Arterial thrombi are platelet rich and composed of a core of platelets on the vessel injury site and a mesh of fibrin covering platelets . (DVT) and pulmonary embolism (PE), affects approximately 300,000 to 600,000 individuals and 60,000 to 100,000 die of VTE each year in the United States [1-4] more than prostate and breast tumor combined . VTE has a Azelaic acid relatively high TLN1 mortality rate of 6% for DVT instances and 12% of PE instances within the 1st month of analysis [6,7]. One-third VTE instances are manifested as PE and 2/3 present with DVT only . Eighty to 90% of pulmonary embolism instances are caused by DVT or a thrombus created in the pelvis . US healthcare system carries a huge burden for treatment of VTE and its complications, which is definitely estimated to be $1.5 billion/year . It is very important to correctly diagnose VTE before instituting an treatment, however, currently available diagnostic methods possess pitfalls and is sometimes misleading . The founded modalities and current gold requirements for evaluation of VTE may be inapplicable in some situations. Ultrasonography (US) offers replaced contrast venography for the analysis Azelaic acid of DVT because of availability, performance, removal of radiation and contrast providers . However, US is dependent on user encounter and also could be jeopardized by mechanical hurdles. US contrast medium is definitely highly allergenic and not suitable for cardiac individuals. It is also not relevant for body cavity and non-occlusive thrombi [12,13]. In individuals with involvement of the vasculature below the knee or in the pelvic veins, in asymptomatic individuals, and in individuals with duplicate veins, US might show false bad results [14-16]. Venography and US can only reflect changes in venous anatomy, which is definitely caused by filling problems and cannot display the metabolic activity of the clot. Since morphologic changes may remain present for years after an episode of DVT, individuals having a prior history of DVT represent challenging to diagnosis because of difficulty in differentiating fresh clots Azelaic acid from residual ones [15,17]. Up to 11% of CT venograms are insufficient for analysis of DVT [10,18] and are not recommended for the initial assessment of DVT due to invasiveness, technical problems and potential complications (e.g., hematoma, allergic reaction to contrast press) . Individuals with implanted electronic devices and intractable claustrophobia or renal failure cannot undergo magnetic resonance imaging (MRI) with contrast media . With the emergence of nuclear medicine Azelaic acid methods, new perspectives were opened early on for analysis of DVT . Initial trials for analysis of DVT using radiolabeled antibodies focusing on fibrin, activated platelets, plasminogen, plasmin, element XIII were not promising because of the long blood circulation time and radioactivity build up in the lungs and problems with timing of availability of the epitope which antibody was designed to bind, causing low clot to blood ratios [21-23]. Later on, studies focusing on specific synthetic peptides focusing on fibrin and platelet receptors have shown more promising results [15,22,24-43], which will be discussed with this review (Number 1). These fresh tracers might be able to aid the currently used modalities for detection of DVT. Open in a separate window Number 1 A schematic look at depicting elements of the venous thrombus and binding sites for different radiotracers. 1. FDG taken up by metabolically active inflammatory cells and platelets. 2. Radiolabeled platelets indicating sites of aggregated platelets. 3. GP IIb/IIIa cyclic RGD peptides (Apcitide, DMP 444, Bitistatin) focusing on GP IIb/IIIa receptors on triggered platelets. 4. TP850 pentapeptide focusing on fibrin chain. 5. 59D8, T2G1, GC4, 64C5 focusing on fibrin chain. 6. Cyclic fibrin binding peptide EP-2104R. 7. DI-80B3 focusing on D-domain of the fibrin. 8. Fibronectin-binding website focusing on lysine residue in fibrin. 9. Recombinant cells plasminogen activatior (rt-PA) binding to C-terminal lysine residue of fibrin. Here, we will discuss currently available and newly.