Frag 176-191, termed Lipolytic Fragment, is the modified version of AOD 9604. It is composed of a structural fragment of growth hormone. According to research, Frag 176-191 may potentially mimic certain characteristics of the parent protein. Fragment 176-191 may increase insulin levels without increasing insulin-like growth factor-1 (IGF-1) levels, which include mitigating carbohydrate metabolism, altering insulin sensitivity, and increasing long bone growth.  Fragment 176-191 peptide is suggested to be a concentrated and stabilized version of the growth hormone-releasing factor—GRF, which may potentially cause a more rapid increase in bodily growth hormone 12.5 times stronger. Fragment 176-191 may stimulate protein synthesis, increase vascularity via nitrogen retention, increase bone mineral density and modify cell aging cycles. It may exert influence in sleep cycles and possibly increase contractile strength via hyperplasia.

 

Research

 

1. Frag 176-191 and Blood Sugar Levels:

Research suggests that Frag 176-191 is a potentially potent synthetic equivalent of the growth hormone and may act to reduce blood sugar levels. This potential is secondary to the increase in plasma insulin levels. Research is ongoing to determine if Frag 176-191 may be employed effectively in research studies using research models of prediabetes and type II diabetes.

 

2. Fragment 176-191 and Cartilage:

Though interest in Frag 176-191 is primarily researched for its potential its lipolytic functions, research is ongoing to determine its other possible impacts. In 2015, research from Korea suggested that Frag 176-191 increases the effects of hyaluronic acid exposure that may promote cartilage regeneration. Studies in rabbits suggested that Frag 176-191 increased cartilage growth laboratory standards, and its combination with hyaluronic acid may produce a more potent effect. The overall result suggests that exposure to Frag 176-191 alone and alongside hyaluronic acid might reduce the disabilities following osteoarthritis.

 

3. Frag 176-191 and Weight:

Fragment 176-191 is commonly referred to as Lipolytic Fragment because of its potential lipolytic potential. This function may possibly be mediated by increased beta-3 adrenergic receptor production (𝛃3-AR or ADRB3). The agonist action of ADRB3 is to accelerate fat burning in fatty tissues and thermogenesis in skeletal muscles. Mouse models genetically induced to not produce ADRB3 appear not to respond to the lipolytic potential of hGH or Frag 176-191. Research suggests that Frag 176-191 action may be accompanied by energy expenditure and weight reduction, amounting to about 50% of reduced weight gain in animal models of obesity over exposure for three weeks. Notably, the weight reduction effect was reported only in obese mice. In lean mice, they appeared to maintain their standard body weight even on exposure to Fragment 176-191. These results suggest that specific lipolysis pathways may be responsible for overriding the effect of ADRB3.

 

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.

B7-33 is the synthetic derivative of H2-relaxin. B7-33 has been suggested to act similarly to h2-relaxin but does not appear to increase the production of cAMP. Its research relevance is suggested in the reduced fibrosis in chronic and acute diseases, such as lung inflammation, heart failure, kidney, etc. B7-33 may also act to reduce scar formation seen in cardiac injuries.

B7-33 is a soluble produced single-chain peptide equivalent of the naturally occurring protein H2-relaxin. B7-33 has been suggested to harbor properties similar to h2-relaxin without increasing the production of cAMP. B7-33 peptide may function to activate ERK1/2 phosphorylation, improve matrix metalloproteinase 2 (MMP2) expression, and extracellular collagen degradation. Despite having a possibly strong affinity for the RXFP-1 receptor, it doesn’t appear to activate the cAMP pathway. Instead, researchers hypothesize that it may activate the pERK pathway—a pathway considered to inhibit the cell cycle in the G1 phase.

The inhibition of the cell cycle progression in RXFP-1 receptor cells by the compound may induce downstream impacts. The anti-fibrotic potential of B7-33 may enhance the pERK1/2 signaling—boosting the synthesis of the enzyme matrix metalloproteinase (MMP)-2, which breaks down collagen. It may be of great advantage that B7-33 does not appear to activate cAMP as cAMP activation may modulate some tumor-promoting action.

 

Peptide Production

B7-33 may be more advantageous in research contexts than the natural H2-relaxin protein as it does not appear to activate the cAMP pathway but may instead hold onto certain anti-fibrotic characteristics. This is one of its advantages as B7-33 production is easy as it has less intricate 2D and 3D structures.

 

B7-33 and Fibrosis

Fibrosis is scarring or the unorganized regeneration of tissues. It is the last stage of several chronic diseases ranging from cardiovascular to lung diseases to cirrhosis of the liver and aberrant wound healing. Fibrosis is considered the primary cause of organ failure. According to research studies, the exposure of H2-relaxin following fibrosis may lead to vasodilatory action and a reduction in the long-term scarring effect of heart damage. That notwithstanding, H2-relaxin may exhibit some setbacks. It may potentially increase heart rate and may increase cancer cell progression. Most of these are linked to the activation of the cAMP pathway, allowing for the research on B7-33 to be relevant and of great import.

According to research by Dr. Akhter Hossain, one of the lead developers of B7-33, it may act to increase MMP-2 production slightly better than H2-relaxin. The results suggest a decrease in cardiac fibrosis in rat models of MI-induced heart failure. Subsequently, it may have improved heart function and reduced long-term symptoms such as heart failure complications. Research suggests that B7-33 reduces scarring in the heart following injury by about 50%. Similar results are reported in mouse models of asthma and lung fibrosis. Scientists introduced B7-33 in mouse models of prostate cancer, and B7-33 did not appear to promote tumor growth.

Scientific studies suggest that coating from B7-33 reduced the thickness of fibrotic capsules by about 50% in six weeks. Further research in B7-33 may aid researchers in preventing the unintentional ancillary action of certain anti-fibrotic molecules to decrease the fibrosis of implanted devices—allowing for more successful device implant.

 

B7-33 and Blood Vessels

Animal model research in male Wistar rats suggests that the compound exhibits the vasoprotective characteristics of serelaxin by promoting bradykinin-mediated endothelium-dependent relaxation in arteries. It may potentially achieve this by increasing endothelium-derived hyperpolarization in vascular beds.

 

B7-33 and Preeclampsia

Preeclampsia, termed Toxemia, is a critical pregnancy condition characterized by high blood pressure and decreased fetal weight. Preeclampsia is complex. In some cases, it may be life-threatening to both the fetus and the mother. Animal studies suggest that B7-33 may help control preeclampsia in severe cases. In this research, B7-33 may act like an RXFP-1 receptor to boost VEGF production in cytotrophoblasts—cells found in the developing fetus that help stimulate blood flow between mother and baby. Therefore, by stimulating VEGF production, B7-33 may potentially enhance blood vessel growth—improving the blood supply between the offspring and mother. Research has supposed that lipidated B7-33 may have a longer half-life.

 

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.

Pinealon is a peptide made up of three amino acid sequences. It is known as a peptide regulator because of its potential capacity to interact with DNA and change gene expression levels. Pinealon may potentially protect cells and tissues from the harmful action of hypoxia.

Compared to other peptides, Pinealon does not appear to bind to cell surfaces or cytoplasmic receptors. As a result, scientists hypothesized that Pinealon may be small enough to circumvent lipid bilayers (such as the cell membrane and nuclear membrane) and interact directly with DNA. According to scientific studies in cell cultures, the peptide may directly permeate cell membranes and nuclear membranes to interact with DNA.

 

Research

 

Pinealon and Cell Aging

Pinealon may impact cell aging cycles in the central nervous system, according to studies. Pinealon and Vesugen, according to a Russian study, may be anabolic in the brain and may reduce the cell aging process when assessed using biological age markers.

According to experts, Pinealon may be active in cells outside the central nervous system. Pinealon may influence muscle irisin synthesis, an adipocytokine produced in skeletal muscles and subcutaneous and visceral adipose areas that protect myocytes during exercise, promote fat burning, and induce telomere extension. As a result, increasing the lifespan of irisin may possibly improve telomere maintenance and assist in the fight against the harmful action of oxidative stress and cell aging.

 

Pinealon and Neuron Protection

Pinealon has been suggested following scientific studies in prenatal rats to protect neurons from oxidative damage while preventing cognitive functioning and motor coordination. The findings suggest a reduction in the accumulation of reactive oxygen species (ROS) and numerous necrotic cells in the brains of the rats studied. The compound appears to control cell cycles by activating proliferation pathways. It may mitigate some of the adverse action of ROS in oxidative stress.

Pinealon has been suggested to boost cell and neuron resilience to hypoxia in adult rats. The peptide appears to achieve this by increasing anti-oxidative enzyme systems and minimizing the excitotoxic action of N-methyl-D-aspartate (NMDA), an amino acid derivative considered to be capable of killing brain cells by over-excitation.

Irisin may promote neuronal differentiation, proliferation, and energy expenditure in the brain. Pinealon appears to raise irisin levels by modulating the gene expression that codes for the enzyme, possibly resulting in higher irisin levels due to the enzyme’s longer half-life.

 

Caspase-3 and Cell Death

Peptide research in animal models of ischemic stroke was suggested to alter cytokine signaling, which may lead to a rise in the levels of caspase-3 enzyme—an enzyme that triggers apoptosis. The peptide may inhibit at least one of the processes that induce cell death by modulating the activities of caspase-3, possibly lowering the impact of oxygen deprivation in stroke. Pinealon appears to mitigate long-term remodeling that may lead to myocardial infarction-related dysfunctions.

Pinealon’s potential in reducing caspase-3 expression are suggested further in studies in skin cells. The peptide may improve cell proliferation in older and young animals by decreasing skin apoptosis.

 

Pinealon and Sleep Regulation

Pinealon, may act to reset the pineal gland, possibly allowing for circadian rhythm disturbance, improved sleep cycle regulation. The capacity of the Pinealon to potentially adjust sleep has been associated with organism age. Irregular sleep may impact metabolic function, as well as cascade of physiological processes, in some ways not yet fully understood. Pinealon’s potential to regulate sleep may support physiological functioning on a macro level.

 

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.

Oxytocin is a nine-amino acid peptide hormone that researchers believe to be generated in the brain and released by the posterior pituitary gland. In its natural state, Oxytocin appears to be a precursor molecule that splits to produce the active hormone. According to research, the peptide may be produced in the retina, adrenal glands, pancreas, and thymus. Although Oxytocin is assumed to be a neurohypophysial hormone, it has been researched in connection with additional activities across various tissues.

Researchers posit that this protein hormone may have two natural roles: it may be a neuropeptide secreted by the brain to function in bonding, sexual reproduction, and delivery. Oxytocin appears to be a blood-borne hormone that may also be generated by the placenta of mammalian females to contribute to neonatal bonding. In males, Oxytocin peptide appears to be generated in the testes and may be involved in match behavior and pair bonding.

 

Research

 

Oxytocin Peptide and Tissue Repair

By potentially acting on inflammatory cytokines, the peptide may impact the severity of inflammation. Scientific research examining lesions and tissue damage on interacting animal models indicated that social contact may have boosted the amount of Oxytocin peptide naturally produced, which appeared to have encouraged the pace of wound healing. A unique study was also conducted to evaluate how antagonism in social interactions may potentially impact wound healing. Research models that were conditionally antagonized against each other exhibited a wound recovery rate of roughly 40%. These models also exhibited reduced amounts of IL-6, tumor necrosis factor-alpha, and IL-1 beta at the site of damage.

 

The Cardiovascular System

Due to Oxytocin’s potential to accelerate wound healing and affect inflammatory cytokines, researchers believe it may possibly exhibit protective actions upon the heart and vascular system. Scientific data suggests that Oxytocin receptor inhibition may cause atherosclerosis in some situations. In rare circumstances, increasing Oxytocin levels in cases of low receptor density might help preserve cardiovascular integrity and reverse atherosclerosis.

According to scientific studies, infusing the compound directly into the heart during ischemia may protect cardiomyocytes from damage or death. According to Jankoski et al., increasing the dose of Oxytocin peptide may help prevent the late-term prevalence of dilated cardiomyopathy. It may help precondition cardiac stem cells to aid in “tissue rejuvenation via differentiation, secretion of cardiomyogenic and protective factors, and aid their fusion with injured cardiomyocytes.”

The peptide in animal studies has been suggested to contribute to diabetes-induced cardiac damage prevention. The peptide appears to inhibit the accumulation and storage of fat cells by up to 19% compared to controls, and fasting glucose levels by approximately 23%. These appear to be the outcome of decreased insulin resistance. The mice models under consideration exhibited less systolic and diastolic dysfunction than controls, resulting in less cardiomyocyte hypertrophy, apoptosis, and fibrosis.

The peptide may also protect other bodily tissues against ischemia. Oxytocin peptide exposure appears to protect against ischemia-reperfusion damage in rat models of priapism via the lowering nitric oxide levels.

 

Oxytocin Peptide and Cognitive Processing

Through scientific investigations, Oxytocin peptide has been suggested to enhance hormone levels related to neuron growth in the prefrontal cortex in maternally deprived mice. Although no overall behavioral changes were observed, the group’s cognitive performance appeared to be increased following Oxytocin exposure. Other studies in mice found that Oxytocin peptide appeared to promote learning in a non-statistically significant way under stressful situations.

 

Oxytocin Peptide and Muscles

Researchers suggest the compound may be a potential auxiliary in muscle cell maintenance and regeneration. It appears to induce a decrease in insulin levels, possibly due muscle atrophy (sarcopenia). According to a Berkeley study, a decline in Oxytocin levels may lead to decreased Oxytocin receptors on muscle stem cells. Upon exposure, the peptide may induce a quick reversal of the muscle-withering action. This may be vital as the muscle requires breakdown and repair for natural maintenance and growth.

 

Oxytocin Peptide and Stress

Epigenetic alterations in Oxytocin peptide were detected in a study of research models undergoing social dysfunction, suggesting that social anxiety may be correlated to degraded Oxytocin signaling. According to research studies in Borderline Personality Disorder (BPD), findings have lately been linked to Oxytocin peptide dysregulation. Research is preclinical, and still in progress.

 

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.

Triptorelin is classified as a synthetic equivalent of GnRH. Therefore, it may potentially enact the anterior pituitary gland to release Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH). If Triptorelin is introduced in a steady-state format and not in a pulsatile way, it may eventually suppress the secretion of LH, FSH, testosterone, and estrogen.

Researchers suggest that Triptorelin may be of most interest in studies on prostate cancer, where exposure to the peptide has been speculated to lower cancer growth by inducing a dip in endogenous testosterone levels. Triptorelin appears to decrease the mortality rate in hormone-sensitive prostate cancer to less than 5% in experimental versus control group comparisons.

Recent research posits that GnRH in symbiont with radiotherapy may potentially exhibit similar action to a total androgen blockade. The blockade of androgen may induce ancillary downstream action, which may potentially be circumvented.

Triptorelin exhibited apparently positive results in reducing urinary tract symptoms in research models of prostate cancer, with the research team reporting that the peptide may have contributed to reducing the frequency of the symptoms from about 54% to about 12%.

 

Scientific Studies

 

Triptorelin and Reproduction, Fertility

Research also suggests that Triptorelin could potentially reduce the prevalence of early menopause in research models that have undergone chemotherapy by approximately 17%. The exposure of this peptide in research models with Adenomyosis might increase the degree of spontaneous pregnancy and potentially improve the outcomes of the disease itself. Identical benefits may be evident in research models with endometriosis.

In endometriosis, triptorelin might act to reduce pain by potentially causing a decrease in the number of nodules in the disease. Research speculates that Triptorelin could potentially improve the outcomes of laparoscopic surgery for endometriosis. It is believed to be specifically effective in potentially increasing the rates of pregnancy after surgery.

In In research models with colorectal endometriosis, Triptorelin appears to potentially decrease pain in about 80% of the subjects and diarrhea in about 60%.

 

Triptorelin and Immune Function

Research in mouse models suggests that LHRH might potentially impact the thymus and the immune system. Cell aging in research models may reduce the LHRH binding sites on the thymus, potentially resulting in a 50% reduction in thymic mass and function.

The LHRH agonist, Triptorelin, may potentially improve proliferation within the thymus and may induce a turnaround in cell aging impacts to some extent.

 

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.

A potential synthetic equivalent of one of collagen’s constituent units is Tripeptide-29, potentially serving as a building block for large collagen molecules. Tripeptide-29 might change the amino acid sequence and relative frequency of a collagen molecule, potentially influencing its superstructure, tertiary, and quaternary properties. Researchers consider collagen to be vital to restoring damaged tissues.

According to speculative research, Tripeptide-29 may have a wide range of physiological impacts. Tripeptide-29 might act as a limited antagonist of collagen receptor-GPVI. Platelet surfaces in this context may be packed with GPVI, the protein considered to be responsible for the early production of blood clots. Collagen fibers are referred to as thrombogenic in this context because they might play a significant part in the collagen-mediated stimulation of the collection of collagen in vascular tissues, which is speculated to be the first stage in tissue repair and clot formation.

Tripeptide-29 might boost GPVI activation, suggesting it could be potentially useful in research related to creating a clotting environment in cases of bleeding and clotting abnormalities.

 

The Roles of Tripeptide-29

Collagen is considered to be one of the most common biological compounds. It is considered to play a role in muscle fibers, skin, ligament and tendon structures, bone, teeth, scar formation, cartilage, cell signaling, transmembrane proteins like integrin and fibronectin, placental structure, and the vitreous humor of the eye.

The Regulation of Tissue Fibrosis

The peptide might suppress the activity of dipeptidyl peptidase-IV in vitro, utilizing fish scales, bovine skin, pig skin, and chicken feet (DPP4). DPP4, speculated to be a cell apoptosis enzyme identified in immunological signaling cells, might hamper growth factors, neuropeptides, chemokines, and vasoactive peptides, since it is speculated to be an inherent element of cell membranes. Its duties are not speculated to be restricted since it appears to be involved in glucose metabolism, which breaks down incretins—a hormone speculated to aid in lowering blood glucose.

DPP4 studies in animal models suggest that it fosters fibrotic growth in organs such as the liver and kidney. Tripeptide-29 might potentially increase cellular glucose absorption and minimize renal fibrosis while also inhibiting DPP4 activity. As a result, various research pathways may have opened up, not only for mitigating diabetes but also as pathologic sequelae.

Tripeptide-29 and Collagen Stability

Tripeptide-29, according to speculative studies, may be effective in potentially modulating collagen stability. Research into the peptide allowed scientists to realize that the final peptide in the tripeptide monomer might potentially modulate the collagen structure (in an A-B-C trend, where C is speculated to have the most influential capacity on collagen stability).

Tripeptide-29 and Skin

The significance of Tripeptide-29 in potentially protecting the skin against cell aging and damage has been the subject of recent studies. The research on Tripeptide-29 peptide suggests promising pathways in potentially reducing cell aging by improving contour, reducing skin deformation, and improving moisture retention.  Tripeptide-29 synergy with certain hexapeptides might improve skin turnover and potentially reduce the development of creasing and wrinkling along the skin surface.

Tripeptide-29 as a Radical Scavenger

Damage caused by free radicals is speculated to be the fundamental cause of tissue and cellular aging. Though various bioprotections exist to counteract the consequences of free radical damage, these barriers appear to reduce in effectivity with time. According to speculative studies, Tripeptide-29 hydrolysate might be a potent radical scavenger.

 

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.