Solriamfetol API Manufacturers
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Looking for Solriamfetol API 178429-62-4?
- Description:
- Here you will find a list of producers, manufacturers and distributors of Solriamfetol. 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:
- Solriamfetol
- Synonyms:
- (2R)-2-amino-3-phenylpropyl carbamate , Solriamfetol
- Cas Number:
- 178429-62-4
- DrugBank number:
- DB14754
- Unique Ingredient Identifier:
- 939U7C91AI
General Description:
Solriamfetol, identified by CAS number 178429-62-4, is a notable compound with significant therapeutic applications. Solriamfetol marketed under the brand name Sunosi by Jazz Pharmaceuticals in the United States is a dopamine and norepinephrine reuptake inhibitor (DNRI) indicated in treating daytime sleepiness associated with narcolepsy or obstructive sleep apnea. Solriamfetol was given FDA approval in 2019.
Indications:
This drug is primarily indicated for: Solriamfetol is indicated for treatment of daytime sleepiness associated with obstructive sleep apnea and narcolepsy, but is not a treatment for the underlying airway obstruction in apnea patients. Its use in specific medical scenarios underscores its importance in the therapeutic landscape.
Metabolism:
Solriamfetol undergoes metabolic processing primarily in: Solriamfetol does not undergo significant metabolism in humans, though less than 1% of solriamfetol is metabolized to N-acetyl solriamfetol. This metabolic pathway ensures efficient processing of the drug, helping to minimize potential toxicity and side effects.
Absorption:
The absorption characteristics of Solriamfetol are crucial for its therapeutic efficacy: Oral bioavailability of solriamfetol is approximately 95%. Peak plasma concentration is reached in 2 hours (with a range of 1.25 to 3 hours) in fasted patients. When solriamfetol is taken with a high fat meal, the time to peak plasma concentration increases to 3 hours. The drug's ability to rapidly penetrate into cells ensures quick onset of action.
Half-life:
The half-life of Solriamfetol is an important consideration for its dosing schedule: 7.1 hours. Other studies have found the mean half life to be 6.1 ± 1.2 hours in fasted subjects and 5.9 ± 1.2 hours in fed subjects. This determines the duration of action and helps in formulating effective dosing regimens.
Protein Binding:
Solriamfetol exhibits a strong affinity for binding with plasma proteins: 13.3% to 19.4% protein bound over a plasma concentration range of 0.059 to 10.1mcg/mL. This property plays a key role in the drug's pharmacokinetics and distribution within the body.
Route of Elimination:
The elimination of Solriamfetol from the body primarily occurs through: 95% of solriamfetol is recovered in urine unchanged by metabolism. Less than 1% of solriamfetol is recovered as N-acetyl solriamfetol. Understanding this pathway is essential for assessing potential drug accumulation and toxicity risks.
Volume of Distribution:
Solriamfetol is distributed throughout the body with a volume of distribution of: 199L. Other studies have found the volume of distribution to be 158.2L ± 37.3L in fasted subjects and 159.8L ± 38.9L in fed subjects. This metric indicates how extensively the drug permeates into body tissues.
Clearance:
The clearance rate of Solriamfetol is a critical factor in determining its safe and effective dosage: Renal clearance is 18.2L/h and total clearance is 19.5L/h. Other studies have found clearance to be 18.4 ± 4.2L/h in fasted subjects and 18.8 ± 4.2L/h in fed subjects. It reflects the efficiency with which the drug is removed from the systemic circulation.
Pharmacodynamics:
Solriamfetol exerts its therapeutic effects through: Solriamfetol weakly binds to dopamine and norepinephrine transporters but not serotonin transporters. Solriamfetol does not bind to dopamine, serotonin, norepinephrine, GABA, adenosine, histamine, orexin, benzodiazepines, or muscarinic and nicotinic receptors. Solriamfetol is also associated with a mean increase of 21 beats per minute (BPM) in heart rate in patients taking 300mg (twice the maximum recommended dose) and 27 BPM in patients taking 900mg (six times the maximum recommended dose). 300mg of solriamfetol does not increase the QTcF interval to a clinically relevant degree. The drug's ability to modulate various physiological processes underscores its efficacy in treating specific conditions.
Mechanism of Action:
Solriamfetol functions by: The specific mechanism of action is unknown but it may be through its activity as a dopamine and norepinephrine reuptake inhibitor. This mechanism highlights the drug's role in inhibiting or promoting specific biological pathways, contributing to its therapeutic effects.
Toxicity:
Categories:
Solriamfetol is categorized under the following therapeutic classes: Acids, Acyclic, Adrenergic Agents, Adrenergic Uptake Inhibitors, Agents producing tachycardia, Agents that produce hypertension, Amino Acids, Amino Acids, Aromatic, Amino Acids, Cyclic, Amino Acids, Peptides, and Proteins, Antidepressive Agents, Central Nervous System Agents, Central Nervous System Depressants, Centrally Acting Sympathomimetics, Dopamine Agents, Dopamine And Norepinephrine Reuptake Inhibitors, Dopamine Uptake Inhibitors, Drugs that are Mainly Renally Excreted, MATE 1 Substrates, MATE substrates, Nervous System, Norepinephrine Reuptake Inhibitor, OCT2 Substrates, Psychoanaleptics, Psychostimulants, Agents Used for ADHD and Nootropics, Wakefulness-Promoting Agents. These classifications highlight the drug's diverse therapeutic applications and its importance in treating various conditions.
Solriamfetol is a type of Central Nervous System Agents
Central Nervous System (CNS) Agents are a crucial category of pharmaceutical Active Pharmaceutical Ingredients (APIs) that specifically target the central nervous system. The CNS encompasses the brain and spinal cord, playing a vital role in regulating and controlling various bodily functions, including cognition, movement, emotions, and sensory perception. These agents are designed to interact with specific receptors, enzymes, or ion channels within the CNS to modulate neural activity and restore normal functioning.
CNS agents comprise a diverse range of pharmaceutical APIs, including analgesics, anesthetics, antipsychotics, sedatives, hypnotics, anti-epileptics, and antidepressants. Each subcategory addresses distinct neurological disorders and conditions. For instance, analgesics alleviate pain by targeting receptors in the brain and spinal cord, while antipsychotics are employed to manage psychosis symptoms in mental illnesses such as schizophrenia.
The development of CNS agents involves rigorous research, molecular modeling, and extensive clinical trials to ensure safety, efficacy, and specific target engagement. Pharmaceutical companies invest significant resources in identifying novel drug targets, synthesizing new compounds, and optimizing their pharmacological properties. These agents undergo rigorous regulatory evaluations and must adhere to stringent quality standards and guidelines.
Given the prevalence of CNS disorders globally, the market demand for effective CNS agents is substantial. The development of innovative CNS APIs not only improves patient outcomes but also provides valuable commercial opportunities for pharmaceutical companies. Continued advancements in CNS agent research and development hold the promise of groundbreaking therapies that can improve the quality of life for individuals affected by neurological conditions.
