PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33984267-7	2021	This conundrum is resolved by demonstrating that four HCV protease inhibitor drugs, simeprevir, vaniprevir, paritaprevir, and grazoprevir inhibit the SARS CoV-2 papain-like protease (PLpro).	Simeprevir	84-94	ORF1a polyprotein;ORF1ab polyprotein	Severe acute respiratory syndrome coronavirus 2	183-188
34903667-10	2021	Simeprevir potently mislocalized KRAS from the PM, reduced the clonogenic potential of pancreatic cancer cell lines in vitro, and abrogated the growth of KRAS-dependent tumors in vivo with enhanced efficacy when combined with MAPK and PI3K inhibitors.	Simeprevir	0-10	KRAS proto-oncogene, GTPase	Homo sapiens	33-37
34903667-10	2021	Simeprevir potently mislocalized KRAS from the PM, reduced the clonogenic potential of pancreatic cancer cell lines in vitro, and abrogated the growth of KRAS-dependent tumors in vivo with enhanced efficacy when combined with MAPK and PI3K inhibitors.	Simeprevir	0-10	KRAS proto-oncogene, GTPase	Homo sapiens	154-158
34815586-9	2022	The docked structures were examined and resulted in the identification of six highly promising DAAs i.e. beclabuvir, elbasvir, paritaprevir, grazoprevir, simeprevir, and asunapevir exhibiting high theoretical binding affinity to Mpro from SARS-CoV-2 in comparison to other DAAs.	Simeprevir	154-164	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	229-233
35167916-11	2022	The most promising candidates among the currently used drugs were zafirlukast and simeprevir with an average binding affinity of -22 kcal/mol for spike proteins originating from various lineages.	Simeprevir	82-92	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	146-151
28520373-0	2012	Simeprevir Therapy and IFNL3 Genotype Simeprevir is a hepatitis C virus (HCV) protease inhibitor used in combination with other drugs to treat chronic hepatitis genotype 1 or 4 infection (1).	Simeprevir	38-48	interferon lambda 3	Homo sapiens	23-28
32640381-7	2020	Caffeic acid and ferulic acid were found to inhibit SARS-CoV-2 membrane protein while the anti-viral agent"s simeprevir and grazoprevir showed a high binding affinity for nucleocapsid protein.	Simeprevir	109-119	nucleocapsid phosphoprotein	Severe acute respiratory syndrome coronavirus 2	171-183
32873185-10	2022	In order to analyse the stability of the binding interactions, the known cysteine protease inhibitors viz, Simeprevir, calpain inhibitor IV and the cathepsin F inhibitor in complex Mpro were subjected to molecular dynamics simulations at 100 ns.	Simeprevir	107-117	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	181-185
32873185-11	2022	Based on the results Simeprevir was found to be a strong inhibitor of SARS-CoV-2 Mpro.	Simeprevir	21-31	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	81-85
32807895-9	2020	Our data showed that Simeprevir and Lumacaftor bind the receptor-binding domain of the Spike protein with high affinity and prevent ACE2 interaction.	Simeprevir	21-31	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	87-92
32807895-9	2020	Our data showed that Simeprevir and Lumacaftor bind the receptor-binding domain of the Spike protein with high affinity and prevent ACE2 interaction.	Simeprevir	21-31	angiotensin converting enzyme 2	Homo sapiens	132-136
28520373-5	2012	The FDA-approved drug label for simeprevir contains information regarding a genetic variant near the IFNL3 gene (a C to T change; rs12979860), which is a strong predictor of response to peginterferon alfa and ribavirin treatment.	Simeprevir	32-42	interferon lambda 3	Homo sapiens	101-106
28520373-7	2012	However, patients of all IFNL3 genotypes had highest SVR rates when being treated with regimens that included simeprevir.	Simeprevir	110-120	interferon lambda 3	Homo sapiens	25-30
30880098-3	2019	The aim of this study was to determine the prevalence of resistance-associated substitutions (RASs) in HCV NS3 gene in patients infected with genotype 1 before therapy with simeprevir.	Simeprevir	173-183	KRAS proto-oncogene, GTPase	Homo sapiens	107-110
30791790-4	2018	For genotype 1, the highest number of ICER comparison corresponds to sofosbuvir (SOF) triple therapy and SOF-based combinations which reported a cost per QALY systematically ranging from negative to lower than US$100,000 when compared with no treatment or dual therapy or Simeprevir triple therapy.	Simeprevir	272-282	cAMP responsive element modulator	Homo sapiens	38-42
30652318-5	2019	In contrast, atorvastatin, bosentan, etoposide, fexofenadine, fluvastatin, glibenclamide and simeprevir were broadly transported by recombinant monkey OATP1B1, OATP1B3 and OATP2B1.	Simeprevir	93-103	solute carrier organic anion transporter family member 1B1	Homo sapiens	151-158
30652318-5	2019	In contrast, atorvastatin, bosentan, etoposide, fexofenadine, fluvastatin, glibenclamide and simeprevir were broadly transported by recombinant monkey OATP1B1, OATP1B3 and OATP2B1.	Simeprevir	93-103	solute carrier organic anion transporter family member 1B3	Homo sapiens	160-167
30652318-5	2019	In contrast, atorvastatin, bosentan, etoposide, fexofenadine, fluvastatin, glibenclamide and simeprevir were broadly transported by recombinant monkey OATP1B1, OATP1B3 and OATP2B1.	Simeprevir	93-103	solute carrier organic anion transporter family member 2B1	Homo sapiens	172-179
30145562-1	2018	INTRODUCTION AND AIM: Approximately 10%-15% of patients with hepatitis C genotype 1 (HCV GT1) experience virological relapse after all-oral antiviral regimen using simeprevir (SMV) and sofosbuvir (SOF).	Simeprevir	164-174	beta-1,4-galactosyltransferase 1	Homo sapiens	89-92
30070722-12	2018	Conclusions: In treatment-naive subjects without cirrhosis, AL-335 + odalasvir + simeprevir for 6-8 weeks was generally safe and highly efficacious against HCV GT1.	Simeprevir	81-91	beta-1,4-galactosyltransferase 1	Homo sapiens	160-163
29451090-3	2018	To investigate the relationships of new direct-acting antiviral drugs, simeprevir/sofosbuvir, with lipid profile and insulin resistance (IR).	Simeprevir	71-81	insulin	Homo sapiens	117-124
30377854-6	2018	The effect of simeprevir and/or odalasvir might be explained by their capacity to inhibit P-glycoprotein.	Simeprevir	14-24	ATP binding cassette subfamily B member 1	Homo sapiens	90-104
30145562-1	2018	INTRODUCTION AND AIM: Approximately 10%-15% of patients with hepatitis C genotype 1 (HCV GT1) experience virological relapse after all-oral antiviral regimen using simeprevir (SMV) and sofosbuvir (SOF).	Simeprevir	176-179	beta-1,4-galactosyltransferase 1	Homo sapiens	89-92
30145562-13	2018	CONCLUSIONS: Treatment with LDV/SOF with/without RBV for 12-24 weeks was very well tolerated and resulted in high SVR 12 rates (96%) in HCV GT1 relapsers to SMV + SOF treatment.	Simeprevir	157-160	beta-1,4-galactosyltransferase 1	Homo sapiens	140-143
29374597-4	2018	Therefore, we examined the association of GHRL gene polymorphisms (rs26312 and rs27647), and its serum level to virologic responses to combined sofosbuvir and Simeprevir therapy for a course of 12 successive weeks in Egyptian chronic hepatitis C (CHC) patients.	Simeprevir	159-169	ghrelin and obestatin prepropeptide	Homo sapiens	42-46
28506030-0	2017	Simeprevir-Based Triple Therapy with Reduced Doses of Pegylated Interferon alpha-2a Plus Ribavirin for Interferon Ineligible Patients with Genotype 1b Hepatitis C Virus.	Simeprevir	0-10	interferon alpha 2	Homo sapiens	64-83
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.	Simeprevir	222-232	interferon lambda 3	Homo sapiens	111-122
29299156-7	2017	Simeprevir down-regulated PI3Kdelta expression and PI3Kdelta inhibition using RNA interference radiosensitized breast cancer cells.	Simeprevir	0-10	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	26-35
29299156-7	2017	Simeprevir down-regulated PI3Kdelta expression and PI3Kdelta inhibition using RNA interference radiosensitized breast cancer cells.	Simeprevir	0-10	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	51-60
29299156-10	2017	Simeprevir showed significant radiosensitizing effect and immune modulatory function by affecting the CD4(+)/CD8(+) ratio of tumor infiltrating lymphocytes.	Simeprevir	0-10	CD4 molecule	Homo sapiens	102-105
29453451-0	2018	Prevalence and impact of baseline resistance-associated substitutions on the efficacy of ledipasvir/sofosbuvir or simeprevir/sofosbuvir against GT1 HCV infection.	Simeprevir	114-124	beta-1,4-galactosyltransferase 1	Homo sapiens	144-147
28877086-7	2017	Baseline NS3-RASs before retreatment were observed in two patients who failed a sofosbuvir/simeprevir regimen: D168V RAS was detected in a genotype-4 patient, whereas the complex RAS-pattern Q80K, I170V, R155K, D168E was observed in a genotype-1a patient.	Simeprevir	91-101	KRAS proto-oncogene, GTPase	Homo sapiens	9-12
28484975-10	2017	The AUC of simeprevir was also dominated by OATP-mediated uptake because of its small Rdif value.	Simeprevir	11-21	solute carrier organic anion transporter family member 1A2	Homo sapiens	44-48
28506030-1	2017	Background/Aims: The present study aimed to evaluate the safety and efficacy of simeprevir-based triple therapy with reduced doses of pegylated interferon (PEG-IFN) and ribavirin for interferon (IFN) ineligible patients, such as elderly and/or cirrhotic patients, and to elucidate the factors contributing to a sustained virologic response (SVR).	Simeprevir	80-90	interferon alpha 1	Homo sapiens	160-163
28506030-1	2017	Background/Aims: The present study aimed to evaluate the safety and efficacy of simeprevir-based triple therapy with reduced doses of pegylated interferon (PEG-IFN) and ribavirin for interferon (IFN) ineligible patients, such as elderly and/or cirrhotic patients, and to elucidate the factors contributing to a sustained virologic response (SVR).	Simeprevir	80-90	interferon alpha 1	Homo sapiens	169-199
28506030-9	2017	Conclusions: Simeprevir-based triple therapy with reduced doses of PEG-IFN and ribavirin was safe and effective for IFN ineligible patients infected with genotype 1b HCV.	Simeprevir	13-23	interferon alpha 1	Homo sapiens	71-74
28506030-9	2017	Conclusions: Simeprevir-based triple therapy with reduced doses of PEG-IFN and ribavirin was safe and effective for IFN ineligible patients infected with genotype 1b HCV.	Simeprevir	13-23	interferon alpha 1	Homo sapiens	116-119
28228479-9	2017	Our findings are consistent with the detection of R155K/D168A in NS3 from virologic failures treated with simeprevir but not grazoprevir.	Simeprevir	106-116	KRAS proto-oncogene, GTPase	Homo sapiens	65-68
28569206-6	2017	RESULTS: The majority of patients with virologic failure had emerging RAVs to all study drugs at the time of failure: in all 22 patients SMV RAVs emerged at NS3 positions 80, 155, 156 and/or 168, consistent with the known SMV resistance profile.	Simeprevir	137-140	KRAS proto-oncogene, GTPase	Homo sapiens	157-160
27896690-1	2017	The disposition of simeprevir (SMV) in humans is characterised by cytochrome P450 3A4 metabolism and hepatic uptake by organic anion transporting polypeptide 1B1/3 (OATP1B1/3).	Simeprevir	19-29	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	66-85
27896690-1	2017	The disposition of simeprevir (SMV) in humans is characterised by cytochrome P450 3A4 metabolism and hepatic uptake by organic anion transporting polypeptide 1B1/3 (OATP1B1/3).	Simeprevir	19-29	solute carrier organic anion transporter family member 1B1	Homo sapiens	165-172
27896690-1	2017	The disposition of simeprevir (SMV) in humans is characterised by cytochrome P450 3A4 metabolism and hepatic uptake by organic anion transporting polypeptide 1B1/3 (OATP1B1/3).	Simeprevir	31-34	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	66-85
27896690-1	2017	The disposition of simeprevir (SMV) in humans is characterised by cytochrome P450 3A4 metabolism and hepatic uptake by organic anion transporting polypeptide 1B1/3 (OATP1B1/3).	Simeprevir	31-34	solute carrier organic anion transporter family member 1B1	Homo sapiens	165-172
27027531-0	2017	IFNL4 polymorphism effects on outcome of simeprevir, peginterferon, and ribavirin therapy for older patients with genotype 1 chronic hepatitis C. AIM: Older patients with chronic hepatitis C have a lower virological response to interferon (IFN)-based treatments compared to younger patients.	Simeprevir	41-51	interferon lambda 4 (gene/pseudogene)	Homo sapiens	0-5
28270091-2	2017	Here, as a model, we focused on the provenance, in the current Italian HCV subtype 1a epidemic, of the NS3 resistance-associated variant (RAV) Q80K, known to interfere with the action of NS3/4A protease inhibitor simeprevir.	Simeprevir	213-223	KRAS proto-oncogene, GTPase	Homo sapiens	103-106
28270091-2	2017	Here, as a model, we focused on the provenance, in the current Italian HCV subtype 1a epidemic, of the NS3 resistance-associated variant (RAV) Q80K, known to interfere with the action of NS3/4A protease inhibitor simeprevir.	Simeprevir	213-223	KRAS proto-oncogene, GTPase	Homo sapiens	187-190
27027531-0	2017	IFNL4 polymorphism effects on outcome of simeprevir, peginterferon, and ribavirin therapy for older patients with genotype 1 chronic hepatitis C. AIM: Older patients with chronic hepatitis C have a lower virological response to interferon (IFN)-based treatments compared to younger patients.	Simeprevir	41-51	interferon alpha 1	Homo sapiens	0-3
26857426-8	2016	The present case report is based on an idea that a regimen containing IFN with simeprevir could be a therapeutic option particularly for those who are likely to be highly sensitive and tolerable to IFN.	Simeprevir	79-89	interferon alpha 1	Homo sapiens	70-73
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.	Simeprevir	59-69	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.	Simeprevir	59-69	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	148-154
26916827-0	2016	Effects of ITPA polymorphism on decrease of hemoglobin during simeprevir, peg-interferon, and ribavirin combination treatment for chronic hepatitis C. AIM: Polymorphisms in the ITPA gene influence anemia during peg-interferon (PEG-IFN) and ribavirin (RBV) therapy, but their effects during triple therapy with simeprevir, PEG-IFN, and RBV are not sufficiently known.	Simeprevir	62-72	inosine triphosphatase	Homo sapiens	11-15
26916827-0	2016	Effects of ITPA polymorphism on decrease of hemoglobin during simeprevir, peg-interferon, and ribavirin combination treatment for chronic hepatitis C. AIM: Polymorphisms in the ITPA gene influence anemia during peg-interferon (PEG-IFN) and ribavirin (RBV) therapy, but their effects during triple therapy with simeprevir, PEG-IFN, and RBV are not sufficiently known.	Simeprevir	62-72	inosine triphosphatase	Homo sapiens	177-181
26916827-0	2016	Effects of ITPA polymorphism on decrease of hemoglobin during simeprevir, peg-interferon, and ribavirin combination treatment for chronic hepatitis C. AIM: Polymorphisms in the ITPA gene influence anemia during peg-interferon (PEG-IFN) and ribavirin (RBV) therapy, but their effects during triple therapy with simeprevir, PEG-IFN, and RBV are not sufficiently known.	Simeprevir	310-320	inosine triphosphatase	Homo sapiens	177-181
26916827-5	2016	In simeprevir plus PEG-IFN/RBV-treated patients, decreases in hemoglobin levels were faster and greater, and the cumulative proportion of patients with ribavirin dose reduction was significantly greater in ITPA genotype CC patients than in CA/AA patients.	Simeprevir	3-13	inosine triphosphatase	Homo sapiens	206-210
26916827-9	2016	CONCLUSION: ITPA polymorphism influences hemoglobin levels and incidence of RVB dose reduction during simeprevir triple therapy, indicating the importance of monitoring anemia during treatment, particularly for ITPA genotype CC patients.	Simeprevir	102-112	inosine triphosphatase	Homo sapiens	12-16
28261382-17	2017	CONCLUSION: Both TVR- and SMV-based triple therapies can be successfully used to treat patients aged 66 years or older with genotype 1b chronic hepatitis C. Genotyping of the IL28B indicates a potential to achieve SVR in these difficult-to-treat elderly patients.	Simeprevir	26-29	interferon lambda 3	Homo sapiens	175-180
28011961-0	2016	Genotypic analysis of HCV 1a by sequencing of the NS3 proteasic region in simeprevir therapy candidates.	Simeprevir	74-84	KRAS proto-oncogene, GTPase	Homo sapiens	50-53
28011961-2	2016	In fact, SIMEPREVIR (SMV) acts as NS3/4A protease inhibitor (PI); its efficacy is, however, reduced in HCV1a patients characterized by NS3Q80K polymorphism.	Simeprevir	9-19	KRAS proto-oncogene, GTPase	Homo sapiens	34-37
28011961-2	2016	In fact, SIMEPREVIR (SMV) acts as NS3/4A protease inhibitor (PI); its efficacy is, however, reduced in HCV1a patients characterized by NS3Q80K polymorphism.	Simeprevir	21-24	KRAS proto-oncogene, GTPase	Homo sapiens	34-37
28011961-3	2016	The aim of this work was to design a genotypic analysis of NS3 protease in order to characterize viral quasispecies in HCV 1a patients before starting the SMV therapy.	Simeprevir	155-158	KRAS proto-oncogene, GTPase	Homo sapiens	59-62
26857426-8	2016	The present case report is based on an idea that a regimen containing IFN with simeprevir could be a therapeutic option particularly for those who are likely to be highly sensitive and tolerable to IFN.	Simeprevir	79-89	interferon alpha 1	Homo sapiens	198-201
26991414-7	2016	RBV dosage affected SVR dose-dependently in patients with the IL28B non-TT genotype treated with SMV triple therapy.	Simeprevir	97-100	interferon lambda 3	Homo sapiens	62-67
27484655-6	2016	The EC50 values of simeprevir in simeprevir-resistant mutants were significantly decreased by combining simeprevir with anti-miR-122.	Simeprevir	19-29	microRNA 122	Homo sapiens	125-132
27484655-6	2016	The EC50 values of simeprevir in simeprevir-resistant mutants were significantly decreased by combining simeprevir with anti-miR-122.	Simeprevir	33-43	microRNA 122	Homo sapiens	125-132
27484655-6	2016	The EC50 values of simeprevir in simeprevir-resistant mutants were significantly decreased by combining simeprevir with anti-miR-122.	Simeprevir	33-43	microRNA 122	Homo sapiens	125-132
27293923-3	2016	Following successful therapy with sofosbuvir, simeprevir, and ribavirin, her insulin requirements decreased and her glycosylated hemoglobin (HgA1c) normalized despite weight gain.	Simeprevir	46-56	insulin	Homo sapiens	77-84
26223482-9	2016	CONCLUSIONS: Hyperbilirubinemia develops at early time points after simeprevir administration in most cases and is dependent on the ITPA genotype.	Simeprevir	68-78	inosine triphosphatase	Homo sapiens	132-136
26353895-2	2016	Simeprevir is metabolized by the cytochrome P450 (CYP) system, primarily CYP3A, and is a substrate for several drug transporters, including the organic anion transporting polypeptides (OATPs).	Simeprevir	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	73-78
26353895-3	2016	It is susceptible to metabolic drug-drug interactions with drugs that are moderate or strong CYP3A inhibitors (e.g. ritonavir and erythromycin) or CYP3A inducers (e.g. rifampin and efavirenz); coadministration of these drugs may increase or decrease plasma concentrations of simeprevir, respectively, and should be avoided.	Simeprevir	275-285	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	93-98
26353895-4	2016	Clinical studies have shown that simeprevir is a mild inhibitor of CYP1A2 and intestinal CYP3A but does not inhibit hepatic CYP3A.	Simeprevir	33-43	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	67-73
26353895-4	2016	Clinical studies have shown that simeprevir is a mild inhibitor of CYP1A2 and intestinal CYP3A but does not inhibit hepatic CYP3A.	Simeprevir	33-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	89-94
26353895-7	2016	Simeprevir is a substrate and inhibitor of the transporters P-glycoprotein (P-gp), breast cancer resistance protein (BCRP) and OATP1B1/3.	Simeprevir	0-10	ATP binding cassette subfamily B member 1	Homo sapiens	60-74
26353895-7	2016	Simeprevir is a substrate and inhibitor of the transporters P-glycoprotein (P-gp), breast cancer resistance protein (BCRP) and OATP1B1/3.	Simeprevir	0-10	ATP binding cassette subfamily B member 1	Homo sapiens	76-80
26353895-7	2016	Simeprevir is a substrate and inhibitor of the transporters P-glycoprotein (P-gp), breast cancer resistance protein (BCRP) and OATP1B1/3.	Simeprevir	0-10	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	83-115
26353895-7	2016	Simeprevir is a substrate and inhibitor of the transporters P-glycoprotein (P-gp), breast cancer resistance protein (BCRP) and OATP1B1/3.	Simeprevir	0-10	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	117-121
26353895-7	2016	Simeprevir is a substrate and inhibitor of the transporters P-glycoprotein (P-gp), breast cancer resistance protein (BCRP) and OATP1B1/3.	Simeprevir	0-10	solute carrier organic anion transporter family member 1B1	Homo sapiens	127-134
26259716-6	2016	Saturation of gut and liver metabolism by CYP3A4, and saturation of hepatic uptake by OATP1B1/3, seem to account for the observed nonlinear PK of simeprevir.	Simeprevir	146-156	solute carrier organic anion transporter family member 1B1	Homo sapiens	86-93
26392483-0	2015	In Vitro Activity of Simeprevir against Hepatitis C Virus Genotype 1 Clinical Isolates and Its Correlation with NS3 Sequence and Site-Directed Mutants.	Simeprevir	21-31	KRAS proto-oncogene, GTPase	Homo sapiens	112-115
28635836-7	2016	The experience in using cePEG-IFN alpha-2b as a component of the three-component AVT regimen (simeprevir, cePEG IFN alfa-2b, and ribavirin) has been published.	Simeprevir	94-104	interferon alpha 1	Homo sapiens	30-33
26668696-8	2015	Patients in the SMV group were older, had higher serum HCV RNA levels, lower hemoglobin, higher prevalence of unfavorable interleukin-28B (IL28B) genotype (rs8099917), and poorer response to previous PEG-IFN and RBV treatment.	Simeprevir	16-19	interferon lambda 3	Homo sapiens	122-137
26668696-8	2015	Patients in the SMV group were older, had higher serum HCV RNA levels, lower hemoglobin, higher prevalence of unfavorable interleukin-28B (IL28B) genotype (rs8099917), and poorer response to previous PEG-IFN and RBV treatment.	Simeprevir	16-19	interferon lambda 3	Homo sapiens	139-144
26392483-1	2015	Simeprevir (TMC435) is a once-daily, single-pill, oral hepatitis C virus (HCV) NS3 protease inhibitor approved for the treatment of chronic HCV infection.	Simeprevir	0-10	KRAS proto-oncogene, GTPase	Homo sapiens	79-82
26392483-1	2015	Simeprevir (TMC435) is a once-daily, single-pill, oral hepatitis C virus (HCV) NS3 protease inhibitor approved for the treatment of chronic HCV infection.	Simeprevir	12-18	KRAS proto-oncogene, GTPase	Homo sapiens	79-82
26392483-5	2015	Naturally occurring NS3 polymorphisms that reduced simeprevir activity, other than Q80K, were uncommon in the simeprevir studies and generally conferred low-level resistance in vitro.	Simeprevir	51-61	KRAS proto-oncogene, GTPase	Homo sapiens	20-23
26392483-5	2015	Naturally occurring NS3 polymorphisms that reduced simeprevir activity, other than Q80K, were uncommon in the simeprevir studies and generally conferred low-level resistance in vitro.	Simeprevir	110-120	KRAS proto-oncogene, GTPase	Homo sapiens	20-23
26392483-9	2015	In conclusion, pretreatment NS3 isolates were generally fully susceptible (FC, <= 2.0) or conferred low-level resistance to simeprevir in vitro (FC, >2.0 and <50).	Simeprevir	127-137	KRAS proto-oncogene, GTPase	Homo sapiens	28-31
26232533-1	2015	The Q80K polymorphism in the hepatitis C virus (HCV) NS3 enzyme reduces susceptibility to simeprevir and other novel protease inhibitors.	Simeprevir	90-100	KRAS proto-oncogene, GTPase	Homo sapiens	53-56
26095167-9	2015	CONCLUSIONS: Considering the effectiveness and safety, simeprevir-based triple therapy will continue to be a useful treatment option in Japan for treatment-naive or prior relapse patients with a favorable IL28B genotype.	Simeprevir	55-65	interferon lambda 3	Homo sapiens	205-210
26075320-1	2015	Favourable efficacy and safety profiles for simeprevir in combination with pegylated interferon alpha (PEG-IFNalpha) and ribavirin (triple therapy) have been shown in clinical trials.	Simeprevir	44-54	interferon alpha 1	Homo sapiens	107-115
26075320-9	2015	The treatment outcome of simeprevir-based triple therapy for HCV genotype 1b patients with prior telaprevir failure depended on the prior response to PEG-IFNalpha and ribavirin.	Simeprevir	25-35	interferon alpha 1	Homo sapiens	154-162
25959702-10	2015	Finally, we detected both natural and on-treatment genotypic resistance to HCV NS3 PIs, including a substantial prevalence of Q80K substitutions associated with decreased susceptibility to simeprevir, a second generation PI.	Simeprevir	189-199	KRAS proto-oncogene, GTPase	Homo sapiens	79-82
26249823-2	2015	The HCV NS3-Q80K polymorphism is associated with resistance to the recently approved NS3 inhibitor simeprevir (SMV) when combined with PEG-interferon and ribavirin (PEG-IFN/RBV) and alternative therapy should be considered for patients with baseline Q80K.	Simeprevir	99-109	KRAS proto-oncogene, GTPase	Homo sapiens	8-11
26249823-2	2015	The HCV NS3-Q80K polymorphism is associated with resistance to the recently approved NS3 inhibitor simeprevir (SMV) when combined with PEG-interferon and ribavirin (PEG-IFN/RBV) and alternative therapy should be considered for patients with baseline Q80K.	Simeprevir	99-109	KRAS proto-oncogene, GTPase	Homo sapiens	85-88
26249823-2	2015	The HCV NS3-Q80K polymorphism is associated with resistance to the recently approved NS3 inhibitor simeprevir (SMV) when combined with PEG-interferon and ribavirin (PEG-IFN/RBV) and alternative therapy should be considered for patients with baseline Q80K.	Simeprevir	111-114	KRAS proto-oncogene, GTPase	Homo sapiens	8-11
26249823-2	2015	The HCV NS3-Q80K polymorphism is associated with resistance to the recently approved NS3 inhibitor simeprevir (SMV) when combined with PEG-interferon and ribavirin (PEG-IFN/RBV) and alternative therapy should be considered for patients with baseline Q80K.	Simeprevir	111-114	KRAS proto-oncogene, GTPase	Homo sapiens	85-88
26096332-2	2015	Combined simeprevir (SMV) and sofosbuvir (SOF) with or without ribavirin (RBV) results in high sustained virological response (SVR) rates along with minimal adverse events (AEs) in patients with hepatitis C genotype 1 (HCV GT1).	Simeprevir	9-19	beta-1,4-galactosyltransferase 1	Homo sapiens	223-226
26488159-9	2015	Contraindicated associations/potential interactions were expected between cART and respectively sofosbuvir (0.2%/0%), sofosbuvir/ledipasvir (0.2%/67.6%), daclatasvir (0%/49.4%), ombitasvir/boosted paritaprevir (with or without dasabuvir) (34.4%/52.2%) and simeprevir (78.8%/0%).	Simeprevir	256-266	CART prepropeptide	Homo sapiens	74-78
26096332-2	2015	Combined simeprevir (SMV) and sofosbuvir (SOF) with or without ribavirin (RBV) results in high sustained virological response (SVR) rates along with minimal adverse events (AEs) in patients with hepatitis C genotype 1 (HCV GT1).	Simeprevir	21-24	beta-1,4-galactosyltransferase 1	Homo sapiens	223-226
26163159-5	2015	The results of co-incubation inhibition assays showed that SMV and ASV strongly inhibited estrone sulfate (5 nM) uptake by OATP2B1, with half maximal inhibitory concentrations of 0.49 +- 0.12 muM and 0.16 +- 0.06 muM, respectively.	Simeprevir	59-62	solute carrier organic anion transporter family member 2B1	Homo sapiens	123-130
26163159-5	2015	The results of co-incubation inhibition assays showed that SMV and ASV strongly inhibited estrone sulfate (5 nM) uptake by OATP2B1, with half maximal inhibitory concentrations of 0.49 +- 0.12 muM and 0.16 +- 0.06 muM, respectively.	Simeprevir	59-62	latexin	Homo sapiens	192-195
26163159-5	2015	The results of co-incubation inhibition assays showed that SMV and ASV strongly inhibited estrone sulfate (5 nM) uptake by OATP2B1, with half maximal inhibitory concentrations of 0.49 +- 0.12 muM and 0.16 +- 0.06 muM, respectively.	Simeprevir	59-62	latexin	Homo sapiens	213-216
26163159-6	2015	Furthermore, it was found that SMV and ASV imposed long-lasting pre-incubation inhibitory effects on OATP2B1 function that enhanced their co-incubation inhibition potencies.	Simeprevir	31-34	solute carrier organic anion transporter family member 2B1	Homo sapiens	101-108
26213689-11	2015	The prevalence of the natural NS3 variant Q80K, associated with resistance to the macrocyclic protease inhibitor simeprevir, was detected in 51.6% of clade I and 0% of clade II (P < .001); clade I showed a lower genetic barrier for Q80K, whereas no sign of selective pressure at any protease inhibitor resistance-associated codon was detected.	Simeprevir	113-123	KRAS proto-oncogene, GTPase	Homo sapiens	30-33
25778747-5	2015	As compared to PRS/SR, treating with an all oral regimen of Sofosbuvir and Simeprevir (SS) for G1/4 and SR for G2/3, increased QALYs by 1 110 451 and reduced deaths by an additional 164 540 at an incremental cost of $80.1 billion and an ICER of $72 169.	Simeprevir	75-85	palmitoyl-protein thioesterase 2	Homo sapiens	95-106
24961662-1	2015	AIM: The efficacy and safety of simeprevir in combination with peginterferon-alpha-2b and ribavirin (PEG IFN-alpha-2b/RBV) were investigated in patients infected with hepatitis C virus (HCV) genotype 1 who were treatment-naive or had previously received interferon (IFN)-based therapy.	Simeprevir	32-42	interferon alpha 1	Homo sapiens	105-108
24961662-11	2015	CONCLUSION: Simeprevir combined with PEG IFN-alpha-2b/RBV was effective in patients infected with HCV genotype 1, both for initial treatment of naive patients and for retreatment of patients in whom previous IFN-based therapy had failed.	Simeprevir	12-22	interferon alpha 1	Homo sapiens	208-211
25389307-1	2015	Hepatitis C virus (HCV) has a naturally occurring polymorphism, Q80K, in the nonstructural protein 3 (NS3) gene encoding the viral protease, which has been associated with reduced susceptibility to the direct-acting antiviral inhibitor simeprevir.	Simeprevir	236-246	KRAS proto-oncogene, GTPase	Homo sapiens	102-105
26248125-4	2015	The Q80K NS3-protease mutation affects sensibility to simeprevir + peg-interferon/ribavirin combinations.	Simeprevir	54-64	KRAS proto-oncogene, GTPase	Homo sapiens	9-12
26135875-0	2015	Development and Validation of Two Screening Assays for the Hepatitis C Virus NS3 Q80K Polymorphism Associated with Reduced Response to Combination Treatment Regimens Containing Simeprevir.	Simeprevir	177-187	KRAS proto-oncogene, GTPase	Homo sapiens	77-80
26135875-1	2015	Persons with hepatitis C virus (HCV) genotype 1a (GT1a) infections harboring a baseline Q80K polymorphism in nonstructural protein 3 (NS3) have a reduced virologic response to simeprevir in combination with pegylated interferon-alfa and ribavirin.	Simeprevir	176-186	KRAS proto-oncogene, GTPase	Homo sapiens	134-137
25770114-9	2015	Simeprevir is also prone to drug interactions because of cytochrome P450(CYP) 3A4, CYP1A2, P-glycoprotein, and OATP1 involvement and is not recommended for use in combination with several HIV antiretrovirals (ARVs).	Simeprevir	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	57-81
25770114-9	2015	Simeprevir is also prone to drug interactions because of cytochrome P450(CYP) 3A4, CYP1A2, P-glycoprotein, and OATP1 involvement and is not recommended for use in combination with several HIV antiretrovirals (ARVs).	Simeprevir	0-10	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	83-89
25770114-9	2015	Simeprevir is also prone to drug interactions because of cytochrome P450(CYP) 3A4, CYP1A2, P-glycoprotein, and OATP1 involvement and is not recommended for use in combination with several HIV antiretrovirals (ARVs).	Simeprevir	0-10	ATP binding cassette subfamily B member 1	Homo sapiens	91-105
25770114-9	2015	Simeprevir is also prone to drug interactions because of cytochrome P450(CYP) 3A4, CYP1A2, P-glycoprotein, and OATP1 involvement and is not recommended for use in combination with several HIV antiretrovirals (ARVs).	Simeprevir	0-10	ornithine aminotransferase pseudogene 1	Homo sapiens	111-116
25963122-1	2015	Aim: Pegylated-interferon/ribavirin/simeprevir (PEG-IFN/RBV/SMV) combination therapy is widely used for hepatitis C virus (HCV) treatment after liver transplantation (LT).	Simeprevir	36-46	interferon alpha 1	Homo sapiens	52-55
25624738-3	2015	Simeprevir received its first global approval in Japan in September 2013 for the treatment of genotype 1 chronic hepatitis C in combination with PEG-IFN and RBV.	Simeprevir	0-10	interferon alpha 1	Homo sapiens	149-152
25624738-5	2015	We experienced a patient with interstitial pneumonitis that was induced by simeprevir with PEG-IFN and RBV therapy for chronic hepatitis C in the early stages of therapy (8 wk after initiating therapy).	Simeprevir	75-85	interferon alpha 1	Homo sapiens	95-98
25624738-6	2015	This is the first case report of interstitial pneumonitis with simeprevir with PEG-IFN and RBV in the world.	Simeprevir	63-73	interferon alpha 1	Homo sapiens	83-86
24005956-3	2014	RESULTS: Compared with the PR48 group, plasma HCV RNA reductions in the simeprevir groups were rapid and more substantial (Week 4: -5.2, -5.2 and -2.9 log10IU/mL for simeprevir 50 mg combined, 100 mg combined, and PR48 groups, respectively).	Simeprevir	72-82	protein phosphatase 2 regulatory subunit B''beta	Homo sapiens	214-218
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.	Simeprevir	33-43	interferon alpha 1	Homo sapiens	6-9
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.	Simeprevir	33-43	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.	Simeprevir	138-148	KRAS proto-oncogene, GTPase	Homo sapiens	50-53
25397486-1	2014	INTRODUCTION: Simeprevir, a new oral NS3/4A protease inhibitor, was recently approved by the FDA and the EMA for the treatment of patients with chronic HCV genotype 1, 4, 5 and 6 infection l. It has been recommended in the 2014 UK Consensus Guidelines as a possible treatment of previously untreated genotype 1a-infected patients.	Simeprevir	14-24	KRAS proto-oncogene, GTPase	Homo sapiens	37-40
24677184-1	2014	UNLABELLED: Treatment guidance for chronic hepatitis C (CHC) released by the American Association for the Study of Liver Diseases (AASLD) and the Infectious Diseases Society of America (IDSA) offers two options for interferon (IFN)-ineligible/intolerant individuals with genotype 1 infection: sofosbuvir/ribavirin (SOF/RBV) for 24 weeks or sofosbuvir/simeprevir (SOF/SMV) for 12 weeks.	Simeprevir	351-361	interferon alpha 1	Homo sapiens	227-230
25349647-7	2014	IL-28B-CC-genotype patients treated with protease inhibitor-based triple-therapy consisting of Boceprevir, Simeprevir, Telaprevir or Vaniprevir showed odds of 3.38, 14.66, 7.84 and 2.91, respectively.	Simeprevir	107-117	interferon lambda 3	Homo sapiens	0-6
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.	Simeprevir	123-126	solute carrier organic anion transporter family member 1B1	Homo sapiens	235-242
25002352-4	2014	The NS3/4A inhibitor simeprevir and NS5B inhibitor sofosbuvir have recently been licensed and can reduce the length of antiviral treatment, improve response rates, and allow for interferon-free regimens for some HCV genotypes.	Simeprevir	21-31	KRAS proto-oncogene, GTPase	Homo sapiens	4-7
24373080-10	2014	The goal of this review to summarize the results and safety of simeprevir, faldaprevir and sofosbuvir, to advise physicians and to inform patients on the benefits and risks of these second-wave IFN-based regimens for HCV genotype infection.	Simeprevir	63-73	interferon alpha 1	Homo sapiens	194-197
24373081-3	2014	Initially, a wave of IFN-based regimen (sofosbuvir, faldaprevir and simeprevir) will be available for treatment of HCV genotype 1.	Simeprevir	68-78	interferon alpha 1	Homo sapiens	21-24
24005956-4	2014	High rapid virologic response rates (83, 90, and 8 % for simeprevir 50 mg combined, 100 mg combined, and PR48 groups, respectively) led to high sustained virologic response rates (77-92 %, compared with 46 % for PR48).	Simeprevir	57-67	protein phosphatase 2 regulatory subunit B''beta	Homo sapiens	212-216
24005956-6	2014	Relapse rates in simeprevir-treated patients were low (8-17 %, compared with 36 % for the PR48 group).	Simeprevir	17-27	protein phosphatase 2 regulatory subunit B''beta	Homo sapiens	90-94
22127068-0	2012	Molecular modeling study on the resistance mechanism of HCV NS3/4A serine protease mutants R155K, A156V and D168A to TMC435.	Simeprevir	117-123	KRAS proto-oncogene, GTPase	Homo sapiens	60-63
22127068-3	2012	Herein, based on the recently determined structure of NS3/4A-TMC435 complex, atomic-level models of the key residue mutated (R155K, A156V and D168A) NS3/4A-TMC435 complexes were constructed.	Simeprevir	61-67	KRAS proto-oncogene, GTPase	Homo sapiens	54-57
22127068-3	2012	Herein, based on the recently determined structure of NS3/4A-TMC435 complex, atomic-level models of the key residue mutated (R155K, A156V and D168A) NS3/4A-TMC435 complexes were constructed.	Simeprevir	61-67	KRAS proto-oncogene, GTPase	Homo sapiens	149-152
22127068-3	2012	Herein, based on the recently determined structure of NS3/4A-TMC435 complex, atomic-level models of the key residue mutated (R155K, A156V and D168A) NS3/4A-TMC435 complexes were constructed.	Simeprevir	156-162	KRAS proto-oncogene, GTPase	Homo sapiens	54-57
22127068-3	2012	Herein, based on the recently determined structure of NS3/4A-TMC435 complex, atomic-level models of the key residue mutated (R155K, A156V and D168A) NS3/4A-TMC435 complexes were constructed.	Simeprevir	156-162	KRAS proto-oncogene, GTPase	Homo sapiens	149-152
22127068-8	2012	These findings could provide some insights into the resistance mechanism of NS3/4A protease mutants to TMC435 and would be critical for the development of novel inhibitors that are less susceptible to drug resistance.	Simeprevir	103-109	KRAS proto-oncogene, GTPase	Homo sapiens	76-79
18678486-0	2008	Structure-activity relationship study on a novel series of cyclopentane-containing macrocyclic inhibitors of the hepatitis C virus NS3/4A protease leading to the discovery of TMC435350.	Simeprevir	175-184	KRAS proto-oncogene, GTPase	Homo sapiens	131-134