Lisdexamfetamine (LDX) is a d-amphetamine (d-AMPH) pro-drug used to treat Attention Deficit and Hyperactivity Disorder (ADHD) and Binge Eating Disorder (BED). After oral administration, lisdexamfetamine dimesylate is rapidly absorbed from the gastrointestinal tract and converted to dextroamphetamine, which is responsible for the drug’s activity. Amphetamines are thought to block the reuptake of norepinephrine and dopamine into the presynaptic neuron and increase the release of these monoamines into the extraneuronal space. Most common adverse reactions in children, adolescents and/or adults with ADHD were anorexia, anxiety, decreased appetite, decreased weight, diarrhea, dizziness, dry mouth, irritability, insomnia, nausea, upper abdominal pain, and vomiting. Agents that alter urinary pH can alter blood levels of amphetamine. Acidifying agents decrease amphetamine blood levels, while alkalinizing agents increase amphetamine blood levels. Needs to adjust Lisdexamfetamine dosage accordingly.

Amphetamine is a potent central nervous system (CNS) stimulant that is used in the treatment of attention deficit hyperactivity disorder (ADHD), narcolepsy, and obesity. Amphetamine was discovered in 1887 and exists as two enantiomers: levoamphetamine and dextroamphetamine. The mode of therapeutic action in ADHD is not known. Amphetamines are thought to block the reuptake of norepinephrine and dopamine into the presynaptic neuron and increase the release of these monoamines into the extraneuronal space. At higher dosages, they cause release of dopamine from the mesocorticolimbic system and the nigrostriatal dopamine systems. Amphetamine may also act as a direct agonist on central 5-HT receptors and may inhibit monoamine oxidase (MAO). In the periphery, amphetamines are believed to cause the release of noradrenaline by acting on the adrenergic nerve terminals and alpha- and beta-receptors. Modulation of serotonergic pathways may contribute to the calming affect. The drug interacts with VMAT enzymes to enhance release of DA and 5-HT from vesicles. It may also directly cause the reversal of DAT and SERT. Several currently prescribed amphetamine formulations contain both enantiomers, including Adderall, Dyanavel XR, and Evekeo, the last of which is racemic amphetamine sulfate. 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.

Brolamfetamine (also known as DOB, bromo-DMA, and 4-bromo-2,5-dimethoxyphenylisopropylamine) is one of a vast number of compounds used recreationally to achieve hallucinogenic effects. Brolamfetamine is one of the most potent hallucinogens, with its hallucinogenic potency directly linked to its abuse potential. Brolamfetamine acts as a partial agonist of 5HT2A, 5HT2B, 5HT2C, and TAAR1 receptors, but it’s psychedelic effects are mainly mediated by its agonistic properties at the 5-HT2A receptor. Animal studies have shown physiologic effects including hypertension, tachycardia, hyperpyrexia, pupillary dilatation, and peripheral vasoconstriction. In general, Brolamfetamine having a similar effect to LSD, with slower onset (up to 3–4 h to peak intoxication) and longer duration of effect (up to 36 h). Brolamfetamine is not commonly available, through periods of higher circulation were reported in Australia in 1983, Ireland in 2003, and in Italy in 2015. Brolamphetamine, as well as many other synthetic hallucinogens, are increasingly being sold as LSD. Internationally Brolamfetamine is a Schedule I drug under the Convention on Psychotropic Substances. Due to its selectivity, Brolamfetamine is often used in scientific research when studying the 5-HT2 receptor subfamily.

4-Methoxymethamphetamine (PMMA, para-Methoxymethamphetamine) is a stimulant and psychedelic drug closely related to the amphetamine-class serotonergic drug para-methoxyamphetamine (PMA). Little is known about the pharmacological properties, metabolism, and toxicity of 4-Methoxymethamphetamine. Because of its structural similarity to para-methoxyamphetamine, which has known toxicity in humans, it is thought to have considerable potential to cause harmful side effects or death in overdose. In the early 2010s, a number of deaths in users of the drug MDMA were linked to misrepresented tablets and capsules of 4-Methoxymethamphetamine. In 2010–2013, a cluster of 29 fatal poisonings related to the toxic designer drug 4-Methoxymethamphetamine was revealed in Norway. The toxicity of PMMA is regarded as substantially higher than for amphetamine, methamphetamine, and MDMA, as indicated by 131 fatal and 31 nonfatal poisonings associated with the abuse of 4-Methoxymethamphetamine worldwide. The toxicity of 4-Methoxymethamphetamine is positively correlated with the 4-Methoxymethamphetamine dose and the blood drug level, but the existing literature indicates that certain human subjects may have an increased risk of 4-Methoxymethamphetamine toxicity. 4-Methoxymethamphetamine, like PMA most likely acts as a selective serotonin releasing agent (SSRA) with weak effects on dopamine and norepinephrine transporters. However, relative to MDMA, it is considerably less effective as a serotonin releaser with properties more akin to a reuptake inhibitor in comparison. It evokes robust hyperthermia while producing only modest hyperactivity and serotonergic neurotoxicity, substantially lower than that caused by MDMA.