Seraspenide, also known as goralatide, is an endogenous tetrapeptide with significant biological activity, widely distributed in various tissues and body fluids. It is hydrolyzed by its precursor thymosin β 4 by prolyl oligopeptidase (POP). The concentration of goratide in the blood is usually within the nanomolar range.
In terms of pharmacokinetics, goralatide is quickly degraded after intravenous administration, with a half-life of only 4 to 5 minutes. It is eliminated from the plasma through two main mechanisms: angiotensin-converting enzyme (ACE)-mediated hydrolysis and glomerular filtration. Among these, ACE-mediated hydrolysis is the primary pathway for goralatide metabolism.
AC-SER-ASP-LYS-PRO-OH is a multifunctional physiological regulator that possesses various biological activities. Early studies showed that goralatide could inhibit the activity of hematopoietic stem cells by preventing them from entering the S phase and keeping them in the G0 phase. More recently, it has been discovered that goralatide can enhance epidermal re-implantation ability and accelerate wound healing in damaged avascular epidermal grafts by promoting angiogenesis. Additionally, goralatide can inhibit the differentiation of bone marrow stem cells into macrophages stimulated by macrophage growth medium (MGM), thus exhibiting anti-inflammatory effects.
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Customized Bottle Caps And Corks:
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Chemical Formula |
C20H33N5O9 |
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Exact Mass |
487.23 |
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Molecular Weight |
487.51 |
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m/z |
487.23 (100.0%), 488.23 (21.6%), 489.23 (2.2%), 489.23 (1.8%), 488.22 (1.8%) |
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Elemental Analysis |
C, 49.27; H, 6.82; N, 14.37; O, 29.54 |
Seraspenide is a bioactive peptide extracted by researchers from the body of gorillas.
1. Antioxidant effect: It has been found to have significant antioxidant activity, which helps to eliminate free radicals and reduce the damage of oxidative stress to cells. This antioxidant effect may help prevent or alleviate diseases related to oxidative stress, such as cardiovascular disease, cancer, and neurodegenerative diseases.
2. Anti inflammatory effect: It may have anti-inflammatory effects, helping to regulate the immune system's response and reduce inflammation. This may have significant implications for the treatment of inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, and asthma.
3. Immunomodulatory effect: It may regulate the activity of the immune system and enhance the body's ability to resist pathogens and diseases. This may be of great significance for improving immune function, preventing infections and autoimmune diseases.
4. Growth promoting effect: It may have a growth promoting effect, helping to promote cell proliferation and tissue repair, accelerating wound healing and fracture healing processes. This may have potential clinical applications for treating trauma, postoperative recovery, and bone related diseases.
5. Neuroprotective effects: may help protect the nervous system from damage and degradation, slowing down the progression of neurodegenerative diseases such as Alzheimer's and Parkinson's disease. This may be achieved through mechanisms such as reducing oxidative stress, inhibiting neuronal apoptosis, and promoting neuronal regeneration.
6. Antibacterial effect: It may have antibacterial activity and help inhibit the growth and reproduction of bacteria, fungi, and viruses. This may be of great significance for the treatment of infectious diseases, such as bacterial infection, fungal infection and viral infection.
7. Antitumor effect: Some preliminary studies have shown that it may have anti-tumor activity, which can inhibit the proliferation and metastasis of tumor cells, and induce tumor cell apoptosis. This provides potential targets and strategies for developing new anti-tumor drugs
There is currently no publicly available literature on the biosynthesis methods of seraspenide for reference. As a relatively new bioactive peptide, its biosynthesis method may require further experimental research and development to draw accurate conclusions.
Generally speaking, the methods for biosynthesis of peptides typically involve genetic engineering and fermentation techniques. Specifically, the biosynthesis of galactide may involve the following steps:
Gene design and cloning: Firstly, it is necessary to design and synthesize a gene sequence that contains the encoding of Goreira peptide. This gene sequence can be designed based on the amino acid sequence of Gorelelutide, typically including messenger RNA (mRNA) coding sequences and appropriate regulatory sequences such as promoters and terminators. Then, clone this gene sequence into an appropriate expression vector for expression in host ce
Host selection: Select suitable host cells for the expression of Goreletin. Common hosts include Escherichia coli, yeast, fungi, or mammalian cells. When selecting host cells, factors such as their expression ability, growth characteristics, and stability in synthesizing target proteins need to be considered.
Transformation and expression: Import an expression vector containing the Goreletin gene into host cells and use appropriate transformation techniques to express it. In general, transformed cells will grow and express target proteins under appropriate culture conditions.
Fermentation production: Utilizing fermentation technology, large-scale cultivation and production of host cells containing the Goreletin gene are carried out. This may involve optimizing the composition of the culture medium, culture conditions (such as temperature, pH, oxygen supply, etc.), fermentation time, and other parameters to obtain high yield and purity of Goreira peptide.
Purification and Separation: By using appropriate purification techniques, extract and purify Goreira peptide from fermentation culture. Common purification methods include affinity chromatography, ion exchange chromatography, gel filtration chromatography, countercurrent chromatography, ultrafiltration and other technologies.
Structure and activity analysis: Perform structural analysis and activity testing on the purified Goreira peptide, including mass spectrometry analysis, amino acid sequence analysis, secondary structure analysis, biological activity testing, etc., to determine its purity and biological activity.
AC-SER-ASP-LYS-PRO-OH is a bioactive peptide with potential medicinal value, so it is crucial to study its pharmacokinetics. Pharmacokinetic studies typically include processes such as drug absorption, distribution, metabolism, and excretion in the body, as well as interactions between drugs and related molecules in the organism. However, there may still be relatively few studies on its pharmacokinetics, as the study of Gorelenide, as a novel bioactive peptide, is still in its early stages.
1. Absorption: Absorption usually occurs in the digestive tract and can be administered orally or by injection. The speed and degree of absorption may be influenced by various factors, such as drug form, route of administration, and intestinal absorption conditions.
2. Distribution: The distribution within the body is influenced by biological barriers and tissue specificity. It may be distributed to various tissues and organs in the bloodstream, and may have specific affinity in some tissues.
3. Metabolism: It may undergo metabolic processes in the body, including enzyme mediated degradation and modification. The properties and metabolic pathways of metabolites may affect the pharmacological and pharmacokinetic properties of Gorelelutide.
4. Excretion: Excretion is usually carried out through the kidneys and/or liver, and may be excreted from the body in the form of urine and/or feces. The excretion rate and pathway may be influenced by various factors, including kidney function, liver function, etc.
5. Drug interactions: May interact with other molecules in the body (such as receptors, proteins, etc.), affecting their pharmacological and pharmacokinetic properties. These interactions may affect the absorption, distribution, metabolism, and excretion processes of Goreletin.
Effect on cardiac fibrosis
1.Inhibit the proliferation of cardiac fibroblasts and collagen synthesis
It can inhibit the proliferation of cardiac fibroblasts and reduce collagen deposition in the heart and kidneys. By upregulating the activity or expression of matrix metalloproteinases (MMPs), it has a significant inhibitory effect on platelet-derived growth factor mediated collagen synthesis in cardiac fibroblasts.
2.Anti-inflammatory effect
It can inhibit TNF - α - induced ICAM-1 expression, monocyte/macrophage infiltration, and inflammatory response in endothelial cells, thereby reducing cardiac fibrosis.
3.Inhibit collagen deposition
It inhibits collagen deposition in target organs through regulation of the signal transduction system, reducing the degree of organ fibrosis caused by pathogenic factors.
4.Improve heart function
Under the condition of acute myocardial infarction with heart failure, it is possible to reduce the total collagen content, decrease macrophage infiltration and the number of TGF - β - positive expression cells, prevent and reverse myocardial fibrosis (reactive fibrosis) in non infarcted areas, and improve cardiac function
5.Reduce heart rupture and mortality after myocardial infarction
It can significantly reduce the incidence and mortality of heart rupture; It reduces the exudation of pro-inflammatory M1 macrophages in cardiac tissue after myocardial infarction, but does not affect the exudation of pro-inflammatory M2 macrophages and neutrophils. The mechanism by which it prevents heart rupture and reduces mortality after acute myocardial infarction is related to the reduction of pro-inflammatory M1 macrophage infiltration and MMP-9 activation.
6.Inhibition of collagen production stimulated by endoplasmic reticulum stress
Weakening endoplasmic reticulum stress-induced collagen production in cardiac fibroblasts by inhibiting CHOP mediated NF - κ B expression.
7.Improving ventricular remodeling after myocardial infarction
The Ac SDKP isoform exerts anti fibrotic effects by inhibiting macrophage bypass activation (M2) in infarcted myocardium, reducing the secretion of a series of molecules such as TGF - β 1, ARG I, and collagen I, thereby improving ventricular remodeling.
What is the difference between this substance and ACE inhibitors?
1. Chemical structure
- Gorelatide: also known as N-acetyl-serine-asparte-lysine-proline - (N-acetyl-Ser-Asp-Lys-Pro), abbreviated as Ac-S-D-K-P. It is an endogenous tetrapeptide with N-terminal acetylation, and its chemical structure contains amino acid residues such as acetyl, serine, aspartic acid, lysine, and proline.
- ACE inhibitors, also known as angiotensin-converting enzyme inhibitors, are a major category of antihypertensive drugs. These types of drugs have diverse structures, but the common feature is their ability to inhibit the activity of angiotensin-converting enzyme (ACE). The specific chemical structure of ACE inhibitors varies depending on the type of drug, but typically contains functional groups that can bind to ACE and inhibit its activity.
2.Mechanism of action
- Gorelatide: It is mainly cleared from the plasma of the human body through two mechanisms: one is the hydrolysis guided by angiotensin-converting enzyme (ACE); The second is glomerular filtration. Among them, ACE mediated hydrolysis is the main pathway for the metabolism of golelatide. Golelatide has various biological activities, including inhibiting the activity of hematopoietic stem cells, promoting angiogenesis, improving epidermal replantation ability, accelerating wound healing in damaged avascular epidermal transplantation, inhibiting the differentiation of bone marrow stem cells into macrophages stimulated by MGM (anti-inflammatory effect), and inhibiting the proliferation of various cells.
- ACE inhibitors: mainly reduce the production of angiotensin II by inhibiting the activity of angiotensin-converting enzyme (ACE), thereby dilating blood vessels and lowering blood pressure. ACE is a key enzyme in the renin-angiotensin system that can convert angiotensin I into angiotensin II, which has strong vasoconstriction and stimulates the release of aldosterone from the adrenal cortex. ACE inhibitors can also improve the function of endothelial cells and blood vessels, promote vasodilation and blood circulation, and potentially improve erectile function.
Synthesis Methods
Solid-Phase Peptide Synthesis (SPPS)
The primary method for seraspenide production is SPPS, a cornerstone of peptide chemistry. The process involves:
Resin Attachment: The C-terminal proline is anchored to a solid support (e.g., Wang resin) via its carboxyl group.
Stepwise Elongation: Amino acids are sequentially added using Fmoc (9-fluorenylmethoxycarbonyl) or Boc (tert-butyloxycarbonyl) protecting groups, with coupling agents like HATU or DIC/HOBt facilitating amide bond formation.
Acetylation: The N-terminal serine is acetylated post-elongation to yield Ac-Ser.
Cleavage and Deprotection: The peptide is released from the resin using trifluoroacetic acid (TFA), removing side-chain protecting groups.
Purification: Reverse-phase high-performance liquid chromatography (RP-HPLC) isolates seraspenide with >95% purity.
Challenges in Synthesis
Racemization: Lysine's ε-amino group can undergo epimerization during coupling, necessitating careful control of pH and temperature.
Aggregation: Hydrophobic interactions between proline and lysine residues may cause peptide aggregation, reducing yields.
Cost: High reagent expenses and low yields (typically 20–40%) increase production costs.
Emerging Alternatives
Enzymatic Synthesis: Transpeptidases or subtilisin variants are being explored for greener, more selective peptide assembly.
Continuous Flow Chemistry: Microfluidic devices enable precise control over reaction conditions, improving scalability.
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