Formation of a blood clot

(© Tatiana Shepeleva -

LAUSANNE, Switzerland — Blood thinners commonly help people with heart-related illnesses, stroke, or at risk for heart attacks. Although they are very effective at preventing blood clots, they also have dangerous side-effects. One of the biggest issues is excessive bleeding and the inability to clot wounds. Now, scientists at the Swiss Federal Institute of Technology Lausanne (EPFL) have created a synthetic blood thinner that stops this life-threatening problem.

Most blood thinners carry out their job in one of two ways. Some blood thinners are anticoagulants (like warfarin and heparin) which work by slowing down the body’s clot-making processes. Others are anti-platelets, like aspirin, which work by blocking proteins or enzymes that cause blood cells and platelets to stick together.

Regardless of how they work, all blood thinners slow down or prevent blood clots from forming. They also prevent normal clotting mechanisms that slow down your bleeding after an injury. As a result, currently available blood thinning drugs can cause serious and sometimes life-threatening bleeding episodes.

How is this new blood thinner different?

EPFL’s new blood thinner is an anticoagulant which works by inhibiting an enzyme called coagulation factor XII (FXII). The first studies hinting at FXII inhibitors as potential blood thinners were conducted a few years ago. These studies show that genetically modified mice deficient in FXII have a significantly lower risk of dangerous blood clots, without having any bleeding side-effects.

Despite this initial discovery however, the ability to suppress FXII in humans is limited. Since scientists can’t create FXII-deficient humans, researchers began looking for ways to create synthetic FXII inhibitors. EPFL is the first group to do so.

“The FXII inhibitor is a variation of a cyclic peptide that we identified in a pool of more than a billion different peptides, using a technique named phage display,” says lead researcher Christian Heinis in a media release.

After identifying how to reduce FXII, the Swiss team enhanced their creation by substituting several of its natural amino acids with synthetic ones.

“This wasn’t a quick task; it took over six years and two generations of PhD students and post-docs to complete,” Heinis adds.

Promising results, but a long way to go

Once the blood thinner was optimized, EPFL teamed up with scientists at the University Hospital of Bern to test it. These studies reveal that the inhibitor effectively blocks clotting without enhancing bleeding. While the inhibitor can likely be used for treating a variety of illnesses, it may be particularly useful in the case of artificial lungs.

“The new FXII inhibitor is a promising candidate for safe thromboprotection in artificial lungs, which are used to bridge the time between lung failure and lung transplantation,” says Heinis. “In these devices, contact of blood proteins with artificial surfaces such as the membrane of the oxygenator or tubing can cause blood clotting.”

This contact-related blood clotting can be especially dangerous and potentially cause death. Further, “contact activation” limits the use of artificial lungs to only a few days or weeks. When researchers test the new blood thinner with artificial lungs, they find that it’s able to effectively reduce clotting without bleeding problems.

Despite the promise of the inhibitor as a blood thinner, however, there is one problem. The current version of the inhibitor is small, making it easily filtered out of the body by the kidneys. Thus, the current version of the inhibitor is not retained in the body for a long time and requires constant infusions.

Heinis and his team are currently working on creating different versions of the inhibitor that will work in the body for longer periods of time.

The study is published in Nature Communications.

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About Brianna Sleezer

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