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Ephedrine works by inducing the release of norepinephrine and hence indirectly activating the α-and β-adrenergic receptors. [11] Chemically, ephedrine is a substituted amphetamine and is the (1R,2S)-enantiomer of β-hydroxy-N-methylamphetamine. [14] Ephedrine was first isolated in 1885 and came into commercial use in 1926.
Amphetamine was first synthesized in 1887 in Germany by Romanian chemist, Lazăr Edeleanu, who named the drug phenylisopropylamine. [4] [3] [18] [2] This concoction was one of a series of compounds related to the plant derivative ephedrine, which had been isolated from the Chinese ephedra plant that same year by Nagai Nagayoshi. [6]
Amphetamine type stimulants (ATS) are a group of synthetic drugs that are chemical derivatives of the parent compound alpha-methylphenethylamine, also known as amphetamine. Common ATS includes amphetamine, methamphetamine , ephedrine , pseudoephedrine , 3,4-methylenedioxymethamphetamine (MDMA), 3,4-methylenedioxyamphetamine (MDA) and 3,4 ...
Subsequently, amphetamine was used in the treatment of narcolepsy, obesity, hay fever, orthostatic hypotension, epilepsy, Parkinson's disease, alcoholism and migraine. [12] [15] The "reinforcing" effects of substituted amphetamines were quickly discovered, and the misuse of substituted amphetamines had been noted as far back as 1936. [15]
Amphetamine [note 2] (contracted from alpha-methylphenethylamine) is a central nervous system ... and decongestants like ephedrine, among other subgroups. ...
β-Hydroxyamphetamines have increased hydrophilicity and lower lipophilicity relative to their amphetamine counterparts owing to their β-hydroxyl group. [ 13 ] [ 14 ] For comparison, the predicted log P (XLogP3) of amphetamine is 1.8, [ 15 ] of β-hydroxyamphetamine is 0.8, [ 16 ] and of cathinone is 1.1. [ 17 ]
Adderall is available as an immediate-release tablet taken two to three times daily every four to six hours or as a long-acting tablet taken without food upon waking up. If you take Adderall late ...
The mechanisms of sympathomimetic drugs can be direct-acting (direct interaction between drug and receptor), such as α-adrenergic agonists, β-adrenergic agonists, and dopaminergic agonists; or indirect-acting (interaction not between drug and receptor), such as MAOIs, COMT inhibitors, release stimulants, and reuptake inhibitors that increase the levels of endogenous catecholamines.
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