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Polyclonal Antibodies

Polyclonal Antibodies

Polyclonal Antibodies

Polyclonal Antibodies

Monoclonal Antibodies

Monoclonal Antibodies

Polyclonal Antibodies

Polyclonal Antibodies

Monoclonal Antibodies

Monoclonal Antibodies

Polyclonal Antibodies

Polyclonal Antibodies

Monoclonal Antibodies

Monoclonal Antibodies

Polyclonal Antibodies

Polyclonal Antibodies

Pivalaldehyde

Pivalonitrile

Pivalonitrile

Pivalonitrile

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Monoclonal Antibodies

Monoclonal Antibodies