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Vasopressin | CAS No: 11000-17-2 | GMP-certified suppliers
A medication that increases blood pressure in adults experiencing vasodilatory shock unresponsive to fluids and catecholamines, supporting critical care management of cardiovascular instability.
Therapeutic categories
Primary indications
- Vasopressin is indicated to increase blood pressure in adults in vasodilatory shock refractory to the application of fluids and catecholamines
Product Snapshot
- Vasopressin is available primarily as injectable solutions suitable for parenteral administration including intravenous, intramuscular, and subcutaneous routes
- It is mainly used in managing vasodilatory shock to increase blood pressure when fluids and catecholamines are insufficient
- Vasopressin products are approved for use in key regulatory markets including the US and Canada
Clinical Overview
Pharmacologically, vasopressin exerts its effects via G-protein-coupled receptors classified as V1 (subtypes V1A), V2, and V3 (formerly V1B). V1 receptors are prevalent in vascular smooth muscle, where vasopressin binding activates phospholipase C, leading to inositol triphosphate and diacylglycerol production that elevate intracellular calcium levels and provoke vasoconstriction. This receptor subtype also mediates central autonomic regulation of blood pressure. V2 receptors, located primarily in renal distal tubules and collecting ducts, promote aquaporin-2 water channel insertion into cell membranes via a cAMP-dependent protein kinase A mechanism, leading to antidiuretic effects. V3 receptors found in the anterior pituitary modulate adrenocorticotropic hormone release and influence central nervous system functions such as memory and behavior.
Key ADME parameters of vasopressin include its peptide nature leading to rapid enzymatic degradation, necessitating parenteral administration. The hormone’s half-life in plasma is short, reflecting swift clearance and metabolism by liver and kidney enzymes.
Safety considerations include the potential for vasopressin to reduce cardiac output in patients with compromised cardiac function. Withdrawal from vasopressin therapy may transiently induce diabetes insipidus, requiring management with desmopressin or supplementary vasopressin. The balance between vasoconstriction and endothelial nitric oxide-mediated vasodilation contributes to patient-specific variability in response.
Vasopressin is marketed under the trade name VASOSTRICT® among others, primarily utilized in intensive care settings for shock management and in endocrinology for diabetes insipidus and related disorders.
From an API sourcing and quality perspective, procurement must ensure compliance with pharmacopeial standards for peptide purity and stability. Rigorous characterization of synthetic or recombinant vasopressin, including assay of peptide integrity, absence of contaminants, and appropriate storage conditions, is critical to support safe and effective formulation development.
Identification & chemistry
| Generic name | Vasopressin |
|---|---|
| Molecule type | Small molecule |
| CAS | 11000-17-2 |
| UNII | Y87Y826H08 |
| DrugBank ID | DB00067 |
Pharmacology
| Summary | Vasopressin is a cyclic nonapeptide hormone that primarily targets V1 (V1a), V2, and V3 (V1b) G-protein-coupled receptors to regulate vascular tone, renal water reabsorption, and stress hormone release. Activation of V1 receptors induces vasoconstriction via phospholipase C signaling and intracellular calcium mobilization, contributing to blood pressure modulation. V2 receptor engagement in renal tubules promotes water reabsorption through aquaporin-2 channel phosphorylation, while V3 receptor activation in the pituitary mediates adrenocorticotropic hormone release during stress. |
|---|---|
| Mechanism of action | Vasopressin, Cyclo (1-6) L-Cysteinyl-L-Tyrosyl-L-PhenylalanylL-Glutaminyl-L-Asparaginyl-L-Cysteinyl-L-Prolyl-L-Arginyl-L-Glycinamide, is a cyclic nonapeptide hormone primarily produced by the supraoptic and periventricular nuclei of the hypothalamus.[A228008, L31413] Vasopressin release is mediated by sensory pathways, in which either a 2% increase in plasma osmolarity or a 10% decrease in blood pressure causes the release of endogenous vasopressin. Upon release, vasopressin mediates a variety of physiological effects, both centrally and systemically, primarily by binding to G-protein-coupled receptors termed V<sub>1</sub> (V<sub>1A</sub>), V<sub>2</sub>, and V<sub>3</sub> (V<sub>1B</sub>). V<sub>1</sub> receptors are abundantly expressed in the brain whereby vasopressin binding can increase blood pressure through autonomic pathways. Peripherally, V<sub>1</sub> is localized in the blood vessels (vascular smooth muscle), platelets, adrenal glands, kidneys, and liver.[A228008, A228018] Vasopressin binding to V<sub>1</sub> causes hydrolysis of phosphatidylinositol-4,5-bisphosphate into inositol triphosphate (IP<sub>3</sub>) and diacylglycerol (DAG) by phospholipase C, which in turn release intracellular calcium and activate protein kinase C (PKC) to open voltage-gated calcium channels (VGCCs) while closing potassium channels. Overall, intracellular calcium levels rise, which bind calmodulin and cause muscular contraction, resulting in vasoconstriction. This is balanced by the apparent ability of vasopressin to induce vasodilation through binding oxytocin receptors and activating endothelial nitric oxide (NO) synthase; NO acts antagonistically to reduce muscle contraction. It is also thought that vasopressin, acting through both V<sub>1</sub> and oxytocin receptors, causes the cardiac release of atrial natriuretic peptide (ANP), which has a negative inotropic effect; indeed, vasopressin tends to decrease heart rate and cardiac output, although the opposite effect has been noted with low doses.[A228013, L31413] V<sub>2</sub> receptors are abundantly expressed in the distal convoluted tubules and the collecting ducts of the kidneys.[A228018, A228023] Vasopressin binding to V<sub>2</sub> causes activation of a G<sub>s</sub> protein that subsequently activates protein kinase A (PKA) through adenylyl cyclase-mediated increase in cyclic adenosine monophosphate (cAMP), which leads to phosphorylation of the water channel aquaporin-2 (AQP2) and its trafficking to the cell surface.[A228018, A228023] Increased AQP2 levels lead to increased water reabsorption and explains vasopressin's antidiuretic effects. V<sub>3</sub> (formerly V<sub>1B</sub>) receptors are primarily located in the anterior pituitary and brain.[A228008, A228018] Vasopressin released during acute stress causes adrenocorticotropic hormone (ACTH) release from the pituitary through V<sub>3</sub> and by potentiating the effects of corticotrophin-releasing factor. Within the brain itself, V<sub>3</sub> activation modulates various effects, including recognition, memory, aggression, anxiety, and depression. Thus, vasopressin can affect a wide variety of physiological processes, often in apparently contradictory ways depending on the patient's dose and physiological state. Vasodilatory shock causes an immediate release of vasopressin from 20 to 200 times its normal serum concentration, which falls again to normal levels in prolonged shock; in this context, normal serum levels are insufficient to control the pathologic vasodilation.[A228013, A228018] In these cases, vasopressin acts to depolarize hyperpolarized vascular smooth muscle cells, restore sensitivity to catecholamines, and inhibit excessive nitric oxide production, primarily through acting through V<sub>1</sub> receptors. Therefore, vasopressin helps decrease the dose requirement for norepinephrine and is routinely administered together with norepinephrine to restore normal blood pressure in shock states.[A228018, L31413] |
| Pharmacodynamics | Vasopressin is a nonapeptide antidiuretic hormone involved in modulating various physiological processes, including autonomic signalling, stress response, behaviour, and memory; the most well-known modulation is of blood pressure.[A110, A111, A112, A113, L31413] Vasopressin acts both within the brain and in the periphery to modulate blood pressure through sympathetic outflow, baroreflex modulation, vasoconstriction, and renal fluid retention.[A228008, A228013, A228018] These mechanisms vary by location and physiological state, leading to occasionally contradictory responses to vasopressin. Although generally safe, vasopressin may worsen cardiac output in patients with impaired cardiac function. The cessation of vasopressin therapy may result in transient reversible diabetes insipidus, which may require additional desmopressin or vasopressin to manage. |
Targets
| Target | Organism | Actions |
|---|---|---|
| Vasopressin V2 receptor | Humans | agonist, regulator |
| Vasopressin V1a receptor | Humans | agonist, regulator |
| Vasopressin V1b receptor | Humans | agonist |
ADME / PK
| Half-life | Vasopressin administered at 0.01-0.1 U/min has an apparent t<sub>1/2</sub> of ≤10 minutes, although half-lives of up to 44 minutes have been reported in the literature. |
|---|---|
| Metabolism | Animal studies suggest that vasopressin is metabolized by serine proteases, carboxypeptidases, and disulphide oxidoreductases, primarily in the liver and kidneys. These cleavage events occur at sites important for vasopressin's activity, and hence the metabolites are expected to be inactive. |
| Route of elimination | Vasopressin is primarily eliminated in the urine, where only 6% of the dose is excreted unchanged. |
| Clearance | Vasopressin has a clearance of 9-25 mL/min/kg in patients with vasodilatory shock receiving 0.01-0.1 U/min of vasopressin. |
Formulation & handling
- Vasopressin is formulated primarily as an injectable solution for intramuscular, subcutaneous, and intravenous administration.
- It is a small molecule with high water solubility and low lipophilicity, indicating good aqueous stability but limited membrane permeability.
- Due to its peptide-like molecular weight, handling should consider aseptic techniques and storage conditions that prevent degradation.
Regulatory status
| Lifecycle | The active pharmaceutical ingredient is protected by multiple patents expiring in 2035 in the United States, with marketed products currently available in the US and Canada. The market is considered to be in a patent-protected phase with limited generic competition. |
|---|
| Markets | US, Canada |
|---|
Supply Chain
| Supply chain summary | Vasopressin is primarily originated by a single originator company with multiple associated branded products marketed mainly in the US and Canada. The patent protections, with expiration dates extending to 2035 in the United States, indicate that generic competition is currently limited or not yet available in these markets. The supply chain involves multiple packagers and pharmaceutical distributors supporting broad availability within North America. |
|---|
Safety
| Toxicity | Vasopressin overdose is expected to present with consequences related to excessive vasoconstriction of peripheral, mesenteric, coronary vascular beds, hyponatremia, and possibly with ventricular tachyarrhythmias, rhabdomyolysis, and gastrointestinal symptoms. As vasopressin is rapidly metabolized and cleared, symptoms will resolve with cessation of vasopressin administration. |
|---|
- Overdose may cause excessive vasoconstriction affecting peripheral, mesenteric, and coronary vascular beds
- Hyponatremia and ventricular tachyarrhythmias have been reported in toxicity cases
- Due to rapid metabolism, adverse effects are typically reversible upon discontinuation
Vasopressin is a type of Vasopressin Analogues
Vasopressin analogues are a subcategory of pharmaceutical active pharmaceutical ingredients (APIs) that mimic the actions of the hormone vasopressin in the human body. Vasopressin, also known as antidiuretic hormone (ADH), plays a crucial role in regulating fluid balance and blood pressure.
These analogues are developed by modifying the structure of vasopressin to enhance its therapeutic properties. They act on specific vasopressin receptors located in various tissues, including the kidneys, blood vessels, and brain. By interacting with these receptors, vasopressin analogues exert a range of effects.
One of the key applications of vasopressin analogues is the treatment of diabetes insipidus, a condition characterized by excessive urine production and excessive thirst. By stimulating the vasopressin receptors in the kidneys, these analogues promote water reabsorption and reduce urine output.
Vasopressin analogues are also utilized in critical care settings to manage hypotension (low blood pressure) and vasodilatory shock. By binding to vasopressin receptors on blood vessels, these analogues induce vasoconstriction, which helps to elevate blood pressure and improve perfusion to vital organs.
In summary, vasopressin analogues are an important class of pharmaceutical APIs that modulate vasopressin receptor activity. Their therapeutic applications range from treating diabetes insipidus to managing hypotension in critical care. By optimizing the structure of vasopressin, these analogues provide targeted and effective treatments for various medical conditions.
Vasopressin (Vasopressin Analogues), classified under Hormonal Agents
Hormonal agents are a prominent category of pharmaceutical active pharmaceutical ingredients (APIs) widely used in the medical field. These substances play a crucial role in regulating and modulating hormonal functions within the body. Hormonal agents are designed to mimic or manipulate the effects of naturally occurring hormones, allowing healthcare professionals to treat various endocrine disorders and hormonal imbalances.
Hormonal agents are commonly employed in the treatment of conditions such as hypothyroidism, hyperthyroidism, diabetes, and hormonal cancers. These APIs work by interacting with specific hormone receptors, either by stimulating or inhibiting their activity, to restore the balance of hormones in the body. They can be administered orally, intravenously, or through other routes depending on the specific medication and patient needs.
Pharmaceutical companies employ rigorous manufacturing processes and quality control measures to ensure the purity, potency, and safety of hormonal agent APIs. These APIs are synthesized using chemical or biotechnological methods, often starting from natural hormone sources or through recombinant DNA technology. Stringent regulatory guidelines are in place to guarantee the efficacy and safety of hormonal agent APIs, ensuring that patients receive high-quality medications.
As the demand for hormone-related therapies continues to grow, ongoing research and development efforts focus on enhancing the effectiveness and reducing the side effects of hormonal agent APIs. This includes the exploration of novel delivery systems, advanced formulations, and targeted drug delivery methods. By continuously advancing our understanding and capabilities in hormonal agents, the medical community can improve patient outcomes and quality of life for individuals with hormonal disorders.
Vasopressin API manufacturers & distributors
Compare qualified Vasopressin API suppliers worldwide. We currently have 4 companies offering Vasopressin API, with manufacturing taking place in 4 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| BCN Peptides | Producer | Spain | Spain | CoA, USDMF | 13 products |
| Hemmo Pharma | Producer | India | India | CoA, USDMF | 13 products |
| Polypeptide Labs | Producer | Sweden | Unknown | CoA, GMP, USDMF | 21 products |
| Reali Tide Biological Tec... | Producer | China | China | BSE/TSE, CoA, MSDS, USDMF | 57 products |
When sending a request, specify which Vasopressin API quality you need: for example EP (Ph. Eur.), USP, JP, BP, or another pharmacopoeial standard, as well as the required grade (base, salt, micronised, specific purity, etc.).
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