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Argipressin acetate is an artificially synthesized cyclic nonapeptide hormone that simulates the action of natural antidiuretic hormone (AVP), exerting dual physiological functions of vasoconstriction and antidiuretic. Its chemical structure consists of nine amino acids, forming a cyclic structure through disulfide bonds between cysteine residues at positions 1 and 6. It contains aromatic amino acids such as tyrosine and phenylalanine, with a molecular formula of C48H69N15O14S2 and a molecular weight of approximately 1144.28.
The drug achieves its function by activating the V1a receptor in vascular smooth muscle and the V2 receptor in renal tubules
Vasoconstriction effect:
After binding to V1a receptors, the phospholipase C (PLC) - inositol triphosphate (IP3) - calcium ion (Ca ² ⁺) signaling pathway is activated, leading to smooth muscle contraction and increased peripheral vascular resistance, thereby raising blood pressure. This mechanism is commonly used to control acute vasodilatory bleeding such as esophageal variceal rupture bleeding.
Antidiuretic effect:
Activating the adenylate cyclase (AC) - cyclic adenosine monophosphate (cAMP) - protein kinase A (PKA) pathway through the V2 receptor promotes membrane insertion of aquaporin 2 (AQP2) in the renal collecting duct, enhances water reabsorption, reduces urine output, and corrects polyuria symptoms of central diabetes insipidus.
Our product
Argipressin Acetate COA
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| Certificate of Analysis | ||
| Compound name | Argipressin Acetate | |
| Grade | Pharmaceutical grade | |
| CAS No. | 129979-57-3 | |
| Quantity | 60g | |
| Packaging standard | PE bag+Al foil bag | |
| Manufacturer | Shaanxi BLOOM TECH Co., Ltd | |
| Lot No. | 202501090069 | |
| 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% | 0.54% |
| 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: | C46H65N15O12S2 |
| Exact Mass: | 1083 |
| Molecular Weight: | 1084 |
| m/z: | 1083 (100.0%), 1084 (49.8%), 1085 (12.1%), 1085 (9.0%), 1084 (5.5%), 1086 (4.5%), 1085 (2.8%), 1085 (2.5%), 1086 (1.9%), 1086 (1.2%), 1087 (1.1%) |
| Elemental Analysis: | C, 50.96; H, 6.04; N, 19.38; O, 17.71; S, 5.91 |
Argipressin acetate, also known as antidiuretic hormone (ADH), is a nine peptide hormone synthesized by neurons in the hypothalamic supraoptic and paraventricular nuclei. It is released into the bloodstream through the pituitary gland and plays a central role in maintaining fluid balance, blood pressure homeostasis, and stress response. Its physiological function is achieved through specific binding to members of the G protein coupled receptor (GPCR) family, with the main receptor subtypes including V1a, V1b, and V2 receptors.
Receptor distribution and functional specificity
The distribution of vasopressin TFA receptor subtypes in tissues is highly selective, determining their functional diversity.
V1a receptor (vasopressin type 1a receptor)
Distribution: Widely distributed in vascular smooth muscle, myocardial cells, liver cells, platelets, and central nervous system (such as hippocampus and amygdala).
Function:
Vasoconstriction: In vascular smooth muscle, vasopressin TFA binds to V1a receptors and activates the phospholipase C (PLC) - inositol triphosphate (IP3) - calcium ion (Ca ² ⁺) signaling pathway, causing an increase in intracellular Ca ² ⁺ concentration, triggering vascular smooth muscle contraction, increasing peripheral vascular resistance, and thus raising blood pressure. This mechanism is particularly important when blood volume is insufficient (such as bleeding or dehydration), as it can quickly maintain circulatory stability.
Cardiac hypertrophy: Activation of V1a receptors in myocardial cells can promote protein synthesis and cell proliferation. Long term excessive stimulation may lead to pathological cardiac hypertrophy, which is associated with the progression of heart failure.
Platelet aggregation: AVP enhances platelet aggregation ability through V1a receptors and participates in the process of thrombosis.
Central regulation: In brain regions such as the hippocampus and amygdala, V1a receptors are involved in learning and memory, emotion regulation, and social behavior control.
V1b receptor (vasopressin type 1b receptor)
Distribution: Mainly distributed in the anterior pituitary gland, pancreatic alpha/beta cells, renal collecting ducts, and central nervous system (such as hypothalamus and prefrontal cortex).
Function:
Release of adrenocorticotropic hormone (ACTH): In the anterior pituitary gland, vasopressin TFA binds to V1b receptors and activates the PLC-IP3-Ca ² ⁺ pathway to stimulate ACTH secretion, which in turn activates the adrenal cortex to secrete cortisol, forming the stress responsive nuclear core of the hypothalamic pituitary adrenal axis (HPA axis).
Glucagon secretion: Activation of V1b receptors in pancreatic alpha cells can promote glucagon release and participate in blood glucose regulation.
Emotion and behavior: The expression of V1b receptors in the central nervous system is related to their regulatory role in anxiety, depression, and aggressive behavior. For example, in patients with severe depression, upregulation of V1b receptor expression in the pituitary gland leads to excessive activation of the HPA axis, exacerbating symptoms of low mood.
V2 receptor (vasopressin type 2 receptor)
Distribution: Specifically expressed in renal collecting duct main cells and distal renal tubular epithelial cells.
Function:
Antidiuretic effect: AVP binds to the V2 receptor and activates the adenylate cyclase (AC) - cyclic adenosine monophosphate (cAMP) - protein kinase A (PKA) signaling pathway, promoting the transport of aquaporin 2 (AQP2) from intracellular vesicles to the luminal membrane, increasing membrane permeability to water, thereby enhancing water reabsorption, reducing urine output, and maintaining fluid osmotic pressure balance.
Regulation of aquaporins: The V2 receptor signaling pathway is also involved in the phosphorylation modification of AQP2 and the maintenance of membrane stability. Long term vasopressin TFA stimulation can upregulate AQP2 expression and enhance the kidney's ability to reabsorb water.
Core signal pathway analysis
AVP receptors activate downstream signaling pathways through different G protein coupling mechanisms, achieving functional specificity:
V1a/V1b receptor signaling pathway (PLC-IP3-Ca ² ⁺ pathway)
Mechanism: Vasopressin TFA binds to V1a/V1b receptors, activating Gq protein and subsequently activating PLC. PLC catalyzes the hydrolysis of phosphatidylinositol 4,5-diphosphate (PIP2) to produce IP3 and diacylglycerol (DAG). IP3 binds to the IP3 receptor on the endoplasmic reticulum, releasing stored Ca ² ⁺ into the cytoplasm and causing an increase in intracellular Ca ² ⁺ concentration; DAG activates protein kinase C (PKC) and participates in the regulation of cell proliferation and differentiation.
Physiological effects:
Vascular smooth muscle contraction (V1a receptor).
ACTH secretion (V1b receptor).
Platelet aggregation (V1a receptor).
V2 receptor signaling pathway (AC cAMP PKA pathway)
Mechanism: After vasopressin TFA binds to the V2 receptor, it activates the Gs protein, which in turn activates AC. AC catalyzes ATP to generate cAMP, which acts as a second messenger to activate PKA. PKA phosphorylates target proteins (such as AQP2), promoting their membrane transport and functional activation.
Physiological effects:
AQP2 membrane insertion enhances renal water reabsorption (V2 receptor).
Long term stimulation can upregulate AQP2 gene expression and increase aquaporin synthesis.
Cross regulation and integration
The synergistic effect of Ca ² ⁺ and cAMP: In renal collecting duct cells, the V2 receptor signaling pathway can activate Rap1 GTPase through the Epac (exchange protein directly activates cAMP) pathway, promoting AQP2 membrane insertion. At the same time, Ca ² ⁺ signaling may enhance PKA activity through calmodulin (CaM), forming a synergistic effect.
Receptor desensitization and internalization: Long term vasopressin TFA stimulation can lead to receptor phosphorylation (such as β - inhibitory protein mediated), trigger receptor internalization, reduce cell sensitivity to argipressin acetate, and form a negative feedback regulatory mechanism.
Pathophysiological significance and clinical application
The abnormality of vasopressin TFA receptor signaling pathway is closely related to various diseases, and intervention strategies targeting receptors have become a hot topic in treatment:
Heart failure
Mechanism: In heart failure, decreased blood volume and decreased renal perfusion pressure over activate vasopressin TFA secretion through non osmotic pressure stimulation (such as atrial baroreceptors), resulting in V1a receptor mediated vasoconstriction and V2 receptor mediated water retention, aggravating pulmonary congestion and hyponatremia.
Treatment: V2 receptor antagonists (such as Tovaptan) can reduce water reabsorption by blocking AVP-V2 receptor binding, improve hyponatremia and fluid retention, and do not activate the renin angiotensin aldosterone system (RAAS) to avoid the risk of electrolyte disorder of traditional diuretics.
Hyponatremia
Mechanism: In the syndrome of abnormal antidiuretic hormone secretion (SIADH), excessive vasopressin TFA secretion leads to water retention and diluted hyponatremia.
Treatment: V2 receptor antagonists can promote free water excretion, correct hyponatremia, and avoid blood volume reduction caused by excessive diuresis.
Anxiety and Depression
Mechanism: V1b receptors play a key role in the overactivation of the HPA axis, and their upregulation is associated with depressive symptoms.
Treatment: Selective V1b receptor antagonists (such as SSR149415) inhibit ACTH secretion, reduce cortisol levels, alleviate anxiety and depressive behavior, and are currently in clinical trials.
Hypertension
Mechanism: V1a receptor mediated vasoconstriction is one of the important mechanisms of hypertension, especially in salt sensitive hypertension where argipressin acetate sensitivity increases.
Treatment: V1a receptor antagonists can reduce peripheral vascular resistance, but their potential side effects on myocardial contractility and platelet function need to be balanced.
Arginine vasopressin achieves multiple physiological functions such as vasoconstriction, water reabsorption, stress response, and emotion regulation through the PLC-IP3-Ca ² ⁺ and AC cAMP PKA signaling pathways via V1a, V1b, and V2 receptor subtypes. The abnormality of its signaling pathway is closely related to diseases such as heart failure, hyponatremia, anxiety, and depression. Selective intervention strategies targeting receptors, such as V2 receptor antagonists and V1b receptor antagonists, provide new directions for clinical treatment. Future research needs to further elucidate the dynamic regulatory mechanisms of receptor subtypes in complex diseases, develop more efficient and low side effect targeted drugs, and explore the potential therapeutic value of the vasopressin TFA signaling pathway in central nervous system diseases.
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