PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
34595388-1	2021	The DOAC Dipstick accurately detects the presence or absence of factor Xa (DXI) and thrombin inhibitor (DTI) classes of direct oral anticoagulants (DOACs) in patients" urine samples on DOAC treatment.	doacs	148-153	coagulation factor II, thrombin	Homo sapiens	84-92
33034105-4	2021	DOACs bind to the fatty acid (FA) site 1 (FA1) of ligand-free HSA, whereas they bind to the FA8 and FA9 sites of heme-Fe(III)- and myristic acid-bound HSA.	doacs	0-5	FA complementation group A	Homo sapiens	42-45
33034105-5	2021	DOACs binding to the FA1 site of ligand-free HSA has been validated by competitive inhibition of heme-Fe(III) recognition.	doacs	0-5	FA complementation group A	Homo sapiens	21-24
33034105-6	2021	Values of the dissociation equilibrium constant for DOACs binding to the FA1 site (ie, calc KDOAC ) derived from in silico docking simulations (ranging between 1.2 x 10-8 M and 1.4 x 10-6 M) agree with those determined experimentally from competitive inhibition of heme-Fe(III) binding (ie, exp KDOAC ; ranging between 2.5 x 10-7 M and 2.2 x 10-6 M).	doacs	52-57	FA complementation group A	Homo sapiens	73-76
34587969-9	2021	We found treatment with DOACs would result in a large reduction in cost ($USD 1447.22 vs. $USD 3374.70) but a small reduction in QALYs (3.07 QALYs vs. 3.09 QALYs) compared with LMWHs over a 5-year time frame, resulting in an ICER of $USD 112895.50/QALYs.	doacs	24-29	cAMP responsive element modulator	Homo sapiens	225-229
34287842-1	2021	Concomitant use of direct oral anticoagulants (DOACs) and medications with inhibition/induction effect on P-gp/CYP3A might increase risk of bleeding/treatment failure, respectively.	doacs	47-52	phosphoglycolate phosphatase	Homo sapiens	106-110
34287842-1	2021	Concomitant use of direct oral anticoagulants (DOACs) and medications with inhibition/induction effect on P-gp/CYP3A might increase risk of bleeding/treatment failure, respectively.	doacs	47-52	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	111-116
34773747-15	2021	CONCLUSIONS: Predictors of DOACs-associated GIB included active cancer, renal impairment, bleeding predisposition, COPD and uncontrolled hypertension.	doacs	27-32	COPD	Homo sapiens	115-119
34568446-5	2021	The primary safety endpoint of major or clinically relevant non-major bleeding was significantly reduced in DOACs as compared to VKAs in both patients with age <75 years (OR: 0.79, 95% CI: 0.70-0.89) and patients with age more than 75 years (OR: 0.75, 95% CI: 0.59-0.96).	doacs	108-113	renin binding protein	Homo sapiens	156-159
34146091-8	2021	Low-dose DOACs vs placebo were associated with significant reductions in MACE (IRR 0.85, 95% CI 0.78-0.91) and myocardial infarction (IRR 0.86, 95% CI 0.78-0.95) and significant increases of major (IRR 2.05, 95% CI 1.50-2.80) or all bleeding (IRR 1.82, 95% CI 1.49-2.22).	doacs	9-14	insulin receptor related receptor	Homo sapiens	198-201
34137279-5	2022	DATA SYNTHESIS: Dexamethasone has the potential to interact with the DOACs via CYP3A4 and/or P-gp induction.	doacs	69-74	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	79-85
34137279-5	2022	DATA SYNTHESIS: Dexamethasone has the potential to interact with the DOACs via CYP3A4 and/or P-gp induction.	doacs	69-74	ATP binding cassette subfamily B member 1	Homo sapiens	93-97
35620356-4	2022	Recently, direct oral anticoagulants (DOACs), such as dabigatran etexilate (a direct thrombin inhibitor) and apixaban, rivaroxaban and edoxaban (direct factor Xa inhibitors), have been developed to overcome these issues.	doacs	38-43	coagulation factor II, thrombin	Homo sapiens	85-93
35620356-4	2022	Recently, direct oral anticoagulants (DOACs), such as dabigatran etexilate (a direct thrombin inhibitor) and apixaban, rivaroxaban and edoxaban (direct factor Xa inhibitors), have been developed to overcome these issues.	doacs	38-43	coagulation factor X	Homo sapiens	152-161
35174529-2	2022	Pharmacokinetics of DOACs are largely influenced by efflux transporters derived from ABC transporters, notably by P-glycoprotein (P-gp).	doacs	20-25	ATP binding cassette subfamily B member 1	Homo sapiens	114-128
35037739-3	2022	DOACs, the preferred anticoagulants in AF, can target factors upstream (FXa) or downstream (thrombin) in the coagulation cascade and mediate differential vascular effects through interaction with protease-activated receptors (PARs).	doacs	0-5	coagulation factor X	Homo sapiens	72-75
35037739-3	2022	DOACs, the preferred anticoagulants in AF, can target factors upstream (FXa) or downstream (thrombin) in the coagulation cascade and mediate differential vascular effects through interaction with protease-activated receptors (PARs).	doacs	0-5	coagulation factor II, thrombin	Homo sapiens	92-100
35425821-5	2022	Preclinical data suggest that only high doses of DOACs are able to mitigate catheter-induced thrombin generation, whereas low dose UFH already do so.	doacs	49-54	coagulation factor II, thrombin	Homo sapiens	93-101
35174529-2	2022	Pharmacokinetics of DOACs are largely influenced by efflux transporters derived from ABC transporters, notably by P-glycoprotein (P-gp).	doacs	20-25	ATP binding cassette subfamily B member 1	Homo sapiens	130-134
33914427-5	2021	These differences between DOACs with almost equal half-life are probably partly due to the differences in dosing interval: twice a day (BID) versus once a day (QD).	doacs	26-31	BH3 interacting domain death agonist	Homo sapiens	136-139
34024021-0	2021	Prothrombin complex concentrate in major bleeding associated with DOACs; an updated systematic review and meta-analysis.	doacs	66-71	coagulation factor II, thrombin	Homo sapiens	0-11
33956281-3	2021	This includes the novel anticoagulants with direct inhibition of the factor Xa mechanism (DOACs).	doacs	90-95	coagulation factor X	Homo sapiens	69-78
33919121-7	2021	The effect of DOACs on the screening coagulation assays such as prothrombin time (PT), activated partial thromboplastin time (APTT), and thrombin time (TT) is directly linked to reagent composition, and clotting time can be different from reagent to reagent, depending on the DOAC"s reagent sensitivity.	doacs	14-19	coagulation factor II, thrombin	Homo sapiens	67-75
33243038-5	2021	The author then discusses the results of two RCTs which separately compared the direct oral factor Xa inhibitors, apixaban or rivaroxaban, with placebo for CAT prophylaxis in ambulatory high-risk cancer patients and found that DOACS reduced VTE but increased bleeding.	doacs	227-232	coagulation factor X	Homo sapiens	92-101
32634728-9	2020	"Switched" patients to DOACs therapy showed an improved FMD (19.0 +- 6.6% vs 3.8 +- 1.3%, p < 0.0001); C-reactive protein (CRP) levels decreased in "switched" patients from 1.4 +- 0.5 to 1.0 +- 0.7 mg/dl (p < 0.05).	doacs	23-28	C-reactive protein	Homo sapiens	103-121
33193842-6	2020	The present study evaluated the capability of DOACs in reducing plasma level of IL-6 in patients suffered from deep vein thrombosis (DVT) of the lower limbs.	doacs	46-51	interleukin 6	Homo sapiens	80-84
33193842-8	2020	We postulate that lowered IL-6 expression in the lymphocytes of DVT patients may mediate the anti-inflammatory action of DOACs.	doacs	121-126	interleukin 6	Homo sapiens	26-30
32949961-1	2020	INTRODUCTION: Direct thrombin inhibitor, dabigatran and factor Xa inhibitors, apixaban, edoxaban, and rivaroxaban (DOACs/NOACs), are currently the first-choice drugs in some indications.	doacs	115-120	coagulation factor II, thrombin	Homo sapiens	21-29
33211254-7	2021	For the comparison of DOAC vs. warfarin (Aim 1), DOACs had comparable risks of IS/SE and major bleeding to warfarin in our present cohort.	doacs	49-54	crystallin beta-gamma domain containing 1	Homo sapiens	41-46
32634728-9	2020	"Switched" patients to DOACs therapy showed an improved FMD (19.0 +- 6.6% vs 3.8 +- 1.3%, p < 0.0001); C-reactive protein (CRP) levels decreased in "switched" patients from 1.4 +- 0.5 to 1.0 +- 0.7 mg/dl (p < 0.05).	doacs	23-28	C-reactive protein	Homo sapiens	123-126
32862668-16	2020	P-glycoprotein inhibition and CYP3A4 induction were independently associated with DDI of antineoplastic agents with DOACs.	doacs	116-121	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
32453015-2	2020	METHODS: SBP was measured in 9051 primary care patients in England on DOACs for atrial fibrillation with postinitiation BP levels available within the Clinical Practice Research Datalink.	doacs	70-75	selenium binding protein 1	Homo sapiens	9-12
32619349-13	2020	Taipan/Ecarin tests may be a solution for VKAs and anti-FXa DOACs, but independent evidence on their value and standardized kits is needed.	doacs	60-65	coagulation factor X	Homo sapiens	56-59
32548560-2	2020	Objective: To evaluate the effects of DOACs on thrombin generation 12 hours after DOAC intake in comparison to baseline and a healthy control group.	doacs	38-43	coagulation factor II, thrombin	Homo sapiens	47-55
32548560-12	2020	While thrombin peak is particularly modified by factor Xa inhibitors, all DOACs prolong the lag time and time to thrombin peak.	doacs	74-79	coagulation factor II, thrombin	Homo sapiens	113-121
32548561-9	2020	Peak thrombin and velocity index show a negative correlation following an exponential regression curve with all anti-Xa DOACs but not with dabigatran.	doacs	120-125	coagulation factor II, thrombin	Homo sapiens	5-13
31539350-16	2020	Conclusions DOAC-Remove effectively reduces DOACs concentration in plasma, which enables FVL testing using APC-R.	doacs	44-49	coagulation factor V	Homo sapiens	89-92
32329770-3	2020	Verapamil hydrochloride and diltiazem hydrochloride are combined P-glycoprotein (P-gp) and CYP3A4 inhibitors and may be associated with increases in the risk of bleeding with DOACs.	doacs	175-180	ATP binding cassette subfamily B member 1	Homo sapiens	81-85
31492462-3	2020	Developed in the early 21st century, DOACs have comparable efficacy to LMWHs, but increase bleeding risk, as the anticoagulant targets (FIIa, FXa) are also essential for physiological hemostasis.	doacs	37-42	coagulation factor X	Homo sapiens	142-145
32862668-16	2020	P-glycoprotein inhibition and CYP3A4 induction were independently associated with DDI of antineoplastic agents with DOACs.	doacs	116-121	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	30-36
31686406-1	2019	INTRODUCTION: Factor Xa-inhibiting direct oral anticoagulants (FXa-DOACs) undergo hepatic metabolism via cytochrome P-450 (CYP450).	doacs	67-72	coagulation factor X	Homo sapiens	14-23
31574017-7	2019	DOACs are inconsistently diagnosed by routine coagulation tests, and reversed by a combination of TXA, PCC and specific antidotes (if available).	doacs	0-5	crystallin gamma D	Homo sapiens	103-106
31686406-1	2019	INTRODUCTION: Factor Xa-inhibiting direct oral anticoagulants (FXa-DOACs) undergo hepatic metabolism via cytochrome P-450 (CYP450).	doacs	67-72	coagulation factor X	Homo sapiens	63-66
31686406-1	2019	INTRODUCTION: Factor Xa-inhibiting direct oral anticoagulants (FXa-DOACs) undergo hepatic metabolism via cytochrome P-450 (CYP450).	doacs	67-72	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	105-121
31686406-1	2019	INTRODUCTION: Factor Xa-inhibiting direct oral anticoagulants (FXa-DOACs) undergo hepatic metabolism via cytochrome P-450 (CYP450).	doacs	67-72	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	123-129
31121158-9	2019	Pretreatment with DOACs clearly limited the impact of thrombin on PAR-1 cleavage in our model, contrary to other anticoagulants, associated with ZO-1 and VE-cadherin expressions.	doacs	18-23	coagulation factor II, thrombin	Homo sapiens	54-62
31520256-7	2019	Drugs interacting with DOACs (P-glycoprotein/CYP3A4) were used by 6460 (20%) of patients.	doacs	23-28	ATP binding cassette subfamily B member 1	Homo sapiens	30-44
31520256-7	2019	Drugs interacting with DOACs (P-glycoprotein/CYP3A4) were used by 6460 (20%) of patients.	doacs	23-28	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	45-51
31327027-3	2019	Direct oral anticoagulants (DOACs)-direct thrombin inhibitor dabigatran, and direct oral factor Xa inhibitors rivaroxaban, apixaban, and edoxaban-are currently frequently used for the prevention and treatment of VTE in adult population.	doacs	28-33	coagulation factor II, thrombin	Homo sapiens	42-50
31010298-3	2019	Over the past years, several direct oral anticoagulants (DOACs) targeting FXa have been developed.	doacs	57-62	coagulation factor X	Homo sapiens	74-77
31010298-6	2019	Direct inhibition of FXa by DOACs could be beneficial in these conditions.	doacs	28-33	coagulation factor X	Homo sapiens	21-24
31010298-7	2019	This is a narrative review that focuses on the cellular effects of FXa in various cell types and conditions, as well as on the possible pleiotropic effects of FXa-targeting DOACs.	doacs	173-178	coagulation factor X	Homo sapiens	159-162
31309520-10	2019	Across the two cohorts, the risk of bleeding was lower in patients being treated with DOACs rather than warfarin (10/4574 vs. 42/8161 event/person-years, respectively, IRR 0.42 95% CI 0.19-0.86).	doacs	86-91	insulin receptor related receptor	Homo sapiens	168-171
31330558-9	2019	The T-TAS AR chip AUC result is useful for assessing the efficacy of DOACs and warfarin in AF patients undergoing catheter ablation, and it is also a potential independent predictor of periprocedural bleeding events and avoidance of thrombosis in patients having undergone total knee arthroplasty.	doacs	69-74	THAS	Homo sapiens	6-9
31121158-5	2019	Our hypothesis is that DOACs may limit the effects of thrombin on endothelial cells (of the BBB) alteration by a mechanism probably involving PAR-1 activation.	doacs	23-28	coagulation factor II, thrombin	Homo sapiens	54-62
31121158-5	2019	Our hypothesis is that DOACs may limit the effects of thrombin on endothelial cells (of the BBB) alteration by a mechanism probably involving PAR-1 activation.	doacs	23-28	coagulation factor II thrombin receptor	Homo sapiens	142-147
31121158-8	2019	Depending on the anticoagulant used, we observed three profiles of response of the endothelial cells after thrombin exposure: i) dabigatran treatment allowed maintaining the tightness of the endothelial monolayer; ii) other DOACs limited thrombin-induced alteration of the endothelial monolayer; and iii) pretreatment with warfarin and heparin did not protect from thrombin-induced BBB breakdown.	doacs	224-229	coagulation factor II, thrombin	Homo sapiens	238-246
31121158-8	2019	Depending on the anticoagulant used, we observed three profiles of response of the endothelial cells after thrombin exposure: i) dabigatran treatment allowed maintaining the tightness of the endothelial monolayer; ii) other DOACs limited thrombin-induced alteration of the endothelial monolayer; and iii) pretreatment with warfarin and heparin did not protect from thrombin-induced BBB breakdown.	doacs	224-229	coagulation factor II, thrombin	Homo sapiens	238-246
31121158-9	2019	Pretreatment with DOACs clearly limited the impact of thrombin on PAR-1 cleavage in our model, contrary to other anticoagulants, associated with ZO-1 and VE-cadherin expressions.	doacs	18-23	coagulation factor II thrombin receptor	Homo sapiens	66-71
31121158-9	2019	Pretreatment with DOACs clearly limited the impact of thrombin on PAR-1 cleavage in our model, contrary to other anticoagulants, associated with ZO-1 and VE-cadherin expressions.	doacs	18-23	tight junction protein 1	Homo sapiens	145-149
31121158-9	2019	Pretreatment with DOACs clearly limited the impact of thrombin on PAR-1 cleavage in our model, contrary to other anticoagulants, associated with ZO-1 and VE-cadherin expressions.	doacs	18-23	cadherin 5	Homo sapiens	154-165
31121158-10	2019	In conclusion, DOACs seem to limit the alteration of the monolayer of endothelial cells of the BBB mediated by the thrombin/PAR-1 pathway.	doacs	15-20	coagulation factor II, thrombin	Homo sapiens	115-123
31121158-10	2019	In conclusion, DOACs seem to limit the alteration of the monolayer of endothelial cells of the BBB mediated by the thrombin/PAR-1 pathway.	doacs	15-20	coagulation factor II thrombin receptor	Homo sapiens	124-129
31113643-9	2019	Bioaccumulation risk should be considered if DOACs are prescribed in PAH and CTEPH patients, especially the risk of drug-drug interaction mediated by P-glycoprotein and cytochrome 3A4 with targeted therapies.	doacs	45-50	ATP binding cassette subfamily B member 1	Homo sapiens	150-164
33843889-2	2019	Two of the most widely used direct oral anticoagulants (DOACs), rivaroxaban and apixaban, are factor Xa inhibitors.	doacs	56-61	coagulation factor X	Homo sapiens	94-103
31266079-2	2019	This study examined the ability of direct oral anticoagulants (DOACs), apixaban and rivaroxaban, to inhibit the release of TF+MV from two cell lines (MDA-MB-231 and AsPC-1) as well as cell proliferation.Activation of the cells with fXa (10 nM) enhanced the release of TF+MV but was suppressed in the presence of either DOAC.	doacs	63-68	coagulation factor X	Homo sapiens	232-235
30929299-2	2019	While the anticancer effects of LMWHs have been extensively studied in preclinical cancer models, the effects of FXa-targeting DOACs on cancer progression remain to be studied.	doacs	127-132	coagulation factor X	Homo sapiens	113-116
30985986-6	2019	However, lacking is accessibility to a detection method that is able to quantify low levels of anti-FXa DOACs.	doacs	104-109	coagulation factor X	Homo sapiens	100-103
31216588-2	2019	Although the long history of anticoagulant drugs has been characteristically shaped by coumarin and heparin derivatives, a new generation of direct oral anticoagulants (DOACs), which specifically inhibit thrombin or activated factor X, combine many advantages of their progenitor drugs, and hence are prepotently revolutionizing the landscape of antithrombotic therapy.	doacs	169-174	coagulation factor II, thrombin	Homo sapiens	204-212
31489274-2	2019	DOACs act by specifically targeting a single coagulation factor, such as Factor Xa or thrombin.	doacs	0-5	coagulation factor X	Homo sapiens	73-82
31489274-2	2019	DOACs act by specifically targeting a single coagulation factor, such as Factor Xa or thrombin.	doacs	0-5	coagulation factor II, thrombin	Homo sapiens	86-94
31045726-4	2019	Rapid identification of DOACs in the blood will allow timely reversal of factor Xa inhibitors and direct thrombin inhibitors when necessary.	doacs	24-29	coagulation factor X	Homo sapiens	73-82
31045726-4	2019	Rapid identification of DOACs in the blood will allow timely reversal of factor Xa inhibitors and direct thrombin inhibitors when necessary.	doacs	24-29	coagulation factor II, thrombin	Homo sapiens	105-113
31195999-1	2019	BACKGROUND: Clinical trials have demonstrated that direct oral anticoagulants (DOACs) are at least non-inferior to warfarin in reducing the risk of stroke/systemic embolism (SE) among patients with non-valvular atrial fibrillation (NVAF), but the comparative risk of major bleeding varies between DOACs and warfarin.	doacs	79-84	squalene epoxidase	Homo sapiens	174-176
30857168-2	2019	DOACs directly and reversibly inhibit activated factor X or thrombin and can interfere with other pathophysiological processes such as inflammation, lipid metabolism, and bone turnover.	doacs	0-5	coagulation factor II, thrombin	Homo sapiens	60-68
30485173-9	2019	DOACs" use was associated with falsely low APCR ratios (i.e. FVL-like effect) and somewhat unexpectedly, anti-Xa agents apixaban and rivaroxaban were also associated with lower AT and higher PS values.	doacs	0-5	coagulation factor V	Homo sapiens	61-64
31014373-1	2019	BACKGROUND: Prothrombin complex concentrate (PCC) is widely used to reverse the action of direct oral anticoagulants (DOACs) in accordance with current guidelines and because of a lack of specific reversal agents.	doacs	118-123	coagulation factor II, thrombin	Homo sapiens	12-23
30362966-3	2019	Most DOACs act by directly binding to and inhibiting the effects of factor Xa.	doacs	5-10	coagulation factor X	Homo sapiens	68-77
30362966-4	2019	Andexanet alfa (Andexxa, Portola Pharmaceuticals, San Francisco, CA) is a modified form of factor Xa that acts as a decoy binding entity for DOACs, thereby allowing endogenous factor Xa to perform its normal clotting functions.	doacs	141-146	coagulation factor X	Homo sapiens	91-100
30362966-4	2019	Andexanet alfa (Andexxa, Portola Pharmaceuticals, San Francisco, CA) is a modified form of factor Xa that acts as a decoy binding entity for DOACs, thereby allowing endogenous factor Xa to perform its normal clotting functions.	doacs	141-146	coagulation factor X	Homo sapiens	176-185
31523979-1	2019	The effect of direct oral anticoagulants (DOACs) on laboratory tests dependent on the production of their targets, factor IIa and factor Xa (FXa), is a well-known problem and can cause both false positive and negative results.	doacs	42-47	coagulation factor X	Homo sapiens	130-139
30950652-6	2019	We performed a multivariable logistic regression, adjusting for age, sex, race/ethnicity, region, zip code-linked household income, and clinical covariates to identify factors associated with the use of DOACs.	doacs	203-208	death associated protein kinase 3	Homo sapiens	98-101
30665674-2	2019	Thus, current DOACs in use (e.g., dabigatran, a direct thrombin inhibitor, and apixaban and rivaroxaban, both direct Xa inhibitors), affect a wide variety of coagulation assays, including those used in LA investigation.	doacs	14-19	coagulation factor II, thrombin	Homo sapiens	55-63
31523979-1	2019	The effect of direct oral anticoagulants (DOACs) on laboratory tests dependent on the production of their targets, factor IIa and factor Xa (FXa), is a well-known problem and can cause both false positive and negative results.	doacs	42-47	coagulation factor X	Homo sapiens	141-144
30359834-5	2019	We included all adult patients with isolated blunt pelvic fractures who were managed nonoperatively and received thromboprophylaxis with either LMWH or DOACs (Factor-Xa inhibitor or direct thrombin inhibitor).	doacs	152-157	coagulation factor X	Homo sapiens	159-168
30697449-1	2018	In recent years, the options for anticoagulant therapy have examined new direct oral anticoagulants (DOACs) comprising direct thrombin inhibitors (dabigatran) and direct factor Xa inhibitors (rivaroxaban, apixaban, and edoxaban).	doacs	101-106	coagulation factor II, thrombin	Homo sapiens	126-134
30848768-1	2019	Direct oral anticoagulants (DOACs), including the direct thrombin inhibitor dabigatran and the direct factor Xa inhibitors rivaroxaban, apixaban and edoxaban have at least comparable efficacy as vitamin K antagonists along with a better safety profile, reflected by a lower incidence of intracranial hemorrhage.	doacs	28-33	coagulation factor II, thrombin	Homo sapiens	57-65
30176116-17	2018	By enabling the t-PA cofactor function of FXabeta in plasma, DOACs also enhance fibrinolysis.	doacs	61-66	plasminogen activator, tissue type	Homo sapiens	16-20
30581412-7	2018	Older AEDs, acting on cytochrome P450 isoenzymes, and especially on CYP3A4, such as phenobarbital, phenytoin, and carbamazepine are more likely to significantly reduce the anticoagulant effect of DOACs (especially rivaroxaban, apixaban, and edoxaban).	doacs	196-201	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	68-74
30292948-1	2018	Direct Oral Anticoagulants (DOACs) available for the treatment and prevention of thromboembolic diseases include dabigatran, a direct thrombin (IIa) inhibitor, and apixaban, edoxaban and rivaroxaban, which are direct inhibitors of Stuart factor (Xa).	doacs	28-33	coagulation factor II, thrombin	Homo sapiens	134-142
30075986-1	2018	Direct oral anticoagulants (DOACs) are small molecule inhibitors of the coagulation proteases thrombin and factor Xa that demonstrate comparable efficacy to warfarin for several common indications, while causing less serious bleeding.	doacs	28-33	coagulation factor II, thrombin	Homo sapiens	94-102
30135185-1	2018	Anticoagulants such as unfractionated heparin (UFH), low-molecular-weight heparins (LMWHs), fondaparinux, and direct oral anticoagulants (DOACs) targeting thrombin (IIa) or factor Xa (FXa) are widely used in prevention and treatment of thromboembolic disorders.	doacs	138-143	coagulation factor II, thrombin	Homo sapiens	155-163
30148651-1	2018	INTRODUCTION: The landscape of therapeutic anticoagulation has changed dramatically over the past decade, with availability of direct oral anticoagulants (DOACs), which inhibit factor Xa or thrombin.	doacs	155-160	coagulation factor X	Homo sapiens	177-186
30148651-1	2018	INTRODUCTION: The landscape of therapeutic anticoagulation has changed dramatically over the past decade, with availability of direct oral anticoagulants (DOACs), which inhibit factor Xa or thrombin.	doacs	155-160	coagulation factor II, thrombin	Homo sapiens	190-198
30787949-2	2018	This overview of systematic reviews presents the baseline results for efficacy and safety of the new direct oral anticoagulants (DOACs) thrombin inhibitors, and activated factor X (Xa) inhibitors in patients with DVT.	doacs	129-134	coagulation factor II, thrombin	Homo sapiens	136-144
30415235-5	2018	CYP2C9 and VKORC1 polymorphisms are essential determinants in the genotype-guided dosing of warfarin and may distinguish patients who would benefit from switching to direct oral anticoagulants (DOACs).	doacs	194-199	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30415235-5	2018	CYP2C9 and VKORC1 polymorphisms are essential determinants in the genotype-guided dosing of warfarin and may distinguish patients who would benefit from switching to direct oral anticoagulants (DOACs).	doacs	194-199	vitamin K epoxide reductase complex subunit 1	Homo sapiens	11-17
30073093-1	2018	Direct oral anticoagulants (DOACs) are a new class of anticoagulants that directly inhibit either thrombin or factor Xa in the coagulation cascade.	doacs	28-33	coagulation factor II, thrombin	Homo sapiens	98-106
30073093-1	2018	Direct oral anticoagulants (DOACs) are a new class of anticoagulants that directly inhibit either thrombin or factor Xa in the coagulation cascade.	doacs	28-33	coagulation factor X	Homo sapiens	110-119
29572341-4	2018	This work aimed to assess potential P-gp-mediated drug-drug interactions between PDE5is and DOACs using in vitro methods.	doacs	92-97	ATP binding cassette subfamily B member 1	Homo sapiens	36-40
29572341-4	2018	This work aimed to assess potential P-gp-mediated drug-drug interactions between PDE5is and DOACs using in vitro methods.	doacs	92-97	phosphodiesterase 5A	Homo sapiens	81-85
29572341-5	2018	A cellular model of drug transport assay, using P-gp-overexpressing Madin-Darby canine kidney cells (transfected with the human P-gp gene), was used to determine the bidirectional permeabilities of two DOACs (rivaroxaban and apixaban) in the absence and presence of increasing concentrations (0.5-100 microM) of three PDE5is (sildenafil, tadalafil, and vardenafil).	doacs	202-207	ATP binding cassette subfamily B member 1	Homo sapiens	48-52
29572341-5	2018	A cellular model of drug transport assay, using P-gp-overexpressing Madin-Darby canine kidney cells (transfected with the human P-gp gene), was used to determine the bidirectional permeabilities of two DOACs (rivaroxaban and apixaban) in the absence and presence of increasing concentrations (0.5-100 microM) of three PDE5is (sildenafil, tadalafil, and vardenafil).	doacs	202-207	ATP binding cassette subfamily B member 1	Homo sapiens	128-132
29072911-5	2018	Efforts are now underway to develop DOACs that inhibit components of the intrinsic and extrinsic coagulation cascades upstream of thrombin and fX.	doacs	36-41	coagulation factor II, thrombin	Homo sapiens	130-138
29274758-2	2018	The DOACs are P-glycoprotein (P-gp) and cytochrome p-450 (CYP3A4) substrates.	doacs	4-9	ATP binding cassette subfamily B member 1	Homo sapiens	14-28
29274758-2	2018	The DOACs are P-glycoprotein (P-gp) and cytochrome p-450 (CYP3A4) substrates.	doacs	4-9	ATP binding cassette subfamily B member 1	Homo sapiens	30-34
29274758-2	2018	The DOACs are P-glycoprotein (P-gp) and cytochrome p-450 (CYP3A4) substrates.	doacs	4-9	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	40-56
29274758-2	2018	The DOACs are P-glycoprotein (P-gp) and cytochrome p-450 (CYP3A4) substrates.	doacs	4-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-64
29297662-7	2017	Since then, the FDA has approved 5 direct-acting oral anticoagulants (DOACs) that inhibit single coagulation factors (factor Xa and thrombin).	doacs	70-75	coagulation factor II, thrombin	Homo sapiens	132-140
29636974-4	2018	However, it is important to be aware that plasma levels of DOACs are affected by drugs that alter the cell efflux transporter P-glycoprotein and/or cytochrome P450.	doacs	59-64	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	148-163
29176379-3	2018	Hence, we aim to study the effect and variability of DOACs on thrombin generation via the calibrated automated thrombogram.	doacs	53-58	coagulation factor II, thrombin	Homo sapiens	62-70
29176379-13	2018	Thrombin generation can measure the anticoagulation effect of commonly used DOACs, with each drug having a unique thrombin generation profile.	doacs	76-81	coagulation factor II, thrombin	Homo sapiens	0-8
29176379-13	2018	Thrombin generation can measure the anticoagulation effect of commonly used DOACs, with each drug having a unique thrombin generation profile.	doacs	76-81	coagulation factor II, thrombin	Homo sapiens	114-122
28895074-1	2018	BACKGROUND: Pharmacokinetics of direct oral anticoagulants (DOACs) are influenced by ATP-binding cassette (ABC) transporters such as P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP).	doacs	60-65	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	85-105
28895074-1	2018	BACKGROUND: Pharmacokinetics of direct oral anticoagulants (DOACs) are influenced by ATP-binding cassette (ABC) transporters such as P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP).	doacs	60-65	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	107-110
28895074-1	2018	BACKGROUND: Pharmacokinetics of direct oral anticoagulants (DOACs) are influenced by ATP-binding cassette (ABC) transporters such as P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP).	doacs	60-65	ATP binding cassette subfamily B member 1	Homo sapiens	133-147
28895074-1	2018	BACKGROUND: Pharmacokinetics of direct oral anticoagulants (DOACs) are influenced by ATP-binding cassette (ABC) transporters such as P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP).	doacs	60-65	ATP binding cassette subfamily B member 1	Homo sapiens	149-153
28895074-1	2018	BACKGROUND: Pharmacokinetics of direct oral anticoagulants (DOACs) are influenced by ATP-binding cassette (ABC) transporters such as P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP).	doacs	60-65	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	159-191
28895074-1	2018	BACKGROUND: Pharmacokinetics of direct oral anticoagulants (DOACs) are influenced by ATP-binding cassette (ABC) transporters such as P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP).	doacs	60-65	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	193-197
29633739-4	2018	The anticoagulant or antithrombotic armamentarium entails several anticoagulants such as heparin, coumarins, fondaparinux, and the recently developed DOACs inhibiting either activated factor Xa (i.e., rivaroxaban, apixaban, edoxaban) or thrombin (i.e., dabigatran), as well as aspirin, i.e., the oldest antiplatelet drug to be ever discovered and used in clinical practice.	doacs	150-155	coagulation factor X	Homo sapiens	184-193
29633739-4	2018	The anticoagulant or antithrombotic armamentarium entails several anticoagulants such as heparin, coumarins, fondaparinux, and the recently developed DOACs inhibiting either activated factor Xa (i.e., rivaroxaban, apixaban, edoxaban) or thrombin (i.e., dabigatran), as well as aspirin, i.e., the oldest antiplatelet drug to be ever discovered and used in clinical practice.	doacs	150-155	coagulation factor II, thrombin	Homo sapiens	237-245
29325495-4	2018	In this regard, the direct oral factor Xa or thrombin inhibitors (DOACs) have emerged as potential alternatives in the management of patients with cancer-associated VTE, albeit findings from randomized controlled studies with a direct head-to-head comparison of DOACs with LMWH, the current standard of care, are still lacking.	doacs	66-71	coagulation factor II, thrombin	Homo sapiens	45-53
29031817-8	2018	Recent studies have focused on the high-alert medications among ABCG2 substrates (defined as those with high risk of adverse events), such as tyrosine kinase inhibitors (TKIs) and direct oral anti-coagulants (DOACs).	doacs	209-214	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	64-69
26984934-2	2017	Thus, we planned to elucidate the adequate prothrombin time (PT) test for the evaluation of the anticoagulant effects of various DOACs.	doacs	129-134	coagulation factor II, thrombin	Homo sapiens	43-54
28689334-1	2017	Direct oral anticoagulants (DOACs) are novel direct-acting medications that are selective for either thrombin or activated factor X.	doacs	28-33	coagulation factor II, thrombin	Homo sapiens	101-109
29849330-3	2017	The DOACs also include the factor Xa inhibitors rivaroxaban, apixaban, and edoxaban.	doacs	4-9	coagulation factor X	Homo sapiens	27-36
28929298-4	2017	More recently, two classes of direct oral anticoagulant agents (DOACs) have been investigated for the prevention and management of venous thromboembolic events: the direct factor Xa inhibitors rivaroxaban, apixaban and edoxaban, and the direct thrombin inhibitor dabigatran.	doacs	64-69	coagulation factor II, thrombin	Homo sapiens	244-252
28639463-6	2017	This review discusses adverse drug reactions to the traditional anticoagulants, warfarin and heparin, and the newer direct oral anticoagulants (DOACs) such as the thrombin inhibitor, dabigatran, and the factor Xa inhibitors, rivaroxaban, apixaban, and edoxaban.	doacs	144-149	coagulation factor II, thrombin	Homo sapiens	163-171
30046690-2	2017	The clinical application of thrombin generation assay (TGA) in monitoring the effect of DOACs has not been well established.	doacs	88-93	coagulation factor II, thrombin	Homo sapiens	28-36
28979172-2	2017	Although there is an approved reversal agent for the direct thrombin inhibitor dabigatran, a specific reversal agent for the anti-factor Xa (FXa) DOACs has yet to be licensed.	doacs	146-151	coagulation factor X	Homo sapiens	125-139
28979172-2	2017	Although there is an approved reversal agent for the direct thrombin inhibitor dabigatran, a specific reversal agent for the anti-factor Xa (FXa) DOACs has yet to be licensed.	doacs	146-151	coagulation factor X	Homo sapiens	141-144
28979172-4	2017	Andexanet alfa is a FXa decoy designed to reverse all anticoagulants that act through this part of the coagulation cascade including anti-FXa DOACs, such as apixaban, edoxaban and rivaroxaban, and indirect FXa inhibitors such as low-molecular-weight heparins.	doacs	142-147	coagulation factor X	Homo sapiens	20-23
28713563-2	2017	The DOACs include dabigatran, which inhibits thrombin, and rivaroxaban, apixaban, and edoxaban, which inhibit factor Xa.	doacs	4-9	coagulation factor II, thrombin	Homo sapiens	45-53
28390791-1	2017	Edoxaban is the most recently approved factor Xa inhibitor within the class of direct oral anticoagulants (DOACs).	doacs	107-112	coagulation factor X	Homo sapiens	39-48
28471371-1	2017	Several direct oral anticoagulants (DOACs), including direct thrombin and factor Xa inhibitors, have been approved as alternatives to vitamin K antagonist anticoagulants.	doacs	36-41	coagulation factor II, thrombin	Homo sapiens	61-69
28769570-1	2017	Reversal agents for direct oral anticoagulants (DOACs), including factor X inhibitors and direct thrombin inhibitors, are a major concern in clinical practice.	doacs	48-53	coagulation factor II, thrombin	Homo sapiens	97-105
28678302-3	2017	Generally, assays that employ clot based principles, or methods that require thrombin or Factor Xa activation or substrates may be affected by the presence of DOACS.	doacs	159-164	coagulation factor II, thrombin	Homo sapiens	77-85
28678302-3	2017	Generally, assays that employ clot based principles, or methods that require thrombin or Factor Xa activation or substrates may be affected by the presence of DOACS.	doacs	159-164	coagulation factor X	Homo sapiens	89-98
28196633-4	2017	Direct oral anticoagulants (DOACs) including Factor Xa inhibitors (rivaroxaban, apixaban and edoxaban) and thrombin inhibitor (dabigatran) are poised to replace warfarin.	doacs	28-33	coagulation factor X	Homo sapiens	45-54
28713563-2	2017	The DOACs include dabigatran, which inhibits thrombin, and rivaroxaban, apixaban, and edoxaban, which inhibit factor Xa.	doacs	4-9	coagulation factor X	Homo sapiens	110-119
28552490-6	2017	Various assays are also developed such as platelet aggregometry techniques for evaluating drug induced- aggregates or methods allowing measurement of the drug activity to its targeted coagulation factors such as: heparin to thrombin or Factor Xa; DOACs to Thrombin or Factor Xa (Dabigatran to thrombin and DiXaIs, Rivaroxaban, Apixaban, and Edoxaban, to Factor Xa).	doacs	247-252	coagulation factor II, thrombin	Homo sapiens	256-264
28581331-3	2017	Over the past decade, direct oral anticoagulants (DOACs) (eg, direct thrombin inhibitor and factor Xa [FXa] inhibitors) have been adopted as alternatives to warfarin due to their clinical advantages and efficacy for the treatment of thrombosis.	doacs	50-55	coagulation factor X	Homo sapiens	103-106
28122753-3	2017	Current DOACs work by either directly blocking thrombin (dabigatran) or inhibiting factor Xa (apixaban, edoxaban, and rivaroxaban).	doacs	8-13	coagulation factor II, thrombin	Homo sapiens	47-92
27988438-3	2017	Direct oral anticoagulants (DOACs) targeting thrombin and factor Xa are currently widely use to prevent and treat venous and arterial thromboembolism.	doacs	28-33	coagulation factor II, thrombin	Homo sapiens	45-53
27988438-3	2017	Direct oral anticoagulants (DOACs) targeting thrombin and factor Xa are currently widely use to prevent and treat venous and arterial thromboembolism.	doacs	28-33	coagulation factor X	Homo sapiens	58-67
28215696-2	2017	Absorption and elimination of DOACs are dependent on the permeability glycoprotein (P-gp) efflux transporter protein system, and DOACs are substrates of the hepatic cytochrome P 450 3A4 (CYP3A4) enzymes.	doacs	30-35	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	165-185
27780803-5	2017	Second, emerging data that naturally occurring polyphosphates activate the contact system and that this system is critical for thrombus stabilization and growth have identified factor XII (FXII) and FXI as targets for new anticoagulants that may be even safer than the DOACs.	doacs	269-274	coagulation factor XI	Homo sapiens	189-192
28412908-2	2017	METHOD: In this paper, we focus on news in the use of direct oral anticoagulants (DOACS), a group of synthetic low molecular weight drugs capable of directly and specifically inhibiting either activated factor X or both free and fibrin- bound thrombin.	doacs	82-87	coagulation factor II, thrombin	Homo sapiens	243-251
28413976-1	2017	BACKGROUND: The Direct Oral Anticoagulants (DOACs) represent a new generation of antithrombotic agents, providing direct inhibition of either thrombin (factor IIa; FIIa) or activated factor X (FXa).	doacs	44-49	coagulation factor II, thrombin	Homo sapiens	142-150
28413976-1	2017	BACKGROUND: The Direct Oral Anticoagulants (DOACs) represent a new generation of antithrombotic agents, providing direct inhibition of either thrombin (factor IIa; FIIa) or activated factor X (FXa).	doacs	44-49	coagulation factor X	Homo sapiens	193-196
27893182-5	2017	SUMMARY: Background The direct oral anticoagulants (DOACs) dabigatran and rivaroxaban are both substrates of the P-glycoprotein (P-gp) transporter, encoded by the ABCB1 gene.	doacs	52-57	ATP binding cassette subfamily B member 1	Homo sapiens	113-127
27893182-5	2017	SUMMARY: Background The direct oral anticoagulants (DOACs) dabigatran and rivaroxaban are both substrates of the P-glycoprotein (P-gp) transporter, encoded by the ABCB1 gene.	doacs	52-57	ATP binding cassette subfamily B member 1	Homo sapiens	129-133
27893182-5	2017	SUMMARY: Background The direct oral anticoagulants (DOACs) dabigatran and rivaroxaban are both substrates of the P-glycoprotein (P-gp) transporter, encoded by the ABCB1 gene.	doacs	52-57	ATP binding cassette subfamily B member 1	Homo sapiens	163-168
27917715-4	2017	The direct oral anticoagulants (DOACs) inhibiting factor Xa or thrombin activity represent an alternative for heparins and VKAs.	doacs	32-37	coagulation factor X	Homo sapiens	50-59
27917715-4	2017	The direct oral anticoagulants (DOACs) inhibiting factor Xa or thrombin activity represent an alternative for heparins and VKAs.	doacs	32-37	coagulation factor II, thrombin	Homo sapiens	63-71
28215696-2	2017	Absorption and elimination of DOACs are dependent on the permeability glycoprotein (P-gp) efflux transporter protein system, and DOACs are substrates of the hepatic cytochrome P 450 3A4 (CYP3A4) enzymes.	doacs	30-35	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	187-193
28215696-2	2017	Absorption and elimination of DOACs are dependent on the permeability glycoprotein (P-gp) efflux transporter protein system, and DOACs are substrates of the hepatic cytochrome P 450 3A4 (CYP3A4) enzymes.	doacs	129-134	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	165-185
28215696-2	2017	Absorption and elimination of DOACs are dependent on the permeability glycoprotein (P-gp) efflux transporter protein system, and DOACs are substrates of the hepatic cytochrome P 450 3A4 (CYP3A4) enzymes.	doacs	129-134	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	187-193
28215696-3	2017	Therefore, drug-interactions may occur when DOACs are administered with drugs affecting the activity of P-gp or CYP3A4 systems.	doacs	44-49	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	112-118
28781287-8	2017	The emerging oral antithrombotic compounds such as direct oral anticoagulants (DOACs), which have the potential to inhibit factor Xa, do not require laboratory monitoring.	doacs	79-84	coagulation factor X	Homo sapiens	123-132
27692605-1	2016	In the past decade Direct Oral Anti-Coagulants (DOACs), targeting Thrombin or Factor Xa, have enormously facilitated the daily treatment of all relevant patients, including those requiring lifelong therapy.	doacs	48-53	coagulation factor II, thrombin	Homo sapiens	66-74
28215696-11	2017	CONCLUSION: The combination of DOACs with carbamazepine, an inducer of P-gp and CYP3A4-activity, should be avoided since the anticoagulant effect is decreased.	doacs	31-36	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	80-86
27692605-1	2016	In the past decade Direct Oral Anti-Coagulants (DOACs), targeting Thrombin or Factor Xa, have enormously facilitated the daily treatment of all relevant patients, including those requiring lifelong therapy.	doacs	48-53	coagulation factor X	Homo sapiens	78-87
27592622-2	2016	The DOACs include dabigatran, which inhibits thrombin, and rivaroxaban, apixaban, and edoxaban, which inhibit factor Xa.	doacs	4-9	coagulation factor II, thrombin	Homo sapiens	45-53
25619266-4	2016	Direct oral anticoagulants (DOACs), including the factor Xa inhibitors rivaroxaban, apixaban and edoxaban, and the direct thrombin inhibitor dabigatran etexilate, have been developed to address limitations associated with traditional anticoagulant therapy.	doacs	28-33	coagulation factor X	Homo sapiens	50-59
27435452-6	2016	This current article assesses the interactions that do or may occur with the DOACs, particularly with respect to the P-gp and CYP3A4 systems.	doacs	77-82	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	126-132
27909544-6	2016	The DOACs include the direct thrombin inhibitor dabigatran and the direct factor Xa inhibitors rivaroxaban, apixaban, and edoxaban.	doacs	4-9	coagulation factor II, thrombin	Homo sapiens	29-37
27512489-1	2016	Direct oral anticoagulants (DOACs or NOACs -non-vitamin K oral anticoagulants), as the name suggests, are oral anticoagulants with a direct inhibitory action either against factor X or factor II (thrombin).	doacs	28-33	coagulation factor II, thrombin	Homo sapiens	196-204
30609341-2	2016	Direct oral anticoagulants (DOACs), including direct anti-Xa and a thrombin inhibitor, have been introduced and provide advantages over warfarin.	doacs	28-33	coagulation factor II, thrombin	Homo sapiens	67-75
27255713-4	2016	The direct-acting oral anticoagulants (DOACs), i.e. the thrombin inhibitor dabigatran and the factor Xa inhibitors rivaroxaban, apixaban and edoxaban, are given in fixed doses, do not need laboratory monitoring, have fewer drug-drug interactions and are therefore much easier to take.	doacs	39-44	coagulation factor II, thrombin	Homo sapiens	56-64
26964028-2	2016	As of today, these direct oral anticoagulants (DOACs) include dabigatran etexilate (thrombin inhibitor) and apixaban, edoxaban and rivaroxaban (inhibitors of FXa).	doacs	47-52	coagulation factor II, thrombin	Homo sapiens	84-92
26964028-2	2016	As of today, these direct oral anticoagulants (DOACs) include dabigatran etexilate (thrombin inhibitor) and apixaban, edoxaban and rivaroxaban (inhibitors of FXa).	doacs	47-52	coagulation factor X	Homo sapiens	158-161
27146462-7	2016	RESULTS: Prothrombin time (PT) and activated partial thromboplastin time (aPTT) are variably affected by the DOACs and dependent of the coagulation assays used.	doacs	109-114	coagulation factor II, thrombin	Homo sapiens	9-20
26739579-6	2016	The two classes of DOACs and the drugs they are comprised of are factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) and direct thrombin inhibitor (dabigatran).	doacs	19-24	coagulation factor X	Homo sapiens	65-74
26739579-6	2016	The two classes of DOACs and the drugs they are comprised of are factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) and direct thrombin inhibitor (dabigatran).	doacs	19-24	coagulation factor II, thrombin	Homo sapiens	131-139
26492202-1	2016	Direct oral anticoagulants (DOACs), including the direct thrombin inhibitor, dabigatran, and the direct factor Xa (FXa) inhibitors, rivaroxaban, apixaban and edoxaban, are approved for thromboembolism prevention and treatment.	doacs	28-33	coagulation factor II, thrombin	Homo sapiens	57-65
26037286-4	2015	RESULTS: The study revealed an up to 3-fold increased risk of hemorrhagic stroke in patients receiving DOACs (OR 3.45, 95% CI 1.62 to 7.37, P=0.001, and I(2)=0%) or PAR-1 antagonists (OR 2.60, 95% CI 1.18 to 5.69, P=0.02, and I(2)=0%) in addition to antiplatelet therapy compared to those with antiplatelet therapy alone.	doacs	103-108	Prader Willi/Angelman region RNA 1	Homo sapiens	165-170
26370208-2	2015	Current guidelines recommend that the vitamin K antagonist warfarin or direct oral anticoagulants (DOACs), such as the approved direct thrombin inhibitor dabigatran and the approved direct factor Xa inhibitors apixaban, rivaroxaban, and edoxaban, should be used for thromboprophylaxis in patients with nonvalvular AF at risk for stroke or systemic embolic events (SEE).	doacs	99-104	coagulation factor II, thrombin	Homo sapiens	135-143
25903537-3	2015	Recently, direct oral anticoagulants (DOACs), including the Factor Xa inhibitors rivaroxaban, apixaban and edoxaban, and the direct thrombin inhibitor dabigatran etexilate, have been developed to address limitations associated with traditional anticoagulant therapy.	doacs	38-43	coagulation factor X	Homo sapiens	60-69
25488466-11	2015	Only DOACs showed a significant reduction in the composite outcome of fatal recurrent VTE and fatal bleeding when compared to placebo, IRR 0.40 (95% CI, 0.14-1.0, p=0.03).	doacs	5-10	insulin receptor related receptor	Homo sapiens	135-138
24861794-1	2014	Direct oral anticoagulants (DOACs), direct inhibitors of thrombin or factor Xa (FXa), are increasingly used in clinical practice for the prevention of thromboembolic complications in patients with non-valvular atrial fibrillation (NVAF) and for therapy of venous thromboembolism (VTE).	doacs	28-33	coagulation factor X	Homo sapiens	69-78
24301324-5	2014	Such assays are increasingly used in clinical routine and their daily use is triggered by the advent of the novel direct oral anticoagulants (DOACs) as an alternative for vitamin K antagonist (VKA) treatment, which are dabigatran, rivaroxaban and apixaban, and by the advent of prasugrel or ticagrelor as an alternative for clopidogrel with regard to platelet P2Y12 receptor inhibition.	doacs	142-147	purinergic receptor P2Y12	Homo sapiens	360-365
26637711-1	2015	The major practical advantage of the direct oral anticoagulants (DOACs), comprising the thrombin inhibitor dabigatran and the factor Xa inhibitors apixaban, edoxaban, and rivaroxaban, over vitamin K antagonists is their fixed dosing without the need for laboratory monitoring.	doacs	65-70	coagulation factor II, thrombin	Homo sapiens	88-96