NAD+ peptide also acts as a means of communication between cells. NAD+ has been suggested to act as an extracellular signaling molecule and helps regulate pivotal physiological functions. These functions include the activity of the intestine, bladder, neurons, and blood vessels. Research into the peptide has also implicated its activity in energy conversion, immune mediation, regulation of circadian rhythm, and timely DNA repair. NAD+ is an important biomolecule, but endogenous production appears to level off and then decline over time, which signifies its importance in age-related disease research.

What Does NAD+ Research Suggest?

1. Anti-Aging Potential of NAD+
Mitochondria is the powerhouse of the cells. It controls processes that generate ATP, which is a form of energy currency. In addition, it is considered to help in several intracellular signaling processes and regulates innate immunity. Mitochondria senescence may lead to decreased cellular metabolism, heightened inflammation, and accelerated cell aging. These processes may lead to certain conditions which have been linked to age-related physiological decline, and it may also induce organ dysfunction and altered tissue repair processes in cases of injury or damage.

Processes that can modulate or accelerate the actions of mitochondria may reverse the biological clock. Researcher speculate that NAD+ may be a critical component of mitochondrial function. A decline in the levels of NAD+ has been suggested to interrupt signaling pathways to the nucleus by promoting a pseudohypoxic state. These changes may undergo reversal with adequate supplementation of NAD+. NAD+ supplementation has been hypothesized to mitigate or reverse decline in mitochondrial action.

NAD+ supplementation may lead to the activation of SIRT1. SIRT1 is a gene that produces an enzyme called Sirtuin-1. It is also known as NAD+-dependent Deacetylase Sirtuin-1. Sirtuin-1 acts as a co-mediator for cellular processes. These may include improved metabolism, cellular longevity, and reduced inflammation.

2. Neurodegenerative Conditions
NAD+ released by the nerve endings acts as a signaling molecule. Due to its antioxidant, anti-inflammatory, and regenerative potential, it has been hypothesized to exhibit significant neuroprotective characteristics. NAD+ appears to act on the mitochondrial energy generation pathways and reduces the production of Reactive Oxygen Species (ROS). ROS are toxic molecules that lead to the generation of biologically healthy molecules. ROS increases significantly over time and is considered to be a pathogenic process in the onset of age-related conditions. Findings in animal models of Parkinson’s disease suggest that NAD+ supplementation may potentially reduce ROS. It also may improve the survival of dopamine-producing cells in the brain. Researchers report that it appeared to effectively reduce the motor deficits seen in the animal models of Parkinson’s disease.

3. Muscle Function:
Muscle cell proliferation is considered to decline over time as well. This decline appears to be a direct consequence of mitochondrial dysfunction and NAD+ decline. A fall in mitochondrial gene expression may lead to reduced oxidative phosphorylation. A decrease in oxidative phosphorylation may lead to reduced energy production by mitochondria. Animal research suggests that NAD+ supplementation may potentially help improve gene expression and energy generation.

NAD+ supplementation appears to help stabilize the activity of Peroxisome Proliferator-activated Receptor Gamma Coactivator 1-alpha (PGC-1-alpha). Stabilization of this gene may effect muscle growth similar to regular physical activity. Also, increased oxidative stress and inflammation may potentially induce a decline in muscle mass. NAD+ supplementation may potentiate an improvement in the survival of muscle fibers.

4. NAD+ and Inflammation
Nicotinamide phosphoribosyltransferase (NAMPT) is an enzyme-linked to inflammation. Several cancers are considered to lead to an over-expression of this enzyme. It is also linked to type 2 diabetes, Non-Alcoholic Fatty Liver Disease (NAFLD), and obesity. NAD+ supplementation may potentially cause a dramatic decline in the levels of NAMPT.

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.

Thymosin Beta-4 has been documented by researchers to potentially play a role in protecting, regenerating, and remodeling damaged tissue cells. After any tissue injury, it is believed that Thymosin Beta-4 may be released by damaged cells to protect them and reduce the inflammatory process. This peptide is believed to be present in every tissue except red cells.

Studies suggest that the first gene coding to occur (the process by which DNA and RNA dictate how and which cells need to form) after cell damage is Thymosin Beta-4. The formation of new blood vessels is believed to be essential to promote tissue repair. Damaged cells are believed to require early nutrients and supportive chemicals to reverse the damage. Thymosin Beta-4 is believed to have an angiogenic quality speculated to stimulate the migration and proliferation of endothelial cells.

TB-500 (Thymosin Beta-4) Mode of Action

This peptide is believed to work by regulating the actin protein. Actin, a highly abundant protein, contributes to the formation of contractile filaments of muscle cells. In addition to its speculated essential role in muscle contractions, this globular protein is believed to perform many non-muscle interactions. These cellular functions, speculated to include locomotion, phagocytosis, chemotaxis, and cytokinesis, make actin involved in more protein-to-protein interactions than any other protein. Actin is believed to represent a significant component of cellular structure, making up more than 10% of cell proteins.

Thymosin Beta-4 is believed to bind and sequester the actin proteins, preventing long filament formation. Avoidance of active polymerization is speculated to keep actin available to perform its functions to the optimum. It is believed to increase the number of freely available actin molecules, considering actin as the critical protein of muscles.

Besides its speculated impact on actin, Thymosin Beta-4 is believed to perform various biological activities in different cellular pathways. Downregulating the inflammatory cascade being the most prominent of them. Moreover, the peptide is believed to promote cell survival and cell migration. Thymosin Beta-4 is suggested to support develop new blood vessels (angiogenesis) and stem cell maturation.

Thymosin Beta-4 is also suggested to cover the remaining aspects of wound healing in one way or another. Following the inhibition of tissue inflammation, it is believed to reduce apoptosis and cytotoxic damage in cells. Thymosin Beta-4 is believed to minimize the number of myofibroblasts to reduce scarring. Research studies in animals suggest the potential to potentially prevent tissue damage and promote wound healing.

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.

Tesamorelin, also known as TH9507, is  a synthetic growth hormone-releasing factor agonist that may stimulate the production and release of endogenous growth hormone. It is comprised of all 44 amino acids of GHRH with a trans3-hexenoic acid group. Additionally, it is speculated to be more robust and stable than GHRH and may be resistant to cleavage by the dipeptidyl aminopeptidase enzyme. Tesamorelin is believed to activate the GHRH receptor in the pituitary gland, causing the synthesis and release of growth hormone-releasing hormone. This hormone, in turn, is speculated to act on several cells, including hepatocytes, to stimulate the production of insulin-like growth factor 1 (IGF-1). IGF-1 is considered to mediate many of the effects of growth hormones, including liver growth, suppression of programmed cell death, impaired glucose tolerance, and lipolysis.

Ipamorelin is a synthetic pentapeptide with distinct and specific growth hormone (GH) release properties, potentially as impactful as researchers suggest GHRP-6 is. It is believed to stimulate GH release via GHRP-like receptors, and surprisingly, it may not release ACTH or cortisol at levels significantly different from those observed after GHRH stimulation. This action is speculated to make ipamorelin potentially the first GHRH agonist specific for GH release, similar to GHRH. Ipamorelin appears to work in a completely different way to stimulate the release of growth hormones. It is suggested to bind to ghrelin receptors in the pituitary gland without affecting other hormones in the body. Ghrelin, which it interacts with, is believed to have profound metabolic regulatory effects, including increased or decreased hunger, suppression of the breakdown of accumulated fat, and most importantly, the release of growth hormone from the pituitary gland.

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 FOXO4-DRI?

FOXO4-DRI, also known as Proxofim is a synthetic peptide developed by Dutch research teams. It contains a specific peptide antagonist named FOXO4-DRI. It is a modified protein type designed to trigger the selective death of aged cells. The discovery of this peptide analog has accentuated the attempts for cell aging reversal. Data suggests promising results during its initial testing in mice. FOXO4-DRI peptide bears the potential to promote cell longevity, possibly reduce physiological impacts linked to the onset of dementia, and suppress tumor development.

How does it work?

Cellular biologists have suggested that cells exhaust after 70 divisions and can no longer produce new cells. There does not appear to be any way to induce the continual division of cells without decay. Eliminating aged cells may make space for younger cell development, in a process called autophagy. Damaged cells tend to spread the decay process as well. Aged, decayed cells are considered to be suitable for nothing as they produce no energy. In addition, they keep occupying space within and between cells, hindering the growth of surrounding cells.

FOXO4-DRI peptide appears to work by removing these senescent cells that have outlived their efficacy. Considered to be the most effective senolytic agent to date; the peptide may potentially cease the communication of cells with p53 genes and convey signals that the cell is damaged and needs to be cleared by autophagy. Stem cells are considered to produce new cells after the death and clearance of aged cells. An increase in new cells to replace the aged ones may culminate in better overall physiological functioning.

Research Implications from FOXO4-DRI

Anti-Aging Impacts on Cells

Mitochondria is known as the ‘powerhouse of the cell’ as it is considered to primarily produce energy. The energy currency of an organism is called Adenosine Triphosphate (ATP). The organisms produce it inside the mitochondria due to several complex reactions. Lysosomes are responsible for removing cellular debris, and work as a dustbin of cells to remove aged and dead cells. If any of these structures becomes compromised, physiological functions are considered to decline. Studies found that test mice became healthier as compared to the control group. Mice in the test group achieved better energy levels, biomarkers for physiological function such as replenishment of follicle development, improved kidney function, and cell cycling with this protein.

Diabetes Research

FOXO proteins are considered to regulate insulin signaling and insulin-like growth factors (IGF). FOXO proteins may control cell growth, metabolism, and differentiation by acting on IGF. Future research may explore the effects of FOXO proteins in insulin signaling. This action may have correlative impacts on diabetes and its related complications.

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.

Research and isolation of Follistatin, a protein that is naturally produced, has led researchers to develop a synthetic version called Follistatin-344. The primary speculation is that Follistatin-344 peptide antagonizes the function of TGF-β. The TGF-β family comprises Follicle Stimulating Hormone (FSH), Myostatin, and Activin. In addition to potentially inhibiting TGF-β, Follistatin-344 might act on the IGF-1/Insulin pathway.

Follistatin-344 Peptide Research

Follistatin-344 peptide has been employed in research studies with a variety of focuses, though it is primarily examined within the context of muscle cells.

1. Muscle Cell Growth: As mentioned, myostatin functions to reduce muscle mass, and is a member of the TGF-1 family that inhibits the growth and differentiation of muscle fibers. There are suggestions that Follistatin-344 peptide may exert potent anti-myostatin action. Speculative research on mice lacking myostatin indicates that the peptide may induce greater muscle mass development. Additionally, speculative studies on Follistatin-344 peptide have suggested a remarkable increase in muscle mass without the involvement of other muscle-building factors. Follistatin-344 has been suggested to increase muscle bulk through two main mechanisms: hypertrophy and hyperplasia. Hypertrophy leads to an increase in the size of individual muscle cells, while hyperplasia increases the number of muscle fibers.

2. Speculative Effects on Diabetes Mellitus Type 1 diabetes, considered to result from a reduced expression of insulin-secreting beta-pancreatic cells, leads to reduced insulin secretion and poor glucose metabolism. Follistatin-344 peptide, following studies in animal research models, appears to lead to an increase in beta-pancreatic cells. The exposure of Follistatin-344 peptide in animal models resulted in a remarkable rise in the life expectancy of mice and a reduction in diabetes-related micro- or macro-vascular complications.

3. Follistatin-344 peptide and Breast Cancer Speculative research on the effects and levels of Follistatin in female research models of breast cancer  involved Reverse Transcription Polymerase Chain Reaction (RT-PCR) to check natural peptide levels. Results taken from females with under-expressed Follistatin indicated that only a few had normal or higher levels of Follistatin. Higher levels of Follistatin could be associated with a lower incidence of disease metastasis and a better prognosis.

4. Speculative Effects on Esophageal and Liver Cancer Barrett’s esophagus, a premalignant condition, involves transforming cells in the lower esophagus. Bone Morphogenetic Protein (BMP) might be a primary factor behind the metaplasia of the esophagus. Speculative research suggests that Follistatin may counteract the action of BMP and potentially prevent the development of esophageal cancer. Additionally, liver fibrosis, a condition predisposing to hepatocellular carcinoma, might see a significant improvement in the lifespan of liver cells (hepatocytes) with Follistatin. The peptide was suggested to reduce the risk of liver fibrosis by 32%, potentially leading to a reduction in the risk of hepatocellular carcinoma.

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 AHK-Cu Peptide?

AHK-Cu is a short peptide with three amino acids attached to a copper molecule (Ala-His-Lys-Cu).  AHK-Cu peptide, also known as copper peptide, has been isolated in blood samples. This peptide may be responsible, in part, for growth and development of cells in the blood vessels. It has also been researched in relation to the generation of new blood vessels (angiogenesis). These actions of the AHK-Cu peptide are posited to be due to its potential to stimulate the production of another peptide called the Vascular Endothelial Growth Factor (VEGF). Producing new blood cells may help supply blood to biological structures such as skin and hair follicles, and may stimulate their development.

Researchers have also studied AHK-Cu in relation to its potential impact on Growth Factor Beta-1. Through its potential impact on Growth Factor Beta-1 and VEGF, AHK-Cu peptide may activate the replication and development of fibroblast cells. Fibroblasts are cells abundantly found in biological structures, including skin, hair follicles, and blood vessels. Fibroblasts are considered to activate the production of proteins such as elastin and collagen, essential participants of the extracellular matrix in the skin.

Research on AHK-Cu Peptide

Follicle Growth and Maintenance

AHK-Cu peptide may potentiate immense growth on follicle development and maintenance. Researchers suggest it may supplement follicle density by preventing possible loss and by stimulating new growth. Follicles may be found in highly vascular structures, areas where extensive network of blood vessels are concentrated, to supply blood to developing follicles. The supply of blood is considered to be crucial because follicles undergo a rapid cell turnover and appear to depend on the supply of blood and nutrients in the process. Along those same lines, blood supply has been suggested to limit the production of, and stability of existing follicles. AHK-Cu peptide may potentially promote new blood vessel development by triggering the release of VEGF.

Another important phenomenon that may potentially damage follicle development is the excessive conversion of testosterone to dihydrotestosterone (DHT). Researchers consider it to be a potentially critical pathology in certain conditions characterized by immense hair loss. AHK-Cu peptide might be relevant in these contexts, as researchers suggest it may prevent the conversion of testosterone to DHT. Second, it may potentially down-regulate the action of DHT on hair follicle receptors.

The hair follicles appear to undergo three main phases of growth: anagen, catagen, and telogen phase. The anagen phase is the growth phase of follicles, and is a highly active phase. Research suggests that AHK-Cu peptide may ‘trap’ the follicles in the anagen phase of the growth cycle and maintain that phase for a considerable duration (certain research findings suggest upwards of a year).

Cell Aging and Skin Structure

A subset of skin cells, fibroblasts are deemed responsible for the secretion of skin proteins such as collagen and elastin. These proteins are considered to lend the skin structure flexibility, and suppleness. Cell aging in the skin may lead to rapid decline in the number of fibroblasts. As a result, the amount of collagen and elastin endogenously produced begins to decline as well, introducing irregularities and textural inconsistencies in the skin and developing creases along the skin surface.

AHK-Cu peptide may potentiate the reversal of cell aging by triggering the growth and development of new fibroblasts. Once there are enough fibroblasts in the extracellular matrix of the skin, natural elastin and collagen production may follow. Research suggests that AHK-Cu may potentially stimulate the production of Type 1 collagen by up to 300%.

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.