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ALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE FOR INFORMATIONAL AND EDUCATIONAL PURPOSES ONLY. The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body. These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law.

Is Sermorelin Worth It?

Sermorelin Acetate and Aging

Growth hormone is a Goldilocks hormone, which is to say that it has an optimal level for producing the best outcomes. Too much GH increases morbidity and mortality, but so does too little. There is good evidence to suggest that at least part of the reason we age is because growth hormone levels decline over time, leaving us with sub-optimal levels of this important messenger. This decline in GH levels is referred to as somatopause and it has become a major focus of anti-aging science and research.

Somatopause is defined by the common symptoms we associate with aging: difficulty maintaining muscle mass, increased fat deposition, loss of bone density, declining energy and libido, higher cholesterol levels, and changes in skin texture and elasticity. Exercise helps to prevent these aging effects precisely because it keeps GH levels high, but more and more research suggests that exercise can only do so much to offset the roughly 40% decline in GH levels that occurs between the ages of 20 and 701. Supplementation may, in fact, be necessary to achieve optimal GH levels. This, ironically, increases exercise capacity, which makes it easier to maintain GH levels moving forward.

It was initially thought that Sermorelin and similar peptides simply reduced the effects of aging without actually prolonging life. For instance, Sermorelin improved muscle mass and body composition, but researchers thought it unlikely that the peptide could help us live longer. Research in mice, however, shows that Sermorelin, specifically, does improve longevity. The improvement is interesting however, as the research revealed a dramatic increase in average life expectancy but no change in maximum life expectancy2.

The above research is consistent with the idea that Sermorelin helps to maintain optimal body chemistry and thus maximizes lifespan. It does not extend maximum life expectancy, but it does help more individuals to get closer to their maximum lifespan. What is more, Sermorelin improves health and general function, meaning that individuals are more active and functional during their extended lives.

The benefits of Sermorelin in reducing the effects of aging include, but are not limited to:

  • improved metabolism,
  • improved body composition (more muscle and less fat),
  • improved immune function,
  • enhanced wound healing,
  • better cardiac function, and
  • improves sleep.

Sermorelin, Sleep and the Brain

Fifteen years ago, orexins were identified as central regulators of energy homeostasis. Research indicates that orexins are key modulators of the sleep-wake cycle and that these neuropeptides also affect feelings of satiety and hunger. Given their role in energy homeostasis, it was hypothesized that orexin levels are likely regulated, at least in part, by the growth hormone axis. Recent research supports this fact and suggests that growth hormone releasing hormone analogues, such as sermorelin, may be effective in treating conditions in which orexin release is dysfunctional (e.g. narcolepsy) [1].

What is PT141 and How Does it Work?

Primary Benefits of PT-141 in Summary According to Research

Enhanced Sexual Arousal: PT-141’s mechanism of action as a melanocortin receptor agonist may lead to increased sexual arousal and desire in individuals with FSAD. By targeting specific neural pathways involved in sexual behavior, PT-141 may help improve sexual sensitivity and responsiveness to sexual stimuli, leading to a heightened sense of arousal.

Improved Erectile Function: For men with ED, PT-141 has shown promise in clinical studies as a potential treatment for enhancing erectile function. By promoting vasodilation in the genital area, PT-141 can increase blood flow to the penis, potentially aiding in achieving and maintaining erections necessary for satisfactory sexual performance.

Localized Action: PT-141’s effects are primarily localized to the genital region, which helps minimize systemic side effects that might be associated with widespread vasodilation. This localized action makes PT-141 different from some other medications used to address sexual dysfunctions.Potential Alternative to Existing Treatments: For individuals who do not respond well to or cannot tolerate other treatments for sexual dysfunctions, PT-141 offers a potential alternative approach. Its unique mechanism of action makes it distinct from other medications like phosphodiesterase type 5 (PDE5) inhibitors commonly used for ED.

Psychological Benefits: By enhancing sexual desire and function, PT-141 may have positive psychological effects, boosting self-esteem and overall sexual satisfaction.

Mechanism of Action: PT-141 works by stimulating specific melanocortin receptors in the brain, particularly the melanocortin 4 receptor (MC4R), which plays a key role in regulating sexual function and behavior. Upon administration, PT-141 binds to MC4R, leading to the activation of downstream signaling pathways.

Peptides and Tanning Research

How Does UV Light Cause Tanning?

UV light causes tanning, which is to say and increase of the skin pigment melanin, by stimulating a cellular process mediated by the tumor-suppressor gene p53[1]. The whole point of this process is to protect skin cells against UV light, which can damage DNA and lead to problems like cancer, cell death, and the breakdown of extracellular matrix proteins (e.g., collagen) in the skin. This latter effect is what leads to observable skin aging in the form of wrinkles, lines, lost elasticity, and more.The pathway is activated when UV light damages DNA in the upper layers of the skin. The damage done to the DNA results in stabilization and activation of the p53 tumor suppressor protein. This, in turn, promotes activation of proopiomelanocortin (POMC). POMC is cleaved to product alpha-melanocyte stimulating hormone (α-MSH), which then binds to the melanocortin 1 receptor (MC1R). This causes melanocytes to both produce more melanin as well as divide and increase in number. Together, these effects cause an increase in melanin pigment leading to darkening of the skin. The melanin then absorbs the harmful UV light preventing further DNA damage[2].Note that tanning via UV light does not occur until after DNA damage has occurred. This means that the potential for cancer development is already present before tanning occurs because DNA damage has already occurred. Therefore doctors have warned against UV-based tanning for years. The only solution, until recently, has been to avoid UV light entirely by either staying out of the sun or by wearing sunscreen. Unfortunately, recent research shows that sunscreen has problems of its own such as damaging coral reefs and potentially causing hormone dysregulation[3]. The current research is focused on promoting melanin production without exposure to UV light, thus gaining the benefits of melanin protection without first inducing DNA damage.

The New Solution to Sunless Tanning

If scientists could stimulate tanning without the DNA damage that jumpstarts the natural process, then we could experience the benefits of tanning without any of the risks. Research into the tanning pathway has been of interest for several decades now, in part because of the discovery of melanotan and the melanocortin receptor system. Interestingly, melanotan was developed as a sunless tanning agent and then became of interest for an entirely different purpose. It’s ability to protect the skin against UV damage was almost completely forgotten as its ability to stimulate sexual arousal became the focus of melanotan research. Much later, research shifted again and melanotan became a front-runner in sunless tanning research. This peptide has since inspired the exploration and development of other peptides for sunless tanning research. Some of those peptides are discussed below along with other compounds associated with sunless tanning.

How Does PT-141 Work?

What is PT-141 and How Does PT-141 Work?

PT-141 is a heavily modified derivative of a natural hormone called alpha-melanocyte stimulating hormone (α-MSH). In the most general sense, PT-141 works directly through the nervous system to increase sexual desire, arousal, and satisfaction. It does this by mimicking some, but not all, of the properties of α-MSH. To understand in more detail how does PT-141 work, it is necessary to understand the melanocortin system and the peptides that interact with it.

What Is a Melanocortin?

In the quest to understand how PT-141-works, it is necessary to understand how the melanocortin system works. All melanocortin’s are peptide hormones, which is to say proteins (made up of amino acids). The group gets its name from the parent molecule, proopiomelanocortin (POMC), that all other melanocortin’s are derived from. POMC is made in the pituitary gland, which is part of the brain and a critical center for controlling growth, the sleep/wake cycle, sexual desire, hunger, and more. Natural melanocortin’s made from POMC include melanocyte-stimulating hormone (MSH) and adrenocorticotropic hormone (ACTH). MSH has long been associated with sexual arousal and changes in appetite.

What is NAD+? How Does it Work?

NAD+ is the second most abundant cofactor in the human body. Anti-aging therapies are becoming more mainstream as aging is now more often being viewed as a disease. Now that this transition is happening, the ability for NAD+ to activate PARPS, Sirtuins, and help with immune dysregulation has been thoroughly investigated and NAD+ and its precursors have been highly popularized. The clinical importance of maintaining cellular NAD+ levels was established early in the last century with the finding that pellagra, a disease characterized by diarrhea, dermatitis, dementia and death, could be cured with foods containing the NAD+ precursor niacin.

Additionally, cellular concentrations of NAD+ have been shown to decrease under conditions of increased oxidative damage such as occur during aging Altered levels of NAD+ have been found to accompany several disorders associated with increased oxidative/free radical damage including diabetes, heart disease, age-related vascular dysfunction, ischemic brain injury, misfolded neuronal proteins, and Alzheimer’s dementia. Interventions targeted at restoring NAD+ has been shown in animal models to support healthy aging and improve metabolic function, and dementia.

A need for NAD+ in muscle development, homeostasis, and aging

In a review study, researchers discuss the recent data that document conserved roles for NAD+ in skeletal muscle development, regeneration, aging, and disease as well as interventions targeting skeletal muscle and affecting NAD+ that suggest promising therapeutic benefits. The researchers also highlight gaps in our knowledge and propose avenues of future investigation to better understand why and how NAD+ regulates skeletal muscle biology.

How Does NAD+ Depletion Impact Aging?

Introduction – What is NAD+?

NAD+ (Nicotinamide Adenine Dinucleotide) is a vital coenzyme found in all living cells, playing a crucial role in cellular metabolism and energy production. Structurally, NAD+ consists of two nucleotides joined through their phosphate groups, with one nucleotide containing an adenine base and the other a nicotinamide base. Functionally, NAD+ is essential in redox reactions, acting as an electron carrier. It cycles between its oxidized form (NAD+), which can accept electrons, and its reduced form (NADH), which carries and donates electrons to other molecules. This electron transfer is fundamental in cellular respiration processes like glycolysis, the citric acid cycle, and oxidative phosphorylation, all of which generate ATP, the primary energy currency of cells. Beyond energy production, NAD+ is involved in DNA repair, gene expression regulation, and maintaining genome integrity. It also activates sirtuins, a family of proteins linked to aging, inflammation, and stress resistance.

Biologically, NAD+ is crucial for converting nutrients into energy and ensuring cellular health. Its levels naturally decline with age and boosting NAD+ has been associated with improved health span and lifespan in various organisms. Adequate NAD+ levels are necessary for optimal cell function and survival. Given its significance, NAD+ precursors like nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) have become popular dietary supplements. Ongoing research aims to understand how increasing NAD+ levels can affect aging and age-related diseases, highlighting its potential in promoting healthy aging and optimal cellular function.

What happens when NAD+ levels are low?

When NAD+ levels are low, several adverse effects can occur due to its essential role in cellular processes. One of the primary consequences is a decline in cellular energy production, as NAD+ is crucial for converting nutrients into ATP, the cell’s main energy currency. This energy deficit can lead to increased fatigue, reduced physical performance, and general lethargy. Additionally, low NAD+ levels impair the function of sirtuins, proteins that regulate inflammation, stress resistance, and cellular repair. This impairment can accelerate aging and increase susceptibility to age-related diseases.

Furthermore, insufficient NAD+ hinders DNA repair processes, leading to genomic instability and a higher risk of mutations and cancers. The decline in NAD+ also affects mitochondrial function, potentially resulting in neurodegenerative diseases and cognitive decline due to reduced brain cell protection and maintenance. Metabolic health can be compromised as well, increasing the risk of conditions such as obesity, diabetes, and cardiovascular diseases. Overall, maintaining adequate NAD+ levels is crucial for sustaining energy production, cellular health, and longevity, and its deficiency can have wide-ranging negative impacts on overall health and well-being.

Peptides and Tanning Research

How Does UV Light Cause Tanning?

UV light causes tanning, which is to say and increase of the skin pigment melanin, by stimulating a cellular process mediated by the tumor-suppressor gene p53[1]. The whole point of this process is to protect skin cells against UV light, which can damage DNA and lead to problems like cancer, cell death, and the breakdown of extracellular matrix proteins (e.g., collagen) in the skin. This latter effect is what leads to observable skin aging in the form of wrinkles, lines, lost elasticity, and more.The pathway is activated when UV light damages DNA in the upper layers of the skin. The damage done to the DNA results in stabilization and activation of the p53 tumor suppressor protein. This, in turn, promotes activation of proopiomelanocortin (POMC). POMC is cleaved to product alpha-melanocyte stimulating hormone (α-MSH), which then binds to the melanocortin 1 receptor (MC1R). This causes melanocytes to both produce more melanin as well as divide and increase in number. Together, these effects cause an increase in melanin pigment leading to darkening of the skin. The melanin then absorbs the harmful UV light preventing further DNA damage[2].Note that tanning via UV light does not occur until after DNA damage has occurred. This means that the potential for cancer development is already present before tanning occurs because DNA damage has already occurred. Therefore doctors have warned against UV-based tanning for years. The only solution, until recently, has been to avoid UV light entirely by either staying out of the sun or by wearing sunscreen. Unfortunately, recent research shows that sunscreen has problems of its own such as damaging coral reefs and potentially causing hormone dysregulation[3]. The current research is focused on promoting melanin production without exposure to UV light, thus gaining the benefits of melanin protection without first inducing DNA damage.

The New Solution to Sunless Tanning

If scientists could stimulate tanning without the DNA damage that jumpstarts the natural process, then we could experience the benefits of tanning without any of the risks. Research into the tanning pathway has been of interest for several decades now, in part because of the discovery of melanotan and the melanocortin receptor system. Interestingly, melanotan was developed as a sunless tanning agent and then became of interest for an entirely different purpose. It’s ability to protect the skin against UV damage was almost completely forgotten as its ability to stimulate sexual arousal became the focus of melanotan research. Much later, research shifted again and melanotan became a front-runner in sunless tanning research. This peptide has since inspired the exploration and development of other peptides for sunless tanning research. Some of those peptides are discussed below along with other compounds associated with sunless tanning.

Ipamorelin Cost

Ipamorelin Cost: What to Know in 2024

Ipamorelin, the short, synthetic agonist of the growth hormone secretaogue (GHS) receptor, is one of the most selective growth hormone (GH) increasing peptides available for research. Given ipamorelin prices, it is also one of the least expensive. Ipamorelin prices top out at less than $100 dollars in most cases for a 5 mg vial, making it among the most affordable GHS agonists and a favorite for researchers investigating the effects of GHS stimulation on growth, muscle function, bone health, diabetes, and postoperative ileus. Given the benefits of ipamorelin, the potential applications, and the low cost of this peptide it is surprising that more research isn’t being done to drive the science forward.

What Is Ipamorelin?

Ipamorelin is a synthetic, highly selective agonist of the GHS receptor originally developed by Novo Nordisk for the treatment of postoperative ileus. Ipamorelin was derived from growth hormone releasing peptide-1, which is itself a derivative of the natural protein hormone ghrelin. Ghrelin, often referred to as the hunger hormone, is produced by the stomach and stimulates the intake of food. It also activates cells in the anterior pituitary gland, increasing levels of neuropeptide Y and growth hormone. Ghrelin plays important roles in reward cognition, learning, memory, the sleep-wake cycle, and energy metabolism.

Ipamorelin is just five amino acids (Aib-His-D-2Nal-D-Phe-Lys ) long and easy to produce via recombinant techniques. This is one of the reasons ipamorelin prices are so affordable. It retains some, but not all of ghrelin’s properties, a feature that makes ipamorelin more selective than ghrelin and thus potentially more useful.

Peptide Sequence: Aib-His-D-2Nal-D-Phe-Lys

Molecular Formula: C38H49N9O5

Molecular Weight: 711.868 g/mol

PubChem CID: 9831659

CAS Number: 170851-70-4

Ipamorelin vs CJC-1295

Ipamorelin vs CJC-1295

CJC-1295 and ipamorelin are both growth hormone secretagogues, though how they naturally raise growth hormone levels differs. Despite their differences in mechanism of action, these two peptides share a lot in common. That’s not to say that their effects are identical by any means though. For the discerning researcher, knowing the differences between these two peptides is critical to experimental design and so it is important to explore precisely how they differ. Additionally, the differences in their mechanisms of action mean that these two peptides might be synergistic in certain research applications and so those potential synergies are worth knowing.

Ipamorelin vs CJC-1295: Mechanism of Action

Ipamorelin is a growth hormone secretagogue receptor (GHS-R) agonist, which means it mimics the effects of ghrelin. Ipamorelin was derived from GHRP-1, which was itself derived as one of six (6) different molecules from ghrelin. As an agonist of the GHS-R, ipamorelin activates cells in the anterior pituitary gland to cause growth hormone release. It also binds to GHS-R subtypes in other areas of the brain to regulate reward cognition, learning, memory, the sleep-wake cycle, taste sensation, and glucose metabolism.

CJC-1295 is a derivative of growth hormone releasing hormone (GHRH) and binds to the GHRH-R in the anterior pituitary gland. As a GHRH-R agonist, CJC-1295 has fewer direct effects than ipamorelin because there is no GHRH-R outside of the anterior pituitary gland. Thus, CJC-1295 primarily causes an increase in growth hormone levels. The increase in growth hormone, however, has secondary effects that will be discussed in greater detail.

Ipamorelin vs CJC-1295: Structure

Ipamorelin is a much smaller molecule when compared to CJC-1295, but CJC-1295 offers the ability to be modified easily through the addition of a molecule known as DAC. DAC, or the drug affinity complex, can drastically alter the half-life of CJC-1295 and thus offers an easy means of tailoring the activity of the peptide. Both peptides must be administered Sub-Q for optimal results as there is extensive degradation in the GI tract as well as first-pass metabolism in the liver.

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