Ipamorelin is a derivative of the growth hormone-releasing peptide-1, which is derived from the natural protein hormone ghrelin. Ghrelin is often termed the hunger hormone. The stomach produces ghrelin, and its exposure appears to stimulate caloric intake. The cells in the anterior pituitary gland are speculated to be activated by ghrelin, which might increase the levels of growth hormone and neuropeptide Y. Ghrelin is of speculated significant value in cognitive function, energy metabolism, and may influence the sleep-wake cycle.

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

Molecular Formula: C₃₈H₄₉N₉O₅

Molecular Weight: 711.868 g/mol

 

Ipamorelin Peptide Mode of Action

The GHS receptor, also called the ghrelin receptor, is highly expressed in the anterior pituitary gland and hypothalamus. Growth hormone is released from the anterior pituitary gland as the agonists bind to the GHS-R in the pituitary gland. Five of the most active GHS-R binding amino acids appear to be present in Ipamorelin, making this short peptide the smallest known GHS-R agonist. The exposure to Ipamorelin in animal models reportedly resulted in the stimulation and the release of neuropeptide Y, which may lead to an increased appetite, decreased pain perception, and changes in energy metabolism.

 

Food Intake

The specific receptors required for stimulating the release of neuropeptide Y are situated in the hypothalamus, and the binding to the GHS-R might trigger the release of this peptide. The release of neuropeptide Y is associated with an increase in food intake. Therefore, it might alter food preferences, thereby increasing the storage of energy as fat.

 

Pain Perception

Research suggests the potential of Ipamorelin in reducing neuropathic pain, the pain associated with nerve dysfunction, and reducing visceral pain, the gastrointestinal tract, and organ pain. Research studies in rats indicate a reduction in pain perception by as much as 2-fold.

 

Bone

Some research studies in rats suggest an association of Ipamorelin with the regulation of bone turnover and promotion of mineralization of existing bones and the formation of new bones. Research in rats suggests the effectiveness of Ipamorelin in offsetting the effects of substances like corticosteroids and certain conditions considered to compromise bone density and increase bone formation by as much as four-fold. In addition, Ipamorelin has been suggested to prevent aberrant fat deposition seen with high corticosteroid levels and prevent bone loss.

 

Ipamorelin Peptide & Heart Function

The relationship between ghrelin and heart function is a complicated one. However, research in cell cultures and research in animal models indicate that ghrelin may help protect the heart after a heart attack or other cardiac damages. Furthermore, it might also be that ghrelin produced in minute amounts in the vascular system may help in reducing the scar formation and the successive hypertrophy of the heart. This might thereby put a stop to the long-term consequences of heart damage and also heart failure.

 

Gender Differences in Ipamorelin Peptide Responses

Research studies conducted in mice, rats, and pigs suggest that the peptide may exhibit objectively larger benefits in females than males. The relative lack of testosterone in females compared to males has been hypothesized to be the foundation for why the peptide may potentially be more effective in females. The lower levels of testosterone have been associated with a decrease in muscle anabolism and lower bone mineral density. Research studies are ongoing to confirm any other reasons associated with the higher potential effectiveness of the peptide in females.

 

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.

Adipotide is a peptidomimetic compound having the molecular sequence of CKGGRAKDC-GG-D(KLAKLAK)2. The molecule has been suggested to mediate selective apoptosis of blood vessels, which supply adipocytes, thus causing weight loss in rhesus monkeys and mice. White adipocytes may be formed due to excess energy consumption compared to utilization. The targeted blood vessels upon Adipotide peptide exposure appears to undergo atrophy (shrinkage), leading to apoptosis (cell death), hence preventing blood supply to the white fat cells. Therefore, the adipocytes might suffer from an ischemic injury due to oxygen and nutrient deprivation and finally undergo apoptotic cell death.

The stereochemical structure of the molecule might allow it to bind to two cognate receptors (prohibitin and ANXA-2) found exclusively on blood vessels of white adipose tissues. High tissue specificity might prevent it from targeting brown fat tissues. Thus it may potentially not influence adaptive brown fat thermogenesis, which is crucial, especially for newborn organisms who can conserve only limited heat. The body surface area to volume ratio might promote high rates of heat loss in such cases.

 

Adipotide and Obesity

In 2008, epidemiological studies suggested that various conditions may be intricately linked to hypertension, hyperlipidemia, metabolic syndrome, NIDDM (Non-Insulin Dependent Diabetes Mellitus), cerebrovascular accidents, myocardial infarction, and cancers. Interestingly, morbidity might be determined by the distribution of adipose tissues within the organism. Abdominal fat might be more harmful in certain areas of placement due to higher lipolytic function. Adipose tissue comprises lipid storing adipocytes (cells) and vascular macrophages, and preadipocytes. An increase in adipose mass might be caused by excess lipid deposition in adipocytes leading to hypertrophy and subsequent hyperplasia. It might further trigger the infiltration of macrophages and conversion of preadipocytes to adipocytes. The blood supply might also promote this microenvironment. Adipotide has been suggested by researchers to target this blood supply, thereby causing irreversible ischemic injury and apoptosis of adipose tissues.

 

Selected Research Studies

In 2004 a study named “Reversal of obesity by targeted ablation of adipose tissue” by Mikhail G Kolonin et al. observed that targeted apoptosis in the vascular bed of white adipose tissue may potentially mitigate obesity. Obese mice exposed to a peptide sequence CKGGRAKDC binds to a multifunctional vascular membrane protein called prohibitin. It appeared to induce a decrease in adipose tissue mass and normalization of overall metabolic processes without any significant ancillary impact.

In 2011, research entitled “A Peptidomimetic Targeting White Fat Causes Weight Loss and Improved Insulin Resistance in Obese Monkeys” by Kirstin F. Barnhart et al. established the ligand-directed peptidomimetic named Adipotide (with sequence CKGGRAKDC-GG-D(KLAKLAK)2 ) as a prototype of anti-obesity peptides in obese monkeys. Adipotide was observed to induce apoptosis in the vasculature of white adipose tissue leading to rapid weight loss, improved insulin and renal function in the monkeys.

In 2011, Fernanda I. Staquicinia et al. analyzed vascular marker(s) for different organs in their work entitled “Vascular ligand-receptor mapping by direct combinatorial selection in cancer patients.” The survey included 2.35 × 106 motifs from a peptide library in research models of cancer, uncovering ligand-receptors specific to particular vascular beds. Among the four native ligand-receptors found, two appeared to be native ligand-receptors (cathepsin B/apolipoprotein E3 and integrin α4/annexin A4) that existed across tissues. The other two exhibited tissue-specific prevalence – prohibitin/annexin A2 exclusive for the white adipose tissue and RAGE/leukocyte proteinase-3 found in bone metastases. Thus prohibitin and ANXA-2 might be found to be receptors specific for vasculature of white fat tissue.

 

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 Sermorelin and CJC-1295 are peptide derivatives of growth hormone-releasing hormone (GHRH) and are often compared regarding their properties and functions. In addition to the number of actions they share, CJC-1295 and Sermorelin also appear to exhibit differences. Sermorelin is also known as GHRH 1-29, the first 29 amino acids from a large growth hormone-releasing hormone is the structure of Sermorelin. The structure of CJC-1295 also appears to consist of the first 29 amino acids of GHRH, but the difference might be that there is a modification in some of the amino acids.

 

The Structure of CJC-1295

Sequence: Tyr-D-Ala-Asp-Ala-Ile-Phe-Thr-Gln-Ser-Tyr-Arg-Lys-Val-Leu-Ala-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Leu-Ser-Arg

Molecular Formula: C₁₅₂H₂₅₂N₄₄O₄₂

Molecular Weight: 3367.954 g/mol

 

The Structure of Sermorelin

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

Molecular Formula: C₁₄₉H₂₄₆N₄₄O₄₂S

Molecular Weight: 3357.933 g/mol

 

Clearance and Structure

GRF (1-29) indicates the growth hormone-releasing factor (1-29), and is another name for Sermorelin. The modified form of GRF (1-29), which is sometimes speculated to be known as Mod GRF (1-29) or tetrasubstituted GRF (1-29), is another name for CJC-1295. The potency of the first 29 amino acids of GHRH is speculated to be the same as the potency of the full 44 amino acids of GHRH. Still, the natural metabolic clearance processes may clear very rapidly. To decrease the clearance rate and boost the half-life, Sermorelin can be modified so that CJC-1295 can be made more resistant to enzymatic cleavage. Research studies indicate that Sermorelin’s half-life is somewhere around five minutes, while the half-life of CJC-1295 appears to be 30 minutes.

 

DAC or no DAC?

The modification in CJC-1295 is often be done by adding a lysine residue and DAC, i.e., a chemical structure, to the carboxy-terminal end. DAC stands for drug affinity complex. The role of DAC is to help bind the molecules that it is attached to with the blood protein albumin. This action may help them extend the half-life of these compounds and extend their duration of action. With DAC, the time of total clearance of CJC-1295 might roughly increase from 1 hour to more than 96 hours.

 

Plasma Growth Hormone: CJC-1295 vs Sermorelin

The levels of Growth Hormone in the blood are suggested to be raised under the influence of both Sermorelin and CJC-1295, by the stimulation of the growth hormone-releasing hormone receptor in the anterior pituitary gland. Since both Sermorelin and CJC-1295 might operate at the level of the receptor of GHRH, they may preserve the normal pulsatile function of Growth Hormone secretion. However, Sermorelin appears to provides the more natural ebb and flow of Growth Hormone as it appears to be cleared much faster as compared to CJC-1295. The best way to explain the two peptides and their effects on the Growth Hormone curve is that both might raise the Growth Hormone levels and also both raise the preserving peaks and troughs, while the overall amount of time spent at the higher Growth Hormone levels might be extended by CJC-1295. In other words, it might be that the sharp peaks are turned into plateaus to some extent by the CJC-1295. With this, the effects of Growth Hormone may potentially be boosted substantially, and the physiology may also be altered to some degree. Still, one of the main reasons to prefer Sermorelin over the peptide CJC-1295 is that Sermorelin might provide the most speculated natural ebb and flow pattern.

 

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.

TB-500, also recognized as Thymosin Beta 4 or Tβ4, is been involved in various research endeavors to understand its mode of action and full physiological impact. TB-500 is an oligopeptide comprised of 43 amino acids, with an approximate molecular weight of 4.9 kDa. It is found distributed across various tissues, excluding Erythrocytes (red blood cells).

Initially identified as a protein isolate from the thymus gland, Thymosin Beta 4 belongs to the Thymosins family, characterized by acidic and lightweight molecules contributing to cell production. By modulating the polymerization of actin proteins, TB-500 may potentially impact cell differentiation and movement. It may either encourage or inhibit the formation of filaments by gathering actin monomers, affecting the differentiation of pluripotent stem cells into diverse cell types like bone cells or neurons. Researchers suggest that Thymosin Beta 4 might influence the formation of new blood vessels and cell migration by manipulating actin, highlighted a potential in wound healing.

The hypothesized impacts of Thymosin Beta 4 range from tissue repair, scar prevention, inhibition of cell death, microbial growth, and inflammation. Studies on externally derived TB-500 indicate accelerated healing of injured cardiac, corneal, and dermal tissues, emphasizing its wound healing potential.

Thymosin Beta 4 has been suggested to host potential anti-inflammatory characteristics, impacting nitric oxide and prostaglandin EP4 release in cell models exposed to reactive oxygen species. TB-500 molecules are considered to be osteoclastogenic, they may play a role in bone production and enhance the stimulus-response of interleukins and pro-inflammatory cytokines in periodontium cells.

Research suggests Thymosin Beta 4 inhibits the activation of NF-κB in murine macrophages and influences the release of the anti-inflammatory peptide fragment acSDKP7. The complex mechanism governing the splitting of acSDKP7 from TB-500 involves specific peptidases, including hydrolysis by meprin – alpha. Thymosin Beta 4 exhibits potential in research studying fibrotic scarring in various organs, potentially reducing inflammation in rodents with pulmonary fibrosis.

 

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 the realm of peptide research, there is a prevailing focus on exploring peptide influence in cell migration, proliferation, and tissue repair. Researchers suggest that peptides exhibiting tissue repair potential are a key area of interest, with BPC-157 garnering significant repute in research studies relating to that focus. This article aims to provide insights into some fundamental aspects of BPC-157 peptides, as proposed by study findings.

BPC-157, which stands for Body Protection Compound, also known as Bepecin and PL10, is a stable synthetic gastric peptide comprising fifteen amino acids, forming a pentadecapeptide. Notably, BPC-157 has no structural resemblance to natural gastric peptides, being a synthetic variant derived from gastric juice. Despite its synthetic nature, BPC-157 purportedly exhibits enhanced stability, enduring gastric acid breakdown for a minimum of 24 hours.

 

Research in BPC-157 Peptide

BPC, being a naturally occurring element in the body, has been suggested, in various research studies on animal models, the potential to enhance tissue repairing processes. Its potential efficacy extends beyond intestinal repair, showcasing similar reparative outcomes in various body tissues. Studies on the healing mechanisms of BPC-157 suggest an association, to some extent, with Growth Hormone.

In terms of fibroblast activity, research findings propose that BPC-157 peptide concentrations may impact the relocation of fibroblasts, potentially prompting the migration of more fibroblasts with elevated BPC levels. Earlier studies have hinted at BPC-157’s role in managing collagen fragments, affecting Fibroblasts’ function and influencing the deposition and maintenance of collagen. Scientific data indicates that BPC-157 may significantly accelerate fibroblasts’ migration, potentially leading to a threefold increase in fibroblast reproduction following exposure.

Regarding tendon healing, studies suggest that BPC-157 contributes to the enhanced recovery of transversely cut rodents’ Achilles tendons, restoring the entire integrity of the tendon. Similar effects were observed in the case of ligament injuries in rodents, with injuries healing within three months of surgical intervention after exposure to BPC-157.

Research findings also propose that BPC-157 may potentiate a positive impact on brain healing, particularly in cases of inflammation, hemorrhage, and edema, as well as traumatic brain damage and severe brain pathologies resulting from gastrointestinal/liver lesions or insulin and NSAID overdose. BPC-157’s speculated benefits extend to aiding in the healing of blood vessel damage, showcasing potential for angiogenesis (the formation of new blood vessels) and inhibiting and reversing the formation of blood clots due to abdominal aorta anastomosis.

Research suggests that BPC-157 acquires significant healing properties in various tissues such as skeletal muscles, bones, tendons, and ligaments. Additionally, they propose that BPC-157 might play a role as a promoter or modifier of the body’s natural healing system. In speculative terms, BPC-157 peptide is associated with various physiological action, including bone healing, repairing skin damage, muscle injury, and healing the sciatic nerve.

 

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.

GHRP-6 is a hexapeptide that is derived synthetically from met-enkephalin. This hexapeptide was identified almost a decade ago and is the first to be studied in animal test subjects. It consists of a chain of six unnatural D amino acids named L – Histidine, D – Tryptophan, L – Alanine, L – Tryptophan, D – Phenylalanine, and L – Lysine.

It is a member of the Growth Hormone Secretagogue family, which is a substance that results in the secretion of a different substance. There is no structural similarity between GHRP-6 peptide and Growth Hormone Releasing Hormone (GHRH). It appears to work by using some specific receptors that are available at the hypothalamic or the pituitary level. Studies are suggesting the presence of GHRP-6 peptide in various peripheral tissues like the adrenal, heart, testis, ovary, skeletal muscle, and lung.

GHRP-6 peptide shows cytoprotective potential related to non-growth hormones, such as cardioprotective, neuroprotective, hepatoprotective, and anti-inflammatory effects.

 

Structure of GHRP-6 Peptide

Molecular Formula: C₄₆H₅₆N₁₂O₆
Molecular Weight : 873 g/mol
Sequence: His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
CAS Number: 87616-84-0

 

GHRP-6 Peptide Mechanism of Action

The animal test subject studies have suggested that ghrelin, i.e., the “hunger hormone,” may be stimulated by Growth Hormone Releasing Peptide – 6. The stimulation may be completed via the ghrelin receptor, which acts at the hypothalamus or the pituitary level via specific receptors that are not similar to the endogenous Growth Hormone Releasing Hormone (GHRH) and thereby signals an increased production of Growth Hormone (GH).  In response to the production of the Growth Hormone, Insulin-like Growth Factor-1 (IGF-1) is considered to be produced by the liver. The IGF-1 may be necessary for the promotion of cell proliferation and the prevention of cell death.

 

Research in GHRP-6 Peptide

The animal test subject studies were carried out to study the GHRP-6 peptide. Various theoretical actions of the GHRP-6 peptide are suggested in the studies since it appears to increase the production of the growth hormone from the pituitary gland and may thereby mimic the ghrelin, i.e., the hunger hormone considered to protect the hormone neurons.

 

Enhancement of the Healing Process and Aesthetic Outcome of the Wounds

GHRP-6 peptide is suggested to exert an impact on the accumulation of the extracellular matrix proteins, which thereby attenuated the inflammation of the wound, accelerated the wound closure, and improved the aesthetic outcome of the wound. The attenuation of the immunoinflammatory mediators, their effector cells, and the reduction of fibrosis-inducing cytokines have appear to be involved in the GHRP-6 peptide pharmacodynamics in the rat experiments that were based on the clean full-thickness controlled wounds. The combined action of these mechanisms may act to modulate the fibroblast’s response to injury, resulting in precocious closure with reduced scarring. The most appreciable observation is that these mechanisms have not shown any interference with the angiogenic repopulation or the reepithelialization process. The successive studies have signified the potential of various GHRPs to ameliorate the systemic and the local inflammatory processes by inhibiting the action of NF-κB. This results in the expression of the pro-inflammatory cytokines and acting as a chemokine receptor antagonist.

 

GHRP-6 Peptide Experimental Studies

The studies in a rat model with liver cirrhosis have suggested that GHRP-6 peptide may exhibit certain antifibrotic effects. The parenchymal fibrotic induration was prevented by GHRP-6 peptide in more than 85% of the cohort, while in 75%, the accumulated fibrotic material was removed. In a microarray experiment, the differentially expressed genes indicated the modulation of gene expression associated with redox metabolism by the GHRP-6. Exposure to GHRP-6 peptide was suggested to induce pharmacological benefits in varied experiments conducted during the last 15 years. Growth Hormone Releasing Peptide – 6 has also been suggested to host cytoprotective potential, encompassing the cardiac and the extracardiac organs. The numerous experimental scenarios that included reperfusion/ ischemia have suggested that GHRP-6 peptide exhibits antiapoptotic and antiestrogenic properties.

 

Muscle Cell Growth

GHRP-6 peptide has been suggested to promote the anabolic environment. The increased production of the insulin-like growth factor 1 (IGF-1) and the release of the growth hormone (GH) from the pituitary gland are the factors associated with gaining muscle mass. The protein synthesis in the body is considered to be increased with the increase in these factors.

 

Weight

The peptide has also been suggested to have a close association with fat loss after its influence in the organism; the body may be enabled to burn fat at a more optimal rate. GHRP-6 peptide has been suggested to improve metabolic rate, which may improve overall functioning associated with an equalized weight.

 

Cell Aging

Collagen production has been speculated to increase following exposure to GHRP-6 peptide, which consequently promotes lean muscle mass and enhanced energy levels. Growth Hormone Releasing Peptide – 6 has also been suggested to enhance the ability of the internal systems to repair old and worn-out cells and improve the function of joints and tissues.

 

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.