Fragment 176-191 exhibits unique potential to stimulate the metabolism of adipose tissue. A similar molecule, AOD 9604 modifies the peptide Fragment 176-191 of the growth hormone hGH by adding a tyrosine residue to the N-terminus. Research findings suggest AOD 9604 may potentially prove more effective in triggering the dissolution of fat cells, than AOD 9401, which preceded it. It has been suggested to follow the same mechanistic pathway for a fat breakdown as hGH. It may also inhibit the conversion of food fat proteins.

Studies explored the impact of exposure to Fragment 176-191 in mice, and they posited that the peptide may have reduced the fat burden in the exposed animals through induction of weight loss. The precise reason for this finding is not yet completely understood. However, scientists opine that the binding of the peptide to beta(3)-adrenergic receptors on the surface of white adipose tissues may trigger the fat metabolism process.

These receptors are strongly associated with fat metabolism. The peptide binding to the cognate receptors may induce downstream signaling for mobilizing the stored fat cells to a usable state by increasing the rate of metabolism. Interestingly, studies in mice that genetically lack β-3-adrenergic receptors also observed fat loss, possibly through apoptosis of the white adipose tissues.

Fragment 176-191 and Cardiac Disease

The burden of fat, if relieved, may lead to a cascade of beneficial downstream actions, most prominently on the cardiovascular system and the heart. Fragment 176-191 may potentially impact cardiac function by mobilizing fat and reducing obesity. One considered pathology of cardiac disease is obesity, and these pathways appear to be independent of β-3-adrenergic receptors and may contribute to improving general metabolism and cardiac function.

Joint Pain and Function

Studies involving Fragment 176-191 have suggested that it may directly impact the proliferation of cells which comprise cartilage. Directly introducing the peptide into arthritic joints in rats was reported to reduce pain perception and appeared to decrease movement disability.  Scientific examination and microscopic cartilage structure analysis in the affected joints have suggested positive impact upon exposure to Fragment 176-191 in rat models of osteoarthritis.

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.

Semax Peptide and Neurogenesis

Semax is a synthetic analog of adrenocorticotropic hormone (ACTH) comprising amino acids 4 through10 of ACTH. Semax peptide appears to stimulate neurogenesis, as suggested by observations in studies involving rats. Researchers propose that the exposure of rats to Semax peptide may upregulate BDNF protein by approximately 1.4 fold, coupled with a 1.6 fold increase in trkB tyrosine phosphorylation. Additionally, there seems to be a simultaneous improvement in exon III BDNF and trkB mRNA levels, respectively, by 3 and 2 folds in the rat hippocampus. Rats subjected to this peptide exhibit a notable increase in the number of conditioned avoidance reactions, indicating the peptide’s potential influence on enhancing cognitive brain functions through the hippocampal BDNF/trkB system.

In studies exploring memory improvement, Semax peptide and a considered anti-amnesic compound were proposed to beneficially impact murine models of amnesia upon combined exposure, except for cases induced by maximal electroshock. There seems to be a bell-shaped reversible concentration-dependent effect equation for Semax, while the anti-amnesic displayed a linear relationship. Researchers suggest that both substances might help suppress the ortho-and antidromic population response surges of CA1 pyramidal neurons of survival hippocampal slices in rats. Notably, the anti-amnesic, compared to Semax peptide, may have improved oxygen consumption in rat brain mitochondria, displaying a linear concentration-effect response.

Regarding the protective potential of Semax peptide on cerebral blood vessels during oxygen deprivation, research findings propose that intranasal exposure to Semax for six days may reduce cortical infarction levels, potentially enhancing the retention and performance of conditioned passive avoidance responses. Semax, researchers suggest, might decrease Vegfa mRNA levels in the frontal cortex and hippocampus following occlusion, indicating its potential to prevent hypoxia-induced Vegfa gene expression at the early stages of global cerebral ischemia. Moreover, the speculative effects of Semax on VEGF-b and Vegf-d genes suggest a noticeable activation, potentially reducing the adverse effects of ischemia and enhancing a positive impact from Semax on ischemic stroke.

Semax Peptide and the Vascular System

Semax appears to alter the expression of several genes in the vascular system, according to speculative research data. Studies propose that Semax may promote vessel formation and stabilization around 24 hours after occlusion, influencing the activation of blood cells about 24 hours post occlusion. Histological studies seem to support these hypotheses suggesting that Semax may improve neuroglia, blood vessel endothelium, and progenitor cells in the subventricular zone, possibly preventing neurological disturbances and excess NO production in the rat brain cortex.

Research indicates that Semax may potentially exert a protective effect against metal-induced cell toxicity and displays a high affinity for Copper II ions. Researchers propose that Semax might induce reduced copper-induced cytotoxicity, as observed in SHSY5Y neuroblastoma and RBE4 endothelial cell lines.

The findings suggest that Semax may normalize the circadian locomotor rhythm in rats, increasing its amplitude, shifting the acrophase, and changing the spectral characteristics. Researchers suggest that the rhythm-synchronizing chronotropic activity might be a part of the specific effect of this potential cognitive enhancer.

Additional Research Implications of Semax

Semax peptide appears to have a concentration-dependent effect on enkephalin-degrading enzymes of serum, exhibiting apparent pronounced effects compared to certain inhibitors of peptidases. Additionally, Semax speculatively inhibits histamine release from mast cell activation, suggesting potential anti-ulcer activity through stabilization of mast cells.

In the realm of neuronal stimulation, research findings propose that Semax peptide may stimulate acetylcholine and exploratory activity. Researchers suggest that Semax peptide may improve the survival of cholinergic basal forebrain neurons in vitro, further stimulating choline acetyltransferase activity in dissociated basal forebrain tissue cultures without affecting the number of GABA-ergic neurons.

Semax peptide might be a potentially relevant candidate for further research in studies on conditions such as ADHD and Rett syndrome. It is proposed that Semax may enhance the effects of psychostimulants on central dopamine release, trigger central brain-derived neurotrophic factor (BDNF) synthesis, and potentially improve selective attention and modulate brain development. The neuroprotective potential of Semax peptide may extend to the immune system, influencing microglia and immune system cells, particularly leukocyte activation.

In the context of glaucomatous optic neuropathy, data suggests that a complex neuroprotective approaches, including Semax peptide exposure, may be employed in research models of normalized ophthalmic tone. The potential efficacy of the peptide may be attributed to Semax’s pathogenetic activity, with neuroprotective and neurotrophic effects speculated to contribute to the observed benefits.

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.

Antigen, Antibody, and Lymphocytic White Blood Cell Recruitment

Researchers suggest that Thymosin Alpha-1 may not over-stimulate cytokine production, setting it apart from other similar agents like interleukin-2 and interferon-alpha.  In the context of cancer and immunodeficiency research models, the peptide has undergone scientific experimentation, with findings suggesting potential enhancement of immune system responsiveness. The peptide may augment the functioning of specific lymphocytes, including the maturation of T cells, T cell-mediated cytotoxicity, and the production of antibiotics and lymphoproliferative responses to mitogens.

The functions may extend to an increase in the activity of Natural Killer Cells, an elevation in cytotoxic T cell levels, and the expression of Th1 type cytokines. It is proposed that Thymosin Alpha-1 peptide might impact the differentiation pathway of T cells, influencing the maturation of thymocytes in the thymus and the diversion of helper CD4+ cells and CD8 cytotoxic suppressor cell sublineages. These are then considered to further differentiate in peripheral lymphoid tissues.

Thymosin Alpha-1 and Immunomodulatory Action

Experiments conducted on thymocytes and mouse cells suggest that Thymosin Alpha-1 may reduce apoptosis of immune cells and increase stem cell expansion in immunosuppressed mice. Research observations indicate an increase in thymopoetic cytokines IL-15, IL-7, and IFN-alpha in response to Thymosin Alpha-1.

The effectiveness of Thymosin Alpha-1 may potentially be linked to different immunological effects where an enhanced or stimulated immune response is needed. In situations like cancers and bacterial, fungal, and viral infections, and in instances of immunocompromised and vaccinated cases, it is suggested to play a role. Researchers suggest that the killing of tumors and virus-infected cells may be facilitated by the coordinated action of CD8 cytotoxic Tc1 cells, CD4 helper Th1 cells, and NK cells. Activated Dendritic Cells may enhance antigen presentation, potentially increasing antibody production, a particularly crucial effect in immunocompromised models to respond effectively to vaccination.

Molecules with the potential to stimulate immune responses, known as antigens, are considered to generate specific responses from B cells in the immune system, producing antibodies or immunoglobulins in response to antigen exposure.

Thymosin Alpha-1’s immunomodulatory potential, researchers indicate, may include promoting Treg cells and inducing IDO1 to ameliorate intestinal inflammation and respiratory allergy. This hypothesis aligns with the maintenance of diplomatic relations between microbial communities and mammals.

Thymosin Alpha-1 might enhance immunosurveillance by boosting the production of MHCs and possibly disable virus immune system cloaking techniques. It is suggested to increase the visibility of viral antigens to the immune system, potentially reducing viral replication and aiding in immune surveillance.

Tumors and ACE Enzymes

Research experiments suggest that Thymosin Alpha-1 increases protein expression on the surface of tumor cells or virally infected cells. It is proposed that this might involve the expression of antigens such as beta two microglobulins, MHC Class 1, and MHC Class 2, as well as antigens specific to tumors. Researchers posit that the peptide partially restores mucociliary clearance and enhances the normal ciliary beating dynamics.

Data indicates that Thymosin Alpha-1 may exhibit inhibitory impacts on angiotensin-converting enzyme (ACE), and it is speculated to interact with ACE domains through hydrogen, hydrophobic, and electrostatic forces. Speculation extends to an improved outcome in viral pneumonia patients who continue the use of ACEi during viral pneumonia.

Thymosin Alpha-1 and Tissue Repair, Cell Migration

Thymosin Alpha-1 is also suggested to stimulate endothelial cell migration, angiogenesis, and wound healing. Research studies suggest that it may stimulate angiogenesis and accelerate wound healing. Thymosin Alpha-1 in combination with IFN-α2b, research studies indicate, may have more significant effects than IFN-α2b alone in research models of normal serum ALT levels and the clearance of Hepatitis C Virus RNA. The speculation is that Thymosin Alpha-1 may increase intracellular Glutathione, exhibiting powerful antioxidant impact, particularly in eliminating superoxide radicals when compared with antioxidant assays.

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.

Regarding the Thymus Gland

Researchers suggest that a functional thymus gland may improve immunity against infections, potentially helping to prevent cancer and enhancing lifespan. Speculatively, the thymus gland and the hormones it secretes could act as an elixir, boosting immunity and contributing to the regulation of cell aging. Each lobe of the thymus gland, speculated to be the main immune organ, appears bumpy due to smaller sections called lobules. These lobules are thought to facilitate the incubation and development of T cells crucial for immunity. Nascent T cells appear to travel from the bone marrow to the thymus, undergoing “thymic maturation.” They are suggested to be selected for efficiency and mature into CD4+ “helper” or CD8+ “killer” lymphocytes, playing diverse key roles in vaccination response, resistance to viral infections, allergies, autoimmunity, inflammatory cascade, tissue repair.

The thymus is speculated to produce immune regulators called cytokines, which, if produced in excess, might lead to a “cytokine storm,” which may have detrimental impacts on its function. The thymus is also speculated to secrete hormones, namely thymosins, thymopoiten, and thymulin peptides, and interleukins. Thymosin may help regulate cell aging and maintain immune balance. The only method to assess thymic function is considered to be through T and B-lymphocyte tests to assess immune status.

Thymic Dysfunction

Strategies to regenerate thymic activity are suggested to be crucial for surviving infections and preventing cancer cell proliferation. Research into thymic activity suggests that specific nutrients and plant compounds may play essential roles in supporting thymus function. Zinc, speculated to play a crucial role in growth and development. Zinc deficiency is suggested to cause reduced T cell function, slower wound healing, and other immune system defects. Vitamin A is also suggested to support the thymus and stimulate the immune response. High-dose vitamin C, speculatively, may maintain the size and weight of the thymus and increase the number of T cells. Selenium is proposed to boost immunity against viruses and cancer. Astragaloside IV, a plant extract, is suggested to have various biochemically active compounds that enhance telomerase activity and exhibit antioxidant, anti-inflammatory, and immunoregulatory effects.

Research data indicates that thymus and spleen extracts may impact inflammation, tissue repair processes, mitigate viral infection, and inhibit cancer cell proliferation. Thymic Protein A (TPA), isolated from calf thymus, is suggested to exert potential immune-modulating and antiviral properties, supporting CD4+ helper T lymphocytes and reversing thymus atrophy.

Thymic Peptides: TB-500, IGF-1 and Thymosin Alpha-1

Thymic peptides are suggested to help restore and balance the immune response. Thymalin, the synthetic version of thymulin, is suggested by researchers to reduce inflammation, increase T cell activity, raise immunoglobulin A, and exert neuroprotective potential. A thymus gland derivative, Thymosin Beta 4 (TB-500), is suggested to protect against viral infections, enhance tissue regeneration for wound healing, and promote bone remodeling from fractures. Thymosin Alpha-1 is suggested to act as a potent immune regulator, supporting immune function against chronic viruses and fungal infections. Hormones such as growth hormone and insulin-like growth factor (IGF-1) are suggested to improve the function of thymus cells and may influence thymus gland size. Animal studies suggest that boosting IGF-1 may restore thymic size and function and may increase T cell count.

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.

Dr. Windebank et al. evaluated neurological impact using a murine model for MGF overexpression. Breeding of transgenic mice was done to help constitutively overexpress MGF in the hippocampus and the subventricular region of the brain – these are the areas of the brain speculated to be associated with neural development and differentiation (neurogenesis). The histological study suggested an extremely high concentration of BrdU, a synthetic marker for detecting proliferating cells in live tissues, in these portions of the mice brain tissues. This represents high levels of cell proliferation and growth in the specific domains of the brain.

A different batch of double transgenic mice was then bred such that the animals produced MGF under certain conditions only when activated by the presence of a triggering agent added to their drinking water. Researchers depended on this new population of mice to study the long-term influence of increased neural MGF production when produced at 1, 3, or 12 months old. Behavioral studies and further histological assays were then conducted at 24 months. Mice showing high Mechano Growth Factor production not only showed signs of neurogenesis but also greater resistance to age-associated neural degeneration, as posited by their improved olfactory responses. They also appeared to display greater speed and higher success in cognitive tests.

The speculated efficiency of MGF was observed to be age-dependent, as suggested in the study. Early induction of MGF production appeared to have resulted in a more dramatic proliferation of BrdU+ cells and further neurological improvement throughout adult life. If MGF production was not stimulated before 12 months of the age of mice, there appeared to be no significant histological or behavioral differences compared to the control group.

As per current research, the cellular site of action or MGF mechanisms is unknown, and further studies are suggested to be needed to deep dive into the cellular and behavioral potential of the Mechano Growth Factor on neurogenesis.

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.

Chemical Makeup and Specifications

PT-141 peptide, also recognized as Bremelanotide, has a molecular mass of 1025.2 grams per mol. Its chemical formula is C₅₀H₆₈N₁₄O₁₀. The systematic name (IUPAC) for Bremelanotide is (3S 6S 9R 12S 15S)-15-[(N-acetyl-L-norleucyl)amino]- 9-bynzyl-6-{3-[(diaminomethylidine)amino]propyl}-12-(1H-imidazol-5-ylmethyl)-3-(1H-indol-3-ylmethyl)-2,5,8,11,14,17-hexaoxo-1,4,7,10,13,18-hexaa zacyclotricosane-23-carboxylic acid. The half-life of a compound, speculatively defined as the time it may take for the compound to reduce half of its potency value, is speculated to be approximately 2 hours for Bremelanotide.

The Biochemical Process

Researchers suggest that Bremelanotide may directly influence the central nervous system. Animal studies suggested that the molecule may stimulate both synthesis and activation of the MC-4R and MC-3R melanocortin receptors. Findings suggest that the reaction itself may control certain signals from the brain to internal systems. The signals regulating blood flow and inflammatory response may be specifically suppressed. Once the switch to these specific receptors gets altered by the molecule, the brain may be enabled to moderate the signals better.

Hemorrhagic Shock and Bremelanotide Interaction

It is suggested that Bremelanotide may help control proper blood circulation in the brain through the stimulation of neural flexes. Hemorrhagic shock, characterized from a ‘lower tissue perfusion’ or the introduction of oxygen to the tissue directly, may worsen due to an increased lack of oxygen to the area over time. Hemorrhagic shock may be classified into the following four types:

• Neurogenic
• Cardiogenic
• Septic (or ‘vasogenic’)
• Hypovolemic

These four types may be difficult to mitigate individually, even at a cellular level, as the responses may be different between two individual cells. Bremelanotide research and impacts on hemorrhagic shock has been studied to date on animal research models only. The studies were conducted in a controlled and stabilized environment, and some findings indicated maladjustment via the triggering of an increase in blood pressure of some of the animal models observed.

Bremelanotide Research Implications

Bremelanotide is a direct derivative of the peptide hormone Melanotan II, which is a synthetic peptide initially developed to induce the increase of melatonin production. During the course of development, researchers noticed a curious impact that peptide exposure seemed to be inducing in both male and female species under observation. Melanotan II appeared to stimulate sexual arousal in the female subset and appeared to induce erections in males on a spontaneous basis. Stemming from these research observations, Bremelanotide has also studied within the context of libido and arousal signaling within the brain of animal research models of both sexes.

The influence of Bremelanotide on the libido of either sex has been suggested to work via different pathways when compared to alternative approaches which aim to alter the blood flow to the sex organs. Instead, Bremelanotide has been speculated to trigger sexual desire by invigorating the parts of the brain that control sexual desire, thereby improving libido in the animal research models observed.

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.