About IVD

Thiopurine S-methyltransferase (TPMT) is a crucial enzyme responsible for the inactivation of thiopurine drugs through S-methylation. These drugs — including azathioprine, mercaptopurine, and thioguanine — are widely used in clinical practice, especially in hematology, oncology, gastroenterology, and transplantology. Thiopurines are prodrugs that require metabolic activation to exert their cytotoxic or immunosuppressive effects. The balance between

The year 2025 confirmed the growing trend of personalized medicine, in which molecular biological diagnostics is no longer an add-on but is becoming a standard tool for clinical decision-making. Take a look at which specific items from our portfolio might be useful for you.   Thrombosis Prevention and Metabolic Pathways – HEMO line The diagnosis

While HLA-B27 is by far the strongest and most well-known genetic marker linked with ankylosing spondylitis, several other genetic factors also contribute to disease susceptibility and can provide additional diagnostic or research insights. 1. HLA-B27 (primary marker) Present in ~90% of patients with AS of European ancestry. Not causative by itself — about 5–10% of

The human leukocyte antigen HLA-B27 is a variant of the class I major histocompatibility complex (MHC I) molecule. It is encoded by the HLA-B locus on chromosome 6 and expressed on almost all nucleated cells. Role in Health and Disease HLA-B27’s normal function is to present peptide antigens (derived from both self and non-self proteins)

Factor V’s role in coagulation Coagulation factor V is a key plasma glycoprotein in the blood-clotting cascade. In its activated form (Factor Va), it acts as a cofactor for Factor Xa, accelerating the conversion of prothrombin (Factor II) into thrombin. Thrombin then cleaves fibrinogen, resulting in fibrin formation — the fibrous mesh that gives structure to

Warfarin is one of the most commonly prescribed oral anticoagulants worldwide. It is highly effective in preventing and treating thromboembolic disorders, but achieving the right dose is challenging — too low a dose may leave patients at risk of clot formation, while too high a dose can cause serious bleeding. One of the key reasons

Lecanemab belongs to the antibody-based treatment approach as might be easily derived from its name Lecanemab where specifically the mab end cap refers to a monoclonal antibody. Lecanemab is registered commercially as Leqembi® and it has been approved by the FDA (Food and Drug Administration) in an accelerated approval pathway in January 2023 however this status changed in the summer of this year when the FDA converted the Leqembi® to traditional approval [1], [2]⁠.

Dihydropyrimidine dehydrogenase (DPD; coded by the DPYD gene) is an initial and rate-limiting enzyme of uracil catabolism, consequently essential for elimination of fluoropyrimidine-based chemotherapeutics (fluorouracil, capecitabine, tegafur, flucytosine).

Genetic polymorphism of cytochrome 450 (CYP) drug-metabolizing enzymes leads to inter-individual variability in the plasma concentrations of many drugs. Inter-individual variability among patients is a major clinical problem, as it can cause serious adverse drug reactions or therapeutic failures.