U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

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Status:
Investigational
Source:
INN:cathinone [INN]
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)


Cathinone is one of the biologically active alkaloids found in the khat shrub (Catha edulis). Due to its psychoactive properties, khat has been known and utilized for ages by the inhabitants of East Africa and the northeastern parts of Arabian Peninsula. In many regions, chewing of freshly collected khat leaves (thus liberating cathinone, which affects the central nervous system) is considered a matter of culture and local tradition. Because of their structural similarity to amphetamine, cathinone and its analogs are often denoted as “natural amphetamines”, and the only structural difference between amphetamine and cathinone is the presence of a carbonyl group in the α-position of cathinone’s side chain. Similar to amphetamine, cathinone and its analogs are characterized by stimulating, euphoric, and empathogenic properties. Due to their effects on the central nervous system, the first synthetic cathinone derivatives were synthesized for medicinal purposes in the early twentieth century, but they began attracting wider attention around the year 2000. At that time, synthetic cathinones were included in a broader group of psychoactive compounds denoted as “legal drugs” or “designer drugs”
Status:
Other

Class (Stereo):
CHEMICAL (RACEMIC)

Status:
US Previously Marketed
Source:
Synatan by Irwin, Neisler (Mallinckrodt)
(1955)
Source URL:
First approved in 1955
Source:
Synatan by Irwin, Neisler (Mallinckrodt)
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)


DEXTROAMPHETAMINE TANNATE is a salt of dextroamphetamine, amphetamine enantiomer. It is used as CNS stimulant in the treatment of attention deficit hyperactivity disorder.
Status:
US Previously Marketed
Source:
Benzaldehyde U.S.P.
(1921)
Source URL:
First marketed in 1921
Source:
Benzaldehyde U.S.P.
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)


Benzaldehyde is the simplest and possibly the most industrially useful member of the family of aromatic aldehydes. Benzaldehyde exists in nature, primarily in combined forms such as a glycoside in almond, apricot, cherry, and peach seeds. The characteristic benzaldehyde odor of oil of bitter almond occurs because of trace amounts of free benzaldehyde formed by hydrolysis of the glycoside amygdalin. Benzaldehyde is a versatile intermediate because of its reactive aldehyde hydrogen, its carbonyl group, and the benzene ring. Benzaldehyde is formed from phenylpyruvic acid, derived by the aminotransferase activity on phenylalanine, in the presence of high levels of Mn2+, and contributes to the generation of flavor compound during cheese ripening. Benzaldehyde is a synthetic flavoring substance, sanctioned by the U.S. Food and Drug Administration (FDA) to be generally recognized as safe (GRAS) for foods. Benzaldehyde is also recognized as safe for use as a bee repellant in the harvesting of honey. Benzaldehyde's most important use is in organic synthesis, where it is the raw material utilized to produce various aldehydes. Because Benzaldehyde rapidly metabolizes to Benzoic Acid in the skin, the available dermal irritation and sensitization data demonstrating no adverse reactions to Benzoic Acid were considered supportive of the safety of Benzaldehyde.
Amphetamine is also prescribed in enantiopure and prodrug form as dextroamphetamine and lisdexamfetamine respectively. Lisdexamfetamine is structurally different from amphetamine, and is inactive until it metabolizes into dextroamphetamine. Dextroamphetamine is useful for those with ADHD and Narcolepsy. It improves self-control for people who have a hard time naturally controlling themselves. Dextroamphetamine aids a person learning and memory of words, and perhaps makes the brain stronger. When a person given dextroamphetamine is tested, their brain is extremely active in the brain parts required for the test and radically less active in other parts. Short practice sessions with dextroamphetamine have a greater effect on learning than sessions without dextroamphetamine. Dextroamphetamine raises decision-making scores, improves choices, and changes beliefs about rewards; at the same time, dextroamphetamine barely—if at all—affects guesses of time. Those who feel lower amounts of joy from dextroamphetamine have greater impulsivity improvements compared to those who feel extreme happiness. The drug should be avoided for those who have hypersensitivity to amphetamines, a history of drug abuse, cardiovascular diseases, hypertensive disease, hyperthyroidism, or in those with glaucoma. In 1935, the medical community became aware of the stimulant properties of amphetamine, specifically dextroamphetamine, and in 1937 Smith, Kline, and French introduced Dexedrine tablets, under the tradename Dexedrine. In the United States, Dexedrine tablets were approved to treat narcolepsy, attention disorders, depression, and obesity. Dexedrine, along with other sympathomimetic, was eventually classified as schedule II, the most restrictive category possible for a drug with recognized medical uses. The exact mechanism of action is not known. Dextroamphetamine stimulates the release of norepinephrine from central adrenergic receptors. At higher dosages, it causes release of dopamine from the mesocorticolimbic system and the nigrostriatal dopamine systems by reversal of the monoamine transporters. Dextroamphetamine may also act as a direct agonist on central 5-HT receptors and may inhibit monoamine oxidase (MAO). Modulation of serotonergic pathways may contribute to the calming effect.
Amphetamine is also prescribed in enantiopure and prodrug form as dextroamphetamine and lisdexamfetamine respectively. Lisdexamfetamine is structurally different from amphetamine, and is inactive until it metabolizes into dextroamphetamine. Dextroamphetamine is useful for those with ADHD and Narcolepsy. It improves self-control for people who have a hard time naturally controlling themselves. Dextroamphetamine aids a person learning and memory of words, and perhaps makes the brain stronger. When a person given dextroamphetamine is tested, their brain is extremely active in the brain parts required for the test and radically less active in other parts. Short practice sessions with dextroamphetamine have a greater effect on learning than sessions without dextroamphetamine. Dextroamphetamine raises decision-making scores, improves choices, and changes beliefs about rewards; at the same time, dextroamphetamine barely—if at all—affects guesses of time. Those who feel lower amounts of joy from dextroamphetamine have greater impulsivity improvements compared to those who feel extreme happiness. The drug should be avoided for those who have hypersensitivity to amphetamines, a history of drug abuse, cardiovascular diseases, hypertensive disease, hyperthyroidism, or in those with glaucoma. In 1935, the medical community became aware of the stimulant properties of amphetamine, specifically dextroamphetamine, and in 1937 Smith, Kline, and French introduced Dexedrine tablets, under the tradename Dexedrine. In the United States, Dexedrine tablets were approved to treat narcolepsy, attention disorders, depression, and obesity. Dexedrine, along with other sympathomimetic, was eventually classified as schedule II, the most restrictive category possible for a drug with recognized medical uses. The exact mechanism of action is not known. Dextroamphetamine stimulates the release of norepinephrine from central adrenergic receptors. At higher dosages, it causes release of dopamine from the mesocorticolimbic system and the nigrostriatal dopamine systems by reversal of the monoamine transporters. Dextroamphetamine may also act as a direct agonist on central 5-HT receptors and may inhibit monoamine oxidase (MAO). Modulation of serotonergic pathways may contribute to the calming effect.
Amphetamine is also prescribed in enantiopure and prodrug form as dextroamphetamine and lisdexamfetamine respectively. Lisdexamfetamine is structurally different from amphetamine, and is inactive until it metabolizes into dextroamphetamine. Dextroamphetamine is useful for those with ADHD and Narcolepsy. It improves self-control for people who have a hard time naturally controlling themselves. Dextroamphetamine aids a person learning and memory of words, and perhaps makes the brain stronger. When a person given dextroamphetamine is tested, their brain is extremely active in the brain parts required for the test and radically less active in other parts. Short practice sessions with dextroamphetamine have a greater effect on learning than sessions without dextroamphetamine. Dextroamphetamine raises decision-making scores, improves choices, and changes beliefs about rewards; at the same time, dextroamphetamine barely—if at all—affects guesses of time. Those who feel lower amounts of joy from dextroamphetamine have greater impulsivity improvements compared to those who feel extreme happiness. The drug should be avoided for those who have hypersensitivity to amphetamines, a history of drug abuse, cardiovascular diseases, hypertensive disease, hyperthyroidism, or in those with glaucoma. In 1935, the medical community became aware of the stimulant properties of amphetamine, specifically dextroamphetamine, and in 1937 Smith, Kline, and French introduced Dexedrine tablets, under the tradename Dexedrine. In the United States, Dexedrine tablets were approved to treat narcolepsy, attention disorders, depression, and obesity. Dexedrine, along with other sympathomimetic, was eventually classified as schedule II, the most restrictive category possible for a drug with recognized medical uses. The exact mechanism of action is not known. Dextroamphetamine stimulates the release of norepinephrine from central adrenergic receptors. At higher dosages, it causes release of dopamine from the mesocorticolimbic system and the nigrostriatal dopamine systems by reversal of the monoamine transporters. Dextroamphetamine may also act as a direct agonist on central 5-HT receptors and may inhibit monoamine oxidase (MAO). Modulation of serotonergic pathways may contribute to the calming effect.
Amphetamine is also prescribed in enantiopure and prodrug form as dextroamphetamine and lisdexamfetamine respectively. Lisdexamfetamine is structurally different from amphetamine, and is inactive until it metabolizes into dextroamphetamine. Dextroamphetamine is useful for those with ADHD and Narcolepsy. It improves self-control for people who have a hard time naturally controlling themselves. Dextroamphetamine aids a person learning and memory of words, and perhaps makes the brain stronger. When a person given dextroamphetamine is tested, their brain is extremely active in the brain parts required for the test and radically less active in other parts. Short practice sessions with dextroamphetamine have a greater effect on learning than sessions without dextroamphetamine. Dextroamphetamine raises decision-making scores, improves choices, and changes beliefs about rewards; at the same time, dextroamphetamine barely—if at all—affects guesses of time. Those who feel lower amounts of joy from dextroamphetamine have greater impulsivity improvements compared to those who feel extreme happiness. The drug should be avoided for those who have hypersensitivity to amphetamines, a history of drug abuse, cardiovascular diseases, hypertensive disease, hyperthyroidism, or in those with glaucoma. In 1935, the medical community became aware of the stimulant properties of amphetamine, specifically dextroamphetamine, and in 1937 Smith, Kline, and French introduced Dexedrine tablets, under the tradename Dexedrine. In the United States, Dexedrine tablets were approved to treat narcolepsy, attention disorders, depression, and obesity. Dexedrine, along with other sympathomimetic, was eventually classified as schedule II, the most restrictive category possible for a drug with recognized medical uses. The exact mechanism of action is not known. Dextroamphetamine stimulates the release of norepinephrine from central adrenergic receptors. At higher dosages, it causes release of dopamine from the mesocorticolimbic system and the nigrostriatal dopamine systems by reversal of the monoamine transporters. Dextroamphetamine may also act as a direct agonist on central 5-HT receptors and may inhibit monoamine oxidase (MAO). Modulation of serotonergic pathways may contribute to the calming effect.