Curcumin sulfate API Manufacturers
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Looking for Curcumin sulfate API 339286-19-0?
- Description:
- Here you will find a list of producers, manufacturers and distributors of Curcumin sulfate. You can filter on certificates such as GMP, FDA, CEP, Written Confirmation and more. Send inquiries for free and get in direct contact with the supplier of your choice.
- API | Excipient name:
- Curcumin sulfate
- Synonyms:
- Curcumin monosulfate , Curcumin sulphate
- Cas Number:
- 339286-19-0
- DrugBank number:
- DB14635
- Unique Ingredient Identifier:
- 160DHE331M
General Description:
Curcumin sulfate is a chemical compound identified by the CAS number 339286-19-0. It is known for its distinct pharmacological properties and applications.
Indications:
This drug is primarily indicated for: No approved therapeutic indications. Its use in specific medical scenarios underscores its importance in the therapeutic landscape.
Metabolism:
Curcumin sulfate undergoes metabolic processing primarily in: Initially, curcumin undergoes rapid intestinal metabolism to form curcumin glucuronide and curcumin sulfate via O-conjugation. Other metabolites formed include tetrahydrocurcumin, hexahydrocurcumin, and hexahydrocurcuminol via reduction . Curcumin may also undergo intensive second metabolism in the liver where the major metabolites were glucuronides of tetrahydrocurcumin and hexahydrocurcumin, with dihydroferulic acid and traces of ferulic acid as further metabolites . Hepatic metabolites are expected to be excreted in the bile . Certain curcumin metabolites, such as tetrahydrocurcumin, retain anti-inflammatory and antioxidant properties . This metabolic pathway ensures efficient processing of the drug, helping to minimize potential toxicity and side effects.
Absorption:
The absorption characteristics of Curcumin sulfate are crucial for its therapeutic efficacy: Curcumin displays poor absorption into the gastrointestinal tract. In a rat study, oral administration of a single dose of 2 g of curcumin resulted in a plasma concentration of less than 5 μg/mL, indicating poor absorption from the gut . The drug's ability to rapidly penetrate into cells ensures quick onset of action.
Half-life:
The half-life of Curcumin sulfate is an important consideration for its dosing schedule: No pharmacokinetic data available. This determines the duration of action and helps in formulating effective dosing regimens.
Protein Binding:
Curcumin sulfate exhibits a strong affinity for binding with plasma proteins: No pharmacokinetic data available. This property plays a key role in the drug's pharmacokinetics and distribution within the body.
Route of Elimination:
The elimination of Curcumin sulfate from the body primarily occurs through: Following oral administration of curcumin to rats at a dose of 1 g/kg bw, about 75% of dose was excreted in the faeces and only traces of the compound was detected in the urine . When a single 400 mg dose of curcumin was administered orally to rats, about 60% was absorbed and 40% was excreted unchanged in the faeces over an period of 5 days . Intraperitoneal administration resulted in fecal excretion of 73% and biliary excretion of 11% . Understanding this pathway is essential for assessing potential drug accumulation and toxicity risks.
Volume of Distribution:
Curcumin sulfate is distributed throughout the body with a volume of distribution of: Following oral administration of radio-labelled curcumin to rats, radioactivity was detected in the liver and kidneys . This metric indicates how extensively the drug permeates into body tissues.
Clearance:
The clearance rate of Curcumin sulfate is a critical factor in determining its safe and effective dosage: No pharmacokinetic data available. It reflects the efficiency with which the drug is removed from the systemic circulation.
Pharmacodynamics:
Curcumin sulfate exerts its therapeutic effects through: Intravenous application of 25 mg/kg bw curcumin to rats resulted in an increase in bile flow by 80 and 120% . In the rat model of inflammation, curcumin was shown to inhibit edema formation. In nude mouse that had been injected subcutaneously with prostate cancer cells, administration of curcumin caused a marked decrease in the extent of cell proliferation, a significant increase of apoptosis and micro-vessel density . Curcumin may exert choleretic effects by increasing biliary excretion of bile salts, cholesterol, and bilirubin, as well as increasing bile solubility . Curcumin inhibited arachidonic acid-induced platelet aggregation _in vitro_ . The drug's ability to modulate various physiological processes underscores its efficacy in treating specific conditions.
Mechanism of Action:
Curcumin sulfate functions by: Curcumin acts as a scavenger of oxygen species, such as hydroxyl radical, superoxide anion, and singlet oxygen and inhibit lipid peroxidation as well as peroxide-induced DNA damage . Curcumin mediates potent anti-inflammatory agent and anti-carcinogenic actions via modulating various signalling molecules. It suppresses a number of key elements in cellular signal transduction pathways pertinent to growth, differentiation, and malignant transformation; it was demonstrated _in vitro_ that curcumin inhibits protein kinases, c-Jun/AP-1 activation, prostaglandin biosynthesis, and the activity and expression of the enzyme cyclooxygenase (COX)-2 . This mechanism highlights the drug's role in inhibiting or promoting specific biological pathways, contributing to its therapeutic effects.
Toxicity:
Classification:
Curcumin sulfate belongs to the class of organic compounds known as curcuminoids. These are aromatic compounds containing a curcumin moiety, which is composed of two aryl buten-2-one (feruloyl) chromophores joined by a methylene group, classified under the direct parent group Curcuminoids. This compound is a part of the Organic compounds, falling under the Phenylpropanoids and polyketides superclass, and categorized within the Diarylheptanoids class, specifically within the Linear diarylheptanoids subclass.
Categories:
Curcumin sulfate is categorized under the following therapeutic classes: Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2B6 Inhibitors, Cytochrome P-450 CYP2B6 Inhibitors (strength unknown), Cytochrome P-450 CYP2C19 Inhibitors, Cytochrome P-450 CYP2C19 inhibitors (strength unknown), Cytochrome P-450 CYP2C9 Inhibitors, Cytochrome P-450 CYP2C9 Inhibitors (strength unknown), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (strength unknown), Cytochrome P-450 CYP3A Inhibitors, Cytochrome P-450 CYP3A4 Inhibitors, Cytochrome P-450 CYP3A4 Inhibitors (strength unknown), Cytochrome P-450 CYP3A5 Inhibitors, Cytochrome P-450 CYP3A5 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors. These classifications highlight the drug's diverse therapeutic applications and its importance in treating various conditions.
Curcumin sulfate is a type of Anti-inflammatory Agents
Anti-inflammatory agents are a crucial category of pharmaceutical active pharmaceutical ingredients (APIs) used to treat various inflammatory conditions. These agents play a vital role in alleviating pain, reducing swelling, and controlling inflammation in the body. They are widely employed in the management of diverse medical conditions, including arthritis, autoimmune disorders, asthma, and skin conditions like dermatitis.
Anti-inflammatory APIs primarily function by inhibiting the production of specific enzymes called cyclooxygenases (COX) and lipoxygenases (LOX). These enzymes are responsible for the synthesis of pro-inflammatory molecules known as prostaglandins and leukotrienes, respectively. By suppressing the activity of COX and LOX, anti-inflammatory agents effectively curtail the production of these inflammatory mediators, thereby mitigating inflammation.
Common examples of anti-inflammatory APIs include non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, aspirin, and naproxen. These agents exhibit analgesic, antipyretic, and anti-inflammatory properties. Another group of anti-inflammatory APIs includes corticosteroids, such as prednisone and dexamethasone, which are synthetic hormones that modulate the body's immune response to control inflammation.
In conclusion, anti-inflammatory agents are a vital category of pharmaceutical APIs widely used to manage inflammation-related disorders. They target enzymes involved in the synthesis of pro-inflammatory molecules, effectively reducing pain and swelling. NSAIDs and corticosteroids are commonly prescribed anti-inflammatory APIs due to their efficacy in controlling inflammation.