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Koen Augustyns - One of the best experts on this subject based on the ideXlab platform.

  • Prolyl peptidases related to dipeptidyl peptidase IV: potential of specific inhibitors in drug discovery.
    Current Topics in Medicinal Chemistry, 2007
    Co-Authors: Pieter Van Der Veken, Achiel Haemers, Koen Augustyns
    Abstract:

    Dipeptidyl peptidase IV (DPP IV) is a validated target for the treatment of type 2 diabetes, with several inhibitors currently in phase 3 clinical trials. This review will mainly focus on proline-specific dipeptidyl peptidases related to DPP IV: fibroblast activation protein (FAP), dipeptidyl peptidase 8 (DPP8), dipeptidyl peptidase 9 (DPP9) and dipeptidyl peptidase II (DPP II). The biochemical and biological properties of these enzymes will be discussed, as well as the therapeutic potential of their inhibition. The development of potent and selective inhibitors for each of these peptidases will be described.

  • Synthesis and dipeptidyl peptidase inhibition of N -(4-substituted-2,4-diaminobutanoyl)piperidines
    Bioorganic & Medicinal Chemistry Letters, 2006
    Co-Authors: Anna Soroka, Pieter Van Der Veken, Ingrid De Meester, Anne-marie Lambeir, Simon Scharpé, Achiel Haemers, Marie-berthe Maes, Koen Augustyns
    Abstract:

    In this paper, we report the synthesis of diastereomerically pure N-(4-substituted-2,4-diaminobutanoyl)piperidines. These compounds were prepared to investigate the influence of the 4-substitution on the dipeptidyl peptidase II (DPP II) activity and selectivity of the parent N-(2,4-diaminobutanoyl)piperidine. The (4S)-methyl compound showed subnanomolar inhibition, comparable with the parent compound. The (4R)-methyl group or bigger substituents decreased the activity.

  • Dipeptidyl peptidase II and leukocyte cell death.
    Biochemical Pharmacology, 2006
    Co-Authors: Marie-berthe Maes, Pieter Van Der Veken, Anne-marie Lambeir, Simon Scharpé, Koen Augustyns, Wim Martinet, Dorien M. Schrijvers, Guido R.y. De Meyer, Ingrid De Meester
    Abstract:

    Abstract Dipeptidyl peptidase (DPP) II (E.C. 3.4.14.2) is an intracellular protease that releases, preferably at acidic pH, N-terminal dipeptides from oligopeptides with Pro or Ala in the penultimate position. The natural substrates and the physiological role of DPPII remain unclear. The aim of the present study was to investigate the involvement of DPPII activity in different forms of cell death (apoptosis, necrosis and autophagy) in human leukocytes. We determined specific DPP activities in leukocytes. Compared to other subpopulations of peripheral blood mononuclear cells (PBMC), we observed relatively high DPPII specific activity in monocytic cells, opening new perspectives for further investigation of the DPPII functions. A second intriguing finding was that DPPII specific activity increased during necrosis, whereas induction of apoptosis or autophagy did not affect any of the dipeptidyl peptidase activities. Finally, we showed that inhibition of DPPII (>90%) using the in vitro applicable, highly potent ( K i of 0.082 ± 0.048 nM) and selective DPPII inhibitor UAMC00039, did not induce any form of cell death in leukocytes. These data are of importance for a more precise interpretation of the in vitro and in vivo effects of other dipeptidyl peptidase inhibitors.

  • Kinetic investigation of human dipeptidyl peptidase II (DPPII)-mediated hydrolysis of dipeptide derivatives and its identification as quiescent cell proline dipeptidase (QPP)/dipeptidyl peptidase 7 (DPP7).
    The Biochemical journal, 2005
    Co-Authors: Marie-berthe Maes, Kristel Senten, Pieter Van Der Veken, Anne-marie Lambeir, Simon Scharpé, Koen Augustyns, Kambiz Gilany, Barbara Leiting, Ingrid De Meester
    Abstract:

    The presence of DPPII (dipeptidyl peptidase II; E.C. 3.4.14.2) has been demonstrated in various mammalian tissues. However, a profound molecular and catalytic characterization, including substrate selectivity, kinetics and pH-dependence, has not been conducted. In the present study, DPPII was purified from human seminal plasma to apparent homogeneity with a high yield (40%) purification scheme, including an inhibitor-based affinity chromatographic step. The inhibitor lysyl-piperidide (K(i) approximately 0.9 microM at pH 5.5) was chosen, as it provided a favourable affinity/recovery ratio. The human enzyme appeared as a 120 kDa homodimer. Mass spectrometric analysis after tryptic digestion together with a kinetic comparison indicate strongly its identity with QPP (quiescent cell proline dipeptidase), also called dipeptidyl peptidase 7. pH profiles of both kcat and kcat/K(m) clearly demonstrated that DPPII/QPP possesses an acidic and not a neutral optimum as was reported for QPP. Kinetic parameters of the human natural DPPII for dipeptide-derived chromogenic [pNA (p-nitroanilide)] and fluorogenic [4Me2NA (4-methoxy-2-naphthylamide)] substrates were determined under different assay conditions. DPPII preferred the chromogenic pNA-derived substrates over the fluorogenic 4Me2NA-derived substrates. Natural human DPPII showed high efficiency towards synthetic substrates containing proline at the P1 position and lysine at P2. The importance of the P1' group for P2 and P1 selectivity was revealed, explaining many discrepancies in the literature. Furthermore, substrate preferences of human DPPII and dipeptidyl peptidase IV were compared based on their selectivity constants (kcat/K(m)). Lys-Pro-pNA (k(cat)/K(m) 4.1x10(6) s(-1) x M(-1)) and Ala-Pro-pNA (kcat/K(m) 2.6x10(6) s(-1) x M(-1)) were found to be the most sensitive chromogenic substrates for human DPPII, but were less selective than Lys-Ala-pNA (kcat/K(m) 0.4x10(6) s(-1) x M(-1)).

  • Kinetic investigation of human dipeptidyl peptidase II (DPPII)-mediated hydrolysis of dipeptide derivatives and its identification as quiescent cell proline dipeptidase (QPP)/dipeptidyl peptidase 7 (DPP7)
    Biochemical Journal, 2005
    Co-Authors: Marie-berthe Maes, Kristel Senten, Pieter Van Der Veken, Anne-marie Lambeir, Simon Scharpé, Koen Augustyns, Kambiz Gilany, Barbara Leiting, Ingrid De Meester
    Abstract:

    The presence of DPPII (dipeptidyl peptidase II; E.C. 3.4.14.2) has been demonstrated in various mammalian tissues. However, a profound molecular and catalytic characterization, including substrate selectivity, kinetics and pH-dependence, has not been conducted. In the present study, DPPII was purified from human seminal plasma to apparent homogeneity with a high yield (40%) purification scheme, including an inhibitor-based affinity chromatographic step. The inhibitor lysyl-piperidide (Ki~0.9 μM at pH 5.5) was chosen, as it provided a favourable affinity/recovery ratio. The human enzyme appeared as a 120 kDa homodimer. Mass spectrometric analysis after tryptic digestion together with a kinetic comparison indicate strongly its identity with QPP (quiescent cell proline dipeptidase), also called dipeptidyl peptidase 7. pH profiles of both kcat and kcat/Km clearly demonstrated that DPPII/QPP possesses an acidic and not a neutral optimum as was reported for QPP. Kinetic parameters of the human natural DPPII for dipeptide-derived chromogenic [pNA (p-nitroanilide)] and fluorogenic [4Me2NA (4-methoxy-2-naphthylamide)] substrates were determined under different assay conditions. DPPII preferred the chromogenic pNA-derived substrates over the fluorogenic 4Me2NA-derived substrates. Natural human DPPII showed high efficiency towards synthetic substrates containing proline at the P1 position and lysine at P2. The importance of the P1′ group for P2 and P1 selectivity was revealed, explaining many discrepancies in the literature. Furthermore, substrate preferences of human DPPII and dipeptidyl peptidase IV were compared based on their selectivity constants (kcat/Km). Lys-Pro-pNA (kcat/Km 4.1×106 s−1·M−1) and Ala-Pro-pNA (kcat/Km 2.6×106 s−1· M−1) were found to be the most sensitive chromogenic substrates for human DPPII, but were less selective than Lys-Ala-pNA (kcat/Km 0.4×106 s−1·M−1).

Ingrid De Meester - One of the best experts on this subject based on the ideXlab platform.

  • Dipeptidyl peptidase II (DPPII), a review
    Clinica Chimica Acta, 2007
    Co-Authors: Marie-berthe Maes, Simon Scharpé, Ingrid De Meester
    Abstract:

    Abstract An increasing number of biological processes appear to be regulated by Pro-specific N-terminal processing. The proline-specific dipeptidyl peptidases (DPPs) like DPPIV, fibroblast activation protein α (FAP), DPPII, DPP8 and DPP9, because of their preference for cleavage after X-Pro in vitro, are likely to be involved in many of these processes. These DPPs are emerging as an important protease family with roles in the regulation of signaling by peptide hormones. Dipeptidyl peptidase II (DPPII, E.C. 3.4.14.2) is an intracellular protease that localizes to the vesicular system. It releases, preferably at acidic pH, N-terminal dipeptides from oligopeptides with Pro or Ala in the penultimate position. Despite the fact that the physiological role of DPPII still has not been elucidated, several suggestions were made on possible functions of the enzyme depending on its localization in different cells, body fluids and organs. DPPII was a.o. suggested to be involved in the processes of cell differentiation and in the protection from cell death, and to have a role in the degradation of collagen fragments, myofibrillar proteins and short neuropeptides. Moreover, changes in the level and distribution of the enzyme provided clues indicating additional roles in disease-related processes. Here we review the DPPII literature, aiming to bring more clarity in the disperse data on this subject and give a state of the art on DPPII research.

  • Synthesis and dipeptidyl peptidase inhibition of N -(4-substituted-2,4-diaminobutanoyl)piperidines
    Bioorganic & Medicinal Chemistry Letters, 2006
    Co-Authors: Anna Soroka, Pieter Van Der Veken, Ingrid De Meester, Anne-marie Lambeir, Simon Scharpé, Achiel Haemers, Marie-berthe Maes, Koen Augustyns
    Abstract:

    In this paper, we report the synthesis of diastereomerically pure N-(4-substituted-2,4-diaminobutanoyl)piperidines. These compounds were prepared to investigate the influence of the 4-substitution on the dipeptidyl peptidase II (DPP II) activity and selectivity of the parent N-(2,4-diaminobutanoyl)piperidine. The (4S)-methyl compound showed subnanomolar inhibition, comparable with the parent compound. The (4R)-methyl group or bigger substituents decreased the activity.

  • Dipeptidyl peptidase II and leukocyte cell death.
    Biochemical Pharmacology, 2006
    Co-Authors: Marie-berthe Maes, Pieter Van Der Veken, Anne-marie Lambeir, Simon Scharpé, Koen Augustyns, Wim Martinet, Dorien M. Schrijvers, Guido R.y. De Meyer, Ingrid De Meester
    Abstract:

    Abstract Dipeptidyl peptidase (DPP) II (E.C. 3.4.14.2) is an intracellular protease that releases, preferably at acidic pH, N-terminal dipeptides from oligopeptides with Pro or Ala in the penultimate position. The natural substrates and the physiological role of DPPII remain unclear. The aim of the present study was to investigate the involvement of DPPII activity in different forms of cell death (apoptosis, necrosis and autophagy) in human leukocytes. We determined specific DPP activities in leukocytes. Compared to other subpopulations of peripheral blood mononuclear cells (PBMC), we observed relatively high DPPII specific activity in monocytic cells, opening new perspectives for further investigation of the DPPII functions. A second intriguing finding was that DPPII specific activity increased during necrosis, whereas induction of apoptosis or autophagy did not affect any of the dipeptidyl peptidase activities. Finally, we showed that inhibition of DPPII (>90%) using the in vitro applicable, highly potent ( K i of 0.082 ± 0.048 nM) and selective DPPII inhibitor UAMC00039, did not induce any form of cell death in leukocytes. These data are of importance for a more precise interpretation of the in vitro and in vivo effects of other dipeptidyl peptidase inhibitors.

  • Inhibition of Dipeptidyl-Peptidase IV catalyzed peptide truncation by Vildagliptin ((2S)-{[(3-hydroxyadamantan-1-yl)amino]acetyl}-pyrrolidine-2-carbonitrile).
    Biochemical Pharmacology, 2005
    Co-Authors: Inger Brandt, Ingrid De Meester, Simon Scharpé, Marie-berthe Maes, Jurgen Joossens, Xin Chen, Anne-marie Lambeir
    Abstract:

    Abstract Vildagliptin (NVP-LAF237/(2S)-{[(3-hydroxyadamantan-1-yl)amino]acetyl}-pyrrolidine-2-carbonitrile) was described as a potent, selective and orally bio-available Dipeptidyl-Peptidase IV (DPP IV, EC 3.4.14.5) inhibitor [Villhauer EB, Brinkman JA, Naderi GB, Burkey BF, Dunning BE, Prasad K, et al.1-[[(3-Hydroxy-1-adamantyl)amino]acetyl]-2-cyano-(S)-pyrrolidine: a potent, selective, and orally bioavailable dipeptidyl peptidase IV inhibitor with antihyperglycemic properties. J Med Chem 2003;46:2774–89]. Phase III clinical trials for the use of this compound in the treatment of Type 2 diabetes were started in the first quarter of 2004. In this paper, we report on (1) the kinetics of binding, (2) the type of inhibition, (3) the selectivity with respect to other peptidases, and (4) the inhibitory potency on the DPP IV catalyzed degradation of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and substance P. Vildagliptin behaved as a slow-binding DPP IV inhibitor with an association rate constant of 1.4 × 105 M−1 s−1 and a Ki of 17 nM. It is a micromolar inhibitor for Dipeptidyl-Peptidase 8 and does not significantly inhibit Dipeptidyl-Peptidase II (EC 3.4.11.2), prolyl oligopeptidase (EC 3.4.21.26), aminopeptidase P (EC 3.4.11.9) or aminopeptidase M (EC 3.4.11.2). There was no evidence for substrate specific inhibition of DPP IV by Vildagliptin or for important allosteric factors affecting the inhibition constant in presence of GIP and GLP-1.

  • Kinetic investigation of human dipeptidyl peptidase II (DPPII)-mediated hydrolysis of dipeptide derivatives and its identification as quiescent cell proline dipeptidase (QPP)/dipeptidyl peptidase 7 (DPP7).
    The Biochemical journal, 2005
    Co-Authors: Marie-berthe Maes, Kristel Senten, Pieter Van Der Veken, Anne-marie Lambeir, Simon Scharpé, Koen Augustyns, Kambiz Gilany, Barbara Leiting, Ingrid De Meester
    Abstract:

    The presence of DPPII (dipeptidyl peptidase II; E.C. 3.4.14.2) has been demonstrated in various mammalian tissues. However, a profound molecular and catalytic characterization, including substrate selectivity, kinetics and pH-dependence, has not been conducted. In the present study, DPPII was purified from human seminal plasma to apparent homogeneity with a high yield (40%) purification scheme, including an inhibitor-based affinity chromatographic step. The inhibitor lysyl-piperidide (K(i) approximately 0.9 microM at pH 5.5) was chosen, as it provided a favourable affinity/recovery ratio. The human enzyme appeared as a 120 kDa homodimer. Mass spectrometric analysis after tryptic digestion together with a kinetic comparison indicate strongly its identity with QPP (quiescent cell proline dipeptidase), also called dipeptidyl peptidase 7. pH profiles of both kcat and kcat/K(m) clearly demonstrated that DPPII/QPP possesses an acidic and not a neutral optimum as was reported for QPP. Kinetic parameters of the human natural DPPII for dipeptide-derived chromogenic [pNA (p-nitroanilide)] and fluorogenic [4Me2NA (4-methoxy-2-naphthylamide)] substrates were determined under different assay conditions. DPPII preferred the chromogenic pNA-derived substrates over the fluorogenic 4Me2NA-derived substrates. Natural human DPPII showed high efficiency towards synthetic substrates containing proline at the P1 position and lysine at P2. The importance of the P1' group for P2 and P1 selectivity was revealed, explaining many discrepancies in the literature. Furthermore, substrate preferences of human DPPII and dipeptidyl peptidase IV were compared based on their selectivity constants (kcat/K(m)). Lys-Pro-pNA (k(cat)/K(m) 4.1x10(6) s(-1) x M(-1)) and Ala-Pro-pNA (kcat/K(m) 2.6x10(6) s(-1) x M(-1)) were found to be the most sensitive chromogenic substrates for human DPPII, but were less selective than Lys-Ala-pNA (kcat/K(m) 0.4x10(6) s(-1) x M(-1)).

Pieter Van Der Veken - One of the best experts on this subject based on the ideXlab platform.

  • Prolyl peptidases related to dipeptidyl peptidase IV: potential of specific inhibitors in drug discovery.
    Current Topics in Medicinal Chemistry, 2007
    Co-Authors: Pieter Van Der Veken, Achiel Haemers, Koen Augustyns
    Abstract:

    Dipeptidyl peptidase IV (DPP IV) is a validated target for the treatment of type 2 diabetes, with several inhibitors currently in phase 3 clinical trials. This review will mainly focus on proline-specific dipeptidyl peptidases related to DPP IV: fibroblast activation protein (FAP), dipeptidyl peptidase 8 (DPP8), dipeptidyl peptidase 9 (DPP9) and dipeptidyl peptidase II (DPP II). The biochemical and biological properties of these enzymes will be discussed, as well as the therapeutic potential of their inhibition. The development of potent and selective inhibitors for each of these peptidases will be described.

  • Synthesis and dipeptidyl peptidase inhibition of N -(4-substituted-2,4-diaminobutanoyl)piperidines
    Bioorganic & Medicinal Chemistry Letters, 2006
    Co-Authors: Anna Soroka, Pieter Van Der Veken, Ingrid De Meester, Anne-marie Lambeir, Simon Scharpé, Achiel Haemers, Marie-berthe Maes, Koen Augustyns
    Abstract:

    In this paper, we report the synthesis of diastereomerically pure N-(4-substituted-2,4-diaminobutanoyl)piperidines. These compounds were prepared to investigate the influence of the 4-substitution on the dipeptidyl peptidase II (DPP II) activity and selectivity of the parent N-(2,4-diaminobutanoyl)piperidine. The (4S)-methyl compound showed subnanomolar inhibition, comparable with the parent compound. The (4R)-methyl group or bigger substituents decreased the activity.

  • Dipeptidyl peptidase II and leukocyte cell death.
    Biochemical Pharmacology, 2006
    Co-Authors: Marie-berthe Maes, Pieter Van Der Veken, Anne-marie Lambeir, Simon Scharpé, Koen Augustyns, Wim Martinet, Dorien M. Schrijvers, Guido R.y. De Meyer, Ingrid De Meester
    Abstract:

    Abstract Dipeptidyl peptidase (DPP) II (E.C. 3.4.14.2) is an intracellular protease that releases, preferably at acidic pH, N-terminal dipeptides from oligopeptides with Pro or Ala in the penultimate position. The natural substrates and the physiological role of DPPII remain unclear. The aim of the present study was to investigate the involvement of DPPII activity in different forms of cell death (apoptosis, necrosis and autophagy) in human leukocytes. We determined specific DPP activities in leukocytes. Compared to other subpopulations of peripheral blood mononuclear cells (PBMC), we observed relatively high DPPII specific activity in monocytic cells, opening new perspectives for further investigation of the DPPII functions. A second intriguing finding was that DPPII specific activity increased during necrosis, whereas induction of apoptosis or autophagy did not affect any of the dipeptidyl peptidase activities. Finally, we showed that inhibition of DPPII (>90%) using the in vitro applicable, highly potent ( K i of 0.082 ± 0.048 nM) and selective DPPII inhibitor UAMC00039, did not induce any form of cell death in leukocytes. These data are of importance for a more precise interpretation of the in vitro and in vivo effects of other dipeptidyl peptidase inhibitors.

  • Kinetic investigation of human dipeptidyl peptidase II (DPPII)-mediated hydrolysis of dipeptide derivatives and its identification as quiescent cell proline dipeptidase (QPP)/dipeptidyl peptidase 7 (DPP7).
    The Biochemical journal, 2005
    Co-Authors: Marie-berthe Maes, Kristel Senten, Pieter Van Der Veken, Anne-marie Lambeir, Simon Scharpé, Koen Augustyns, Kambiz Gilany, Barbara Leiting, Ingrid De Meester
    Abstract:

    The presence of DPPII (dipeptidyl peptidase II; E.C. 3.4.14.2) has been demonstrated in various mammalian tissues. However, a profound molecular and catalytic characterization, including substrate selectivity, kinetics and pH-dependence, has not been conducted. In the present study, DPPII was purified from human seminal plasma to apparent homogeneity with a high yield (40%) purification scheme, including an inhibitor-based affinity chromatographic step. The inhibitor lysyl-piperidide (K(i) approximately 0.9 microM at pH 5.5) was chosen, as it provided a favourable affinity/recovery ratio. The human enzyme appeared as a 120 kDa homodimer. Mass spectrometric analysis after tryptic digestion together with a kinetic comparison indicate strongly its identity with QPP (quiescent cell proline dipeptidase), also called dipeptidyl peptidase 7. pH profiles of both kcat and kcat/K(m) clearly demonstrated that DPPII/QPP possesses an acidic and not a neutral optimum as was reported for QPP. Kinetic parameters of the human natural DPPII for dipeptide-derived chromogenic [pNA (p-nitroanilide)] and fluorogenic [4Me2NA (4-methoxy-2-naphthylamide)] substrates were determined under different assay conditions. DPPII preferred the chromogenic pNA-derived substrates over the fluorogenic 4Me2NA-derived substrates. Natural human DPPII showed high efficiency towards synthetic substrates containing proline at the P1 position and lysine at P2. The importance of the P1' group for P2 and P1 selectivity was revealed, explaining many discrepancies in the literature. Furthermore, substrate preferences of human DPPII and dipeptidyl peptidase IV were compared based on their selectivity constants (kcat/K(m)). Lys-Pro-pNA (k(cat)/K(m) 4.1x10(6) s(-1) x M(-1)) and Ala-Pro-pNA (kcat/K(m) 2.6x10(6) s(-1) x M(-1)) were found to be the most sensitive chromogenic substrates for human DPPII, but were less selective than Lys-Ala-pNA (kcat/K(m) 0.4x10(6) s(-1) x M(-1)).

  • Kinetic investigation of human dipeptidyl peptidase II (DPPII)-mediated hydrolysis of dipeptide derivatives and its identification as quiescent cell proline dipeptidase (QPP)/dipeptidyl peptidase 7 (DPP7)
    Biochemical Journal, 2005
    Co-Authors: Marie-berthe Maes, Kristel Senten, Pieter Van Der Veken, Anne-marie Lambeir, Simon Scharpé, Koen Augustyns, Kambiz Gilany, Barbara Leiting, Ingrid De Meester
    Abstract:

    The presence of DPPII (dipeptidyl peptidase II; E.C. 3.4.14.2) has been demonstrated in various mammalian tissues. However, a profound molecular and catalytic characterization, including substrate selectivity, kinetics and pH-dependence, has not been conducted. In the present study, DPPII was purified from human seminal plasma to apparent homogeneity with a high yield (40%) purification scheme, including an inhibitor-based affinity chromatographic step. The inhibitor lysyl-piperidide (Ki~0.9 μM at pH 5.5) was chosen, as it provided a favourable affinity/recovery ratio. The human enzyme appeared as a 120 kDa homodimer. Mass spectrometric analysis after tryptic digestion together with a kinetic comparison indicate strongly its identity with QPP (quiescent cell proline dipeptidase), also called dipeptidyl peptidase 7. pH profiles of both kcat and kcat/Km clearly demonstrated that DPPII/QPP possesses an acidic and not a neutral optimum as was reported for QPP. Kinetic parameters of the human natural DPPII for dipeptide-derived chromogenic [pNA (p-nitroanilide)] and fluorogenic [4Me2NA (4-methoxy-2-naphthylamide)] substrates were determined under different assay conditions. DPPII preferred the chromogenic pNA-derived substrates over the fluorogenic 4Me2NA-derived substrates. Natural human DPPII showed high efficiency towards synthetic substrates containing proline at the P1 position and lysine at P2. The importance of the P1′ group for P2 and P1 selectivity was revealed, explaining many discrepancies in the literature. Furthermore, substrate preferences of human DPPII and dipeptidyl peptidase IV were compared based on their selectivity constants (kcat/Km). Lys-Pro-pNA (kcat/Km 4.1×106 s−1·M−1) and Ala-Pro-pNA (kcat/Km 2.6×106 s−1· M−1) were found to be the most sensitive chromogenic substrates for human DPPII, but were less selective than Lys-Ala-pNA (kcat/Km 0.4×106 s−1·M−1).

Simon Scharpé - One of the best experts on this subject based on the ideXlab platform.

  • Dipeptidyl peptidase II (DPPII), a review
    Clinica Chimica Acta, 2007
    Co-Authors: Marie-berthe Maes, Simon Scharpé, Ingrid De Meester
    Abstract:

    Abstract An increasing number of biological processes appear to be regulated by Pro-specific N-terminal processing. The proline-specific dipeptidyl peptidases (DPPs) like DPPIV, fibroblast activation protein α (FAP), DPPII, DPP8 and DPP9, because of their preference for cleavage after X-Pro in vitro, are likely to be involved in many of these processes. These DPPs are emerging as an important protease family with roles in the regulation of signaling by peptide hormones. Dipeptidyl peptidase II (DPPII, E.C. 3.4.14.2) is an intracellular protease that localizes to the vesicular system. It releases, preferably at acidic pH, N-terminal dipeptides from oligopeptides with Pro or Ala in the penultimate position. Despite the fact that the physiological role of DPPII still has not been elucidated, several suggestions were made on possible functions of the enzyme depending on its localization in different cells, body fluids and organs. DPPII was a.o. suggested to be involved in the processes of cell differentiation and in the protection from cell death, and to have a role in the degradation of collagen fragments, myofibrillar proteins and short neuropeptides. Moreover, changes in the level and distribution of the enzyme provided clues indicating additional roles in disease-related processes. Here we review the DPPII literature, aiming to bring more clarity in the disperse data on this subject and give a state of the art on DPPII research.

  • Synthesis and dipeptidyl peptidase inhibition of N -(4-substituted-2,4-diaminobutanoyl)piperidines
    Bioorganic & Medicinal Chemistry Letters, 2006
    Co-Authors: Anna Soroka, Pieter Van Der Veken, Ingrid De Meester, Anne-marie Lambeir, Simon Scharpé, Achiel Haemers, Marie-berthe Maes, Koen Augustyns
    Abstract:

    In this paper, we report the synthesis of diastereomerically pure N-(4-substituted-2,4-diaminobutanoyl)piperidines. These compounds were prepared to investigate the influence of the 4-substitution on the dipeptidyl peptidase II (DPP II) activity and selectivity of the parent N-(2,4-diaminobutanoyl)piperidine. The (4S)-methyl compound showed subnanomolar inhibition, comparable with the parent compound. The (4R)-methyl group or bigger substituents decreased the activity.

  • Dipeptidyl peptidase II and leukocyte cell death.
    Biochemical Pharmacology, 2006
    Co-Authors: Marie-berthe Maes, Pieter Van Der Veken, Anne-marie Lambeir, Simon Scharpé, Koen Augustyns, Wim Martinet, Dorien M. Schrijvers, Guido R.y. De Meyer, Ingrid De Meester
    Abstract:

    Abstract Dipeptidyl peptidase (DPP) II (E.C. 3.4.14.2) is an intracellular protease that releases, preferably at acidic pH, N-terminal dipeptides from oligopeptides with Pro or Ala in the penultimate position. The natural substrates and the physiological role of DPPII remain unclear. The aim of the present study was to investigate the involvement of DPPII activity in different forms of cell death (apoptosis, necrosis and autophagy) in human leukocytes. We determined specific DPP activities in leukocytes. Compared to other subpopulations of peripheral blood mononuclear cells (PBMC), we observed relatively high DPPII specific activity in monocytic cells, opening new perspectives for further investigation of the DPPII functions. A second intriguing finding was that DPPII specific activity increased during necrosis, whereas induction of apoptosis or autophagy did not affect any of the dipeptidyl peptidase activities. Finally, we showed that inhibition of DPPII (>90%) using the in vitro applicable, highly potent ( K i of 0.082 ± 0.048 nM) and selective DPPII inhibitor UAMC00039, did not induce any form of cell death in leukocytes. These data are of importance for a more precise interpretation of the in vitro and in vivo effects of other dipeptidyl peptidase inhibitors.

  • Inhibition of Dipeptidyl-Peptidase IV catalyzed peptide truncation by Vildagliptin ((2S)-{[(3-hydroxyadamantan-1-yl)amino]acetyl}-pyrrolidine-2-carbonitrile).
    Biochemical Pharmacology, 2005
    Co-Authors: Inger Brandt, Ingrid De Meester, Simon Scharpé, Marie-berthe Maes, Jurgen Joossens, Xin Chen, Anne-marie Lambeir
    Abstract:

    Abstract Vildagliptin (NVP-LAF237/(2S)-{[(3-hydroxyadamantan-1-yl)amino]acetyl}-pyrrolidine-2-carbonitrile) was described as a potent, selective and orally bio-available Dipeptidyl-Peptidase IV (DPP IV, EC 3.4.14.5) inhibitor [Villhauer EB, Brinkman JA, Naderi GB, Burkey BF, Dunning BE, Prasad K, et al.1-[[(3-Hydroxy-1-adamantyl)amino]acetyl]-2-cyano-(S)-pyrrolidine: a potent, selective, and orally bioavailable dipeptidyl peptidase IV inhibitor with antihyperglycemic properties. J Med Chem 2003;46:2774–89]. Phase III clinical trials for the use of this compound in the treatment of Type 2 diabetes were started in the first quarter of 2004. In this paper, we report on (1) the kinetics of binding, (2) the type of inhibition, (3) the selectivity with respect to other peptidases, and (4) the inhibitory potency on the DPP IV catalyzed degradation of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and substance P. Vildagliptin behaved as a slow-binding DPP IV inhibitor with an association rate constant of 1.4 × 105 M−1 s−1 and a Ki of 17 nM. It is a micromolar inhibitor for Dipeptidyl-Peptidase 8 and does not significantly inhibit Dipeptidyl-Peptidase II (EC 3.4.11.2), prolyl oligopeptidase (EC 3.4.21.26), aminopeptidase P (EC 3.4.11.9) or aminopeptidase M (EC 3.4.11.2). There was no evidence for substrate specific inhibition of DPP IV by Vildagliptin or for important allosteric factors affecting the inhibition constant in presence of GIP and GLP-1.

  • Kinetic investigation of human dipeptidyl peptidase II (DPPII)-mediated hydrolysis of dipeptide derivatives and its identification as quiescent cell proline dipeptidase (QPP)/dipeptidyl peptidase 7 (DPP7).
    The Biochemical journal, 2005
    Co-Authors: Marie-berthe Maes, Kristel Senten, Pieter Van Der Veken, Anne-marie Lambeir, Simon Scharpé, Koen Augustyns, Kambiz Gilany, Barbara Leiting, Ingrid De Meester
    Abstract:

    The presence of DPPII (dipeptidyl peptidase II; E.C. 3.4.14.2) has been demonstrated in various mammalian tissues. However, a profound molecular and catalytic characterization, including substrate selectivity, kinetics and pH-dependence, has not been conducted. In the present study, DPPII was purified from human seminal plasma to apparent homogeneity with a high yield (40%) purification scheme, including an inhibitor-based affinity chromatographic step. The inhibitor lysyl-piperidide (K(i) approximately 0.9 microM at pH 5.5) was chosen, as it provided a favourable affinity/recovery ratio. The human enzyme appeared as a 120 kDa homodimer. Mass spectrometric analysis after tryptic digestion together with a kinetic comparison indicate strongly its identity with QPP (quiescent cell proline dipeptidase), also called dipeptidyl peptidase 7. pH profiles of both kcat and kcat/K(m) clearly demonstrated that DPPII/QPP possesses an acidic and not a neutral optimum as was reported for QPP. Kinetic parameters of the human natural DPPII for dipeptide-derived chromogenic [pNA (p-nitroanilide)] and fluorogenic [4Me2NA (4-methoxy-2-naphthylamide)] substrates were determined under different assay conditions. DPPII preferred the chromogenic pNA-derived substrates over the fluorogenic 4Me2NA-derived substrates. Natural human DPPII showed high efficiency towards synthetic substrates containing proline at the P1 position and lysine at P2. The importance of the P1' group for P2 and P1 selectivity was revealed, explaining many discrepancies in the literature. Furthermore, substrate preferences of human DPPII and dipeptidyl peptidase IV were compared based on their selectivity constants (kcat/K(m)). Lys-Pro-pNA (k(cat)/K(m) 4.1x10(6) s(-1) x M(-1)) and Ala-Pro-pNA (kcat/K(m) 2.6x10(6) s(-1) x M(-1)) were found to be the most sensitive chromogenic substrates for human DPPII, but were less selective than Lys-Ala-pNA (kcat/K(m) 0.4x10(6) s(-1) x M(-1)).

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