Australian and US researchers have genetically engineered a novel antithrombotic drug, which binds only to activated platelets at the site of a thrombus.

By only binding to activated platelets, not sealing platelets, there is no risk of bleeding complications with the recombinant fusion protein known as Targ-TAP.

Targ-TAP consists of a single-chain antibody that targets and blocks the activated GPIIb/IIIa complex on platelets, and tick anticoagulant peptide (TAP), a potent direct inhibitor of factor Xa.

Baker Heart and Diabetes Institute and Harvard Medical School have jointly filed an application for a patent on Targ-TAP.

Speaking at the ISTH Congress in Melbourne, the Baker Institute’s Dr Xiaowei Wang said the challenge with current anti-platelet and anticoagulant drugs for VTE prophylaxis was the risk of bleeding complications.

She said the specific binding affinity of Targ-TAP to activated platelets had been demonstrated in both mouse and human blood.

Targ-TAP does not increase bleeding time or blood volume loss and had been shown to inhibit both arterial and venous thrombosis.

“We first looked at it as a treatment for arterial thrombosis. But a lot of models for thrombosis in the pre-clinical setting are very fast and so we also looked at the venous side of things where it usually takes a bit of time to build up.”

“We found out you can use Targ-TAP as a prevention and because of that we are now going back and looking at whether or not this drug is probably more suited to, for example, people with a previous PE or VTE who have to take a flight from Australia to Europe. It is a high-risk event,” she said.

Dr Wang said the goal was that Targ-TAP could replace a heparin or warfarin injection and avoid any bleeding risk.

The subcutaneous injection of Targ-TAP had a circulating half-life of about 10 hours – an improvement on less than three hours for intravenous administration.

She said the next research steps would include looking at the toxicology of the drug, humanising the peptide and further extending its circulating half-life.