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Cocaine

Group: Stimulants
Nicknames: sniff, charlie, C, snow, white, yay, rock, crack
Last reviewed: October 2026

Pharmacology

Cocaine is a serotonin-noradrenaline-dopamine reuptake inhibitor (SNDRI), which increases levels of these neurotransmitters in the gap (‘synapse’) between nerve cells. It does this by blocking the monoamine transporters SERT (serotonin), DAT (dopamine), and NET (noradrenaline/norepinephrine). Blocking these transporters prevents neurotransmitters from re-entering the nerve cell, leading to accumulation at the synapse where they activate their receptors to produce cocaine’s stimulating effects.

The way that powder cocaine produces its effects is the same as crack cocaine; the difference is that powder is usually snorted, while crack is usually smoked.

In the liver, cocaine is broken down into the inactive benzoylecgonine metabolite. However, when cocaine is taken alongside alcohol, some cocaine and benzoylecgonine can be converted into cocaethylene: an active stimulant which lasts longer than cocaine and is associated with a significantly increased risk in heart failure.

Contrary to popular belief, evidence does not suggest that cocaethylene is any more toxic to the heart than cocaine itself. Instead, the combination of cocaine and alcohol can lead to individuals taking more of both, while alcohol disrupts the metabolism of cocaine leading to higher levels of cocaine sticking around in the bloodstream for a longer time. Overall, this puts more pressure on the brain and body than cocaine alone, increasing overall health risks.

Cocaine is non-selective with a slight preference for DAT over NET and SERT, though it is mostly studied in relation to dopamine. Compared to amphetamines, which compete for dopamine through the transporter, cocaine directly sticks to and blocks DAT. However, scientists remain unsure if cocaine both inhibits and reverses dopamine transport, causing dopamine to be ejected from nerve cells into the synapse, in a similar way to amphetamines. This uncertainty comes from the fact that ‘atypical’ dopamine reuptake inhibitors, like bupropion and modafinil, do not produce euphoric and reinforcing effects to the same extent.

Sodium channels are blocked by cocaine in a similar way to local anaesthetics like novocaine, which stops sodium from entering the nerve cells. This quickly prevents tactile and pain signals from reaching the brain, leading to cocaine’s common numbing sensation. However, other substances (like procaine, also known by its commercial name ‘novocaine’) can be cut into cocaine to simulate a similarly numbing effect.

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