PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
34560933-1	2021	In capillary electrophoresis an enantioseparation of daclatasvir (DCV) was observed in case of heptakis(2,6-di-O-methyl)-beta-CD, heptakis(2-O-methyl)-beta-CD and beta-CD, while two peaks with a plateau were noted for heptakis(2,3,6-tri-O-methyl)-beta-CD and heptakis(2,3-di-O-methyl)-beta-CD indicating a slow equilibrium.	daclatasvir	53-64	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	121-128
34560933-1	2021	In capillary electrophoresis an enantioseparation of daclatasvir (DCV) was observed in case of heptakis(2,6-di-O-methyl)-beta-CD, heptakis(2-O-methyl)-beta-CD and beta-CD, while two peaks with a plateau were noted for heptakis(2,3,6-tri-O-methyl)-beta-CD and heptakis(2,3-di-O-methyl)-beta-CD indicating a slow equilibrium.	daclatasvir	53-64	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	151-158
34560933-1	2021	In capillary electrophoresis an enantioseparation of daclatasvir (DCV) was observed in case of heptakis(2,6-di-O-methyl)-beta-CD, heptakis(2-O-methyl)-beta-CD and beta-CD, while two peaks with a plateau were noted for heptakis(2,3,6-tri-O-methyl)-beta-CD and heptakis(2,3-di-O-methyl)-beta-CD indicating a slow equilibrium.	daclatasvir	53-64	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	163-170
34560933-1	2021	In capillary electrophoresis an enantioseparation of daclatasvir (DCV) was observed in case of heptakis(2,6-di-O-methyl)-beta-CD, heptakis(2-O-methyl)-beta-CD and beta-CD, while two peaks with a plateau were noted for heptakis(2,3,6-tri-O-methyl)-beta-CD and heptakis(2,3-di-O-methyl)-beta-CD indicating a slow equilibrium.	daclatasvir	53-64	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	247-254
34560933-1	2021	In capillary electrophoresis an enantioseparation of daclatasvir (DCV) was observed in case of heptakis(2,6-di-O-methyl)-beta-CD, heptakis(2-O-methyl)-beta-CD and beta-CD, while two peaks with a plateau were noted for heptakis(2,3,6-tri-O-methyl)-beta-CD and heptakis(2,3-di-O-methyl)-beta-CD indicating a slow equilibrium.	daclatasvir	53-64	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	285-292
34560933-6	2021	Higher order complexes between DCV and heptakis(2,6-di-O-methyl)-beta-CD were corroborated by mass spectrometry.	daclatasvir	31-34	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	65-72
31858513-1	2020	NS5A-P32 deletion (P32del) is a resistance-associated amino acid change that has recently gained popularity in direct-acting antiviral treatment for chronic hepatitis C. Although not yet detected in naive patients, it appears in 5 to 10% of hepatitis C genotype 1b patients who fail to respond to daclatasvir/asunaprevir and sofosbuvir/ledipasvir treatments.	daclatasvir	297-308	inhibitor of growth family member 2	Homo sapiens	5-8
33857308-0	2021	Erratum to: SD1000: High Sustained Viral Response Rate in 1361 Patients With Hepatitis C Genotypes 1, 2, 3, and 4 Using a Low-cost Fixed-dose Combination Tablet of Generic Sofosbuvir and Daclatasvir: A Multicenter Phase III Clinical Trial.	daclatasvir	187-198	hepatitis c genotypes 1, 2, 3, and 4	None	77-113
32804853-1	2021	OBJECTIVES: To evaluate the effect of generic sofosbuvir and daclatasvir (SOF/DCV) treatment on the glycemic state and insulin resistance as well as lipid profiles of those who achieved sustained virological response (SVR) in diabetic chronic hepatitis C virus (CHC) patients.	daclatasvir	61-72	insulin	Homo sapiens	119-126
35379125-2	2022	METHODS: The transport of daclatasvir, as well as the standard rhodamine 123 by P-gp across the rat intestine, was studied in vitro using the non-everted sac method.	daclatasvir	26-37	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	80-84
35379125-6	2022	RESULTS: The inhibitory effect of atorvastatin on Pgp activity and expression was manifested by increased serosal transport of the standard rhodamine 123, as well as daclatasvir.	daclatasvir	166-177	phosphoglycolate phosphatase	Rattus norvegicus	50-53
35379125-11	2022	CONCLUSION: Atorvastatin has a significant effect on P-gp mediated intestinal transport of daclatasvir, however, it did not affect the systemic bioavailability of a single oral dose of daclatasvir.	daclatasvir	91-102	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	53-57
34997607-10	2022	Daclatasvir showed site dependent intestinal absorption in a manner suggesting its affection by P-gp efflux.	daclatasvir	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	96-100
33218024-7	2020	Furthermore, three of the top 30 drugs with strong affinity prediction for the TMPRSS2 are anti-hepatitis C virus (HCV) drugs, including ombitasvir, daclatasvir, and paritaprevir.	daclatasvir	149-160	transmembrane serine protease 2	Homo sapiens	79-86
32982753-14	2020	However, SOF/VEL+RBV achieved a high SVR rate in cirrhotic patients then SOF+DCV+RBV.	daclatasvir	77-80	small integral membrane protein 1 (Vel blood group)	Homo sapiens	9-16
32486887-0	2020	Peripheral Expression of CXCL10 Gene in Chronic Hepatitis C Patients Treated with Sofosbuvir, Daclatasvir, and Ribavirin.	daclatasvir	94-105	C-X-C motif chemokine ligand 10	Homo sapiens	25-31
32486887-6	2020	In this study we analyzed the expression levels of CXCL10 mRNA in the 90 chronic HCV patients using quantitative PCR (qPCR) prior, after, and during therapy with sofosbuvir/ribavirin (SOF+RBV) and sofosbuvir/daclatasvir/ribavirin (SOF+DCV+RBV), and further, the results were analyzed relative to treatment response.	daclatasvir	235-238	C-X-C motif chemokine ligand 10	Homo sapiens	51-57
32486887-10	2020	Comparing the 2 regimens, the reduction in peripheral CXCL10 expression was more pronounced in patients undergoing SOF+DCV+RBV therapy.	daclatasvir	119-122	C-X-C motif chemokine ligand 10	Homo sapiens	54-60
31959479-1	2020	BACKGROUND: Daclatasvir (DCV) is a HCV NS5A inhibitor whose plasma exposure may be influenced by co-administration with inducers or inhibitors of CYP3A4 such as many antiretrovirals.	daclatasvir	12-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	146-152
31863490-8	2020	We have studied the expression levels of one of these antiviral effectors, TRIM22 in response to sofosbuvir (SOF) and daclatasvir (DAC) in combination with RBV, using quantitative PCR in the peripheral blood mononuclear cells (PBMCs) of HCV-infected patients.	daclatasvir	118-129	tripartite motif containing 22	Homo sapiens	75-81
31863490-8	2020	We have studied the expression levels of one of these antiviral effectors, TRIM22 in response to sofosbuvir (SOF) and daclatasvir (DAC) in combination with RBV, using quantitative PCR in the peripheral blood mononuclear cells (PBMCs) of HCV-infected patients.	daclatasvir	131-134	tripartite motif containing 22	Homo sapiens	75-81
31959479-1	2020	BACKGROUND: Daclatasvir (DCV) is a HCV NS5A inhibitor whose plasma exposure may be influenced by co-administration with inducers or inhibitors of CYP3A4 such as many antiretrovirals.	daclatasvir	25-28	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	146-152
31914336-5	2020	Moreover, DCV-TRIO lacks differentiation from its earlier-launched DAA rivals, presents an inconvenient twice-daily dosing schedule and is not recommended in patients with advanced liver and kidney disease.	daclatasvir	10-13	trio Rho guanine nucleotide exchange factor	Homo sapiens	14-18
31846553-7	2020	RESULTS: Twenty of 43 (46.5%) daclatasvir+asunaprevir (DCV+ASV)-treated patients with virologic failure had no RASs at baseline, 3 (15%) acquired P32 deletion RASs.	daclatasvir	30-41	inhibitor of growth family member 2	Homo sapiens	146-149
32012839-5	2020	Compared with "Treat at F3"; "Treat at F0" exhibited an ICER of US$3780.20/QALY and US$15,145.98/QALY under the DCV+ASV regimen and PegIFN-based regimen; respectively.	daclatasvir	112-115	cAMP responsive element modulator	Homo sapiens	56-60
31527804-9	2019	However, the hsa-miR146b-5p expression in CD14+ monocytes of SVR patients treated with DCV and ASV was comparable to that in monocytes of non-SVR patients treated with DCV and ASV.	daclatasvir	87-90	CD14 molecule	Homo sapiens	42-46
31951178-8	2020	RESULTS: SOF and DAC exerted a potent antifibrotic effect evidenced by their activity against hyaluronic acid HA and metalloproteinase MMP-9 significantly (P<=0.001).	daclatasvir	17-20	matrix metallopeptidase 9	Homo sapiens	135-140
31645655-0	2020	Effect of CYP3A5*3 genetic variant on the metabolism of direct-acting antivirals in vitro: a different effect on asunaprevir versus daclatasvir and beclabuvir.	daclatasvir	132-143	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	10-16
31645655-1	2020	Direct-acting antivirals, asunaprevir (ASV), daclatasvir (DCV), and beclabuvir (BCV) are known to be mainly metabolized by CYP3A enzymes; however, the differences in the detailed metabolic activities of CYP3A4 and CYP3A5 on these drugs are not well clarified.	daclatasvir	45-56	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	203-209
31645655-1	2020	Direct-acting antivirals, asunaprevir (ASV), daclatasvir (DCV), and beclabuvir (BCV) are known to be mainly metabolized by CYP3A enzymes; however, the differences in the detailed metabolic activities of CYP3A4 and CYP3A5 on these drugs are not well clarified.	daclatasvir	45-56	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	214-220
31645655-1	2020	Direct-acting antivirals, asunaprevir (ASV), daclatasvir (DCV), and beclabuvir (BCV) are known to be mainly metabolized by CYP3A enzymes; however, the differences in the detailed metabolic activities of CYP3A4 and CYP3A5 on these drugs are not well clarified.	daclatasvir	58-61	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	203-209
31645655-1	2020	Direct-acting antivirals, asunaprevir (ASV), daclatasvir (DCV), and beclabuvir (BCV) are known to be mainly metabolized by CYP3A enzymes; however, the differences in the detailed metabolic activities of CYP3A4 and CYP3A5 on these drugs are not well clarified.	daclatasvir	58-61	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	214-220
31645655-2	2020	The aim of the present study was to elucidate the relative contributions of CYP3A4 and CYP3A5 to the metabolism of ASV, DCV, and BCV, as well as the effect of CYP3A5*3 genetic variant in vitro.	daclatasvir	120-123	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	76-82
31914336-3	2020	Currently, several DAA options are available on the market.Areas covered: This review focuses on the pharmacokinetics, efficacy, tolerability and safety profile of DCV-TRIO, a twice-daily fixed-dose combination of daclatasvir, asunaprevir and beclabuvir approved in Japan for the treatment of genotype 1 HCV infection.Expert opinion: The DCV-TRIO combination achieved good response rates in genotype 1 patients (SVR12 >= 95% in naive subtype 1b), independently from IL28B genotype, cirrhotic status and prior interferon exposure.	daclatasvir	164-167	trio Rho guanine nucleotide exchange factor	Homo sapiens	168-172
31914336-3	2020	Currently, several DAA options are available on the market.Areas covered: This review focuses on the pharmacokinetics, efficacy, tolerability and safety profile of DCV-TRIO, a twice-daily fixed-dose combination of daclatasvir, asunaprevir and beclabuvir approved in Japan for the treatment of genotype 1 HCV infection.Expert opinion: The DCV-TRIO combination achieved good response rates in genotype 1 patients (SVR12 >= 95% in naive subtype 1b), independently from IL28B genotype, cirrhotic status and prior interferon exposure.	daclatasvir	164-167	trio Rho guanine nucleotide exchange factor	Homo sapiens	342-346
31914336-3	2020	Currently, several DAA options are available on the market.Areas covered: This review focuses on the pharmacokinetics, efficacy, tolerability and safety profile of DCV-TRIO, a twice-daily fixed-dose combination of daclatasvir, asunaprevir and beclabuvir approved in Japan for the treatment of genotype 1 HCV infection.Expert opinion: The DCV-TRIO combination achieved good response rates in genotype 1 patients (SVR12 >= 95% in naive subtype 1b), independently from IL28B genotype, cirrhotic status and prior interferon exposure.	daclatasvir	164-167	interferon lambda 3	Homo sapiens	466-471
32367815-10	2020	CONCLUSIONS: Body weight and serum albumin were the major determinants of daclatasvir V/F in this population.	daclatasvir	74-85	albumin	Homo sapiens	35-42
31481446-4	2019	Lopinavir, ritonavir, saquinavir, atazanavir, maraviroc, ledipasvir, and daclatasvir inhibited the efflux of a model ABCB1 substrate, rhodamine 123 (RHD123), in Caco-2 cells and rat-derived PCIS.	daclatasvir	73-84	ATP binding cassette subfamily B member 1	Homo sapiens	117-122
31380801-3	2019	However, DCV[3] and DCV[4] crystallized in the centrosymmetric space group P21/c which excludes their application as nonlinear optical materials in the crystalline state.	daclatasvir	20-23	H3 histone pseudogene 16	Homo sapiens	75-78
30848363-9	2019	CONCLUSIONS: Many patients treated with the DCV/ASV/BCV regimen have a history of a failure to achieve SVR with previous IFN-free DAA therapy.	daclatasvir	44-47	interferon alpha 1	Homo sapiens	121-124
30848363-11	2019	In addition, most patients with a history of failure with IFN-free DAA therapy, particularly the DCV/ASV regimen, showed resistance to this regimen.	daclatasvir	97-100	interferon alpha 1	Homo sapiens	58-61
29094205-0	2018	Association between alanine aminotransferase elevation and UGT1A1*6 polymorphisms in daclatasvir and asunaprevir combination therapy for chronic hepatitis C. BACKGROUND: Liver damage presented as alanine aminotransferase (ALT) elevation and high ALT-caused treatment discontinuation occurs with high frequency in Japanese patients receiving daclatasvir plus asunaprevir (DCV/ASV) therapy for hepatitis C virus (HCV) infection, and its mechanism is unknown.	daclatasvir	85-96	glutamic--pyruvic transaminase	Homo sapiens	20-44
31291311-0	2019	Single nucleotide polymorphisms associated with elevated alanine aminotransferase in patients receiving asunaprevir plus daclatasvir combination therapy for chronic hepatitis C. AIMS: Drug-induced liver damage characterized by serum alanine aminotransferase (ALT) elevation often occurs in direct-acting antiviral (DAA) combination therapy for chronic hepatitis C virus (HCV) infection.	daclatasvir	121-132	glutamic--pyruvic transaminase	Homo sapiens	57-81
31291311-9	2019	CONCLUSIONS: CYP3A4 rs4646437 was found to be significantly and independently associated with ALT elevation in Japanese patients receiving ASV plus DCV therapy.	daclatasvir	148-151	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	13-19
30467710-4	2019	In chronic experiments, we found that nicotine and PACAP both reduced DCV and DC diameters and that this effect was likewise prevented by CST.	daclatasvir	70-73	adenylate cyclase activating polypeptide 1	Rattus norvegicus	51-56
30467710-9	2019	We conclude that CST regulates DCV quanta by acutely inhibiting catecholamine secretion and chronically increasing expression of CgA after nicotinic stimulation and CgB and SgII after PACAPergic stimulation.	daclatasvir	31-34	chromogranin A	Rattus norvegicus	129-132
30906544-0	2019	Changes in serum LDL, PCSK9 and microRNA-122 in patients with chronic HCV infection receiving Daclatasvir/Asunaprevir.	daclatasvir	94-105	proprotein convertase subtilisin/kexin type 9	Homo sapiens	22-27
30906544-10	2019	In summary, treatment of HCV with Daclatasvir/Asunaprevir resulted in elevated LDL, and relative miR122 and PCSK9-A levels in serum appeared to have some association with LDL increase.	daclatasvir	34-45	microRNA 122	Homo sapiens	97-103
30906544-10	2019	In summary, treatment of HCV with Daclatasvir/Asunaprevir resulted in elevated LDL, and relative miR122 and PCSK9-A levels in serum appeared to have some association with LDL increase.	daclatasvir	34-45	proprotein convertase subtilisin/kexin type 9	Homo sapiens	108-113
30266283-0	2019	Real-world effectiveness of daclatasvir plus sofosbuvir and velpatasvir/sofosbuvir in hepatitis C genotype 2 and 3.	daclatasvir	28-39	c genotype 2 and 3	None	96-114
30067145-0	2018	Decreased CD4+CD25+CD127dim/- Regulatory T Cells and T Helper 17 Cell Responsiveness to Toll-Like Receptor 2 in Chronic Hepatitis C Patients with Daclatasvir Plus Asunaprevir Therapy.	daclatasvir	146-157	CD4 molecule	Homo sapiens	10-13
30067145-11	2018	These data suggested that daclatasvir plus asunaprevir therapy resulted in the decreased responsiveness of Tregs/Th17 cells to TLR2 stimulation in chronic hepatitis C patients, which might provide a novel mechanism underlying DAA-induced immunoregulation.	daclatasvir	26-37	toll like receptor 2	Homo sapiens	127-131
29864695-5	2018	The linear ranges were 1-20 mug mL-1 for SOF and 0.6-6 mug mL-1 for DCS with correlation coefficients >=0.9995.	daclatasvir	68-71	L1 cell adhesion molecule	Mus musculus	32-54
29500489-0	2018	Potent viral suppression and improvements in alpha-fetoprotein and measures of fibrosis in Japanese patients receiving a daclatasvir/asunaprevir/beclabuvir fixed-dose combination for the treatment of HCV genotype-1 infection.	daclatasvir	121-132	alpha fetoprotein	Homo sapiens	45-62
29500489-3	2018	METHODS: Treatment-naive or interferon-experienced UNITY-3 patients with HCV GT-1 who received twice-daily DCV-TRIO were assessed for fibrosis [FibroTest; FibroScan; fibrosis-4 index (FIB-4), aspartate-aminotransferase-to-platelet-ratio index] and AFP at baseline and Weeks 4 (FIB-4 only), 12 or 24 post-treatment.	daclatasvir	107-110	trio Rho guanine nucleotide exchange factor	Homo sapiens	111-115
29500489-8	2018	CONCLUSIONS: DCV-TRIO administered for 12 weeks to Japanese patients with primarily GT-1b infection achieved a high SVR12 rate and resulted in improved measures of hepatic fibrosis and serum AFP that may reduce the risk of future liver disease progression and hepatocellular carcinoma, particularly in those with compensated cirrhosis.	daclatasvir	13-16	trio Rho guanine nucleotide exchange factor	Homo sapiens	17-21
29500489-8	2018	CONCLUSIONS: DCV-TRIO administered for 12 weeks to Japanese patients with primarily GT-1b infection achieved a high SVR12 rate and resulted in improved measures of hepatic fibrosis and serum AFP that may reduce the risk of future liver disease progression and hepatocellular carcinoma, particularly in those with compensated cirrhosis.	daclatasvir	13-16	alpha fetoprotein	Homo sapiens	191-194
29353349-8	2018	Daclatasvir has low-to-moderate clearance with the predominant route of elimination via cytochrome P450 3A4-mediated metabolism and P-glycoprotein excretion and intestinal secretion.	daclatasvir	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	88-107
29353349-10	2018	As a result, the dose of daclatasvir should be reduced from 60 to 30 mg once daily when co-administered with strong inhibitors of cytochrome P450 3A4.	daclatasvir	25-36	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	130-149
29353349-12	2018	The dose of daclatasvir should be increased from 60 to 90 mg once daily when co-administered with moderate inducers of cytochrome P450 3A4.	daclatasvir	12-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	119-138
29353349-13	2018	Co-administration of daclatasvir with strong inducers of cytochrome P450 3A4 is contraindicated.	daclatasvir	21-32	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	57-76
29353349-16	2018	In vitro, daclatasvir is a weak-to-moderate inhibitor of transporters including organic cation transporter 1, P-glycoprotein, organic transporting polypeptide 1B1, organic transporting polypeptide 1B3, and breast cancer resistance protein, although in clinical studies, daclatasvir has not altered the pharmacokinetics of concomitantly administered drugs that are substrates of these transporters to an appreciable degree, except for rosuvastatin.	daclatasvir	10-21	solute carrier family 22 member 1	Homo sapiens	80-108
29353349-16	2018	In vitro, daclatasvir is a weak-to-moderate inhibitor of transporters including organic cation transporter 1, P-glycoprotein, organic transporting polypeptide 1B1, organic transporting polypeptide 1B3, and breast cancer resistance protein, although in clinical studies, daclatasvir has not altered the pharmacokinetics of concomitantly administered drugs that are substrates of these transporters to an appreciable degree, except for rosuvastatin.	daclatasvir	10-21	ATP binding cassette subfamily B member 1	Homo sapiens	110-200
29855221-1	2018	Areas covered: This article reviews the pharmacodynamic and pharmacokinetic properties of the DCV-TRIO combination.	daclatasvir	94-97	trio Rho guanine nucleotide exchange factor	Homo sapiens	98-102
29454794-9	2018	Compared with an HCV genotype 1a recombinant, HCV genotype 6a recombinants of strains HK2 and HK6a were equally sensitive to daclatasvir, elbasvir, velpatasvir, pibrentasvir, and sofosbuvir, but less sensitive to ledipasvir, ombitasvir, and dasabuvir.	daclatasvir	125-136	hexokinase 2	Homo sapiens	86-89
30431653-0	2019	Polymorphism in interferon lambda3/interleukin-28B gene and risk to noncirrhotic chronic hepatitis C genotype 3 virus infection and its effect on the response to combined daclatasvir and sofosbuvir therapy.	daclatasvir	171-182	interferon lambda 3	Homo sapiens	16-34
30431653-0	2019	Polymorphism in interferon lambda3/interleukin-28B gene and risk to noncirrhotic chronic hepatitis C genotype 3 virus infection and its effect on the response to combined daclatasvir and sofosbuvir therapy.	daclatasvir	171-182	interferon lambda 3	Homo sapiens	35-50
30431653-2	2019	The present study was, therefore, initiated to investigate the association of polymorphism in interferon lambda3 (IFNL3) also known as interleukin-28B (IL-28B) gene with chronic HCV infection and association of these polymorphic variants with the combination daclatasvir and sofosbuvir HCV therapy response.	daclatasvir	259-270	interferon lambda 3	Homo sapiens	94-112
30431653-2	2019	The present study was, therefore, initiated to investigate the association of polymorphism in interferon lambda3 (IFNL3) also known as interleukin-28B (IL-28B) gene with chronic HCV infection and association of these polymorphic variants with the combination daclatasvir and sofosbuvir HCV therapy response.	daclatasvir	259-270	interferon lambda 3	Homo sapiens	114-119
30431653-2	2019	The present study was, therefore, initiated to investigate the association of polymorphism in interferon lambda3 (IFNL3) also known as interleukin-28B (IL-28B) gene with chronic HCV infection and association of these polymorphic variants with the combination daclatasvir and sofosbuvir HCV therapy response.	daclatasvir	259-270	interferon lambda 3	Homo sapiens	135-150
30431653-2	2019	The present study was, therefore, initiated to investigate the association of polymorphism in interferon lambda3 (IFNL3) also known as interleukin-28B (IL-28B) gene with chronic HCV infection and association of these polymorphic variants with the combination daclatasvir and sofosbuvir HCV therapy response.	daclatasvir	259-270	interferon lambda 3	Homo sapiens	152-158
30253037-0	2018	Association of IL-1beta, IL-1RN, and ESR1 genes polymorphism with risk of infection and response to sofosbuvir plus daclatasvir combination therapy in hepatitis C virus genotype-4 patients.	daclatasvir	116-127	estrogen receptor 1	Homo sapiens	37-41
30344416-6	2018	P32 deletion, an NS5A RAS, has been gradually noticed in patients with DCV/ASV failure.	daclatasvir	71-74	inhibitor of growth family member 2	Homo sapiens	0-3
29094205-0	2018	Association between alanine aminotransferase elevation and UGT1A1*6 polymorphisms in daclatasvir and asunaprevir combination therapy for chronic hepatitis C. BACKGROUND: Liver damage presented as alanine aminotransferase (ALT) elevation and high ALT-caused treatment discontinuation occurs with high frequency in Japanese patients receiving daclatasvir plus asunaprevir (DCV/ASV) therapy for hepatitis C virus (HCV) infection, and its mechanism is unknown.	daclatasvir	85-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
29094205-5	2018	CONCLUSIONS: Through the analysis we suggest that the A allele in UGT1A1 rs4148323 (UGT1A1*6), which is highly prevalent in the Japanese population, should be considered a risk for the development of DCV/ASV therapy-induced ALT elevation.	daclatasvir	200-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
29094205-5	2018	CONCLUSIONS: Through the analysis we suggest that the A allele in UGT1A1 rs4148323 (UGT1A1*6), which is highly prevalent in the Japanese population, should be considered a risk for the development of DCV/ASV therapy-induced ALT elevation.	daclatasvir	200-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
29094205-6	2018	Pretreatment SNP testing of UGT1A1*6 might be beneficial for the prediction of liver damage induced by DCV/ASV or even by DCV/ASV plus beclabuvir.	daclatasvir	103-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
29094205-6	2018	Pretreatment SNP testing of UGT1A1*6 might be beneficial for the prediction of liver damage induced by DCV/ASV or even by DCV/ASV plus beclabuvir.	daclatasvir	122-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
29484572-11	2018	CONCLUSION: Low-dose Sofosbuvir and full-dose Daclatasvir are safe and effective in treating CHC in patients with CKD with eGFR less than 30 mL/min/1.73 m2.	daclatasvir	46-57	CD59 molecule (CD59 blood group)	Homo sapiens	144-149
29790402-7	2018	DCV levels were influenced by CYP24A1 rs2248359T>C polymorphism at 2 weeks and VDR Cdx2 A>G at 1 month of treatment.	daclatasvir	0-3	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	30-37
29790402-7	2018	DCV levels were influenced by CYP24A1 rs2248359T>C polymorphism at 2 weeks and VDR Cdx2 A>G at 1 month of treatment.	daclatasvir	0-3	vitamin D receptor	Homo sapiens	82-85
29790402-7	2018	DCV levels were influenced by CYP24A1 rs2248359T>C polymorphism at 2 weeks and VDR Cdx2 A>G at 1 month of treatment.	daclatasvir	0-3	caudal type homeobox 2	Homo sapiens	86-90
28892235-11	2018	In conclusion, this analysis showed high response rates in HCV genotype 1-infected patients treated with daclatasvir, ASV, and BCV irrespective of RBV use, prior interferon-based therapy, or restriction on non-cirrhotic patients, IL28B genotype, or baseline resistance-associated variants.	daclatasvir	105-116	interferon lambda 3	Homo sapiens	230-235
29327780-8	2018	The pooled SVR rates for GT1 were 89.9% (95% CI 88.6-91.1, I2  = 55.1%) with daclatasvir/asunaprevir (DCV/ASV) and 98.1% (95% CI 97.0-99.0, I2  = 41.0%) with ledipasvir/sofosbuvir +- ribavirin (LDV/SOF +- RBV).	daclatasvir	77-88	beta-1,4-galactosyltransferase 1	Homo sapiens	25-28
29414007-7	2018	Under the optimum conditions, the linear ranges of calibration curves were 0.2-30 and 6-120 ng mL-1 for DCS and LDS, respectively with correlation coefficients >=0.9998.	daclatasvir	104-107	L1 cell adhesion molecule	Mus musculus	95-99
29414007-8	2018	The detection limits were 0.047 and 1.939 ng mL-1 for DCS and LDS, respectively indicating ultrasensitivity of the proposed method.	daclatasvir	54-57	L1 cell adhesion molecule	Mus musculus	45-49
29869645-1	2018	The fixed-dose tablet combination of daclatasvir (30 mg)/asunaprevir (200 mg)/beclabuvir (75 mg), DCV-TRIO, is one of the latest drugs in the pipeline of interferon-free direct-acting antiviral hepatitis C virus (HCV) therapies.	daclatasvir	37-48	trio Rho guanine nucleotide exchange factor	Homo sapiens	102-106
29869645-1	2018	The fixed-dose tablet combination of daclatasvir (30 mg)/asunaprevir (200 mg)/beclabuvir (75 mg), DCV-TRIO, is one of the latest drugs in the pipeline of interferon-free direct-acting antiviral hepatitis C virus (HCV) therapies.	daclatasvir	98-101	trio Rho guanine nucleotide exchange factor	Homo sapiens	102-106
29869645-3	2018	Results from the UNITY 1, 2, 3 and 4 phase III clinical trials showed that DCV-TRIO exhibited high sustained virologic responses at 12 weeks (between 92% and 100% for HCV GT-1 treatment-naive patients).	daclatasvir	75-78	trio Rho guanine nucleotide exchange factor	Homo sapiens	79-83
29869645-5	2018	Further research should focus on more real-life data on DCV-TRIO and on developing a pill regimen that works on other HCV genotypes with high genetic barriers and that is available at a reduced cost.	daclatasvir	56-59	trio Rho guanine nucleotide exchange factor	Homo sapiens	60-64
28815329-1	2018	BACKGROUND: In Japan, daclatasvir (DCV) and asunaprevir (ASV) therapy was the first IFN-free treatment to be approved, and thousands of patients have since been successfully treated, with an SVR rate of around 90%.	daclatasvir	22-33	interferon alpha 1	Homo sapiens	84-87
28815329-1	2018	BACKGROUND: In Japan, daclatasvir (DCV) and asunaprevir (ASV) therapy was the first IFN-free treatment to be approved, and thousands of patients have since been successfully treated, with an SVR rate of around 90%.	daclatasvir	35-38	interferon alpha 1	Homo sapiens	84-87
29327780-8	2018	The pooled SVR rates for GT1 were 89.9% (95% CI 88.6-91.1, I2  = 55.1%) with daclatasvir/asunaprevir (DCV/ASV) and 98.1% (95% CI 97.0-99.0, I2  = 41.0%) with ledipasvir/sofosbuvir +- ribavirin (LDV/SOF +- RBV).	daclatasvir	102-105	beta-1,4-galactosyltransferase 1	Homo sapiens	25-28
28884930-5	2018	Among the 6 patients receiving lead-in injections, viral relapse occurred in 2 patients who had an unfavorable IFN-lambda3-related gene single nucleotide polymorphism allele; both patients had been previously treated with simeprevir, and HCV carrying NS5A-L31V/Y93H mutations had emerged after DCV/ASV.	daclatasvir	294-297	interferon lambda 3	Homo sapiens	111-122
29255971-0	2018	Effects of a Fixed-Dose Co-Formulation of Daclatasvir, Asunaprevir, and Beclabuvir on the Pharmacokinetics of a Cocktail of Cytochrome P450 and Drug Transporter Substrates in Healthy Subjects.	daclatasvir	42-53	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	124-139
28834042-7	2018	RESULTS: In 69 (81.2%) patients who received DCV/ASV and achieved a sustained virologic response at 24 weeks after the end of treatment (SVR24), TC and LDL-C increased significantly from baseline to p24w.	daclatasvir	45-48	component of oligomeric golgi complex 2	Homo sapiens	152-157
29743792-14	2018	Further wider-scale studies are needed to evaluate the actual role of IL18 polymorphisms in treatment response with sofosbuvir/daclatasvir.	daclatasvir	127-138	interleukin 18	Homo sapiens	70-74
29111569-8	2018	In contrast, addition of either mTOR inhibitor to DAC induced a 30% reduction in antiviral activity in GT1b cells (P <= .01 vs DAC alone).	daclatasvir	50-53	mechanistic target of rapamycin kinase	Homo sapiens	32-36
29111569-8	2018	In contrast, addition of either mTOR inhibitor to DAC induced a 30% reduction in antiviral activity in GT1b cells (P <= .01 vs DAC alone).	daclatasvir	130-133	mechanistic target of rapamycin kinase	Homo sapiens	32-36
29091211-0	2017	Influence of ABCB11 and HNF4alpha genes on daclatasvir plasma concentration: preliminary pharmacogenetic data from the Kineti-C study.	daclatasvir	43-54	hepatocyte nuclear factor 4 alpha	Homo sapiens	24-33
28834042-10	2018	At 12w, TC and LDL-C increased to a greater degree in patients receiving SOF/LDV than in those receiving DCV/ASV or SOF/RBV.	daclatasvir	105-108	component of oligomeric golgi complex 2	Homo sapiens	15-20
29111569-6	2018	RESULTS: Addition of either mTOR inhibitor to the DAA daclatasvir (DAC) resulted in a 30% increase in antiviral activity compared to DAC alone for HCV GT2a, GT3a, and GT4a (all P <= .01).	daclatasvir	67-70	mechanistic target of rapamycin kinase	Homo sapiens	28-32
29111569-6	2018	RESULTS: Addition of either mTOR inhibitor to the DAA daclatasvir (DAC) resulted in a 30% increase in antiviral activity compared to DAC alone for HCV GT2a, GT3a, and GT4a (all P <= .01).	daclatasvir	133-136	mechanistic target of rapamycin kinase	Homo sapiens	28-32
28370350-11	2017	CONCLUSIONS: Twelve weeks of DCV-TRIO was well tolerated and provided 100% SVR12 in treatment-naive and treatment-experienced patients with genotype-1 infection, with or without cirrhosis, including those with baseline NS5A-L31 or NS5A-Y93 resistance-associated substitutions.	daclatasvir	29-32	trio Rho guanine nucleotide exchange factor	Homo sapiens	33-37
29091211-3	2017	Objectives: We investigated the association between daclatasvir plasma concentrations at 2 weeks and 1 month of therapy and genetic variants (SNPs) in genes encoding transporters and nuclear factors (ABCB1, ABCB11 and HNF4alpha).	daclatasvir	52-63	ATP binding cassette subfamily B member 1	Homo sapiens	200-205
29091211-3	2017	Objectives: We investigated the association between daclatasvir plasma concentrations at 2 weeks and 1 month of therapy and genetic variants (SNPs) in genes encoding transporters and nuclear factors (ABCB1, ABCB11 and HNF4alpha).	daclatasvir	52-63	ATP binding cassette subfamily B member 11	Homo sapiens	207-213
29091211-3	2017	Objectives: We investigated the association between daclatasvir plasma concentrations at 2 weeks and 1 month of therapy and genetic variants (SNPs) in genes encoding transporters and nuclear factors (ABCB1, ABCB11 and HNF4alpha).	daclatasvir	52-63	hepatocyte nuclear factor 4 alpha	Homo sapiens	218-227
29091211-6	2017	HNF4alpha 975 C > G polymorphism was found to be associated with the daclatasvir plasma concentrations at 2 weeks (P = 0.009) and 1 month of therapy (P = 0.006).	daclatasvir	72-83	hepatocyte nuclear factor 4 alpha	Homo sapiens	0-9
29085787-0	2017	Increase in Albumin by Daclatasvir/asunaprevir Therapy is Correlated with Decrease in Aspartate Transaminase.	daclatasvir	23-34	solute carrier family 17 member 5	Homo sapiens	86-108
29085787-8	2017	CONCLUSION: DCV/ASV therapy resulted in an increase in albumin levels in SVR patients, which was significantly correlated with a decrease in AST levels.	daclatasvir	12-15	solute carrier family 17 member 5	Homo sapiens	141-144
28797106-9	2017	Serum AFP levels decreased to similar levels between PEG-IFN/RBV and DCV/ASV groups following the achievement of viral eradication.	daclatasvir	69-72	alpha fetoprotein	Homo sapiens	6-9
27943563-4	2017	Patients without SVR12 were offered retreatment based on the DAA resistance profile at failure; patients with resistance to <=1 DCV-TRIO component received DCV-TRIO + RBV for 12 weeks.	daclatasvir	131-134	trio Rho guanine nucleotide exchange factor	Homo sapiens	135-139
27943563-9	2017	All 15 patients retreated with DCV-TRIO + RBV for 12 weeks achieved SVR12.	daclatasvir	31-34	trio Rho guanine nucleotide exchange factor	Homo sapiens	35-39
27943563-12	2017	Non-SVR12 was not associated with emergence of NS3 or NS5B RAS and retreatment with DCV-TRIO + RBV for 12 weeks led to SVR in all patients.	daclatasvir	84-87	trio Rho guanine nucleotide exchange factor	Homo sapiens	88-92
28380010-1	2017	The DNA intercalating dye Hoechst 33342 or its close analog DCV are actively removed from cells by the multidrug resistance transporter ABCG2, a protein overexpressed in metastatic cells and somatic stem cells.	daclatasvir	60-63	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	136-141
26733671-7	2017	Successful QUAD therapy as well as successful IFN-free DCV/ASV regimen resulted in an improved functional NK cell response (degranulation and TRAIL expression) to in vitro stimulation with IFNalpha.	daclatasvir	55-58	interferon alpha 1	Homo sapiens	46-49
26733671-7	2017	Successful QUAD therapy as well as successful IFN-free DCV/ASV regimen resulted in an improved functional NK cell response (degranulation and TRAIL expression) to in vitro stimulation with IFNalpha.	daclatasvir	55-58	TNF superfamily member 10	Homo sapiens	142-147
26733671-7	2017	Successful QUAD therapy as well as successful IFN-free DCV/ASV regimen resulted in an improved functional NK cell response (degranulation and TRAIL expression) to in vitro stimulation with IFNalpha.	daclatasvir	55-58	interferon alpha 1	Homo sapiens	189-197
27932311-7	2017	RESULTS: Short exposure of HCV-infected cells to daclatasvir reduced viral assembly and induced clustering of structural proteins with non-structural HCV proteins, including core, E2, NS4B, and NS5A.	daclatasvir	49-60	polyprotein;protein F	Hepatitis C virus genotype 1	184-188
27502287-2	2017	METHODS: In this phase 3 study, DCV-TRIO for 12 weeks and daclatasvir plus asunaprevir (DUAL) for 24 weeks were studied in Japanese patients infected with HCV genotype 1 (99 % genotype 1b).	daclatasvir	32-35	trio Rho guanine nucleotide exchange factor	Homo sapiens	36-40
27502287-3	2017	RESULTS: SVR12 rates >=95 % were achieved in both treatment-naive (N = 152) and interferon-experienced (N = 65) cohorts treated with DCV-TRIO for 12 weeks and were comparable across patient subgroups, including patients aged >=65 years and those with cirrhosis.	daclatasvir	136-139	trio Rho guanine nucleotide exchange factor	Homo sapiens	140-144
27502287-5	2017	In the absence of baseline resistance-associated polymorphisms at positions NS5A-Y93H or -L31, SVR12 rates were 98 % with DCV-TRIO or DUAL.	daclatasvir	122-125	trio Rho guanine nucleotide exchange factor	Homo sapiens	126-130
27502287-6	2017	Among genotype 1b-infected patients with baseline Y93H or L31 polymorphisms, 35/38 (92 %) DCV-TRIO recipients, and 7/16 (44 %) DUAL recipients achieved SVR12.	daclatasvir	90-93	trio Rho guanine nucleotide exchange factor	Homo sapiens	94-98
27502287-7	2017	Adverse events, mostly liver related, led to treatment discontinuation in 10 % of DCV-TRIO recipients.	daclatasvir	82-85	trio Rho guanine nucleotide exchange factor	Homo sapiens	86-90
27502287-8	2017	In this group, SVR12 was achieved by 3/9 patients who discontinued before Week 4 and by 12/12 patients who completed >=4 weeks of DCV-TRIO.	daclatasvir	133-136	trio Rho guanine nucleotide exchange factor	Homo sapiens	137-141
27502287-9	2017	Treatment-related serious adverse events occurred in 4 and 3 % of DCV-TRIO and DUAL recipients, respectively.	daclatasvir	66-69	trio Rho guanine nucleotide exchange factor	Homo sapiens	70-74
27502287-12	2017	CONCLUSION: SVR12 was achieved by 96 % of Japanese patients with HCV genotype 1 infection after 12 weeks of treatment with the DCV-TRIO regimen.	daclatasvir	127-130	trio Rho guanine nucleotide exchange factor	Homo sapiens	131-135
27890790-11	2017	LAY SUMMARY: IFN-free therapy with oral direct-acting antiviral drugs (daclatasvir and asunaprevir) for HCV infection showed similar tolerability and antiviral efficacy in patients aged >=80years as in younger patients (patients aged >=70 and <80years and patients aged <70years), with an SVR rate over 90% and no severe adverse effects.	daclatasvir	71-82	interferon alpha 1	Homo sapiens	13-16
27530469-7	2017	DDI are more likely to occur with 3D regimen, daclatasvir, simeprevir and ledipasvir, as they are all both substrates and inhibitors of P-gp and/or CYP3A4, than with sofosbuvir.	daclatasvir	46-57	ATP binding cassette subfamily B member 1	Homo sapiens	136-140
27530469-7	2017	DDI are more likely to occur with 3D regimen, daclatasvir, simeprevir and ledipasvir, as they are all both substrates and inhibitors of P-gp and/or CYP3A4, than with sofosbuvir.	daclatasvir	46-57	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	148-154
27664109-4	2016	DCV may be the object of a DDI via the induction or inhibition of cytochrome P450 (CYP) 3A4 and/or P-glycoprotein (P-gp) by the concomitant medication, or the precipitant of a DDI via DCV-based induction/inhibition of CYP 3A4 or inhibition of P-gp, organic anion transporting polypeptide 1B1/B3, and/or breast cancer resistance protein.	daclatasvir	0-3	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	66-91
27348464-13	2016	In scenario analysis, including GT1b patients with and without cirrhosis who were Y93H mutation-negative, the ICER of OBV/PTV/r vs DCV/ASV was below the Japanese willingness-to-pay threshold of JPY 5 million/QALY, while the ICER of SOF/LDV vs OBV/PTV/r was above this threshold; thus, OBV/PTV/r was cost-effective.	daclatasvir	131-134	beta-1,4-galactosyltransferase 1	Homo sapiens	32-35
27798211-2	2017	When combined with the CYP3A4 substrate daclatasvir, the daclatasvir dosage should be reduced from 60 to 30 mg once daily.	daclatasvir	57-68	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	23-29
27664109-4	2016	DCV may be the object of a DDI via the induction or inhibition of cytochrome P450 (CYP) 3A4 and/or P-glycoprotein (P-gp) by the concomitant medication, or the precipitant of a DDI via DCV-based induction/inhibition of CYP 3A4 or inhibition of P-gp, organic anion transporting polypeptide 1B1/B3, and/or breast cancer resistance protein.	daclatasvir	0-3	ATP binding cassette subfamily B member 1	Homo sapiens	99-113
27664109-4	2016	DCV may be the object of a DDI via the induction or inhibition of cytochrome P450 (CYP) 3A4 and/or P-glycoprotein (P-gp) by the concomitant medication, or the precipitant of a DDI via DCV-based induction/inhibition of CYP 3A4 or inhibition of P-gp, organic anion transporting polypeptide 1B1/B3, and/or breast cancer resistance protein.	daclatasvir	0-3	ATP binding cassette subfamily B member 1	Homo sapiens	115-119
27664109-4	2016	DCV may be the object of a DDI via the induction or inhibition of cytochrome P450 (CYP) 3A4 and/or P-glycoprotein (P-gp) by the concomitant medication, or the precipitant of a DDI via DCV-based induction/inhibition of CYP 3A4 or inhibition of P-gp, organic anion transporting polypeptide 1B1/B3, and/or breast cancer resistance protein.	daclatasvir	0-3	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	218-225
27664109-4	2016	DCV may be the object of a DDI via the induction or inhibition of cytochrome P450 (CYP) 3A4 and/or P-glycoprotein (P-gp) by the concomitant medication, or the precipitant of a DDI via DCV-based induction/inhibition of CYP 3A4 or inhibition of P-gp, organic anion transporting polypeptide 1B1/B3, and/or breast cancer resistance protein.	daclatasvir	0-3	phosphoglycolate phosphatase	Homo sapiens	243-291
27664109-4	2016	DCV may be the object of a DDI via the induction or inhibition of cytochrome P450 (CYP) 3A4 and/or P-glycoprotein (P-gp) by the concomitant medication, or the precipitant of a DDI via DCV-based induction/inhibition of CYP 3A4 or inhibition of P-gp, organic anion transporting polypeptide 1B1/B3, and/or breast cancer resistance protein.	daclatasvir	0-3	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	303-335
27652142-7	2016	Subgroup analysis showed the rate of RVR and SVR24 in high-dose daclatasvir (60 mg/day) group were slightly higher than the overall results; the rate of RVR in low-dose daclatasvir (10 mg/day) group was also higher than the control group, but its SVR24 rate was similar between the two groups.	daclatasvir	64-75	nuclear receptor subfamily 1 group D member 2	Homo sapiens	37-40
27664109-4	2016	DCV may be the object of a DDI via the induction or inhibition of cytochrome P450 (CYP) 3A4 and/or P-glycoprotein (P-gp) by the concomitant medication, or the precipitant of a DDI via DCV-based induction/inhibition of CYP 3A4 or inhibition of P-gp, organic anion transporting polypeptide 1B1/B3, and/or breast cancer resistance protein.	daclatasvir	184-187	ATP binding cassette subfamily B member 1	Homo sapiens	99-113
27664109-4	2016	DCV may be the object of a DDI via the induction or inhibition of cytochrome P450 (CYP) 3A4 and/or P-glycoprotein (P-gp) by the concomitant medication, or the precipitant of a DDI via DCV-based induction/inhibition of CYP 3A4 or inhibition of P-gp, organic anion transporting polypeptide 1B1/B3, and/or breast cancer resistance protein.	daclatasvir	184-187	ATP binding cassette subfamily B member 1	Homo sapiens	115-119
27652142-7	2016	Subgroup analysis showed the rate of RVR and SVR24 in high-dose daclatasvir (60 mg/day) group were slightly higher than the overall results; the rate of RVR in low-dose daclatasvir (10 mg/day) group was also higher than the control group, but its SVR24 rate was similar between the two groups.	daclatasvir	169-180	nuclear receptor subfamily 1 group D member 2	Homo sapiens	153-156
27492209-8	2016	Daclatasvir and asunaprevir were stopped because this was suspected to be a side-effect of these drugs, but the patient nonetheless went on to develop severe thrombocytopenia (platelet count 17,000/muL), which needed transfusions.	daclatasvir	0-11	tripartite motif containing 37	Homo sapiens	198-201
27484655-7	2016	A similar reduction in EC50 in daclatasvir-resistant mutants was achieved by combining daclatasvir with anti-miR-122.	daclatasvir	31-42	microRNA 122	Homo sapiens	109-116
27388424-12	2016	CONCLUSIONS: Herein, we have reported the outcomes of HCV-associated OLP in patients who received successful treatment with IFN-free DAAs, using the DCV/ASV combination therapy.	daclatasvir	149-152	interferon alpha 1	Homo sapiens	124-127
26574180-10	2016	CONCLUSION: Successful viral eradication by IFN-free daclatasvir and asunaprevir therapy could lead to improved liver function parameters and reduced liver fibrosis markers and AFP levels.	daclatasvir	53-64	interferon alpha 1	Homo sapiens	44-47
26574180-10	2016	CONCLUSION: Successful viral eradication by IFN-free daclatasvir and asunaprevir therapy could lead to improved liver function parameters and reduced liver fibrosis markers and AFP levels.	daclatasvir	53-64	alpha fetoprotein	Homo sapiens	177-180
27029743-4	2016	Cytochrome P450s were the main enzymes involved in the metabolism of daclatasvir.	daclatasvir	69-80	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
26018228-7	2016	CONCLUSION: DCV staining may be used to discriminate subsets of CD34+ cells similarly to other methods which have previously defined different functional properties that can be related to the characterization, resolution, and purification of primitive hematopoietic stem cells in combination with specific useful markers for multicolor flow cytometric measurements.	daclatasvir	12-15	CD34 molecule	Homo sapiens	64-68
26572539-5	2016	Quantification of NE and EPI-storing dense core (DC) vesicles (DCV) revealed decreased DCV numbers in chromaffin cells in Chga-KO mice.	daclatasvir	63-66	chromogranin A	Mus musculus	122-126
26572539-6	2016	For both cell types, the DCV diameter in Chga-KO mice was less (100-200 nm) than in WT mice (200-350 nm).	daclatasvir	25-28	chromogranin A	Mus musculus	41-45
26572539-8	2016	Chga-KO mice showed an ~47 % increase in DCV/DC ratio, implying vesicle swelling due to increased osmotically active free catecholamines.	daclatasvir	41-44	chromogranin A	Mus musculus	0-4
26292191-0	2016	Relationships between serum asunaprevir concentration and alanine aminotransferase elevation during daclatasvir plus asunaprevir for chronic HCV genotype 1b infection.	daclatasvir	100-111	glutamic--pyruvic transaminase	Homo sapiens	58-82
26292191-1	2016	Alanine aminotransferase (ALT) elevations were the most frequent adverse events during all-oral combinations with daclatasvir and asunaprevir for patients with hepatitis C virus (HCV) infection, but the underline mechanisms are unclear.	daclatasvir	114-125	glutamic--pyruvic transaminase	Homo sapiens	0-24
26760453-13	2016	CONCLUSION: IFN- and RBV-free treatment with SOF/DCV was well tolerated and achieved SVR12 in all HIV/HCV with advanced liver disease.	daclatasvir	49-52	interferon alpha 1	Homo sapiens	12-16
27022224-15	2016	Among both daclatasvir and telaprevir treatment groups, across GT1b- or GT1a-infected patients, lower response rates were observed in patients with IL28B non-CC and cirrhosis - factors known to affect response to pegIFN/RBV.	daclatasvir	11-22	interferon lambda 3	Homo sapiens	148-153
26440999-11	2016	CONCLUSION: Cost-effectiveness conclusions are similar for patients treated in the chronic hepatitis C and CC disease stages, with DCV + ASV expected to be cost-saving versus standard of care in Japan for patients with HCV genotype 1b patients who have failed prior therapy or are IFN-ineligible/intolerant.	daclatasvir	131-134	interferon alpha 1	Homo sapiens	281-284
25904097-1	2016	BACKGROUND: Resistance-associated variants (RAVs) reduce the efficacy of interferon (IFN)-free therapy with asunaprevir and daclatasvir for patients infected with hepatitis C virus (HCV) genotype 1b.	daclatasvir	124-135	interferon alpha 1	Homo sapiens	73-90
27750228-1	2016	In Japan, in September 2014, IFN-free asunaprevir (ASV) and daclatasvir (DCV) became available for combination therapy.	daclatasvir	73-76	interferon alpha 1	Homo sapiens	29-32
26313445-2	2015	This Phase III study (COMMAND-4; AI444-042) evaluated the efficacy and safety of daclatasvir (DCV), a pan-genotypic HCV NS5A inhibitor, with pegylated interferon-alpha2a/ribavirin (PEG-IFN/RBV) in treatment-naive patients with HCV GT4 infection.	daclatasvir	81-92	interferon alpha 2	Homo sapiens	151-169
26544203-11	2015	The ICER of DCV/ASV compared to PR was US$ 16,635/QALY at a total treatment price of US$ 77,419; US$11,581 /QALY at a price of US$ 58,065; US$ 6,375/QALY at a price of US$ 38,710; and US$ 1,364 /QALY at a price of US$ 19,355.	daclatasvir	12-15	cAMP responsive element modulator	Homo sapiens	4-8
26744738-8	2015	Daclatasvir and asunaprevir are substrates for cytochrome P450 3A4 enzymatic pathway; thus, there is a substantial potential for drug interactions.	daclatasvir	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	47-66
26711745-9	2015	The retreatment of resistant viruses that emerged using DCV monotherapy with DCV-NS5A-Syn resulted in a multilog drop and rebound in HCV similar to the initial decline and rebound observed with DCV alone on wild-type (WT) virus.	daclatasvir	56-59	synemin	Homo sapiens	86-89
26711745-9	2015	The retreatment of resistant viruses that emerged using DCV monotherapy with DCV-NS5A-Syn resulted in a multilog drop and rebound in HCV similar to the initial decline and rebound observed with DCV alone on wild-type (WT) virus.	daclatasvir	77-80	synemin	Homo sapiens	86-89
26711745-9	2015	The retreatment of resistant viruses that emerged using DCV monotherapy with DCV-NS5A-Syn resulted in a multilog drop and rebound in HCV similar to the initial decline and rebound observed with DCV alone on wild-type (WT) virus.	daclatasvir	77-80	synemin	Homo sapiens	86-89
26711745-10	2015	A triple combination of DCV, NS5A-Syn, and a DAA targeting the NS3 or NS5B protein cleared the cells of viruses that are highly resistant to DCV.	daclatasvir	141-144	KRAS proto-oncogene, GTPase	Homo sapiens	63-66
26711745-11	2015	Our data support the observation that the cooperative interaction of DCV and NS5A-Syn potentiates both the genotype coverage and resistance barrier of DCV, offering an additional DAA option for combination therapy and tools for explorations of NS5A function.	daclatasvir	151-154	synemin	Homo sapiens	82-85
25704315-2	2015	We herein report a case of progressive SCH with acute cellular rejection (ACR) and bacterial infection, which was successfully treated using IFN-free therapy with daclatasvir and asunaprevir.	daclatasvir	163-174	interferon alpha 1	Homo sapiens	141-144
26313445-4	2015	DCV-treated patients with undetectable HCV RNA at weeks 4 and 12 (eRVR) received 24 weeks of DCV plus PEG-IFN/RBV; those without eRVR received an additional 24 weeks of PEG-IFN/RBV.	daclatasvir	0-3	endogenous retrovirus group 3 member 1, envelope	Homo sapiens	66-70
26313445-4	2015	DCV-treated patients with undetectable HCV RNA at weeks 4 and 12 (eRVR) received 24 weeks of DCV plus PEG-IFN/RBV; those without eRVR received an additional 24 weeks of PEG-IFN/RBV.	daclatasvir	0-3	endogenous retrovirus group 3 member 1, envelope	Homo sapiens	129-133
24943406-1	2015	Daclatasvir (DCV) and asunaprevir (ASV) are NS5A and NS3 protease-targeted antivirals respectively, currently under development for the treatment of chronic hepatitis C virus (HCV) infection.	daclatasvir	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	53-56
25080450-6	2015	RESULTS: Overall, eRVR was achieved by 54.4% (80/147) of genotype 1-infected patients receiving daclatasvir 20 mg, 54.1% (79/146) receiving 60 mg versus 13.9% (10/72) receiving placebo.	daclatasvir	96-107	endogenous retrovirus group 3 member 1, envelope	Homo sapiens	18-22
25770426-0	2015	DIP1 plays an antiviral role against DCV infection in Drosophila melanogaster.	daclatasvir	37-40	DISCO Interacting Protein 1	Drosophila melanogaster	0-4
25770426-7	2015	This study demonstrated that dip1 is a novel antiviral gene that restricts DCV replication in vitro and in vivo.	daclatasvir	75-78	DISCO Interacting Protein 1	Drosophila melanogaster	29-33
24943406-1	2015	Daclatasvir (DCV) and asunaprevir (ASV) are NS5A and NS3 protease-targeted antivirals respectively, currently under development for the treatment of chronic hepatitis C virus (HCV) infection.	daclatasvir	13-16	KRAS proto-oncogene, GTPase	Homo sapiens	53-56
24943406-9	2015	In these patients, HCV RNA rebounded with ASV- and DCV- double resistant variants (NS3 D168A/V plus NS5A L31M and Y93H).	daclatasvir	51-54	KRAS proto-oncogene, GTPase	Homo sapiens	83-86
25546252-9	2015	However, DCV impairs late steps in PI4KA activation that requires NS5A expressed in the context of the HCV polyprotein.	daclatasvir	9-12	phosphatidylinositol 4-kinase alpha	Homo sapiens	35-40
25764674-3	2015	In September 2014, the first IFN-free DAAs, daclatasvir (DCV) and asunaprevir (ASV), were launched and the antiviral therapy for IFN intolerant/ineligible patients became to be possible.	daclatasvir	44-55	interferon alpha 1	Homo sapiens	29-32
25764674-3	2015	In September 2014, the first IFN-free DAAs, daclatasvir (DCV) and asunaprevir (ASV), were launched and the antiviral therapy for IFN intolerant/ineligible patients became to be possible.	daclatasvir	44-55	interferon alpha 1	Homo sapiens	129-132
25764674-3	2015	In September 2014, the first IFN-free DAAs, daclatasvir (DCV) and asunaprevir (ASV), were launched and the antiviral therapy for IFN intolerant/ineligible patients became to be possible.	daclatasvir	57-60	interferon alpha 1	Homo sapiens	29-32
25529083-4	2015	A PEG-IFN/RBV-based regimen with simeprevir or daclatasvir is based on response-guided therapy and its efficacy depends on predictors of response to IFN.	daclatasvir	47-58	interferon alpha 1	Homo sapiens	6-9
26549010-0	2015	Daclatasvir for the treatment of chronic hepatitis C. INTRODUCTION: Following more than 20 years of Interferon (IFN)-based treatment for hepatitis C virus (HCV), the understanding of viral life cycle led to the development of new antiviral drugs directly targeting HCV replication steps.	daclatasvir	0-11	interferon alpha 1	Homo sapiens	112-115
26549010-1	2015	Daclatasvir (DCV) is a potent inhibitor of non-structural NS5A HCV protein with pangenotypic activity and low-moderate barrier to resistance suitable for IFN-free combination with other direct acting antivirals (DAAs).	daclatasvir	0-11	interferon alpha 1	Homo sapiens	154-157
26549010-1	2015	Daclatasvir (DCV) is a potent inhibitor of non-structural NS5A HCV protein with pangenotypic activity and low-moderate barrier to resistance suitable for IFN-free combination with other direct acting antivirals (DAAs).	daclatasvir	13-16	interferon alpha 1	Homo sapiens	154-157
26549010-4	2015	EXPERT OPINION: DCV in combination with other DAAs has provided IFN-free regimens with increased efficacy and tolerability.	daclatasvir	16-19	interferon alpha 1	Homo sapiens	64-67
25529083-4	2015	A PEG-IFN/RBV-based regimen with simeprevir or daclatasvir is based on response-guided therapy and its efficacy depends on predictors of response to IFN.	daclatasvir	47-58	interferon alpha 1	Homo sapiens	149-152
25529083-6	2015	In HCV-1a infected patients, the K80Q mutation in NS3 or the presence of NS5A variants at baseline are associated with poor response with simeprevir- or daclatasvir-containing regimens respectively.	daclatasvir	153-164	KRAS proto-oncogene, GTPase	Homo sapiens	50-53
23916491-5	2013	The results showed that Ran was upregulated in S2 cells in response to DCV infection.	daclatasvir	71-74	RAN, member RAS oncogene family	Homo sapiens	24-27
24612030-8	2014	Importantly, it seems that the IL28B status of the patients may influence the presence of Y93H mutations, resulting in different treatment responses to daclatasvir.	daclatasvir	152-163	interferon lambda 3	Homo sapiens	31-36
25059552-2	2014	Daclatasvir combined with peginterferon alpha-2a and ribavirin in Japanese patients infected with genotype 1b HCV achieved sustained virological response (SVR) in 100% of treatment-naive patients, due to high rates of favorable IL28B allele and genotype 1b.	daclatasvir	0-11	interferon lambda 3	Homo sapiens	228-233
25059552-6	2014	IFN-free regimens including daclatasvir and asunaprevir for genotype 1 null responders should be tailored to subtype, and preexisting NS5A-resistant variants should be evaluated carefully before choosing the drugs.	daclatasvir	28-39	interferon alpha 1	Homo sapiens	0-4
24867984-6	2014	The results of our coincubation inhibition assays have shown that all tested DAAs could inhibit OATP1B1 functions and that SMV, ASV, and DCV (to a lesser extent), but not SFV, exhibited long-lasting preincubation inhibitory effects on OATP1B1 functions.	daclatasvir	137-140	solute carrier organic anion transporter family member 1B1	Homo sapiens	235-242
23177287-3	2013	DCV as triple therapy in combination with pegylated interferon and ribavirin resulted in a high rate of early virologic response in treatment-naive patients with genotype 1 infection; as quadruple therapy in combination with asunaprevir (BMS-650032, NS3 protease inhibitor), pegylated interferon, and ribavirin, it resulted in a high rate of sustained virologic response in genotype 1 prior null responders.	daclatasvir	0-3	KRAS proto-oncogene, GTPase	Homo sapiens	250-253
23504694-12	2013	CONCLUSION: The treatment failure of daclatasvir and asunaprevir in HCV GT1a patients was associated with both NS5A and NS3 resistance variants in prior null responders.	daclatasvir	37-48	KRAS proto-oncogene, GTPase	Homo sapiens	120-123
23803447-7	2013	DCV infection activated the JAK/STAT pathway by 1 hour post incubation.	daclatasvir	0-3	hopscotch	Drosophila melanogaster	28-31
23803447-7	2013	DCV infection activated the JAK/STAT pathway by 1 hour post incubation.	daclatasvir	0-3	Signal-transducer and activator of transcription protein at 92E	Drosophila melanogaster	32-36
23803447-11	2013	CONCLUSIONS: In conclusion, the present study demonstrates that DCV infection may activate phagocytosis, JAK/STAT pathway and Imd pathway in the early host-virus interactions.	daclatasvir	64-67	hopscotch	Drosophila melanogaster	105-108
23803447-11	2013	CONCLUSIONS: In conclusion, the present study demonstrates that DCV infection may activate phagocytosis, JAK/STAT pathway and Imd pathway in the early host-virus interactions.	daclatasvir	64-67	Signal-transducer and activator of transcription protein at 92E	Drosophila melanogaster	109-113
23803447-11	2013	CONCLUSIONS: In conclusion, the present study demonstrates that DCV infection may activate phagocytosis, JAK/STAT pathway and Imd pathway in the early host-virus interactions.	daclatasvir	64-67	immune deficiency	Drosophila melanogaster	126-129
8344234-8	1993	Similarly, the faster velocities of DCV (V70, V80, and V90 velocities) were significantly slowed in both the VWF and non-VWF groups.	daclatasvir	36-39	von Willebrand factor	Homo sapiens	109-112
23358451-4	2013	In syd-2 loss of function mutants, the normal polarized localization of INS-22 neuropeptide-containing DCVs in motor neurons is disrupted, and DCVs accumulate in the cell body and dendrites.	daclatasvir	103-107	Liprin-alpha	Caenorhabditis elegans	3-8
23358451-4	2013	In syd-2 loss of function mutants, the normal polarized localization of INS-22 neuropeptide-containing DCVs in motor neurons is disrupted, and DCVs accumulate in the cell body and dendrites.	daclatasvir	103-107	putative insulin-like peptide alpha-type 2	Caenorhabditis elegans	72-78
23358451-4	2013	In syd-2 loss of function mutants, the normal polarized localization of INS-22 neuropeptide-containing DCVs in motor neurons is disrupted, and DCVs accumulate in the cell body and dendrites.	daclatasvir	143-147	Liprin-alpha	Caenorhabditis elegans	3-8
23358451-5	2013	Time-lapse microscopy and kymograph analysis of mobile DCVs revealed that syd-2 mutants exhibit decreased numbers of DCVs moving in both anterograde and retrograde directions, and a corresponding increase in stationary DCVs in both axon commissures and dendrites.	daclatasvir	55-59	Liprin-alpha	Caenorhabditis elegans	74-79
23358451-6	2013	In addition, DCV run lengths and velocities were decreased in both axon commissures and dendrites of syd-2 mutants.	daclatasvir	13-16	Liprin-alpha	Caenorhabditis elegans	101-106
23358451-7	2013	This study shows that SYD-2 promotes bi-directional mobility of DCVs and identifies SYD-2 as a novel regulator of DCV trafficking and polarized distribution.	daclatasvir	64-67	Liprin-alpha	Caenorhabditis elegans	22-27
22706796-2	2012	The aim of this article is to report the first ever use of daclatasvir (DCV; also known as BMS-790052), a potent orally administered nonstructural 5A replication complex inhibitor, in combination with peginterferon alpha (PEG-IFNalpha) and ribavirin in an LT recipient.	daclatasvir	59-70	interferon alpha 1	Homo sapiens	226-234
22706796-2	2012	The aim of this article is to report the first ever use of daclatasvir (DCV; also known as BMS-790052), a potent orally administered nonstructural 5A replication complex inhibitor, in combination with peginterferon alpha (PEG-IFNalpha) and ribavirin in an LT recipient.	daclatasvir	72-75	interferon alpha 1	Homo sapiens	226-234
14764620-3	2004	POAG caused by DCV at MYOC has been termed "myocilin glaucoma".	daclatasvir	15-18	myocilin	Homo sapiens	22-26
14764620-3	2004	POAG caused by DCV at MYOC has been termed "myocilin glaucoma".	daclatasvir	15-18	myocilin	Homo sapiens	44-52
14764620-4	2004	Clinically, DCV at MYOC may manifest as a typical POAG, normal tension glaucoma, or ocular hypertension without glaucoma.	daclatasvir	12-15	myocilin	Homo sapiens	19-23
14764620-7	2004	DCV at MYOC cause POAG in interaction with environmental factors and DCV at other loci.	daclatasvir	0-3	myocilin	Homo sapiens	7-11
14764620-8	2004	Most DCV at MYOC are relatively young, and the Gln368Stop mutation is exclusively European in origin.	daclatasvir	5-8	myocilin	Homo sapiens	12-16
14764620-9	2004	The overall frequency of DCV at MYOC is similar among African, Caucasian and Asian probands with POAG.	daclatasvir	25-28	myocilin	Homo sapiens	32-36
14764620-10	2004	Because of this fact and the higher prevalence of POAG in African descendants compared with Caucasians or Asians, the overall frequency of DCV at MYOC is several-fold higher in the general population of African descendants, which is in part responsible for their higher prevalence of POAG.	daclatasvir	139-142	myocilin	Homo sapiens	146-150
8597299-5	1995	Quantitative analysis revealed that 4-8% of the mossy terminal profiles examined (n = 350) contained CCK-labeled DCVs, which corresponded to 0.03-0.2 labeled DCVs per 100 microns2 of neuropil.	daclatasvir	113-117	cholecystokinin	Rattus norvegicus	101-104
8597299-5	1995	Quantitative analysis revealed that 4-8% of the mossy terminal profiles examined (n = 350) contained CCK-labeled DCVs, which corresponded to 0.03-0.2 labeled DCVs per 100 microns2 of neuropil.	daclatasvir	158-162	cholecystokinin	Rattus norvegicus	101-104
12438120-2	2002	Current evidence indicates that CAPS functions selectively in DCV exocytosis by interacting with DCVs, the plasma membrane, and protein components of the fusion machinery.	daclatasvir	97-101	calcyphosine	Homo sapiens	32-36
8344234-8	1993	Similarly, the faster velocities of DCV (V70, V80, and V90 velocities) were significantly slowed in both the VWF and non-VWF groups.	daclatasvir	36-39	von Willebrand factor	Homo sapiens	121-124
33768560-0	2021	Association between interleukin 28B polymorphism and sustained virological response to sofosbuvir plus daclatasvir in chronic hepatitis C genotype 4 Egyptian patients.	daclatasvir	103-114	interferon lambda 3	Homo sapiens	20-35
1655654-5	1991	The faster DCVs and the sensory median nerve conduction velocity were significantly slowed in the VWF(+) and VWF(-) groups.	daclatasvir	11-15	von Willebrand factor	Homo sapiens	98-101
1655654-5	1991	The faster DCVs and the sensory median nerve conduction velocity were significantly slowed in the VWF(+) and VWF(-) groups.	daclatasvir	11-15	von Willebrand factor	Homo sapiens	109-112
33768560-3	2021	We aimed to evaluate the usefulness of the reference single nucleotide polymorphism (rs12979860) interleukin 28B (CC genotype) for predicting sustained virological response to sofosbuvir plus daclatasvir in Egyptian patients infected with HCV-4.	daclatasvir	192-203	interferon lambda 3	Homo sapiens	97-112
33768560-9	2021	WHAT IS NEW AND CONCLUSION: Our results suggest that IL28B genotype contributes to the prediction of response to sofosbuvir plus daclatasvir.	daclatasvir	129-140	interferon lambda 3	Homo sapiens	53-58
34890854-1	2022	The separation of daclatasvir and its R,R,R,R-enantiomer was studied by capillary electrophoresis using various randomly methylated beta-CDs and the single isomer heptakis(2,6-di-O-methyl)-beta-CD (2,6-DM-beta-CD) as chiral selectors in an acidic background electrolyte.	daclatasvir	18-29	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	189-196
34890854-1	2022	The separation of daclatasvir and its R,R,R,R-enantiomer was studied by capillary electrophoresis using various randomly methylated beta-CDs and the single isomer heptakis(2,6-di-O-methyl)-beta-CD (2,6-DM-beta-CD) as chiral selectors in an acidic background electrolyte.	daclatasvir	18-29	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	205-212
34890854-3	2022	HPLC and NMR analyses confirmed that the presence of a high 2,6-DM-beta-CD content in the CDs enables to achieve the migration order R,R,R,R-enantiomer > daclatasvir.	daclatasvir	154-165	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	67-74