Eptifibatide peptide, its molecular weight is 994.19, molecular formula is C35H49N11O9S2, CAS 188627-80-7. It is composed of 9 amino acids and is a disulfide linked cyclic polypeptide with a similar structure to oxytocin, but with modifications made to the positions 1, 2, 4, and 8 on the molecular structure of oxytocin. One cysteine residue undergoes N-terminal deamination to generate 3-mercaptopropionic acid, two L-tyrosine residues are modified to D-tyrosine, ethoxy replaces phenol, four threonine residues replace glutamine, and eight ornithine residues replace leucine.
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Eptifibatide COA
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| Certificate of Analysis | ||
| Compound name | Eptifibatide | |
| Grade | Pharmaceutical grade | |
| CAS No. | 188627-80-7 | |
| Quantity | 70g | |
| Packaging standard | PE bag+Al foil bag | |
| Manufacturer | Shaanxi BLOOM TECH Co., Ltd | |
| Lot No. | 202601090078 | |
| MFG | Jan 9th 2026 | |
| EXP | Jan 8th 2029 | |
| Structure |
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| Item | Enterprise standard | Analysis result |
| Appearance | White or almost white powder | Conformed |
| Water content | ≤5.0% | 0.54% |
| Loss on drying | ≤1.0% | 0.42% |
| Heavy Metals | Pb≤0.5ppm | N.D. |
| As≤0.5ppm | N.D. | |
| Hg≤0.5ppm | N.D. | |
| Cd≤0.5ppm | N.D. | |
| Purity (HPLC) | ≥99.0% | 99.98% |
| Single impurity | <0.8% | 0.52% |
| Total microbial count | ≤750cfu/g | 95 |
| E. Coli | ≤2MPN/g | N.D. |
| Salmonella | N.D. | N.D. |
| Ethanol (by GC) | ≤5000ppm | 500ppm |
| Storage |
Store in a sealed, dark, and dry place below -20°C |
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| Chemical Formula | C35H49N11O9S2 |
| Exact Mass | 831 |
| Molecular Weight | 832 |
| m/z | 831 (100.0%), 832 (37.9%), 833 (9.0%), 833 (7.0%), 832 (4.1%), 834 (3.4%), 833 (1.8%), 832 (1.6%), 833 (1.1%) |
| Elemental Analysis | 831 (100.0%), 832 (37.9%), 833 (9.0%), 833 (7.0%), 832 (4.1%), 834 (3.4%), 833 (1.8%), 832 (1.6%), 833 (1.1%) |
Eptifibatide peptide, as an important antiplatelet drug, plays a crucial role in the treatment of cardiovascular diseases. Its mechanism of action mainly revolves around precise regulation of soterocyte aggregation process, effectively inhibiting thrmbus formation and improving cardiovascular domain by specifically blocking key pathways.
Specific blockade of glycoprotein IIb/IIIa receptor binding to fibrinogen
Soterocyte aggregation is the core process of thrombois, and glycoprotein IIb/IIIa receptors play a crucial role in this process. When the vascular wall is damaged or there is an inflammatory response, the subendothelial collagen tissue is exposed, and soterocytes bind to the collagen tissue through the Ib and IIa/IIIa receptors on their cell membrane glycoproteins, causing soterocyte adhesion. Subsequently, under the influence of some stimulating factors, soterocytes are further activated. The glycoprotein IIb/IIIa receptors on the activated soterocyte surface undergo conformational changes, exposing binding sites to fibrinogen. Fibrinogen, as a bridging molecule, can simultaneously bind to multiple soterocyte glycoprotein IIb/IIIa receptors, causing soterocytes to crosslink and aggregate, forming blood clots.
It is a highly selective glycoprotein IIb/IIIa receptor antagonist that can specifically bind to the glycoprotein IIb/IIIa receptor on the surface of soterocytes, competitively blocking the binding site between fibrinogen and the receptor. This inhibitory effect prevents soterocytes from forming aggregates through fibrinogen bridging, cutting off the critical pathway of soterocyte aggregation from the source. For example, in patients with acute cornary syndrome, cornary artery thrombois is the main cause of myocardial ischemia and even myocardial infarction.
Etriptide effectively inhibits soterocyte aggregation and reduces the risk of thrombois through the aforementioned mechanism, thereby reversing the ischemic state caused by thrombois. Related studies have shown that the inhibitory effect on soterocyte aggregation has the characteristics of rapid onset and reversibility. After intravenous administration, it can quickly reach an effective blood drug concentration, significantly inhibit soterocyte domain within 1 hour, and its effect can last for 2-4 hours. After discontinuation, soterocyte domain can gradually recover, which gives it a unique advantage in clinical situations where rapid antiplatelet action is required and there may be a risk of bleeding.
Information sources: 39Drug Tong, Minfukang, Baidu Baike.
Inhibition of soterocyte activating factor
Soterocyte activating factor is an important inflammatory mediator and soterocyte activator that can induce soterocyte activation, further promoting soterocyte aggregation and thrmbus formation. During the occurrence and development of cardiovascular disease, inflammation and soterocyte activation interact and promote each other, forming a vicious cycle. For example, the instability of atherosclerotic plaque is closely related to local inflammatory response. A variety of cytokines and mediators released by inflammatory cells can activate soterocytes, and activated soterocytes will release more inflammatory mediators, exacerbate inflammatory response, and promote plaque rupture and thrombois.
It can exert its effect by inhibiting soterocyte activation induced by soterocyte activating factor. It can interfere with the binding of soterocyte activating factors to soterocyte surface receptors, thereby blocking signaling pathways and inhibiting soterocyte activation processes. Specifically, intrifiban can inhibit the mobilization of calcium ions in soterocytes, suppress the release of soterocyte particulate matter, and collectively inhibit soterocyte activation and aggregation. For example, during the perioperative period of percutaneous cornary intervention (PCI), catheterization may damage the endothelium of blood vessels, activate soterocytes and coagulation systems, leading to increased release of soterocyte activating factors. The application can effectively inhibit the action of soterocyte activating factor, reduce soterocyte activation, and lower the risk of stent thrombois and other vascular complications.
Source of information: 39 Medicine Tong, Miaoshou Doctor.
Regulating the domain of endothelial cells in blood vessels
The integrity and normal domain of vascular endothelium are important conditions for maintaining smooth vascular walls and unobstructed blood flow. In cardiovascular diseases, endothelial cells are often damaged, leading to endothelial dysfunction. Endothelial dysfunction is characterized by a decrease in vasodilator substances released by endothelial cells, an increase in vasoconstrictor substances, and a decrease in the anti thrombotic ability of endothelial cells, which can easily promote soterocyte aggregation and thrombois.
It has a certain regulatory effect on the domain of vascular endothelial cells. On the one hand, it can stimulate endothelial cell proliferation and promote the repair of damaged blood vessel walls.
When the vascular endothelium is damaged, it can activate the proliferation related signaling pathway of endothelial cells, promote the migration and proliferation of endothelial cells, and help restore the integrity of the vascular endothelium. For example, in patients with cornary atherosclerosis, vascular eptifibatide peptide injury is an important link in the occurrence and development of atherosclerosis. It can reduce the formation and progression of atherosclerotic plaque by promoting endothelial cell repair. On the other hand, it can stimulate endothelial cells to release vasodilators such as nitric oxide (NO). NO is an important endothelial relaxing factor that can diffuse to vascular smooth muscle cells, causing vasodilation, while also inhibiting soterocyte aggregation and adhesion, reducing the risk of thrombois. By regulating endothelial cell domain, improving the diastolic state of blood vessels, reducing blood viscosity, and thus improving blood circulation.
Information source: 39Drug Tong, Baidu Baike.
Anti inflammatory effect
Inflammatory reaction plays an important role in atherosclerosis and thrombois. In atherosclerotic plaque, there are a large number of inflammatory cell infiltration, such as monocytes, T lymphocytes, etc. These inflammatory cells can release various inflammatory factors, such as tumor necrosis factor - α (TNF - α), interleukin-6 (IL-6), etc. These inflammatory factors can not only activate vascular endothelial cells and immune cells, aggravate the inflammatory response, but also promote soterocyte activation and aggregation, and promote thrmbus formation.
Etriptide has certain anti-inflammatory effects, which can reduce inflammatory reactions and alleviate tissue damage.
It can inhibit the release of inflammatory factors, such as by suppressing the release of inflammatory factors during soterocyte activation and reducing the level of inflammatory factors in the blood. At the same time, it can also regulate the domain of immune cells, inhibit the infiltration of immune cells such as monocytes and T lymphocytes into the vascular wall, reduce the aggregation of inflammatory cells in the vascular wall, and further alleviate the inflammatory response. For example, in patients with acute cornary syndrome, the activation of inflammatory response is one of the important factors leading to worsening of the condition. Its anti-inflammatory effect can reduce the damage of inflammatory response to blood vessels, decrease the risk of thrombois, and improve the prognosis of patients.
Information source: 39Drug Tong, Baidu Baike.
The impact on hemorheology
Abnormal hemorheology also plays an important role in the occurrence and development of cardiovascular diseases. Factors such as increased blood viscosity and enhanced red blood cell aggregation can lead to increased blood flow resistance, slowed blood flow velocity, and increased risk of thrombois.
It can effectively inhibit soterocyte activation and aggregation, and reduce blood viscosity. By inhibiting soterocyte aggregation, the aggregation state of soterocytes in the blood is reduced, resulting in an increase in blood fluidity. Meanwhile, the regulatory effect of intrifiban on endothelial cell domain also contributes to improving hemorheology. For example, it promotes the release of vasodilators such as NO from endothelial cells, causing vasodilation and reducing resistance to blood flow, further improving blood circulation. This improvement in blood rheology helps prevent thrombois and reduce the occurrence of cardiovascular events.
By specifically blocking the binding of glycoprotein IIb/IIIa receptors to fibrinogen, inhibiting the action of soterocyte activating factor, regulating endothelial cell domain, exerting anti-inflammatory effects, and having a positive impact on hemorheology, various mechanisms of action are effectively employed to inhibit soterocyte aggregation and thrmbus formation, and improve cardiovascular domain. These mechanisms of action work together and provide a solid theoretical foundation for their application in the treatment of cardiovascular diseases. In clinical practice, fully understanding the mechanism of action of eptifibatide peptide can help doctors use the drug more reasonably, improve treatment efficacy, and reduce the risk of adverse reactions.
Information sources: 39 Medicine Tong, Minfukang.
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