Profiles of direct oral anticoagulants and clinical usage—dosage and dose regimen differences

Abstract The availability of direct oral anticoagulants (DOACs) has caused a paradigm shift in thrombosis management. DOAC profiles do not differ greatly, though they are quite different from that of warfarin, whereas their dosage and dose regimens are not consistent. The direct thrombin inhibitor d...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Ieko, Masahiro [verfasserIn] Naitoh, Sumiyoshi Yoshida, Mika Takahashi, Nobuhiko

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	Anticoagulant therapy Direct oral anticoagulant (DOAC) Warfarin Stroke prevention in atrial fibrillation (SPAF) Relative potency

Anmerkung:	© Ieko et al. 2016

Übergeordnetes Werk:	Enthalten in: Journal of Intensive Care - London : BioMed Central, 2013, 4(2016), 1 vom: 10. März
Übergeordnetes Werk:	volume:4 ; year:2016 ; number:1 ; day:10 ; month:03

Links:	Volltext

DOI / URN:	10.1186/s40560-016-0144-5

Katalog-ID:	SPR036660639

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520			\|a Abstract The availability of direct oral anticoagulants (DOACs) has caused a paradigm shift in thrombosis management. DOAC profiles do not differ greatly, though they are quite different from that of warfarin, whereas their dosage and dose regimens are not consistent. The direct thrombin inhibitor dabigatran seems to obstruct tenase by inhibiting thrombin generated in the initial phase and feedback to the amplification phase of cell-based coagulation reactions. Factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) mainly inhibit factor Xa activity of the prothrombinase complex in the propagation phase. The dose regimens of these inhibitors can be classified into once (rivaroxaban, edoxaban) and twice (dabigatran, apixaban) daily. On the other hand, their plasma elimination half-life times are similar, which can be explained by differences in the type of aimed anticoagulation, such as persistent (e.g., warfarin) and intermittent (e.g., low-molecular-weight heparin). Because of the differences among DOACs, an indicator is necessary to compare them. We investigated relative potency to compare dosage and intensity by calculation of conversion using a profile comprised of molecular weight, bioavailability, protein-binding rate, inhibitory constant, and dosage. We found that the relative potencies were different, with that of apixaban higher than edoxaban (60 mg) and nearly twice that of rivaroxaban. However, dabigatran could not be evaluated with this profile, likely due to its different mode of action. These results suggest that rivaroxaban and apixaban differ in regard to anticoagulation type, as the former shows persistent and the latter intermittent anticoagulation.
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allfields	10.1186/s40560-016-0144-5 doi (DE-627)SPR036660639 (SPR)s40560-016-0144-5-e DE-627 ger DE-627 rakwb eng Ieko, Masahiro verfasserin aut Profiles of direct oral anticoagulants and clinical usage—dosage and dose regimen differences 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ieko et al. 2016 Abstract The availability of direct oral anticoagulants (DOACs) has caused a paradigm shift in thrombosis management. DOAC profiles do not differ greatly, though they are quite different from that of warfarin, whereas their dosage and dose regimens are not consistent. The direct thrombin inhibitor dabigatran seems to obstruct tenase by inhibiting thrombin generated in the initial phase and feedback to the amplification phase of cell-based coagulation reactions. Factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) mainly inhibit factor Xa activity of the prothrombinase complex in the propagation phase. The dose regimens of these inhibitors can be classified into once (rivaroxaban, edoxaban) and twice (dabigatran, apixaban) daily. On the other hand, their plasma elimination half-life times are similar, which can be explained by differences in the type of aimed anticoagulation, such as persistent (e.g., warfarin) and intermittent (e.g., low-molecular-weight heparin). Because of the differences among DOACs, an indicator is necessary to compare them. We investigated relative potency to compare dosage and intensity by calculation of conversion using a profile comprised of molecular weight, bioavailability, protein-binding rate, inhibitory constant, and dosage. We found that the relative potencies were different, with that of apixaban higher than edoxaban (60 mg) and nearly twice that of rivaroxaban. However, dabigatran could not be evaluated with this profile, likely due to its different mode of action. These results suggest that rivaroxaban and apixaban differ in regard to anticoagulation type, as the former shows persistent and the latter intermittent anticoagulation. Anticoagulant therapy (dpeaa)DE-He213 Direct oral anticoagulant (DOAC) (dpeaa)DE-He213 Warfarin (dpeaa)DE-He213 Stroke prevention in atrial fibrillation (SPAF) (dpeaa)DE-He213 Relative potency (dpeaa)DE-He213 Naitoh, Sumiyoshi aut Yoshida, Mika aut Takahashi, Nobuhiko aut Enthalten in Journal of Intensive Care London : BioMed Central, 2013 4(2016), 1 vom: 10. März (DE-627)771390440 (DE-600)2739853-5 2052-0492 nnns volume:4 year:2016 number:1 day:10 month:03 https://dx.doi.org/10.1186/s40560-016-0144-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2016 1 10 03
spelling	10.1186/s40560-016-0144-5 doi (DE-627)SPR036660639 (SPR)s40560-016-0144-5-e DE-627 ger DE-627 rakwb eng Ieko, Masahiro verfasserin aut Profiles of direct oral anticoagulants and clinical usage—dosage and dose regimen differences 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ieko et al. 2016 Abstract The availability of direct oral anticoagulants (DOACs) has caused a paradigm shift in thrombosis management. DOAC profiles do not differ greatly, though they are quite different from that of warfarin, whereas their dosage and dose regimens are not consistent. The direct thrombin inhibitor dabigatran seems to obstruct tenase by inhibiting thrombin generated in the initial phase and feedback to the amplification phase of cell-based coagulation reactions. Factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) mainly inhibit factor Xa activity of the prothrombinase complex in the propagation phase. The dose regimens of these inhibitors can be classified into once (rivaroxaban, edoxaban) and twice (dabigatran, apixaban) daily. On the other hand, their plasma elimination half-life times are similar, which can be explained by differences in the type of aimed anticoagulation, such as persistent (e.g., warfarin) and intermittent (e.g., low-molecular-weight heparin). Because of the differences among DOACs, an indicator is necessary to compare them. We investigated relative potency to compare dosage and intensity by calculation of conversion using a profile comprised of molecular weight, bioavailability, protein-binding rate, inhibitory constant, and dosage. We found that the relative potencies were different, with that of apixaban higher than edoxaban (60 mg) and nearly twice that of rivaroxaban. However, dabigatran could not be evaluated with this profile, likely due to its different mode of action. These results suggest that rivaroxaban and apixaban differ in regard to anticoagulation type, as the former shows persistent and the latter intermittent anticoagulation. Anticoagulant therapy (dpeaa)DE-He213 Direct oral anticoagulant (DOAC) (dpeaa)DE-He213 Warfarin (dpeaa)DE-He213 Stroke prevention in atrial fibrillation (SPAF) (dpeaa)DE-He213 Relative potency (dpeaa)DE-He213 Naitoh, Sumiyoshi aut Yoshida, Mika aut Takahashi, Nobuhiko aut Enthalten in Journal of Intensive Care London : BioMed Central, 2013 4(2016), 1 vom: 10. März (DE-627)771390440 (DE-600)2739853-5 2052-0492 nnns volume:4 year:2016 number:1 day:10 month:03 https://dx.doi.org/10.1186/s40560-016-0144-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2016 1 10 03
allfields_unstemmed	10.1186/s40560-016-0144-5 doi (DE-627)SPR036660639 (SPR)s40560-016-0144-5-e DE-627 ger DE-627 rakwb eng Ieko, Masahiro verfasserin aut Profiles of direct oral anticoagulants and clinical usage—dosage and dose regimen differences 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ieko et al. 2016 Abstract The availability of direct oral anticoagulants (DOACs) has caused a paradigm shift in thrombosis management. DOAC profiles do not differ greatly, though they are quite different from that of warfarin, whereas their dosage and dose regimens are not consistent. The direct thrombin inhibitor dabigatran seems to obstruct tenase by inhibiting thrombin generated in the initial phase and feedback to the amplification phase of cell-based coagulation reactions. Factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) mainly inhibit factor Xa activity of the prothrombinase complex in the propagation phase. The dose regimens of these inhibitors can be classified into once (rivaroxaban, edoxaban) and twice (dabigatran, apixaban) daily. On the other hand, their plasma elimination half-life times are similar, which can be explained by differences in the type of aimed anticoagulation, such as persistent (e.g., warfarin) and intermittent (e.g., low-molecular-weight heparin). Because of the differences among DOACs, an indicator is necessary to compare them. We investigated relative potency to compare dosage and intensity by calculation of conversion using a profile comprised of molecular weight, bioavailability, protein-binding rate, inhibitory constant, and dosage. We found that the relative potencies were different, with that of apixaban higher than edoxaban (60 mg) and nearly twice that of rivaroxaban. However, dabigatran could not be evaluated with this profile, likely due to its different mode of action. These results suggest that rivaroxaban and apixaban differ in regard to anticoagulation type, as the former shows persistent and the latter intermittent anticoagulation. Anticoagulant therapy (dpeaa)DE-He213 Direct oral anticoagulant (DOAC) (dpeaa)DE-He213 Warfarin (dpeaa)DE-He213 Stroke prevention in atrial fibrillation (SPAF) (dpeaa)DE-He213 Relative potency (dpeaa)DE-He213 Naitoh, Sumiyoshi aut Yoshida, Mika aut Takahashi, Nobuhiko aut Enthalten in Journal of Intensive Care London : BioMed Central, 2013 4(2016), 1 vom: 10. März (DE-627)771390440 (DE-600)2739853-5 2052-0492 nnns volume:4 year:2016 number:1 day:10 month:03 https://dx.doi.org/10.1186/s40560-016-0144-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2016 1 10 03
allfieldsGer	10.1186/s40560-016-0144-5 doi (DE-627)SPR036660639 (SPR)s40560-016-0144-5-e DE-627 ger DE-627 rakwb eng Ieko, Masahiro verfasserin aut Profiles of direct oral anticoagulants and clinical usage—dosage and dose regimen differences 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ieko et al. 2016 Abstract The availability of direct oral anticoagulants (DOACs) has caused a paradigm shift in thrombosis management. DOAC profiles do not differ greatly, though they are quite different from that of warfarin, whereas their dosage and dose regimens are not consistent. The direct thrombin inhibitor dabigatran seems to obstruct tenase by inhibiting thrombin generated in the initial phase and feedback to the amplification phase of cell-based coagulation reactions. Factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) mainly inhibit factor Xa activity of the prothrombinase complex in the propagation phase. The dose regimens of these inhibitors can be classified into once (rivaroxaban, edoxaban) and twice (dabigatran, apixaban) daily. On the other hand, their plasma elimination half-life times are similar, which can be explained by differences in the type of aimed anticoagulation, such as persistent (e.g., warfarin) and intermittent (e.g., low-molecular-weight heparin). Because of the differences among DOACs, an indicator is necessary to compare them. We investigated relative potency to compare dosage and intensity by calculation of conversion using a profile comprised of molecular weight, bioavailability, protein-binding rate, inhibitory constant, and dosage. We found that the relative potencies were different, with that of apixaban higher than edoxaban (60 mg) and nearly twice that of rivaroxaban. However, dabigatran could not be evaluated with this profile, likely due to its different mode of action. These results suggest that rivaroxaban and apixaban differ in regard to anticoagulation type, as the former shows persistent and the latter intermittent anticoagulation. Anticoagulant therapy (dpeaa)DE-He213 Direct oral anticoagulant (DOAC) (dpeaa)DE-He213 Warfarin (dpeaa)DE-He213 Stroke prevention in atrial fibrillation (SPAF) (dpeaa)DE-He213 Relative potency (dpeaa)DE-He213 Naitoh, Sumiyoshi aut Yoshida, Mika aut Takahashi, Nobuhiko aut Enthalten in Journal of Intensive Care London : BioMed Central, 2013 4(2016), 1 vom: 10. März (DE-627)771390440 (DE-600)2739853-5 2052-0492 nnns volume:4 year:2016 number:1 day:10 month:03 https://dx.doi.org/10.1186/s40560-016-0144-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2016 1 10 03
allfieldsSound	10.1186/s40560-016-0144-5 doi (DE-627)SPR036660639 (SPR)s40560-016-0144-5-e DE-627 ger DE-627 rakwb eng Ieko, Masahiro verfasserin aut Profiles of direct oral anticoagulants and clinical usage—dosage and dose regimen differences 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ieko et al. 2016 Abstract The availability of direct oral anticoagulants (DOACs) has caused a paradigm shift in thrombosis management. DOAC profiles do not differ greatly, though they are quite different from that of warfarin, whereas their dosage and dose regimens are not consistent. The direct thrombin inhibitor dabigatran seems to obstruct tenase by inhibiting thrombin generated in the initial phase and feedback to the amplification phase of cell-based coagulation reactions. Factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) mainly inhibit factor Xa activity of the prothrombinase complex in the propagation phase. The dose regimens of these inhibitors can be classified into once (rivaroxaban, edoxaban) and twice (dabigatran, apixaban) daily. On the other hand, their plasma elimination half-life times are similar, which can be explained by differences in the type of aimed anticoagulation, such as persistent (e.g., warfarin) and intermittent (e.g., low-molecular-weight heparin). Because of the differences among DOACs, an indicator is necessary to compare them. We investigated relative potency to compare dosage and intensity by calculation of conversion using a profile comprised of molecular weight, bioavailability, protein-binding rate, inhibitory constant, and dosage. We found that the relative potencies were different, with that of apixaban higher than edoxaban (60 mg) and nearly twice that of rivaroxaban. However, dabigatran could not be evaluated with this profile, likely due to its different mode of action. These results suggest that rivaroxaban and apixaban differ in regard to anticoagulation type, as the former shows persistent and the latter intermittent anticoagulation. Anticoagulant therapy (dpeaa)DE-He213 Direct oral anticoagulant (DOAC) (dpeaa)DE-He213 Warfarin (dpeaa)DE-He213 Stroke prevention in atrial fibrillation (SPAF) (dpeaa)DE-He213 Relative potency (dpeaa)DE-He213 Naitoh, Sumiyoshi aut Yoshida, Mika aut Takahashi, Nobuhiko aut Enthalten in Journal of Intensive Care London : BioMed Central, 2013 4(2016), 1 vom: 10. März (DE-627)771390440 (DE-600)2739853-5 2052-0492 nnns volume:4 year:2016 number:1 day:10 month:03 https://dx.doi.org/10.1186/s40560-016-0144-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2016 1 10 03
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source	Enthalten in Journal of Intensive Care 4(2016), 1 vom: 10. März volume:4 year:2016 number:1 day:10 month:03
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topic_facet	Anticoagulant therapy Direct oral anticoagulant (DOAC) Warfarin Stroke prevention in atrial fibrillation (SPAF) Relative potency
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author	Ieko, Masahiro
spellingShingle	Ieko, Masahiro misc Anticoagulant therapy misc Direct oral anticoagulant (DOAC) misc Warfarin misc Stroke prevention in atrial fibrillation (SPAF) misc Relative potency Profiles of direct oral anticoagulants and clinical usage—dosage and dose regimen differences
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topic_title	Profiles of direct oral anticoagulants and clinical usage—dosage and dose regimen differences Anticoagulant therapy (dpeaa)DE-He213 Direct oral anticoagulant (DOAC) (dpeaa)DE-He213 Warfarin (dpeaa)DE-He213 Stroke prevention in atrial fibrillation (SPAF) (dpeaa)DE-He213 Relative potency (dpeaa)DE-He213
topic	misc Anticoagulant therapy misc Direct oral anticoagulant (DOAC) misc Warfarin misc Stroke prevention in atrial fibrillation (SPAF) misc Relative potency
topic_unstemmed	misc Anticoagulant therapy misc Direct oral anticoagulant (DOAC) misc Warfarin misc Stroke prevention in atrial fibrillation (SPAF) misc Relative potency
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title	Profiles of direct oral anticoagulants and clinical usage—dosage and dose regimen differences
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title_full	Profiles of direct oral anticoagulants and clinical usage—dosage and dose regimen differences
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title_sort	profiles of direct oral anticoagulants and clinical usage—dosage and dose regimen differences
title_auth	Profiles of direct oral anticoagulants and clinical usage—dosage and dose regimen differences
abstract	Abstract The availability of direct oral anticoagulants (DOACs) has caused a paradigm shift in thrombosis management. DOAC profiles do not differ greatly, though they are quite different from that of warfarin, whereas their dosage and dose regimens are not consistent. The direct thrombin inhibitor dabigatran seems to obstruct tenase by inhibiting thrombin generated in the initial phase and feedback to the amplification phase of cell-based coagulation reactions. Factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) mainly inhibit factor Xa activity of the prothrombinase complex in the propagation phase. The dose regimens of these inhibitors can be classified into once (rivaroxaban, edoxaban) and twice (dabigatran, apixaban) daily. On the other hand, their plasma elimination half-life times are similar, which can be explained by differences in the type of aimed anticoagulation, such as persistent (e.g., warfarin) and intermittent (e.g., low-molecular-weight heparin). Because of the differences among DOACs, an indicator is necessary to compare them. We investigated relative potency to compare dosage and intensity by calculation of conversion using a profile comprised of molecular weight, bioavailability, protein-binding rate, inhibitory constant, and dosage. We found that the relative potencies were different, with that of apixaban higher than edoxaban (60 mg) and nearly twice that of rivaroxaban. However, dabigatran could not be evaluated with this profile, likely due to its different mode of action. These results suggest that rivaroxaban and apixaban differ in regard to anticoagulation type, as the former shows persistent and the latter intermittent anticoagulation. © Ieko et al. 2016
abstractGer	Abstract The availability of direct oral anticoagulants (DOACs) has caused a paradigm shift in thrombosis management. DOAC profiles do not differ greatly, though they are quite different from that of warfarin, whereas their dosage and dose regimens are not consistent. The direct thrombin inhibitor dabigatran seems to obstruct tenase by inhibiting thrombin generated in the initial phase and feedback to the amplification phase of cell-based coagulation reactions. Factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) mainly inhibit factor Xa activity of the prothrombinase complex in the propagation phase. The dose regimens of these inhibitors can be classified into once (rivaroxaban, edoxaban) and twice (dabigatran, apixaban) daily. On the other hand, their plasma elimination half-life times are similar, which can be explained by differences in the type of aimed anticoagulation, such as persistent (e.g., warfarin) and intermittent (e.g., low-molecular-weight heparin). Because of the differences among DOACs, an indicator is necessary to compare them. We investigated relative potency to compare dosage and intensity by calculation of conversion using a profile comprised of molecular weight, bioavailability, protein-binding rate, inhibitory constant, and dosage. We found that the relative potencies were different, with that of apixaban higher than edoxaban (60 mg) and nearly twice that of rivaroxaban. However, dabigatran could not be evaluated with this profile, likely due to its different mode of action. These results suggest that rivaroxaban and apixaban differ in regard to anticoagulation type, as the former shows persistent and the latter intermittent anticoagulation. © Ieko et al. 2016
abstract_unstemmed	Abstract The availability of direct oral anticoagulants (DOACs) has caused a paradigm shift in thrombosis management. DOAC profiles do not differ greatly, though they are quite different from that of warfarin, whereas their dosage and dose regimens are not consistent. The direct thrombin inhibitor dabigatran seems to obstruct tenase by inhibiting thrombin generated in the initial phase and feedback to the amplification phase of cell-based coagulation reactions. Factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) mainly inhibit factor Xa activity of the prothrombinase complex in the propagation phase. The dose regimens of these inhibitors can be classified into once (rivaroxaban, edoxaban) and twice (dabigatran, apixaban) daily. On the other hand, their plasma elimination half-life times are similar, which can be explained by differences in the type of aimed anticoagulation, such as persistent (e.g., warfarin) and intermittent (e.g., low-molecular-weight heparin). Because of the differences among DOACs, an indicator is necessary to compare them. We investigated relative potency to compare dosage and intensity by calculation of conversion using a profile comprised of molecular weight, bioavailability, protein-binding rate, inhibitory constant, and dosage. We found that the relative potencies were different, with that of apixaban higher than edoxaban (60 mg) and nearly twice that of rivaroxaban. However, dabigatran could not be evaluated with this profile, likely due to its different mode of action. These results suggest that rivaroxaban and apixaban differ in regard to anticoagulation type, as the former shows persistent and the latter intermittent anticoagulation. © Ieko et al. 2016
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title_short	Profiles of direct oral anticoagulants and clinical usage—dosage and dose regimen differences
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We investigated relative potency to compare dosage and intensity by calculation of conversion using a profile comprised of molecular weight, bioavailability, protein-binding rate, inhibitory constant, and dosage. We found that the relative potencies were different, with that of apixaban higher than edoxaban (60 mg) and nearly twice that of rivaroxaban. However, dabigatran could not be evaluated with this profile, likely due to its different mode of action. 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Profiles of direct oral anticoagulants and clinical usage—dosage and dose regimen differences

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