PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
23143088-1	2012	UNLABELLED: The aim of the present study was to investigate if flumazenil blood-brain barrier transport and binding to the benzodiazepine site on the gamma-aminobutyric acid A (GABA(A)) receptor complex is altered in an experimental model of epilepsy and subsequently to study if changes in P-glycoprotein (P-gp)-mediated efflux of flumazenil at the blood-brain barrier may confound interpretation of (11)C-flumazenil PET in epilepsy.	Flumazenil	63-73	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	291-305
23143088-1	2012	UNLABELLED: The aim of the present study was to investigate if flumazenil blood-brain barrier transport and binding to the benzodiazepine site on the gamma-aminobutyric acid A (GABA(A)) receptor complex is altered in an experimental model of epilepsy and subsequently to study if changes in P-glycoprotein (P-gp)-mediated efflux of flumazenil at the blood-brain barrier may confound interpretation of (11)C-flumazenil PET in epilepsy.	Flumazenil	63-73	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	307-311
23143088-13	2012	P-gp inhibition by tariquidar treatment increased brain concentrations of flumazenil in both groups, but B(max) estimates were not influenced, suggesting that (11)C-flumazenil scanning is not confounded by alterations in P-gp function.	Flumazenil	74-84	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-4
23143088-13	2012	P-gp inhibition by tariquidar treatment increased brain concentrations of flumazenil in both groups, but B(max) estimates were not influenced, suggesting that (11)C-flumazenil scanning is not confounded by alterations in P-gp function.	Flumazenil	165-175	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-4
29243592-7	2012	Hypnotic effects of ECK-E and the EtOAc fraction were fully inhibited by flumazenil, a specific GABAA-BZD receptor antagonist.	Flumazenil	73-83	Eph receptor A2	Mus musculus	20-25
22771461-9	2012	The sleep-promoting effects and changes in c-Fos induced by magnolol were reversed by flumazenil, an antagonist at the benzodiazepine site of the GABA(A) receptor.	Flumazenil	86-96	FBJ osteosarcoma oncogene	Mus musculus	43-48
22720038-8	2012	The effects of nitrazepam in the Usp46 mutant and KO mice were antagonized by flumazenil.	Flumazenil	78-88	ubiquitin specific peptidase 46	Mus musculus	33-38
22455873-0	2012	[11C]Flumazenil brain uptake is influenced by the blood-brain barrier efflux transporter P-glycoprotein.	Flumazenil	5-15	phosphoglycolate phosphatase	Mus musculus	89-103
22455873-3	2012	The purpose of this study was to investigate whether [11C]flumazenil is a P-gp substrate.	Flumazenil	53-68	phosphoglycolate phosphatase	Mus musculus	74-78
22455873-9	2012	RESULTS: Mdr1a/1b dKO mice had approximately 70% higher [11C]flumazenil uptake in the brain than WT mice.	Flumazenil	61-71	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	9-14
22455873-13	2012	CONCLUSIONS: The present study showed that [11C]flumazenil is a P-gp substrate in rodents.	Flumazenil	43-58	phosphoglycolate phosphatase	Mus musculus	64-68
22455873-14	2012	Consequently, altered cerebral [11C]flumazenil uptake, as observed in epilepsy, may not reflect solely GABAA receptor density changes but also changes in P-gp activity.	Flumazenil	36-46	phosphoglycolate phosphatase	Mus musculus	154-158
21945440-5	2011	The hypnotic activity of ILTG was fully inhibited by flumazenil (FLU), a specific gamma-aminobutyric acid type A (GABA(A))-benzodiazepine (BZD) receptor antagonist.	Flumazenil	53-63	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	114-152
21788318-11	2011	JM-1232(-) suppressed the action potential discharge in the CA1 pyramidal neurons during theta-burst stimulation, which was reversed by flumazenil.	Flumazenil	136-146	carbonic anhydrase 1	Mus musculus	60-63
21518336-6	2011	The anti-epileptic effect of magnolol was reversed by the GABA(A)/benzodiazepine receptor antagonist flumazenil.	Flumazenil	101-111	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	58-89
22384252-2	2012	To study GABA signaling in vivo, we recently used a novel positron emission tomography (PET) paradigm measuring the change in binding of the benzodiazepine (BDZ) site radiotracer [(11)C]flumazenil associated with increases in extracellular GABA induced via GABA membrane transporter (GAT1) blockade with tiagabine.	Flumazenil	186-196	solute carrier family 6 member 1	Homo sapiens	284-288
21945440-5	2011	The hypnotic activity of ILTG was fully inhibited by flumazenil (FLU), a specific gamma-aminobutyric acid type A (GABA(A))-benzodiazepine (BZD) receptor antagonist.	Flumazenil	65-68	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	114-152
21321274-10	2011	Compounds that were previously thought to be transported by P-gp in rodents, such as p-MPPF, WAY-100635, and flumazenil, cannot be considered substrates of human P-gp.	Flumazenil	109-119	phosphoglycolate phosphatase	Homo sapiens	162-166
20623764-8	2011	Coinfusion of flumazenil with ALLO into the hippocampal CA3 region, but not into the central amygdala, blocked the antidepressant-like effects of ALLO.	Flumazenil	14-24	carbonic anhydrase 3	Rattus norvegicus	56-59
20147571-8	2011	This was confirmed in human positron emission tomography studies, in which [(11)C]flumazenil uptake following a single dose of 1 mg MRK-409 was comparable to that of placebo, indicating that occupancy of GABA(A) receptor benzodiazepine binding sites by MRK-409 was below the limits of detection (i.e. <10%).	Flumazenil	82-92	mitogen-activated protein kinase kinase kinase 20	Homo sapiens	132-135
20113637-11	2010	The mRNA expression of NPY receptor Y2 increased by 1 or 2 times in the flumazenil, the nifedipine and the topiramate treatment groups when compared with the FZP-tolerance group.	Flumazenil	72-82	neuropeptide Y	Rattus norvegicus	23-26
20670676-10	2010	Neurosteroid withdrawal-induced seizure exacerbation, diazepam insensitivity, and flumazenil efficacy in the kindling model were reversed by inhibition of Egr3.	Flumazenil	82-92	early growth response 3	Mus musculus	155-159
20069292-4	2010	RESULTS: We show that this radiotracer has a high in vitro specificity for PBR/TSPO versus central benzodiazepine receptors, as reflected by the drastic reduction of its binding to target tissue by addition of PK11195 or PBR111, while addition of flumazenil does not affect binding.	Flumazenil	247-257	translocator protein	Homo sapiens	75-78
20069292-4	2010	RESULTS: We show that this radiotracer has a high in vitro specificity for PBR/TSPO versus central benzodiazepine receptors, as reflected by the drastic reduction of its binding to target tissue by addition of PK11195 or PBR111, while addition of flumazenil does not affect binding.	Flumazenil	247-257	translocator protein	Homo sapiens	79-83
20691671-12	2010	Furthermore, the expressions level of BDNF was significantly increased in the baicalein with flumazenil-treated group compared to the baicalein- or flumazenil-treated groups in the hippocampus after an acquisition trial.	Flumazenil	93-103	brain derived neurotrophic factor	Mus musculus	38-42
20691671-12	2010	Furthermore, the expressions level of BDNF was significantly increased in the baicalein with flumazenil-treated group compared to the baicalein- or flumazenil-treated groups in the hippocampus after an acquisition trial.	Flumazenil	148-158	brain derived neurotrophic factor	Mus musculus	38-42
16875845-3	2006	We tested the hypothesis that individuals affected by the GABRG2(R43Q) mutation have reduced binding to the GABA(A) receptor complex using positron emission tomography (PET) and the benzodiazepine receptor ligand [(11)C]-flumazenil.	Flumazenil	221-231	gamma-aminobutyric acid type A receptor subunit gamma2	Homo sapiens	58-64
19285093-3	2009	Increased expression of alpha4-containing GABAR was verified by a relative insensitivity of GABA (EC(20))-gated current to modulation by the benzodiazepine (BZ) lorazepam (0.01-100 microM), and potentiation of current by flumazenil and RO15-4513, characteristic of alpha4betagamma2 pharmacology.	Flumazenil	221-231	immunoglobulin binding protein 1	Homo sapiens	24-30
19299782-7	2009	The inhibitory effects of midazolam on UII-evoked norepinephrine release were significantly attenuated by flumazenil, a benzodiazepine site antagonist.	Flumazenil	106-116	urotensin 2	Rattus norvegicus	39-42
19141300-0	2009	Reduced benzodiazepine tolerance, but increased flumazenil-precipitated withdrawal in AMPA-receptor GluR-A subunit-deficient mice.	Flumazenil	48-58	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	100-106
19141300-7	2009	Withdrawal symptoms, precipitated by flumazenil (20 mg/kg, s.c.) 48 h after discontinuation of the flurazepam treatment, were enhanced in the GluR-A-/- mice.	Flumazenil	37-47	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	142-148
18615011-6	2009	GAT1 blockade resulted in significant increases in mean (+/- SD) [(11)C]flumazenil-binding potential (BP(ND)) over baseline in brain regions representing the major functional domains of the cerebral cortex: association cortex +15.2+/-20.2% (p=0.05), sensory cortex +13.5+/-15.5% (p=0.03) and limbic (medial temporal lobe, MTL) +16.4+/-20.2% (p=0.03).	Flumazenil	72-82	solute carrier family 6 member 1	Homo sapiens	0-4
18499303-13	2008	treatment with flumazenil (1mg/kg) blocked the anxiolytic-like effects of N/OFQ (10pmol; i.c.v.	Flumazenil	15-25	prepronociceptin	Mus musculus	74-79
18346513-3	2008	RESULTS: Relative to the control subjects, the [(11)C]flumazenil binding potentials (BPs) were significantly higher in the cerebral cortex and cerebellum in the 5 patients with the deletion and in the 1 patient with a UBE3A mutation, and were less frequently or barely increased in adult patients with the deletion and in the patient with IDs.	Flumazenil	54-64	ubiquitin protein ligase E3A	Homo sapiens	218-223
17570441-8	2007	In addition, the anxiolytic-like properties of sinapic acid examined in the EPM test were blocked by flumazenil or bicuculline, which are GABA(A) antagonists.	Flumazenil	101-111	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	138-145
16844276-13	2006	COX-2 inhibitors also antagonized the effect of flumazenil (4 mg/kg)- against PTZ-induced convulsions further confirming the GABAergic mechanism.	Flumazenil	48-58	cytochrome c oxidase II, mitochondrial	Mus musculus	0-5
19704033-4	2009	MRK-016 gave good receptor occupancy after oral dosing in rats, with the dose required to produce 50% occupancy being 0.39 mg/kg and a corresponding rat plasma EC(50) value of 15 ng/ml that was similar to the rhesus monkey plasma EC(50) value of 21 ng/ml obtained using [(11)C]flumazenil positron emission tomography.	Flumazenil	277-287	mitogen-activated protein kinase kinase kinase 20	Homo sapiens	0-3
19203567-4	2009	flumazenil on midazolam apparent oral clearance (a surrogate marker of CYP3A activity).	Flumazenil	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	71-76
19203567-18	2009	flumazenil can be used in conjunction with oral midazolam for CYP3A phenotyping.	Flumazenil	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	62-67
17301177-6	2007	The surface numbers of diazepam binding sites (alpha/gamma2 subunits) assessed by [3H]flumazenil binding were reduced in the PRIP-DKO mice as compared with those of wild-type mice, whereas the cell surface GABA binding sites (alpha/beta subunits, assessed by [3H]muscimol binding) were increased in PRIP-DKO mice.	Flumazenil	86-96	phospholipase C-like 1	Mus musculus	125-129
16168444-8	2006	Interestingly, benzodiazepine receptor antagonist flumazenil (5 ng/rat, icv), augmented the orexin-A (30 nM/rat, icv) induced hyperphagia; the effect may be attributed to the intrinsic activity of the agent.	Flumazenil	50-60	hypocretin neuropeptide precursor	Rattus norvegicus	92-100
16878489-1	2006	It is established that bicuculline, picrotoxin, and flumazenil (agents blocking different sites of GABA receptor) decrease the anxiolytic effect of piracetam as manifested in the conflict situation test.	Flumazenil	52-62	GABA type A receptor-associated protein	Homo sapiens	99-112
14602800-9	2003	Conversely, the CBR agonist clonazepam and the CBR antagonist flumazenil did not affect testosterone secretion.	Flumazenil	62-72	cannabinoid receptor 1	Homo sapiens	47-50
15582681-13	2004	The inhibition of U50 tolerance by melatonin was reversed by the chronic treatment with flumazenil (0.1 mg/kg), a benzodiazepine receptor antagonist and picrotoxin (1 mg/kg), a GABAA-gated chloride channel blocker.	Flumazenil	88-98	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	177-182
14749435-6	2004	At all of the ages, selective stimulation of PBR by diazepam in the presence of flumazenil prolonged GABA(A) mIPSCs in a PK11195- and finasteride-sensitive manner.	Flumazenil	80-90	translocator protein	Rattus norvegicus	45-48
11132744-5	2000	RESULTS: Total resistive work spent on the upstream segment of the nasal route per minute (Wn) (J x min(-1)) was greater during midazolam sedation (3.6 +/- 2.9) than while awake (1.6 +/- 0.9) and after flumazenil antagonism (1.7 +/- 0.6), respectively (mean +/- SD) (P < 0.05).	Flumazenil	202-212	CD59 molecule (CD59 blood group)	Homo sapiens	100-107
11602679-7	2001	Activation of central benzodiazepine receptors preceded the IL1beta step because flumazenil inhibited Dyn but not IL1beta antianalgesia.	Flumazenil	81-91	interleukin 1 beta	Mus musculus	60-67
11602679-7	2001	Activation of central benzodiazepine receptors preceded the IL1beta step because flumazenil inhibited Dyn but not IL1beta antianalgesia.	Flumazenil	81-91	prodynorphin	Mus musculus	102-105
11669460-6	2001	TJ-24-induced SI behavior was significantly blocked by the GABA(A)/BZP receptor inverse agonist Ro 15-4513 and the GABA(A)/BZP receptor antagonist flumazenil.	Flumazenil	147-157	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	115-135
12621596-6	2003	However, TRH produced equal or greater symptom and physiological responses compared with flumazenil, suggesting that flumazenil may act as a panicogen in PD via a GABAergic mechanism rather than via a cognitively mediated response to somatic symptoms.	Flumazenil	117-127	thyrotropin releasing hormone	Homo sapiens	9-12
11826609-0	2002	Flumazenil responsive ornithine transcarbamylase deficiency encephalopathy: clinical and radiographic features.	Flumazenil	0-10	ornithine transcarbamylase	Homo sapiens	22-48
11704264-6	2001	of flumazenil, a benzodiazepine receptor antagonist, 20 min before the injection of DBI (i.c.v.)	Flumazenil	3-13	diazepam binding inhibitor	Mus musculus	84-87
10805336-2	2000	We found an inverse relationship between [11C]flumazenil and [11C]raclopride binding in the putamen of symptomatic patients, and interpret this result as GABA receptor upregulation.	Flumazenil	46-56	GABA type A receptor-associated protein	Homo sapiens	154-167
11164073-6	2000	Significant changes in arousal, posture and oro-nasal activity were induced by CRH, whereas FLU alone had no effect but appeared to reduce some responses to CRH.	Flumazenil	92-95	corticotropin releasing hormone	Sus scrofa	157-160
11009473-8	2000	Protection and increased ROS signals with flumazenil (10 microM) were abolished with the thiol reductant N-(2-mercaptopropionyl)-glycine (2-MPG, 800 microM), an antioxidant (cell death: 2-MPG + flumazenil, 55 +/- 12%, n = 6; ROS signals: 2-MPG + flumazenil, 0.11 +/- 0.19, n = 6).	Flumazenil	42-52	N-methylpurine DNA glycosylase	Gallus gallus	140-143
11009473-8	2000	Protection and increased ROS signals with flumazenil (10 microM) were abolished with the thiol reductant N-(2-mercaptopropionyl)-glycine (2-MPG, 800 microM), an antioxidant (cell death: 2-MPG + flumazenil, 55 +/- 12%, n = 6; ROS signals: 2-MPG + flumazenil, 0.11 +/- 0.19, n = 6).	Flumazenil	42-52	N-methylpurine DNA glycosylase	Gallus gallus	188-191
11009473-8	2000	Protection and increased ROS signals with flumazenil (10 microM) were abolished with the thiol reductant N-(2-mercaptopropionyl)-glycine (2-MPG, 800 microM), an antioxidant (cell death: 2-MPG + flumazenil, 55 +/- 12%, n = 6; ROS signals: 2-MPG + flumazenil, 0.11 +/- 0.19, n = 6).	Flumazenil	42-52	N-methylpurine DNA glycosylase	Gallus gallus	188-191
11009473-8	2000	Protection and increased ROS signals with flumazenil (10 microM) were abolished with the thiol reductant N-(2-mercaptopropionyl)-glycine (2-MPG, 800 microM), an antioxidant (cell death: 2-MPG + flumazenil, 55 +/- 12%, n = 6; ROS signals: 2-MPG + flumazenil, 0.11 +/- 0.19, n = 6).	Flumazenil	194-204	N-methylpurine DNA glycosylase	Gallus gallus	140-143
11009473-8	2000	Protection and increased ROS signals with flumazenil (10 microM) were abolished with the thiol reductant N-(2-mercaptopropionyl)-glycine (2-MPG, 800 microM), an antioxidant (cell death: 2-MPG + flumazenil, 55 +/- 12%, n = 6; ROS signals: 2-MPG + flumazenil, 0.11 +/- 0.19, n = 6).	Flumazenil	194-204	N-methylpurine DNA glycosylase	Gallus gallus	140-143
11057525-8	2000	Subsequent testing with DMCM confirmed that a benzodiazepine inverse agonist can induce Fos-LI in most of the same brain regions as observed following ethanol withdrawal, and that this change in Fos protein can be attenuated by pretreatment with flumazenil (5.0 mg/kg).	Flumazenil	246-256	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-198
10899945-6	2000	The PBR antagonist PK11195 (10(-6) M) suppressed the stimulatory action of both TTN and Ro 5-4864 on [(3)H]thymidine incorporation, whereas the central-type benzodiazepine receptor antagonist flumazenil (10(-6) M) had no effect.	Flumazenil	192-202	translocator protein	Rattus norvegicus	4-7
11057525-5	2000	In addition, flumazenil effects on Fos-LI were measured in a group of animals treated with the BZD inverse agonist DMCM (0.75 and 1.0 mg/kg).	Flumazenil	13-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
11057525-8	2000	Subsequent testing with DMCM confirmed that a benzodiazepine inverse agonist can induce Fos-LI in most of the same brain regions as observed following ethanol withdrawal, and that this change in Fos protein can be attenuated by pretreatment with flumazenil (5.0 mg/kg).	Flumazenil	246-256	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
11021974-7	2000	The effect of diazepam on both behaviour and NPY-LI was antagonized by flumazenil (15 mg/kg).	Flumazenil	71-81	neuropeptide Y	Rattus norvegicus	45-48
9715814-0	1998	Diazepam-treated female rats: flumazenil- and PK 11195-induced withdrawal in the hippocampus CA1.	Flumazenil	30-40	carbonic anhydrase 1	Rattus norvegicus	93-96
10353632-9	1999	The effects of DBI and ODN in group-housed mice were significantly blocked by flumazenil (33 nmol, i.c.v.).	Flumazenil	78-88	diazepam binding inhibitor	Mus musculus	15-18
10353632-10	1999	Moreover, the effect of flumazenil in socially isolated mice was significantly attenuated by DBI and ODN (10 nmol, i.c.v.).	Flumazenil	24-34	diazepam binding inhibitor	Mus musculus	93-96
11198048-5	2000	Flumazenil given prior to FG-7142 blocked LLP in all but one of the amygdala efferent pathways, suggesting benzodiazepine receptor dependence of initiation of LLP.	Flumazenil	0-10	LLP homolog, long-term synaptic facilitation factor	Homo sapiens	42-45
11198048-5	2000	Flumazenil given prior to FG-7142 blocked LLP in all but one of the amygdala efferent pathways, suggesting benzodiazepine receptor dependence of initiation of LLP.	Flumazenil	0-10	LLP homolog, long-term synaptic facilitation factor	Homo sapiens	159-162
11198048-9	2000	At the same time LLP only in the right amygdalo-PAG pathway was reduced by Flumazenil.	Flumazenil	75-85	LLP homolog, long-term synaptic facilitation factor	Homo sapiens	17-20
10582800-0	1999	Preserved benzodiazepine receptors in Alzheimer"s disease measured with C-11 flumazenil PET and I-123 iomazenil SPECT in comparison with CBF.	Flumazenil	77-87	RNA polymerase III subunit K	Homo sapiens	72-76
10343173-5	1999	The effect of diazepam on the stress-induced decrease in hippocampal glucocorticoid receptor mRNA was reversed by Ro-15-1788, suggesting that it is mediated by central benzodiazepine receptors, i.e. GABA-A.	Flumazenil	114-124	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	69-92
9987027-9	1999	Diazepam-induced ataxia in alpha 6 -/- mice could be reversed by the benzodiazepine site antagonist flumazenil, indicating the involvement of the remaining alpha 1 beta 2/3 gamma 2 GABAA receptors of the granule cells.	Flumazenil	100-110	gamma-aminobutyric acid (GABA) A receptor, subunit alpha 6	Mus musculus	27-36
10942971-2	1998	In the present study we investigated the role of carboxylesterases for the metabolism of flumazenil.	Flumazenil	89-99	carboxylesterase 1	Homo sapiens	49-66
9610949-0	1998	Supraspinal flumazenil inhibits the antianalgesic action of spinal dynorphin A (1-17).	Flumazenil	12-22	prodynorphin	Mus musculus	67-84
10942971-9	1998	PMSF, a specific inhibitor for serine proteases and mammalian acetylcholinesterase, completely inhibited the formation of flumazenil -acid and the flumazenil methylester at a concentration of 100 microM.	Flumazenil	122-132	acetylcholinesterase (Cartwright blood group)	Homo sapiens	62-82
9467187-6	1998	Moreover, flumazenil facilitates learning and memory perhaps by modulating the release of PAF and consequently attenuated alprazolam and BN-50730-(PAF receptor antagonist)-induced retrograde amnesia.	Flumazenil	10-20	patchy fur	Mus musculus	90-93
9493872-3	1998	Both flumazenil and baclofen induced a decrease in the cAMP content.	Flumazenil	5-15	cathelicidin antimicrobial peptide	Rattus norvegicus	55-59
9467187-6	1998	Moreover, flumazenil facilitates learning and memory perhaps by modulating the release of PAF and consequently attenuated alprazolam and BN-50730-(PAF receptor antagonist)-induced retrograde amnesia.	Flumazenil	10-20	platelet-activating factor receptor	Mus musculus	147-159
8972548-4	1996	In contrast, progesterone (1 mg/kg, for 9 days) produced a significant antistress effect, which was blocked by GABA-A antagonists picrotoxin (1 mg/kg) and bicuculline (1 mg/kg), but not by flumazenil (2 mg/kg), a specific benzodiazepine (BZD) antagonist.	Flumazenil	189-199	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	111-117
9313947-12	1997	Bmax values for [3H]-flumazenil binding in the subiculum, CA1, CA2, CA3, hilus and dentate gyrus were all found to be significantly reduced in HS compared with controls and significant increases in affinity were observed in the subiculum, hilus and dentate gyrus.	Flumazenil	21-31	carbonic anhydrase 2	Homo sapiens	63-66
9313947-12	1997	Bmax values for [3H]-flumazenil binding in the subiculum, CA1, CA2, CA3, hilus and dentate gyrus were all found to be significantly reduced in HS compared with controls and significant increases in affinity were observed in the subiculum, hilus and dentate gyrus.	Flumazenil	21-31	carbonic anhydrase 3	Homo sapiens	68-71
9272753-9	1997	The increase in punished responding produced by NPY was not altered by administration of the benzodiazepine antagonist flumazenil and only partially blocked by the picrotoxinin receptor ligand isopropylbicyclophosphate (10 and 15 microg/kg).	Flumazenil	119-129	neuropeptide Y	Homo sapiens	48-51
8944400-9	1996	Analysis of baboon data from Ator and Griffiths (1986) revealed apparent pKB values for flumazenil antagonism of the discriminative stimulus effects of lorazepam that were lower than the pKB values for either zopiclone or CL 218,872.	Flumazenil	88-98	protein tyrosine kinase 2 beta	Homo sapiens	73-76
8985717-0	1996	Flumazenil attenuates the pituitary response to CRH in healthy males.	Flumazenil	0-10	corticotropin releasing hormone	Homo sapiens	48-51
8985717-3	1996	ACTH response was significantly lower after flumazenil administration than after saline or midazolam.	Flumazenil	44-54	proopiomelanocortin	Homo sapiens	0-4
8946426-4	1996	The present studies attempted to further characterize the behavioral effects of medial septal injections of flumazenil to an endogenous negative modulator of the GABAA/BDZ receptor complex, diazepam binding inhibitor (DBI).	Flumazenil	108-118	diazepam binding inhibitor	Rattus norvegicus	190-216
8946426-4	1996	The present studies attempted to further characterize the behavioral effects of medial septal injections of flumazenil to an endogenous negative modulator of the GABAA/BDZ receptor complex, diazepam binding inhibitor (DBI).	Flumazenil	108-118	diazepam binding inhibitor	Rattus norvegicus	218-221
8944400-11	1996	The apparent pA2 and pKB values obtained in the present review were similar across behavioral assays, except that, in squirrel monkeys, flumazenil pKB values for antagonism of benzodiazepine-induced decreases in schedule-controlled behavior were lower than pKB values obtained from drug discrimination studies.	Flumazenil	136-146	protein tyrosine kinase 2 beta	Homo sapiens	147-150
8944400-11	1996	The apparent pA2 and pKB values obtained in the present review were similar across behavioral assays, except that, in squirrel monkeys, flumazenil pKB values for antagonism of benzodiazepine-induced decreases in schedule-controlled behavior were lower than pKB values obtained from drug discrimination studies.	Flumazenil	136-146	protein tyrosine kinase 2 beta	Homo sapiens	147-150
8613963-5	1996	Double-immunolabeling experiments using 5- and 10-nm gold particles suggest that after chronic flumazenil treatment, receptor subunit assemblies containing the alpha1/gamma2 and alpha6/delta subunits may be replaced by a receptor assembly containing the alpha1/delta subunits.	Flumazenil	95-105	adrenoceptor alpha 1D	Homo sapiens	160-190
8818332-2	1996	Chronic benzodiazepine treatment of rat cerebellar granule cells induced a transient down-regulation of the gamma-aminobutyric acidA (GABAA) receptor alpha 1 subunit protein, that was dose-dependent (1 nM-1 microM) and prevented by the benzodiazepine antagonist flumazenil (1 microM).	Flumazenil	262-272	gamma-aminobutyric acid type A receptor subunit alpha 1	Rattus norvegicus	108-157
8873540-9	1996	With addition of flumazenil, slope and VE50 increased to 1.47 +/- 0.37 l.min-1.mmHg-1 (P < 0.05) and 16.4 +/- 2.0l.min-1 (P < 0.05); after placebo, the respective values of 1.02 +/- 0.19 l.min-1.mmHg-1 and 12.5 +/- 1.2 l.min-1 did not differe significantly from their values during combined alfentanil and midazolam administration.	Flumazenil	17-27	CD59 molecule (CD59 blood group)	Homo sapiens	73-78
8873540-9	1996	With addition of flumazenil, slope and VE50 increased to 1.47 +/- 0.37 l.min-1.mmHg-1 (P < 0.05) and 16.4 +/- 2.0l.min-1 (P < 0.05); after placebo, the respective values of 1.02 +/- 0.19 l.min-1.mmHg-1 and 12.5 +/- 1.2 l.min-1 did not differe significantly from their values during combined alfentanil and midazolam administration.	Flumazenil	17-27	CD59 molecule (CD59 blood group)	Homo sapiens	118-123
8873540-9	1996	With addition of flumazenil, slope and VE50 increased to 1.47 +/- 0.37 l.min-1.mmHg-1 (P < 0.05) and 16.4 +/- 2.0l.min-1 (P < 0.05); after placebo, the respective values of 1.02 +/- 0.19 l.min-1.mmHg-1 and 12.5 +/- 1.2 l.min-1 did not differe significantly from their values during combined alfentanil and midazolam administration.	Flumazenil	17-27	CD59 molecule (CD59 blood group)	Homo sapiens	118-123
8873540-9	1996	With addition of flumazenil, slope and VE50 increased to 1.47 +/- 0.37 l.min-1.mmHg-1 (P < 0.05) and 16.4 +/- 2.0l.min-1 (P < 0.05); after placebo, the respective values of 1.02 +/- 0.19 l.min-1.mmHg-1 and 12.5 +/- 1.2 l.min-1 did not differe significantly from their values during combined alfentanil and midazolam administration.	Flumazenil	17-27	CD59 molecule (CD59 blood group)	Homo sapiens	118-123
8857601-5	1996	and the influence of the GABAA receptor agonist muscimol and the antagonist to BZD receptors flumazenil on GnRH gene expression.	Flumazenil	93-103	gonadotropin releasing hormone 1	Rattus norvegicus	107-111
8857601-7	1996	The administration of flumazenil produced a small increase in GnRH mRNA while the inhibitory effect of ODN on GnRH mRNA levels was completely prevented by the administration of this BZD antagonist.	Flumazenil	22-32	gonadotropin releasing hormone 1	Rattus norvegicus	62-66
8613963-5	1996	Double-immunolabeling experiments using 5- and 10-nm gold particles suggest that after chronic flumazenil treatment, receptor subunit assemblies containing the alpha1/gamma2 and alpha6/delta subunits may be replaced by a receptor assembly containing the alpha1/delta subunits.	Flumazenil	95-105	adrenoceptor alpha 1D	Homo sapiens	254-266
35246037-11	2022	An increase in IL-1beta mRNA levels due to postinjury application of midazolam was reversible by flumazenil administration.	Flumazenil	97-107	interleukin 1 alpha	Homo sapiens	15-23
8624588-0	1996	[The effect of diazepam and flumazenil on pulsatile secretion of prolactin and LH in women].	Flumazenil	28-38	prolactin	Homo sapiens	65-74
8624588-1	1996	The authors examined the effect of diazepam and flumazenil on prolactin and LH secretion in women.	Flumazenil	48-58	prolactin	Homo sapiens	62-71
7579146-1	1995	We examined the effects of the benzodiazepine antagonist, flumazenil, on epileptiform discharges evoked in the hippocampal CA1 region in vitro.	Flumazenil	58-68	carbonic anhydrase 1	Homo sapiens	123-126
7862733-1	1994	The anxiolytic-like effect of (-)-nicotine (1.9 mumol/kg, IP) on the elevated plus-maze in CD1 mice was blocked by the benzodiazepine receptor antagonist flumazenil (1 and 10 mumol/kg, IP).	Flumazenil	154-164	CD1 antigen complex	Mus musculus	91-94
7814832-0	1994	Flumazenil effects on growth hormone response to gamma-hydroxybutyric acid.	Flumazenil	0-10	growth hormone 1	Homo sapiens	22-36
8039271-0	1994	Effect of flumazenil on basal and naloxone-stimulated ACTH and cortisol release in humans.	Flumazenil	10-20	proopiomelanocortin	Homo sapiens	54-58
8039271-11	1994	Flumazenil had no effect on ACTH and cortisol release when given alone; flumazenil area under the ACTH/time curve (pmol/L.min) = -36.5 +/- 63.5 compared with placebo = -53.5 +/- 31.8, flumazenil area under the cortisol/time curve (nmol/L.min x 10(-3)) = - 2.4 +/- 2.4 compared with placebo -0.56 +/- 1.4.	Flumazenil	72-82	proopiomelanocortin	Homo sapiens	98-102
1654569-1	1991	The aim of the present study was to determine whether melatonin-induced depression of locomotor activity in hamsters is time-dependent and to analyze the inhibitory effects of the central-type benzodiazepine (BZP) antagonist Ro 15-1788 on melatonin-induced depression of locomotor behavior.	Flumazenil	225-235	zinc finger E-box binding homeobox 1	Homo sapiens	180-213
1936896-9	1991	The intensity of the abstinence syndrome induced by flumazenil was attenuated by L-PIA, CPA NECA, TP and 8-PTP.	Flumazenil	52-62	protein tyrosine phosphatase, receptor type, U	Mus musculus	107-110
2109472-3	1990	administration, both drugs are rapidly distributed into similar distribution volumes, from which they are cleared with a comparable short elimination half-life (t1/2 beta) in the range of 1 h (flumazenil) to 3 h (midazolam).	Flumazenil	193-203	interleukin 1 receptor like 1	Homo sapiens	161-170
2109476-5	1990	It is recommended that flumazenil be administered carefully by titration in increments of 0.1 mg.min-1 to avoid emergence reactions by awakening too fast (tachycardia, hypertension).	Flumazenil	23-33	CD59 molecule (CD59 blood group)	Homo sapiens	97-102
23799902-5	2013	KEY RESULTS: We find the sensitivity of GABAA R to zolpidem, midazolam and DMCM significantly reduced in TMN neurons from gamma2F77I mice, but modulatory activities of diazepam, chlordiazepoxide and flumazenil not affected.	Flumazenil	199-209	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2	Mus musculus	40-47
35440709-5	2022	In contrast, the inhibitory interneuron marker parvalbumin covaried with GABAA receptor-subunit genes GABRA1, GABRB2 and GABRG2, and their distribution tracked (11C)flumazenil binding.	Flumazenil	165-175	parvalbumin	Homo sapiens	47-58
8592140-6	1996	The alpha 1 subunit contributes the high-affinity binding of [3H]Ro 15-1788 (flumazenil) and the diazepam-sensitive binding of [3H]Ro 15-4513.	Flumazenil	77-87	adrenoceptor alpha 1D	Homo sapiens	4-11
8748046-3	1995	Our previous studies revealed the ability of flumazenil (a benzodiazepine antagonist) to counteract GHB effects on GH secretion.	Flumazenil	45-55	growth hormone 1	Homo sapiens	100-102
7838917-3	1994	To examine this possibility we determined whether the BZD receptor antagonist flumazenil could antagonize the effects of CCK-4 (50 micrograms) in healthy volunteers.	Flumazenil	78-88	protein tyrosine kinase 7 (inactive)	Homo sapiens	121-126
8391018-3	1993	An additional inhibition study (pretreatment with 0.15 mg/kg of flumazenil) was performed on one of the volunteers, which resulted in an average gray matter K1/k2 estimate of 0.68 +/- 0.08 ml/ml (linear three-compartment model, nine brain regions).	Flumazenil	64-74	keratin 1	Homo sapiens	157-162
8471371-6	1993	Flumazenil data were best interpreted by a monoexponential function, with a mean terminal elimination half-life of 35.3 (13.8) min, a total plasma clearance of 20.6 (6.9) ml min-1 kg-1 and apparent volume of distribution at steady state of 1.0 (0.2) litre kg-1.	Flumazenil	0-10	CD59 molecule (CD59 blood group)	Homo sapiens	174-184
1637608-3	1992	The sedative effects of midazolam and antagonism by flumazenil resulted in alterations in EEG, P300 and psychometric tests (syndrome short test, letter cancellation, choice reaction and recognition).	Flumazenil	52-62	E1A binding protein p300	Homo sapiens	95-99
1325067-3	1992	Flumazenil Ro15-1788) reversed the effect of flunitrazepam suggesting the reduction in dopamine D1 receptor binding in the striatum was mediated via GABA-Bz-Cl channel complex.	Flumazenil	0-10	dopamine receptor D1	Mus musculus	87-107
2554616-5	1989	Systemic flumazepil administration contributed to the memory trace reproduction against the background of GABA-A receptors activation by muscimol in the dose of 0.5 mg/kg.	Flumazenil	9-19	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	106-112
2769267-4	1989	Synthetic TTN injected intracerebroventricularly into rats induces a proconflict activity (IC50 0.8 nmol/rat) that is prevented by the specific "peripheral" benzodiazepine (BZ) receptor antagonist isoquinoline carboxamide, PK 11195, but not by the "central" BZ receptor antagonist imidazobenzodiazepine, flumazenil.	Flumazenil	304-314	diazepam binding inhibitor	Rattus norvegicus	10-13
3033417-2	1987	High concentrations of clonazepam (3.16 X 10(-5) and 10(-4) M) caused an inhibition of alpha-MSH release and this effect was reversed by the central-type benzodiazepine-receptor antagonist Ro 15-1788.	Flumazenil	189-199	proopiomelanocortin	Homo sapiens	87-96
2570433-2	1989	These impairments can be reversed by appropriate agents such as the cholinesterase inhibitor physostigmine in the case of scopolamine or the benzodiazepine antagonist Ro 15-1788 in the case of lorazepam.	Flumazenil	167-177	butyrylcholinesterase	Homo sapiens	68-82
2855121-5	1988	However, both Ro 15-1788 and beta-CCE blocked the antagonism of ethanol"s effects by Ro 15-4513, suggesting a role for the GABA receptor complex in the actions of ethanol.	Flumazenil	14-24	GABA type A receptor-associated protein	Homo sapiens	123-136
3128805-0	1988	Corticotropin releasing factor and amphetamine exaggerate partial agonist properties of benzodiazepine antagonist Ro 15-1788 in the conflict test.	Flumazenil	114-124	corticotropin releasing hormone	Rattus norvegicus	0-30
3023014-7	1986	Ro 15-1788 (100 nM), a selective antagonist of the central type of benzodiazepine-binding sites (added to the perifusion system 30 min before DZ and then during the whole period of DZ perifusion), completely abolished (P less than 0.01) the inhibitory effect of DZ (10 nM) on the TRH-induced TSH and GH responses.	Flumazenil	0-10	thyrotropin releasing hormone	Rattus norvegicus	280-283
3000525-2	1985	Prior administration of RO 15-1788 blocked the effects of chlordiazepoxide on basal plasma AVP as well as picrotoxin-evoked changes in plasma AVP and blood pressure.	Flumazenil	24-34	arginine vasopressin	Homo sapiens	91-94
3000525-2	1985	Prior administration of RO 15-1788 blocked the effects of chlordiazepoxide on basal plasma AVP as well as picrotoxin-evoked changes in plasma AVP and blood pressure.	Flumazenil	24-34	arginine vasopressin	Homo sapiens	142-145
6421562-8	1984	The benzodiazepin antagonist Ro 15-1788 represents a valuable diagnostic aid in ascertained or suspect cases of benzodiazepin intoxications.	Flumazenil	29-39	activation induced cytidine deaminase	Homo sapiens	73-76
2868143-1	1985	Intracisternally administered cholecystokinin produced long lasting hypothermia in mice, and the hypothermic effect was significantly antagonized by benzodiazepines like chlordiazepoxide and diazepam and by a benzodiazepine antagonist, Ro 15-1788, that were administered intraperitoneally.	Flumazenil	236-246	cholecystokinin	Mus musculus	30-45
2859382-0	1985	Reversal of antinociceptive effect of cholecystokinin by benzodiazepines and a benzodiazepine antagonist, Ro 15-1788.	Flumazenil	106-116	cholecystokinin	Mus musculus	38-53
2859382-5	1985	Benzodiazepines and Ro 15-1788 seem to inhibit the release of opioid peptides induced by cholecystokinin.	Flumazenil	20-30	cholecystokinin	Mus musculus	89-104
33143464-4	2021	The effect of selective receptor antagonist GABAA on anticonvulsant activity was investigated with flumazenil.	Flumazenil	99-109	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	44-49
6304714-7	1983	DBI is a competitive inhibitor for the binding of [3H]diazepam, [3H]flunitrazepam, beta-[3H]carboline propyl esters, and 3H-labeled Ro 15-1788.	Flumazenil	132-142	diazepam binding inhibitor, acyl-CoA binding protein	Homo sapiens	0-3
6287328-0	1982	Benzodiazepine antagonist Ro 15-1788 counteracts the prolactin-lowering effects of other benzodiazepines in rats.	Flumazenil	26-36	prolactin	Rattus norvegicus	53-62
32386503-4	2021	RESULTS: The results demonstrated that the neuropharmacological activities of beta-CBP may involve benzodiazepine/GABAergic receptors, since the pre-treatment of beta-CBP (200 mg/kg) associated with flumazenil (5 mg/kg, benzodiazepine receptor antagonist) and bicuculline (1 mg/kg, selective GABAA receptor antagonist) reestablished the anxiety parameters in the elevated plus-maze test, as well as the results of reduced latency to consume food in the novelty suppressed feeding test.	Flumazenil	199-209	CREB binding protein	Mus musculus	83-86
32386503-4	2021	RESULTS: The results demonstrated that the neuropharmacological activities of beta-CBP may involve benzodiazepine/GABAergic receptors, since the pre-treatment of beta-CBP (200 mg/kg) associated with flumazenil (5 mg/kg, benzodiazepine receptor antagonist) and bicuculline (1 mg/kg, selective GABAA receptor antagonist) reestablished the anxiety parameters in the elevated plus-maze test, as well as the results of reduced latency to consume food in the novelty suppressed feeding test.	Flumazenil	199-209	CREB binding protein	Mus musculus	167-170
32446885-8	2020	The midazolam-mediated inhibition of VEGF-induced intracellular events was reversed by treatment with the GABAA receptor antagonist flumazenil.	Flumazenil	132-142	vascular endothelial growth factor A	Mus musculus	37-41
32752296-5	2020	MF1-promoted GABA currents were blocked by flumazenil (10 mum) treatment, suggesting that MF1 enhances receptor function via the benzodiazepine recognition site.	Flumazenil	43-53	forkhead box C1	Mus musculus	0-3
32752296-5	2020	MF1-promoted GABA currents were blocked by flumazenil (10 mum) treatment, suggesting that MF1 enhances receptor function via the benzodiazepine recognition site.	Flumazenil	43-53	forkhead box C1	Mus musculus	90-93
30454851-11	2019	Specifically, similar to the effect of BZD, the overexpression of DHHC12 in the BLA exerted a significant anxiolytic action, which was prevented by flumazenil.	Flumazenil	148-158	zinc finger DHHC-type palmitoyltransferase 12	Rattus norvegicus	66-72
32059939-6	2020	The anxiolytic-like effect of mast-L was attenuated by flumazenil (antagonist of benzodiazepine binding site) and WAY100635 (selective antagonist of 5-HT1A receptors) pretreatments.	Flumazenil	55-65	microtubule associated serine/threonine kinase-like	Mus musculus	30-36
32210319-0	2020	GluN2A-selective positive allosteric modulator-nalmefene-flumazenil reverses ketamine-fentanyl-dexmedetomidine-induced anesthesia and analgesia in rats.	Flumazenil	57-67	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	0-6
31430640-7	2020	We found that flumazenil, a selective antagonist of GABA receptor, could effectively increase the survival of the tested animals, which provides a potential therapy for future clinical applications.	Flumazenil	14-24	GABA type A receptor-associated protein	Homo sapiens	52-65
31123329-9	2019	This enzymatic experiment clearly showed that K393 exerts enzymatic inhibition against NAMPT.	Flumazenil	46-50	nicotinamide phosphoribosyltransferase	Homo sapiens	87-92
28969445-9	2018	Treatment with flumazenil also significantly increased TNF-alpha and IL-6 levels in immobilisation stress-free mice treated with IM38.	Flumazenil	15-25	tumor necrosis factor	Mus musculus	55-64
30003929-9	2019	Flumazenil (a neutral allosteric antagonist at GABAA receptor) prolonged KET sleep and blocked p-MEK upregulation, indicating the involvement of this receptor as a negative modulator.	Flumazenil	0-10	midkine	Mus musculus	97-100
30381406-4	2018	Our functional brain imaging using PET with [18F]fluorodeoxyglucose and [18F] flumazenil revealed that the brain dysfunction induced by PAM is closely aligned to disruption of neurotransmitter-related neuronal activity and functional correlation in the region of the limbic system rather than to decrease of metabolic activity of neurons in the injection area.	Flumazenil	78-88	peptidylglycine alpha-amidating monooxygenase	Mus musculus	136-139
29782207-2	2018	Midazolam inhibited VEGF-induced elevation of intracellular Ca2+, generation of reactive oxygen species (ROS), and transglutaminase activation in HRECs; these effects were reversed by the GABA, type A (GABAA) receptor antagonist flumazenil but not by the translocator protein antagonist PK11195.	Flumazenil	229-239	vascular endothelial growth factor A	Mus musculus	20-24
28969445-9	2018	Treatment with flumazenil also significantly increased TNF-alpha and IL-6 levels in immobilisation stress-free mice treated with IM38.	Flumazenil	15-25	interleukin 6	Mus musculus	69-73
28577050-8	2017	Pretreatment with flumazenil (FLU) did not reverse the anticonvulsive effect of VRB; however, it was able to upregulate BDNF and COX-2 genes and downregulate c-fos.	Flumazenil	18-28	brain derived neurotrophic factor	Homo sapiens	120-124
29232839-6	2017	However, the sedative-hypnotic effects were blocked by the type A GABA (GABAA) receptor antagonists bicuculline and flumazenil.	Flumazenil	116-126	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	72-77
28577050-8	2017	Pretreatment with flumazenil (FLU) did not reverse the anticonvulsive effect of VRB; however, it was able to upregulate BDNF and COX-2 genes and downregulate c-fos.	Flumazenil	18-28	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	129-134
28577050-8	2017	Pretreatment with flumazenil (FLU) did not reverse the anticonvulsive effect of VRB; however, it was able to upregulate BDNF and COX-2 genes and downregulate c-fos.	Flumazenil	18-28	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	158-163
28577050-8	2017	Pretreatment with flumazenil (FLU) did not reverse the anticonvulsive effect of VRB; however, it was able to upregulate BDNF and COX-2 genes and downregulate c-fos.	Flumazenil	30-33	brain derived neurotrophic factor	Homo sapiens	120-124
28577050-8	2017	Pretreatment with flumazenil (FLU) did not reverse the anticonvulsive effect of VRB; however, it was able to upregulate BDNF and COX-2 genes and downregulate c-fos.	Flumazenil	30-33	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	129-134
28577050-8	2017	Pretreatment with flumazenil (FLU) did not reverse the anticonvulsive effect of VRB; however, it was able to upregulate BDNF and COX-2 genes and downregulate c-fos.	Flumazenil	30-33	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	158-163
28551554-7	2017	Ketanserin (6mug), a 5-HT2A/C receptor antagonist, and flumazenil (6mug), a GABAA receptor antagonist, abolished the antihyperalgesic effect of mexicanolide 1 (3mug).	Flumazenil	55-65	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	76-81
28111292-4	2017	Midazolam-induced p-MEK1/2 upregulation was prevented by pretreatment (30min) with flumazenil (10mg/kg), indicating the involvement of GABAA receptors.	Flumazenil	83-93	mitogen-activated protein kinase kinase 1	Mus musculus	20-26
28111292-4	2017	Midazolam-induced p-MEK1/2 upregulation was prevented by pretreatment (30min) with flumazenil (10mg/kg), indicating the involvement of GABAA receptors.	Flumazenil	83-93	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	135-140
28111292-6	2017	Notably, during midazolam-induced sleep the content of inactivated p-Thr286 MEK1, which can dampen ERK1/2 activation, was increased (+33% to +149%) through a mechanism sensitive to flumazenil (10mg/kg).	Flumazenil	181-191	mitogen-activated protein kinase kinase 1	Mus musculus	76-80
28111292-6	2017	Notably, during midazolam-induced sleep the content of inactivated p-Thr286 MEK1, which can dampen ERK1/2 activation, was increased (+33% to +149%) through a mechanism sensitive to flumazenil (10mg/kg).	Flumazenil	181-191	mitogen-activated protein kinase 3	Mus musculus	99-105
28111292-7	2017	Midazolam also increased MKP-3 (+13% to +73%) content and this upregulation was prevented by flumazenil (10mg/kg); an effect suggesting ERK inactivation because MKP-3 is the phosphatase selective for ERK1/2 dephosphorylation.	Flumazenil	93-103	mitogen-activated protein kinase 1	Mus musculus	136-139
28111292-7	2017	Midazolam also increased MKP-3 (+13% to +73%) content and this upregulation was prevented by flumazenil (10mg/kg); an effect suggesting ERK inactivation because MKP-3 is the phosphatase selective for ERK1/2 dephosphorylation.	Flumazenil	93-103	dual specificity phosphatase 6	Mus musculus	161-166
28111292-7	2017	Midazolam also increased MKP-3 (+13% to +73%) content and this upregulation was prevented by flumazenil (10mg/kg); an effect suggesting ERK inactivation because MKP-3 is the phosphatase selective for ERK1/2 dephosphorylation.	Flumazenil	93-103	mitogen-activated protein kinase 3	Mus musculus	200-206
28215510-4	2017	We explored the therapeutic potential of flumazenil (FLUM), a GABAAR antagonist working at the benzodiazepine binding site that has FDA approval.	Flumazenil	41-51	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2	Mus musculus	62-68
26875558-6	2016	In addition, we found that the inhibitory effect of diazepam was also completely blocked by pretreatment with a specific CBR antagonist, flumazenil.	Flumazenil	137-147	cannabinoid receptor 1	Rattus norvegicus	121-124
26661244-1	2017	Studies in rodents suggest that flumazenil is a P-glycoprotein substrate at the blood-brain barrier.	Flumazenil	32-42	ATP binding cassette subfamily B member 1	Homo sapiens	48-62
26661244-2	2017	This study aimed to assess whether [11C]flumazenil is a P-glycoprotein substrate in humans and to what extent increased P-glycoprotein function in epilepsy may confound interpretation of clinical [11C]flumazenil studies used to assess gamma-aminobutyric acid A receptors.	Flumazenil	40-50	ATP binding cassette subfamily B member 1	Homo sapiens	56-70
26661244-9	2017	In conclusion, although [11C]flumazenil appears to be a (weak) P-glycoprotein substrate in humans, this does not seem to affect its role as a tracer for assessing gamma-aminobutyric acid A receptor density.	Flumazenil	24-39	ATP binding cassette subfamily B member 1	Homo sapiens	63-77
27573669-9	2016	These effects of (-)-alpha-pinene on sleep and inhibitory synaptic response were mimicked by zolpidem, acting as a modulator for GABAA-BZD receptors, and fully antagonized by flumazenil, an antagonist for GABAA-BZD receptor.	Flumazenil	175-185	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	205-210
24643139-8	2014	In the mechanistic studies, effects of propofol, amyloid-beta protein (Abeta), and GABA receptor antagonist flumazenil on caspase-3 activation and opening of the mitochondrial permeability transition pore were assessed in H4 human neuroglioma and mouse neuroblastoma cells by western blot analysis and flow cytometry.	Flumazenil	108-118	GABA type A receptor-associated protein	Homo sapiens	83-96
26949686-7	2016	While he was alert, electroencephalogram showed the reversal of slow wave into beta range fast activity and F-18 flumazenil positron emission tomography (PET) showed increased GABAergic receptor activity in both frontoparietotemporal cortices.	Flumazenil	113-123	mastermind like domain containing 1	Homo sapiens	108-112
26592470-3	2016	We first determined that flumazenil (100 nM-100 muM, IC50=~1 muM) acted as a negative modulator, reducing GABA (10 muM)-gated current in the presence of 100 nM THP (to increase receptor efficacy), assessed with whole cell patch clamp recordings of recombinant alpha4beta2delta expressed in HEK-293 cells.	Flumazenil	25-35	latexin	Homo sapiens	48-51
26592470-3	2016	We first determined that flumazenil (100 nM-100 muM, IC50=~1 muM) acted as a negative modulator, reducing GABA (10 muM)-gated current in the presence of 100 nM THP (to increase receptor efficacy), assessed with whole cell patch clamp recordings of recombinant alpha4beta2delta expressed in HEK-293 cells.	Flumazenil	25-35	latexin	Homo sapiens	61-64
26592470-3	2016	We first determined that flumazenil (100 nM-100 muM, IC50=~1 muM) acted as a negative modulator, reducing GABA (10 muM)-gated current in the presence of 100 nM THP (to increase receptor efficacy), assessed with whole cell patch clamp recordings of recombinant alpha4beta2delta expressed in HEK-293 cells.	Flumazenil	25-35	latexin	Homo sapiens	61-64
26592470-5	2016	Flumazenil (10 muM) decreased surface expression of alpha4F by ~60%, while increasing its intracellular accumulation, after 48 h. Reduced surface expression of alpha4beta2delta after flumazenil treatment was confirmed by decreases in the current responses to 100 nM of the GABA agonist gaboxadol.	Flumazenil	0-10	latexin	Homo sapiens	15-18
26592470-5	2016	Flumazenil (10 muM) decreased surface expression of alpha4F by ~60%, while increasing its intracellular accumulation, after 48 h. Reduced surface expression of alpha4beta2delta after flumazenil treatment was confirmed by decreases in the current responses to 100 nM of the GABA agonist gaboxadol.	Flumazenil	183-193	latexin	Homo sapiens	15-18
24643139-8	2014	In the mechanistic studies, effects of propofol, amyloid-beta protein (Abeta), and GABA receptor antagonist flumazenil on caspase-3 activation and opening of the mitochondrial permeability transition pore were assessed in H4 human neuroglioma and mouse neuroblastoma cells by western blot analysis and flow cytometry.	Flumazenil	108-118	caspase 3	Homo sapiens	122-131
24183322-3	2013	Flumazenil acts as a benzodiazepine receptor antagonist (subunits alpha1, alpha2, alpha3, and alpha5) or partial agonist (subunits alpha4 and alpha6).	Flumazenil	0-10	adrenoceptor alpha 1D	Homo sapiens	66-72
23752092-5	2013	The effect of MCP-1 was not dependent on the activation of its receptor CCR2, while it was blocked by flumazenil, the antagonist of benzodiazepine sites.	Flumazenil	102-112	C-C motif chemokine ligand 2	Homo sapiens	14-19
23320076-0	2013	Increases in [3H]muscimol and [3H]flumazenil binding in the dorsolateral prefrontal cortex in schizophrenia are linked to alpha4 and gamma2S mRNA levels respectively.	Flumazenil	34-44	immunoglobulin binding protein 1	Homo sapiens	122-128
23806621-10	2013	The GABAA inverse agonist, FG-7142, reduced sociability and this was reversed by the GABAA antagonist, flumazenil and dcycloserine, but not by clozapine, or the GABAA benzodiazepine anxiolytic, alprazolam.	Flumazenil	103-113	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	4-9
24096829-4	2013	Furthermore, the effects of FTA on PTZ-induced seizure and c-Fos expression were reversed by the GABAA/benzodiazepine receptor-selective antagonist flumazenil.	Flumazenil	148-158	FBJ osteosarcoma oncogene	Mus musculus	59-64