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  • Writer's pictureCiaran Farrelly


*This post has been edited for context, it was originally published on

It all starts with a seed. The seed of a willow tree in this case. For centuries alchemists, witch doctors and some time later, chemists have been using aspirin and it’s derivatives to cure fever, aches and pains. More recently the blood thinning properties of aspirin have proven it to maintain it’s place as a mainstay of modern medicine.

In the early days of ‘aspirin’ usage, the bark of the willow tree was used in teas and tinctures to relieve the symptoms of fever and pains. In the nineteenth century chemists started isolating the active ingredient (Salicylic Acid) from bark and before long it had been patented and was being sold.

Initially, although it proved a powerful analgesic (painkiller), there were some unwanted side effects. These side effects most notably included heavy wear and tear on the stomach and intestines.

A major breakthrough came when slight alterations to the chemical structure was made.

For those unfamiliar to chemical structures (otherwise known as normal people) it may be hard to tell the difference, or at least understand how that change makes any difference. And the key is it doesn’t. It doesn’t really change the way it works, just how aggressive it is. The structure on the right is the structure of Aspirin as it’s consumed today. This small change in structure reduced the somewhat problematic stomach and intestinal bleeding. Not too shabby.

That’s all very well, but how does aspirin work?

Good question. First of all I have to tell you a little bit about prostaglandins. These are a family of reasonably complex molecules which have a plethora of roles in the body, but for this piece we can consider them as pain signallers. Your brain notes a high level of prostaglandins in a particular area and starts shouting “Hey! Hey! You’re in pain! THIS HURTS”. Aspirin blocks the production of these prostaglandins and so reduces your body’s pain response. Thats the bottom line, in a general sense. Happy with that answer? Great, you can stop here, not yet satisfied? Even better…

Cyclooxygenase 3d structure
This is a COX enzyme, and yes I’m well aware it looks like a four year old went nuts with some silly string

These prostaglandins we’ve been talking about are the trigger to your pain response, but how does Aspirin stop their production? To understand that we have to look at the prostaglandin production line, so to speak. Prostaglandins are the final product of a series of reactions from more basic building blocks. Each step in the production is carried out by a specific enyzyme, which specialises in precisely that specific reaction, or a set of very similar reactions.

The enzyme of interest in Aspirins case is the cyclooxygenase or COX (yep, seriously) enzyme. Enzymes comes in all shapes and sizes, but the key part is that they work by having an active site, where a particular reaction can occur with incredible efficiency. The precursor arrives at the active site, a reaction occurs, and the product is released. Aspirin works by getting into this active site and irreversibly binding to it, essentially jamming the cogs of this prostaglandin making machine. By stopping this reaction, the prostaglandins do not become fully formed and cannot do their job as pain signallers. Bang and the pain is gone!


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