Dr. Windebank et al. evaluated neurological impact using a murine model for MGF overexpression. Breeding of transgenic mice was done to help constitutively overexpress MGF in the hippocampus and the subventricular region of the brain – these are the areas of the brain speculated to be associated with neural development and differentiation (neurogenesis). The histological study suggested an extremely high concentration of BrdU, a synthetic marker for detecting proliferating cells in live tissues, in these portions of the mice brain tissues. This represents high levels of cell proliferation and growth in the specific domains of the brain.

A different batch of double transgenic mice was then bred such that the animals produced MGF under certain conditions only when activated by the presence of a triggering agent added to their drinking water. Researchers depended on this new population of mice to study the long-term influence of increased neural MGF production when produced at 1, 3, or 12 months old. Behavioral studies and further histological assays were then conducted at 24 months. Mice showing high Mechano Growth Factor production not only showed signs of neurogenesis but also greater resistance to age-associated neural degeneration, as posited by their improved olfactory responses. They also appeared to display greater speed and higher success in cognitive tests.

The speculated efficiency of MGF was observed to be age-dependent, as suggested in the study. Early induction of MGF production appeared to have resulted in a more dramatic proliferation of BrdU+ cells and further neurological improvement throughout adult life. If MGF production was not stimulated before 12 months of the age of mice, there appeared to be no significant histological or behavioral differences compared to the control group.

As per current research, the cellular site of action or MGF mechanisms is unknown, and further studies are suggested to be needed to deep dive into the cellular and behavioral potential of the Mechano Growth Factor on neurogenesis.

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Chemical Makeup and Specifications

PT-141 peptide, also recognized as Bremelanotide, has a molecular mass of 1025.2 grams per mol. Its chemical formula is C₅₀H₆₈N₁₄O₁₀. The systematic name (IUPAC) for Bremelanotide is (3S 6S 9R 12S 15S)-15-[(N-acetyl-L-norleucyl)amino]- 9-bynzyl-6-{3-[(diaminomethylidine)amino]propyl}-12-(1H-imidazol-5-ylmethyl)-3-(1H-indol-3-ylmethyl)-2,5,8,11,14,17-hexaoxo-1,4,7,10,13,18-hexaa zacyclotricosane-23-carboxylic acid. The half-life of a compound, speculatively defined as the time it may take for the compound to reduce half of its potency value, is speculated to be approximately 2 hours for Bremelanotide.

The Biochemical Process

Researchers suggest that Bremelanotide may directly influence the central nervous system. Animal studies suggested that the molecule may stimulate both synthesis and activation of the MC-4R and MC-3R melanocortin receptors. Findings suggest that the reaction itself may control certain signals from the brain to internal systems. The signals regulating blood flow and inflammatory response may be specifically suppressed. Once the switch to these specific receptors gets altered by the molecule, the brain may be enabled to moderate the signals better.

Hemorrhagic Shock and Bremelanotide Interaction

It is suggested that Bremelanotide may help control proper blood circulation in the brain through the stimulation of neural flexes. Hemorrhagic shock, characterized from a ‘lower tissue perfusion’ or the introduction of oxygen to the tissue directly, may worsen due to an increased lack of oxygen to the area over time. Hemorrhagic shock may be classified into the following four types:

• Neurogenic
• Cardiogenic
• Septic (or ‘vasogenic’)
• Hypovolemic

These four types may be difficult to mitigate individually, even at a cellular level, as the responses may be different between two individual cells. Bremelanotide research and impacts on hemorrhagic shock has been studied to date on animal research models only. The studies were conducted in a controlled and stabilized environment, and some findings indicated maladjustment via the triggering of an increase in blood pressure of some of the animal models observed.

Bremelanotide Research Implications

Bremelanotide is a direct derivative of the peptide hormone Melanotan II, which is a synthetic peptide initially developed to induce the increase of melatonin production. During the course of development, researchers noticed a curious impact that peptide exposure seemed to be inducing in both male and female species under observation. Melanotan II appeared to stimulate sexual arousal in the female subset and appeared to induce erections in males on a spontaneous basis. Stemming from these research observations, Bremelanotide has also studied within the context of libido and arousal signaling within the brain of animal research models of both sexes.

The influence of Bremelanotide on the libido of either sex has been suggested to work via different pathways when compared to alternative approaches which aim to alter the blood flow to the sex organs. Instead, Bremelanotide has been speculated to trigger sexual desire by invigorating the parts of the brain that control sexual desire, thereby improving libido in the animal research models observed.

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.

Both peptides are structural analogs of ghrelin, a natural peptide hormone produced in the gastrointestinal tract. Ghrelin is suggested to promote the release of growth hormone (GH) from the pituitary gland and regulate hunger hormone signaling in the brain, and it is often referred to as the “hunger hormone.” Similarly, the peptides are speculated to perform the same function by associating with the growth hormone secretagogue receptor.

Growth Hormone Releasing Hormone (GHRH)

GHRH is suggested to interact with the Growth Hormone Secretagogue Receptor (GHS-R). Researchers speculate that this interaction may have a wide spread of impacts, including cognitive function and associations, sleep-wake cycle, memory, glucose metabolism, reward centers, and taste sensation. GHS-R activation and stimulation are suggested to lead to alteration in energy metabolism, shifting from catabolism to anabolism. This shift is speculated to be mediated through an increase in the release of growth hormone. GHS-Rs appear to be prevalent both on the pituitary gland and hypothalamus. Therefore, both Ipamorelin and GHRP-2 are speculated to associate with the receptors and promote a two-way increase in GH release. GH release is suggested to be directly enhanced upon peptide-GHSR association on the pituitary glands. Hypothalamic stimulation is considered to enhance the release of GHRH, which, in turn, binds to cognate receptors on the pituitary gland and improves GH release.

The shift in the energy balance does not appear to be a straightforward catabolic-to-anabolic change. These peptides, speculated to be fat-burning in nature, are suggested by researchers to act on adipocytes to enhance the mobilization of stored fat. Simultaneously, there is an impetus for muscle and tissue repair and building, better known as lean body mass formation. Thus, the alteration in energy homeostasis may act to cause a complex alterations in lean body mass formation and thereby anabolism of tissues.

Preserving Growth Hormone Physiology

Ipamorelin and GHRH-2 are suggested to be similar in their mechanism of alteration in physiologic levels of GH. Before significant research was conducted on synthetic peptides, research studies focused on directly supplementing growth hormone, which appeared to bring about a direct impact in the positive action of hormone but disrupted the natural physiological level of the same. Growth hormone is considered to show a gradual surge and decrease in levels in a twenty-four-hour physiological cycle. Exogenous supplementation of the hormone in animal models appeared to result in sharp surges and falls in the hormone level, and thus its biological effect did not sustain long. Maintenance of the normal pulsatile expression cycle of GH is suggested to help overcome the detrimental impact of sudden GH surges, such as cardiac damage, joint pain, swelling, and acromegaly. Introduction of Ipamorelin and GHRP-2 blend is speculated to enhance the physiologic mechanisms of growth hormone release without producing an excess of the hormone. Thus, the natural hormone level is suggested to be maintained and may help to overcome the effects of sudden hormone spikes considered to be triggered by direct supplementation of growth hormone.

Action of Growth Hormone

Despite the name’s connotation, researchers suggest that the hormone plays a more profound and crucial role in influencing the physiological process beyond the development and growth of long bones in animals. The hormone is speculated to have various crucial roles, such as glucose metabolism, promoting lean mass development, tissue repair and muscle growth, fat metabolism, cardiac function, proper kidney function, liver function, and bone development. Across animal species studies, a decrease in GH has been associated with the cell aging cycle. This decline in hormone levels is speculated to be both the cause and outcome of cell aging processes. Studies have suggested that exogenous supplementation of the hormone may perhaps delay cell aging. Research conducted at the Well-Being Institute at the University of Cambridge suggested that a decrease in growth hormone level between delineated age groupings declines by a factor of about 20. The decrease in hormone level appears to be accompanied by a reduction in muscle mass, change in brain function, increased levels of blood sugar, and many more. The direct supplementation of external growth hormone may detrimentally impact the organism. Hence, alternative approaches like synthetic peptides have gained prominence within research communities for evaluating the cell aging influence and impacts of continued growth hormone production upon natural declination.

Molecular Differences Between Ipamorelin and GHRP-2

The mode of action of Ipamorelin and GHRH-2 is speculated to be essentially the same stimulation of GHS-R. Interestingly, their molecular structures are different, and they exhibit different secondary potentials. Their unique structural features appear to contribute towards their varied functional modalities. Both peptides are suggested to help in muscle cell proliferation, but GHRP-2 is suggested to help improve muscle growth and breakdown even during starvation by preventing muscle breakdown. GHRP-2 has been observed to inactivate Atrogin-2 and MURF1 proteins in studies conducted on yaks. These proteins are considered to promote muscle degradation. Thus, it follows that their inactivation may serve to prevent muscle degradation.

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.

Sermorelin peptide has been evaluated in research studies to determine its impact on growth hormone secretion. Research in the peptide has lead to a diverse set of hypotheses related to the peptide’s physiological impact, summarized here:

• Potential anti-fibrotic impact on cardiac tissues post-attack
• Potential increase in bone density
• Potential improvement in renal function
• Potential in neurological dysfunction including dementia
• Potential reductive action in seizure activity
• Potential regulation of sleep/wake cycles

Sermorelin Peptide and Sleep Research

Animal study findings observed the peptide to potentially reverse the impact of cell aging on the circadian rhythm and sleep-wake cycle. The production of growth hormone and slow-wave sleep purportedly decreases with time, by about two to threefold. Sermorelin peptide exposure was suggested to induce slow-wave sleep, which in turn may promote increased production of growth hormone.

Orexins, considered to be metabolic regulators of the sleep-wake cycle, may potentially be influenced by Sermorelin peptide. The growth hormone axis has been conjectured to regulate orexin levels, thereby influencing energy homeostasis. Recent observations suggest the regulation of orexins by Sermorelin peptide. The peptide was evaluated by research teams within the context of conditions arising from dysfunctional orexin release, such as a neurological disorder known as narcolepsy, which adversely affects the sleep-wake pattern.

Orexin-Sermorelin Correlation

The brain appears to possess relatively fewer abundant orexin neurons, estimated to be about 10,000 to 20,000. Orexin neurons, also known as hypocretin, appear prevalent throughout the brain and spinal cord. Cognate receptors for orexin may also be present throughout the nervous system. Orexin receptors are often termed as “multi-tasking” as they may potentially regulate metabolism, energy homeostasis, sleep-wake patterns, feeding behavior, mood, cognitive ability, and reward systems. Dysregulation experienced in the oxinergic system may potentially lead to pathological conditions. Due to its speculated regulation of fat metabolism, a deficiency in orexin receptors may cause obesity and narcolepsy. On the other hand, an excess of the receptors could lead to a significant alteration in reward-seeking behavior. Modulation of orexin may bring positive outcomes in mitigating the onset of specific conditions. Sermorelin peptide might indirectly promote orexin neurons and thus increase the overall level of orexin in the nervous system.

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 Epitalon?

Epitalon, also known as Epithalon or Epithalamide, is a tetrapeptide secreted from the pineal gland. It comprises Alanine, Glycine, Aspartic acid, and Glutamic acid. The peptide is speculated to mimic the naturally occurring pineal hormone called Epithalamin. The molecule is thought to bind to and induce the sensitivity of the hypothalamus towards the natural hormone, thereby regulating the circadian rhythm and controlling melatonin production. Positive speculative influences have been suggested in the areas of cell aging, and thereby potentially improving life expectancy, and inhibiting the proliferation of cancer cells (with animal research studies conducted in breast, prostate, and colon cancers).

Mode of Action

Telomeres, sequences present towards the end of the chromosomes, may undergo shortening with each round of replication due to the basal expression and activity of the telomerase enzyme. In subsequent cellular divisions, the sequences may shorten, leading to the loss of crucial DNA elements from the chromosomes. Epitalon is believed to help activate the telomerase enzyme, which may maintain telomeric length and potentially reverse the cell aging process. This mechanism may allow cells to continue dividing, contributing to a greater level of physiological function.

Epitalon and Cell Aging

Cell aging is the natural physiological phenomenon whereby cells undergoing repeated cycles of division may ultimately shorten their telomere length beyond the Hayflick limit. These cells might lose some of the beneficial DNA required for proper propagation, leading to cellular senescence, the onset of aging, and age-related conditions such as cardiovascular diseases and potentially untimely death. Aging cells may either leak out accumulated toxins into the surrounding system or undergo self-degradation (apoptosis or programmed cell death). However, sometimes such aged cells, instead of perishing, might turn rogue and adversely affect tissues of various organs like kidneys, lungs, liver, brain, and heart, causing the onset of diseases.

Epitalon Research

Scientists have examined murine models of the early onset of aging to speculate the effect of Epitalon. Genetically modified mice were used for the research, displaying shortened lengths of telomeres and leading to the early onset of aging. These animals exhibited various physiological impairments like shrinkage in the size of the brain, atrophied spleens, damaged intestines, loss of the sense of smell, and so on. These models were exposed to Epitalon and monitored. One month post-exposure, they exhibited apparent dramatic improvement in physiological parameters. At the molecular level, the chromosomes exhibited a greater length of telomeres, possibly due to enhanced telomerase activity. The exposed animals exhibited the formation of new neurons, growth in the size of the spleen, and regained the sense of smell.

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.

The GHK-Cu peptide has been speculated to reduce the formation of DHT in hair follicles. There appear to be two forms in which the 5-alpha reductase exists: Type 1 which plays a role in the hair follicles and Type 2 which plays a role in the prostate tissue. 5-alpha Reductase appears to be inhibited by the pro-pecia (finasteride), thereby improving follicle growth. Although the pro-pecia appears to be more significant for the Type 2 forms, it may control the enlargement of the prostate. In context to the Type 1 5-AR, they appear to be better inhibited by the increasing copper ions in skin cells, thereby controlling the damage to the hair growth. As per the research conducted by the different researchers, copper ions in the may potentially inhibit the Type 1 5-AR by up to 90%. It is also suggested that Type 2 form may be less efficiently inhibited by copper ions. Hence, it can be hypothesized that the 5-AR may be specifically inhibited by copper ions.

Iron Toxicity and GHK-Cu Peptide

After significant caloric ingestion, levels of iron appear to increase, thereby saturating Transferrin. The excessive iron may circulate as free iron in the blood and may be toxic upon direct exposure for the target organs. The Ferritin may release the GHK-Cu (2+) reduced iron by 87%. Approximately, 4500 atoms of iron per protein molecules may be stored in Ferritin, considered to be a catalyst of the lipid peroxidation, thereby producing a slew of free radicals, resulting in the damage of cell membrane, protein and DNA. The entry of free iron in the cells and its accumulation in the mitochondria may disrupt the process of oxidative phosphorylation, may catalyse the lipid peroxidation forming free radicals and hence, may cause cell death.

Cell proliferation and Tissue Repair

Research conducted by different scientists has suggested that the miR-399-5p expression may be downregulated by GHK. In the cells, the anti-apoptotic potential of GHK appears to be partially reversed due to the overexpression of miR-399-5p. The research also suggests that the downregulation of miR-339-5p speculated to be induced by GHK may involve the p38 MAPK pathways. The miR-399-5p/ VEGFA have also been hypothesized to play a role in the prevention of neuronal apoptosis as a consequence of the ICH injury. In the cells, the miR-399-5p expression may possibly be downregulated by GHK and the miR-399-5p appears overexpressed, which may reverse any anti-apoptotic potential of GHK.

GHK-Cu and Inflammation Studies

GHK has been isolated in urine, saliva and plasma. It occurs naturally, and appears to form complexes with copper readily, and may regulate the metabolism of the copper. The copper (II) chelation and the GHK tripeptide, together form the GHK-Cu, may accelerate the processes of wound healing, regeneration, anti-inflammatory actions and anti-oxidant potential. The level of the TNF-α and TGF-β, the acute phase inflammatory cytokines, may be lowered following GHK-Cu exposure, thereby resulting in the oxidative damage and hence, the suppression of inflammation.

In one research study, it was suggested that the GHK-Cu exposure to the animal models increased the superoxide dismutase and decreased the production of the reactive oxygen species. Also the production of IL-6 and TNF-α appeared to be decreased as a result of the suppression of the p39 MAPK and NF-κB p65 in the in-vitro model. The results of the studies have suggested that the LPS-induced phosphorylation of NF- κB p65 may be also inhibited by GHK-Cu. Additional studies have reported that the GHK-Cu may potentially inhibit the NF-κB pathway in inflammatory bowel diseases and chronic inflammatory diseases.

With all these points, it has been suggested by researchers that the GHK-Cu has the potential to improve the growth of hair follicles, as it appears to reduce the negative impacts such as inflammation and iron toxicity, and may promote processes such as cell proliferation and blood circulation close to the site of follicle development.

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.