Researchers at the University of Birmingham have identified a protein that appears to play a key role in forming blood clots.
Small cells called platelets circulate in the blood and respond to injury by becoming sticky and sending out tiny "arms" that latch onto other platelets and the surface of the injury, forming a clot.
Lead researcher Yotis Senis claim to have identified a protein called CD148 that controls the stickiness of blood.
During the study, the research team compared platelets from mice engineered to lack CD148, with those from normal mice.
They found that platelets from mice deficient in the protein were more lethargic in responding to injury, sent out fewer arms and formed smaller clots.
"CD148 looks very promising as a realistic target for new drug development," New Scientist quoted Jeremy Pearson, Associate Medical Director at the British Heart Foundation as saying.
For the safety of any future blood-thinning medicine, removing CD148 didn't cause any dangerous bleeding. This may be because several other pathways can also trigger clotting.
The blood-thinners like aspirin inhibited all these pathways until the body removes the platelet from the circulation.
They can trigger dangerous bleeding in some patients, particularly in the stomach.
"They're a blunt instrument," said Senis.
Senis revealed that a drug that reversibly blocked CD148 would be safer because it would only affect one pathway, dampening clotting but leaving some control over bleeding.
The study appears in journal Blood.