What Is Adipotide (FTPP)?

Adipotide, also known as Prohibitin-TP01 and abbreviated as FTPP, is a synthetically made proapoptotic peptide with a unique function, potentially targeting and affecting various types of fat cells. Speculative research suggests that Adipotide might aim to reduce the number of fat cells by impacting the blood supply to adipocytes. It is suggested to target proteins present on the walls of blood vessels supplying adipocytes, potentially interfering with and disrupting the blood supply, resulting in the reabsorption and metabolism of fat cells.

According to research, Adipotide FTPP might selectively target the blood vessels supplying fat cells while potentially sparing other blood vessels responsible for supplying organs and tissues. Research conducted on monkeys, indicates that Adipotide may be associated with weight loss and potentially influence insulin sensitivity, thereby speculatively contributing to the management of conditions like type 2 diabetes.

Weight

Starting in 2011, research was initiated on Adipotide to explore its potential impact on weight loss. Details from preclinical research on Rhesus monkeys suggest that the exposure to Adipotide resulted in a targeted and highly selective apoptosis of blood vessels supplying white fat adipocytes. This process lead to the ischemic death of affected adipocytes, causing significant weight loss.

Researchers have suggested an intriguing side effect, where exposure to Adipotide reduced weight through fat loss and also decreased overall food consumption in test animals, suggesting a role in appetite reduction and weight loss. The selectivity of Adipotide in targeting the vasculature of fat cells suggests that the presence of a protein receptor called Prohibitin might play a role. Prohibitin is considered to be selectively present in the vasculature of fat and cancer cells, and Adipotide may interact with this protein to induce apoptosis in white adipocytes.

Cancer

The sustenance of cancer cells might depend on their blood supply. In cancer research, targeting the blood supply of cancer cells has been explored. Adipotide has been suggested to interact with protein receptor Prohibitin, found on the walls of blood vessels supplying cancer cells. Adipotide might target cancer cells, leading to their death by ischemia.

Considering that pProhibitin is selectively present in cancer and fat cells, the study of Adipotide in anti-cancer research might yield positive results, as suggested by advanced studies which indicate that Adipotide selectively targets cancer cells while protecting surrounding cells and tissues.

Glucose Tolerance

Glucose tolerance refers to the biological response of higher-than-usual glucose levels. A test called OGTT, or the oral glucose tolerance test, measures this response through introduction of a set amount of high glucose and measuring corresponding blood glucose levels. Research suggests that if Adipotide leads to significant weight loss by burning white adipocytes, it might potentially contribute to changes in body mass index and, speculatively, improved insulin sensitivity. In essence, Adipotide might cause a decline in fatty cells and could potentially lead to fat loss.

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.

Semaglutide, aka GLP-1: What is it?

Semaglutide or GLP-1 is a naturally occurring peptide suggested to lower blood sugar levels, modulating insulin production and release. It is a 30-31 amino acid sequence short peptide. The primary function of Semaglutide (GLP-1) appears to be to regulate blood sugar levels by enhancing insulin secretion. Semaglutide appears to upregulate the transcription of the insulin genes and therefore prevents a pathological rise in blood sugar levels by protecting insulin stores. Although the primary research surrounding Semaglutide is based on its speculated anti-diabetic characteristics, newer studies are reviewing its role in other dimensions.

Semaglutide has been linked with neurotrophic effects in the brain and central nervous system. Semaglutide appears to decrease appetite in the gastrointestinal (GI) system by delaying gastric emptying and reducing intestinal motility. Preliminary research has suggested impacts of Semaglutide on the heart, fat, muscles, bones, liver, lungs, and kidneys. The main focus of Semaglutide research has been diabetes and appetite inhibition, and subsequent investigations focus on the possible cardiovascular impacts of the peptide. More prevalent and thus less robust research focuses on the potential of Semaglutide to stave off neurodegenerative disease. Though this latter area of research is the most recent, it is also the quick-growing domain of Semaglutide investigations which suggest the peptide may act to prevent the accumulation of amyloid-beta plaques in the context of Alzheimer’s disease research.

Blood Sugar Regulation – the Incretin Effect

One of the speculated ways Semaglutide appears to induce a drop in blood sugar levels is by the “incretin effect.” Incretins are hormones released by the gastrointestinal tract. These hormones are secreted in response to high glucose levels in the blood and act to bring down their levels.

The two most important regulators for incretin release appear to be GLP-1. Even though the circulatory levels of the other regulator, i.e. GIP, appear higher than that of Semaglutide, it appears more potent out of the two, particularly in very high blood sugar levels. Considered to be foremost expert, Dr. Holst has studied this effect, the link between GLP-1 and incretin, and its potency in rodent models.

A GLP-1 receptor has been observed on the surface of pancreatic beta cells, suggested that GLP-1 enhances the exocytosis of insulin from the pancreas. When mixed with sulfonylurea compounds, GLP-1 may potentially increase insulin secretion. It may be enough to cause mild hypoglycemia in up to 40% of research models. Moreover, increased insulin secretion is associated with several trophic results, such as better protein synthesis, a decrease in the breakdown of protein, and enhanced uptake of amino acids by skeletal muscle.

GLP-1 and The Brain

Secondary research on Semaglutide suggests it may have a neuroprotective role in the CNS and the brain. Exposure to Semaglutide may improve cognitive function and protect against certain neurodegenerative diseases like Alzheimer’s disease. This potential was observed when the introduced of Semaglutide in mice with specific genetic defects appeared to induce an improvement in learning deficit as well as enhanced their associative and spatial learning.

GLP-1 and its analogs have been suggested to reduce amyloid-beta deposition in the brain and the beta-amyloid precursor protein found in the neurons. Since the deposition of these beta-amyloid plaques in brain tissue appears to be the primary pathology resulting in Alzheimer’s disease, Semaglutide may be relevant to Alzheimer research.

GLP-1 and The Hunger Hormone Signaling

Investigations in mice models suggested that direct introduction of Semaglutide into the brains of laboratory murine models appeared to reduce the drive to eat and inhibit food intake. Semaglutide may enhance satiety via hunger hormone (ghrelin) signaling, and reducing appetite. Recent studies have suggested that Semaglutide receptor agonists may induce gradual linear weight loss in mice. Over an extended period, this weight loss was associated with significant improvement in cardiovascular risk factors and reduced hemoglobin A1C levels. The latter is a proxy marker for the severity of diabetes and the quality of blood sugar control.

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 Syn-AKE Peptide?

The Syn-AKE peptide is a synthetic analog of the protein Waglerin-1. It is a 21 amino acid protein isolated from tropidolaemus wagleri. However, Syn-AKE includes only three of the amino acids which are present in the original endogenous sequence. It represents the perceived active portion of the protein and appears to produce similar action as that of the original Waglerin-1, but researchers assert that it appears to act in a controlled way.

What Are Syn-peptides?

Syn-peptides are synthetically developed peptides similar in structure to a naturally occurring peptide. They typically appear to assume the action of the naturally occurring form. Peptides are short proteins which research posits may indeed be short enough to cross the skin barrier in certain organisms.

How Does Syn-AKE Peptide Work?

Syn-AKE peptide is designed to mimic paralytic action. The Syn-AKE peptide was developed with close structural similarities to the Waglerin-1 peptide. The Waglerin-1 peptide was proposed to induce paralysis in laboratory studies, and the synthetic peptide may potentially produce a similar effect via its chemically similar structure. Researchers believe the molecule may small enough to penetrate the skin barrier. However, only tiny quantities of the molecule has been hypothesized to be able to penetrate muscle cells beneath the skin structure.

Waglerin-1 has been proposed by various researchers to induce sodium uptake by muscle cells by interacting with the mnAchR receptor. Preventing sodium uptake may block the transmission of nerve impulses to the muscles, and the muscles remain relaxed.

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 Semaglutide Peptide?

Semaglutide, or the Glucagon-like Peptide (GLP-1), is a naturally-occurring peptide hormone. It is a very short peptide of about 30 or 31 peptides only. The natural function of the endogenous peptide is proposed to be the regulation of blood glucose levels at an average value by interfering with natural insulin production and secretion. It appears, peculiarly, to mediate this insulin-altering function. Semaglutide peptide has been suggested by researchers to protect the beta cell insulin stores in the pancreas by upregulating the insulin gene transcription.

Apart from this main hypothesis of Semaglutide peptide, it also has neurotrophic potential on the brain and the central nervous system, which researchers are exploring in more depth. Semaglutide peptide appears to play a potentially significant role in hunger and appetite regulation in the gastrointestinal tract (GIT), potentially inducing the delay of gastric emptying and reduction of intestinal motility.

Recent studies on the Semaglutide peptide have suggested its potential action may be as far reaching as in liver, kidneys, lungs, muscles, bones, fat, and the heart function. Even though the Semaglutide peptide has mainly been investigated in the context of diabetes research, newer studies suggest its potential in cardiovascular and neurodegenerative disease research as well.

Even though this development requires additional research, some studies suggest potential in the context of Alzheimer’s disease research by slowing down the accumulation of amyloid-beta plaques in the brain, which is considered to be the primary pathology of the disease. Research conducted on the mechanism of action of the Semaglutide peptide suggested two significant mechanisms by which it appears to mediate most of its potential. These two mechanisms are described under separate headings below:

The “Incretin Effect”

One of the essential hypothetical modes of action of Semaglutide- according to research conducted by Dr. Holst- is the “incretin effect.” Incretins are a group of metabolic hormones secreted by the gastrointestinal tract. The incretins are involved in decreasing the circulating blood sugar levels. Apart from gastrointestinal peptide (GIP), researchers suggest that Semaglutide or GLP-1 may potentially be the more important regulator of these hormones in the GIT.

The Semaglutide or GLP-1 receptors have been posited to exist on pancreatic beta cells, directly stimulating insulin release from the pancreas. This increased insulin secretion has been linked with other metabolic actions like increased amino acid uptake by muscle cells and increased protein synthesis and breakdown.

Studies conducted on murine models suggested that exposure to Semaglutide peptide appeared to reduce hunger levels and food intake in mice, which resulted in weight loss. This weight loss was also linked to reduced cardiovascular disease risk and decreased HbA1C levels.

Beta Cell Protection

The pancreatic beta cells are the central insulin-secreting cells. Therefore, their destruction, downregulation, or apoptosis due to any reason may possibly be a pathology of diabetes. Some compelling research on diabetic mice models has suggested that Semaglutide peptide may act upon the pancreatic beta cells in two ways. Firstly, GLP-1 may possibly stimulate the growth and proliferation of new beta cells from their progenitors in the pancreatic duct epithelium. Secondly, GLP-1 may potentially inhibit the apoptosis of these cells by inhibiting the inflammatory cytokines involved in the process. The net effect of these two actions may tip the balance towards a more significant number of pancreatic beta cells, potentially allowing them to protect the pancreas against insults that harm beta cells.

Semaglutide Peptide and The Brain

Speculative research into the peptide suggests its potentially in directing the progress of neurodegenerative diseases, specifically Alzheimer’s. It is hypothesized that the GLP-1 receptors in the brain may reduce the deposition of beta-amyloid plaques, which is the primary pathology involved in Alzheimer’s disease. Studies on rats suggested that the exposure to Semaglutide peptide appeared to improve associative and spatial learning in mice with genetic defects.

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.

AICAR’s Involvement in Insulin Resistance

Research study claims suggest that inflammation in adipose tissue might lead to alterations in insulin sensitivity. Research speculates that mitigating this inflammation may hypothetically enhance glucose metabolism and homeostasis without notable alterations in weight. AICAR, through unspecified pathways related to SIRT1 and macrophages, is speculated to have a role in reducing inflammation in adipose tissue. In research involving undisclosed diabetic and control mice, AICAR has been linked to a reduction in inflammatory responses by activating AMP kinase. This activation may potentially improve insulin sensitivity, energy homeostasis, lipid metabolism, and inflammatory markers.

Insights into Anti-Cancer Research and AICAR

AMPK’s conjectured impact on tumor growth and spread is presumed to be variable in different contexts. Supposedly, in certain instances, it might slow down tumor invasion, while in others, it might accentuate tumor growth. Some research implies that extended activation of the enzyme might hypothetically lead to cancer cell death by slowing cancer cell metabolism, rendering them more susceptible to environmental influences. Scientists are exploring the potential of AICAR peptides alongside other anticancer compounds to evaluate possible effectiveness against cancer cell proliferation.

AICAR Peptide and Anti-Inflammatory Action

The purported anti-inflammatory potential of AMPK activators have been the subject of exploration. AICAR, sharing potential metformin-like actions in various inflammatory conditions, is speculated to hold promise in autoimmune and inflammatory disorders. Studies in mice suggest that AICAR might decrease inflammation in colitis models. This anti-inflammatory potential may be attributed to its role as a central inhibitor of immune responses, potentially reducing nuclear factor kappa B (NF-κB) activation in macrophages and certain cytokines.

AICAR Peptide and the Heart

Inflammation of cardiovascular tissue is presumed to be the primary pathology in numerous heart diseases, including atherosclerosis. Inflammation and vascular smooth muscle proliferation may be critical factors in the failure of stent placement and other cardiovascular conditions. Therefore, controlling vascular inflammation may hypothetically reduce both short-term and long-term complications of stent placement without resorting to alternative compounds that might increase bleeding risk.

The main hypothesis that researchers hold for the AICAR peptide is that via AMPK activation, the peptide may potentially suppress specific immune responses assumed to lead to atherosclerosis. In this scenario, AICAR might mitigate the supposed risk of developing atherosclerotic plaques resulting from macrophage proliferation, hypothetically reducing the prevalence of heart diseases.

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.

PTD-DBM Peptide Discovery

In South Korea, researchers conducted studies on a condition referred to as androgenetic alopecia. Research into this condition reportedly prompted Professor Choi Kang-yeol of Yonsei University and a team of researchers to explore a protein associated with follicle loss in androgenetic alopecia, namely CXXC5. The protein’s identification led to the discovery of the PTD-DBM peptide, which researchers suggest might interact with this protein to potentially alter the mechanism of follicle loss in the disease. It is also speculated to indirectly promote hair follicle growth in lab animals exposed to the peptide.

Mechanism Of Action

PTD-DBM peptide purportedly interferes with an endogenous protein, CXXC5, believed to be involved in the mechanism of hair loss. CXXC-type zinc finger protein 5 (CXXC5) is described as a negative regulator of the Wnt/β-catenin pathway, a key pathway in wound healing and hair regeneration. Allegedly, the protein CXXC5 binds to the Dishevelled protein, impeding the growth of hair follicles and leading to hair loss. This is the point at which research into the PTD-DBM peptide may become relevant, as it is suggested to activate the Wnt/β-catenin pathway by interfering with the binding of CXXC5 with the Dishevelled (Dvl) protein. The claim is that PTD-DBM may promote the growth of new hair follicles and potentially inhibit the loss of existing follicles. Moreover, there are speculative assertions about its ability to induce wound repair through wound-induced hair neogenesis (WIHN).

PTD-DBM Peptide In Wound-Healing

The Wnt/β-catenin pathway is considered common to cutaneous wound healing, dermal fibrosis, and follicle regrowth. Researchers suggest that CXXC-type zinc finger protein 5 (CXXC5) may serve as a negative feedback regulator of the Wnt/β-catenin pathway by interacting with the Dishevelled (Dvl) protein. The speculation researchers have made is that the PTD-DBM peptide may act as a common link between the protein CXXC5 and the Wnt/β-catenin pathway. Experiments on laboratory animals imply that inhibiting the CXXC5 protein might lead to accelerated cutaneous wound healing and enhanced keratin 14 and collagen synthesis. The assertion is that the PTD-DBM peptide links with the protein CXXC5, interfering with the regulation of the Wnt/β-catenin pathway and bringing about the wound-healing potential of the peptide.

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.