A newly engineered protein may be an effective way to reverse the effects of anticoagulants, scientists report in a new study. The protein, which they named FXaI16L, is also able to trigger blood clotting even in the presence of anticoagulants.

This, the scientists argue, may eventually be an effective way of rapidly clotting blood in emergencies. It is most relevant in accidents where the victims are taking anti-coagulants. The researchers published their results in Nature Medicine.

Blood clotting is a natural response in humans to prevent loss of dangerous amounts of blood as a result of injuries. However, if this process is deregulated, it can lead to several, life-threatening conditions. Stroke is one such condition.

Blood clots prevent the flow of blood. In cases where there is an obstruction in blood flow to the brain, an ischemic stroke occurs. Physiologically, when blood flow is obstructed, nutrients and oxygen fail to reach a specific part of the brain which leads to the death of those brain cells.

As a result, stroke patients usually experience drooping of the face, slurring of speech, and numbness in limbs. These are tell-tale signs of stroke and need immediate treatment. If left unchecked, a stroke may lead to more severe debilities, brain injuries, and even death.

In most cases – especially the mild ones – stroke can be treated with drugs that reduce cholesterol and blood pressure and those that remove and prevent future blood clots. These anticoagulants directly inhibit the coagulation factor Xa (FXa) to prevent clotting.

However, these have to be carefully used because they up the risk of excessive bleeding from accidents or emergency medical procedures.

Thus, the study aims to develop a molecule that can restore blood clotting rapidly to respond to emergency situations.

In their experiments, they used mouse models treated with anticoagulants. They focused on the ability of FXaI16L, a protein from a genetic variant of FXa, to promote blood clotting after treatment with an anticoagulant.

Remarkably, they found that injecting FXaI16L into these mouse models can reverse the anticoagulant effects, even in the presence of the anticoagulants.

Further, because FXaI16L is still an enzyme, it inherently has higher levels of activity compared to small, non-enzymatic molecule drug candidates that are currently in development.

Their findings represent a new molecule that can rapidly clot blood even in the presence of anticoagulants. Currently, the team is undergoing further research and trials to ensure the validity and efficacy of their drug candidate.

Study lead Rodney Camire Ph.D. said their next steps would be to test the approach in large animals to help determine whether this variant is effective and safe, and may progress to clinical trials. MIMS