For a long time now scientists have understood the dangers of nicotine addiction. Also for a long time, they’ve been trying to find an effective treatment for it. And while nicotine gum and patches and other devices around now to help stop people from smoking are good, they’re still failing for many millions of people who want to stop but can’t.

However, thanks to a group of scientists at Scripps Research, that could all be about to change as they’ve developed an engineered enzyme that might just do the trick. What this enzyme does is it breaks down nicotine in the bloodstream before it has a chance to reach the brain. This reduces the want for nicotine and as a result, reverses the signs of nicotine dependence.





While the study has only been carried out on nicotine-dependent rats so far, it shows great promise for helping humans kick the habit also. “This is a very exciting approach because it can reduce nicotine dependence without inducing cravings and other severe withdrawal symptoms, and it works in the bloodstream, not the brain, so its side effects should be minimal,” explains Olivier George, Ph.D., principal investigator on the study and associate professor at Scripps Research.

It’s estimated that as many as 60 percents of those who try cigarettes become regular smokers. And even today, with all the aids in place, around 75 percent of those who try to quit, end up relapsing. This technique of reversing nicotine dependence by stopping the drug reaching the brain has been considered as a treatment for a long time. However, previous efforts have never been effective enough.

The enzyme used in this study is called NicA2-J1. It was chosen as it clearly has the ability to reduce nicotine blood levels in rats. One experiment involved rats spending 21 hours a day for 12 days in a chamber where they had access to intravenous nicotine by simply pressing a lever. By learning to self-administer the drug in such a way, the rats soon became dependent on it.





After the 12 days had passed, the rats were only allowed nicotine every 48 hours. This led to the animals experiencing withdrawals in between. However, those treated with the highest dose of NicA2-J1 had very low nicotine blood levels and withdrawal symptoms were significantly reduced.

Normally when an animal that’s nicotine dependent is suddenly deprived of the drug, withdrawal symptoms appear almost instantly. “It’s like quitting ‘cold turkey’ — the subject will feel horrible,” says George. “However, what’s unique about this enzyme is that it removes enough nicotine to reduce the level of dependence, but leaves enough to keep the animals from going into severe withdrawal.”

Another hallmark characteristic that goes alongside nicotine dependence is the need to seek the drug even though they know the serious consequences associated with it (i.e. impairment of lung function and a higher risk of cancer as well as many others). Remarkably, from the study, the researchers revealed that NicA2-J1 could, in fact, help reduce this compulsive motivation. The team found that as the animals learned there was a 30 percent chance of being shocked when pressing the nicotine inducing lever, those treated with NicA2-J1 were much quicker to reduce their lever presses.





The researchers also looked at the rats’ susceptibility to relapse after going without nicotine for 10 days. They then injected them with the drug to re-awaken their desire for it. On top of that, they restored access to the lever press. Rats who went untreated showed a significant increase in the number of lever presses, while those treated with NicA2-J1 pressed it far less.

With such promising results, the researchers are now keen to test NicA2-J1 on humans and are pushing to get it to clinical trial. Until then, they will continue to study the enzyme’s properties to get a much deeper understanding of all it can be used for.

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