PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33900318-7	2021	Ritonavir, Arbidol, and Saquinavir presented the best performance when binding to a dimer, which was independent of the protonated state of Hie41 (protonated at Nepsilon) and Hid41 (protonated at Ndelta), and these findings suggest that Chloroquine may not effectively inhibit the activity of dimeric Mpro in vivo.	umifenovir	11-18	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	301-305
33900318-6	2021	Ritonavir, Arbidol, and Chloroquine consistently showed an outstanding binding ability to monomeric Mpro under various methods.	umifenovir	11-18	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	100-104
33900318-8	2021	Furthermore, three common hot-spot residues of Met165, Hie41, and Gln189 of monomeric Mpro systems dominated the binding of Ritonavir, Arbidol, and Chloroquine.	umifenovir	135-142	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	86-90
33900318-9	2021	In dimeric Mpro, Gln189, Met165, and Met49 contributed significantly to binding with Ritonavir, Arbidol, and Saquinavir; therefore, Gln189 and Met165 might serve as the focus in the discovery and development of anti-COVID-19 drugs.	umifenovir	96-103	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	11-15
33750821-3	2021	The endosomal acidification inhibitors (8P9R and chloroquine) can synergistically enhance the activity of arbidol, a spike-ACE2 fusion inhibitor, against SARS-CoV-2 and SARS-CoV in cells.	umifenovir	106-113	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	117-122
33750821-3	2021	The endosomal acidification inhibitors (8P9R and chloroquine) can synergistically enhance the activity of arbidol, a spike-ACE2 fusion inhibitor, against SARS-CoV-2 and SARS-CoV in cells.	umifenovir	106-113	angiotensin converting enzyme 2	Homo sapiens	123-127
33750821-4	2021	In vivo studies indicate that 8P9R or the combination of repurposed drugs (umifenovir also known as arbidol, chloroquine and camostat which is a TMPRSS2 inhibitor), simultaneously interfering with the two entry pathways of coronaviruses, can significantly suppress SARS-CoV-2 replication in hamsters and SARS-CoV in mice.	umifenovir	75-85	transmembrane serine protease 2	Homo sapiens	145-152
33750821-4	2021	In vivo studies indicate that 8P9R or the combination of repurposed drugs (umifenovir also known as arbidol, chloroquine and camostat which is a TMPRSS2 inhibitor), simultaneously interfering with the two entry pathways of coronaviruses, can significantly suppress SARS-CoV-2 replication in hamsters and SARS-CoV in mice.	umifenovir	100-107	transmembrane serine protease 2	Homo sapiens	145-152
33688584-3	2021	Comparing to those under trial/temporarily used antivirus drugs (i.e., umifenovir, lopinavir), ceftriaxone, cefotaxime, and cefuroxime show higher binding affinities to the N-terminal domain of N protein (N-NTD), C-terminal domain of N protein (N-CTD), and receptor-binding domain of S protein (S-RBD).	umifenovir	71-81	nucleocapsid phosphoprotein	Severe acute respiratory syndrome coronavirus 2	173-174
33387467-9	2021	Molecular dynamics (MD) simulation-based analyses demonstrate that arbidol binds and stabilizes at the receptor-binding domain (RBD)/ACE2 interface with a high affinity.	umifenovir	67-74	ace2	None	133-137
33387467-11	2021	Analyses of the detailed decomposition of energy components and binding affinities revealed a substantial increase in the affinity between the RBD and ACE2 in the arbidol-bound RBD/ACE2 complex, suggesting that arbidol generates favorable interactions between them.	umifenovir	163-170	ace2	None	151-155
33387467-11	2021	Analyses of the detailed decomposition of energy components and binding affinities revealed a substantial increase in the affinity between the RBD and ACE2 in the arbidol-bound RBD/ACE2 complex, suggesting that arbidol generates favorable interactions between them.	umifenovir	163-170	ace2	None	181-185
33387467-11	2021	Analyses of the detailed decomposition of energy components and binding affinities revealed a substantial increase in the affinity between the RBD and ACE2 in the arbidol-bound RBD/ACE2 complex, suggesting that arbidol generates favorable interactions between them.	umifenovir	211-218	ace2	None	151-155
33387467-11	2021	Analyses of the detailed decomposition of energy components and binding affinities revealed a substantial increase in the affinity between the RBD and ACE2 in the arbidol-bound RBD/ACE2 complex, suggesting that arbidol generates favorable interactions between them.	umifenovir	211-218	ace2	None	181-185
33387467-13	2021	Furthermore, key residues of the RBD and ACE2 that interact with arbidol were identified, opening the door for developing therapeutic strategies and higher-efficacy arbidol derivatives or lead drug candidates.	umifenovir	65-72	ace2	None	41-45
33387467-13	2021	Furthermore, key residues of the RBD and ACE2 that interact with arbidol were identified, opening the door for developing therapeutic strategies and higher-efficacy arbidol derivatives or lead drug candidates.	umifenovir	165-172	ace2	None	41-45
33688584-3	2021	Comparing to those under trial/temporarily used antivirus drugs (i.e., umifenovir, lopinavir), ceftriaxone, cefotaxime, and cefuroxime show higher binding affinities to the N-terminal domain of N protein (N-NTD), C-terminal domain of N protein (N-CTD), and receptor-binding domain of S protein (S-RBD).	umifenovir	71-81	nucleocapsid phosphoprotein	Severe acute respiratory syndrome coronavirus 2	194-195
33688584-3	2021	Comparing to those under trial/temporarily used antivirus drugs (i.e., umifenovir, lopinavir), ceftriaxone, cefotaxime, and cefuroxime show higher binding affinities to the N-terminal domain of N protein (N-NTD), C-terminal domain of N protein (N-CTD), and receptor-binding domain of S protein (S-RBD).	umifenovir	71-81	nucleocapsid phosphoprotein	Severe acute respiratory syndrome coronavirus 2	194-195
33688584-3	2021	Comparing to those under trial/temporarily used antivirus drugs (i.e., umifenovir, lopinavir), ceftriaxone, cefotaxime, and cefuroxime show higher binding affinities to the N-terminal domain of N protein (N-NTD), C-terminal domain of N protein (N-CTD), and receptor-binding domain of S protein (S-RBD).	umifenovir	71-81	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	284-285
33584285-8	2020	Finally, we also found that arbidol reduced serum levels of pro-inflammatory factors such as TNF-alpha and IL-6 induced by fecal dilution.	umifenovir	28-35	tumor necrosis factor	Mus musculus	93-102
33584285-8	2020	Finally, we also found that arbidol reduced serum levels of pro-inflammatory factors such as TNF-alpha and IL-6 induced by fecal dilution.	umifenovir	28-35	interleukin 6	Mus musculus	107-111
32866534-0	2020	Scaffold morphing of arbidol (umifenovir) in search of multi-targeting therapy halting the interaction of SARS-CoV-2 with ACE2 and other proteases involved in COVID-19.	umifenovir	21-28	angiotensin converting enzyme 2	Homo sapiens	122-126
32394467-7	2020	Neuraminidase inhibitors such as oseltamivir, peramivir, and zanamivir are invalid for 2019-nCoV and are not recommended for treatment but protease inhibitors such as lopinavir/ritonavir (LPV/r) inhibit the progression of MERS-CoV disease and can be useful for patients of COVID-19 and, in combination with Arbidol, has a direct antiviral effect on early replication of SARS-CoV.	umifenovir	307-314	neuraminidase 1	Homo sapiens	0-13
33347311-5	2021	The inhibitors of the virus entry to cells and RdRp, such as Arbidol, remdesivir, favipiravir, EIDD-2081, and ribavirin, are in clinical trials, while most of the protease inhibitors are mainly calculated by molecular docking technology, which needs in vivo and in vitro experiments to prove the effect for SARS-CoV-2.	umifenovir	61-68	ORF1a polyprotein;ORF1ab polyprotein	Severe acute respiratory syndrome coronavirus 2	47-51
33720612-6	2020	Umifenovir is antiviral agent, it belongs to fusion inhibitors, interacts with SARS-CoV-2 spike protein.	umifenovir	0-10	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	90-95
32866534-0	2020	Scaffold morphing of arbidol (umifenovir) in search of multi-targeting therapy halting the interaction of SARS-CoV-2 with ACE2 and other proteases involved in COVID-19.	umifenovir	30-40	angiotensin converting enzyme 2	Homo sapiens	122-126
32324898-7	2020	The ADR could be explained by the use of lopinavir/ ritonavir and umifenovir by 63.8% and 18.1%, respectively.	umifenovir	66-76	aldo-keto reductase family 1 member B	Homo sapiens	4-7
32574262-7	2020	Treatment with IFN-alpha2b with or without arbidol significantly reduced the duration of detectable virus in the upper respiratory tract and in parallel reduced duration of elevated blood levels for the inflammatory markers IL-6 and CRP.	umifenovir	43-50	interleukin 6	Homo sapiens	224-228
32474860-2	2020	On the basis of clinical practice and in-vitro studies, we postulated that post-exposure prophylaxis (PEP) using Arbidol is associated with decreased infection among individuals exposed to confirmed cases of COVID-19 infection.	umifenovir	113-120	prolyl endopeptidase	Homo sapiens	102-105
32474860-8	2020	The Cox regression based on the data of the family members and health care workers with Arbidol or not showed that Arbidol PEP was a protective factor against the development of COVID-19 (HR 0.025, 95% CI 0.003-0.209, P=0.0006 for family members and HR 0.056, 95% CI 0.005-0.662, P=0.0221 for health care workers).	umifenovir	88-95	prolyl endopeptidase	Homo sapiens	123-126
32474860-8	2020	The Cox regression based on the data of the family members and health care workers with Arbidol or not showed that Arbidol PEP was a protective factor against the development of COVID-19 (HR 0.025, 95% CI 0.003-0.209, P=0.0006 for family members and HR 0.056, 95% CI 0.005-0.662, P=0.0221 for health care workers).	umifenovir	115-122	prolyl endopeptidase	Homo sapiens	123-126
32574262-7	2020	Treatment with IFN-alpha2b with or without arbidol significantly reduced the duration of detectable virus in the upper respiratory tract and in parallel reduced duration of elevated blood levels for the inflammatory markers IL-6 and CRP.	umifenovir	43-50	C-reactive protein	Homo sapiens	233-236
24400440-0	2013	Arbidol exhibits strong inhibition towards UDP-glucuronosyltransferase (UGT) 1A9 and 2B7.	umifenovir	0-7	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	43-88
29642580-7	2018	Arbidol shows increasing cytotoxicity when tested in various cell lines, in the order: Huh-7 < HBCA < PS < UKF-NB-4 < Vero with CC50 values ranging from 18.69 +- 0.1 to 89.72 +- 0.19 microM.	umifenovir	0-7	MIR7-3 host gene	Homo sapiens	87-92
26843065-6	2016	We have aimed to locate the protonated (Arp) and unprotonated (Arb) forms of arbidol in a model membrane system.	umifenovir	77-84	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	40-43
32955901-7	2020	RESULTS AND CONCLUSION: The similarity between hemagglutinin and spike proteins were reported due to the fact that inhibition properties of Arbidol and its 39 analogues were examined in detail against hemagglutinin esterase and spike glycoproteins.	umifenovir	140-147	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	65-70
32955901-7	2020	RESULTS AND CONCLUSION: The similarity between hemagglutinin and spike proteins were reported due to the fact that inhibition properties of Arbidol and its 39 analogues were examined in detail against hemagglutinin esterase and spike glycoproteins.	umifenovir	140-147	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	228-233
32955901-9	2020	The interaction mechanism was clarified between arbidol and spike proteins.	umifenovir	48-55	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	60-65
32955901-10	2020	Phenylalanine, tyrosine, glycine, lysine, and aspartic acid were found to be the headliner amino acids in the interactions between Arbidol and binding domains of spike glycoproteins in the SARS-CoV2 (Tab.	umifenovir	131-138	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	162-167
29895962-6	2018	Moreover, ARB inhibits pseudoviruses expressing the ZIKV Envelope glycoprotein.	umifenovir	10-13	endogenous retrovirus group K member 20	Homo sapiens	57-78
24769245-5	2014	This could impact on the virus itself, and/or on cellular functions or critical steps in virus-cell interactions, thereby positioning ARB as both a direct-acting antiviral (DAA) and a host-targeting agent (HTA).	umifenovir	134-137	hepatocellular carcinoma associated transcript 5	Homo sapiens	184-210
24400440-9	2013	Given that arbidol exhibits strong inhibition towards UGT1A9 and UGT2B7, clinical monitoring should be given when arbidol was co-administered with drugs mainly undergoing UGT1A9, UGT2B7-mediated metabolism.	umifenovir	11-18	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	171-177
24400440-9	2013	Given that arbidol exhibits strong inhibition towards UGT1A9 and UGT2B7, clinical monitoring should be given when arbidol was co-administered with drugs mainly undergoing UGT1A9, UGT2B7-mediated metabolism.	umifenovir	11-18	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	179-185
24400440-9	2013	Given that arbidol exhibits strong inhibition towards UGT1A9 and UGT2B7, clinical monitoring should be given when arbidol was co-administered with drugs mainly undergoing UGT1A9, UGT2B7-mediated metabolism.	umifenovir	114-121	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	65-71
24400440-1	2013	The aim of the present study was to investigate arbidol"s inhibition towards UDP-glucuronosyltransferase (UGT) 1A9 and 2B7.	umifenovir	48-55	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	77-122
24400440-2	2013	The nonspecific probe substrate 4-methylumbelliferone (4-MU) and recombinant UGT enzymes (UGT1A9, UGT2B7) were firstly used to evaluate the inhibition of arbidol towards UGT1A9 and UGT2B7.	umifenovir	154-161	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	77-80
24400440-2	2013	The nonspecific probe substrate 4-methylumbelliferone (4-MU) and recombinant UGT enzymes (UGT1A9, UGT2B7) were firstly used to evaluate the inhibition of arbidol towards UGT1A9 and UGT2B7.	umifenovir	154-161	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	90-96
24400440-2	2013	The nonspecific probe substrate 4-methylumbelliferone (4-MU) and recombinant UGT enzymes (UGT1A9, UGT2B7) were firstly used to evaluate the inhibition of arbidol towards UGT1A9 and UGT2B7.	umifenovir	154-161	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	98-104
24400440-2	2013	The nonspecific probe substrate 4-methylumbelliferone (4-MU) and recombinant UGT enzymes (UGT1A9, UGT2B7) were firstly used to evaluate the inhibition of arbidol towards UGT1A9 and UGT2B7.	umifenovir	154-161	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	170-176
24400440-2	2013	The nonspecific probe substrate 4-methylumbelliferone (4-MU) and recombinant UGT enzymes (UGT1A9, UGT2B7) were firstly used to evaluate the inhibition of arbidol towards UGT1A9 and UGT2B7.	umifenovir	154-161	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	181-187
24400440-3	2013	Furthermore, specific substrates of UGT1A9 and UGT2B7 propofol and zidovudine (AZT) were used to determine the inhibition of arbidol towards UGT1A9 and UGT2B7.	umifenovir	125-132	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	141-147
24400440-3	2013	Furthermore, specific substrates of UGT1A9 and UGT2B7 propofol and zidovudine (AZT) were used to determine the inhibition of arbidol towards UGT1A9 and UGT2B7.	umifenovir	125-132	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	152-158
24400440-6	2013	Arbidol was demonstrated to exhibit competitive inhibition towards UGT1A9 and UGT2B7 without substate-dependent behaviour.	umifenovir	0-7	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	67-73
24400440-6	2013	Arbidol was demonstrated to exhibit competitive inhibition towards UGT1A9 and UGT2B7 without substate-dependent behaviour.	umifenovir	0-7	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	78-84
24400440-9	2013	Given that arbidol exhibits strong inhibition towards UGT1A9 and UGT2B7, clinical monitoring should be given when arbidol was co-administered with drugs mainly undergoing UGT1A9, UGT2B7-mediated metabolism.	umifenovir	11-18	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	54-60
24400440-9	2013	Given that arbidol exhibits strong inhibition towards UGT1A9 and UGT2B7, clinical monitoring should be given when arbidol was co-administered with drugs mainly undergoing UGT1A9, UGT2B7-mediated metabolism.	umifenovir	11-18	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	65-71
23357765-10	2013	CYP3A4 was the major isoform involved in arbidol metabolism, whereas the other P450s and flavin-containing monooxygenases (FMOs) played minor roles.	umifenovir	41-48	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
23987067-3	2013	5-nitroistnin and arbidol had no effect on basal activity, but synergistically increased in a concentration-dependent manner the spermine NONO-induced activation of this enzyme.	umifenovir	18-25	non-POU domain containing octamer binding	Homo sapiens	138-142
23987067-4	2013	5-Nitroisatin and arbidol, like YC-1, sensitized guanylyl cyclase towards nitric oxide (NO) and produced a leftward shift of the spermine NONO concentration response curve.	umifenovir	18-25	RNA binding motif single stranded interacting protein 1	Homo sapiens	32-36
23987067-4	2013	5-Nitroisatin and arbidol, like YC-1, sensitized guanylyl cyclase towards nitric oxide (NO) and produced a leftward shift of the spermine NONO concentration response curve.	umifenovir	18-25	non-POU domain containing octamer binding	Homo sapiens	138-142
23357765-11	2013	These results indicated possible drug interactions between arbidol and CYP3A4 inhibitors and inducers.	umifenovir	59-66	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	71-77
10222830-3	1999	Arbidole-treated patients with lower baseline immunity showed improvement in immunological parameters (in the counts of CD4 and CD8 lymphocytes, B lymphocytes, in the levels of serum immunoglobulins).	umifenovir	0-8	CD4 molecule	Homo sapiens	120-123
23488780-0	2013	Glucuronidation of the broad-spectrum antiviral drug arbidol by UGT isoforms.	umifenovir	53-60	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	64-67
23488780-1	2013	OBJECTIVES: The aim of this work was to identify the uridine glucuronosyltransferase (UGT) isoforms involved in the metabolism of the broad-spectrum antiviral drug arbidol.	umifenovir	164-171	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	53-84
23488780-1	2013	OBJECTIVES: The aim of this work was to identify the uridine glucuronosyltransferase (UGT) isoforms involved in the metabolism of the broad-spectrum antiviral drug arbidol.	umifenovir	164-171	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	86-89
23488780-3	2013	The glucuronidation activity of commercially recombinant UGT isoforms towards arbidol was screened.	umifenovir	78-85	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	57-60
23488780-4	2013	A combination of kinetic analysis and chemical inhibition study was used to determine the UGT isoforms involved in arbidol"s glucuronidation.	umifenovir	115-122	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	90-93
23488780-7	2013	Assessment of a panel of recombinant UGT isoforms revealed that UGT1A1, UGT1A3 and UGT1A9 could catalyse the glucuronidation of arbidol.	umifenovir	128-135	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	37-40
23488780-7	2013	Assessment of a panel of recombinant UGT isoforms revealed that UGT1A1, UGT1A3 and UGT1A9 could catalyse the glucuronidation of arbidol.	umifenovir	128-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
23488780-7	2013	Assessment of a panel of recombinant UGT isoforms revealed that UGT1A1, UGT1A3 and UGT1A9 could catalyse the glucuronidation of arbidol.	umifenovir	128-135	UDP glucuronosyltransferase family 1 member A3	Homo sapiens	72-78
23488780-7	2013	Assessment of a panel of recombinant UGT isoforms revealed that UGT1A1, UGT1A3 and UGT1A9 could catalyse the glucuronidation of arbidol.	umifenovir	128-135	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	83-89
23488780-8	2013	Kinetic analysis and chemical inhibition study demonstrated that UGT1A9 was the predominant UGT isoform involved in arbidol glucuronidation in HLMs.	umifenovir	116-123	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	65-71
23488780-8	2013	Kinetic analysis and chemical inhibition study demonstrated that UGT1A9 was the predominant UGT isoform involved in arbidol glucuronidation in HLMs.	umifenovir	116-123	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	65-68
23488780-9	2013	CONCLUSIONS: The major contribution of UGT1A9 towards arbidol glucuronidation was demonstrated in this study.	umifenovir	54-61	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	39-45
19575005-10	2009	Treatment with arbidol reduced histopathological changes, decreased viral load and viral antigen levels, and modulated the level of serum TNF-alpha.	umifenovir	15-22	tumor necrosis factor	Homo sapiens	138-147
10222830-3	1999	Arbidole-treated patients with lower baseline immunity showed improvement in immunological parameters (in the counts of CD4 and CD8 lymphocytes, B lymphocytes, in the levels of serum immunoglobulins).	umifenovir	0-8	CD8a molecule	Homo sapiens	128-131
34898207-0	2021	Modeling the Structure-Activity Relationship of Arbidol Derivatives and Other SARS-CoV-2 Fusion Inhibitors Targeting the S2 Segment of the Spike Protein.	umifenovir	48-55	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	139-144
34911144-3	2022	Arbidol can affect the activity of CYP3A4, which is also a key metabolic enzyme of MP by competitive inhibition, and which is easy to aggravate the side effects of MP.	umifenovir	0-7	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	35-41
34130375-3	2021	Thus, in this current computational study we carried out molecular docking experiments to assess the bridging potentials of some commercial drugs such as chloroquine, hydroxychloroquine, lopinavir, ritonavir, nafamostat, camostat, famotidine, umifenovir, nitazoxanide, ivermectin, and fluvoxamine at the interface between human ACE2 and the coronavirus spike glycoprotein complex.	umifenovir	243-253	angiotensin converting enzyme 2	Homo sapiens	328-332
35044216-5	2022	The SA-decreasing effect of ARB was demonstrated to result from its inhibitory effect on sialyltransferases (ST), ST3GAL4 and ST6GAL1 of 16-HBE cells.	umifenovir	28-31	ST3 beta-galactoside alpha-2,3-sialyltransferase 4	Homo sapiens	114-121
35044216-5	2022	The SA-decreasing effect of ARB was demonstrated to result from its inhibitory effect on sialyltransferases (ST), ST3GAL4 and ST6GAL1 of 16-HBE cells.	umifenovir	28-31	ST6 beta-galactoside alpha-2,6-sialyltransferase 1	Homo sapiens	126-133
35044216-10	2022	ARB is the first antiviral drug on the market that was found to possess ST inhibiting function; this will provide crucial evidence for the clinical usages of ARB, such as in combination with neuraminidase (NA) inhibitors to exert optimized antiviral effect etc.	umifenovir	0-3	neuraminidase 1	Homo sapiens	191-204
35044216-10	2022	ARB is the first antiviral drug on the market that was found to possess ST inhibiting function; this will provide crucial evidence for the clinical usages of ARB, such as in combination with neuraminidase (NA) inhibitors to exert optimized antiviral effect etc.	umifenovir	158-161	neuraminidase 1	Homo sapiens	191-204
35097067-9	2022	During the treatment, the lymphocyte count, ESR, IL-6, serum ferritin, LDH, CK-MB, hs-CRP and D-dimer levels all improved gradually, indicating that both Arbidol and methylprednisolone therapy were contributed to improving the condition of COVID-19 patients.	umifenovir	154-161	interleukin 6	Homo sapiens	49-53
35097067-9	2022	During the treatment, the lymphocyte count, ESR, IL-6, serum ferritin, LDH, CK-MB, hs-CRP and D-dimer levels all improved gradually, indicating that both Arbidol and methylprednisolone therapy were contributed to improving the condition of COVID-19 patients.	umifenovir	154-161	C-reactive protein	Homo sapiens	86-89
34126092-10	2021	A good quality cohort showed lower CRP levels in Arbidol (ARB) + IFN group vs. IFN only group.	umifenovir	49-56	C-reactive protein	Homo sapiens	35-38
34126092-10	2021	A good quality cohort showed lower CRP levels in Arbidol (ARB) + IFN group vs. IFN only group.	umifenovir	58-61	C-reactive protein	Homo sapiens	35-38