PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
19604081-0	2009	Relevance of CYP2D6 -1584C>G polymorphism for thioridazine:mesoridazine plasma concentration ratio in psychiatric patients.	Thioridazine	49-61	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	13-19
19923256-7	2010	Extracted ion chromatograms of metabolites observed for albendazole, amiodarone, astemizole, thioridazine, mesoridazine, and danazol showed marked differences in the regioselectivity of CYP2J2 and CYP3A4.	Thioridazine	93-105	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	186-192
19923256-7	2010	Extracted ion chromatograms of metabolites observed for albendazole, amiodarone, astemizole, thioridazine, mesoridazine, and danazol showed marked differences in the regioselectivity of CYP2J2 and CYP3A4.	Thioridazine	93-105	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	197-203
19604081-5	2009	Therefore, the aim of this study was to analyze the relationship between the presence of the CYP2D6 -1584C>G polymorphism and the plasma concentrations of thioridazine and its metabolites in a previously studied population of patients in order to evaluate the implications for CYP2D6 hydroxylation capacity.	Thioridazine	158-170	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	93-99
19604081-6	2009	MATERIALS & METHODS: The CYP2D6 -1584C>G polymorphism was determined by using a PCR-RFLP method in 61 Caucasian psychiatric patients receiving thioridazine monotherapy.	Thioridazine	150-162	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	29-35
19604081-7	2009	RESULTS: Among patients with two active CYP2D6 genes, there were significant differences in the thioridazine:mesoridazine plasma concentrations ratio (p < 0.05) among the three CYP2D6 -1584C>G genotype groups.	Thioridazine	96-108	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	40-46
19604081-7	2009	RESULTS: Among patients with two active CYP2D6 genes, there were significant differences in the thioridazine:mesoridazine plasma concentrations ratio (p < 0.05) among the three CYP2D6 -1584C>G genotype groups.	Thioridazine	96-108	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	180-186
19604081-8	2009	Moreover, in this group of patients the thioridazine:mesoridazine ratio was lower (p < 0.05) in carriers of CYP2D6 -1584G allele than in patients homozygous for CYP2D6 -1584C allele.	Thioridazine	40-52	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	111-117
19482014-5	2009	Formation of reactive intermediates of chlorpromazine and thioridazine was primarily mediated by heterologously expressed recombinant CYP2D6, and to a less extent, CYP1A2.	Thioridazine	58-70	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	134-140
19482014-5	2009	Formation of reactive intermediates of chlorpromazine and thioridazine was primarily mediated by heterologously expressed recombinant CYP2D6, and to a less extent, CYP1A2.	Thioridazine	58-70	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	164-170
19604081-3	2009	However, the impact this SNP in the CYP2D6 promoter region has on plasma levels of patients taking CYP2D6 substrates, such as thioridazine, has not been studied.	Thioridazine	126-138	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	36-42
19604081-8	2009	Moreover, in this group of patients the thioridazine:mesoridazine ratio was lower (p < 0.05) in carriers of CYP2D6 -1584G allele than in patients homozygous for CYP2D6 -1584C allele.	Thioridazine	40-52	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	164-170
19604081-10	2009	CONCLUSION: According to the present results the concentration ratio of thioridazine to mesoridazine was related to the CYP2D6 -1584C>G polymorphism.	Thioridazine	72-84	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	120-126
19604081-3	2009	However, the impact this SNP in the CYP2D6 promoter region has on plasma levels of patients taking CYP2D6 substrates, such as thioridazine, has not been studied.	Thioridazine	126-138	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	99-105
19604081-4	2009	Previously, we showed the validity of the mesoridazine:thioridazine ratio to assess CYP2D6 activity in clinical settings.	Thioridazine	55-67	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	84-90
18836185-9	2008	CONCLUSIONS: The present study indicates that reversal of methicillin resistance by thioridazine in MRSA may be explained by a reduced transcription of mecA and blaZ, resulting in a reduced protein level of PBP2a.	Thioridazine	84-96	Beta-lactamase regulatory sensor-transducer BlaR1	Staphylococcus aureus	161-165
19902987-10	2009	Therapeutic drug monitoring has been strongly recommended for many antipsychotics, including haloperidol, chlorpromazine, fluphenazine, perphenazine, risperidone and thioridazine, which are all metabolized by CYP2D6.	Thioridazine	166-178	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	209-215
17561380-3	2008	In the current study, we investigated the influence of chronic treatment with clozapine and other antipsychotics (thioridazine,sulpiride and risperidone) on TSPO binding in cell cultures and rat tissues.	Thioridazine	114-126	translocator protein	Rattus norvegicus	157-161
17676390-5	2008	Peptide degradation rate (optimum pH and temperature of 7.4 and 37 degrees C, respectively) was concentration-dependent inhibited by known aminopeptidase inhibitors (puromycin, bacitracin, and bestatin, and to a lesser extent by thioridazine).	Thioridazine	229-241	carboxypeptidase Q	Homo sapiens	139-153
17460606-8	2007	Plasma concentrations of thioridazine are influenced by age, smoking, and CYP2D6 genotype, but CYP2D6 genotype does not appear to influence on-treatment QTc interval.	Thioridazine	25-37	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	74-80
17056009-0	2006	hERG K+ channel blockade by the antipsychotic drug thioridazine: An obligatory role for the S6 helix residue F656.	Thioridazine	51-63	ETS transcription factor ERG	Homo sapiens	0-4
17501721-7	2007	The pharmacological profile of NOX4 was distinct from other NOX isoforms: DPI (diphenyleneiodonium chloride) and thioridazine inhibited the enzyme efficiently, whereas apocynin and gliotoxin did not (IC(50)>100 muM).	Thioridazine	113-125	NADPH oxidase 4	Homo sapiens	31-35
17056009-2	2006	Although thioridazine is known to inhibit cardiac hERG K(+) channels there is little mechanistic information on this action.	Thioridazine	9-21	ETS transcription factor ERG	Homo sapiens	50-54
17056009-3	2006	We have investigated in detail hERG K(+) channel current (I(hERG)) blockade by thioridazine and identified a key molecular determinant of blockade.	Thioridazine	79-91	ETS transcription factor ERG	Homo sapiens	31-35
17056009-3	2006	We have investigated in detail hERG K(+) channel current (I(hERG)) blockade by thioridazine and identified a key molecular determinant of blockade.	Thioridazine	79-91	ETS transcription factor ERG	Homo sapiens	60-64
17056009-5	2006	Thioridazine inhibited I(hERG) tails at -40mV following a 2s depolarization to +20mV with an IC(50) value of 80nM.	Thioridazine	0-12	ETS transcription factor ERG	Homo sapiens	25-29
17056009-7	2006	Thioridazine block of I(hERG) was only weakly voltage-dependent, though the time dependence of I(hERG) inhibition indicated contingency of blockade upon channel gating.	Thioridazine	0-12	ETS transcription factor ERG	Homo sapiens	24-28
17056009-8	2006	The S6 helix point mutation F656A almost completely abolished, and the Y652A mutation partially attenuated, I(hERG) inhibition by thioridazine.	Thioridazine	130-142	ETS transcription factor ERG	Homo sapiens	110-114
17056009-9	2006	In summary, thioridazine is one of the most potent hERG K(+) channel blockers amongst antipsychotics, exhibiting characteristics of a preferential open/activated channel blocker and binding at a high affinity site in the hERG channel pore.	Thioridazine	12-24	ETS transcription factor ERG	Homo sapiens	51-55
17056009-9	2006	In summary, thioridazine is one of the most potent hERG K(+) channel blockers amongst antipsychotics, exhibiting characteristics of a preferential open/activated channel blocker and binding at a high affinity site in the hERG channel pore.	Thioridazine	12-24	ETS transcription factor ERG	Homo sapiens	221-225
16685461-0	2006	Effect of thioridazine on gap junction intercellular communication in connexin 43-expressing cells.	Thioridazine	10-22	gap junction protein alpha 1	Homo sapiens	70-81
16685461-7	2006	Western blot analysis of connexin 43 in a membrane-enriched fraction of WB-F344 cells treated with thioridazine revealed decreased amounts of unphosphorylated connexin 43, and appearance of a phosphorylated connexin 43 band that co-migrated with a "hyperphosphorylated" connexin 43 band present in TPA-inhibited cells.	Thioridazine	99-111	gap junction protein, alpha 1	Rattus norvegicus	25-36
16685461-7	2006	Western blot analysis of connexin 43 in a membrane-enriched fraction of WB-F344 cells treated with thioridazine revealed decreased amounts of unphosphorylated connexin 43, and appearance of a phosphorylated connexin 43 band that co-migrated with a "hyperphosphorylated" connexin 43 band present in TPA-inhibited cells.	Thioridazine	99-111	gap junction protein, alpha 1	Rattus norvegicus	159-170
16685461-7	2006	Western blot analysis of connexin 43 in a membrane-enriched fraction of WB-F344 cells treated with thioridazine revealed decreased amounts of unphosphorylated connexin 43, and appearance of a phosphorylated connexin 43 band that co-migrated with a "hyperphosphorylated" connexin 43 band present in TPA-inhibited cells.	Thioridazine	99-111	gap junction protein, alpha 1	Rattus norvegicus	159-170
16685461-7	2006	Western blot analysis of connexin 43 in a membrane-enriched fraction of WB-F344 cells treated with thioridazine revealed decreased amounts of unphosphorylated connexin 43, and appearance of a phosphorylated connexin 43 band that co-migrated with a "hyperphosphorylated" connexin 43 band present in TPA-inhibited cells.	Thioridazine	99-111	gap junction protein, alpha 1	Rattus norvegicus	159-170
15826185-1	2005	Poly(benzyl ether) dendrons having a focal triazole unit (Gntrz: trz = triazole; n = generation number = 0-2) were found to react with (MeSO(3))(2)Fe to form dendritic coordination polymers ([Fe(Gntrz)(3)](MeSO(3))(2).2H(2)O) that undergo the thermal spin transition.	Thioridazine	60-63	spindlin 1	Homo sapiens	251-255
16805946-9	2006	CYP2D6 is an important catalyst of the oxidation of chlorpromazine, thioridazine, risperidone and haloperidol.	Thioridazine	68-80	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-6
16675310-1	2006	Resolution of racemic thioridazine obtained from Thioril tablets (Cipla Ltd., Goa, India) into its enantiomers has been achieved by HPLC using a beta-cyclodextrin (CD)-bonded stationary phase.	Thioridazine	22-34	tripartite motif containing 47	Homo sapiens	78-81
16675310-1	2006	Resolution of racemic thioridazine obtained from Thioril tablets (Cipla Ltd., Goa, India) into its enantiomers has been achieved by HPLC using a beta-cyclodextrin (CD)-bonded stationary phase.	Thioridazine	49-56	tripartite motif containing 47	Homo sapiens	78-81
16117689-4	2005	Like chlorpromazine and thioridazine, fluphenazine may be oxidized by retinal cytochrome P450 and/or myeloperoxidase to an electrophile, producing injury in susceptible patients.	Thioridazine	24-36	myeloperoxidase	Homo sapiens	101-116
16272405-3	2006	The results indicate that CYP1A2 and CYP3A4 are the main enzymes responsible for 5-sulfoxidation and N-demethylation (34-52%), whereas CYP2D6 is the basic enzyme that catalyzes mono-2- and di-2-sulfoxidation of thioridazine in human liver (49 and 64%, respectively).	Thioridazine	211-223	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	26-32
16272405-3	2006	The results indicate that CYP1A2 and CYP3A4 are the main enzymes responsible for 5-sulfoxidation and N-demethylation (34-52%), whereas CYP2D6 is the basic enzyme that catalyzes mono-2- and di-2-sulfoxidation of thioridazine in human liver (49 and 64%, respectively).	Thioridazine	211-223	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	37-43
16272405-3	2006	The results indicate that CYP1A2 and CYP3A4 are the main enzymes responsible for 5-sulfoxidation and N-demethylation (34-52%), whereas CYP2D6 is the basic enzyme that catalyzes mono-2- and di-2-sulfoxidation of thioridazine in human liver (49 and 64%, respectively).	Thioridazine	211-223	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	135-141
16272405-6	2006	In contrast to promazine and perazine, CYP2C19 insignificantly contributes to the N-demethylation of thioridazine.	Thioridazine	101-113	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
16472104-8	2006	However, after co-administration of drugs such as quinidine, propafenone and thioridazine (potent inhibitors of CYP2D6), the NE-100 AUC(oral) ratios predicted from the dispersion model was much greater than those from well-stirred model.	Thioridazine	77-89	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	112-118
16328041-8	2006	Caspase-3 expression, a typical mediator of apoptosis, was markedly increased following a 4-h exposure of B16 cells to thioridazine (25 microM and 50 microM).	Thioridazine	119-131	caspase 3	Mus musculus	0-9
16294502-7	2005	Thioridazine (CAS 50-52-2) was used as internal standard.	Thioridazine	0-12	BCAR1 scaffold protein, Cas family member	Homo sapiens	14-17
15695070-1	2005	The alpha1A- and alpha1B-adrenoceptor affinity of the typical (chlorpromazine, haloperidol, pimozide, thioridazine and trifluoperazine) and atypical (clozapine, olanzapine, quetiapine, risperidone and sertindole) antipsychotics was determined by competition binding at alpha1A- and alpha1B-adrenoceptors in rat submaxillary gland and liver.	Thioridazine	102-114	adrenoceptor alpha 1B	Rattus norvegicus	17-37
15795647-4	2005	Thioridazine suppressed the pseudocholinesterase activity of human serum by up to 19% during the 120-minute incubation period, and this effect was more pronounced at higher thioridazine concentrations.	Thioridazine	0-12	butyrylcholinesterase	Homo sapiens	28-48
15795647-4	2005	Thioridazine suppressed the pseudocholinesterase activity of human serum by up to 19% during the 120-minute incubation period, and this effect was more pronounced at higher thioridazine concentrations.	Thioridazine	173-185	butyrylcholinesterase	Homo sapiens	28-48
15795647-5	2005	These findings suggest that thioridazine may prolong the serum half-life of cocaine by inhibiting the pseudocholinesterase-mediated catabolism of cocaine to ecgonine methyl ester.	Thioridazine	28-40	butyrylcholinesterase	Homo sapiens	102-122
16051556-8	2005	Thioridazine, perphenazine, trifluoperazine, and chlorpromazine blocked hERG potassium channels with the following IC(50) values: IC(50) values were 224 +/- 42 nM for thioridazine, 1003 +/- 71 nM for perphenazine, 1406 +/- 124 nM for trifluoperazine, and 1561 +/- 281 nM for chloropromazine.	Thioridazine	167-179	ETS transcription factor ERG	Homo sapiens	72-76
16051556-9	2005	Inhibition of hERG channels by thioridazine was characterized by significant changes in voltage dependence, the value of V(1/2), the half-maximal activation potential, and shift into negative potential, that is, the amount of block was greater at more positive potential.	Thioridazine	31-43	ETS transcription factor ERG	Homo sapiens	14-18
16051556-6	2005	Therefore, we investigated the effects of four distinct phenothiazine drugs (thioridazine, chlorpromazine, trifluoperazine, and perphenazine) on hERG channel expressed in chinese hamster ovary (CHO) cells.	Thioridazine	77-89	ETS transcription factor ERG	Homo sapiens	145-149
15489264-8	2004	We show that some antihistaminic compounds (hydroxyzine and promethazine) and other pharmacological compounds with a related structure (including thioridazine and sertraline) kill tumor cells and significantly decrease the level of TCTP.	Thioridazine	146-158	tumor protein, translationally-controlled 1	Homo sapiens	232-236
16051556-8	2005	Thioridazine, perphenazine, trifluoperazine, and chlorpromazine blocked hERG potassium channels with the following IC(50) values: IC(50) values were 224 +/- 42 nM for thioridazine, 1003 +/- 71 nM for perphenazine, 1406 +/- 124 nM for trifluoperazine, and 1561 +/- 281 nM for chloropromazine.	Thioridazine	0-12	ETS transcription factor ERG	Homo sapiens	72-76
15572279-5	2005	Thioridazine (Ki=15 microM) was the most potent inhibitor of the rat CYP2D among the drugs studied, whose effect was more pronounced than that of the other neuroleptics tested: phenothiazines (Ki=18-23 microM), haloperidol (Ki=32 microM), sertindole (Ki=51 microM) or risperidone (Ki=165 microM).	Thioridazine	0-12	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	69-74
15374578-5	2004	Typical antipsychotics haloperidol, thioridazine and chlorpromazine non-selectively inhibited [(14)C]glycine uptake mediated by GlyT1a and GlyT2 with potency of 9-21 microM.	Thioridazine	36-48	solute carrier family 6 member 5	Homo sapiens	139-144
15542767-6	2004	In contrast, Kir1.1 and Kir2.1 channels were insensitive to ethanol and various SSRIs and antipsychotics, although thioridazine weakly inhibited Kir1.1 channels.	Thioridazine	115-127	potassium inwardly-rectifying channel, subfamily J, member 1	Mus musculus	145-151
15107661-3	2004	Sexual dysfunction related to hyperprolactinemia is commonly described, but ejaculatory disturbance due to potent alpha1 adrenergic antagonism may also occur, and has been reported frequently with certain typical antipsychotics such as thioridazine, but rarely with atypical antipsychotics.	Thioridazine	236-248	adrenoceptor alpha 1D	Homo sapiens	114-120
15260906-1	2004	The role of certain drug metabolizing enzymes in cardiotoxicity, such as CYP2D6 for thioridazine, has been suggested.	Thioridazine	84-96	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	73-79
14997012-11	2004	After 4-h exposure to thioridazine (25 and 50 microM), a 25- to 30-fold increase in caspase-3 activity in neuroblastoma cells was noted.	Thioridazine	22-34	caspase 3	Homo sapiens	84-93
15076020-3	2004	Sexual dysfunction related to hyperprolactinemia is commonly described, but ejaculatory disturbance due to potent alpha1 adrenergic antagonism may also occur, and has been reported frequently with certain typical antipsychotics such as thioridazine, but rarely with atypical antipsychotics.	Thioridazine	236-248	adrenoceptor alpha 1D	Homo sapiens	114-120
12957233-10	2003	According to plasma IC50, THIO, CPZ and CLO are potent cholinesterase inhibitors.	Thioridazine	26-30	butyrylcholinesterase	Rattus norvegicus	55-69
12566082-11	2003	TFP, TMX and thioridazine inhibited the activity of Kv1.3 channels only when applied extracellularly.	Thioridazine	13-25	potassium voltage-gated channel subfamily A member 3	Homo sapiens	52-57
12682803-0	2003	Thioridazine steady-state plasma concentrations are influenced by tobacco smoking and CYP2D6, but not by the CYP2C9 genotype.	Thioridazine	0-12	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	86-92
12682803-2	2003	The disposition of thioridazine has been related to the CYP2D6 phenotype.	Thioridazine	19-31	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	56-62
12682803-3	2003	The present study aimed to evaluate the influence of CYP2D6 and CYP2C9 genotypes, and tobacco smoking on steady-state thioridazine plasma levels.	Thioridazine	118-130	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	53-59
12682803-3	2003	The present study aimed to evaluate the influence of CYP2D6 and CYP2C9 genotypes, and tobacco smoking on steady-state thioridazine plasma levels.	Thioridazine	118-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
12682803-6	2003	RESULTS: The median dose-corrected, steady-state plasma concentrations (C/D) of thioridazine were related to the number of functional CYP2D6 alleles ( P<0.01), being 15.2, 7.2, 4.0, 4.2 nmol/l per milligram in subjects with no, one, two, and three or more functional CYP2D6 genes, respectively.	Thioridazine	80-92	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	134-140
12682803-6	2003	RESULTS: The median dose-corrected, steady-state plasma concentrations (C/D) of thioridazine were related to the number of functional CYP2D6 alleles ( P<0.01), being 15.2, 7.2, 4.0, 4.2 nmol/l per milligram in subjects with no, one, two, and three or more functional CYP2D6 genes, respectively.	Thioridazine	80-92	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	270-276
12682803-12	2003	CONCLUSION: The results show that the plasma concentrations of thioridazine and its metabolites are influenced by tobacco smoking and the CYP2D6 genotype, and support the dose-dependent inhibition of CYP2D6 by thioridazine.	Thioridazine	63-75	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	138-144
12682803-12	2003	CONCLUSION: The results show that the plasma concentrations of thioridazine and its metabolites are influenced by tobacco smoking and the CYP2D6 genotype, and support the dose-dependent inhibition of CYP2D6 by thioridazine.	Thioridazine	63-75	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	200-206
12682803-12	2003	CONCLUSION: The results show that the plasma concentrations of thioridazine and its metabolites are influenced by tobacco smoking and the CYP2D6 genotype, and support the dose-dependent inhibition of CYP2D6 by thioridazine.	Thioridazine	210-222	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	138-144
12682803-12	2003	CONCLUSION: The results show that the plasma concentrations of thioridazine and its metabolites are influenced by tobacco smoking and the CYP2D6 genotype, and support the dose-dependent inhibition of CYP2D6 by thioridazine.	Thioridazine	210-222	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	200-206
12208554-8	2002	5-Sulfoxidation of these drugs may be mediated by different isoenzymes, e.g. CYP2D1 (promazine and perazine), CYP2B2 (perazine) and CYP1A2 (thioridazine).	Thioridazine	140-152	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	132-138
12442016-1	2002	PURPOSE: We evaluated the calcium channel blocking activity of thioridazine, clomipramine and fluoxetine in isolated rat vas deferens and determined their relative order of potency.	Thioridazine	63-75	arginine vasopressin	Rattus norvegicus	121-124
12503836-9	2002	CYP2D6 enzyme hydroxylation capacity, evaluated by debrisoquine metabolic ratio (MR) (p < 0.05) and thioridazine/mesoridazine ratio (p < 0.05), was also correlated with QTc intervals.	Thioridazine	103-115	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-6
12503836-12	2002	Patients with impaired CYP2D6 enzyme activity due to enzyme inhibition by thioridazine might be more prone to increased risk of sudden death due to torsade de pointes type cardiac dysrhythmia.	Thioridazine	74-86	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	23-29
12083975-1	2002	Many antipsychotics, including perphenazine, zuclopenthixol, thioridazine, haloperidol and risperidone, are metabolised to a significant extent by the polymorphic cytochrome P450 (CYP) 2D6, which shows large interindividual variation in activity.	Thioridazine	61-73	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	163-188
12176106-7	2002	We found that sertindole, pimozide and thioridazine displayed little (<10-fold) or no selectivity for dopamine D(2) or 5-HT(2A) receptors relative to their HERG channel affinities.	Thioridazine	39-51	5-hydroxytryptamine receptor 2A	Homo sapiens	124-129
12176106-7	2002	We found that sertindole, pimozide and thioridazine displayed little (<10-fold) or no selectivity for dopamine D(2) or 5-HT(2A) receptors relative to their HERG channel affinities.	Thioridazine	39-51	potassium voltage-gated channel subfamily H member 2	Homo sapiens	159-163
12065442-5	2002	KM values spanned an 80-fold range from 0.12 microM (CYP2D6-catalyzed thioridazine S-oxidation) to 9.8 microM (CYP2C19-catalyzed imipramine N-demethylation).	Thioridazine	70-82	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	53-59
12065442-5	2002	KM values spanned an 80-fold range from 0.12 microM (CYP2D6-catalyzed thioridazine S-oxidation) to 9.8 microM (CYP2C19-catalyzed imipramine N-demethylation).	Thioridazine	70-82	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	111-118
11976278-6	2002	We conclude that thioridazine interacts with the inner membrane of mitochondria, more likely close to its surface, acquiring antioxidant activity toward processes with potential implications in apoptosis such as O2*- accumulation, as well as LPO, MPT and associated release of cytochrome c.	Thioridazine	17-29	lactoperoxidase	Homo sapiens	242-245
11976278-6	2002	We conclude that thioridazine interacts with the inner membrane of mitochondria, more likely close to its surface, acquiring antioxidant activity toward processes with potential implications in apoptosis such as O2*- accumulation, as well as LPO, MPT and associated release of cytochrome c.	Thioridazine	17-29	cytochrome c, somatic	Homo sapiens	277-289
10780978-1	2000	To investigate the effects of various chemical classes of antipsychotic drugs: haloperidol, thioridazine, pimozide and clozapine, on the G-protein-activated inwardly rectifying K(+) (GIRK) channels, we carried out Xenopus oocyte functional assays with GIRK1 and GIRK2 mRNAs or GIRK1 and GIRK4 mRNAs.	Thioridazine	92-104	potassium inwardly rectifying channel subfamily J member 3 S homeolog	Xenopus laevis	137-181
11411819-14	2001	Of the conventional antipsychotics, chlorpromazine and thioridazine have the greatest alpha1-adrenergic affinity and have been most frequently reported to be associated with priapism.	Thioridazine	55-67	adrenoceptor alpha 1D	Homo sapiens	86-92
10942178-0	2000	Use of the mesoridazine/thioridazine ratio as a marker for CYP2D6 enzyme activity.	Thioridazine	24-36	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	59-65
10942178-1	2000	Thioridazine is metabolized in humans by CYP2D6 to mesoridazine, which is an active metabolite.	Thioridazine	0-12	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	41-47
10942178-4	2000	The goal of this study was to evaluate the use of the mesoridazine/thioridazine ratio for the estimation of CYP2D6 enzyme capacity.	Thioridazine	67-79	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	108-114
10942178-10	2000	Therefore, the authors suggest that the measurement of thioridazine and its metabolite might be a useful tool to assess CYP2D6 activity during treatment.	Thioridazine	55-67	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	120-126
11802093-0	2001	Effect of thioridazine dosage on the debrisoquine hydroxylation phenotype in psychiatric patients with different CYP2D6 genotypes.	Thioridazine	10-22	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	113-119
11802093-8	2001	The CYP2D6 hydroxylation capacity was inhibited by thioridazine as determined by the debrisoquine MR.	Thioridazine	51-63	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	4-10
11802093-9	2001	This inhibition was reversible by thioridazine withdrawal, and thus seems to be dose dependent and related to CYP2D6 genotype.	Thioridazine	34-46	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	110-116
11802093-10	2001	One must consider the effects of thioridazine dosage on CYP2D6, because it may influence the metabolism of concomitant drugs or produce clinically important adverse effects such as cardiotoxicity.	Thioridazine	33-45	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	56-62
11686961-19	2001	Compared to chlormethiazole, thioridazine was significantly inferior when assessed on some items of the CAPE and the Crichton Geriatric Behavioural Rating Scales.	Thioridazine	29-41	structural maintenance of chromosomes 2	Homo sapiens	104-108
11128236-7	2000	For those taking haloperidol or thioridazine, prolactin levels decreased when participants were on placebo.	Thioridazine	32-44	prolactin	Homo sapiens	46-55
10855463-5	2000	At the second blood sampling, after addition of thioridazine (260 mg/day), which is a strong CYP2D6 inhibitor, concentrations of venlafaxine were further increased (2.76 mg/l), and concentrations of O-desmethylvenlafaxine decreased (0.22 mg/l).	Thioridazine	48-60	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	93-99
10780978-1	2000	To investigate the effects of various chemical classes of antipsychotic drugs: haloperidol, thioridazine, pimozide and clozapine, on the G-protein-activated inwardly rectifying K(+) (GIRK) channels, we carried out Xenopus oocyte functional assays with GIRK1 and GIRK2 mRNAs or GIRK1 and GIRK4 mRNAs.	Thioridazine	92-104	potassium inwardly rectifying channel subfamily J member 3 S homeolog	Xenopus laevis	183-187
10796547-20	2000	Compared to chlormethiazole, thioridazine was significantly inferior when assessed on some items of the CAPE and the Crichton Geriatric Behavioural Rating Scales.	Thioridazine	29-41	structural maintenance of chromosomes 2	Homo sapiens	104-108
10410249-2	1999	In general, PDH phosphatase was more strongly inhibited than PDC by the calmodulin antagonists with the following potency order: fluphenazine > chlorpromazine > thioridazine > triflupromazine.	Thioridazine	167-179	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	12-15
10587283-6	1999	In conclusion, fluvoxamine markedly interferes with the metabolism of THD, probably at the CYP2C19 and/or CYP1A2 enzyme level.	Thioridazine	70-73	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
10587283-6	1999	In conclusion, fluvoxamine markedly interferes with the metabolism of THD, probably at the CYP2C19 and/or CYP1A2 enzyme level.	Thioridazine	70-73	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	106-112
10608490-6	1999	Thioridazine decreased the total CYP content and reduced CYP2C11, CYP2E1, and CYP3A.	Thioridazine	0-12	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	33-36
10608490-6	1999	Thioridazine decreased the total CYP content and reduced CYP2C11, CYP2E1, and CYP3A.	Thioridazine	0-12	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	57-64
10608490-6	1999	Thioridazine decreased the total CYP content and reduced CYP2C11, CYP2E1, and CYP3A.	Thioridazine	0-12	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	66-72
10608490-6	1999	Thioridazine decreased the total CYP content and reduced CYP2C11, CYP2E1, and CYP3A.	Thioridazine	0-12	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	78-83
10410249-2	1999	In general, PDH phosphatase was more strongly inhibited than PDC by the calmodulin antagonists with the following potency order: fluphenazine > chlorpromazine > thioridazine > triflupromazine.	Thioridazine	167-179	calmodulin 1	Homo sapiens	72-82
9435993-12	1997	As potent inhibitors of CYP2D6, both paroxetine and fluoxetine have the potential to increase the plasma concentrations of antipsychotic medications metabolised through this enzyme, including perphenazine, haloperidol, thioridazine and risperidone in patients who are CYP2D6 extensive metabolisers.	Thioridazine	219-231	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	24-30
10229929-5	1999	It is suggested that thioridazine alone or in combination with caffeine may exert its synergistic effect on melphalan cytotoxicity to cultured human lymphocytes not only indirectly, i.e. as a strong calmodulin inhibitor by facilitating the intracellular retention of melphalan, but also directly by reaction with nucleic acids and by causing scissions in and damage to them.	Thioridazine	21-33	calmodulin 1	Homo sapiens	199-209
9352572-9	1997	One patient homozygous for the defective allele CYP2D6*5 had the second highest and highest plasma concentrations of S(+)-mianserin and R-desmethylmianserin, respectively, before thioridazine coadministration, and exhibited little increase in plasma concentration of the drugs after thioridazine coadministration.	Thioridazine	179-191	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	48-54
9352572-9	1997	One patient homozygous for the defective allele CYP2D6*5 had the second highest and highest plasma concentrations of S(+)-mianserin and R-desmethylmianserin, respectively, before thioridazine coadministration, and exhibited little increase in plasma concentration of the drugs after thioridazine coadministration.	Thioridazine	283-295	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	48-54
9352572-10	1997	These results suggest that thioridazine specifically inhibits the metabolism of S(+)-mianserin and R-desmethylmianserin, probably through inhibition of CYP2D6, but not R(-)-mianserin.	Thioridazine	27-39	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	152-158
8946674-2	1996	This probably occurred in an individual with genetically reduced capacity for oxidative drug metabolism, specifically via thioridazine"s interference with the hepatic cytochrome P450IID6 isoenzyme (CYP2D6).	Thioridazine	122-134	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	198-204
9169102-0	1997	Serotonin decreases cytoskeletal and cytosolic glycolytic enzymes and the levels of ATP and glucose 1,6-bisphosphate in skin, which is prevented by the calmodulin antagonists thioridazine and clotrimazole.	Thioridazine	175-187	calmodulin 1	Rattus norvegicus	152-162
9143866-5	1997	The substrates of CYP2D6 such as thioridazine, amitriptyline and metoprolol inhibited the O-demethylation of codeine preferentially, while the substrates of CYP3A4 such as cyclosporine A, midazolam and erythromycin were all strong inhibitors of the N-demethylation of codeine.	Thioridazine	33-45	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	18-24
9143866-5	1997	The substrates of CYP2D6 such as thioridazine, amitriptyline and metoprolol inhibited the O-demethylation of codeine preferentially, while the substrates of CYP3A4 such as cyclosporine A, midazolam and erythromycin were all strong inhibitors of the N-demethylation of codeine.	Thioridazine	33-45	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	157-163
15251546-7	1996	Discontinuing the thioridazine therapy resulted in normalization of the serum PRL and resolution of the pituitary abnormality.	Thioridazine	18-30	prolactin	Homo sapiens	78-81
8905336-5	1996	Trifluoperazine (0.5-1%) and thioridazine (2%), potent calmodulin antagonists, in Pluronic F-127 base substantially prevented the development of 2-chloroethylethyl sulfide-induced skin lesions.	Thioridazine	29-41	calmodulin 2	Mus musculus	55-65
8653995-3	1996	Cytochrome P450IID6 (CYP2D6) is involved in the formation of thioridazine 2-sulfoxide (2-SO) from thioridazine and also probably partially in the formation of thioridazine 5-sulfoxide (5-SO), but not in the formation of thioridazine 2-sulfone (2-SO2) from thioridazine 2-SO.	Thioridazine	61-73	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	21-27
8653995-4	1996	Significant correlations between the mephenytoin enantiomeric ratio and concentrations of thioridazine and metabolites suggest that cytochrome P450IIC19 could contribute to the biotransformation of thioridazine into yet-unknown metabolites, other than thioridazine 2-SO, thioridazine 2-SO2, or thioridazine 5-SO.	Thioridazine	90-102	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	143-152
8653995-4	1996	Significant correlations between the mephenytoin enantiomeric ratio and concentrations of thioridazine and metabolites suggest that cytochrome P450IIC19 could contribute to the biotransformation of thioridazine into yet-unknown metabolites, other than thioridazine 2-SO, thioridazine 2-SO2, or thioridazine 5-SO.	Thioridazine	198-210	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	143-152
7756324-2	1995	In our study, induction of 2",3"-cyclic-nucleotide 3"-phosphohydrolase (CNP), which was considered to be a membrane-associated enzyme closely associated with myelination, was inhibited with supplementation of thioridazine, followed by an increase in the relative concentration of longer chain fatty acids in cell membrane lipids, indicating that thioridazine causes impaired differentiation in the glial stem cell system.	Thioridazine	209-221	2',3'-cyclic nucleotide 3' phosphodiesterase	Homo sapiens	27-70
8542328-8	1995	Haloperidol, thioridazine and risperidone also markedly increased Fos expression in the lateral septum.	Thioridazine	13-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
7756324-2	1995	In our study, induction of 2",3"-cyclic-nucleotide 3"-phosphohydrolase (CNP), which was considered to be a membrane-associated enzyme closely associated with myelination, was inhibited with supplementation of thioridazine, followed by an increase in the relative concentration of longer chain fatty acids in cell membrane lipids, indicating that thioridazine causes impaired differentiation in the glial stem cell system.	Thioridazine	209-221	2',3'-cyclic nucleotide 3' phosphodiesterase	Homo sapiens	72-75
7756324-2	1995	In our study, induction of 2",3"-cyclic-nucleotide 3"-phosphohydrolase (CNP), which was considered to be a membrane-associated enzyme closely associated with myelination, was inhibited with supplementation of thioridazine, followed by an increase in the relative concentration of longer chain fatty acids in cell membrane lipids, indicating that thioridazine causes impaired differentiation in the glial stem cell system.	Thioridazine	346-358	2',3'-cyclic nucleotide 3' phosphodiesterase	Homo sapiens	27-70
7756324-2	1995	In our study, induction of 2",3"-cyclic-nucleotide 3"-phosphohydrolase (CNP), which was considered to be a membrane-associated enzyme closely associated with myelination, was inhibited with supplementation of thioridazine, followed by an increase in the relative concentration of longer chain fatty acids in cell membrane lipids, indicating that thioridazine causes impaired differentiation in the glial stem cell system.	Thioridazine	346-358	2',3'-cyclic nucleotide 3' phosphodiesterase	Homo sapiens	72-75
7669826-5	1995	Fluphenazine and thioridazine caused an increase of PLA2 activity in rat brain both after a single dose and long-term administration.	Thioridazine	17-29	phospholipase A2 group IB	Rattus norvegicus	52-56
21153182-4	1995	This stimulatory effect of insulin could be prevented by treatment with calmodulin antagonists trifluoperazine, thioridazine or CGS 9343 B (a potent and selective inhibitor of calmodulin activity), which strongly suggests that calmodulin is involved in this action of insulin.	Thioridazine	112-124	insulin	Homo sapiens	27-34
21153182-4	1995	This stimulatory effect of insulin could be prevented by treatment with calmodulin antagonists trifluoperazine, thioridazine or CGS 9343 B (a potent and selective inhibitor of calmodulin activity), which strongly suggests that calmodulin is involved in this action of insulin.	Thioridazine	112-124	calmodulin 1	Homo sapiens	72-82
21153182-4	1995	This stimulatory effect of insulin could be prevented by treatment with calmodulin antagonists trifluoperazine, thioridazine or CGS 9343 B (a potent and selective inhibitor of calmodulin activity), which strongly suggests that calmodulin is involved in this action of insulin.	Thioridazine	112-124	calmodulin 1	Homo sapiens	176-186
21153182-4	1995	This stimulatory effect of insulin could be prevented by treatment with calmodulin antagonists trifluoperazine, thioridazine or CGS 9343 B (a potent and selective inhibitor of calmodulin activity), which strongly suggests that calmodulin is involved in this action of insulin.	Thioridazine	112-124	calmodulin 1	Homo sapiens	176-186
8224738-3	1993	Electron microscopic studies have revealed that calmodulin (CaM) antagonists, trifluoperazine, thioridazine, pimozide and CGS 9343B, were most effective in preserving muscle structure.	Thioridazine	95-107	calmodulin 1	Rattus norvegicus	48-58
7898773-4	1994	5-HT2A receptors: risperidone (9.07) > spiperone > chlorpromazine > clozapine > thioridazine = fluphenazine > haloperidol (6.03).	Thioridazine	92-104	5-hydroxytryptamine receptor 2A	Rattus norvegicus	0-6
7898773-5	1994	5-HT2C receptors: clozapine (7.19) > chlorpromazine > risperidone > thioridazine > fluphenazine > spiperone > haloperidol (< 4.00).	Thioridazine	77-89	5-hydroxytryptamine receptor 2C	Rattus norvegicus	0-6
8302284-1	1994	P-type Ca2+ channels in cerebellar Purkinje neurons and N-type Ca2+ channels in sympathetic neurons were found to be inhibited by D2 dopamine receptor antagonists with diverse structures, including phenothiazines (chlorpromazine and thioridazine), diphenylbutylpiperidines (fluspirilene and pimozide), butyrophenones (haloperidol and spiperone), and a piperazine (fluphenazine).	Thioridazine	233-245	dopamine receptor D2	Homo sapiens	130-150
8224738-3	1993	Electron microscopic studies have revealed that calmodulin (CaM) antagonists, trifluoperazine, thioridazine, pimozide and CGS 9343B, were most effective in preserving muscle structure.	Thioridazine	95-107	calmodulin 1	Rattus norvegicus	60-63
2055234-7	1991	These results indicate that the action of thioridazine during electromechanical coupling in the human and rat vas deferens may involve more than its blockade of voltage gated Ca2+ channels.	Thioridazine	42-54	arginine vasopressin	Rattus norvegicus	110-113
1672374-5	1991	The neuroleptics thioridazine and chlorpromazine also decreased thrombin-stimulated [3H]IP2 and [3H]IP3 production but not [3H]IP1 in human platelets, whereas haloperidol had no significant effect.	Thioridazine	17-29	coagulation factor II, thrombin	Homo sapiens	64-72
1672374-5	1991	The neuroleptics thioridazine and chlorpromazine also decreased thrombin-stimulated [3H]IP2 and [3H]IP3 production but not [3H]IP1 in human platelets, whereas haloperidol had no significant effect.	Thioridazine	17-29	inhibitor of nuclear factor kappa B kinase regulatory subunit gamma	Homo sapiens	88-91
1663111-3	1991	Other calmodulin antagonists, such as trifluoperazine, thioridazine, and W-7, also inhibited the Ni(2+)-stimulated phosphatase activity.	Thioridazine	55-67	calmodulin 1	Homo sapiens	6-16
2386945-13	1990	We conclude that pimozide and thioridazine may be useful in the control of estradiol- and polypeptide hormone-induced growth of ER-positive and ER-negative human breast tumors.	Thioridazine	30-42	estrogen receptor 1	Homo sapiens	128-130
2386945-13	1990	We conclude that pimozide and thioridazine may be useful in the control of estradiol- and polypeptide hormone-induced growth of ER-positive and ER-negative human breast tumors.	Thioridazine	30-42	estrogen receptor 1	Homo sapiens	144-146
2315954-0	1990	Modulation of the course of CCl4-induced liver injury by the anti-calmodulin drug thioridazine.	Thioridazine	82-94	calmodulin 1	Rattus norvegicus	66-76
1971007-3	1990	All three atypical neuroleptics studied increased PEK mRNA in the following order: anterior-CPU, thioridazine greater than clozapine and molindone; medial-CPU, thioridazine and molindone greater than clozapine; and NAc, thioridazine much greater than molindone and clozapine.	Thioridazine	97-109	proenkephalin	Rattus norvegicus	50-53
1971007-3	1990	All three atypical neuroleptics studied increased PEK mRNA in the following order: anterior-CPU, thioridazine greater than clozapine and molindone; medial-CPU, thioridazine and molindone greater than clozapine; and NAc, thioridazine much greater than molindone and clozapine.	Thioridazine	160-172	proenkephalin	Rattus norvegicus	50-53
1971007-3	1990	All three atypical neuroleptics studied increased PEK mRNA in the following order: anterior-CPU, thioridazine greater than clozapine and molindone; medial-CPU, thioridazine and molindone greater than clozapine; and NAc, thioridazine much greater than molindone and clozapine.	Thioridazine	160-172	proenkephalin	Rattus norvegicus	50-53
2315954-0	1990	Modulation of the course of CCl4-induced liver injury by the anti-calmodulin drug thioridazine.	Thioridazine	82-94	C-C motif chemokine ligand 4	Rattus norvegicus	28-32
2315954-6	1990	TDZ administration decreased calcium liver content in CCl4-poisoned animals but did not change the intensity of CCl4-induced fatty liver.	Thioridazine	0-3	C-C motif chemokine ligand 4	Rattus norvegicus	54-58
2315954-9	1990	TDZ-lowering effects on body temperature might also be a determinant in the delaying effects of this drug on the onset of CCl4-induced necrosis.	Thioridazine	0-3	C-C motif chemokine ligand 4	Rattus norvegicus	122-126
34571136-0	2021	Thioridazine reverts the phenotype in cellular and Drosophila models of amyotrophic lateral sclerosis by enhancing TDP-43 aggregate clearance.	Thioridazine	0-12	TAR DNA-binding protein-43 homolog	Drosophila melanogaster	115-121
2606333-0	1989	Treatment of frostbite with the calmodulin antagonists thioridazine and trifluoperazine.	Thioridazine	55-67	calmodulin 1	Homo sapiens	32-42
2606333-2	1989	Thioridazine and trifluoperazine, which have been previously found in this laboratory to be the most effective calmodulin antagonists in treatment of burns, are shown here to be also effective in the treatment of frostbite.	Thioridazine	0-12	calmodulin 1	Homo sapiens	111-121
34472703-0	2022	Revisiting the molecular interactions between the tumor protein TCTP and the drugs sertraline/thioridazine.	Thioridazine	94-106	tumor protein, translationally-controlled 1	Homo sapiens	64-68
34472703-2	2022	The direct interaction of TCTP with the drugs sertraline and thioridazine has been reported in vitro by SPR experiments to be in the ~30-50 microM Kd range (Amson et al.	Thioridazine	61-73	tumor protein, translationally-controlled 1	Homo sapiens	26-30
34472703-2	2022	The direct interaction of TCTP with the drugs sertraline and thioridazine has been reported in vitro by SPR experiments to be in the ~30-50 microM Kd range (Amson et al.	Thioridazine	61-73	sepiapterin reductase	Homo sapiens	104-107
34472703-7	2022	Here, we combined NMR, TSA, SPR, BLI and ITC techniques to probe the molecular interactions between TCTP with the drugs sertraline and thioridazine.	Thioridazine	135-147	sepiapterin reductase	Homo sapiens	28-31
34472703-7	2022	Here, we combined NMR, TSA, SPR, BLI and ITC techniques to probe the molecular interactions between TCTP with the drugs sertraline and thioridazine.	Thioridazine	135-147	tumor protein, translationally-controlled 1	Homo sapiens	100-104
34571136-10	2021	Our findings have important implications as thioridazine cleared TDP-43 aggregates and recovered TDP-43 functionality.	Thioridazine	44-56	TAR DNA-binding protein-43 homolog	Drosophila melanogaster	65-71
34571136-10	2021	Our findings have important implications as thioridazine cleared TDP-43 aggregates and recovered TDP-43 functionality.	Thioridazine	44-56	TAR DNA-binding protein-43 homolog	Drosophila melanogaster	97-103
2576023-17	1989	Our results suggest that, in the peripheral nervous system of the rat, haloperidol and sulpiride act as antagonists of DA2 receptors while chlorpromazine and thioridazine antagonized DA1 receptors.	Thioridazine	158-170	RT1 class II, locus Da	Rattus norvegicus	183-186
35399625-5	2022	After thioridazine treatment, levels of glutathione, and BRCA2, RAD51, and ERCC1 proteins were decreased.	Thioridazine	6-18	BRCA2 DNA repair associated	Homo sapiens	57-62
35399625-5	2022	After thioridazine treatment, levels of glutathione, and BRCA2, RAD51, and ERCC1 proteins were decreased.	Thioridazine	6-18	RAD51 recombinase	Homo sapiens	64-69
35399625-5	2022	After thioridazine treatment, levels of glutathione, and BRCA2, RAD51, and ERCC1 proteins were decreased.	Thioridazine	6-18	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	75-80
35153769-5	2021	Blasts t (6; 11) KMT2A-AFDN rearranged, both from cell lines and primary samples, were shown to be significantly highly responsive to the combination of venetoclax and thioridazine, with the synergy being induced by a dramatic increase of mitochondrial depolarization that triggered blast apoptosis.	Thioridazine	168-180	lysine methyltransferase 2A	Homo sapiens	17-22
35153769-5	2021	Blasts t (6; 11) KMT2A-AFDN rearranged, both from cell lines and primary samples, were shown to be significantly highly responsive to the combination of venetoclax and thioridazine, with the synergy being induced by a dramatic increase of mitochondrial depolarization that triggered blast apoptosis.	Thioridazine	168-180	afadin, adherens junction formation factor	Homo sapiens	23-27
2604739-4	1989	Thioridazine was a potent linear mixed-type inhibitor of P-450b-dependent 7-pentoxyresorufin O-depentylase activity in phenobarbital-induced rat liver.	Thioridazine	0-12	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	57-63
2604739-8	1989	This finding is consistent with the relative capacity of thioridazine to inhibit oxidase activities catalyzed by P-450b and P-450c.	Thioridazine	57-69	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	113-119
2604739-8	1989	This finding is consistent with the relative capacity of thioridazine to inhibit oxidase activities catalyzed by P-450b and P-450c.	Thioridazine	57-69	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	124-130
34415167-2	2021	Herein, we employed an integrative approach by combining NMR, X-ray crystallography, and enzyme inhibition kinetics to understand the inhibition modes of three hAOX1 inhibitors-thioridazine, benzamidine, and raloxifene.	Thioridazine	177-189	aldehyde oxidase 1	Homo sapiens	160-165
2714615-6	1989	Of all the compounds investigated here, the most effective were trifluoperazine and thioridazine, which are also known as the more potent calmodulin antagonists.	Thioridazine	84-96	calmodulin 1	Rattus norvegicus	138-148
2474349-6	1989	The putative calmodulin antagonists, chlorpromazine, promethazine, thioridazine (phenothiazines) and W-7 (a naphthalene sulphonamide) all inhibited histamine release in the presence of divalent cations in both untreated cells and in RPMC depleted of their intracellular calcium.	Thioridazine	67-79	calmodulin 1	Rattus norvegicus	13-23
2805571-0	1989	Prevention of anaphylactoid shock in the rat by the calmodulin antagonist thioridazine.	Thioridazine	74-86	calmodulin 1	Rattus norvegicus	52-62
2848236-2	1988	Being added from the mucous or serous membranes, Ca channel blocker (fendiline) and calmodulin antagonist (thioridazine) inhibit the water effect of ADH.	Thioridazine	107-119	calmodulin 1	Homo sapiens	84-94
2849726-2	1988	(+)-Thioridazine was shown to have 2.7 and 4.5 times higher affinity than (-)-thioridazine for D2 and alpha-1 receptors, respectively.	Thioridazine	0-16	solute carrier family 3 member 1	Rattus norvegicus	95-119
2849726-2	1988	(+)-Thioridazine was shown to have 2.7 and 4.5 times higher affinity than (-)-thioridazine for D2 and alpha-1 receptors, respectively.	Thioridazine	74-90	solute carrier family 3 member 1	Rattus norvegicus	95-119
3509283-2	1987	Thioridazine hapten was coupled to bovine serum albumin, whereas the haptens for mesoridazine and sulforidazine were coupled to porcine thyroglobulin.	Thioridazine	0-12	albumin	Oryctolagus cuniculus	42-55
3039914-9	1987	A variety of structurally diverse calmodulin antagonists examined were also found to effectively protect P-450Ch7 alpha from deactivation; these include calmidazolium and tamoxifen (IC50 = 25 to 50 microM), chlorpromazine, thioridazine, amitriptyline, imipramine, and the naphthalene sulfonamide compound W-7 (IC50 = 50 to 300 microM).	Thioridazine	223-235	calmodulin 1	Rattus norvegicus	34-44
2892222-6	1987	There was a positive correlation between serum neuroleptic and prolactin concentrations for the patients taking haloperidol (r = 0.620, P less than 0.001) or thioridazine (r = 0.542, P less than 0.001).	Thioridazine	158-170	prolactin	Homo sapiens	63-72
2885243-1	1987	Ca2+ channel blocker (sensit) and calmodulin antagonists (thioridazine, perphenazine, oxyprothepine) applied to the mucosal side of frog urinary bladder, weakened the response of epithelial cells to vasopressin.	Thioridazine	58-70	calmodulin 1	Homo sapiens	34-44
2885243-1	1987	Ca2+ channel blocker (sensit) and calmodulin antagonists (thioridazine, perphenazine, oxyprothepine) applied to the mucosal side of frog urinary bladder, weakened the response of epithelial cells to vasopressin.	Thioridazine	58-70	arginine vasopressin	Homo sapiens	199-210
3484705-0	1986	Thioridazine enhances lysosomal accumulation of epidermal growth factor and toxicity of conjugates of epidermal growth factor with Pseudomonas exotoxin.	Thioridazine	0-12	epidermal growth factor	Homo sapiens	48-71
3484705-0	1986	Thioridazine enhances lysosomal accumulation of epidermal growth factor and toxicity of conjugates of epidermal growth factor with Pseudomonas exotoxin.	Thioridazine	0-12	epidermal growth factor	Homo sapiens	102-125
3484705-4	1986	The release of radioactivity associated with [125I]EGF into medium was slow in the presence of thioridazine.	Thioridazine	95-107	epidermal growth factor	Homo sapiens	51-54
3484705-1	1986	Thioridazine, a phenothiazine calmodulin inhibitor, aggravated the cytotoxic effect of a conjugate (EGF-PE) of epidermal growth factor (EGF) coupled with Pseudomonas exotoxin against cultured HeLa cells.	Thioridazine	0-12	calmodulin 1	Homo sapiens	30-40
3484705-5	1986	The Percoll gradient centrifugation pattern showed that thioridazine delayed both the appearance of [125I]EGF in lysosomes and the disappearance of [125I]EGF from the lysosomes.	Thioridazine	56-68	epidermal growth factor	Homo sapiens	106-109
3484705-5	1986	The Percoll gradient centrifugation pattern showed that thioridazine delayed both the appearance of [125I]EGF in lysosomes and the disappearance of [125I]EGF from the lysosomes.	Thioridazine	56-68	epidermal growth factor	Homo sapiens	154-157
3484705-1	1986	Thioridazine, a phenothiazine calmodulin inhibitor, aggravated the cytotoxic effect of a conjugate (EGF-PE) of epidermal growth factor (EGF) coupled with Pseudomonas exotoxin against cultured HeLa cells.	Thioridazine	0-12	epidermal growth factor	Homo sapiens	100-103
3484705-1	1986	Thioridazine, a phenothiazine calmodulin inhibitor, aggravated the cytotoxic effect of a conjugate (EGF-PE) of epidermal growth factor (EGF) coupled with Pseudomonas exotoxin against cultured HeLa cells.	Thioridazine	0-12	epidermal growth factor	Homo sapiens	111-134
3484705-7	1986	Thioridazine was found to inhibit lysosomal enzyme activities of cathepsin B and acid phosphatase, but not beta-hexosaminidase when cell extracts were treated with the drug.	Thioridazine	0-12	cathepsin B	Homo sapiens	65-76
3484705-1	1986	Thioridazine, a phenothiazine calmodulin inhibitor, aggravated the cytotoxic effect of a conjugate (EGF-PE) of epidermal growth factor (EGF) coupled with Pseudomonas exotoxin against cultured HeLa cells.	Thioridazine	0-12	epidermal growth factor	Homo sapiens	136-139
3484705-9	1986	The potentiating action of EGF-PE by thioridazine is discussed in relation to the altered lysosomal function in treated cells.	Thioridazine	37-49	epidermal growth factor	Homo sapiens	27-30
3484705-3	1986	By using iodinated epidermal growth factor ( [125I]EGF), the effect of thioridazine on intracellular transport of EGF was examined.	Thioridazine	71-83	epidermal growth factor	Homo sapiens	114-117
6720732-0	1984	Interactions between thioridazine and bromocriptine in a patient with a prolactin-secreting pituitary adenoma.	Thioridazine	21-33	prolactin	Homo sapiens	72-81
4065553-1	1985	Thioridazine was found to increase the serum prolactin level as well as the tumor size of a prolactin--secreting pituitary chromophobe adenoma in a schizophrenic man.	Thioridazine	0-12	prolactin	Homo sapiens	45-54
4065553-1	1985	Thioridazine was found to increase the serum prolactin level as well as the tumor size of a prolactin--secreting pituitary chromophobe adenoma in a schizophrenic man.	Thioridazine	0-12	prolactin	Homo sapiens	92-101
6720732-4	1984	His serum prolactin level fell to the 400 ng/ml range during bromocriptine therapy but rose whenever the antipsychotic thioridazine was added to his regimen.	Thioridazine	119-131	prolactin	Homo sapiens	10-19
6652340-4	1983	The anti-haemolytic effect of low concentrations of chlorpromazine or thioridazine was diminished by previous exposure of red cells to neuraminidase and/or trypsin.	Thioridazine	70-82	neuraminidase 1	Homo sapiens	135-148
6137352-1	1983	Syndrome malin refers to neuroleptic malignant syndrome (NMS), a combination of extrapyramidal symptoms, hyperthermia, autonomic dysfunction, hypertension, and coma, which has been reported primarily with haloperidol administration, but also with fluphenazine, thiothixene, and thioridazine.	Thioridazine	278-290	NHL repeat containing E3 ubiquitin protein ligase 1	Homo sapiens	9-14
7247630-0	1981	Motility, Parkinsonism, and prolactin with thiothixene and thioridazine.	Thioridazine	59-71	prolactin	Homo sapiens	28-37
7178223-5	1982	The most potent inhibitors of AHH activity were captan, BHA, chlorpromazine, thioridazine, disulfiram and menadione.	Thioridazine	77-89	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	30-33
6170412-5	1981	Chlorpromazine, trifluoperazine, thioridazine, chlorprothixene and amitriptyline inhibited amylase secretion stimulated by carbachol, A-23187, and cholecystokinin-pancreozymin but not that elicited by dibutyryl cyclic AMP secretin or vasoactive intestinal peptide (VIP).	Thioridazine	33-45	vasoactive intestinal peptide	Homo sapiens	265-268
23087-6	1978	Relative prolactin-stimulating potency in humans of chlorpromazine, thioridazine, trifluoperazine, butaperazine, and haloperidol correlated well with their relative clinical potencies.	Thioridazine	68-80	prolactin	Homo sapiens	9-18
7308732-0	1981	Oxidation of human oxyhemoglobin by thioridazine and related drugs in the presence of ceruloplasmin.	Thioridazine	36-48	ceruloplasmin	Homo sapiens	86-99
6932868-0	1980	The effect of thioridazine on prolactin levels in acutely schizophrenic patients: challenge-dose and steady-state levels.	Thioridazine	14-26	prolactin	Homo sapiens	30-39
6932868-1	1980	Prolactin (PRL) levels in unmedicated male patients with acute schizophrenia were within normal range at baseline, increased five fold after a challenge dose of thioridazine, did not significantly increase further after therapeutic dosages, and remained elevated for the duration of treatment.	Thioridazine	161-173	prolactin	Homo sapiens	0-9
6932868-1	1980	Prolactin (PRL) levels in unmedicated male patients with acute schizophrenia were within normal range at baseline, increased five fold after a challenge dose of thioridazine, did not significantly increase further after therapeutic dosages, and remained elevated for the duration of treatment.	Thioridazine	161-173	prolactin	Homo sapiens	11-14
6932868-2	1980	The rise in PRL levels was significantly correlated with the steady-state plasma levels of thioridazine and/or mesoridazine.	Thioridazine	91-103	prolactin	Homo sapiens	12-15
702341-4	1978	An increase in spin-probe immobilization was induced by each drug with approximate relative potencies given by the order: desmethylchlorpromazine congruent to thioridazine congruent to fluphenazine congruent to prochlorperazine congruent to trifluoperazine greater than acetophenazine congruent to triflupromazine congruent to chlorpromazine greater than promazine greater than promethazine greater than perphenazine.	Thioridazine	159-171	spindlin 1	Homo sapiens	15-19
849673-0	1977	Prolactin and psychophysiologic measures after single doses of thioridazine.	Thioridazine	63-75	prolactin	Homo sapiens	0-9
1027573-2	1976	Introduction of melleril to rats with toxic CCl4-induced hepatitis (CCl4 dosage of 0.15 ml per 100 g body weight) depresses free activity of acid phosphatase, this fall, however, failing to reach the corresponding values in intact animals.	Thioridazine	16-24	C-C motif chemokine ligand 4	Rattus norvegicus	44-48
1027573-2	1976	Introduction of melleril to rats with toxic CCl4-induced hepatitis (CCl4 dosage of 0.15 ml per 100 g body weight) depresses free activity of acid phosphatase, this fall, however, failing to reach the corresponding values in intact animals.	Thioridazine	16-24	C-C motif chemokine ligand 4	Rattus norvegicus	68-72
1259521-6	1976	Serum prolactin levels tended to be higher with thioridazine than on equivalent doses of chlorpromazine or trifluoperazine hydrochloride.	Thioridazine	48-60	prolactin	Homo sapiens	6-15
4775864-2	1973	The effects of chlorpromazine, haloperidol, and thioridazine on brain noradrenaline content elevated by previous administration of MAO inhibitors.	Thioridazine	48-60	monoamine oxidase A	Rattus norvegicus	131-134
239221-0	1975	Effect of thioridazine, clozapine and other antipsychotics on the kinetic state of tyrosine hydroxylase and on the turnover rate of dopamine in striatum and nucleus accumbens.	Thioridazine	10-22	tyrosine hydroxylase	Rattus norvegicus	83-103
1171660-1	1975	The binding of thioridazine, northioridazine, mesoridazine and sulforidazine to bovine serum albumin is studied by means of equilibrium dialysis.	Thioridazine	15-27	albumin	Homo sapiens	87-100
1120175-4	1975	We have found that thioridazine is as effective as chlorpromazine, trifluperazine, and prolixin enanthate in increasing serum prolactin levels in unmediated schizophrenic patients, indicating it is an effective dopamine-blocking agent.	Thioridazine	19-31	prolactin	Homo sapiens	126-135
4421012-1	1974	Part 5: Products of autoxidation and photo-oxidation of thioridazine hydrochloride.	Thioridazine	56-82	tankyrase	Homo sapiens	0-6
813887-1	1975	In reaction mixture containing 0,1 M NaCl and acetylcholine used as substrate, the kinetics of the inhibition of bovine erythrocyte acetylcholinesterase (EC 3.1.1.7) by thioridazine hydrochloride and thiazinamium methylsulfate imply the simultaneous binding of two thioridazine or thiazinamium molecules at the free enzyme and of two thioridazine molecules at the acetylated enzyme.	Thioridazine	169-195	acetylcholinesterase	Bos taurus	132-152
813887-1	1975	In reaction mixture containing 0,1 M NaCl and acetylcholine used as substrate, the kinetics of the inhibition of bovine erythrocyte acetylcholinesterase (EC 3.1.1.7) by thioridazine hydrochloride and thiazinamium methylsulfate imply the simultaneous binding of two thioridazine or thiazinamium molecules at the free enzyme and of two thioridazine molecules at the acetylated enzyme.	Thioridazine	169-181	acetylcholinesterase	Bos taurus	132-152
239662-0	1975	Thioridazine stimulates prolactin secretion in man.	Thioridazine	0-12	prolactin	Homo sapiens	24-33
239662-2	1975	We decided to test, indirectly, thioridazine"s effects on another brain dopaminergic system, the tuberoinfundibular tract, which regulates prolactin secretion by stimulating hypothalamic secretion of prolactin-inhibiting factor.	Thioridazine	32-44	prolactin	Homo sapiens	139-148
239662-2	1975	We decided to test, indirectly, thioridazine"s effects on another brain dopaminergic system, the tuberoinfundibular tract, which regulates prolactin secretion by stimulating hypothalamic secretion of prolactin-inhibiting factor.	Thioridazine	32-44	prolactin	Homo sapiens	200-209
239662-6	1975	It is concluded that thioridazine is a potent dopamine antagonist in the tuberoinfundibular system, and it is suggested that this system"s regulation of prolactin secretion may provide a useful method for studying antipsychotic drug effects in man.	Thioridazine	21-33	prolactin	Homo sapiens	153-162
4798098-2	1973	The influence of MAO inhibitors on the behavioral actions of chlorpromazine, haloperidol, and thioridazine.	Thioridazine	94-106	monoamine oxidase A	Rattus norvegicus	17-20
32694422-10	2020	The immune response induced by cytokines (as interferon-gamma, interleukin-6, and tumor necrosis factor-alpha) was significantly stronger in mice treated with thioridazine + loratadine + R848.	Thioridazine	159-171	interferon gamma	Mus musculus	45-61
33665638-1	2021	The aberrant expression of dopamine receptors (DRDs) in acute myeloid leukemia (AML) cells has encouraged the repurposing of DRD antagonists such as thioridazine (TDZ) as anti-leukemic agents.	Thioridazine	149-161	dopamine receptor D2	Homo sapiens	47-50
33665638-1	2021	The aberrant expression of dopamine receptors (DRDs) in acute myeloid leukemia (AML) cells has encouraged the repurposing of DRD antagonists such as thioridazine (TDZ) as anti-leukemic agents.	Thioridazine	163-166	dopamine receptor D2	Homo sapiens	47-50
33969139-10	2021	Nisin and/or Thioridazine decreased PI3K/AKT mRNA and protein expression in hepatocellular carcinoma cells (HCC).	Thioridazine	13-25	AKT serine/threonine kinase 1	Homo sapiens	41-44
33969139-11	2021	Also Nisin and/or Thioridazine decreased anti-oxidative SIRT1/NRF2 mRNA expression.	Thioridazine	18-30	sirtuin 1	Homo sapiens	56-61
33969139-11	2021	Also Nisin and/or Thioridazine decreased anti-oxidative SIRT1/NRF2 mRNA expression.	Thioridazine	18-30	NFE2 like bZIP transcription factor 2	Homo sapiens	62-66
4875479-0	1967	[Thioridazine and its metabolites TPD-6 and TPO-33 Sandoz in the treatment of depressive states].	Thioridazine	1-13	thyroid peroxidase	Homo sapiens	44-47
33238129-3	2020	Knockdown of the key peroxisomal FAO enzyme, acyl-CoA oxidase 1 (ACOX1), as well as treatment with the peroxisomal FAO inhibitor thioridazine, specifically suppresses the oxidative respiration of persister cells and significantly decreases their emergence.	Thioridazine	129-141	acyl-CoA oxidase 1	Homo sapiens	65-70
33238129-4	2020	Consistently, a combination treatment of BRAF/MEK inhibitors with thioridazine in human-melanoma-bearing mice results in a durable anti-tumor response.	Thioridazine	66-78	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	41-45
33238129-4	2020	Consistently, a combination treatment of BRAF/MEK inhibitors with thioridazine in human-melanoma-bearing mice results in a durable anti-tumor response.	Thioridazine	66-78	mitogen-activated protein kinase kinase 7	Homo sapiens	46-49
32694422-10	2020	The immune response induced by cytokines (as interferon-gamma, interleukin-6, and tumor necrosis factor-alpha) was significantly stronger in mice treated with thioridazine + loratadine + R848.	Thioridazine	159-171	interleukin 6	Mus musculus	63-76
32694422-10	2020	The immune response induced by cytokines (as interferon-gamma, interleukin-6, and tumor necrosis factor-alpha) was significantly stronger in mice treated with thioridazine + loratadine + R848.	Thioridazine	159-171	tumor necrosis factor	Mus musculus	82-109
32064022-0	2020	Thioridazine Induces Cardiotoxicity via Reactive Oxygen Species-Mediated hERG Channel Deficiency and L-Type Calcium Channel Activation.	Thioridazine	0-12	ETS transcription factor ERG	Homo sapiens	73-77
32931582-0	2020	Thioridazine requires calcium influx to induce MLL-AF6-rearranged AML cell death.	Thioridazine	0-12	lysine methyltransferase 2A	Homo sapiens	47-50
32931582-0	2020	Thioridazine requires calcium influx to induce MLL-AF6-rearranged AML cell death.	Thioridazine	0-12	afadin, adherens junction formation factor	Homo sapiens	51-54
32931582-3	2020	We performed a high-throughput drug-screening assay of 1280 compounds and identified thioridazine (TDZ), a drug that was highly selective for the t(6;11)(q27;q23) MLL-AF6 (6;11)AML rearrangement, which mediates a dramatically poor (below 20%) survival rate.	Thioridazine	85-97	lysine methyltransferase 2A	Homo sapiens	163-166
32931582-3	2020	We performed a high-throughput drug-screening assay of 1280 compounds and identified thioridazine (TDZ), a drug that was highly selective for the t(6;11)(q27;q23) MLL-AF6 (6;11)AML rearrangement, which mediates a dramatically poor (below 20%) survival rate.	Thioridazine	85-97	afadin, adherens junction formation factor	Homo sapiens	167-170
32931582-3	2020	We performed a high-throughput drug-screening assay of 1280 compounds and identified thioridazine (TDZ), a drug that was highly selective for the t(6;11)(q27;q23) MLL-AF6 (6;11)AML rearrangement, which mediates a dramatically poor (below 20%) survival rate.	Thioridazine	99-102	lysine methyltransferase 2A	Homo sapiens	163-166
32931582-3	2020	We performed a high-throughput drug-screening assay of 1280 compounds and identified thioridazine (TDZ), a drug that was highly selective for the t(6;11)(q27;q23) MLL-AF6 (6;11)AML rearrangement, which mediates a dramatically poor (below 20%) survival rate.	Thioridazine	99-102	afadin, adherens junction formation factor	Homo sapiens	167-170
32447223-6	2020	Mice untreated or treated with Tio alone developed the most intense parasitemia, highest parasitic load, elevated IL-10, IL-17, IFN-gamma, and TNF-alpha plasma levels, increased N-acetylglucosaminidase and myeloperoxidase activity in the liver and skeletal muscle, as well as severe myositis and liver inflammation (P < 0.05).	Thioridazine	31-34	interleukin 10	Mus musculus	114-119
32447223-6	2020	Mice untreated or treated with Tio alone developed the most intense parasitemia, highest parasitic load, elevated IL-10, IL-17, IFN-gamma, and TNF-alpha plasma levels, increased N-acetylglucosaminidase and myeloperoxidase activity in the liver and skeletal muscle, as well as severe myositis and liver inflammation (P < 0.05).	Thioridazine	31-34	interleukin 17A	Mus musculus	121-126
32447223-6	2020	Mice untreated or treated with Tio alone developed the most intense parasitemia, highest parasitic load, elevated IL-10, IL-17, IFN-gamma, and TNF-alpha plasma levels, increased N-acetylglucosaminidase and myeloperoxidase activity in the liver and skeletal muscle, as well as severe myositis and liver inflammation (P < 0.05).	Thioridazine	31-34	interferon gamma	Mus musculus	128-137
32447223-6	2020	Mice untreated or treated with Tio alone developed the most intense parasitemia, highest parasitic load, elevated IL-10, IL-17, IFN-gamma, and TNF-alpha plasma levels, increased N-acetylglucosaminidase and myeloperoxidase activity in the liver and skeletal muscle, as well as severe myositis and liver inflammation (P < 0.05).	Thioridazine	31-34	tumor necrosis factor	Mus musculus	143-152
32447223-6	2020	Mice untreated or treated with Tio alone developed the most intense parasitemia, highest parasitic load, elevated IL-10, IL-17, IFN-gamma, and TNF-alpha plasma levels, increased N-acetylglucosaminidase and myeloperoxidase activity in the liver and skeletal muscle, as well as severe myositis and liver inflammation (P < 0.05).	Thioridazine	31-34	myeloperoxidase	Mus musculus	206-221
32309275-11	2020	Thus, it was possible to verify that thioridazine and trifluoperazine tend to increase the stability of the BCL-2 protein and can compete for the binding site with the BH3 peptide.	Thioridazine	37-49	BCL2 apoptosis regulator	Homo sapiens	108-113
32829256-4	2020	Our results reveal that thioridazine and its identified photoproducts (mesoridazine and sulforidazine) have high biological activity on the virus Mpro.	Thioridazine	24-36	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	146-150
32064022-3	2020	The present study was aimed at exploring the long-term effects of THIO on the hERG and L-type calcium channels, both of which are relevant to the development of QT prolongation.	Thioridazine	66-70	ETS transcription factor ERG	Homo sapiens	78-82
32064022-9	2020	The ROS scavenger N-acetyl cysteine (NAC) significantly attenuated hERG reduction induced by THIO and abolished the upregulation of ER stress marker proteins.	Thioridazine	93-97	ETS transcription factor ERG	Homo sapiens	67-71
32064022-10	2020	Meanwhile, THIO increased the degradation of hERG channels via disrupting hERG-Hsp70 interactions.	Thioridazine	11-15	ETS transcription factor ERG	Homo sapiens	45-49
32064022-10	2020	Meanwhile, THIO increased the degradation of hERG channels via disrupting hERG-Hsp70 interactions.	Thioridazine	11-15	ETS transcription factor ERG	Homo sapiens	74-78
32064022-17	2020	In conclusion, dysfunction of hERG channel proteins and activation of L-type calcium channels via ROS production might be the ionic mechanisms for QT prolongation induced by THIO.	Thioridazine	174-178	ETS transcription factor ERG	Homo sapiens	30-34
30737777-0	2019	Targeting the TLK1/NEK1 DDR axis with Thioridazine suppresses outgrowth of androgen independent prostate tumors.	Thioridazine	38-50	NIMA related kinase 1	Homo sapiens	19-23
31645049-10	2020	RESULTS: D2R antagonists thioridazine, pimozide, haloperidol, and remoxipride decrease spheroid formation behaviors at a selective 100 nmol/L concentration, while D2R agonists PHNO, sumanirole, and ropinirole increase the formation of spheroids.	Thioridazine	25-37	dopamine receptor D2	Homo sapiens	9-12
31645049-10	2020	RESULTS: D2R antagonists thioridazine, pimozide, haloperidol, and remoxipride decrease spheroid formation behaviors at a selective 100 nmol/L concentration, while D2R agonists PHNO, sumanirole, and ropinirole increase the formation of spheroids.	Thioridazine	25-37	dopamine receptor D2	Homo sapiens	163-166
31822725-1	2019	Several recent publications demonstrated that DRD2-targeting antipsychotics such as thioridazine induce proliferation arrest and apoptosis in diverse cancer cell types including those derived from brain, lung, colon, and breast.	Thioridazine	84-96	dopamine receptor D2	Homo sapiens	46-50
31822725-4	2019	Further, DRD2 stimulation with quinpirole, a DRD2 agonist, promotes self-renewal, even in cell lines in which thioridazine does not inhibit self-renewal.	Thioridazine	110-122	dopamine receptor D2	Homo sapiens	9-13
30737777-0	2019	Targeting the TLK1/NEK1 DDR axis with Thioridazine suppresses outgrowth of androgen independent prostate tumors.	Thioridazine	38-50	tousled like kinase 1	Homo sapiens	14-18
30737777-5	2019	Following DNA damage, addition of the TLK specific inhibitor, thioridazine (THD), impairs ATR and Chk1 activation, establishing the existence of a ADT > TLK1 > NEK1 > ATR > Chk1, DDR pathway, while its abrogation leads to apoptosis.	Thioridazine	62-74	ATR serine/threonine kinase	Homo sapiens	90-93
30737777-5	2019	Following DNA damage, addition of the TLK specific inhibitor, thioridazine (THD), impairs ATR and Chk1 activation, establishing the existence of a ADT > TLK1 > NEK1 > ATR > Chk1, DDR pathway, while its abrogation leads to apoptosis.	Thioridazine	62-74	checkpoint kinase 1	Homo sapiens	98-102
30737777-5	2019	Following DNA damage, addition of the TLK specific inhibitor, thioridazine (THD), impairs ATR and Chk1 activation, establishing the existence of a ADT > TLK1 > NEK1 > ATR > Chk1, DDR pathway, while its abrogation leads to apoptosis.	Thioridazine	62-74	tousled like kinase 1	Homo sapiens	153-157
30737777-5	2019	Following DNA damage, addition of the TLK specific inhibitor, thioridazine (THD), impairs ATR and Chk1 activation, establishing the existence of a ADT > TLK1 > NEK1 > ATR > Chk1, DDR pathway, while its abrogation leads to apoptosis.	Thioridazine	62-74	NIMA related kinase 1	Homo sapiens	160-164
30737777-5	2019	Following DNA damage, addition of the TLK specific inhibitor, thioridazine (THD), impairs ATR and Chk1 activation, establishing the existence of a ADT > TLK1 > NEK1 > ATR > Chk1, DDR pathway, while its abrogation leads to apoptosis.	Thioridazine	62-74	ATR serine/threonine kinase	Homo sapiens	167-170
30737777-5	2019	Following DNA damage, addition of the TLK specific inhibitor, thioridazine (THD), impairs ATR and Chk1 activation, establishing the existence of a ADT > TLK1 > NEK1 > ATR > Chk1, DDR pathway, while its abrogation leads to apoptosis.	Thioridazine	62-74	checkpoint kinase 1	Homo sapiens	173-177
30816566-9	2019	Thioridazine, unlike promazine, inhibited phosphorylation of AMPK in a dose dependent manner.	Thioridazine	0-12	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	61-65
31172995-4	2019	The results with the monomer of hAOX1 allowed to shed some light on the role played by thioridazine and two malonate ions that are co-crystalized in the recent X-ray structure of hAOX1.	Thioridazine	87-99	aldehyde oxidase 1	Homo sapiens	32-37
31172995-4	2019	The results with the monomer of hAOX1 allowed to shed some light on the role played by thioridazine and two malonate ions that are co-crystalized in the recent X-ray structure of hAOX1.	Thioridazine	87-99	aldehyde oxidase 1	Homo sapiens	179-184
30928383-5	2019	In addition we found that TRAMP mice treated with the TLK inhibitor, thioridazine (THD), following castration did not recover cancerous growth of their prostates.	Thioridazine	69-81	translocating chain-associating membrane protein 1	Mus musculus	26-31
30928383-5	2019	In addition we found that TRAMP mice treated with the TLK inhibitor, thioridazine (THD), following castration did not recover cancerous growth of their prostates.	Thioridazine	69-81	tousled-like kinase 2 (Arabidopsis)	Mus musculus	54-57
30816566-12	2019	CONCLUSIONS: Some dopamine receptor antagonists such as thioridazine can induce differentiation of CSC-like cells by inhibiting phosphorylation of AMPK.	Thioridazine	56-68	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	147-151
30816566-13	2019	Binding to DRD2 or DRD4 might have mediated the action of thioridazine involved in the differentiation of CSC-like cells.	Thioridazine	58-70	dopamine receptor D2	Homo sapiens	11-15
30816566-13	2019	Binding to DRD2 or DRD4 might have mediated the action of thioridazine involved in the differentiation of CSC-like cells.	Thioridazine	58-70	dopamine receptor D4	Homo sapiens	19-23
30382490-4	2019	METHODS: The effect of trifluperazine, chlorpromazine, perphenazine, thioridazine and promethazine on rat liver AOX was measured spectrophotometrically.	Thioridazine	69-81	acyl-CoA oxidase 1	Rattus norvegicus	112-115
30678307-5	2019	Notably, through whole gene expression screening with THD treatment, frizzled (Fzd) proteins, a family of G-protein-coupled receptors, were found, suggesting the participation of Wnt/beta-catenin signaling.	Thioridazine	54-57	frizzled class receptor 1	Homo sapiens	79-82
31007848-4	2019	To this end, we queried the Connectivity Map with an AXL gene signature which revealed a class of dopamine receptors antagonists named phenothiazines (Thioridazine, Fluphenazine and Trifluoperazine) typically used as anti-psychotics.	Thioridazine	151-163	AXL receptor tyrosine kinase	Homo sapiens	53-56
30678307-5	2019	Notably, through whole gene expression screening with THD treatment, frizzled (Fzd) proteins, a family of G-protein-coupled receptors, were found, suggesting the participation of Wnt/beta-catenin signaling.	Thioridazine	54-57	catenin beta 1	Homo sapiens	183-195
30678307-6	2019	After THD treatment, Fzd-1 and GSK3beta-S9 phosphorylation (inactivated form) was reduced to promote beta-catenin degradation, which attenuated P62 inhibition.	Thioridazine	6-9	frizzled class receptor 1	Homo sapiens	21-26
30678307-6	2019	After THD treatment, Fzd-1 and GSK3beta-S9 phosphorylation (inactivated form) was reduced to promote beta-catenin degradation, which attenuated P62 inhibition.	Thioridazine	6-9	glycogen synthase kinase 3 beta	Homo sapiens	31-39
30678307-6	2019	After THD treatment, Fzd-1 and GSK3beta-S9 phosphorylation (inactivated form) was reduced to promote beta-catenin degradation, which attenuated P62 inhibition.	Thioridazine	6-9	catenin beta 1	Homo sapiens	101-113
30678307-6	2019	After THD treatment, Fzd-1 and GSK3beta-S9 phosphorylation (inactivated form) was reduced to promote beta-catenin degradation, which attenuated P62 inhibition.	Thioridazine	6-9	nucleoporin 62	Homo sapiens	144-147
30678307-9	2019	Moreover, treatment with THD combined with temozolomide (TMZ) engendered increased LC3-II expression and caspase-3 activity, indicating promising drug synergism.	Thioridazine	25-28	caspase 3	Homo sapiens	105-114
30678307-10	2019	In conclusion, THD induces autophagy in GBM cells by not only upregulating AMPK activity, but also enhancing P62-mediated autophagy and apoptosis through Wnt/beta-catenin signaling.	Thioridazine	15-18	nucleoporin 62	Homo sapiens	109-112
30678307-10	2019	In conclusion, THD induces autophagy in GBM cells by not only upregulating AMPK activity, but also enhancing P62-mediated autophagy and apoptosis through Wnt/beta-catenin signaling.	Thioridazine	15-18	catenin beta 1	Homo sapiens	158-170
30182339-0	2018	In silico screening for ERalpha down modulators identifies thioridazine as an anti-proliferative agent in primary, 4OH-tamoxifen-resistant and Y537S ERalpha-expressing breast cancer cells.	Thioridazine	59-71	estrogen receptor 1	Homo sapiens	24-31
30678307-0	2019	Thioridazine Enhances P62-Mediated Autophagy and Apoptosis Through Wnt/beta-Catenin Signaling Pathway in Glioma Cells.	Thioridazine	0-12	nucleoporin 62	Homo sapiens	22-25
30678307-0	2019	Thioridazine Enhances P62-Mediated Autophagy and Apoptosis Through Wnt/beta-Catenin Signaling Pathway in Glioma Cells.	Thioridazine	0-12	catenin beta 1	Homo sapiens	71-83
30182339-8	2018	RESULTS: We found that mitoxantrone and thioridazine induced ERalpha downmodulation and prevented MCF-7 BC cell proliferation.	Thioridazine	40-52	estrogen receptor 1	Homo sapiens	61-68
30182339-10	2018	Thioridazine also reduced the ERalpha content and prevented cell proliferation in primary, Tam-resistant and genome-edited Y537S ERalpha expressing BC cells.	Thioridazine	0-12	estrogen receptor 1	Homo sapiens	30-37
30182339-10	2018	Thioridazine also reduced the ERalpha content and prevented cell proliferation in primary, Tam-resistant and genome-edited Y537S ERalpha expressing BC cells.	Thioridazine	0-12	estrogen receptor 1	Homo sapiens	129-136
30182339-11	2018	CONCLUSIONS: We suggest that modulation of the intracellular ERalpha concentration in BC cells can be exploited in in silico screens to identify anti-BC drugs and uncover a re-purposing opportunity for thioridazine in the treatment of primary and metastatic ET resistant BCs.	Thioridazine	202-214	estrogen receptor 1	Homo sapiens	61-68
30182339-0	2018	In silico screening for ERalpha down modulators identifies thioridazine as an anti-proliferative agent in primary, 4OH-tamoxifen-resistant and Y537S ERalpha-expressing breast cancer cells.	Thioridazine	59-71	estrogen receptor 1	Homo sapiens	149-156
28454238-6	2017	The effect of the DRD2 antagonist, thioridazine, on the proliferation of the AGS gastric cancer cells was determined.	Thioridazine	35-47	dopamine receptor D2	Homo sapiens	18-22
30131338-0	2018	Thioridazine inhibits self-renewal in breast cancer cells via DRD2-dependent STAT3 inhibition, but induces a G1 arrest independent of DRD2.	Thioridazine	0-12	dopamine receptor D2	Homo sapiens	62-66
30131338-0	2018	Thioridazine inhibits self-renewal in breast cancer cells via DRD2-dependent STAT3 inhibition, but induces a G1 arrest independent of DRD2.	Thioridazine	0-12	signal transducer and activator of transcription 3	Homo sapiens	77-82
30131338-4	2018	The inhibition of self-renewal by thioridazine in these cells is mediated by DRD2 inhibition.	Thioridazine	34-46	dopamine receptor D2	Homo sapiens	77-81
29960166-0	2018	ROS mediated ER stress induces Bax-Bak dependent and independent apoptosis in response to Thioridazine.	Thioridazine	90-102	BCL2 associated X, apoptosis regulator	Homo sapiens	31-34
29960166-0	2018	ROS mediated ER stress induces Bax-Bak dependent and independent apoptosis in response to Thioridazine.	Thioridazine	90-102	BCL2 antagonist/killer 1	Homo sapiens	35-38
29960166-5	2018	TDZ treatment induced nuclear condensation, mitochondrial membrane potential loss, mitochondrial cytochrome c release, activation of caspase-9 and caspase-3 substantiating mitochondrial pathways of apoptosis in cells.	Thioridazine	0-3	cytochrome c, somatic	Homo sapiens	97-109
29960166-5	2018	TDZ treatment induced nuclear condensation, mitochondrial membrane potential loss, mitochondrial cytochrome c release, activation of caspase-9 and caspase-3 substantiating mitochondrial pathways of apoptosis in cells.	Thioridazine	0-3	caspase 9	Homo sapiens	133-142
29960166-5	2018	TDZ treatment induced nuclear condensation, mitochondrial membrane potential loss, mitochondrial cytochrome c release, activation of caspase-9 and caspase-3 substantiating mitochondrial pathways of apoptosis in cells.	Thioridazine	0-3	caspase 3	Homo sapiens	147-156
29960166-6	2018	TDZ induced ROS generation and up-regulation of ER stress linked proteins, such as CHOP, BiP etc.	Thioridazine	0-3	heat shock protein family A (Hsp70) member 5	Homo sapiens	89-92
29960166-7	2018	ER stress and apoptosis caused by TDZ were prevented by ROS inhibitor N-acetyl-L-cysteine (NAC) and protein synthesis inhibitor cycloheximide.	Thioridazine	34-37	X-linked Kx blood group	Homo sapiens	91-94
29960166-13	2018	Conclusively, TDZ induced Bax-Bak dependent and independent apoptosis by enhancing ROS production followed by ER stress.	Thioridazine	14-17	BCL2 associated X, apoptosis regulator	Homo sapiens	26-29
29960166-13	2018	Conclusively, TDZ induced Bax-Bak dependent and independent apoptosis by enhancing ROS production followed by ER stress.	Thioridazine	14-17	BCL2 antagonist/killer 1	Homo sapiens	30-33
29344260-0	2017	DR2 blocker thioridazine: A promising drug for ovarian cancer therapy.	Thioridazine	12-24	dopamine receptor D2	Mus musculus	0-3
29344260-3	2017	Thioridazine, a DR2 blocker, has antineoplastic activity in a variety of cancer cells.	Thioridazine	0-12	dopamine receptor D2	Mus musculus	16-19
29344260-5	2017	It was revealed that the DR2 blocker thioridazine induced cell death in a dose-dependent manner in ovarian cancer cells.	Thioridazine	37-49	dopamine receptor D2	Mus musculus	25-28
29344260-11	2017	The present study demonstrated that the DR2 blocker thioridazine exhibited anticancer effects in vitro and in vivo, suggesting that thioridazine may be used as a potential drug in ovarian cancer therapy.	Thioridazine	52-64	dopamine receptor D2	Mus musculus	40-43
29344260-11	2017	The present study demonstrated that the DR2 blocker thioridazine exhibited anticancer effects in vitro and in vivo, suggesting that thioridazine may be used as a potential drug in ovarian cancer therapy.	Thioridazine	132-144	dopamine receptor D2	Mus musculus	40-43
28649130-1	2017	Recent evidence shows that dopamine D2-like receptor (D2DR) antagonists, such as trifluoperazine and thioridazine, are effective for cancer therapy and inhibition of cancer stem-like cells (CSCs).	Thioridazine	101-113	dopamine receptor D2	Homo sapiens	54-58
30127400-7	2018	Finally, Thioridazinehydrochloride (TDZ), a potent antipsychotic drug against Schizophrenia was selected and its efficiency in inhibiting IkappaBalpha protein degradation and NF-kappaB activation was experimentally validated.	Thioridazine	9-34	NFKB inhibitor alpha	Homo sapiens	138-150
30127400-7	2018	Finally, Thioridazinehydrochloride (TDZ), a potent antipsychotic drug against Schizophrenia was selected and its efficiency in inhibiting IkappaBalpha protein degradation and NF-kappaB activation was experimentally validated.	Thioridazine	36-39	NFKB inhibitor alpha	Homo sapiens	138-150
30093531-1	2018	We completed a phase 1 dose-escalation trial to evaluate the safety of a dopamine receptor D2 (DRD2) antagonist thioridazine (TDZ), in combination with cytarabine.	Thioridazine	112-124	dopamine receptor D2	Homo sapiens	73-93
30093531-1	2018	We completed a phase 1 dose-escalation trial to evaluate the safety of a dopamine receptor D2 (DRD2) antagonist thioridazine (TDZ), in combination with cytarabine.	Thioridazine	112-124	dopamine receptor D2	Homo sapiens	95-99
30093531-1	2018	We completed a phase 1 dose-escalation trial to evaluate the safety of a dopamine receptor D2 (DRD2) antagonist thioridazine (TDZ), in combination with cytarabine.	Thioridazine	126-129	dopamine receptor D2	Homo sapiens	95-99
33052635-0	2018	Thioridazine upregulates programmed cell death 4 to induce apoptosis in nasopharyngeal carcinoma through the PI3K/Akt signalling pathway.	Thioridazine	0-12	programmed cell death 4	Homo sapiens	25-48
33052635-0	2018	Thioridazine upregulates programmed cell death 4 to induce apoptosis in nasopharyngeal carcinoma through the PI3K/Akt signalling pathway.	Thioridazine	0-12	AKT serine/threonine kinase 1	Homo sapiens	114-117
33052635-2	2018	This study aimed to investigate the link between PDCD4 and THZ in the regulation of nasopharyngeal cancer (NPC) cell proliferation.	Thioridazine	59-62	programmed cell death 4	Homo sapiens	49-54
33052635-9	2018	Furthermore, PDCD4-siRNA antagonized THZ treatment and promoted NPC cell proliferation.	Thioridazine	37-40	programmed cell death 4	Homo sapiens	13-18
33052635-11	2018	In conclusion, our findings show that THZ and PDCD4 exert antagonistic effects on NPC cell proliferation, probably through the PI3K/Akt pathway.	Thioridazine	38-41	AKT serine/threonine kinase 1	Homo sapiens	132-135
33052635-12	2018	Moreover, these results provide an insight into the mechanism by which THZ targets PDCD4 in NPC cell lines and suggest that the ectopic expression of PDCD4 is a potential therapeutic strategy.	Thioridazine	71-74	programmed cell death 4	Homo sapiens	83-88
33052635-12	2018	Moreover, these results provide an insight into the mechanism by which THZ targets PDCD4 in NPC cell lines and suggest that the ectopic expression of PDCD4 is a potential therapeutic strategy.	Thioridazine	71-74	programmed cell death 4	Homo sapiens	150-155
28806703-0	2017	NOX4-mediated ROS production induces apoptotic cell death via down-regulation of c-FLIP and Mcl-1 expression in combined treatment with thioridazine and curcumin.	Thioridazine	136-148	NADPH oxidase 4	Homo sapiens	0-4
28806703-0	2017	NOX4-mediated ROS production induces apoptotic cell death via down-regulation of c-FLIP and Mcl-1 expression in combined treatment with thioridazine and curcumin.	Thioridazine	136-148	CASP8 and FADD like apoptosis regulator	Homo sapiens	81-87
28806703-0	2017	NOX4-mediated ROS production induces apoptotic cell death via down-regulation of c-FLIP and Mcl-1 expression in combined treatment with thioridazine and curcumin.	Thioridazine	136-148	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	92-97
28806703-6	2017	Among apoptosis-related proteins, thioridazine plus curcumin induced down-regulation of c-FLIP and Mcl-1 expression at the post-translational levels in a proteasome-dependent manner.	Thioridazine	34-46	CASP8 and FADD like apoptosis regulator	Homo sapiens	88-94
28806703-6	2017	Among apoptosis-related proteins, thioridazine plus curcumin induced down-regulation of c-FLIP and Mcl-1 expression at the post-translational levels in a proteasome-dependent manner.	Thioridazine	34-46	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	99-104
28806703-7	2017	Augmentation of proteasome activity was related to the up-regulation of proteasome subunit alpha 5 (PSMA5) expression in curcumin plus thioridazine-treated cells.	Thioridazine	135-147	proteasome 20S subunit alpha 5	Homo sapiens	72-98
28806703-7	2017	Augmentation of proteasome activity was related to the up-regulation of proteasome subunit alpha 5 (PSMA5) expression in curcumin plus thioridazine-treated cells.	Thioridazine	135-147	proteasome 20S subunit alpha 5	Homo sapiens	100-105
28806703-8	2017	Combined treatment with curcumin and thioridazine produced intracellular ROS in a NOX4-dependent manner, and ROS-mediated activation of Nrf2/ARE signaling played a critical role in the up-regulation of PSMA5 expression.	Thioridazine	37-49	NADPH oxidase 4	Homo sapiens	82-86
28806703-8	2017	Combined treatment with curcumin and thioridazine produced intracellular ROS in a NOX4-dependent manner, and ROS-mediated activation of Nrf2/ARE signaling played a critical role in the up-regulation of PSMA5 expression.	Thioridazine	37-49	proteasome 20S subunit alpha 5	Homo sapiens	202-207
28806703-9	2017	Furthermore, ectopic expression of c-FLIP and Mcl-1 inhibited apoptosis in thioridazine and curcumin-treated cells.	Thioridazine	75-87	CASP8 and FADD like apoptosis regulator	Homo sapiens	35-41
28806703-9	2017	Furthermore, ectopic expression of c-FLIP and Mcl-1 inhibited apoptosis in thioridazine and curcumin-treated cells.	Thioridazine	75-87	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	46-51
28806703-10	2017	Therefore, we demonstrated that thioridazine plus curcumin induces proteasome activity by up-regulating PSMA5 expression via NOX4-mediated ROS production and that down-regulation of c-FLIP and Mcl-1 expression post-translationally is involved in apoptosis.	Thioridazine	32-44	proteasome 20S subunit alpha 5	Homo sapiens	104-109
28806703-10	2017	Therefore, we demonstrated that thioridazine plus curcumin induces proteasome activity by up-regulating PSMA5 expression via NOX4-mediated ROS production and that down-regulation of c-FLIP and Mcl-1 expression post-translationally is involved in apoptosis.	Thioridazine	32-44	NADPH oxidase 4	Homo sapiens	125-129
28806703-10	2017	Therefore, we demonstrated that thioridazine plus curcumin induces proteasome activity by up-regulating PSMA5 expression via NOX4-mediated ROS production and that down-regulation of c-FLIP and Mcl-1 expression post-translationally is involved in apoptosis.	Thioridazine	32-44	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	193-198
28454238-10	2017	Furthermore, the DRD2 antagonist, thioridazine, inhibited the growth of AGS gastric cancer cells.	Thioridazine	34-46	dopamine receptor D2	Homo sapiens	17-21
28039773-0	2017	Synthesis and SAR evaluation of novel thioridazine derivatives active against drug-resistant tuberculosis.	Thioridazine	38-50	sarcosine dehydrogenase	Homo sapiens	14-17
28228218-0	2017	[Thioridazine Sensitizes Apoptotic Effect of TRAIL in Human Lung Cancer PC9 Cells Through ER Stress Mediated Up-regulation of DR5].	Thioridazine	1-13	TNF superfamily member 10	Homo sapiens	45-50
28228218-0	2017	[Thioridazine Sensitizes Apoptotic Effect of TRAIL in Human Lung Cancer PC9 Cells Through ER Stress Mediated Up-regulation of DR5].	Thioridazine	1-13	proprotein convertase subtilisin/kexin type 9	Homo sapiens	72-75
28228218-0	2017	[Thioridazine Sensitizes Apoptotic Effect of TRAIL in Human Lung Cancer PC9 Cells Through ER Stress Mediated Up-regulation of DR5].	Thioridazine	1-13	TNF receptor superfamily member 10b	Homo sapiens	126-129
28228218-2	2017	This study is to observe the proliferation inhibition effect of TRAIL sensitized by thioridazine on PC9 cells through endoplasmic reticulum (ER) stress mediated up-regulation of death receptor 5 (DR5) and investigate its mechanism.	Thioridazine	84-96	TNF superfamily member 10	Homo sapiens	64-69
28228218-2	2017	This study is to observe the proliferation inhibition effect of TRAIL sensitized by thioridazine on PC9 cells through endoplasmic reticulum (ER) stress mediated up-regulation of death receptor 5 (DR5) and investigate its mechanism.	Thioridazine	84-96	proprotein convertase subtilisin/kexin type 9	Homo sapiens	100-103
28228218-2	2017	This study is to observe the proliferation inhibition effect of TRAIL sensitized by thioridazine on PC9 cells through endoplasmic reticulum (ER) stress mediated up-regulation of death receptor 5 (DR5) and investigate its mechanism.	Thioridazine	84-96	TNF receptor superfamily member 10b	Homo sapiens	178-194
28228218-2	2017	This study is to observe the proliferation inhibition effect of TRAIL sensitized by thioridazine on PC9 cells through endoplasmic reticulum (ER) stress mediated up-regulation of death receptor 5 (DR5) and investigate its mechanism.	Thioridazine	84-96	TNF receptor superfamily member 10b	Homo sapiens	196-199
28228218-3	2017	METHODS: PC9 cells were treated with different concentrations of thioridazine and TRAIL alone or in combination.	Thioridazine	65-77	proprotein convertase subtilisin/kexin type 9	Homo sapiens	9-12
28228218-6	2017	RESULTS: Thioridazine inhibited the proliferation of PC9 cells in a dose-dependent manner (P&lt;0.05).	Thioridazine	9-21	proprotein convertase subtilisin/kexin type 9	Homo sapiens	53-56
28228218-7	2017	Thioridazine increased the inhibition and apoptosis of PC9 cells and up-regulated the expression of cell-surface DR5 induced by TRAIL.	Thioridazine	0-12	proprotein convertase subtilisin/kexin type 9	Homo sapiens	55-58
28228218-7	2017	Thioridazine increased the inhibition and apoptosis of PC9 cells and up-regulated the expression of cell-surface DR5 induced by TRAIL.	Thioridazine	0-12	TNF receptor superfamily member 10b	Homo sapiens	113-116
28228218-7	2017	Thioridazine increased the inhibition and apoptosis of PC9 cells and up-regulated the expression of cell-surface DR5 induced by TRAIL.	Thioridazine	0-12	TNF superfamily member 10	Homo sapiens	128-133
28228218-8	2017	Flow cytometry showed that compared with TRAIL group, combination group of TRAIL and thioridazine increased cell apoptotic rates significantly (P&lt;0.05).	Thioridazine	85-97	TNF superfamily member 10	Homo sapiens	41-46
28228218-9	2017	Western blotting indicated that compared with TRAIL group, expressions of Cleaved-caspase-8, Cleaved-PARP and DR5 increased significantly in combination group of TRAIL and thioridazine.	Thioridazine	172-184	TNF superfamily member 10	Homo sapiens	46-51
28228218-9	2017	Western blotting indicated that compared with TRAIL group, expressions of Cleaved-caspase-8, Cleaved-PARP and DR5 increased significantly in combination group of TRAIL and thioridazine.	Thioridazine	172-184	caspase 8	Homo sapiens	82-91
28228218-9	2017	Western blotting indicated that compared with TRAIL group, expressions of Cleaved-caspase-8, Cleaved-PARP and DR5 increased significantly in combination group of TRAIL and thioridazine.	Thioridazine	172-184	collagen type XI alpha 2 chain	Homo sapiens	101-105
28228218-9	2017	Western blotting indicated that compared with TRAIL group, expressions of Cleaved-caspase-8, Cleaved-PARP and DR5 increased significantly in combination group of TRAIL and thioridazine.	Thioridazine	172-184	TNF receptor superfamily member 10b	Homo sapiens	110-113
28228218-11	2017	CONCLUSIONS: Thioridazine enhanced proliferation inhibition effect of TRAIL in PC9 cells may be facilitated through ER stress mediated upregulation of DR5.	Thioridazine	13-25	TNF superfamily member 10	Homo sapiens	70-75
28228218-11	2017	CONCLUSIONS: Thioridazine enhanced proliferation inhibition effect of TRAIL in PC9 cells may be facilitated through ER stress mediated upregulation of DR5.	Thioridazine	13-25	proprotein convertase subtilisin/kexin type 9	Homo sapiens	79-82
28228218-11	2017	CONCLUSIONS: Thioridazine enhanced proliferation inhibition effect of TRAIL in PC9 cells may be facilitated through ER stress mediated upregulation of DR5.	Thioridazine	13-25	TNF receptor superfamily member 10b	Homo sapiens	151-154
28000884-8	2017	The expression of some apoptosis genes (Bax and caspase-3) was upregulated after treatment with THIO, while that of the anti-apoptosis gene Bcl-2 was downregulated.	Thioridazine	96-100	BCL2 associated X, apoptosis regulator	Homo sapiens	40-43
28182008-0	2017	Thioridazine enhances sensitivity to carboplatin in human head and neck cancer cells through downregulation of c-FLIP and Mcl-1 expression.	Thioridazine	0-12	CASP8 and FADD like apoptosis regulator	Homo sapiens	111-117
28182008-0	2017	Thioridazine enhances sensitivity to carboplatin in human head and neck cancer cells through downregulation of c-FLIP and Mcl-1 expression.	Thioridazine	0-12	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	122-127
28182008-4	2017	Combined treatment with carboplatin and thioridazine induced downregulation of Mcl-1 and c-FLIP expression.	Thioridazine	40-52	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	79-84
28182008-4	2017	Combined treatment with carboplatin and thioridazine induced downregulation of Mcl-1 and c-FLIP expression.	Thioridazine	40-52	CASP8 and FADD like apoptosis regulator	Homo sapiens	89-95
28182008-5	2017	Ectopic expression of Mcl-1 and c-FLIP inhibited carboplatin plus thioridazine-induced apoptosis.	Thioridazine	66-78	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	22-27
28182008-5	2017	Ectopic expression of Mcl-1 and c-FLIP inhibited carboplatin plus thioridazine-induced apoptosis.	Thioridazine	66-78	CASP8 and FADD like apoptosis regulator	Homo sapiens	32-38
28182008-6	2017	We found that augmentation of proteasome activity had a critical role in downregulation of Mcl-1 and c-FLIP expression at the post-translational level in carboplatin plus thioridazine-treated cells.	Thioridazine	171-183	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	91-96
28182008-6	2017	We found that augmentation of proteasome activity had a critical role in downregulation of Mcl-1 and c-FLIP expression at the post-translational level in carboplatin plus thioridazine-treated cells.	Thioridazine	171-183	CASP8 and FADD like apoptosis regulator	Homo sapiens	101-107
28182008-7	2017	Furthermore, carboplatin plus thioridazine induced upregulation of the expression of proteasome subunit alpha 5 (PSMA5) through mitochondrial reactive oxygen species (ROS)-dependent nuclear factor E2-related factor 2 (Nrf2) activation.	Thioridazine	30-42	proteasome 20S subunit alpha 5	Homo sapiens	85-111
28182008-7	2017	Furthermore, carboplatin plus thioridazine induced upregulation of the expression of proteasome subunit alpha 5 (PSMA5) through mitochondrial reactive oxygen species (ROS)-dependent nuclear factor E2-related factor 2 (Nrf2) activation.	Thioridazine	30-42	proteasome 20S subunit alpha 5	Homo sapiens	113-118
28182008-7	2017	Furthermore, carboplatin plus thioridazine induced upregulation of the expression of proteasome subunit alpha 5 (PSMA5) through mitochondrial reactive oxygen species (ROS)-dependent nuclear factor E2-related factor 2 (Nrf2) activation.	Thioridazine	30-42	NFE2 like bZIP transcription factor 2	Homo sapiens	218-222
28182008-9	2017	Collectively, our study demonstrates that combined treatment with carboplatin and thioridazine induces apoptosis through proteasomal degradation of Mcl-1 and c-FLIP by upregulation of Nrf2-dependent PSMA5 expression.	Thioridazine	82-94	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	148-153
28182008-9	2017	Collectively, our study demonstrates that combined treatment with carboplatin and thioridazine induces apoptosis through proteasomal degradation of Mcl-1 and c-FLIP by upregulation of Nrf2-dependent PSMA5 expression.	Thioridazine	82-94	CASP8 and FADD like apoptosis regulator	Homo sapiens	158-164
28182008-9	2017	Collectively, our study demonstrates that combined treatment with carboplatin and thioridazine induces apoptosis through proteasomal degradation of Mcl-1 and c-FLIP by upregulation of Nrf2-dependent PSMA5 expression.	Thioridazine	82-94	NFE2 like bZIP transcription factor 2	Homo sapiens	184-188
28182008-9	2017	Collectively, our study demonstrates that combined treatment with carboplatin and thioridazine induces apoptosis through proteasomal degradation of Mcl-1 and c-FLIP by upregulation of Nrf2-dependent PSMA5 expression.	Thioridazine	82-94	proteasome 20S subunit alpha 5	Homo sapiens	199-204
28520378-0	2012	Thioridazine Therapy and CYP2D6 Genotypes Thioridazine is an antipsychotic used in the treatment of schizophrenia and psychosis.	Thioridazine	42-54	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	25-31
28520378-4	2012	The CYP2D6 enzyme is involved in metabolizing thioridazine.	Thioridazine	46-58	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	4-10
28520378-6	2012	In individuals with low CYP2D6 activity, standard doses of thioridazine may lead to higher drug levels in the plasma, and increase the risk of cardiac arrhythmias.	Thioridazine	59-71	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	24-30
28520378-7	2012	The FDA-approved drug label for thioridazine states that thioridazine is contraindicated in individuals who are known to have reduced levels of CYP2D6 activity.	Thioridazine	32-44	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	144-150
28520378-7	2012	The FDA-approved drug label for thioridazine states that thioridazine is contraindicated in individuals who are known to have reduced levels of CYP2D6 activity.	Thioridazine	57-69	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	144-150
28520378-8	2012	The label also states it is contraindicated to coadminister thioridazine with drugs that inhibit CYP2D6 (e.g., fluoxetine, paroxetine) or inhibit the metabolism of thioridazine (e.g., fluvoxamine, propranolol, and pindolol) (1).	Thioridazine	60-72	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	97-103
28000884-8	2017	The expression of some apoptosis genes (Bax and caspase-3) was upregulated after treatment with THIO, while that of the anti-apoptosis gene Bcl-2 was downregulated.	Thioridazine	96-100	caspase 3	Homo sapiens	48-57
28000884-8	2017	The expression of some apoptosis genes (Bax and caspase-3) was upregulated after treatment with THIO, while that of the anti-apoptosis gene Bcl-2 was downregulated.	Thioridazine	96-100	BCL2 apoptosis regulator	Homo sapiens	140-145
27422209-9	2016	However, thioridazine and rifapentine in a ratio of 1:3 enhanced the killing of M. tuberculosis H37Ra within the human monocyte-derived macrophages (THP-1) compared to the single drug treatments.	Thioridazine	9-21	GLI family zinc finger 2	Homo sapiens	149-154
27453171-10	2016	Thioridazine and irradiation treatment induced G0/G1 phases cell cycle arrest through down-regulation of CDK4 and cyclinD1.	Thioridazine	0-12	cyclin dependent kinase 4	Homo sapiens	105-109
27212019-8	2016	Both compounds reached in vivo CNS concentrations compatible with NOX inhibition and thioridazine significantly decreased superoxide levels in the spinal cord of SOD1(G93A) mice in vivo.	Thioridazine	85-97	superoxide dismutase 1, soluble	Mus musculus	162-166
27212019-10	2016	Thioridazine, but not perphenazine, dampened the increase of microglia markers in SOD1(G93A) mice.	Thioridazine	0-12	superoxide dismutase 1, soluble	Mus musculus	82-86
27453171-10	2016	Thioridazine and irradiation treatment induced G0/G1 phases cell cycle arrest through down-regulation of CDK4 and cyclinD1.	Thioridazine	0-12	cyclin D1	Homo sapiens	114-122
27453171-11	2016	In addition, thioridazine and irradiation treatment induced apoptosis through up-regulation of cleaved capase-3 and 9, as well as an increase in the expression of Bax and Bak and a decrease in the expression of Bcl-2 and Bcl-xl.	Thioridazine	13-25	BCL2 associated X, apoptosis regulator	Homo sapiens	163-166
27453171-11	2016	In addition, thioridazine and irradiation treatment induced apoptosis through up-regulation of cleaved capase-3 and 9, as well as an increase in the expression of Bax and Bak and a decrease in the expression of Bcl-2 and Bcl-xl.	Thioridazine	13-25	BCL2 antagonist/killer 1	Homo sapiens	171-174
27453171-11	2016	In addition, thioridazine and irradiation treatment induced apoptosis through up-regulation of cleaved capase-3 and 9, as well as an increase in the expression of Bax and Bak and a decrease in the expression of Bcl-2 and Bcl-xl.	Thioridazine	13-25	BCL2 apoptosis regulator	Homo sapiens	211-216
27453171-11	2016	In addition, thioridazine and irradiation treatment induced apoptosis through up-regulation of cleaved capase-3 and 9, as well as an increase in the expression of Bax and Bak and a decrease in the expression of Bcl-2 and Bcl-xl.	Thioridazine	13-25	BCL2 like 1	Homo sapiens	221-227
27453171-12	2016	Furthermore, thioridazine and irradiation treatment inhibited the PI3K-AKT-mTOR pathway and up-regulated the expression of p53.	Thioridazine	13-25	AKT serine/threonine kinase 1	Homo sapiens	71-74
27453171-12	2016	Furthermore, thioridazine and irradiation treatment inhibited the PI3K-AKT-mTOR pathway and up-regulated the expression of p53.	Thioridazine	13-25	mechanistic target of rapamycin kinase	Homo sapiens	75-79
27453171-12	2016	Furthermore, thioridazine and irradiation treatment inhibited the PI3K-AKT-mTOR pathway and up-regulated the expression of p53.	Thioridazine	13-25	tumor protein p53	Homo sapiens	123-126
27398159-14	2016	CONCLUSION: Taken together, all the data in the present study suggested that the THIO plus MPA might act as the suppressor of tumor growth in ECa by inhibiting the PI3K/AKT signal transduction pathway, which was mediated by PRB, DRD2 and EGFR.	Thioridazine	81-85	dopamine receptor D2	Homo sapiens	229-233
27398159-14	2016	CONCLUSION: Taken together, all the data in the present study suggested that the THIO plus MPA might act as the suppressor of tumor growth in ECa by inhibiting the PI3K/AKT signal transduction pathway, which was mediated by PRB, DRD2 and EGFR.	Thioridazine	81-85	epidermal growth factor receptor	Homo sapiens	238-242
26682943-5	2016	RESULTS: A strong inhibition (IC50 value &lt;15 muM) was observed for clofazimine (P-gp, BCRP and MRP1), thioridazine (BCRP), timcodar (P-gp, BSEP and MRP1) and SQ109 (P-gp and BCRP).	Thioridazine	105-117	phosphoglycolate phosphatase	Homo sapiens	136-140
27249081-11	2016	CONCLUSIONS: Higher vigilance for ARS is warranted during use of clozapine, chlorprothixene, thioridazine, and haloperidol.	Thioridazine	93-105	secreted LY6/PLAUR domain containing 1	Homo sapiens	34-37
26820562-7	2016	The CD spectra showed binding of thioridazine into thioredoxin 1 and suggested partial helix unfolding, which most probably concerns helix 3.	Thioridazine	33-45	thioredoxin	Homo sapiens	51-62
27408917-5	2016	TLK1 effectors, gallic acid (GA) and thioridazine (THD) activate and inhibit the kinase, respectively, and the data report on the impact of these compounds and the significance of TLK1 to DNA break repair and the survival of human salivary acinar cells.	Thioridazine	37-49	tousled like kinase 1	Homo sapiens	180-184
27408917-5	2016	TLK1 effectors, gallic acid (GA) and thioridazine (THD) activate and inhibit the kinase, respectively, and the data report on the impact of these compounds and the significance of TLK1 to DNA break repair and the survival of human salivary acinar cells.	Thioridazine	51-54	tousled like kinase 1	Homo sapiens	180-184
26682943-5	2016	RESULTS: A strong inhibition (IC50 value &lt;15 muM) was observed for clofazimine (P-gp, BCRP and MRP1), thioridazine (BCRP), timcodar (P-gp, BSEP and MRP1) and SQ109 (P-gp and BCRP).	Thioridazine	105-117	ATP binding cassette subfamily B member 11	Homo sapiens	142-146
26258683-4	2015	We identified the FDA-approved antipsychotic drug thioridazine as an EAG2 channel blocker that reduces xenografted MB growth and metastasis, and present a case report of repurposing thioridazine for treating a human patient.	Thioridazine	50-62	potassium voltage-gated channel subfamily H member 5	Homo sapiens	69-73
26682943-5	2016	RESULTS: A strong inhibition (IC50 value &lt;15 muM) was observed for clofazimine (P-gp, BCRP and MRP1), thioridazine (BCRP), timcodar (P-gp, BSEP and MRP1) and SQ109 (P-gp and BCRP).	Thioridazine	105-117	ATP binding cassette subfamily C member 1	Homo sapiens	151-155
26682943-5	2016	RESULTS: A strong inhibition (IC50 value &lt;15 muM) was observed for clofazimine (P-gp, BCRP and MRP1), thioridazine (BCRP), timcodar (P-gp, BSEP and MRP1) and SQ109 (P-gp and BCRP).	Thioridazine	105-117	phosphoglycolate phosphatase	Homo sapiens	136-140
26706948-0	2015	[Mechanism of Killing Effect of Thioridazine on Human Lung Cancer PC9 Cells].	Thioridazine	32-44	proprotein convertase subtilisin/kexin type 9	Homo sapiens	66-69
26706948-2	2015	So we choose PC9 cell lines as the research object, the aim is to oberve the killing effect of thioridazine on PC9 cells and investigate its possible mechanism.	Thioridazine	95-107	proprotein convertase subtilisin/kexin type 9	Homo sapiens	13-16
26706948-2	2015	So we choose PC9 cell lines as the research object, the aim is to oberve the killing effect of thioridazine on PC9 cells and investigate its possible mechanism.	Thioridazine	95-107	proprotein convertase subtilisin/kexin type 9	Homo sapiens	111-114
26706948-3	2015	METHODS: After being treated with different concentrations of thioridazine, the proliferation of PC9 cells was determined by methyl thiazolyltetrazolium (MTT) assay.	Thioridazine	62-74	proprotein convertase subtilisin/kexin type 9	Homo sapiens	97-100
26706948-6	2015	RESULTS: The proliferation of PC9 cells was significantly inhibited by thioridazine in a dose- and time-dependent manner.	Thioridazine	71-83	proprotein convertase subtilisin/kexin type 9	Homo sapiens	30-33
26706948-9	2015	Western blot analysis showed that, compared with the control group, thioridazine reduced the expressions of CyclinD1, Bcl-2 and Bcl-xl (P&lt;0.01) and increased the expression of Bax (P&lt;0.01).	Thioridazine	68-80	cyclin D1	Homo sapiens	108-116
26706948-9	2015	Western blot analysis showed that, compared with the control group, thioridazine reduced the expressions of CyclinD1, Bcl-2 and Bcl-xl (P&lt;0.01) and increased the expression of Bax (P&lt;0.01).	Thioridazine	68-80	BCL2 apoptosis regulator	Homo sapiens	118-123
26706948-9	2015	Western blot analysis showed that, compared with the control group, thioridazine reduced the expressions of CyclinD1, Bcl-2 and Bcl-xl (P&lt;0.01) and increased the expression of Bax (P&lt;0.01).	Thioridazine	68-80	BCL2 like 1	Homo sapiens	128-134
26706948-9	2015	Western blot analysis showed that, compared with the control group, thioridazine reduced the expressions of CyclinD1, Bcl-2 and Bcl-xl (P&lt;0.01) and increased the expression of Bax (P&lt;0.01).	Thioridazine	68-80	BCL2 associated X, apoptosis regulator	Homo sapiens	179-182
26706948-10	2015	In the mean time, thioridazine promoted the activities of Caspase-3, Caspase-8 and Caspase-9 (P&lt;0.01).	Thioridazine	18-30	caspase 3	Homo sapiens	58-67
26706948-10	2015	In the mean time, thioridazine promoted the activities of Caspase-3, Caspase-8 and Caspase-9 (P&lt;0.01).	Thioridazine	18-30	caspase 8	Homo sapiens	69-78
26706948-10	2015	In the mean time, thioridazine promoted the activities of Caspase-3, Caspase-8 and Caspase-9 (P&lt;0.01).	Thioridazine	18-30	caspase 9	Homo sapiens	83-92
26706948-11	2015	CONCLUSIONS: The mechanism of thioridazine inhibiting the proliferation of PC9 cells may be related to stimulation of Caspase apoptotic pathway, down-regulation of CyclinD1, Bcl-2, Bcl-xl and up-regulation of Bax.	Thioridazine	30-42	proprotein convertase subtilisin/kexin type 9	Homo sapiens	75-78
26706948-11	2015	CONCLUSIONS: The mechanism of thioridazine inhibiting the proliferation of PC9 cells may be related to stimulation of Caspase apoptotic pathway, down-regulation of CyclinD1, Bcl-2, Bcl-xl and up-regulation of Bax.	Thioridazine	30-42	cyclin D1	Homo sapiens	164-172
26706948-11	2015	CONCLUSIONS: The mechanism of thioridazine inhibiting the proliferation of PC9 cells may be related to stimulation of Caspase apoptotic pathway, down-regulation of CyclinD1, Bcl-2, Bcl-xl and up-regulation of Bax.	Thioridazine	30-42	BCL2 apoptosis regulator	Homo sapiens	174-179
26706948-11	2015	CONCLUSIONS: The mechanism of thioridazine inhibiting the proliferation of PC9 cells may be related to stimulation of Caspase apoptotic pathway, down-regulation of CyclinD1, Bcl-2, Bcl-xl and up-regulation of Bax.	Thioridazine	30-42	BCL2 like 1	Homo sapiens	181-187
26706948-11	2015	CONCLUSIONS: The mechanism of thioridazine inhibiting the proliferation of PC9 cells may be related to stimulation of Caspase apoptotic pathway, down-regulation of CyclinD1, Bcl-2, Bcl-xl and up-regulation of Bax.	Thioridazine	30-42	BCL2 associated X, apoptosis regulator	Homo sapiens	209-212
26322824-2	2015	We report the first crystal structures of human AOX1, substrate free (2.6-A resolution) and in complex with the substrate phthalazine and the inhibitor thioridazine (2.7-A resolution).	Thioridazine	152-164	aldehyde oxidase 1	Homo sapiens	48-52
26095429-8	2015	Thioridazine was also found to markedly inhibit tumor proliferation and induce tumor cell apoptosis in vivo as shown by the lower Ki67 index and increase in TUNEL-positive cells.	Thioridazine	0-12	antigen identified by monoclonal antibody Ki 67	Mus musculus	130-134
26264841-0	2015	Molecular dynamics and density functional studies on the metabolic selectivity of antipsychotic thioridazine by cytochrome P450 2D6: Connection with crystallographic and metabolic results.	Thioridazine	96-108	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	112-131
26264841-4	2015	The sulfur atom attached to the phenothiazine ring is preferentially oxidized mainly by CYP2D6, that is, the 2-sulfoxide is a major metabolite, and interestingly this metabolite shows more potent activity against dopamine D2 receptors than THD.	Thioridazine	240-243	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	88-94
26264841-9	2015	2006, 34, 471) reported a kinetic study of THD formed by CYP2D6.	Thioridazine	43-46	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	57-63
26264841-15	2015	2015, 290, 5092) revealed the crystallographic structure of THD with CYP2D6.	Thioridazine	60-63	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	69-75
26013584-6	2015	Addition of an electron-attracting substituent in position 2 of the C ring extended the inhibitory activity to NOX1 and NOX3, with thioridazine being the most potent inhibitor.	Thioridazine	131-143	NADPH oxidase 1	Homo sapiens	111-115
26013584-6	2015	Addition of an electron-attracting substituent in position 2 of the C ring extended the inhibitory activity to NOX1 and NOX3, with thioridazine being the most potent inhibitor.	Thioridazine	131-143	NADPH oxidase 3	Homo sapiens	120-124
25832589-4	2015	After 20-muM thioridazine treatment for 24 h, the protein level of DRD2 in SiHa cells was analyzed by Western blots, apoptosis was detected with the phosphatidylserine externalization and comet assay, and necrosis was detected by measuring high-mobility group box 1 protein (HMGB1).	Thioridazine	13-25	dopamine receptor D2	Homo sapiens	67-71
26271665-0	2015	Erratum to: Thioridazine specifically sensitizes drug-resistant cancer cells through highly increase in apoptosis and P-gp inhibition.	Thioridazine	12-24	phosphoglycolate phosphatase	Homo sapiens	118-122
24952635-0	2014	Thioridazine inhibits angiogenesis and tumor growth by targeting the VEGFR-2/PI3K/mTOR pathway in ovarian cancer xenografts.	Thioridazine	0-12	kinase insert domain receptor	Homo sapiens	69-76
25832589-0	2015	Dopamine D2 receptor blocker thioridazine induces cell death in human uterine cervical carcinoma cell line SiHa.	Thioridazine	29-41	dopamine receptor D2	Homo sapiens	0-20
25832589-1	2015	AIM: The aim of this study was to explore the correlation of dopamine D2 receptor (DRD2) and the development of uterine cervical cancer, and the effect of thioridazine (an antagonist of DRD2) on the SiHa cell line.	Thioridazine	155-167	dopamine receptor D2	Homo sapiens	186-190
25832589-6	2015	In vitro, DRD2 blocker thioridazine treatment resulted in death of SiHa cells with the expression of DRD2 significantly regulated down (P &lt; 0.05), and thioridazine significantly induced SiHa apoptosis (P = 0.016) and necrosis (P &lt; 0.01).	Thioridazine	23-35	dopamine receptor D2	Homo sapiens	10-14
25832589-6	2015	In vitro, DRD2 blocker thioridazine treatment resulted in death of SiHa cells with the expression of DRD2 significantly regulated down (P &lt; 0.05), and thioridazine significantly induced SiHa apoptosis (P = 0.016) and necrosis (P &lt; 0.01).	Thioridazine	23-35	dopamine receptor D2	Homo sapiens	101-105
25832589-6	2015	In vitro, DRD2 blocker thioridazine treatment resulted in death of SiHa cells with the expression of DRD2 significantly regulated down (P &lt; 0.05), and thioridazine significantly induced SiHa apoptosis (P = 0.016) and necrosis (P &lt; 0.01).	Thioridazine	154-166	dopamine receptor D2	Homo sapiens	10-14
26124671-8	2015	Treatment of HCC cells with thioridazine displays a dose-dependent response in HCC cell lines SNU449, LM3, and Huh7.	Thioridazine	28-40	MIR7-3 host gene	Homo sapiens	111-115
26124671-9	2015	Thioridazine treatment reduced cell viability and sphere formation of HCC cell lines through induction of G0/G1 cell cycle arrest and suppression of stemness genes CD133, OCT4, and EpCam.	Thioridazine	0-12	prominin 1	Homo sapiens	164-169
26124671-9	2015	Thioridazine treatment reduced cell viability and sphere formation of HCC cell lines through induction of G0/G1 cell cycle arrest and suppression of stemness genes CD133, OCT4, and EpCam.	Thioridazine	0-12	POU class 5 homeobox 1	Homo sapiens	171-175
26124671-9	2015	Thioridazine treatment reduced cell viability and sphere formation of HCC cell lines through induction of G0/G1 cell cycle arrest and suppression of stemness genes CD133, OCT4, and EpCam.	Thioridazine	0-12	epithelial cell adhesion molecule	Homo sapiens	181-186
26178512-2	2015	METHODS: CCK-8 assay was employed for detecting the influence of THIO plus MPA on the proliferation and apoptosis of endometrial cancer cells (ISK &amp; KLE).	Thioridazine	65-69	potassium voltage-gated channel subfamily E regulatory subunit 1	Homo sapiens	143-146
25907934-9	2015	Thioridazine treatment of the cells resulted in up-regulated PDCD4 mRNA expression and down-regulated mRNA expressions of CCND1, CDK4, c-MYC, BCL2, CASPASE3, PARP1 and EIF4A, increased PDCD4 protein expression and reduced p-AKT protein expression.	Thioridazine	0-12	programmed cell death 4	Homo sapiens	61-66
25907934-9	2015	Thioridazine treatment of the cells resulted in up-regulated PDCD4 mRNA expression and down-regulated mRNA expressions of CCND1, CDK4, c-MYC, BCL2, CASPASE3, PARP1 and EIF4A, increased PDCD4 protein expression and reduced p-AKT protein expression.	Thioridazine	0-12	cyclin D1	Homo sapiens	122-127
25907934-9	2015	Thioridazine treatment of the cells resulted in up-regulated PDCD4 mRNA expression and down-regulated mRNA expressions of CCND1, CDK4, c-MYC, BCL2, CASPASE3, PARP1 and EIF4A, increased PDCD4 protein expression and reduced p-AKT protein expression.	Thioridazine	0-12	cyclin dependent kinase 4	Homo sapiens	129-133
25907934-9	2015	Thioridazine treatment of the cells resulted in up-regulated PDCD4 mRNA expression and down-regulated mRNA expressions of CCND1, CDK4, c-MYC, BCL2, CASPASE3, PARP1 and EIF4A, increased PDCD4 protein expression and reduced p-AKT protein expression.	Thioridazine	0-12	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	135-140
25907934-9	2015	Thioridazine treatment of the cells resulted in up-regulated PDCD4 mRNA expression and down-regulated mRNA expressions of CCND1, CDK4, c-MYC, BCL2, CASPASE3, PARP1 and EIF4A, increased PDCD4 protein expression and reduced p-AKT protein expression.	Thioridazine	0-12	BCL2 apoptosis regulator	Homo sapiens	142-146
25907934-9	2015	Thioridazine treatment of the cells resulted in up-regulated PDCD4 mRNA expression and down-regulated mRNA expressions of CCND1, CDK4, c-MYC, BCL2, CASPASE3, PARP1 and EIF4A, increased PDCD4 protein expression and reduced p-AKT protein expression.	Thioridazine	0-12	caspase 3	Homo sapiens	148-156
25907934-9	2015	Thioridazine treatment of the cells resulted in up-regulated PDCD4 mRNA expression and down-regulated mRNA expressions of CCND1, CDK4, c-MYC, BCL2, CASPASE3, PARP1 and EIF4A, increased PDCD4 protein expression and reduced p-AKT protein expression.	Thioridazine	0-12	poly(ADP-ribose) polymerase 1	Homo sapiens	158-163
25907934-9	2015	Thioridazine treatment of the cells resulted in up-regulated PDCD4 mRNA expression and down-regulated mRNA expressions of CCND1, CDK4, c-MYC, BCL2, CASPASE3, PARP1 and EIF4A, increased PDCD4 protein expression and reduced p-AKT protein expression.	Thioridazine	0-12	eukaryotic translation initiation factor 4A2	Homo sapiens	168-173
25907934-9	2015	Thioridazine treatment of the cells resulted in up-regulated PDCD4 mRNA expression and down-regulated mRNA expressions of CCND1, CDK4, c-MYC, BCL2, CASPASE3, PARP1 and EIF4A, increased PDCD4 protein expression and reduced p-AKT protein expression.	Thioridazine	0-12	programmed cell death 4	Homo sapiens	185-190
25907934-9	2015	Thioridazine treatment of the cells resulted in up-regulated PDCD4 mRNA expression and down-regulated mRNA expressions of CCND1, CDK4, c-MYC, BCL2, CASPASE3, PARP1 and EIF4A, increased PDCD4 protein expression and reduced p-AKT protein expression.	Thioridazine	0-12	AKT serine/threonine kinase 1	Homo sapiens	224-227
25907934-10	2015	CONCLUSION: Thioridazine inhibits the proliferation and induces apoptosis of SW480 cells by up-regulating PDCD4 and inhibiting PI3K/Akt pathway.	Thioridazine	12-24	programmed cell death 4	Homo sapiens	106-111
25907934-10	2015	CONCLUSION: Thioridazine inhibits the proliferation and induces apoptosis of SW480 cells by up-regulating PDCD4 and inhibiting PI3K/Akt pathway.	Thioridazine	12-24	AKT serine/threonine kinase 1	Homo sapiens	132-135
24989930-0	2014	Thioridazine specifically sensitizes drug-resistant cancer cells through highly increase in apoptosis and P-gp inhibition.	Thioridazine	0-12	ATP binding cassette subfamily B member 1	Homo sapiens	106-110
24989930-3	2014	By studying cleaved PARP, annexin V staining, and Hoechst staining, we found that THIO largely increased apoptosis specifically in KBV20C cells, suggesting that the difference in sensitization between the resistant and sensitive cells can be attributed to the ability of THIO to induce apoptosis.	Thioridazine	82-86	poly(ADP-ribose) polymerase 1	Homo sapiens	20-24
24989930-3	2014	By studying cleaved PARP, annexin V staining, and Hoechst staining, we found that THIO largely increased apoptosis specifically in KBV20C cells, suggesting that the difference in sensitization between the resistant and sensitive cells can be attributed to the ability of THIO to induce apoptosis.	Thioridazine	82-86	annexin A5	Homo sapiens	26-35
24989930-4	2014	THIO could also inhibit p-glycoprotein (P-gp) activity in the resistant KBV20C cells.	Thioridazine	0-4	ATP binding cassette subfamily B member 1	Homo sapiens	24-38
24989930-4	2014	THIO could also inhibit p-glycoprotein (P-gp) activity in the resistant KBV20C cells.	Thioridazine	0-4	ATP binding cassette subfamily B member 1	Homo sapiens	40-44
24989930-7	2014	As observed in a single treatment with THIO, the sensitization mechanism induced by the co-treatment also involves both apoptosis and P-gp inhibition.	Thioridazine	39-43	ATP binding cassette subfamily B member 1	Homo sapiens	134-138
24952635-0	2014	Thioridazine inhibits angiogenesis and tumor growth by targeting the VEGFR-2/PI3K/mTOR pathway in ovarian cancer xenografts.	Thioridazine	0-12	mechanistic target of rapamycin kinase	Homo sapiens	82-86
24952635-5	2014	In addition, thioridazine inhibited the phosphorylation of the signaling molecules downstream of phosphatidylinositol-3"-kinase (PI3K), including Akt, phosphoinositide-dependent protein kinase 1 (PDK1), and mammalian target of rapamycin (mTOR), during ovarian tumor progression via vascular endothelial growth factor receptor 2 (VEGFR-2).	Thioridazine	13-25	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	97-127
24952635-5	2014	In addition, thioridazine inhibited the phosphorylation of the signaling molecules downstream of phosphatidylinositol-3"-kinase (PI3K), including Akt, phosphoinositide-dependent protein kinase 1 (PDK1), and mammalian target of rapamycin (mTOR), during ovarian tumor progression via vascular endothelial growth factor receptor 2 (VEGFR-2).	Thioridazine	13-25	AKT serine/threonine kinase 1	Homo sapiens	146-149
24952635-5	2014	In addition, thioridazine inhibited the phosphorylation of the signaling molecules downstream of phosphatidylinositol-3"-kinase (PI3K), including Akt, phosphoinositide-dependent protein kinase 1 (PDK1), and mammalian target of rapamycin (mTOR), during ovarian tumor progression via vascular endothelial growth factor receptor 2 (VEGFR-2).	Thioridazine	13-25	pyruvate dehydrogenase kinase 1	Homo sapiens	151-194
24952635-5	2014	In addition, thioridazine inhibited the phosphorylation of the signaling molecules downstream of phosphatidylinositol-3"-kinase (PI3K), including Akt, phosphoinositide-dependent protein kinase 1 (PDK1), and mammalian target of rapamycin (mTOR), during ovarian tumor progression via vascular endothelial growth factor receptor 2 (VEGFR-2).	Thioridazine	13-25	pyruvate dehydrogenase kinase 1	Homo sapiens	196-200
24952635-5	2014	In addition, thioridazine inhibited the phosphorylation of the signaling molecules downstream of phosphatidylinositol-3"-kinase (PI3K), including Akt, phosphoinositide-dependent protein kinase 1 (PDK1), and mammalian target of rapamycin (mTOR), during ovarian tumor progression via vascular endothelial growth factor receptor 2 (VEGFR-2).	Thioridazine	13-25	mechanistic target of rapamycin kinase	Homo sapiens	207-236
24952635-5	2014	In addition, thioridazine inhibited the phosphorylation of the signaling molecules downstream of phosphatidylinositol-3"-kinase (PI3K), including Akt, phosphoinositide-dependent protein kinase 1 (PDK1), and mammalian target of rapamycin (mTOR), during ovarian tumor progression via vascular endothelial growth factor receptor 2 (VEGFR-2).	Thioridazine	13-25	mechanistic target of rapamycin kinase	Homo sapiens	238-242
24952635-5	2014	In addition, thioridazine inhibited the phosphorylation of the signaling molecules downstream of phosphatidylinositol-3"-kinase (PI3K), including Akt, phosphoinositide-dependent protein kinase 1 (PDK1), and mammalian target of rapamycin (mTOR), during ovarian tumor progression via vascular endothelial growth factor receptor 2 (VEGFR-2).	Thioridazine	13-25	kinase insert domain receptor	Homo sapiens	282-327
24952635-5	2014	In addition, thioridazine inhibited the phosphorylation of the signaling molecules downstream of phosphatidylinositol-3"-kinase (PI3K), including Akt, phosphoinositide-dependent protein kinase 1 (PDK1), and mammalian target of rapamycin (mTOR), during ovarian tumor progression via vascular endothelial growth factor receptor 2 (VEGFR-2).	Thioridazine	13-25	kinase insert domain receptor	Homo sapiens	329-336
24952635-6	2014	These results provide convincing evidence that thioridazine regulates endothelial cell function and subsequent angiogenesis by inhibiting VEGFR-2/PI3K/mTOR signal transduction.	Thioridazine	47-59	kinase insert domain receptor	Homo sapiens	138-145
24952635-6	2014	These results provide convincing evidence that thioridazine regulates endothelial cell function and subsequent angiogenesis by inhibiting VEGFR-2/PI3K/mTOR signal transduction.	Thioridazine	47-59	mechanistic target of rapamycin kinase	Homo sapiens	151-155
24556678-0	2014	Antipsychotic agent thioridazine sensitizes renal carcinoma Caki cells to TRAIL-induced apoptosis through reactive oxygen species-mediated inhibition of Akt signaling and downregulation of Mcl-1 and c-FLIP(L).	Thioridazine	20-32	TNF superfamily member 10	Homo sapiens	74-79
24604290-5	2014	Thioridazine treatment induced nuclear fragmentation, increased the proportion of sub-G1 phase cells, and elevated the percentage of Annexin V-positive cells, suggesting the occurrence of apoptosis.	Thioridazine	0-12	annexin A5	Homo sapiens	133-142
24604290-6	2014	Moreover, thioridazine induced gastric cancer cell apoptosis in a caspase-dependent manner, as shown by a decrease in the precursors of casapse-9, caspase-8 and caspase-3, and by the ability of the caspase inhibitor Z-VAD-FMK to reverse the cytotoxic effect of thioridazine.	Thioridazine	10-22	caspase 8	Homo sapiens	147-156
24604290-6	2014	Moreover, thioridazine induced gastric cancer cell apoptosis in a caspase-dependent manner, as shown by a decrease in the precursors of casapse-9, caspase-8 and caspase-3, and by the ability of the caspase inhibitor Z-VAD-FMK to reverse the cytotoxic effect of thioridazine.	Thioridazine	10-22	caspase 3	Homo sapiens	161-170
24692704-4	2014	The inhibition of the ABCB1 transporter in the presence of the newly-developed phenothiazines was greater than that for the known ABCB1 inhibitors thioridazine and verapamil.	Thioridazine	147-159	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	22-27
24692704-4	2014	The inhibition of the ABCB1 transporter in the presence of the newly-developed phenothiazines was greater than that for the known ABCB1 inhibitors thioridazine and verapamil.	Thioridazine	147-159	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	130-135
24417241-0	2014	Allosteric effects of erythromycin pretreatment on thioridazine block of hERG potassium channels.	Thioridazine	51-63	ETS transcription factor ERG	Homo sapiens	73-77
24417241-3	2014	Experiments were conducted to determine if concomitant exposure to two potent pore hERG blockers, thioridazine and terfenadine and a weak hERG blocker, erythromycin, would result in an additive, synergistic or inhibitory effect.	Thioridazine	98-110	ETS transcription factor ERG	Homo sapiens	83-87
24417241-6	2014	KEY RESULTS: Pre-exposure of cells to erythromycin resulted in an approximately 14-22-fold rightward shift in the hERG concentration-response curve for thioridazine and terfenadine respectively.	Thioridazine	152-164	ETS transcription factor ERG	Homo sapiens	114-118
24556678-10	2014	Collectively, our study demonstrates that thioridazine enhances TRAIL-mediated apoptosis via the ROS-mediated inhibition of Akt signaling and the downregulation of c-FLIP(L) and Mcl-1 at the post-translational level.	Thioridazine	42-54	TNF superfamily member 10	Homo sapiens	64-69
24556678-10	2014	Collectively, our study demonstrates that thioridazine enhances TRAIL-mediated apoptosis via the ROS-mediated inhibition of Akt signaling and the downregulation of c-FLIP(L) and Mcl-1 at the post-translational level.	Thioridazine	42-54	AKT serine/threonine kinase 1	Homo sapiens	124-127
24556678-10	2014	Collectively, our study demonstrates that thioridazine enhances TRAIL-mediated apoptosis via the ROS-mediated inhibition of Akt signaling and the downregulation of c-FLIP(L) and Mcl-1 at the post-translational level.	Thioridazine	42-54	CASP8 and FADD like apoptosis regulator	Homo sapiens	164-173
24556678-10	2014	Collectively, our study demonstrates that thioridazine enhances TRAIL-mediated apoptosis via the ROS-mediated inhibition of Akt signaling and the downregulation of c-FLIP(L) and Mcl-1 at the post-translational level.	Thioridazine	42-54	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	178-183
24556678-0	2014	Antipsychotic agent thioridazine sensitizes renal carcinoma Caki cells to TRAIL-induced apoptosis through reactive oxygen species-mediated inhibition of Akt signaling and downregulation of Mcl-1 and c-FLIP(L).	Thioridazine	20-32	AKT serine/threonine kinase 1	Homo sapiens	153-156
24556678-0	2014	Antipsychotic agent thioridazine sensitizes renal carcinoma Caki cells to TRAIL-induced apoptosis through reactive oxygen species-mediated inhibition of Akt signaling and downregulation of Mcl-1 and c-FLIP(L).	Thioridazine	20-32	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	189-194
24556678-0	2014	Antipsychotic agent thioridazine sensitizes renal carcinoma Caki cells to TRAIL-induced apoptosis through reactive oxygen species-mediated inhibition of Akt signaling and downregulation of Mcl-1 and c-FLIP(L).	Thioridazine	20-32	CASP8 and FADD like apoptosis regulator	Homo sapiens	199-205
24556678-2	2014	However, the effect of thioridazine on tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) sensitization has not yet been studied.	Thioridazine	23-35	TNF superfamily member 10	Homo sapiens	96-101
24556678-3	2014	Here, we investigated the ability of thioridazine to sensitize TRAIL-mediated apoptosis.	Thioridazine	37-49	TNF superfamily member 10	Homo sapiens	63-68
24556678-5	2014	We found that thioridazine downregulated c-FLIP(L) and Mcl-1 expression at the post-translational level via an increase in proteasome activity.	Thioridazine	14-26	CASP8 and FADD like apoptosis regulator	Homo sapiens	41-50
24556678-5	2014	We found that thioridazine downregulated c-FLIP(L) and Mcl-1 expression at the post-translational level via an increase in proteasome activity.	Thioridazine	14-26	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	55-60
24556678-6	2014	The overexpression of c-FLIP(L) and Mcl-1 overcame thioridazine plus TRAIL-induced apoptosis.	Thioridazine	51-63	CASP8 and FADD like apoptosis regulator	Homo sapiens	22-31
24556678-6	2014	The overexpression of c-FLIP(L) and Mcl-1 overcame thioridazine plus TRAIL-induced apoptosis.	Thioridazine	51-63	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	36-41
24556678-7	2014	We further observed that thioridazine inhibited the Akt signaling pathway.	Thioridazine	25-37	AKT serine/threonine kinase 1	Homo sapiens	52-55
24556678-9	2014	Furthermore, thioridazine increased the production of reactive oxygen species (ROS) in Caki cells, and ROS scavengers (N-acetylcysteine, glutathione ethyl ester, and trolox) inhibited thioridazine plus TRAIL-induced apoptosis, as well as Akt inhibition and the downregulation of c-FLIP(L) and Mcl-1.	Thioridazine	13-25	TNF superfamily member 10	Homo sapiens	202-207
24556678-9	2014	Furthermore, thioridazine increased the production of reactive oxygen species (ROS) in Caki cells, and ROS scavengers (N-acetylcysteine, glutathione ethyl ester, and trolox) inhibited thioridazine plus TRAIL-induced apoptosis, as well as Akt inhibition and the downregulation of c-FLIP(L) and Mcl-1.	Thioridazine	13-25	AKT serine/threonine kinase 1	Homo sapiens	238-241
24556678-9	2014	Furthermore, thioridazine increased the production of reactive oxygen species (ROS) in Caki cells, and ROS scavengers (N-acetylcysteine, glutathione ethyl ester, and trolox) inhibited thioridazine plus TRAIL-induced apoptosis, as well as Akt inhibition and the downregulation of c-FLIP(L) and Mcl-1.	Thioridazine	13-25	CASP8 and FADD like apoptosis regulator	Homo sapiens	279-288
24556678-9	2014	Furthermore, thioridazine increased the production of reactive oxygen species (ROS) in Caki cells, and ROS scavengers (N-acetylcysteine, glutathione ethyl ester, and trolox) inhibited thioridazine plus TRAIL-induced apoptosis, as well as Akt inhibition and the downregulation of c-FLIP(L) and Mcl-1.	Thioridazine	13-25	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	293-298
23476805-2	2013	Chlorpromazine was the only antipsychotic that inhibited CYP1A2 activity (IC50 = 9.5  mu M), whilst levomepromazine, chlorpromazine, and thioridazine significantly decreased CYP2D6-mediated formation of 1"-hydroxybufuralol (IC50 range, 3.5-25.5  mu M).	Thioridazine	137-149	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	174-180
24292587-5	2013	Drug accumulation by MDR mouse T-lymphoma cells was moderately modified in the presence of thioridazine derivatives.	Thioridazine	91-103	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	21-24
24292587-6	2013	Thioridazine induced apoptosis of the MDR cancer cell line, but there was no significant apoptotic effect on the PC3 cell line.	Thioridazine	0-12	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	38-41
24152992-6	2013	RESULTS: A 48 hours exposure to thioridazine was followed by a significant increase of [Ca2+](i) (30 microM), decrease of forward scatter (30 microM), and increase of annexin-V-binding (&gt;=12 microM).	Thioridazine	32-44	annexin A5	Homo sapiens	167-176
23165143-10	2013	Sertraline and thioridazine interfere with this repressive feedback by targeting directly TPT1/TCTP and inhibiting its binding to MDM2, restoring wildtype p53 function.	Thioridazine	15-27	tumor protein, translationally-controlled 1	Homo sapiens	90-94
23165143-10	2013	Sertraline and thioridazine interfere with this repressive feedback by targeting directly TPT1/TCTP and inhibiting its binding to MDM2, restoring wildtype p53 function.	Thioridazine	15-27	tumor protein, translationally-controlled 1	Homo sapiens	95-99
23165143-10	2013	Sertraline and thioridazine interfere with this repressive feedback by targeting directly TPT1/TCTP and inhibiting its binding to MDM2, restoring wildtype p53 function.	Thioridazine	15-27	MDM2 proto-oncogene	Homo sapiens	130-134
23165143-10	2013	Sertraline and thioridazine interfere with this repressive feedback by targeting directly TPT1/TCTP and inhibiting its binding to MDM2, restoring wildtype p53 function.	Thioridazine	15-27	tumor protein p53	Homo sapiens	155-158
24130798-2	2013	Cytochrome c was irradiated with UV light for 120 min, over a pH range from 4.0 to 8.0, in the absence and in the presence of different concentrations of thioridazine (TR) and fluphenazine (FP).	Thioridazine	154-166	cytochrome c, somatic	Homo sapiens	0-12
23476805-5	2013	Thioridazine displayed a Ki of 1.75  mu M and an inhibitory potency of 1.57 on CYP2D6, suggesting a potential to induce in vivo interactions.	Thioridazine	0-12	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	79-85
23238017-2	2012	We have identified distinct derivatives of medicinal active phenothiazines, namely mepazine, thioridazine, and promazine, as small molecule inhibitors of the MALT1 protease.	Thioridazine	93-105	MALT1 paracaspase	Homo sapiens	158-172
22985512-0	2012	Inhibition of peroxisomal beta-oxidation by thioridazine increases the amount of VLCFAs and Abeta generation in the rat brain.	Thioridazine	44-56	amyloid beta precursor protein	Rattus norvegicus	92-97
23022044-6	2012	Thioridazine suppressed phosphorylation of the signaling regulators downstream of the focal adhesion kinase (FAK) through alphavbeta3 integrin, which also include Akt, phosphoinositide-dependent protein kinase 1 (PDK-1), mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (p70S6K), but had no effect on VEGF-stimulated extracellular signal-regulated kinase (ERK) phosphorylation.	Thioridazine	0-12	AKT serine/threonine kinase 1	Homo sapiens	163-166
23022044-6	2012	Thioridazine suppressed phosphorylation of the signaling regulators downstream of the focal adhesion kinase (FAK) through alphavbeta3 integrin, which also include Akt, phosphoinositide-dependent protein kinase 1 (PDK-1), mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (p70S6K), but had no effect on VEGF-stimulated extracellular signal-regulated kinase (ERK) phosphorylation.	Thioridazine	0-12	pyruvate dehydrogenase kinase 1	Homo sapiens	168-211
23022044-6	2012	Thioridazine suppressed phosphorylation of the signaling regulators downstream of the focal adhesion kinase (FAK) through alphavbeta3 integrin, which also include Akt, phosphoinositide-dependent protein kinase 1 (PDK-1), mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (p70S6K), but had no effect on VEGF-stimulated extracellular signal-regulated kinase (ERK) phosphorylation.	Thioridazine	0-12	pyruvate dehydrogenase kinase 1	Homo sapiens	213-218
23022044-6	2012	Thioridazine suppressed phosphorylation of the signaling regulators downstream of the focal adhesion kinase (FAK) through alphavbeta3 integrin, which also include Akt, phosphoinositide-dependent protein kinase 1 (PDK-1), mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (p70S6K), but had no effect on VEGF-stimulated extracellular signal-regulated kinase (ERK) phosphorylation.	Thioridazine	0-12	mechanistic target of rapamycin kinase	Homo sapiens	221-250
23022044-6	2012	Thioridazine suppressed phosphorylation of the signaling regulators downstream of the focal adhesion kinase (FAK) through alphavbeta3 integrin, which also include Akt, phosphoinositide-dependent protein kinase 1 (PDK-1), mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (p70S6K), but had no effect on VEGF-stimulated extracellular signal-regulated kinase (ERK) phosphorylation.	Thioridazine	0-12	mechanistic target of rapamycin kinase	Homo sapiens	252-256
23022044-6	2012	Thioridazine suppressed phosphorylation of the signaling regulators downstream of the focal adhesion kinase (FAK) through alphavbeta3 integrin, which also include Akt, phosphoinositide-dependent protein kinase 1 (PDK-1), mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (p70S6K), but had no effect on VEGF-stimulated extracellular signal-regulated kinase (ERK) phosphorylation.	Thioridazine	0-12	ribosomal protein S6 kinase B1	Homo sapiens	288-294
23022044-6	2012	Thioridazine suppressed phosphorylation of the signaling regulators downstream of the focal adhesion kinase (FAK) through alphavbeta3 integrin, which also include Akt, phosphoinositide-dependent protein kinase 1 (PDK-1), mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (p70S6K), but had no effect on VEGF-stimulated extracellular signal-regulated kinase (ERK) phosphorylation.	Thioridazine	0-12	vascular endothelial growth factor A	Homo sapiens	318-322
23022044-6	2012	Thioridazine suppressed phosphorylation of the signaling regulators downstream of the focal adhesion kinase (FAK) through alphavbeta3 integrin, which also include Akt, phosphoinositide-dependent protein kinase 1 (PDK-1), mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (p70S6K), but had no effect on VEGF-stimulated extracellular signal-regulated kinase (ERK) phosphorylation.	Thioridazine	0-12	mitogen-activated protein kinase 1	Homo sapiens	334-371
23022044-6	2012	Thioridazine suppressed phosphorylation of the signaling regulators downstream of the focal adhesion kinase (FAK) through alphavbeta3 integrin, which also include Akt, phosphoinositide-dependent protein kinase 1 (PDK-1), mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (p70S6K), but had no effect on VEGF-stimulated extracellular signal-regulated kinase (ERK) phosphorylation.	Thioridazine	0-12	mitogen-activated protein kinase 1	Homo sapiens	373-376
23203067-5	2012	Daunomycin, doxorubicin, thioridazine, and trifluoperazine showed strong affinity to the S1 site, which is a central cavity formed between three domains of CASQ2.	Thioridazine	25-37	calsequestrin 2	Canis lupus familiaris	156-161
23022044-0	2012	Anti-angiogenic effects of thioridazine involving the FAK-mTOR pathway.	Thioridazine	27-39	protein tyrosine kinase 2	Homo sapiens	54-57
23022044-0	2012	Anti-angiogenic effects of thioridazine involving the FAK-mTOR pathway.	Thioridazine	27-39	mechanistic target of rapamycin kinase	Homo sapiens	58-62
23022044-4	2012	Thioridazine also suppressed vascular endothelial growth factor (VEGF)-stimulated HUVEC migration in a dose-time-dependent manner.	Thioridazine	0-12	vascular endothelial growth factor A	Homo sapiens	29-63
23022044-4	2012	Thioridazine also suppressed vascular endothelial growth factor (VEGF)-stimulated HUVEC migration in a dose-time-dependent manner.	Thioridazine	0-12	vascular endothelial growth factor A	Homo sapiens	65-69
23022044-5	2012	We also showed that being treated with thioridazine inhibited VEGF-stimulated proliferation, invasion, and capillary-like structure tube formation in vitro.	Thioridazine	39-51	vascular endothelial growth factor A	Homo sapiens	62-66
23022044-6	2012	Thioridazine suppressed phosphorylation of the signaling regulators downstream of the focal adhesion kinase (FAK) through alphavbeta3 integrin, which also include Akt, phosphoinositide-dependent protein kinase 1 (PDK-1), mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (p70S6K), but had no effect on VEGF-stimulated extracellular signal-regulated kinase (ERK) phosphorylation.	Thioridazine	0-12	protein tyrosine kinase 2	Homo sapiens	86-107
23022044-6	2012	Thioridazine suppressed phosphorylation of the signaling regulators downstream of the focal adhesion kinase (FAK) through alphavbeta3 integrin, which also include Akt, phosphoinositide-dependent protein kinase 1 (PDK-1), mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (p70S6K), but had no effect on VEGF-stimulated extracellular signal-regulated kinase (ERK) phosphorylation.	Thioridazine	0-12	protein tyrosine kinase 2	Homo sapiens	109-112
22985512-4	2012	Under the experimental conditions, thioridazine caused VLCFA accumulation and increases in Abeta(40) content, APP immunoreactivity and APP(751+770) mRNA expressions in the rat cerebral cortex.	Thioridazine	35-47	amyloid beta precursor protein	Rattus norvegicus	91-96
22460505-0	2012	Thioridazine induces apoptosis by targeting the PI3K/Akt/mTOR pathway in cervical and endometrial cancer cells.	Thioridazine	0-12	AKT serine/threonine kinase 1	Homo sapiens	53-56
22460505-0	2012	Thioridazine induces apoptosis by targeting the PI3K/Akt/mTOR pathway in cervical and endometrial cancer cells.	Thioridazine	0-12	mechanistic target of rapamycin kinase	Homo sapiens	57-61
22460505-4	2012	Cell cycle analysis indicated thioridazine induced the down-regulation of cyclin D1, cyclin A and CDK4, and the induction of p21 and p27, a cyclin-dependent kinase inhibitor.	Thioridazine	30-42	cyclin D1	Homo sapiens	74-83
22460505-4	2012	Cell cycle analysis indicated thioridazine induced the down-regulation of cyclin D1, cyclin A and CDK4, and the induction of p21 and p27, a cyclin-dependent kinase inhibitor.	Thioridazine	30-42	cyclin A2	Homo sapiens	85-93
22460505-4	2012	Cell cycle analysis indicated thioridazine induced the down-regulation of cyclin D1, cyclin A and CDK4, and the induction of p21 and p27, a cyclin-dependent kinase inhibitor.	Thioridazine	30-42	cyclin dependent kinase 4	Homo sapiens	98-102
22460505-4	2012	Cell cycle analysis indicated thioridazine induced the down-regulation of cyclin D1, cyclin A and CDK4, and the induction of p21 and p27, a cyclin-dependent kinase inhibitor.	Thioridazine	30-42	H3 histone pseudogene 16	Homo sapiens	125-128
22460505-4	2012	Cell cycle analysis indicated thioridazine induced the down-regulation of cyclin D1, cyclin A and CDK4, and the induction of p21 and p27, a cyclin-dependent kinase inhibitor.	Thioridazine	30-42	dynactin subunit 6	Homo sapiens	133-136
22460505-6	2012	Furthermore, as expected, thioridazine successfully inhibited phosphorylation of Akt, phosphorylation of 4E-BP1 and phosphorylation of p70S6K, which is one of the best characterized targets of the mTOR complex cascade.	Thioridazine	26-38	AKT serine/threonine kinase 1	Homo sapiens	81-84
22460505-6	2012	Furthermore, as expected, thioridazine successfully inhibited phosphorylation of Akt, phosphorylation of 4E-BP1 and phosphorylation of p70S6K, which is one of the best characterized targets of the mTOR complex cascade.	Thioridazine	26-38	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	105-111
22460505-6	2012	Furthermore, as expected, thioridazine successfully inhibited phosphorylation of Akt, phosphorylation of 4E-BP1 and phosphorylation of p70S6K, which is one of the best characterized targets of the mTOR complex cascade.	Thioridazine	26-38	ribosomal protein S6 kinase B1	Homo sapiens	135-141
22460505-6	2012	Furthermore, as expected, thioridazine successfully inhibited phosphorylation of Akt, phosphorylation of 4E-BP1 and phosphorylation of p70S6K, which is one of the best characterized targets of the mTOR complex cascade.	Thioridazine	26-38	mechanistic target of rapamycin kinase	Homo sapiens	197-201
22460505-7	2012	These results suggest that thioridazine effectively suppresses tumor growth activity by targeting the PI3K/Akt/mTOR/p70S6K signaling pathway.	Thioridazine	27-39	AKT serine/threonine kinase 1	Homo sapiens	107-110
22460505-7	2012	These results suggest that thioridazine effectively suppresses tumor growth activity by targeting the PI3K/Akt/mTOR/p70S6K signaling pathway.	Thioridazine	27-39	mechanistic target of rapamycin kinase	Homo sapiens	111-115
22460505-7	2012	These results suggest that thioridazine effectively suppresses tumor growth activity by targeting the PI3K/Akt/mTOR/p70S6K signaling pathway.	Thioridazine	27-39	ribosomal protein S6 kinase B1	Homo sapiens	116-122
21976621-4	2012	The inhibition profiles of 20 known inhibitors of CYP2D6 were characterized in vitro against four clinically relevant CYP2D6 substrates (desipramine, dextromethorphan, metoprolol, and thioridazine) and bufuralol.	Thioridazine	184-196	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	50-56
23406751-6	2012	Chronic treatment of rats with thioridazine diminished the protein level and activity of CYP3A, while risperidone induced this enzyme.	Thioridazine	31-43	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	89-94
22044918-2	2011	Fluphenazine, thioridazine, triflupromazine, chlorpromazine, and promazine reversibly inhibited acetylcholine (100 muM)-induced currents with IC50 values of 3.8; 5.8; 6.1; 10.6 and 18.3 muM, respectively.	Thioridazine	14-26	latexin	Homo sapiens	115-118
22044918-2	2011	Fluphenazine, thioridazine, triflupromazine, chlorpromazine, and promazine reversibly inhibited acetylcholine (100 muM)-induced currents with IC50 values of 3.8; 5.8; 6.1; 10.6 and 18.3 muM, respectively.	Thioridazine	14-26	latexin	Homo sapiens	186-189
22157679-9	2011	The pharmacological compounds sertraline and thioridazine increase the amount of P53 by neutralizing TCTP"s action on the MDM2-P53 axis.	Thioridazine	45-57	transformation related protein 53, pseudogene	Mus musculus	81-84
22157679-9	2011	The pharmacological compounds sertraline and thioridazine increase the amount of P53 by neutralizing TCTP"s action on the MDM2-P53 axis.	Thioridazine	45-57	tumor protein, translationally-controlled 1	Mus musculus	101-105
22157679-9	2011	The pharmacological compounds sertraline and thioridazine increase the amount of P53 by neutralizing TCTP"s action on the MDM2-P53 axis.	Thioridazine	45-57	transformed mouse 3T3 cell double minute 2	Mus musculus	122-126
22157679-9	2011	The pharmacological compounds sertraline and thioridazine increase the amount of P53 by neutralizing TCTP"s action on the MDM2-P53 axis.	Thioridazine	45-57	transformation related protein 53, pseudogene	Mus musculus	127-130
22358097-3	2011	The investigated neuroleptics added to control liver microsomes produced some inhibitory effects on CYP2C11 activity, which were moderate (thioridazine: K(i) = 55), modest (sertindole and perazine: K(i) = 76 and 94 muM, respectively) or week (promazine, levomepromazine, haloperidol and chlorpromazine: K(i) = 285, 280, 223 and 157 muM, respectively).	Thioridazine	139-151	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	100-107
21035837-0	2011	A gene signature-based approach identifies thioridazine as an inhibitor of phosphatidylinositol-3"-kinase (PI3K)/AKT pathway in ovarian cancer cells.	Thioridazine	43-55	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	75-105
21035837-0	2011	A gene signature-based approach identifies thioridazine as an inhibitor of phosphatidylinositol-3"-kinase (PI3K)/AKT pathway in ovarian cancer cells.	Thioridazine	43-55	AKT serine/threonine kinase 1	Homo sapiens	113-116
21035837-3	2011	METHODS: Using in-silico gene signature based approach, we have demonstrated that thioridazine could inhibit phosphatidylinositol-3"-kinase (PI3K)/Akt pathway, and thus exert cytotoxicity in ovarian cancer cells.	Thioridazine	82-94	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	109-139
21035837-3	2011	METHODS: Using in-silico gene signature based approach, we have demonstrated that thioridazine could inhibit phosphatidylinositol-3"-kinase (PI3K)/Akt pathway, and thus exert cytotoxicity in ovarian cancer cells.	Thioridazine	82-94	AKT serine/threonine kinase 1	Homo sapiens	147-150
21035837-6	2011	In SKOV-3 cells, immunoblot using p85 antibody showed that thioridazine could inhibit PI3K signal.	Thioridazine	59-71	phosphoinositide-3-kinase regulatory subunit 2	Homo sapiens	34-37
21035837-7	2011	In addition, thioridazine was found to inhibit p-Akt (Ser 473) in a dose-dependent manner.	Thioridazine	13-25	AKT serine/threonine kinase 1	Homo sapiens	49-52
21035837-9	2011	Exposure to thioridazine induced G(0)/G(1) arrest and down-regulated the cell cycle regulator, Cyclin D1 and CDK4, and up-regulated p21, p16, and p-CDC25A.	Thioridazine	12-24	cyclin D1	Homo sapiens	95-104
22199281-0	2011	Thioridazine induces apoptosis of multidrug-resistant mouse lymphoma cells transfected with the human ABCB1 and inhibits the expression of P-glycoprotein.	Thioridazine	0-12	ATP binding cassette subfamily B member 1	Homo sapiens	102-107
22199281-0	2011	Thioridazine induces apoptosis of multidrug-resistant mouse lymphoma cells transfected with the human ABCB1 and inhibits the expression of P-glycoprotein.	Thioridazine	0-12	ATP binding cassette subfamily B member 1	Homo sapiens	139-153
22199281-3	2011	We have studied thioridazine (TZ), a phenothiazine neuroleptic that is much milder, for activity against multidrug-resistant (MDR) cancer cells, as well as against the overexpressed ABCB1 transporter (P-glycoprotein) that is the cause for the MDR phenotype of these cancer cells.	Thioridazine	30-32	ATP binding cassette subfamily B member 1	Homo sapiens	201-215
22199281-4	2011	MATERIALS AND METHODS: MDR mouse T-lymphoma cells, transfected with the human gene ABCB1 that codes for the transporter ABCB1, were incubated with TZ for various periods of time and examined for evidence of apoptosis.	Thioridazine	147-149	ATP binding cassette subfamily B member 1	Homo sapiens	83-88
22199281-5	2011	Concentrations of TZ were evaluated for activity against the ABCB1 transporter with the aid of an automated ethidium bromide (EB) method.	Thioridazine	18-20	ATP binding cassette subfamily B member 1	Homo sapiens	61-66
22199281-6	2011	RESULTS: TZ induces apoptosis of MDR cancer cell line, as well as inhibits the activity of the overexpressed ABCB1 transporter of these cells.	Thioridazine	9-11	ATP binding cassette subfamily B member 1	Homo sapiens	109-114
21035837-9	2011	Exposure to thioridazine induced G(0)/G(1) arrest and down-regulated the cell cycle regulator, Cyclin D1 and CDK4, and up-regulated p21, p16, and p-CDC25A.	Thioridazine	12-24	cyclin dependent kinase 4	Homo sapiens	109-113
21035837-9	2011	Exposure to thioridazine induced G(0)/G(1) arrest and down-regulated the cell cycle regulator, Cyclin D1 and CDK4, and up-regulated p21, p16, and p-CDC25A.	Thioridazine	12-24	H3 histone pseudogene 16	Homo sapiens	132-135
21035837-9	2011	Exposure to thioridazine induced G(0)/G(1) arrest and down-regulated the cell cycle regulator, Cyclin D1 and CDK4, and up-regulated p21, p16, and p-CDC25A.	Thioridazine	12-24	cyclin dependent kinase inhibitor 2A	Homo sapiens	137-140
21035837-9	2011	Exposure to thioridazine induced G(0)/G(1) arrest and down-regulated the cell cycle regulator, Cyclin D1 and CDK4, and up-regulated p21, p16, and p-CDC25A.	Thioridazine	12-24	cell division cycle 25A	Homo sapiens	148-154
22358097-6	2011	Of the neuroleptics studied, only chronic treatment with levomepromazine, perazine and thioridazine diminished CYP2C11 activity; those effects were positively correlated with the observed decreases in the protein level of the enzyme.	Thioridazine	87-99	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	111-118
23226058-3	2011	For example, individuals with the CYP2D6 loss-of-function genotype are at increased risk for ventricular arrhythmia if treated with usual does of thioridazine.	Thioridazine	146-158	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	34-40
20615392-7	2010	The obtained results indicate that the catalysis of chlorpromazine N-demethylation and 5-sulfoxidation in humans exhibits a stricter CYP1A2 preference compared to the previously tested phenothiazines (promazine, perazine, and thioridazine).	Thioridazine	226-238	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	133-139
20097249-7	2010	Aripiprazole, perphenazine, thioridazine, and fluoxetine were determined to be the potent hCES1 inhibitors.	Thioridazine	28-40	carboxylesterase 1	Homo sapiens	90-95