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Fedratinib
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Looking for Fedratinib API 936091-26-8?
- Description:
- Here you will find a list of producers, manufacturers and distributors of Fedratinib. 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:
- Fedratinib
- Synonyms:
- Cas Number:
- 936091-26-8
- DrugBank number:
- DB12500
- Unique Ingredient Identifier:
- 6L1XP550I6
General Description:
Fedratinib, identified by CAS number 936091-26-8, is a notable compound with significant therapeutic applications. Fedratinib, also known as SAR302503 and TG101348, is a tyrosine kinase inhibitor used to treat intermediate-2 and high risk primary and secondary myelofibrosis. It is an anilinopyrimidine derivative. Fedratinib was granted FDA approval on August 16, 2019.
Indications:
This drug is primarily indicated for: Fedratinib is indicated to treat adults with primary or secondary myelofibrosis that is either intermediate-2 or high risk. Its use in specific medical scenarios underscores its importance in the therapeutic landscape.
Metabolism:
Fedratinib undergoes metabolic processing primarily in: Fedratinib is metabolized by CYP3A4, CYP2C19, and flavin-containing monooxygenase 3. Beyond that, data regarding the metabolism of fedratinib is not readily available. This metabolic pathway ensures efficient processing of the drug, helping to minimize potential toxicity and side effects.
Absorption:
The absorption characteristics of Fedratinib are crucial for its therapeutic efficacy: A 400mg oral dose results in a Cmax of 1804ng/mL and an AUC of 26,870ng/*hr/mL. Fedratinib has a Tmax of 1.75-3 hours. A high fat breakfast does not significantly affect the absorption of fedratinib. The drug's ability to rapidly penetrate into cells ensures quick onset of action.
Half-life:
The half-life of Fedratinib is an important consideration for its dosing schedule: The half life of fedratinib is 41 hours with a terminal half life of 114 hours. This determines the duration of action and helps in formulating effective dosing regimens.
Protein Binding:
Fedratinib exhibits a strong affinity for binding with plasma proteins: Fedratinib is ≥92% protein bound in plasma. This property plays a key role in the drug's pharmacokinetics and distribution within the body.
Route of Elimination:
The elimination of Fedratinib from the body primarily occurs through: An oral dose of fedratinib is 77% eliminated in the feces with 23% as unchanged drug. 5% is eliminated in the urine, with 3% as unchanged drug. Understanding this pathway is essential for assessing potential drug accumulation and toxicity risks.
Volume of Distribution:
Fedratinib is distributed throughout the body with a volume of distribution of: The apparent volume of distribution is 1770L. This metric indicates how extensively the drug permeates into body tissues.
Clearance:
The clearance rate of Fedratinib is a critical factor in determining its safe and effective dosage: The clearance of fedratinib is 13L/h. It reflects the efficiency with which the drug is removed from the systemic circulation.
Pharmacodynamics:
Fedratinib exerts its therapeutic effects through: Fedratinib is a kinase inhibitor that inhibits cell division and induces apoptosis. Patients taking fedratinib may experience anemia, thrombocytopenia, gastrointestinal toxicity, hepatic toxicity, or elevated amylase and lipase. These effects should be managed by reducing the dose, temporarily stopping the medication, or providing transfusions on a case by case basis. The drug's ability to modulate various physiological processes underscores its efficacy in treating specific conditions.
Mechanism of Action:
Fedratinib functions by: Fedratinib is an inhibitor of Janus Activated Kinase 2 (JAK2) and FMS-like tyrosine kinase 3. JAK2 is highly active in myeloproliferative neoplasms like myelofibrosis. Fedratinib's inhibition of JAK2 inhibits phosphorylation of signal transducer and activator of transcription (STAT) 3 and 5, which prevents cell division and induces apoptosis. This mechanism highlights the drug's role in inhibiting or promoting specific biological pathways, contributing to its therapeutic effects.
Toxicity:
Classification:
Fedratinib belongs to the class of organic compounds known as benzenesulfonamides. These are organic compounds containing a sulfonamide group that is S-linked to a benzene ring, classified under the direct parent group Benzenesulfonamides. This compound is a part of the Organic compounds, falling under the Benzenoids superclass, and categorized within the Benzene and substituted derivatives class, specifically within the Benzenesulfonamides subclass.
Categories:
Fedratinib is categorized under the following therapeutic classes: Amides, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, BCRP/ABCG2 Inhibitors, Cytochrome P-450 CYP2C19 Substrates, Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (strength unknown), Cytochrome P-450 CYP3A Substrates, Cytochrome P-450 CYP3A4 Substrates, Cytochrome P-450 Enzyme Inhibitors, Cytochrome P-450 Substrates, Janus-associated kinase (JAK) inhibitors, Kinase Inhibitor, MATE 1 Inhibitors, MATE 2 Inhibitors, MATE inhibitors, OATP1B1/SLCO1B1 Inhibitors, OATP1B3 inhibitors, P-glycoprotein inhibitors, P-glycoprotein substrates, Protein Kinase Inhibitors, Sulfones, Sulfur Compounds, Tyrosine Kinase Inhibitors. These classifications highlight the drug's diverse therapeutic applications and its importance in treating various conditions.
Experimental Properties:
Further physical and chemical characteristics of Fedratinib include:
- Water Solubility: 4µg/mL
Fedratinib is a type of Enzyme Replacements/modifiers
Enzyme replacements/modifiers are a crucial category of pharmaceutical active pharmaceutical ingredients (APIs) utilized in the treatment of various enzyme-related disorders. Enzymes play a vital role in the normal functioning of the body by catalyzing specific biochemical reactions. However, in certain medical conditions, the body may lack or produce dysfunctional enzymes, leading to serious health complications.
Enzyme replacement therapy (ERT) involves administering exogenous enzymes to compensate for the enzyme deficiency in patients. These enzymes are typically derived from natural sources or produced using recombinant DNA technology. By introducing these enzymes into the body, they can effectively substitute the missing or defective enzymes, thereby restoring normal metabolic processes.
On the other hand, enzyme modifiers are API substances that regulate the activity of specific enzymes within the body. These modifiers can either enhance or inhibit the enzyme's function, depending on the therapeutic objective. By modulating enzyme activity, these APIs can restore the balance of enzymatic reactions, leading to improved physiological outcomes.
Enzyme replacements/modifiers have shown remarkable success in treating various genetic disorders, such as Gaucher disease, Fabry disease, and lysosomal storage disorders. Additionally, they have demonstrated potential in managing enzyme deficiencies associated with rare diseases and certain types of cancer.
The development and production of enzyme replacements/modifiers involve rigorous research, formulation optimization, and adherence to stringent quality control measures. Pharmaceutical companies invest substantial resources in developing these APIs to ensure their safety, efficacy, and compliance with regulatory standards.
Overall, enzyme replacements/modifiers represent a vital therapeutic category in modern medicine, offering hope and improved quality of life for patients with enzyme-related disorders.
Fedratinib manufacturers | traders | suppliers
We have 1 companies offering Fedratinib produced in 1 different countries.
Get in contact with the supplier of your choice:
- TAPI from Israel, product country of origin Israel
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