Ambient
Showing 123501–123550 of 146505 results
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Pirquinozol
Molecular Formula : C11H9N3O2
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Pitavastatin (+)-Phenylethylamine Salt
Molecular Formula : C25H24FNO4 • C8H11N
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Pitavastatin (+)-Phenylethylamine Salt
Molecular Formula : C25H24FNO4 • C8H11N
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Pitavastatin (1R)-N-Methyl-2-hydroxyethylamide
Molecular Formula : C29H33FN2O4
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Pitavastatin (1R)-N-Methyl-2-hydroxyethylamide
Molecular Formula : C29H33FN2O4
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Pitavastatin (1R)-N-Methyl-2-hydroxyethylamide
Molecular Formula : C29H33FN2O4
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Pitavastatin (2R)-N-Methyl-2-hydroxypropylamide
Molecular Formula : C28H31FN2O4
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Pitavastatin (2R)-N-Methyl-2-hydroxypropylamide
Molecular Formula : C28H31FN2O4
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Pitavastatin (2R)-N-Methyl-2-hydroxypropylamide
Molecular Formula : C28H31FN2O4
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Pitavastatin Calcium
Molecular Formula : 2 C25 H23 F N O4 . Ca
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Pitavastatin Calcium
Molecular Formula : 2 C25 H23 F N O4 . Ca
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Pitavastatin Calcium
Molecular Formula : 2 C25 H23 F N O4 . Ca
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Pitavastatin Methyl Ester
Molecular Formula : C26 H26 F N O4
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Pitavastatin Methyl Ester
Molecular Formula : C26 H26 F N O4
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Pitavastatin Methyl Ester
Molecular Formula : C26 H26 F N O4
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Pitavastatin N-Methyl,-2-methoxyethylamide
Molecular Formula : C29H33FN2O4
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Pitavastatin N-Methyl,-2-methoxyethylamide
Molecular Formula : C29H33FN2O4
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Pitavastatin N-Methyl,-2-methoxyethylamide
Molecular Formula : C29H33FN2O4
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Pitavastatin-d5 Lactone
Molecular Formula : C25H17D5FNO3
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Pitavastatin-d5 Lactone
Molecular Formula : C25H17D5FNO3
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Pitavastatin-d5 Lactone
Molecular Formula : C25H17D5FNO3
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Pitavastatin-d5 Sodium Salt
Molecular Formula : C25H18D5FNNaO4
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Pitavastatin-d5 Sodium Salt
Molecular Formula : C25H18D5FNNaO4
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Pitavastatin-d5 Sodium Salt
Molecular Formula : C25H18D5FNNaO4
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Pitofenone Hydrochloride
Molecular Formula : C22 H25 N O4 . Cl H
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Pitofenone Hydrochloride
Molecular Formula : C22 H25 N O4 . Cl H
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Pitolisant
Molecular Formula : C17 H26 Cl N O
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Pitolisant
Molecular Formula : C17 H26 Cl N O
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Pitolisant
Molecular Formula : C17 H26 Cl N O
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Pivalaldehyde
Pivalaldehyde
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Pivalic Acid
Molecular Formula : C5 H10 O2
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Pivalic Acid
Molecular Formula : C5 H10 O2
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Pivalic acid-d9
Molecular Formula : C5 D9 H O2
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Pivalic acid-d9
Molecular Formula : C5 D9 H O2
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Pivalic acid-d9
Molecular Formula : C5 D9 H O2
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Pivalimidamide Hydrochloride
Molecular Formula : C5H13ClN2
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Pivalimidamide Hydrochloride
Molecular Formula : C5H13ClN2
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Pivalimidamide Hydrochloride
Molecular Formula : C5H13ClN2
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Pivalonitrile
Pivalonitrile
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Pivalonitrile
Pivalonitrile
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Pivalonitrile
Pivalonitrile
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Pivaloylglycine-13C2,15N
Molecular Formula : C513C2H1315NO3
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Pivaloylglycine-13C2,15N
Molecular Formula : C513C2H1315NO3
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Pivaloylglycine-13C2,15N
Molecular Formula : C513C2H1315NO3
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PIVKA II (1C5), mAb, Mouse
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.
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PIVKA II (1C5), mAb, Mouse
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.
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PIVKA II (1C5), mAb, Mouse
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.
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PIVKA II (2D7), mAb, Mouse
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.
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PIVKA II (2D7), mAb, Mouse
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.
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PIVKA II (2D7), mAb, Mouse
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.