Argipressin acetate, molecular formula C46H65N15O12S2, molecular weight 1084.24 g/mol, appears as a white to off white crystalline powder, with a pH value of about 3.5 and an optical rotation of -23.822 ° (in 1 mol/dm ³ acetic acid solution). Its solubility is excellent, with a solubility of ≥ 360 mg/mL (332.03 mM) in water at room temperature. Storage conditions should be strictly controlled at 2-8 ℃ to avoid degradation. This substance forms a cyclic structure through disulfide bonds (Cys ¹ - Cys ⁶), with an amino acid sequence of H-Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly-NH ₂, where the 8th arginine residue is the source of its name. It has a direct antidiuretic effect on the kidneys, can also contract surrounding sanguis vessels, and cause contraction of the intestines, gallbladder, and bladder. But arginine vasopressin has almost no effect on inducing labor.
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Argipressin Acetate COA
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| Certificate of Analysis | ||
| Compound name |
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| Grade | Pharmaceutical grade | |
| CAS No. | 129979-57-3 | |
| Quantity | 80g | |
| Packaging standard | PE bag+Al foil bag | |
| Manufacturer | Shaanxi BLOOM TECH Co., Ltd | |
| Lot No. | 202501090053 | |
| MFG | Jan 9th 2025 | |
| EXP | Jan 8th 2028 | |
| Structure |
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| Item | Enterprise standard | Analysis result |
| Appearance | White or almost white powder | Conformed |
| Water content | ≤5.0% | 0.45% |
| Loss on drying | ≤1.0% | 0.53% |
| 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% | 99.90% |
| Single impurity | <0.8% | 0.25% |
| Total microbial count | ≤750cfu/g | 80 |
| E. Coli | ≤2MPN/g | N.D. |
| Salmonella | N.D. | N.D. |
| Ethanol (by GC) | ≤5000ppm | 400ppm |
| Storage | Store in a sealed, dark, and dry place below -20°C | |
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| Chemical Formula: | C48H69N15O14S2 |
| Exact Mass: | 1127 |
| Molecular Weight: | 1128 |
| m/z: | 1127 (100.0%), 1128 (51.9%), 1129 (13.2%), 1129 (9.0%), 1128 (5.5%), 1130 (4.7%), 1129 (2.9%), 1129 (2.7%), 1128 (1.6%), 1130 (1.4%), 1130 (1.4%), 1131 (1.2%) |
| Elemental Analysis: | C, 51.10; H, 6.16; N, 18.62; O, 18.43; S, 5.68 |
Argipressin acetate is an artificially synthesized substance similar to natural arginine vasopressin, which changes the structure of natural hormones by removing one amino acid and replacing it with a different amino acid at another position. This medication can help control bleeding by affecting the levels of coagulation factor VIII and Von Willebrand factor in the sanguis, and can improve certain types of nocturia symptoms. This drug is mainly used to treat symptoms such as central diabetes insipidus, nocturnal enuresis, and hemophilia, and can also be used to test the ability of the kidneys to concentrate urine.
Hemostatic effect: treating hemorrhagic diseases
Esophageal variceal rupture and bleeding:
Esophageal variceal bleeding is one of the most serious complications of portal hypertension in liver cirrhosis. Its pathogenesis is the continuous increase of portal vein presure (>12 mmHg), which leads to the formation and rupture of esophageal and gastric varices, causing acute massive bleeding with a mortality rate of up to 20% -30%. AVP, as a first-line drug for treating this disease, has a highly precise and multi-target
synergistic hemostatic mechanism
Visceral hematal constriction: AVP activates the V1a receptor on the membrane of hematal smooth muscle cells, triggers the G protein coupled signaling pathway, activates phospholipase C (PLC), promotes the generation and release of calcium ions from the endoplasmic reticulum calcium pool by inositol triphosphate (IP ∝), and activates protein kinase C (PKC) by diacylglycerol (DAG), ultimately leading to myosin light chain phosphorylation and strong contraction of hematal smooth muscle. This process preferentially acts on visceral sanguis vessels (such as splenic artery and superior mesenteric artery), reducing visceral sanguis flow by 30% -50% and portal vein presure by 15% -25%, thereby reducing the impact of sanguis flow in varicose veins and lowering the risk of rupture.
Hemodynamic optimization: AVP contracts peripheral sanguis vessels, increases mean arterial presure (MAP), increases cardiac afterload, and indirectly reduces portal vein sanguis flow. At the same time, its vasoconstrictive effect can reduce the renal sanguis flow, activate the renin angiotensin aldosterone system (RAAS), further promote the retention of water and sodium, maintain the effective circulating sanguis volume, and avoid the rebound rise of portal vein presure caused by low sanguis volume.
Clinical efficacy: Multiple randomized controlled trials (RCTs) have confirmed that AVP combined with endoscopic therapy (such as ligation and sclerotherapy injection) can significantly improve hemostasis success rate (from 60% to 85%), reduce rebleeding rate (from 40% to 20%), and decrease the need for sanguis transfusion. It has a rapid onset of action (constricting sanguis vessels within 5-10 minutes) and a long-lasting effect (lasting 4-6 hours), especially suitable for stopping acute massive bleeding or transitional hemostasis before endoscopic treatment.
Attention: AVP may cause side effects such as myocardial ischemia and intestinal ischemia. It is necessary to strictly monitor sanguis presure, heart rate, and lactate levels, and avoid high doses (>0.4 U/min) or prolonged use.
Other bleeding control measures
AVP exerts hemostatic effects through multiple mechanisms in diseases with prolonged bleeding time caused by hereditary hemorrhagic telangiectasia (HHT), uremia, cirrhosis, etc
Enhancing platelet activity: AVP activates phospholipase A2 (PLA2) on the platelet membrane through V1a receptors, promoting arachidonic acid metabolism and generating thromboxane A2 (TXA2), which is a potent inducer of platelet aggregation. At the same time, AVP can increase the concentration of calcium ions in platelets, promote actin myosin interaction, enhance platelet deformation and release response, and shorten bleeding time.
Promoting the activity of coagulation factor VIII: AVP regulates endothelial cell function and promotes the release of von Willebrand factor (vWF). As a carrier of coagulation factor VIII, vWF can significantly enhance its stability and activity. In addition, AVP may indirectly promote thrombin production and accelerate fibrin formation by activating the contact phase (such as FXII) in the coagulation cascade reaction.
Clinical application:
HHT: AVP can reduce the frequency and severity of nosebleeds, and improve patients' quality of life.
Uremia: Uremic patients are prone to bleeding due to abnormal platelet function and lack of coagulation factors. AVP combined with erythropoietin (EPO) can significantly correct anemia and improve hemostatic function.
Cirrhosis: In addition to portal hypertension related bleeding, patients with cirrhosis often have coagulation dysfunction. AVP can reduce the risk of bleeding after surgery or invasive procedures through multiple pathways of hemostasis.
Dosage and monitoring: AVP is usually administered intravenously at low doses (0.01-0.04 U/min) and requires regular monitoring of platelet count, prothrombin time (PT), and activated partial thromboplastin time (APTT) to avoid the risk of thrombosis.
Central nervous system regulation
Intracranial presure regulation
The pathological core of high intracranial presure syndrome (such as traumatic brain injury, brain tumor, cerebral hemorrhage) is the increase in intracranial content volume, which leads to an increase in intracranial presure (ICP), causing cerebral herniation and even death. AVP effectively reduces ICP through the following mechanisms:
Cerebral vasoconstriction: AVP activates the V1a receptor of cerebral hematal smooth muscle, triggering vasoconstriction through a calcium dependent signaling pathway, reducing cerebral sanguis flow (CBF) by 10% -20%, thereby reducing brain tissue volume and ICP.
Animal experiments have shown that AVP can reduce the ICP of brain edema model rats from 30 mmHg to 15 mmHg, and the effect lasts for 4-6 hours.
Sanguis brain barrier protection: AVP reduces the expression of hematal endothelial growth factor (VEGF), inhibits the increase in sanguis-brain barrier permeability, and alleviates vasogenic brain edema. Meanwhile, argipressin acetate anti-inflammatory effect can reduce the levels of inflammatory factors such as tumor necrosis factor - α (TNF - α) and interleukin-6 (IL-6), further alleviating cytotoxic brain edema.
Clinical application: AVP is commonly used when traditional intracranial presure lowering drugs such as mannitol and hypertonic saline are ineffective, or as a combination therapy. For example, in patients with traumatic brain injury, AVP combined with hypothermia therapy can significantly reduce ICP and improve neurological function prognosis.
Attention: It is necessary to strictly monitor cerebral perfusion presure (CPP=MAP-ICP) to avoid excessive vasoconstriction leading to CPP<50 mmHg and causing cerebral ischemia.
Physiological activity research
To investigate whether arginine vasopressin acetate has the effect of reducing stress-induced hyperthermia, wireless telemetry technology was used to measure changes in body temperature in rats, and the effects of intraperitoneal injection of arginine vasopressin acetate and arginine vasopressin acetate V1 receptor blocker on stress-induced hyperthermia in rats were observed. The results showed that intraperitoneal injection of arginine vasopressin acetate could significantly reduce stress-induced hyperthermia in rats, while injection of blockers could increase the response to stress-induced hyperthermia. That is to say, acetate arginine vasopressin not only has the effect of reducing stress-induced hyperthermia in rats, but also endogenous substances have a negative regulatory effect on stress-induced hyperthermia.
Establish a neural cell aging experimental research model using serum-free culture of mouse neuroblastoma cells. Observation of the effect of arginine vasopressin acetate on the cell cycle and total protein of experimental neuronal cells during aging using flow cytometry. It was found that acetate arginine vasopressin can produce changes in cell cycle and total cell protein that delay cell aging .
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