Temoporfin API Manufacturers

General Description:

Temoporfin, identified by CAS number 122341-38-2, is a notable compound with significant therapeutic applications. Temoporfin is a photosensitizing agent used in the treatment of squamous cell carcinoma of the head and neck . It was first authorized for market by the European Medicines Agency in October 2001. It is currently available under the brand name Foscan.

Indications:

This drug is primarily indicated for: For use in the treatment of patients with advanced squamous cell carcinoma of the head and neck failing standard therapies and who are unsuitable for radiotherapy, surgery, or systemic chemotherapy . Its use in specific medical scenarios underscores its importance in the therapeutic landscape.

Metabolism:

Temoporfin undergoes metabolic processing primarily in: The exact metabolic reactions Temoporfin undergoes are unknown. The drug metabolites have been identified as conjugates but specific information is unavailable. This metabolic pathway ensures efficient processing of the drug, helping to minimize potential toxicity and side effects.

Absorption:

The absorption characteristics of Temoporfin are crucial for its therapeutic efficacy: Tmax is 2-4 h after intravenous administration . Plasma concentration initially decreases rapidly then slowly rises to reach peak serum concentration . The drug's ability to rapidly penetrate into cells ensures quick onset of action.

Half-life:

The half-life of Temoporfin is an important consideration for its dosing schedule: Terminal plasma half life is 65 h . Elimination of Temoporfin is bi-exponential with the intial phase having a half-life of 30 h and a terminal half-life of 61-88 h . This determines the duration of action and helps in formulating effective dosing regimens.

Protein Binding:

Temoporfin exhibits a strong affinity for binding with plasma proteins: Temoporfin is 85-88% bound to plasma proteins . Temoporfin initially binds and aggregates to an unknown high density protein . This makes up about 70% of the bound drug immediately after administration. The remainder is bound to plasma lipoproteins with 22% bound to high density lipoprotein (HDL), 4% bound to low density lipoprotein (LDL), and 4% bound to very low density lipoprotein (VLDL). Within 24 hours after administration, Temoporfin undergoes redistribution to lipoproteins with about 73% bound to HDL, 8% bound to LDL, and 3% bound to VLDL. Only 17% remains bound to the unknown high density protein after redistribution. This property plays a key role in the drug's pharmacokinetics and distribution within the body.

Route of Elimination:

The elimination of Temoporfin from the body primarily occurs through: Data on elimination in humans is limited . Animal data indicates Temoporfin is eliminated solely by the liver with two conjugated metabolites being excreted through bile. No enterohepatic recirculation has been observed with these metabolites. Understanding this pathway is essential for assessing potential drug accumulation and toxicity risks.

Volume of Distribution:

Temoporfin is distributed throughout the body with a volume of distribution of: The volume of distribution is 0.34-0.46 L/kg . Temoporfin is known to distribute into the tissues and preferentially collects in tumour tissue. This metric indicates how extensively the drug permeates into body tissues.

Clearance:

The clearance rate of Temoporfin is a critical factor in determining its safe and effective dosage: Temoporfin is cleared at a rate of 3.9-4.1 mL/h/kg . It reflects the efficiency with which the drug is removed from the systemic circulation.

Pharmacodynamics:

Temoporfin exerts its therapeutic effects through: Temoporfin is a photosensitizing agent . It enters cancer cells and is activated via light to produce reactive species which destroy the cell. The drug's ability to modulate various physiological processes underscores its efficacy in treating specific conditions.

Mechanism of Action:

Temoporfin functions by: Temoporfin is excited from ground state to the first excited singlet state by the application of 652 nm light . It is then thought to undergo intersystem crossing to an excited triplet state which is longer lived and able to interact with surrounding molecules . It is then thought to produce cytotoxic species by either a Type I or Type II reaction typical of agents used in photodynamic therapy. Type I involves either hydrogen abstraction of electron transfer from the excited photosensitizer to a substrate molecule to produce free radicals or radical ions. Type II reactions involve a similar reaction with oxygen as the substrate to produce reactive oxygen species. These reactive products cause oxidative damage to the cancer cell resulting in cell death. There is evidence that photodynamic therapy with Temoporfin activates macrophages and increases phagocytosis . These activated macrophages also produce more tumour necrosis factor-α (TNF-α) and nitric oxide (NO). It is thought that this increase in macrophage activity contributes to the efficacy of therapy through phagocytosis of cancer cells and increased cell death signalling though TNF-α. The increase in NO production likely contributes to oxidative damage through reactive nitrogen species. This mechanism highlights the drug's role in inhibiting or promoting specific biological pathways, contributing to its therapeutic effects.

Toxicity:

Categories:

Temoporfin is categorized under the following therapeutic classes: Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Biological Factors, Dermatologicals, Heterocyclic Compounds, Fused-Ring, Narrow Therapeutic Index Drugs, Photosensitizing Agents, Pigments, Biological, Porphyrins, Radiation-Sensitizing Agents, Sensitizers Used in Photodynamic/radiation Therapy. These classifications highlight the drug's diverse therapeutic applications and its importance in treating various conditions.