B7-33 – A Peptide with Potent Antifibrotic Properties

B7-33 – A Peptide with Potent Antifibrotic Properties

B7-33 is a single-chain peptide. It is derived from a naturally occurring compound called H2-Relaxin. Relaxin proteins are a family of four proteins comprising Relaxin, Insulin-like peptide 3, H3-relaxin, and insulin-like peptide 5. They all possess pleiotropic actions impacting the cardiovascular system, musculoskeletal system, reproduction system, etc. These proteins perform these actions through four types of receptors, namely (RXFP1/2 and RXFP3/4). Various ligands, such as cAMP and corticotropin-releasing hormone, stimulate these receptors. All these agonists can express antioxidant, anti-inflammatory, and wound healing properties. However, Relaxin, in addition to possessing above mentioned properties, also exhibits antihypertrophic, vasodilator, and angiogenic properties. This is why Relaxin and its derivatives have been of great interest for researchers to explore its further benefits.

 

B7-33 Specifications:

Sequence: VIKLSGRELVRAQIAISGMSTWSKRSL
PubChem CID: 318164840
Synonyms: (B7-33) H2, GTPL9321

 

Mechanism of action

An important property of the B7-33 peptide that helps it exceed its potential compared to the naturally occurring Relaxin protein is its ability to preferentially act through the pERK Pathway instead of the cAMP-mediated pathway. Also, it has a greater affinity to bind to RXFP1 receptors than Relaxin. However, the antifibrotic properties are mediated through RXFP1-angiotensin II type 2 receptors stimulation. It further activates the pERK1/2 pathway, leading to enhanced production of Matrix Metalloproteinase (MMP)-2. These collagen degrading proteins play their role in controlling fibrosis and eventually preventing scarring. This property of B7-33 to act through pERK1/2 without activating the cAMP pathway is significantly important because studies have indicated cAMP to have a tumor-promoting potential which is the most dreadful side effect associated with the full-sequence Relaxin. Another advantage of B7-33 over H2-relaxin protein is its less complicated structure. It makes it less laborious to produce it in the laboratories while still retaining all the useful properties associated with the native Relaxin proteins. This ease of production implies a lower cost of manufacturing as well.

 

Research implications of B7-33

1. Antifibrotic Properties:
Fibrosis or scarring is an unwanted side-effect of healing following an injury which is more significant in chronic inflammatory diseases. Fibrosis in the chronic diseases of the liver, heart, or lungs is the leading cause of organ failure. If only we could control this unorganized tissue regeneration, we could prevent organ failure. A study on H2-relaxin proteins indicated their potential in reducing fibrosis following an ischemic injury to the heart. It demonstrated an immediate vasodilatory effect in the heart that led to a reduction in the long-term scarring.

Though it was the first product that got approved for the treatment of Acute Heart Failure, it wasn’t an ideal therapeutic agent owing to its side effects, i.e., its tumor-promoting effect. And it could only be given by intravenous route. Studies have indicated that the use of B7-33 produces a similar yet more pronounced reduction in fibrosis without activation of the cAMP pathway avoiding the risk of tumors. A study performed on rat models demonstrated that the use of B7-33 led to a reduction in scarring by approximately 50% following an injury. This reduction in fibrosis eventually leads to improved cardiac function with lesser long-term complications associated with heart failure.

2. Blood vessel protection and use in Preeclampsia:
Researchers have indicated that B7-33 possesses vasoprotective properties of Human Relaxin-2 (Serelaxin) against long-term scarring and endothelial dysfunction. It appears to do this through activation of bradykinin-mediated relaxation of arteries that is endothelium-dependent. B7-33 is more selective in its action as compared to Serelaxin and is cheaper as well.

Preeclampsia is a common complication of pregnancy that can prove life-threatening to the mother and the fetus. It leads to high blood pressure in the mother and reduced fetal weight. A recent study provides evidence that B7-33, by stimulating RXFP-1 receptors, leads to enhanced Vascular Endothelial Growth Factor (VEGF) production. VEGF stimulates the production of the cytotrophoblast cells in the fetus, which are responsible for developing blood flow from mother to baby. B7-33 can help improve the fetus’s survival by prolonging the duration of pregnancy in cases where an early delivery of the baby is suggested.

3. Exogenous Implants:
Exogenous-implanted medical devices often fail to perform their function in full efficacy because the body reacts to it as a foreign object and walls it off by stimulating fibrosis around it. This is particularly harmful in cardiac stenting, where fibrosis can lead to implant dysfunction. Experiments have proved that fibrosis is significantly reduced after coating the implant with B7-33, which improves implant efficacy.

 

Disclaimer: The products mentioned are not for human or animal consumption. All the information shared in this article is for educational purposes only.

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Humanin – The Secret to a Never Aging Heart?

Humanin – The Secret to a Never Aging Heart?

What is Humanin?

It is a micro-peptide and consists of a three-turn alpha-helix. It has an asymmetrical structure. The number of amino acids comprising the peptide chain depends on the peptide site. It consists of 21 amino acids produced in mitochondria, and 24 amino acids are made in the cell’s cytosol.

Mitochondria are the cell’s powerhouse and play complex roles in energy production, cellular signaling, and metabolism. Earlier, the mitochondria’s function, maintenance, and biogenesis were assumed to be controlled by the Nucleus. However, newer studies have demonstrated that a few mitochondria possess a genomic sequence of their own, which can be translated into some proteins, which may affect the Nucleus’s genomic expression.

Research done on the genomic sequence of mitochondria has shown that the rRNA possesses Open Reading Frames (ORFs), which can be transcribed and eventually translated into small peptides, which include biological activity. These peptides comprise Humanin (HN), Small Humanin-Like Peptides 1-6 (SHLPs), and Mitochondrial ORF-encoded peptide (MOTS-c). These peptides bind to specific receptors both in and out of the cells and exert various biological effects.

Studies have postulated that the detectable concentration of Humanin in skeletal muscles, hypothalamus, and cortex decline progressively with advancing age in mice and humans. Therefore, Humanin can be considered a biomarker of age. Humanin has many biological functions that include cytoprotective and metabolic roles. The cytoprotective roles include protection against oxidative stress and injury, anti-inflammatory responses, neuroprotection, and cardio-protection. The metabolic protection roles involve metabolic hemostasis, ATP production, reduction in visceral fat, and glucose-stimulated insulin secretion.

Just like the process of aging affects all other structural and functional properties of the body, it affects the heart. It occurs in a histological change in the heart by fibrosis. Myocardial fibrosis can appear either as an age-related physiological change or due to various pathological phenomena such as Myocardial Infarction and ischemic- reperfusion injury. This contributes to cardiac dysfunction. It affects both systolic and diastolic function and eventually progresses to heart failure. The number of fibroblast cells present in cardiac tissue directly correlates with the age of the heart tissue. While considering its ratio to the cardiac striated cells present, this factor shows the extent of age-related degenerative change present in the heart. These fibroblasts lead to the secretion of extracellular matrix proteins such a collagen type 1 that favors fibrosis.

Humanin – Mechanism of Action

The studies have suggested that Humanin exerts its cardioprotective effects by activating the AKT/GSK-3 beta (Glycogen Synthase Kinase) pathway. Humanin also alters the pro-apoptotic factors in the cardiac fibers and prevents cell death. It starts and downregulates varying pathways depending upon the site of action and the type of pathology.
Other factors responsible for causing fibrosis in the heart are FGF-2 (Fibroblast Growth Factor-2), MMP-2 (Matrix Metalloproteinase-2), and Transforming Growth Factor-beta (TGF-beta). These factors tend to increase in the cardiac tissue as age progresses. Studies have confirmed the role of Humanin to attenuate the effect of them all.

Another mechanism associated with age-related cardiac tissue deterioration involves the damage caused by Reactive Oxidative Species (ROS). Excessive Reactive Oxidative Species cause deterioration of the Antioxidant Defense System by depolarizing the mitochondrial membrane. It leads to ATP (Adenosine Triphosphate) hydrolysis and causes swelling of mitochondria. This causes rupture of the outer membrane of mitochondria and eventually the release of pro-apoptotic proteins in the cytosol. Humanin induces enzymes and various small non-enzymatic molecules that lead to an overall reduction of the oxidative stress caused by Reactive Oxygen Species (ROS).

A study performed on aged rats has postulated that chronic administration of exogenous humanin ameliorates myocardial fibrosis and apoptosis. This study indicated an increase in the ratio of cardiac fibers to fibroblasts. It was measured in the percentage of each cell present in a random field chosen after immunofluorescence staining of the cardiac tissue. Picrosirius red staining of the cardiac tissue demonstrated a decrease in the collagen content of the heart tissue, which is a marker of tissue age. Long-term supplementation with humanin has proven to reduce fibroblast proliferation and downregulate the expression of Fibroblast Growth Factor-2 (FGF-2), Matrix Metalloproteinase-2 (MMP-2), and Transforming Growth Factor-beta 1 (TGF-beta 1). It has also been shown to suppress pro-apoptotic factors in the cardiac tissue.
To conclude, the use of Humanin can be a breakthrough in easing cardiac function in a physiologically or a pathologically compromised heart.

 

Disclaimer: The products mentioned are not for human or animal consumption. All the information shared in this article is for educational purposes only.

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ARA-290 – The Holy Grail of Immune Modulation and Neuropathy?

ARA-290 – The Holy Grail of Immune Modulation and Neuropathy?

WHAT IS ARA-290?

ARA-290 is a peptide derivative of erythropoietin (EPO). Erythropoietin is the primary hormone responsible for erythropoiesis, which is the production of new red blood cells. In addition, it is also involved in angiogenesis (production of new blood vessels), cell survival, blood pressure regulation, and neuroprotection in diabetic neuropathy.

ARA-290 provides only a selective range of nociceptive and neuroprotective effects and evades the hemopoietic action. It is of great interest to researchers because of these two properties and their role in wound repair in diabetes and immune modulation in autoimmune diseases. It has cleared phase 2 trials and is currently in phase 3 trials.

RESEARCH IMPLICATIONS OF ARA-290:

BLOOD VESSELS INTEGRITY

ARA-290 plays a significant role in prolonging cell survival and helping Endothelial Colony Forming Cells (ECFCs) repair and rebuild blood vessels after their integrity has been compromised following an injury. Similarly, ARA-290 can protect retinal epithelial cells from ischemic or inflammatory injury, promote repair, and lead to regeneration. This way, it plays a crucial role in the prevention of blindness.

ARA-290 improves migration, proliferation, and homing ability of Endothelial Colony Forming Cells, which favors the targeted repair of blood vessels that have undergone damage. Studies have indicated that ARA-290 augments the effect of endogenous ECFCs and the transplanted exogenous ECFCs to repair and establish the vasculature of ischemic tissues. This can lead to a whole new domain of medical treatment, permitting viable cells to be implanted in the body and making up for irreversible losses.

DOWNREGULATION OF INFLAMMATORY CYTOKINES AND TISSUE PROTECTION

Lately, the surgical management of diabetes was done by transplantation of viable insulin-producing islet cells to make up for insulin deficiency in people with diabetes. This provided a regulated physiological control of diabetes and prevented long-term grave complications of diabetes. However, this method was soon abandoned because this led to the activation of macrophages, implant rejection, and ultimately implant failure. Studies have demonstrated the potential of ARA-290 in suppressing this inflammatory cascade by inhibiting the release of TNF-alpha, IL-6, and IL-12, which prolongs the survival of exogenous Islet cells.

The mechanism behind this inflammatory suppression involves the binding of ARA-290 to the Tissue Protective Receptor (TPR). This altogether reduced the effect of harmful inflammatory mediators, which boost tissue protection. Erythropoietin does play the above role, but it comes with the cost of its hematopoietic and cardiovascular side effects. ARA-290 leads to better wound healing and quick post-injury recovery, reducing morbidity and mortality.

ROLE OF ARA-290 IN IMMUNE SYSTEM REGULATION

There is mounting evidence that supports the role of ARA-290 in immune modulation through the binding of ARA-290 to Tissue Protective Receptors, which are expressed by a wide range of immune cells, including lymphocytes dendritic cells, mast cells, and macrophages.
After binding ARA-290 to the macrophages, it suppresses the release of proinflammatory mediators. This leads to a decrease in pathogen clearance, but it altogether reduces disease severity and prevents long-term morbidity due to chronic inflammation. It also lessens the release of inflammatory chemokines by the macrophages and reduces inflammatory infiltration while favoring resident macrophage recruitment to the site of injury at the same time. This prevents the side effects of inflammation on the surrounding tissues.

Studies have demonstrated the effect of ARA-290 in altering the antigenic property of dendritic cells in such a way that leads to increased long-term resistance against pathogens, to which the host has been exposed already. This forms the foundation of its role in prevention tissue, organ, or graft rejection following transplantation.

This property of ARA-290 can manage chronic inflammatory diseases such as ulcerative colitis by restricting uncontrolled inflammatory processes by selective immune modulation.

Research has shown the effect of ARA-290 in reducing the levels of ANA and anti-dsDNA in Systemic Lupus Erythematous (SLE). The two auto-antibodies are considered the markers of disease progression and indicators of diagnosis in SLE. It also saves the kidney from damage in SLE, which leads to the morbidity associated with SLE. ARA-290 is assumed to become the first-ever targeted treatment for SLE.

ROLE OF ARA-290 IN NOCICEPTION

Neuropathic pain caused by diabetic neuropathy is difficult to control and poorly understood in terms of its underlying pathophysiology. However, research has shown that this can be alleviated by suppressing Innate Repair Receptors (IRR) on which ARA-290 can act. This also inhibits TRPV1 channel (Capsaicin receptor) activity, responsible for the perception of burning pain associated with neuropathy.

Small nerve fiber neuropathy associated with several autoimmune diseases such as sarcoidosis, diabetes, and HIV, leads to loss of tiny nerve fibers and ultimately severe neuropathic burning pain. Studies have shown the treatment with ARA-290 to increase these fibers and significantly control pain.

This attribute of neuropathic pain modulation of ARA-290 is of primary interest and is under phase 3 of clinical trials.

 

Disclaimer: The products mentioned are not for human or animal consumption. All the information shared in this article is for educational purposes only.

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Kisspeptin-10: The Promising Elixir

Kisspeptin-10: The Promising Elixir

Kisspeptin-10 is a newly identified peptide named after the famous chocolate ‘Kisses.’ It is derived from the Kiss-1 gene, which is transcribed into the kiss-1 protein before it is finally transformed into Kisspeptin-10. It is mainly synthesized by two clusters of neuronal cell bodies located in the hypothalamus and produced by neurons in the arcuate nucleus in the brain. These are involved in the negative feedback mechanism by which the gonadotropin-releasing hormone Luteinizing hormone (GnRH/LH) pulse is regulated by testosterone. However, it is produced in other parts of the body.

Kisspeptin-10 regulates several hormone-controlled activities in the body.
It plays a significant role in regulating the hypothalamo-pituitary-gonadal axis, and by doing so, is essential in pubarche (the onset of puberty). It also plays a role in the female reproductive cycle through negative feedback control of gonadotropin-releasing hormone by estrogen and other steroids.

Kisspeptin-10 has several effects on the body, which are discussed below.

Effects of Kisspeptin-10

Reduction in Body Fat
Kisspeptin-10 has been proven to reduce the amount of fat in the body by decreasing the formation and maturation of adipocytes (fat cells). It limits the formation of adipocytes by decreasing the expression of the PPAR-y and CEBP- beta genes, which are involved in both the construction and differentiation of adipocytes.
Kisspeptin-10 affects the formation of fat cells and the breakdown of the cells already formed. It enhances the expression of perilipin and hormone-sensitive lipase, which is the enzyme involved in the breakdown of fat cells.
It also helps to reduce body fat by stimulating leptin, a hormone produced by the adipocytes. Leptin regulates energy balance by suppressing food intake through signals sent to the hypothalamus. When food intake is stopped, the body fat reservoir is utilized, and more fat cells are broken down.

Build Up of Bones
Kisspeptin-10 (KP-10) helps to activate bone-forming cells known as osteoblasts. It does this by increasing the genetic expression of osteo-genes such as the bone morphogenetic protein 2 (BMP2) genes.
Kisspeptin-10 is also involved in activating several transcription factors involved in osteoblasts’ activation. These transcription factors include Runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP), and distal–less homeobox 5 (Dlx5). The activated osteoblasts then form bone cells (osteocytes). Once osteocytes undergo maturation and differentiation, they can then lead to an increase in bone matrix formation and bone mineral density.

Control of Fertility
Kisspeptin-10 is important in regulating the hypothalamo-pituitary-gonadal (HPG) axis, which produces and regulates gonadal hormones like testosterone and estrogen. These hormones are essential for infertility, and they are responsible for the secondary sexual characteristics that accompany puberty.
In the HPG axis, the hypothalamus secretes gonadotropin-releasing hormone (GnRH), which stimulates the pituitary gland to produce gonadotropins (Luteinizing hormone and follicle-stimulating hormone). Luteinizing hormone then stimulates the production of testosterone, while follicle-stimulating hormone stimulates the production of estrogen.
Since 2005, Kisspeptin-10 has been the most significant activator of the HPG axis. Lack of Kisspeptin-10 can weaken fertility and sexual development. In a study, the administration of Kisspeptin-10 induced the rats’ maturation while the administration of its antagonist delayed their maturation.

Potential Neuronal Regeneration
Gonadotropin-releasing hormone (GnRH) has been studied to have demonstrated neuroprotective and neuro-regenerative actions. The widespread incidence of GnRH and GnRH immune-reactive neurons in the cerebral cortex suggest that GnRH can be a neuromodulatory peptide. Immunohistochemistry studies also reveal the presence of a GnRH receptor and messenger RNA in the cerebral cortical neurons of rats’ embryos and adult rats.
Kisspeptin-10 stimulates and regulates the production of GnRH and can be beneficial in patients with brain trauma and spinal cord injuries.

Kisspeptin-10 and Olfaction

Olfaction has a vital role to play in mammalian reproduction. Recent studies have shown that Kisspeptin-10 is present in the amygdala, the central structure in the olfactory system. Immunochemistry also revealed a close relationship between amygdala neurons containing Kisspeptin-10 and dopaminergic neurons, indicating the importance of Kisspeptin-10 in social behaviors like reward, motivation, and appreciation.
A study revealed that male mice injected with Kisspeptin-10 spent most of their time sniffing female mice. In contrast, those injected with testosterone did not investigate females preferentially over males.

Conclusion

Kisspeptin-10 is a unique peptide that plays several essential roles in the body, especially in the reproductive system. Its potential usefulness in the regeneration of neurons makes it a peptide that stands out from others and can be an elixir of life in the future.

 

Disclaimer: The products mentioned are not for human or animal consumption. All the information shared in this article is for educational purposes only.

Role of Copper Peptide in the Improvement of the Growth of Hair Follicle

Copper Peptide is formed as a result of the affinity of the human peptide, GHK (glycyl-L-histidyl-L-lysine) to the Cu(2+) (Copper 2+). In the human body, the Copper Peptide has varied roles like collagen stimulation, anti-inflammatory, and anti-oxidant effects,...

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BPC 157: The Next Delivery Weapon Against COVID-19?

BPC 157: The Next Delivery Weapon Against COVID-19?

BPC 157 is the new hope in the fight against Covid-19. It is a peptide that has demonstrated anti-inflammatory, anti-viral, and cytoprotective effects in several organs in the body.

The Covid-19 pandemic has ravaged the world for quite some years now. Several lives have been claimed, the economy of several nations devastated, and technological advancement has been halted due to this deadly virus. The estimated number of patients confirmed to have the disease has exceeded 266,504,411, and about 5,268,849 deaths have been recorded as of 8th of December, 2021, 3.20 pm CET.

Coronaviruses, a group of respiratory viruses, have been identified as the cause of severe acute respiratory syndrome (SARS). The current pandemic is caused by SARS – CoV-2. The SARS-Cov-2 virus enters the host cell through the S-spike protein by binding to ACE-2 for internalization assisted by TMPRSS2 protease. The invasion of the virus to the endothelial cells of the vascular system, the hepatocytes, the myocytes, and the alveoli cells of the lung results in several inflammatory changes due to pro-inflammatory cytokines like IL-6 and TNF-alpha.
This contributes to the pathogenesis of lung injury commonly associated with the disease, decreased immune response, myocytes damage, and gastrointestinal, neurological, and cardiopulmonary adverse changes.

MECHANISM OF ACTION

Usually, endothelial cells produce nitric oxide by the endothelial nitric oxide synthase (eNOS). This maintains vascular homeostasis, regulates cell growth, promotes apoptosis (cell death), and enhances immune function.

Covid-19 infection can lead to loss of eNOS activity leading to decreased nitric oxide; hence the vascular integrity is destroyed, the immune response becomes suboptimal, and finally, multi-organ failure. Reduction in nitric oxide levels also causes thrombosis and hypertension frequently seen in severe cases of Covid-19 due to the lost vascular integrity.
BPC 157 prevents the destruction of eNOS and promotes the production of nitric oxide. By doing so, BPC 157 helps to maintain vascular integrity and prevent the decrease in immune response caused by the SARS- CoV-2 virus.

Furthermore, BPC-157 prevents the virus from replicating, limiting the virus’s spread in the body, reducing thrombus formation. It can be good prophylaxis in disease conditions like atherosclerosis and any other platelet-endothelial dysfunction. It can also mitigate organ damage caused by the virus. This is further elaborated in the next section.

SYSTEMIC APPLICATION OF BPC 157

BPC 157 acts on specific crucial organs in the body. It protects the brain, the heart, the liver, and the lungs from the adverse effect of the SARS-CoV 2 virus.

BPC 157 NEUROPROTECTIVE ACTIONS

Covid-19 causes inflammation of the brain parenchyma, characterized by infiltration of lymphocytes into the brain and increased blood-brain barrier permeability. It can also damage the brain by reducing blood flow to the brain or disturbing the vascular integrity of the cerebral blood vessels and can even attack the neurons directly.

The resultant sequelae are stroke, loss of smell and taste, loss of consciousness, lack of concentration, headaches, seizures, and even Guillain-Barre syndrome.
BPC 157 can counteract these adverse effects by the following mechanisms based on previous effects in other experiments.

● BPC 157 promotes hippocampal neuron survival and growth.
● Studies have shown that it reduces the damage induced by brain trauma from cuprizone.
● BPC 157 decreased pro-inflammatory gene Cox-2 expression in rat brain lesions.
● It has been proven to be helpful in encephalopathy from alcohol usage and NSAIDs.
Though it is yet to be used in Covid-19 patients, it carries great potential in the management of encephalopathy as well.

BPC 157 CARDIOPROTECTIVE ACTIONS

This is the aspect where BPC 157 has the most promising effects. It prevents the disruption of the vascular integrity and the destruction of myocardial cells by the SARS-CoV 2 virus.
Recent experiments revealed BPC 157 actions on the cardiovascular system, which include:
● BPC 157 reduced the duration of arrhythmias during hypoxia and reoxygenation.
● It can be used to treat and prevent hypertension.
● It prevents pulmonary interstitial edema.
It can be therapeutic for cardiovascular disorders like thromboembolism, coagulopathies, arrhythmias, and pulmonary embolism. It is also helpful in the management of acute respiratory distress syndrome.

ACTION OF BPC 157 ON OTHER ORGANS

In an experiment, rats were subjected to congestive heart failure. Due to this, their serum liver enzymes like alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase were raised, suggesting liver damage.
The rats were then administered BPC 157 for four weeks, and the raised liver enzymes showed a considerable decrease.

BPC 157, based on its proven beneficial effects in other experiments, offers the world a new hope in the fight against the deadly Covid-19 virus. Scientists and medical practitioners worldwide need to pay more attention to this peptide.

 

Disclaimer: The products mentioned are not for human or animal consumption. All the information shared in this article is for educational purposes only.

Role of Copper Peptide in the Improvement of the Growth of Hair Follicle

Copper Peptide is formed as a result of the affinity of the human peptide, GHK (glycyl-L-histidyl-L-lysine) to the Cu(2+) (Copper 2+). In the human body, the Copper Peptide has varied roles like collagen stimulation, anti-inflammatory, and anti-oxidant effects,...

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Epitalon is a peptide that has been majorly studied with respect to its anti-aging influence. The findings have been restricted to animal studies. Hence the efficacy of the molecule in humans is subject to conjecture. The molecule has been shown to reverse the aging...

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What is Thymosin Alpha 1 (Tα1)?

What is Thymosin Alpha 1 (Tα1)?

Thymosin Alpha 1 (Tα1) is a peptide naturally produced by the thymus gland. A pleiotropic peptide stimulates or downregulates inflammation and immune function depending on the host’s state.

What is the Structure of Thymosin Alpha 1 (Tα1)?

Tα1 contains 28 amino acids with a molecular weight of 3KDa, and it is stable at 80–90 °C. The amino acid residues are N-terminally acetylated and proteolytically processed from prothymosin alpha. It was first isolated by Goldstein and coworkers from thymosin fraction 5 derived from calf thymus tissues. The amino acid sequence is as follows:
Ac-Ser-Asp-Ala-Ala-Val-Asp-Thr-Ser-Ser-Glu-Ile-Thr-Thr-Lys-Asp-Leu-Lys-Glu-Lys-Lys-Glu-Val-Val-Glu-Glu-Ala-Glu-Asn-OH

What are the Biological Activities of Thymosin Alpha 1 (Tα1)?

Immunoregulation
Several in vivo and in vitro studies have demonstrated the immune regulating potential of Thymosin Alpha 1 peptide. Tα1 assists in:

● Maturation of T-cells and converts precursor cells into differentiated and mature CD4+ and CD8+ T cells.
● Balancing the levels of CD3/CD4+/CD8+ T cells in the peripheral blood.
● Stimulating the action of Natural Killer (NK) cells and cytotoxic lymphocytes leads to the death of virally infected cells.
● Activating dendritic cells has been proven to reduce mortality in mice infected with aspergillosis.
● Regulating the levels of immune cytokines, such as increasing the levels of IL-2 and decreasing the levels of IL-4, IL-10, and IL-1B.

Antitumor Effects
Tα1 has been shown to reduce tumor cell proliferation in various in vivo and in vitro studies. The tumor models shown to be effective include primary hepatocarcinoma, primary lung adenocarcinoma, breast adenomas, glioblastoma, colorectal cancer, and metastatic spread to the liver and lungs. The antitumor effects of Tα1 are due to its ability to include apoptosis and its impact on a variety of inflammation, immune, and oxidative responses.

Antioxidant Effects
Tα1 reduces oxidative stress by increasing the activity of antioxidants such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). It also reduces molecules responsible for producing free radicals such as malondialdehyde (MDA).

Other Effects
Other biological effects of Tα1 include:
● It has neuro-excitatory effects, and its effect on excitatory transmission in hippocampal neurons has been demonstrated.
● When combined with chemotherapy, it can prevent chemotherapy-included neurotoxicosis.
● It can stimulate endothelial cell migration and angiogenesis. These effects might have some implications in promoting wound healing.
● Due to its immune regulating, anti-inflammatory, and antioxidant effects, the use of Tα1 might be useful in various autoimmune and inflammatory conditions. Such conditions include cystic fibrosis, Lyme disease, and even COVID.

Clinical Applications of Thymosin Alpha 1 (Tα1)?

Tα1 have clinical applications in the following areas:

Cancer Therapy
In a phase II multi-center, randomized open-label study, a combination of Dacarbazine (DTIC) and different doses of Tα1 was given to patients with stage IV melanoma. Results showed that the therapy tripled the response rate and improved the overall survival by three months. Similarly, when combined with transarterial chemoembolization (TACE), the use of Tα1 significantly improved the treatment response and survival rates in patients with unresectable hepatocellular carcinoma.

Hepatitis B Treatment
Tα1 has been approved as a monotherapy for the treatment of hepatitis B in many countries. In Japanese research, giving Tα1 to hepatitis B positive patients lead to seroconversion in up to 21.5% of patients with 48 weeks of therapy. Similarly, in a Chinese patient, Tα1 treatment led to complete remission, defined by normalization of alanine transaminase (ALT) and undetectable HBV DNA, in up to 42.3% of patients.

Hepatitis C Treatment
Tα1 is not effective as a monotherapy for hepatitis C treatment. However, the response rate can increase significantly when used in combination with peg-IFN and ribavirin therapy. HCV is a resistant infection, and even with dual peg-IFN and ribavirin therapy, the response rate can be as low as 50%. Therefore, T might be an effective adjuvant for hepatitis C management.

HIV/AIDS Treatment
The human immunodeficiency virus (HIV) targets body cells that express CD4, such as CD4+ lymphocytes and macrophages. Once the virus develops an affinity for lymphocytes (lymphotropic), it becomes highly efficient in targeting new CD4+ cells and becomes highly virulent. A solid immune response might be one way to prevent the infection and onset of HIV infection. In one study, triple therapy with IFN-α, zidovudine, and T significantly improved CD4+ function and low levels of HIV viral infections.

Summary

Thymosin Alpha 1 (Tα1) is a pleiotropic peptide with various immune-modulating, anti-inflammatory, anti-viral, antioxidant, and antitumor effects. Its potential use in health and disease warrants rigorous clinical research.

 

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Role of Copper Peptide in the Improvement of the Growth of Hair Follicle

Copper Peptide is formed as a result of the affinity of the human peptide, GHK (glycyl-L-histidyl-L-lysine) to the Cu(2+) (Copper 2+). In the human body, the Copper Peptide has varied roles like collagen stimulation, anti-inflammatory, and anti-oxidant effects,...

How does Epitalon reverse aging?

Epitalon is a peptide that has been majorly studied with respect to its anti-aging influence. The findings have been restricted to animal studies. Hence the efficacy of the molecule in humans is subject to conjecture. The molecule has been shown to reverse the aging...

Unique Effect of Sermorelin on Sleep

What is Sermorelin peptide? Sermorelin peptide is a synthetic analog of the naturally occurring growth hormone-releasing hormone (GHRH). GHRH is a 44 amino acid long peptide, and Sermorelin peptide comprises the first 29 amino acids. The shortened peptide is...