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Goralatide is a naturally occurring tetrapeptide, with the chemical name N-acetyl-ser-Asp-Lys-Pro, abbreviated as Ac-S-D-K-P. Its molecular formula is C20H33N5O9, with a molecular weight accurate to 487.5041 daltons, and the CAS accession number is 127103-11-1. The molecule undergoes N-terminal acetylation modification to form a linear peptide structure with a specific spatial conformation. The serine, aspartic acid, lysine, and proline residues in its amino acid sequence are connected by peptide bonds, forming a mixed conformation of β - angle and α - helix in the secondary structure. This structural feature endows it with high affinity binding ability to specific enzymes, such as angiotensin-converting enzyme ACE.
In terms of physical and chemical properties, it appears as a white to off white solid with a density of 1.4 ± 0.1 g/cm ³, a boiling point of 992.0 ± 65.0 ° C (760 mmHg), and a flash point of 553.7 ± 34.3 ° C. Its solubility data shows that the molecule has a solubility of 2 mg/ml in water, and higher solubility in organic solvents such as dichloromethane and N, N-dimethylformamide. This dissolution characteristic requires the use of a water-based buffer system in the development of its formulation, and requires low-temperature storage conditions (-20 ℃) to maintain stability. Its powder form can be stably stored for 1 year, and its solution form can maintain activity for 7 days at 4 ℃.
Our product
Ceftiofur+. COA
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Certificate of Analysis |
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Compound name |
Goralatide | |
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CAS No. |
127103-11-1 | |
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Grade |
Pharmaceutical grade | |
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Quantity |
Customized | |
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Packaging standard |
Customized | |
| Manufacturer | Shaanxi BLOOM TECH Co., Ltd | |
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Lot No. |
20250109001 |
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MFG |
Jan 12th 2025 |
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EXP |
Jan 8th 2029 |
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Structure |
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| TEST STANDARD | GB/T24768-2009 Industry. Stnndard | |
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Item |
Enterprise standard |
Analysis result |
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Appearance |
White or almost white powder |
Conformed |
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Water content |
≤4.5% |
0.30% |
| Loss on drying |
≤1.0% |
0.15% |
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Heavy Metals |
Pb≤0.5ppm |
N.D. |
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As≤0.5ppm |
N.D. | |
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Hg≤0.5ppm |
N.D. | |
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Cd≤0.5ppm |
N.D. | |
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Purity (HPLC) |
≥99.0% |
99.5% |
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Single impurity |
<0.8% |
0.48% |
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Residue on ignition |
<0.20% |
0.064% |
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Total microbial count |
≤750cfu/g |
80 |
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E. Coli |
≤2MPN/g |
N.D. |
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Salmonella |
N.D. | N.D. |
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Ethanol (by GC) |
≤5000ppm |
400ppm |
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Storage |
Store in a sealed, dark and dry place at-20 degrees |
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Metabolic pathways and pharmacokinetic characteristics
1. Metabolic mechanism in vivo
Metabolic studies reveal that it achieves rapid degradation through a dual pathway clearance mechanism:
Enzymatic pathway: Angiotensin converting enzyme (ACE), as the main metabolic enzyme, specifically hydrolyzes the N-terminal acetylserine aspartate bond of golelatide, generating inactive metabolites;
Renal excretion: Unenzymatically hydrolyzed molecules are excreted from the body through glomerular filtration, with a filtration threshold of approximately 60 kDa protein.
In human pharmacokinetic experiments, after intravenous injection of golelatide, its plasma half-life is only 4-5 minutes, and the clearance rate is as high as 1200 ml/min/kg, indicating that the molecule has a very high in vivo metabolic rate. Its apparent distribution volume (Vd) is 0.5 L/kg, indicating limited tissue distribution, mainly confined to the intravascular space.
2. Metabolites and toxicity
Enzymatic metabolites include N-acetylserine, aspartic acid, lysine, and proline, all of which are endogenous amino acids and pose no toxic risks. Acute toxicity studies showed that the maximum tolerated dose (MTD) for a single intravenous injection in rats was 50 mg/kg, and no death or significant organ damage was observed. Long term toxicity study (28 days) confirmed that at a daily dose of 10 mg/kg, pathological examination of major organs (heart, liver, kidney) showed no abnormalities, and blood biochemical indicators (ALT, AST, Cr, BUN) were within normal range.
Formulation development and administration strategy
Delivery system optimization
The current research focuses on delivery strategies that prolong the in vivo action time of golelatide due to its rapid metabolic characteristics
Nanocarrier: Nanoparticles prepared using poly (lactic acid glycolic acid) copolymer (PLGA) can extend the half-life of golelatide to 24 hours and achieve targeted delivery (such as in the heart or kidneys);
Prodrug modification: By esterification or amidation reaction, golelatide is coupled with a macromolecular carrier (such as human serum albumin) to form a prodrug, which slowly releases the active molecule after enzymatic hydrolysis in vivo.
Administration route and dosage
In animal experiments, the administration routes of goralatide include intravenous injection, subcutaneous injection, and local application. For cardiac protection applications, the intravenous injection dose is 1 mg/kg, once a day; For wound healing applications, the local application dose is 0.1 mg/cm ², twice a day. Dose optimization studies have shown that the efficacy of golelatide is dose-dependent, but no additional benefits were observed beyond 10 mg/kg, and there may be an increased risk of bleeding.
Research on the cardioprotective effect
1. Validation of myocardial infarction model
In animal models of myocardial infarction (MI), cardiac protection is achieved by inhibiting myocardial cell apoptosis and promoting angiogenesis. After coronary artery ligation in rats, continuous intraperitoneal injection of golelatide (0.5 mg/kg/d) for 7 days can reduce the infarct area by 28% -32% and increase the left ventricular ejection fraction (LVEF) by 12% -15%. Mechanism studies have shown that this molecule inhibits caspase-3 activity and reduces cardiomyocyte apoptosis by activating the PI3K/Akt pathway; Simultaneously upregulating VEGF-A expression promotes a 40% -45% increase in CD31+vascular density and improves myocardial perfusion.
2. Inhibition of cardiac fibrosis
In the stress overload induced cardiac remodeling model, myocardial fibrosis can be significantly reduced. Four weeks after aortic constriction surgery in mice, Masson staining in the intervention group (1 mg/kg/d) showed a 55% -60% reduction in collagen deposition and a 65% -70% decrease in the number of α - SMA positive myofibroblasts. Its anti fibrotic mechanism involves inhibiting the TGF - β 1/Smad3 signaling pathway, reducing phosphorylated Smad3 levels by 70% -75%, and promoting MMP-2/MMP-9 expression, accelerating extracellular matrix degradation.
Research on the renal protective effect
1. diabetes nephropathy model
In the model of streptozotocin (STZ) - induced diabetes nephropathy, galatide protects renal function through anti-inflammatory and anti fibrosis mechanisms. Continuous intraperitoneal injection of goralatide (0.3 mg/kg/d) for 8 weeks in rats can reduce 24-hour urinary protein excretion rate by 40% -45% and blood creatinine levels by 30% -35%. Pathological examination showed a 55% -60% decrease in glomerular sclerosis index and a 60% -65% decrease in interstitial fibrosis area. Its mechanism of action includes:
Anti inflammatory: Inhibit the NF - κ B pathway and reduce the expression of TNF - α and IL-6 in renal tissue;
Anti fibrosis: Downregulate the expression of CTGF and Collagen IV, and inhibit epithelial mesenchymal transition (EMT).
2. Unilateral ureteral obstruction (UUO) model
In the UUO induced renal interstitial fibrosis model, golelatide can alleviate renal tubular injury and fibrosis. Starting from the 7th day after surgery, rats were intraperitoneally injected with golelatide (0.5 mg/kg/d). After 14 days, the fibrotic area of the obstructed kidney decreased by 50% -55%, and the infiltration of inflammatory cells (CD68+macrophages) decreased by 60% -65%. Mechanism studies have shown that golelatide inhibits the TGF - β 1/Smad2/3 signaling pathway, leading to a 65% -70% decrease in phosphorylated Smad2/3 levels and promoting Smad7 expression, forming a negative feedback regulation.
Research on promoting wound healing
1. Full layer skin defect model
In a rat model of full-thickness skin defects, golelatide accelerates wound healing by promoting re epithelialization and angiogenesis. Postoperative local application of golelatide (0.1 mg/cm ²) can shorten wound closure time by 40% -45% and increase re epithelialization rate by 50% -55%. Immunohistochemical analysis showed that the number of Ki-67 positive keratinocytes in wound tissue increased by 60% -65%, and CD31+vascular density increased by 70% -75%. The mechanism involves:
Promote cell migration: upregulate E-cadherin expression and enhance intercellular adhesion;
Angiogenesis: Activate the VEGFR2/ERK1/2 pathway to promote endothelial cell lumen formation.
2. diabetes foot ulcer model
In the plantar ulcer model of diabetes db/db mice, galatide can improve the healing quality. Local injection of golelatide (0.2 mg/cm ²) after ulcer formation resulted in a 60% -65% reduction in ulcer area and a 40% -45% reduction in scar formation after 14 days. Mechanism studies have shown that golelatide promotes wound tissue normalization by inhibiting the TGF - β 1/Smad3 signaling pathway, reducing the Collagen I/III ratio.
Research on anti-inflammatory and immune regulation
1. Inflammatory bowel disease model
In a mouse colitis model induced by dextran sulfate sodium (DSS), golelatide reduces inflammation by regulating immune cell differentiation. Oral administration of Gorelatide (5 mg/kg/d) during DSS treatment can reduce the Disease Activity Index (DAI) by 50% -55% and the colon length shortening rate by 40% -45%. Flow cytometry analysis showed that the proportion of M1 macrophages (CD11b+F4/80+iNOS+) in colon tissue decreased by 60% -65%, while the proportion of M2 macrophages (CD11b+F4/80+Arg1+) increased by 55% -60%. The mechanism involves inhibiting STAT1 phosphorylation, promoting STAT6 activation, and inducing macrophage polarization.
2. Autoimmune encephalomyelitis (EAE) model
In the EAE mouse model, golelatide can inhibit central nervous system inflammation. Starting from the 7th day after immunization with MOG35-55, intraperitoneal injection of golaglutide (1 mg/kg/d) was administered. After 21 days, the clinical score decreased by 55% -60%, and the demyelination area of the spinal cord decreased by 60% -65%. Immunohistochemical analysis showed that CD4+T cell infiltration in spinal cord tissue decreased by 65% -70%, and IL-17A and IFN - γ expression were down regulated by 70% -75%. The mechanism involves inhibiting Th17 cell differentiation and promoting Treg cell generation.
Research on anti-tumor adjuvant therapy
1. breast cancer model
In the 4T1 breast cancer mouse model, gorelatide enhances the chemotherapy effect by inhibiting the polarization of tumor associated macrophages (TAM). Starting from the 7th day after 4T1 cell inoculation, intraperitoneal injection of golelatide (2 mg/kg/d) combined with paclitaxel (10 mg/kg) was administered. After 21 days, the tumor volume decreased by 60% -65%, and the number of lung metastases decreased by 70% -75%. Flow cytometry analysis showed that the proportion of M2 type TAMs (CD11b+F4/80+CD206+) in tumor tissue decreased by 65% -70%, while the proportion of CD8+T cells increased by 55% -60%.
2. Lung cancer model
In the LLC lung cancer mouse model, golelatide can improve the tumor microenvironment. Starting from the 10th day after LLC cell inoculation, intraperitoneal injection of golelatide (1.5 mg/kg/d) was administered. After 28 days, the tumor growth inhibition rate reached 55% -60%, and the tumor blood vessels normalized (the coverage of surrounding cells increased by 60% -65%). Mechanism studies have shown that golelatide reduces tumor vascular leakage and enhances chemotherapy drug delivery efficiency by inhibiting the PDGF-BB/PDGFR β signaling pathway.
By inhibiting the entry of primitive hematopoietic stem cells into the S phase and immobilizing them in the G0 phase, negative regulation of hematopoietic activity is achieved. In vitro experiments have shown that this molecule can reduce the number of hematopoietic stem cell colony forming units (CFU) by 60% without inducing cell apoptosis. Mechanism studies have shown that by blocking the signal transduction of stem cell specific proliferation stimuli such as SCF and TPO, the expression of Cyclin D1 and CDK4/6 is inhibited, thereby blocking the cell cycle progression.
Significant promotion of angiogenesis can be achieved at nanomolar concentrations. In the chicken embryo chorioallantoic membrane (CAM) model, the treatment group showed an 80% increase in vascular density and functional integrity of neovascularization. Mechanism studies reveal that it promotes endothelial cell migration and luminal formation by activating the VEGFR2/PI3K/Akt pathway in endothelial cells. In addition, upregulation of matrix metalloproteinase-1 (MMP-1) expression can promote extracellular matrix remodeling and provide physical space for angiogenesis.
By inhibiting the differentiation of bone marrow stem cells into macrophages, it exerts anti-inflammatory effects. In the LPS induced inflammation model, treatment with this substance can reduce the number of macrophages by 40% and inhibit the secretion of pro-inflammatory cytokines (TNF - α, IL-6). Its mechanism of action involves blocking the NF - κ B signaling pathway, inhibiting the degradation of I κ B α, and thus suppressing the nuclear translocation of transcription factor p65.
Has inhibitory effects on fibrosis of multiple organs. In the cardiac fibrosis model, collagen deposition can be reduced by 50% and Smad2/3 phosphorylation induced by transforming growth factor - β 1 (TGF - β 1) can be inhibited. In the renal fibrosis model, this substance can reduce the expression of α - smooth muscle actin (α - SMA) and inhibit the activation of myofibroblasts. Its anti fibrotic mechanism involves inhibiting PDGF receptor signaling, blocking fibroblast proliferation and collagen synthesis.
Goralatide, as a multifunctional physiological regulatory factor, has shown broad prospects in the fields of hematopoietic regulation, angiogenesis, anti-inflammatory immunity, and anti fibrosis through its unique chemical structure and mechanism of action. Although its rapid metabolic characteristics limit clinical applications, optimizing the delivery system and modifying prodrugs can significantly prolong its in vivo action time. Although clinical translation still faces challenges such as dosing frequency and biomarker development, with the deepening of mechanism research and breakthroughs in formulation technology, golelatide is expected to become an innovative therapeutic drug for various diseases such as heart disease, chronic kidney disease, and difficult to heal wounds, providing patients with new treatment options.
It is a remarkable tetrapeptide with multifaceted roles in hematopoiesis, immunoregulation, angiogenesis, and tissue repair. Its ability to modulate stem cell proliferation and protect against cytotoxic insults positions it as a potential therapeutic agent in various medical fields. While challenges remain, ongoing research is paving the way for its clinical application, offering hope for improved treatments in oncology, autoimmunity, and regenerative medicine. As our understanding of Goralatide's biology deepens, so too does the potential to harness its power for human health.
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