| Class | Recreational sympathomimetic |
|---|---|
| Chemistry |
Phenylethylamine |
| Routes of administration |
oral, nasal, IM, s.c, IV |
| Absorption |
Good oral bioavailability (about 75%) |
| Solubility |
pKa = 9.9, poor water solubility; good lipid solubility |
| Distribution |
VOD= 4L/kg, 20% protein-bound |
| Metabolism |
Undergoes hepatic metabolism primarily by CYP2D6; CYP1A2, CYP3A4, and CYP2B6 involved to a lesser extent. First step may be oxidative deamination, beta-hydroxylation, or para-hydroxylation. Some metabolites are also psychoactive. A significant amount, estimated to be around a quarter, is excreted unchanged in urine. |
| Elimination |
Minimal free drug is eliminated in the urine |
| Time course of action |
Half-life 4-12 hours |
| Target receptor |
The intracellular receptor TAAR1, which is activated and causes the internalisation or transporter reversal of DAT, NET and SERT (as well as vesicular monoamine transporter VMAT2 and MAO which are inhibited) |
| Mechanism of action |
By increasing the synaptic concentration of noradrenaline and dopamine, amphetamine-like drugs acts as indirect sympathomimetics. Because they act centrally, this effect translates into increased alertness and arousal, as well as broadly adrenaline-like peripheral effects. |
| Clinical effects |
Increased alertness as well as nausea, vomiting, abdominal cramps, hypertension, tachycardia, exacerbation of motor tics, lower seizure threshold |
| Literature reference |
Heal et al (2013) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |