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General Description:

Safinamide, identified by CAS number 133865-89-1, is a notable compound with significant therapeutic applications. Safinamide is for the treatment of parkinson's disease. It was approved in Europe in February 2015, and in the United States on March 21, 2017.

Indications:

This drug is primarily indicated for: Safinamide is indicated as an add-on treatment to levodopa with or without other medicines for Parkinson’s disease. Its use in specific medical scenarios underscores its importance in the therapeutic landscape.

Metabolism:

Safinamide undergoes metabolic processing primarily in: The principal step is mediated by amidases which have not been identified, and produces safinamide acid. It is also metabolized to O-debenzylated safinamide and N-delkylated amine. The N-dealkylated amine is then oxidized to a carboxylic acid and finally glucuronidated. Dealkylation reactions are mediated by cytochrome P450s (CYPs), especially CYP3A4. Safinamide acid binds to organic anion transporter 3 (OAT3), but no clinical relevance of this interaction has been determined. Safinamide also binds to ABCG2 transiently. No other transporter affinities have been found in preliminary studies. This metabolic pathway ensures efficient processing of the drug, helping to minimize potential toxicity and side effects.

Absorption:

The absorption characteristics of Safinamide are crucial for its therapeutic efficacy: Rapid with peak plasma concentrations ranging from 2 to 4 h, total bioavailability is 95%. Food prolonged the rate and did not affect the extent of absorption of safinamide. The drug's ability to rapidly penetrate into cells ensures quick onset of action.

Half-life:

The half-life of Safinamide is an important consideration for its dosing schedule: 22 h. This determines the duration of action and helps in formulating effective dosing regimens.

Protein Binding:

Safinamide exhibits a strong affinity for binding with plasma proteins: 88–90%. This property plays a key role in the drug's pharmacokinetics and distribution within the body.

Route of Elimination:

The elimination of Safinamide from the body primarily occurs through: 76% renal, 1.5% faeces. Understanding this pathway is essential for assessing potential drug accumulation and toxicity risks.

Volume of Distribution:

Safinamide is distributed throughout the body with a volume of distribution of: 1.8 litres/kg. This metric indicates how extensively the drug permeates into body tissues.

Clearance:

The clearance rate of Safinamide is a critical factor in determining its safe and effective dosage: total oral clearance of plasma , which accounts for parent safinamide as well as metabolites, was on average only 17.53 ± 2.71 ml/h × kg. It reflects the efficiency with which the drug is removed from the systemic circulation.

Mechanism of Action:

Safinamide functions by: Safinamide is a unique molecule with multiple mechanisms of action and a very high therapeutic index. It combines potent, selective, and reversible inhibition of MAO-B with blockade of voltage-dependent Na+ and Ca2+ channels and inhibition of glutamate release. Safinamide has neuroprotective and neurorescuing effects in MPTP-treated mice, in the rat kainic acid, and in the gerbil ischemia model. This mechanism highlights the drug's role in inhibiting or promoting specific biological pathways, contributing to its therapeutic effects.

Toxicity:

Classification:

Safinamide belongs to the class of organic compounds known as alpha amino acid amides. These are amide derivatives of alpha amino acids, classified under the direct parent group Alpha amino acid amides. This compound is a part of the Organic compounds, falling under the Organic acids and derivatives superclass, and categorized within the Carboxylic acids and derivatives class, specifically within the Amino acids, peptides, and analogues subclass.

Categories:

Safinamide is categorized under the following therapeutic classes: Agents that produce hypertension, Agents that reduce seizure threshold, Amines, Amino Acids, Amino Acids, Peptides, and Proteins, Anti-Parkinson Drugs, Antidepressive Agents, BCRP/ABCG2 Inhibitors, Benzene Derivatives, Benzyl Compounds, Central Nervous System Depressants, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2C19 Inhibitors, Cytochrome P-450 CYP2C19 inhibitors (strength unknown), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (strength unknown), Cytochrome P-450 CYP3A Inhibitors, Cytochrome P-450 CYP3A Substrates, Cytochrome P-450 CYP3A4 Substrates, Cytochrome P-450 CYP3A5 Inhibitors, Cytochrome P-450 CYP3A5 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytochrome P-450 Substrates, Dopamine Agents, Monoamine Oxidase A Inhibitors for interaction with Monoamine Oxidase A substrates, Monoamine Oxidase B Inhibitors, Monoamine Oxidase Inhibitors, Nervous System, Serotonergic Drugs Shown to Increase Risk of Serotonin Syndrome. These classifications highlight the drug's diverse therapeutic applications and its importance in treating various conditions.