← Back to Drugs A–Z

Amphetamines

Group: Stimulants
Nicknames: speed, sulph, whizz, Adderall, Vyvanse, Elvanse, amfetamine
Last reviewed: October 2026

Pharmacology

Amphetamine exerts its behavioural effects by modulating neurotransmitters in the brain, affecting the monoamine neurotransmitters dopamine, noradrenaline (norepinephrine) and, to a lesser extent, serotonin. Amphetamines mainly act by releasing dopamine and noradrenaline into the ‘synapse’ between nerve endings in the brain and their reuptake is either slowed down or inhibited.

The ‘come-down’ effect is consequently disorientating and unpleasant, interferes with the sleep pattern and can be implicated in impulsive and high-risk behaviours.

Amphetamines increase the amount of dopamine and noradrenaline levels in the synapse, leading to their characteristic stimulatory effects on the brain and heart. They do this by entering nerve cells primarily through the dopamine transporter (DAT) and noradrenaline transporter (NET), outcompeting their respective neurotransmitters and therefore blocking their reuptake. Once inside the neurons, amphetamines activate the trace amine-associated receptor 1 (TAAR1) and the vesicular monoamine transporter-2 (VMAT2). This leads to a blockage and reversal of monoamine neurotransmitter transport, essentially causing nerve cells to empty dopamine and noradrenaline into the synapse where they can activate their respective receptors.

At high doses, amphetamines also block the monoamine oxidase enzymes (MAO-A and MAO-B), slowing down the metabolism of monoamine neurotransmitters.

Altogether, the build up of these neurotransmitters at synapses in the brain lead to enhanced mental focus, greater wakefulness, and improved ability to concentrate, which is helpful for those with ADHD or narcolepsy.

Dexamphetamine has a stronger preference for DAT and TAAR1 than levoamphetamine, making it a more potent stimulant. Levoamphetamine on the other hand causes slightly more cardiac and peripheral (bodily) effects.

During the follicular phase of menstruation (when oestrogen levels are higher) amphetamine effects may be heightened, while effects seem to be reduced during the luteal phase (when progesterone levels are higher).

The oral bioavailability (how well it’s absorbed in the gut) and half-life (how long it sticks around in the body) of dexamphetamine varies with urine acidity. Generally, immediate release amphetamines reach peak concentrations in the blood after 3 hours, while extended release take 7 hours after dosing. Amphetamines are metabolised by enzymes such as CYP2D6, so taking them along with CYP2D6 inhibitors (e.g. some antidepressants, CBD, ritonavir, quinidine) can increase the levels of amphetamines in the body, potentially leading to overdose (commonly known as “overamping” with stimulants).

Lisdexamphetamine is a prodrug of dexamphetamine and is less sensitive to acidity when taken orally. Once absorbed into the blood, lisdexamphetamine is converted into dexamphetamine leading to a more gradual peak and longer duration. Additionally, unlike dexamphetamine, injecting or snorting lisdexamphetamine does not enhance the subjective effects.

Keep This Information Independent

Release is a registered charity. We rely on your support to provide expert, non-judgmental legal and harm reduction guidance to thousands of people every year.

Donate to Release