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Common Blood Thinner Blocks COVID-19 As Effectively As Remdesivir, Study Shows

sars-cov-2 attaching to human cell receptor

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Key Takeaways

  • Heparin is an anticoagulant, a type of medication used to slow the formation of blood clots.
  • New research shows heparin prevents COVID-19 from attaching to host cells in the body and may limit the spread of the virus.
  • Patients who are critically ill from COVID-19 sometimes form damaging blood clots throughout the body and heparin can prevent this from happening.

Heparin, a common blood-thinning medication, is being increasingly used to treat patients with COVID-19. There is evidence that it can prevent some of the damaging effects of COVID-19 illness and even stop COVID-19 from attaching to cells in the body, perhaps as effectively as the drug remdesivir.

In July, researchers from Rensselaer Polytechnic Institute found heparin was just as effective at blocking SARS-CoV-2 infection in cells than remdesivir, an antiviral that received emergency use authorization from the Food and Drug Administration (FDA) to treat COVID-19 back in May. While heparin is FDA-approved to prevent blood clots, remdesivir isn't officially FDA-approved for any condition.

“We’re learning how to block viral infection, and that is knowledge we are going to need if we want to rapidly confront pandemics,” Jonathan Dordick, PhD, lead researcher and a professor of chemical and biological engineering at Rensselaer Polytechnic Institute says in a news release. “The reality is that we don’t have great antivirals. To protect ourselves against future pandemics, we are going to need an arsenal of approaches that we can quickly adapt to emerging viruses.”

What Is Heparin?

Heparin is an anticoagulant, a type of medication used to slow the formation of blood clots within the body. It is most commonly used to prevent blood clots in patients who have had surgery or medical procedures that predispose them to form blood clots. It will not dissolve an existing clot.

Heparin vs. Remdesivir

Researchers of the RPI study, published in Cell Discovery, looked at the concentration of heparin necessary to block 50% of viral infectivity caused by the SARS-CoV-2 virus. This is known as an EC50.

Heparin had an EC50 of 2.1 micromolar, while remdesivir had previously shown an EC50 of 770 nanomolar. The lower the value, the more potent and active the compound is. This means heparin is about a third as active as remdesivir.

Dordick explains this lower potency does not mean heparin is less effective at blocking SARS-CoV-2.

"Heparin and remdesivir have roughly similar virus inhibition," Dordick tells Verywell via email. "An EC50 that is one third as active is basically equivalent, as EC50 values are meant to cover thousands of fold concentration ranges."

He says that while the drugs may be similarly effective at blocking COVID-19, their mechanisms of action are very different.

Remdesivir targets an enzyme responsible for virus replication, preventing SARS-CoV-2 from spreading in cells. Heparin, on the other hand, "tightly binds to the viral spike protein," Dordick says.

Essentially, heparin could serve as a decoy for any SARS-CoV-2 virus in the body. Instead of latching onto human cell receptors, the spike protein on the virus could latch onto heparin. Eventually, it would degrade on its own.

Heparin Is Already Being Used to Treat COVID-19

The RPI study considers the use of heparin to treat COVID-19 early, before someone is really sick. But because of its known use as an anticoagulant, heparin is currently being used to treat some of the sickest COVID-19 patients.

“In critically ill hospitalized patients with COVID-19, the use of heparin in the absence of clinically-proven or suspected thrombus [blood clot] is a matter of debate, since randomized studies are lacking," Jennifer Haythe, MD, a critical care cardiologist at Columbia University Center in New York City, tells Verywell.

Still, Haythe says that because of the high rate of blood clots in these critically ill patients, "many centers are opting to treat patients [with heparin] based on limited data."

Some patients with COVID-19 are at an increased risk for blood clots due to a cascade of widespread inflammation within the body triggered by the infection. When the body is under attack from infection, the immune system releases factors that stop bleeding, just as it would if a person were injured.

Between 8% and 54% of patients with COVID-19 will develop some form of a blood clot, immunologist Lina Velikova, MD, MPH, tells Verywell. This rate is much higher than other critical illnesses such as pneumonia or sepsis.

What This Means For You

The evidence in support of heparin as part of COVID-19 treatment is growing, especially in hospitalized patients. It can prevent the blood clots that complicate recovery and stop the virus from spreading in the body. If you or someone you care for are diagnosed with COVID-19, ask your health care provider what you can do to lower your risk of developing blood clots.

How Is Heparin Administered?

When used in the treatment of COVID-19, heparin can be administered in multiple ways, according to Daniel Goldstein, MD, vice chairman of the department of cardiothoracic surgery at Montefiore Health System in New York.

"Practice varies from institution to institution, but the common approaches include low molecular weight heparins (LMWHs) and IV heparin," Goldstein tells Verywell, adding that bivalirudin and antiplatelets may be used as well.

Low molecular weight heparins (LMWHs) are given as injections in the abdomen once or twice a day. They include drugs like enoxaparin (Lovenox) and dalteparin (Fragmin).

Unfractionated heparin (UFHs), or the IV heparin Goldstein mentions, is generally given by continuous intravenous (IV) infusion. Regular blood samples must be drawn to assess how quickly the blood is forming clots, and the dose of heparin is adjusted based on results. Treatment with UFHs requires more monitoring than LMWHs.

What Are the Risks of Heparin Use?

Heparin causes significant bleeding in between 10% and 15% of patients.

UFHs and LMWHs can also cause a condition known as heparin-induced thrombocytopenia in 0.2% to 5% of patients, in which platelet counts decrease in response to heparin treatment. This is a serious adverse reaction to heparin therapy that further increases the risk for bleeding and requires that the heparin medication be stopped.

If any signs of bleeding occur while on heparin, the medication should be stopped and the prescriber notified immediately.

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