Specificity: Human PIVKA-II. (Cross-reaction: Prothrombin < 0.001%, Thrombin < 0.001%)
Application: ELISA, CLIA. Suitable for use as a detection antibody when paired with CABT-B9009
Isotype: Mouse IgG
Conjugation: Unconjugated. Different conjugations are also available upon request.
Corresponding antigen available: Recombinant Human PIVKA-II.
Summary
Specifications
Antibody Isotype
IgG1
Clone
N12454N
Species Reactivity
Human
Immunogen
Synthetic immunogen
Conjugate
Unconjugated
Applications
Application Notes
ELISA, CLIA We recommend the following antibodies for sandwich immunoassay (Capture - Detection): CABT-B9009 - CABT-L2604 Each laboratory should determine an optimum working titer for use in its particular application. Other applications have not been tested but use in such assays should not necessarily be excluded.
Target
Alternative Names
PROTEIN INDUCED VITAMIN K ANTAGONIST; Des-gamma carboxyprothrombin; protein induced by vitamin K absence/antagonist-II, PIVKA-II
Citations
Publication ()
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Background
PIVKA-II, also known as protein-induced vitamin K absence or antagonist-II, is a biomarker that has gained attention in the field of hepatocellular carcinoma (HCC) and other vitamin K-related disorders. It refers to abnormal forms of clotting factor II (prothrombin) that lack adequate vitamin K-dependent modifications, leading to impaired blood clotting function. Prothrombin in hepatocytes is a vitamin K-dependent protein consisting of three domains: fragment 1, fragment 2, and a protease domain. The N-terminal domain contains 10 glutamate residues that are normally converted into γ-carboxylated glutamate, forming the Gla domain.
Figure 1. Structure of PIVKA-II. (Source: Xing, H. et al., 2016)
The name "PIVKA-II" reflects its origin as an abnormal prothrombin variant. In normal circumstances, prothrombin undergoes post-translational modifications that enable it to function in blood clotting. These modifications are dependent on the availability of vitamin K, which is essential for the carboxylation of specific amino acid residues in prothrombin. However, in conditions associated with vitamin K deficiency or dysfunction, abnormal prothrombin variants, such as PIVKA-II, can be produced.
PIVKA-II has been primarily studied in the context of hepatocellular carcinoma, the most common type of liver cancer. In HCC, PIVKA-II is produced by tumor cells that have lost their ability to properly utilize vitamin K, resulting in the accumulation of undercarboxylated prothrombin variants in the bloodstream. Detecting elevated levels of PIVKA-II in blood samples can be used as a diagnostic marker for HCC, especially in cases where conventional tumor markers like alpha-fetoprotein (AFP) may be less reliable. Moreover, PIVKA-II has shown potential as a prognostic indicator in HCC. Higher PIVKA-II levels have been associated with more advanced stages of the disease, larger tumor sizes, and poorer overall survival rates. Monitoring PIVKA-II levels during treatment and follow-up can provide valuable information about disease progression and treatment response.
Alternative Names
Anti Human protein-induced vitamin K antagonist monoclonal antibody Anti-Human des-gamma carboxyprothrombin (DCP) monoclonal antibody Anti-Human DCP monoclonal antibody Anti-Human protein induced by vitamin K absence/antagonist-II (PIVKA-II) monoclonal antibody
References
1. Xing H, et al. Clinical application of protein induced by vitamin K antagonist-II as a biomarker in hepatocellular carcinoma. Tumor Biology. 2016, 37: 15447-15456.
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References
PIVKA-II as a potential new biomarker for hepatocellular carcinoma – A pilot study
In Vivo
Authors: Svobodova, S., Karlikova, M., Topolcan, O., Pecen, L., Pestova, M., Kott, O., Kucera, R.
Aim: The aim of this study was to evaluate the clinical contribution of protein induced by vitamin K absence (PIVKA-II) for hepatocellular carcinoma (HCC) diagnostics and compare it with alpha-foetoprotein (AFP), a routinely used tumour marker. Materials and Methods: A total of 332 participants were enrolled in this study: 64 with HCC, 48 with liver metastases of colorectal cancer origin, 42 with liver cirrhosis and 178 healthy individuals. Serum levels of PIVKA-II were measured using the chemiluminescent assay of the Architect 1000i System (Abbott, USA) and AFP levels using the chemiluminescent assay by DxI 800 (Beckman Coulter, USA). Results: PIVKA-II achieved better clinical sensitivity than AFP and the difference in this sensitivity was statistically significant. PIVKA-II achieved the best sensitivity (96.9%) in distinguishing between the HCC and control groups with the proposed cut-off value of 60 mAU/ml. Conclusion: Our recommendation is for addition of PIVKA-II to the routine panel of HCC tumour markers.
PIVKA-II serves as a potential biomarker that complements AFP for the diagnosis of hepatocellular carcinoma
Background Hepatocellular carcinoma (HCC) is one of the most common malignant tumors of the digestive system and has high morbidity and mortality rates. It is essential to search new biomarkers to improve the accuracy of early HCC diagnosis. Therefore, we evaluated the diagnostic value of prothrombin induced by vitamin K deficiency or antagonist- II (PIVKA-II) as a potential biomarker that complements α-fetoprotein (AFP) in HCC by detecting the serum PIVKA-II levels. Methods Serum PIVKA-II levels were compared in 168 HCC patients, 150 benign liver disease patients and 153 healthy controls to investigate the PIVKA-II potential to be a HCC biomarker. Receiver operating characteristic curve (ROC) analysis was used to evaluate the value of PIVKA-II in the diagnosis of HCC and its complementary role of AFP. The correlation between serum PIVKA-II levels and clinicopathological characteristics was analyzed to study the value of PIVKA-II in assessing HCC progression and prognosis. Finally, the ability of PIVKA-II in assessing the surgical treatment effects of HCC was studied by comparing the pre- and post-operative serum PIVKA-II levels in 89 HCC patients. Results Serum PIVKA-II levels in HCC patients were significantly higher than that in patients with benign liver disease and healthy controls. The PIVKA-II performance in the diagnosing HCC as an individual biomarker was remarkable. The combined detection of PIVKA-II and AFP improved the diagnostic efficiency of HCC. PIVKA-II retained significant diagnosis capabilities for AFP-negative HCC patients. Significant correlations were found between PIVKA-II expression levels and some clinicopathological characteristics, including tumor size, tumor stage, tumor metastasis, differentiation degree and complications. PIVKA-II expression obviously decreased after surgical resection. Conclusions PIVKA-II is a promising serum biomarker for the HCC diagnosis that can be used as a supplement for AFP. The combined diagnosis of the two markers greatly improved the diagnostic efficiency of HCC. The PIVKA-II levels in HCC patients were widely associated with clinicopathological characteristics representing tumor cell dissemination and/or poor prognosis. PIVKA-II can be used to evaluate the curative effects of HCC resection.