and comprises a chain of 15 amino acids. TB-500 is synthetic form of Thymosin Beta 4, a water-soluble and regenerative compound found abundantly in bio-fluids such as saliva, and cerebrospinal fluid. TB-500 is the isolated (17)LKKTETQ(23) segment of Thymosin Beta 4 and has been researched for its potential to exert similar impacts.

BPC-157 and TB-500 Mechanism of Action

Research suggests that BPC-157 may mediate upregulation of growth hormones, modulate Nitric Oxide synthesis, enhance blood vessel production, and modify collagen production as well as bone proteins. TB-500, on the other hand, is suggested to principally associate with actin, promoting cellular migration and regeneration, and blocking inflammatory chemokines and cytokines.

BPC-157

The role of BPC-157 is centered on its potential ability to increase angiogenesis or the production of blood vessels by modifying the expression of Vascular Endothelial Growth Factor 2 (VEGFR2). This increase in angiogenesis is believed to trigger a cascade of different effects from faster wound healing, improved tendon and bone repair, and tissue regeneration in research subjects. Another suggested action of BPC-157 is its unique potential to enhance the tendon repair process and reduce the recovery time needed for damaged tendons to return to their original strength. BPC-157 is also suggested to show a cytoprotective effect, especially in the gastric mucosa, apart from the liver, pancreas, heart, and brain neurons.

TB-500

The research in TB-500 is based on its potential to bind with actin and improve tissue regeneration, tissue formation, and aid wound healing. It also appears to improve cell migration, re-epithelialization, and angiogenesis that are claimed to be crucial in tissue repair and wound healing. The peptide is also suggested to exhibit an anti-inflammatory effect by suppressing the release of chemokines and cytokines responsible for inflammation. It is currently being studied for its potential cardioprotective and neuroprotective characteristics. In-vitro tests in animal models also suggest the ability of TB-500 to inhibit premature apoptosis or cell death in the heart and the hippocampal region of the brain.

Conclusion of BPC-157 and TB-500

Based on theoretical deductions and scientific findings, both the peptides are speculated to exert action in wound healing and tissue formation. They are suggested to showcase angiogenesis and cytoprotective influence, although they may affect different factors in the process. The difference appears to be that BPC-157 influences tendon and bone repair while TB-500 doesn’t. This suggests it may potentially be more impactful in injuries that damage tendons, ligaments, and bones. It is also claimed to have greater neurological impact compared to the latter. TB-500, on the other hand, is suggested to exhibit anti-inflammatory, cardioprotective, and neuroprotective roles that BPC-157 may lack.

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

Findings from research suggest that substance P, beta-endorphin, and cortisol levels in the hypothalamus and blood plasma may show alterations under DSIP influence. It is proposed to induce changes in other peptides that mediate the acute and long-term stress coping effect. Furthermore, DSIP is believed to regulate opioid-peptidergic systems.

Delta Sleep-Inducing Peptide and Sleep, Circadian Rhythm

The peptide is said to exist in both free and bound forms in the hypothalamus, limbic system, and pituitary gland. It is believed to trigger hypothalamic neural circuitry, increasing LH during sleep, and may help in cases of chronic insomnia, according to speculative research.

A study of research models of chronic insomnia was completed to determine the intermediate effect of the peptide on sleep and daytime performance. Delta Sleep-Inducing Peptide was delivered under placebo-controlled, double-blind conditions for seven successive nights.
Polysomnograms were captured for placebo baseline, beginning and end of Delta sleep-inducing peptide exposure, and one placebo post-exposure at night. The daytime psychological state and mental performance were extensively analyzed before and after 6 Delta sleep-inducing peptide influence. Each model researched IV Delta sleep-inducing peptide, and the findings reported a greater regulation in sleep cycles.

The speculated findings also propose that DSIP may mitigate instances of narcolepsy by reducing the number of sleep attacks during the day and enhancing REM sleep. DSIP was delivered to research models of narcolepsy, with results observed to encompass decreased sleep attack frequency and improved activity, alertness, and performance during the daytime. The peptide was suggested to reduce the sleep period with the enhancement of REM sleep, accentuating circadian and ultradian rhythms.

Delta Sleep-Inducing Peptide and Opioid Withdrawal

It is speculated that DSIP might help deal with opioid withdrawal due to its suggested agonistic activity at opioid receptors. Animal study findings have suggested that DSIP, when delivered directly into the bulbo-mesencephalon-thalamic recruiting system, may trigger slow-wave sleep, and this effect may be reversed by naloxone.

Pain Perception and Depressive Behavior

DSIP is also being evaluated for potential in chronic pain and/or depression research. DSIP has been suggested to exert significant reductions in pain levels and depressive states when introduced. Due to its suggested modulating effect on endogenous opioid-peptidergic systems and its impact on circadian rhythms and cortisol levels, a study was conducted on research models of migraine episodes, vasomotor headaches, chronic tinnitus, psychogenic panic attacks, and depressive states. Delta Sleep-Inducing Peptide was suggested to remarkably lower pain levels in the majority of research models and indicated a significant decrease in depressive states following exposure.

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

Speculations suggest that the peptide is secreted in response to tissue injury, aiding in protecting tissues from inflammatory damage and promoting tissue remodeling and regeneration post-injury. It is theorized to play a significant role in signaling tissue remodeling, specifically in removing damaged or scarred tissue. However there may be a reduction in its concentration, speculated to contribute to increased inflammation, cancerous activity, and tissue destruction.

Copper Peptides Peptide Mechanism of Action

GHK-Cu peptide may influence various pathways through its peptide sequence and copper. It is suggested to attract mast cells and macrophages to the injury site, releasing proteins that stimulate tissue repair. The peptide may primarily increase collagen, elastin, proteoglycans, glycosaminoglycans, and decorin in fibroblasts. It may stimulate metalloproteases and protease inhibitors to remove damaged tissue proteins and decrease the secretion of TGF-beta from fibroblasts, potentially reducing scar formation.

The speculated mechanism proposes that GHK-Cu peptide promotes collagen production by chondrocytes, leading to bone growth and formation. Additionally, it may provide copper for angiogenesis in tissues. The peptide is thought to improve the differentiation and proliferation of axons within neurons, block ferritin channels, and release oxidative iron after tissue injury, potentially blocking iron-catalyzed lipid peroxidation. Thus, copper-peptide-induced tissue repair is theorized to work for various tissues, including skin, hair follicles, stomach lining, intestinal lining, bone tissue, hooves, etc.

GHK-Cu Research Studies

Scientific work suggests that GHK-Cu peptide may affect various aspects, including infection control, wound healing, follicle growth restoration, anti-cancer cell proliferation, and neurological impact.

Wound Healing and Infection Control: Speculative findings propose that the peptide may cause better wound contraction, faster granular tissue development, and improved angiogenesis. Systemic exposure to the peptide might promote healing, and its introduction into the muscle could potentially help repair distant sites.

Anti-Inflammatory Response: Research suggests that GHK-Cu peptide might interact with TNF-alpha and pro-inflammatory cytokines, such as IL-6, in fibroblasts, leading to a significant reduction in inflammation. This may make the peptide suitable for systemic exposure in research on inflammatory skin cell conditions, such as psoriasis.

Follicle Growth Restoration: The peptide has been suggested to have efficacy comparable to other established research compounds in the restoration of follicle growth.

Cognitive Function: The peptide is speculated to promote cognitive function by increasing the migration of hematogenous cells into collagen tubes, producing nerve growth factors, increasing the expression of integrins, and enhancing the regeneration rate of myelinated nerve fibers. A gene expression study suggests that the peptide may induce changes in the expression of fundamental proteins, impacting various biochemical pathways in organs and tissues, including the nervous system.

Anti-Cancer: GHK-Cu has been suggested by researchers to be relevant in research studies of metastatic cancer. It is speculated that higher tissue copper levels may keep cells younger, and GHK-Cu may assist in mediating this effect.

Lungs: Research suggests that the peptide may protect the lungs from acute injury and fibrosis, mitigating damage due to reactive oxygen species (ROS) and inflammatory cytokines. Exposure to GHK-Cu peptide is theorized to reduce inflammatory cell infiltration and interstitial thickness in research models of pulmonary fibrosis, exhibiting potential in research areas of various lung diseases.

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.