PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
20214592-6	2009	CYP2C8 is a major catalyst in the metabolism of paclitaxel, amodiaquine, troglitazone, amiodarone, verapamil and ibuprofen, with a secondary role in the biotransformation of cerivastatin and fluvastatin.	Amodiaquine	60-71	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	0-6
19926036-5	2009	For example, there is a clear association between concentrations of proguanil within plasma and certain genetic polymorphisms of CYP2C19, and genetically established levels of CYP2C8 might have important clinical implications in the toxicity of amodiaquine.	Amodiaquine	245-256	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	129-136
19926036-5	2009	For example, there is a clear association between concentrations of proguanil within plasma and certain genetic polymorphisms of CYP2C19, and genetically established levels of CYP2C8 might have important clinical implications in the toxicity of amodiaquine.	Amodiaquine	245-256	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	176-182
20126327-2	2009	Both subjects were homozygous for the wild type allele of cytochrome P450 2C8, the main enzyme responsible for amodiaquine metabolism.	Amodiaquine	111-122	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	58-77
19074972-0	2009	Novel metabolites of amodiaquine formed by CYP1A1 and CYP1B1: structure elucidation using electrochemistry, mass spectrometry, and NMR.	Amodiaquine	21-32	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	43-49
19184353-6	2009	Histamine fluxes accounted for <25 % of hist-rad fluxes, but this percentage increased after blocking HMT (100 microM amodiaquin) or DAO (100 microM aminoguanidine).	Amodiaquine	121-131	histamine N-methyltransferase	Sus scrofa	105-108
19074972-0	2009	Novel metabolites of amodiaquine formed by CYP1A1 and CYP1B1: structure elucidation using electrochemistry, mass spectrometry, and NMR.	Amodiaquine	21-32	cytochrome P450, family 1, subfamily b, polypeptide 1	Rattus norvegicus	54-60
19074972-9	2009	Three additional new metabolites of amodiaquine and desethylamodiaquine were formed via rCYP1A1 and rCYP1B1.	Amodiaquine	36-47	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	88-95
19074972-9	2009	Three additional new metabolites of amodiaquine and desethylamodiaquine were formed via rCYP1A1 and rCYP1B1.	Amodiaquine	36-47	cytochrome P450, family 1, subfamily b, polypeptide 1	Rattus norvegicus	100-107
29788622-4	2008	Amodiaquine and isoniazid are metabolized polymorphically by CYP2C8 and N-acetyltransferase 2, respectively.	Amodiaquine	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	61-67
18779360-0	2008	Effect of concomitant artesunate administration and cytochrome P4502C8 polymorphisms on the pharmacokinetics of amodiaquine in Ghanaian children with uncomplicated malaria.	Amodiaquine	112-123	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	52-70
29788622-4	2008	Amodiaquine and isoniazid are metabolized polymorphically by CYP2C8 and N-acetyltransferase 2, respectively.	Amodiaquine	0-11	N-acetyltransferase 2	Homo sapiens	72-93
18855526-2	2008	Amodiaquine is mainly metabolized hepatically towards its major active metabolite desethylamodiaquine, by the polymorphic P450 isoform CYP2C8.	Amodiaquine	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	135-141
17361129-0	2007	Amodiaquine metabolism is impaired by common polymorphisms in CYP2C8: implications for malaria treatment in Africa.	Amodiaquine	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	62-68
18444659-2	2008	We investigated in this study the down-regulative effects of 5-caffeoylquinic acid (CQA), the predominant isomer of CHA, on the H(2)O(2-) or TNF-alpha-induced secretion of interleukin (IL)-8, a central pro-inflammatory chemokine involved in the pathogenesis of inflammatory bowel diseases, in human intestinal epithelial Caco-2 cells.	Amodiaquine	84-87	tumor necrosis factor	Homo sapiens	141-150
18444659-2	2008	We investigated in this study the down-regulative effects of 5-caffeoylquinic acid (CQA), the predominant isomer of CHA, on the H(2)O(2-) or TNF-alpha-induced secretion of interleukin (IL)-8, a central pro-inflammatory chemokine involved in the pathogenesis of inflammatory bowel diseases, in human intestinal epithelial Caco-2 cells.	Amodiaquine	84-87	C-X-C motif chemokine ligand 8	Homo sapiens	172-190
18444659-3	2008	After the cells had been pre- and simultaneously treated with CQA, the oversecretion of IL-8 and overexpression of its mRNA induced by H(2)O(2) were significantly suppressed in a dose-dependent manner in the range of 0.25-2.00 mmol/L.	Amodiaquine	62-65	C-X-C motif chemokine ligand 8	Homo sapiens	88-92
18444659-4	2008	We further found that a metabolite of CQA, caffeic acid (CA), but not quinic acid, significantly inhibited the H(2)O(2)-induced IL-8 secretion and its mRNA expression in the same dose-dependent manner.	Amodiaquine	38-41	C-X-C motif chemokine ligand 8	Homo sapiens	128-132
18255358-1	2008	The antimalarial drug amodiaquine is extensively metabolized to N-desethylamodiaquine (DEAQ) by cytochrome P450 2C8 (CYP2C8).	Amodiaquine	22-33	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	96-115
18255358-1	2008	The antimalarial drug amodiaquine is extensively metabolized to N-desethylamodiaquine (DEAQ) by cytochrome P450 2C8 (CYP2C8).	Amodiaquine	22-33	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	117-123
18758509-6	2008	The alkalinizing lysosomotropic drugs chloroquine, hydroxychloroquine, amodiaquine, and azithromycin had a similar effect on the overall production of mature bioactive TGFbeta.	Amodiaquine	71-82	transforming growth factor beta 1	Homo sapiens	168-175
17361129-1	2007	Metabolism of the antimalarial drug amodiaquine (AQ) into its primary metabolite, N-desethylamodiaquine, is mediated by CYP2C8.	Amodiaquine	36-47	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	120-126
17361129-1	2007	Metabolism of the antimalarial drug amodiaquine (AQ) into its primary metabolite, N-desethylamodiaquine, is mediated by CYP2C8.	Amodiaquine	49-51	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	120-126
17361129-2	2007	We studied the frequency of CYP2C8 variants in 275 malaria-infected patients in Burkina Faso, the metabolism of AQ by CYP2C8 variants, and the impact of other drugs on AQ metabolism.	Amodiaquine	112-114	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	118-124
17361129-5	2007	The variant most common in Africans, CYP2C8(*)2, showed defective metabolism of AQ (threefold higher K(m) and sixfold lower intrinsic clearance), and CYP2C8(*)3 had markedly decreased activity.	Amodiaquine	80-82	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	37-43
17361129-6	2007	Considering drugs likely to be coadministered with AQ, the antiretroviral drugs efavirenz, saquinavir, lopinavir, and tipranavir were potent CYP2C8 inhibitors at clinically relevant concentrations.	Amodiaquine	51-53	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	141-147
17361129-7	2007	Variable CYP2C8 activity owing to genetic variation and drug interactions may have important clinical implications for the efficacy and toxicity of AQ.	Amodiaquine	148-150	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	9-15
17222819-5	2007	In conclusion, the present findings suggested that the elevation of endogenous histamine by amodiaquine may thus play a protective role through the regulation of TNF-alpha production in endotoxin-induced hepatic injury mice.	Amodiaquine	92-103	tumor necrosis factor	Mus musculus	162-171
17417075-7	2007	For example, the parameter values for HF alone and with AQ were: Cmax 144 +/- 53 versus 164 +/- 58 microg/L; T1/2beta 142 +/- 23 versus 139 +/- 28 hours; Cl/F 37.3 +/- 13.9 versus 32.3 +/- 11.4 L/h; and metabolic ratio 1.2 +/- 0.5 vs 1.1 +/- 0.6 Similarly, the disposition of HFM was not significantly altered (P > 0.05) after an earlier exposure to amodiaquine.	Amodiaquine	56-58	interleukin 1 receptor like 1	Homo sapiens	109-121
17286541-5	2007	Amodiaquine is almost entirely metabolized by the polymorphic cytochrome P450 (CYP) isoform 2C8 to the pharmacologically active desethylamodiaquine.	Amodiaquine	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	62-77
17222819-0	2007	Effect of amodiaquine, a histamine N-methyltransferase inhibitor, on, Propionibacterium acnes and lipopolysaccharide-induced hepatitis in mice.	Amodiaquine	10-21	histamine N-methyltransferase	Mus musculus	25-54
17222819-1	2007	We examined whether treatment with amodiaquine, a potent inhibitor of histamine N-methyltransferase protects mice from Propionibacterium acnes (P. acnes)-primed and lipopolysaccharide (LPS)-induced hepatitis.	Amodiaquine	35-46	histamine N-methyltransferase	Mus musculus	70-99
17222819-3	2007	Pretreatment with amodiaquine also improved the survival rate of the hepatitis mice, and this improvement was partially associated with the decrease in serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT).	Amodiaquine	18-29	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	168-194
17222819-3	2007	Pretreatment with amodiaquine also improved the survival rate of the hepatitis mice, and this improvement was partially associated with the decrease in serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT).	Amodiaquine	18-29	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	196-199
17222819-3	2007	Pretreatment with amodiaquine also improved the survival rate of the hepatitis mice, and this improvement was partially associated with the decrease in serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT).	Amodiaquine	18-29	glutamic pyruvic transaminase, soluble	Mus musculus	205-229
17222819-3	2007	Pretreatment with amodiaquine also improved the survival rate of the hepatitis mice, and this improvement was partially associated with the decrease in serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT).	Amodiaquine	18-29	glutamic pyruvic transaminase, soluble	Mus musculus	231-234
17222819-4	2007	Amodiaquine partially suppressed increases of tumor necrosis factor (TNF)-alpha in the serum and TNF-alpha mRNA expression in the liver, whereas the expression of interleukin (IL)-18, interferon (IFN)-gamma and IL-12 in the liver was not changed by amodiaquine treatment.	Amodiaquine	0-11	tumor necrosis factor	Mus musculus	46-79
17222819-4	2007	Amodiaquine partially suppressed increases of tumor necrosis factor (TNF)-alpha in the serum and TNF-alpha mRNA expression in the liver, whereas the expression of interleukin (IL)-18, interferon (IFN)-gamma and IL-12 in the liver was not changed by amodiaquine treatment.	Amodiaquine	0-11	tumor necrosis factor	Mus musculus	97-106
17286541-5	2007	Amodiaquine is almost entirely metabolized by the polymorphic cytochrome P450 (CYP) isoform 2C8 to the pharmacologically active desethylamodiaquine.	Amodiaquine	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	79-82
16536934-1	2006	OBJECTIVES: To assess the relationship between the genetic and phenotypic factors linked to the cytochrome P-450 enzyme system and the response to the antimalarial drugs chloroquine, amodiaquine, mefloquine, and proguanil, as well as to determine how certain biological and social factors of the host influence the behavior of this enzymatic complex.	Amodiaquine	183-194	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	96-112
16783563-0	2006	Amodiaquine, its desethylated metabolite, or both, inhibit the metabolism of debrisoquine (CYP2D6) and losartan (CYP2C9) in vivo.	Amodiaquine	0-11	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	91-97
16783563-0	2006	Amodiaquine, its desethylated metabolite, or both, inhibit the metabolism of debrisoquine (CYP2D6) and losartan (CYP2C9) in vivo.	Amodiaquine	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
16783563-1	2006	OBJECTIVE: To study the extent of in vivo inhibition by the antimalarial drug amodiaquine, its active metabolite N-desethylamodiaquine, or both, of the metabolism of four probe drugs of the enzymes CYP2D6, CYP2C19, CYP2C9 and CYP1A2.	Amodiaquine	78-89	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	198-204
16783563-1	2006	OBJECTIVE: To study the extent of in vivo inhibition by the antimalarial drug amodiaquine, its active metabolite N-desethylamodiaquine, or both, of the metabolism of four probe drugs of the enzymes CYP2D6, CYP2C19, CYP2C9 and CYP1A2.	Amodiaquine	78-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	206-213
16783563-1	2006	OBJECTIVE: To study the extent of in vivo inhibition by the antimalarial drug amodiaquine, its active metabolite N-desethylamodiaquine, or both, of the metabolism of four probe drugs of the enzymes CYP2D6, CYP2C19, CYP2C9 and CYP1A2.	Amodiaquine	78-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	215-221
16783563-1	2006	OBJECTIVE: To study the extent of in vivo inhibition by the antimalarial drug amodiaquine, its active metabolite N-desethylamodiaquine, or both, of the metabolism of four probe drugs of the enzymes CYP2D6, CYP2C19, CYP2C9 and CYP1A2.	Amodiaquine	78-89	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	226-232
16783563-10	2006	The effects on CYP2D6 and CYP2C9 activities subsided within a week after intake of amodiaquine as tested by the phenotyping cocktail.	Amodiaquine	83-94	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	15-21
16783563-10	2006	The effects on CYP2D6 and CYP2C9 activities subsided within a week after intake of amodiaquine as tested by the phenotyping cocktail.	Amodiaquine	83-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
16783563-12	2006	CONCLUSION: A single dose of amodiaquine decreased CYP2D6 and CYP2C9 activities significantly compared to baseline values.	Amodiaquine	29-40	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	51-57
16783563-12	2006	CONCLUSION: A single dose of amodiaquine decreased CYP2D6 and CYP2C9 activities significantly compared to baseline values.	Amodiaquine	29-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
16168438-3	2005	The histamine receptor H1 antagonist diphenhydramine, the antimalarial drug amodiaquine, the antifolate drug metoprine, and the anticholinesterase drug tacrine (an early drug for Alzheimer"s disease) are surprisingly all potent HNMT inhibitors, having inhibition constants in the range of 10-100nM.	Amodiaquine	76-87	histamine N-methyltransferase	Homo sapiens	228-232
16359408-3	2005	The pro-drug AQ is transformed by cytochrome P450 CYP2C8 to the active metabolite N-desethylaminodiaquine.	Amodiaquine	13-15	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	50-56
16359408-7	2005	AQ metabolism in patients with CYP2C8*2 may be impaired, and with an increase of AQ based treatment the risk of severe adverse events may mount.	Amodiaquine	0-2	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	31-37
14681337-6	2004	Other classes of drugs that demonstrated inhibition of aldehyde oxidase included phenothiazines, tricyclic antidepressants, tricyclic atypical antipsychotic agents, and dihydropyridine calcium channel blockers, along with some other drugs, including loratadine, cyclobenzaprine, amodiaquine, maprotiline, ondansetron, propafenone, domperidone, quinacrine, ketoconazole, verapamil, tacrine, and salmeterol.	Amodiaquine	279-290	aldehyde oxidase 1	Homo sapiens	55-71
15785959-1	2005	OBJECTIVE: The determination of the prevalence of the CYP2C8 main alleles in a typical set of malaria patients in Zanzibar, as these patients represent a typical population exposed to amodiaquine, an antimalarial mainly metabolized by CYP2C8.	Amodiaquine	184-195	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	54-60
15601807-3	2005	A validated sensitive, moderate-throughput high-performance liquid chromatography/tandem mass spectrometry (HPLC/MS/MS) assay was used to detect N-desethylamodiaquine, the CYP2C8-derived major metabolite of amodiaquine metabolism, using heterologously expressed recombinant CYP2C8 (rhCYP2C8) and pooled human liver microsomes.	Amodiaquine	155-166	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	172-178
15601807-3	2005	A validated sensitive, moderate-throughput high-performance liquid chromatography/tandem mass spectrometry (HPLC/MS/MS) assay was used to detect N-desethylamodiaquine, the CYP2C8-derived major metabolite of amodiaquine metabolism, using heterologously expressed recombinant CYP2C8 (rhCYP2C8) and pooled human liver microsomes.	Amodiaquine	155-166	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	274-280
12082016-9	2002	Further exploration of antimalarial compounds identified the common medicinals chloroquine, quinacrine, and amodiaquine as Tp53-inducers.	Amodiaquine	108-119	tumor protein p53	Homo sapiens	123-127
12903974-1	2003	The non-covalent interactions between the monomeric phenolic compound chlorogenic acid (5-CQA) and bovine serum albumin (BSA), lysozyme, and alpha-lactalbumin were characterized, and their effect on protein properties was examined.	Amodiaquine	90-93	albumin	Homo sapiens	106-119
12903974-1	2003	The non-covalent interactions between the monomeric phenolic compound chlorogenic acid (5-CQA) and bovine serum albumin (BSA), lysozyme, and alpha-lactalbumin were characterized, and their effect on protein properties was examined.	Amodiaquine	90-93	lactalbumin alpha	Homo sapiens	141-158
12397395-7	2002	Blockade of histamine N-methyltransferase by amodiaquin (100 microM) abolished catabolism completely, whereas blockade of diamine oxidase by aminoguanidine (100 microM) was less effective.	Amodiaquine	45-55	histamine N-methyltransferase	Sus scrofa	12-41
11124226-7	2001	Proguanil, cycloguanil, amodiaquine, and desethylamodiaquine inhibited CYP2D6 (K(i) = 6.76, 5.97, 2.1, and 4.13 microM, respectively).	Amodiaquine	24-35	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	71-77
11805197-0	2002	Amodiaquine clearance and its metabolism to N-desethylamodiaquine is mediated by CYP2C8: a new high affinity and turnover enzyme-specific probe substrate.	Amodiaquine	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	81-87
11805197-3	2002	CYP2C8 was the main hepatic isoform that cleared AQ and catalyzed the formation of DEAQ. The extrahepatic P450s, 1A1 and 1B1, also cleared AQ and catalyzed the formation of an unknown metabolite M2.	Amodiaquine	49-51	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	0-6
11805197-3	2002	CYP2C8 was the main hepatic isoform that cleared AQ and catalyzed the formation of DEAQ. The extrahepatic P450s, 1A1 and 1B1, also cleared AQ and catalyzed the formation of an unknown metabolite M2.	Amodiaquine	49-51	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	106-124
11805197-3	2002	CYP2C8 was the main hepatic isoform that cleared AQ and catalyzed the formation of DEAQ. The extrahepatic P450s, 1A1 and 1B1, also cleared AQ and catalyzed the formation of an unknown metabolite M2.	Amodiaquine	85-87	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	0-6
11805197-3	2002	CYP2C8 was the main hepatic isoform that cleared AQ and catalyzed the formation of DEAQ. The extrahepatic P450s, 1A1 and 1B1, also cleared AQ and catalyzed the formation of an unknown metabolite M2.	Amodiaquine	85-87	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	106-124
11805197-7	2002	Both the formation of DEAQ and the clearance of AQ showed excellent correlations (r(2) = 0.98 and 0.95) with 6alpha-hydroxylation of paclitaxel, a marker substrate for CYP2C8.	Amodiaquine	24-26	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	168-174
11805197-9	2002	Docking of AQ into the active site homology models of the CYP2C isoforms showed favorable interactions with CYP2C8, which supported the likelihood of an N-desethylation reaction.	Amodiaquine	11-13	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	108-114
11805197-10	2002	These data show that CYP2C8 is the main hepatic isoform responsible for the metabolism of AQ.	Amodiaquine	90-92	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	21-27
11805197-11	2002	The specificity, high affinity, and high turnover make AQ desethylation an excellent marker reaction for CYP2C8 activity.	Amodiaquine	55-57	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	105-111
10831384-1	2000	A multidrug-resistant strain of Plasmodium yoelii nigeriensis (MDR) showing a wide spectrum of resistance to chloroquine, amodiaquine, mepacrine, mefloquine, halofantrine, quinine, and quinidine was used in this study for in vivo evaluation of the blood schizontocidal activity of pyronaridine, a topoisomerase II inhibitor, in Swiss mice.	Amodiaquine	122-133	malic enzyme complex, mitochondrial	Mus musculus	63-66
11140821-2	2000	Treatment of rats with 10 mg/kg (single dose) amodiaquine resulted in 10% and 63% increases, respectively in the activities of liver superoxide dismutase and glutathione peroxidase (P<0.01), while the activity of liver catalase was significantly reduced by 26% compared to control.	Amodiaquine	46-57	catalase	Rattus norvegicus	222-230
11140821-4	2000	Following multiple dose (10 mg/kg for 4 consecutive days) amodiaquine treatment, activities of superoxide dismutase and glutathione peroxidase were increased by 30% and 133% respectively while catalase activity was decreased by 45%.	Amodiaquine	58-69	catalase	Rattus norvegicus	193-201
11140821-9	2000	The activities of serum aspartate amino transferase, alanine amino transferase, ornithine carbamyl transferase and gamma-glutamyl transferase were significantly increased by both single and multiple doses of amodiaquine treatment (P<0.01).	Amodiaquine	208-219	gamma-glutamyltransferase 1	Rattus norvegicus	115-141
9736572-4	1998	The inclusion of a group at the C-5" position of amodiaquine reduced or eliminated bioactivation, as determined by glutathione conjugate formation in vivo.	Amodiaquine	49-60	hemolytic complement	Mus musculus	32-35
9736572-6	1998	Chemical substitution at the C-5" position also resulted in compounds which underwent slower elimination (<5% of the dose excreted into bile and urine, compared with 50% for amodiaquine) and increased levels of accumulation in tissue (10% of the dose in the liver at 48 h compared with 1% with amodiaquine).	Amodiaquine	177-188	hemolytic complement	Mus musculus	29-32
9736572-6	1998	Chemical substitution at the C-5" position also resulted in compounds which underwent slower elimination (<5% of the dose excreted into bile and urine, compared with 50% for amodiaquine) and increased levels of accumulation in tissue (10% of the dose in the liver at 48 h compared with 1% with amodiaquine).	Amodiaquine	297-308	hemolytic complement	Mus musculus	29-32
9736572-8	1998	The alteration in the disposition following the introduction of the C-5" substituent resulted in an increased duration of antimalarial activity in the mouse compared with that for amodiaquine.	Amodiaquine	180-191	hemolytic complement	Mus musculus	68-71
1346997-6	1992	Cyclosporine A was a potent competitive inhibitor of CQA metabolism, providing initial evidence that formation of metabolite I was catalyzed by proteins of the CYP3 gene family.	Amodiaquine	53-56	peptidylprolyl isomerase F	Homo sapiens	160-164
7714794-3	1995	Glutathione conjugates of AQ and desethylAQ were eliminated in bile after intraportal administration of [3H]AQ (54 mumol/kg, 20 microCi/kg) to anesthetized male CD1 mice.	Amodiaquine	26-28	CD1 antigen complex	Mus musculus	161-164
7816881-5	1994	The cholinesterase inhibitors tacrine (THA) and, to a lesser extent, physostigmine (PHYSO) and amodiaquine (AMDQ), caused an upward shift in the frequency of the resting electrocortical activity, although scopolamine significantly slowed the activity below baseline levels.	Amodiaquine	95-106	butyrylcholinesterase	Homo sapiens	4-18
7816881-5	1994	The cholinesterase inhibitors tacrine (THA) and, to a lesser extent, physostigmine (PHYSO) and amodiaquine (AMDQ), caused an upward shift in the frequency of the resting electrocortical activity, although scopolamine significantly slowed the activity below baseline levels.	Amodiaquine	108-112	butyrylcholinesterase	Homo sapiens	4-18
8145732-13	1994	IC50 values for the HNMT inhibitor amodiaquine were 0.50, 0.48, and 0.40 microM, respectively, for enzyme from these same three sources.	Amodiaquine	35-46	histamine N-methyltransferase	Homo sapiens	20-24
1346997-7	1992	This was substantiated by the finding that CQA metabolism was completely inhibited by a polyclonal antibody directed against a pregnenolone 16 alpha-carbonitrile-inducible cytochrome P-450 of rat liver.	Amodiaquine	43-46	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	172-188
1346997-8	1992	The rate of CQA metabolism correlated significantly to the level of CYP3A4 expression, the rate of cyclosporine A metabolism to each of the primary metabolites (M-1, M-17, and M-21), and the rate of midazolam 4-hydroxylation.	Amodiaquine	12-15	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	68-74
8329010-1	1993	The pharmacokinetics of amodiaquine (AQ, Flavoquine, CAS 6398-98-7) and its metabolites, mono (AQml) and bis-desethyl amodiaquine (AQm2) were investigated in 8 healthy volunteers after an oral dose of 306.2 mg of AQ.	Amodiaquine	24-35	BCAR1 scaffold protein, Cas family member	Homo sapiens	53-56
33588856-1	2021	BACKGROUND: The anti-malarial drug, amodiaquine, a commonly used, long-acting partner drug in artemisinin-based combination therapy, is metabolized to active desethyl-amodiaquine (DEAQ) by cytochrome P450 2C8 (CYP2C8).	Amodiaquine	36-47	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	189-208
33588856-1	2021	BACKGROUND: The anti-malarial drug, amodiaquine, a commonly used, long-acting partner drug in artemisinin-based combination therapy, is metabolized to active desethyl-amodiaquine (DEAQ) by cytochrome P450 2C8 (CYP2C8).	Amodiaquine	36-47	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	210-216
1907425-6	1991	IC50 values for the inhibition of mouse kidney HNMT by amodiaquine and S-adenosyl-L-homocysteine were 1.67 and 11.8 microM, respectively.	Amodiaquine	55-66	histamine N-methyltransferase	Mus musculus	47-51
34438008-0	2021	Development and Characterization of Inhalable Transferrin Functionalized Amodiaquine Nanoparticles - Efficacy in Non-small Cell Lung Cancer (NSCLC) Treatment.	Amodiaquine	73-84	transferrin	Homo sapiens	46-57
34592572-4	2021	We found that de-glycosylation at N331 and N343 drastically reduces the RBD binding to ACE2.	Amodiaquine	34-38	angiotensin converting enzyme 2	Homo sapiens	87-91
34438008-4	2021	In this study, targeting potential of transferrin ligand conjugated inhalable AQ-loaded nanoparticles (Tf-AMQ NPs) was investigated against NSCLC.	Amodiaquine	78-80	transferrin	Homo sapiens	38-49
34438008-6	2021	Cytotoxicity studies in NSCLC cell line with overexpressed transferrin receptors shown significant reduction in IC50 values with Tf-decorated AQ-loaded nanoparticles compared to AQ or non-targeted NPs, along with significant apoptosis induction (caspase assay) and reduced % colony growth in A549 and H1299 cells with Tf-AMQ NP.	Amodiaquine	142-144	transferrin	Homo sapiens	59-70
34438008-6	2021	Cytotoxicity studies in NSCLC cell line with overexpressed transferrin receptors shown significant reduction in IC50 values with Tf-decorated AQ-loaded nanoparticles compared to AQ or non-targeted NPs, along with significant apoptosis induction (caspase assay) and reduced % colony growth in A549 and H1299 cells with Tf-AMQ NP.	Amodiaquine	178-180	transferrin	Homo sapiens	59-70
34438008-8	2021	AQ"s autophagy inhibition ability significantly increased with nanoparticle encapsulation and transferrin conjugation.	Amodiaquine	0-2	transferrin	Homo sapiens	94-105
34438008-9	2021	In conclusion, amodiaquine can be an assuring candidate for repurposing to consider for NSCLC treatment while delivering inhalable transferrin conjugated nanoparticles developed using a scalable HPH process to the target site, thus reducing the dose, side effects.	Amodiaquine	15-26	transferrin	Homo sapiens	131-142
35429395-7	2022	The mdr1-YY haplotype, associated with chloroquine and amodiaquine resistance, decreased over time, while the NY (wildtype) and the NF (modulates response to lumefantrine) haplotypes increased.	Amodiaquine	55-66	ATP binding cassette subfamily B member 1	Homo sapiens	4-8
34808194-5	2021	We found that AQ effectively and significantly increased testosterone production in TM3 and primary Leydig cells through enhanced expression of StAR, CYP11A1, CYP17A1, and 3betaHSD.	Amodiaquine	14-16	steroidogenic acute regulatory protein	Mus musculus	144-148
34808194-5	2021	We found that AQ effectively and significantly increased testosterone production in TM3 and primary Leydig cells through enhanced expression of StAR, CYP11A1, CYP17A1, and 3betaHSD.	Amodiaquine	14-16	cytochrome P450, family 11, subfamily a, polypeptide 1	Mus musculus	150-157
34808194-5	2021	We found that AQ effectively and significantly increased testosterone production in TM3 and primary Leydig cells through enhanced expression of StAR, CYP11A1, CYP17A1, and 3betaHSD.	Amodiaquine	14-16	cytochrome P450, family 17, subfamily a, polypeptide 1	Mus musculus	159-166
34808194-6	2021	Concurrently, AQ dose-dependently increased the expression of 3-hydroxy-3-methylglutaryl-CoA reductase, a key enzyme in the cholesterol synthesis pathway, through induction of the transcriptional and DNA-binding activities of NR4A1, contributing to increased cholesterol synthesis in Leydig cells.	Amodiaquine	14-16	nuclear receptor subfamily 4, group A, member 1	Mus musculus	226-231
34808194-7	2021	Furthermore, AQ increased the expression of fatty acid synthase and diacylglycerol acyltransferase and potentiated de novo synthesis of fatty acids and triglycerides (TG).	Amodiaquine	13-15	fatty acid synthase	Mus musculus	44-63
35132775-0	2022	Scaffold hopping from amodiaquine to novel Nurr1 agonist chemotypes via microscale analogue libraries.	Amodiaquine	22-33	nuclear receptor subfamily 4 group A member 2	Homo sapiens	43-48
35132775-3	2022	To identify novel Nurr1 agonist chemotypes, we have employed the Nurr1 activator amodiaquine as template for microscale analogue library synthesis.	Amodiaquine	81-92	nuclear receptor subfamily 4 group A member 2	Homo sapiens	18-23
35132775-3	2022	To identify novel Nurr1 agonist chemotypes, we have employed the Nurr1 activator amodiaquine as template for microscale analogue library synthesis.	Amodiaquine	81-92	nuclear receptor subfamily 4 group A member 2	Homo sapiens	65-70
35474783-9	2022	Moreover, myricetin caused considerable elevation in the oral exposure of amodiaquine as a CYP2C8 substrate via a slowdown of amodiaquine clearance in the rat model.	Amodiaquine	74-85	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	91-97
35474783-5	2022	In the in vitro study, myricetin showed a substantial effect on CYP2C8 inhibition in human liver microsomes using CYP2C8-catalyzed amodiaquine-N-deethylation as an index reaction.	Amodiaquine	131-142	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	64-70
35474783-5	2022	In the in vitro study, myricetin showed a substantial effect on CYP2C8 inhibition in human liver microsomes using CYP2C8-catalyzed amodiaquine-N-deethylation as an index reaction.	Amodiaquine	131-142	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	114-120
35474783-9	2022	Moreover, myricetin caused considerable elevation in the oral exposure of amodiaquine as a CYP2C8 substrate via a slowdown of amodiaquine clearance in the rat model.	Amodiaquine	126-137	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	91-97
35110426-0	2022	Inhibition of stearoyl-CoA desaturase 1 potentiates anti-tumor activity of amodiaquine in non-small cell lung cancer.	Amodiaquine	75-86	stearoyl-Coenzyme A desaturase 1	Mus musculus	14-39
35110426-4	2022	Here, we found that amodiaquine (AQ) increased autophagosome numbers and LC3BII and p62 at protein levels in A549 lung cancer cells suggesting the blockade of autophagic flux by AQ.	Amodiaquine	20-31	nucleoporin 62	Mus musculus	84-87
35110426-4	2022	Here, we found that amodiaquine (AQ) increased autophagosome numbers and LC3BII and p62 at protein levels in A549 lung cancer cells suggesting the blockade of autophagic flux by AQ.	Amodiaquine	33-35	nucleoporin 62	Mus musculus	84-87
35110426-4	2022	Here, we found that amodiaquine (AQ) increased autophagosome numbers and LC3BII and p62 at protein levels in A549 lung cancer cells suggesting the blockade of autophagic flux by AQ.	Amodiaquine	178-180	nucleoporin 62	Mus musculus	84-87
35110426-5	2022	To identify the key metabolic vulnerability associated with autophagy inhibition by AQ treatment, we then performed transcriptomics analysis in the presence or absence of AQ in A549 lung cancer cells and found stearoyl-CoA desaturase 1 (SCD) 1 was one of the most highly upregulated with AQ exposure.	Amodiaquine	84-86	stearoyl-Coenzyme A desaturase 1	Mus musculus	210-243
35110426-5	2022	To identify the key metabolic vulnerability associated with autophagy inhibition by AQ treatment, we then performed transcriptomics analysis in the presence or absence of AQ in A549 lung cancer cells and found stearoyl-CoA desaturase 1 (SCD) 1 was one of the most highly upregulated with AQ exposure.	Amodiaquine	171-173	stearoyl-Coenzyme A desaturase 1	Mus musculus	210-243
35110426-5	2022	To identify the key metabolic vulnerability associated with autophagy inhibition by AQ treatment, we then performed transcriptomics analysis in the presence or absence of AQ in A549 lung cancer cells and found stearoyl-CoA desaturase 1 (SCD) 1 was one of the most highly upregulated with AQ exposure.	Amodiaquine	288-290	stearoyl-Coenzyme A desaturase 1	Mus musculus	210-243
35110426-6	2022	The induction of SCD1 by AQ exposure at both protein and mRNA level suggests that SCD1 could represent a potential therapeutic target of AQ treatment.	Amodiaquine	25-27	stearoyl-Coenzyme A desaturase 1	Mus musculus	17-21
35110426-6	2022	The induction of SCD1 by AQ exposure at both protein and mRNA level suggests that SCD1 could represent a potential therapeutic target of AQ treatment.	Amodiaquine	25-27	stearoyl-Coenzyme A desaturase 1	Mus musculus	82-86
35110426-6	2022	The induction of SCD1 by AQ exposure at both protein and mRNA level suggests that SCD1 could represent a potential therapeutic target of AQ treatment.	Amodiaquine	137-139	stearoyl-Coenzyme A desaturase 1	Mus musculus	17-21
35110426-6	2022	The induction of SCD1 by AQ exposure at both protein and mRNA level suggests that SCD1 could represent a potential therapeutic target of AQ treatment.	Amodiaquine	137-139	stearoyl-Coenzyme A desaturase 1	Mus musculus	82-86
35110426-8	2022	Taken together, our study identified SCD1 could be a new therapeutic target upon autophagy inhibition by AQ exposure.	Amodiaquine	105-107	stearoyl-Coenzyme A desaturase 1	Mus musculus	37-41
3337739-2	1988	Amodiaquine was clearly the most potent HMT inhibitor followed by quinacrine, chlorhexidine, alcuronium and chloroquine.	Amodiaquine	0-11	histamine N-methyltransferase	Rattus norvegicus	40-43
6380785-5	1984	The mefloquine-resistant Camp strain remained sensitive to chloroquine and amodiaquine, and became slightly more resistant to quinine; there was increased sensitivity to pyrimethamine.	Amodiaquine	75-86	cathelicidin antimicrobial peptide	Homo sapiens	25-29
4028443-7	1985	The Kii for inhibition of the RBC enzyme by amodiaquine, an HNMT inhibitor, was 1.0 X 10(-7) mol/l, while the Kis value was 0.48 X 10(-7) mol/l.	Amodiaquine	44-55	histamine N-methyltransferase	Homo sapiens	60-64
3832018-1	1985	Four compounds: amodiaquine, quinacrine, 1,4-(tele)-methylhistamine and metoprine, which in vitro effectively inhibit histamine N-methyltransferase (HMT) activity, were tested for their effects on histamine (HI) levels in the rat brain and ex vivo HMT activity.	Amodiaquine	16-27	histamine N-methyltransferase	Rattus norvegicus	118-147
3832018-1	1985	Four compounds: amodiaquine, quinacrine, 1,4-(tele)-methylhistamine and metoprine, which in vitro effectively inhibit histamine N-methyltransferase (HMT) activity, were tested for their effects on histamine (HI) levels in the rat brain and ex vivo HMT activity.	Amodiaquine	16-27	histamine N-methyltransferase	Rattus norvegicus	149-152
3832018-3	1985	Amodiaquine, quinacrine and 1,4-(tele)-methyl-HI weakly inhibited HMT activity ex vivo and they failed to alter HI levels in the rat brain.	Amodiaquine	0-11	histamine N-methyltransferase	Rattus norvegicus	66-69
33507465-9	2021	In the same vein, we found that amodiaquine substantially increased the level of phosphorylated P38 Mapk.	Amodiaquine	32-43	mitogen-activated protein kinase 14	Mus musculus	96-104
7110523-1	1982	The effects of histamine and amodiaquine (a drug known to inhibit histamine-N-methyltransferase) on pulsatile growth hormone (GH) secretion were determined in unanaesthetized male rats.	Amodiaquine	29-40	gonadotropin releasing hormone receptor	Rattus norvegicus	110-124
7110523-1	1982	The effects of histamine and amodiaquine (a drug known to inhibit histamine-N-methyltransferase) on pulsatile growth hormone (GH) secretion were determined in unanaesthetized male rats.	Amodiaquine	29-40	gonadotropin releasing hormone receptor	Rattus norvegicus	126-128
7256355-1	1981	The antimalarial agent, amodiaquine, is a potent inhibitor of AChE (Ki = 1.50 x 10(-9) M, pH 7.4, 25 degrees C).	Amodiaquine	24-35	acetylcholinesterase (Cartwright blood group)	Homo sapiens	62-66
7256355-2	1981	Both the protonated diethylamino and phenolic hydroxyl functions of amodiaquine are necessary for interaction with AChE.	Amodiaquine	68-79	acetylcholinesterase (Cartwright blood group)	Homo sapiens	115-119
7256355-3	1981	This suggests that the inhibition of AChE by amodiaquine may involve binding of the protonated diethylamino and phenolic hydroxyl functions to the anionic and esteric sites of the enzyme respectively.	Amodiaquine	45-56	acetylcholinesterase (Cartwright blood group)	Homo sapiens	37-41
7256355-4	1981	The anti-AChE property of amodiaquine may be related in some way to the gastrointestinal and central nervous system disturbances frequently encountered when large doses of amodiaquine are used for the treatment of malaria.	Amodiaquine	26-37	acetylcholinesterase (Cartwright blood group)	Homo sapiens	9-13
7256355-4	1981	The anti-AChE property of amodiaquine may be related in some way to the gastrointestinal and central nervous system disturbances frequently encountered when large doses of amodiaquine are used for the treatment of malaria.	Amodiaquine	172-183	acetylcholinesterase (Cartwright blood group)	Homo sapiens	9-13
33875422-10	2021	Between one in three and one in six individuals harbored reduced activity alleles of CYP2A6, CYP2B6, CYP2D6 and CYP2C8 with important implications for artemisinin, chloroquine and amodiaquine therapy.	Amodiaquine	180-191	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	85-91
33875422-10	2021	Between one in three and one in six individuals harbored reduced activity alleles of CYP2A6, CYP2B6, CYP2D6 and CYP2C8 with important implications for artemisinin, chloroquine and amodiaquine therapy.	Amodiaquine	180-191	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	93-99
33875422-10	2021	Between one in three and one in six individuals harbored reduced activity alleles of CYP2A6, CYP2B6, CYP2D6 and CYP2C8 with important implications for artemisinin, chloroquine and amodiaquine therapy.	Amodiaquine	180-191	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	101-107
33875422-10	2021	Between one in three and one in six individuals harbored reduced activity alleles of CYP2A6, CYP2B6, CYP2D6 and CYP2C8 with important implications for artemisinin, chloroquine and amodiaquine therapy.	Amodiaquine	180-191	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	112-118
6789797-1	1980	Amodiaquine, 10(-5) M, totally inhibited the activity of histamine-methyltransferase (HMT) in the rat brain.	Amodiaquine	0-11	histamine N-methyltransferase	Rattus norvegicus	86-89
33507465-11	2021	These results collectively suggest that amodiaquine can augment tyrosine hydroxylase expression via phosphorylated P38 Mapk while negatively regulating the phosphorylated Akt in protein expression.	Amodiaquine	40-51	tyrosine hydroxylase	Mus musculus	64-84
33507465-11	2021	These results collectively suggest that amodiaquine can augment tyrosine hydroxylase expression via phosphorylated P38 Mapk while negatively regulating the phosphorylated Akt in protein expression.	Amodiaquine	40-51	mitogen-activated protein kinase 14	Mus musculus	115-123
33507465-11	2021	These results collectively suggest that amodiaquine can augment tyrosine hydroxylase expression via phosphorylated P38 Mapk while negatively regulating the phosphorylated Akt in protein expression.	Amodiaquine	40-51	thymoma viral proto-oncogene 1	Mus musculus	171-174
33629841-2	2021	We have systematically studied the structure-activity relationship of the 4-amino-7-chloroquinoline scaffold contained in Nurr1 activators amodiaquine and chloroquine and discovered fragment-like analogues that activated Nurr1 in several cellular settings.	Amodiaquine	139-150	nuclear receptor subfamily 4 group A member 2	Homo sapiens	122-127
33629841-2	2021	We have systematically studied the structure-activity relationship of the 4-amino-7-chloroquinoline scaffold contained in Nurr1 activators amodiaquine and chloroquine and discovered fragment-like analogues that activated Nurr1 in several cellular settings.	Amodiaquine	139-150	nuclear receptor subfamily 4 group A member 2	Homo sapiens	221-226
32924342-0	2020	Beneficial Effect of Chloroquine and Amodiaquine on Type 1 Diabetic Tubulopathy by Attenuating Mitochondrial Nox4 and Endoplasmic Reticulum Stress.	Amodiaquine	37-48	NADPH oxidase 4	Mus musculus	109-113
33441761-6	2021	Further studies on cytochrome b5 (CYB5), an alternative NADH-dependent electron donor indicated particularly strong support of CYP2C8-dependent amodiaquine N-deethylation by CYB5 and this was confirmed by genetic CYB5 single- and POR/CYB5 double-knockout.	Amodiaquine	144-155	cytochrome b5 type A	Homo sapiens	19-32
33441761-6	2021	Further studies on cytochrome b5 (CYB5), an alternative NADH-dependent electron donor indicated particularly strong support of CYP2C8-dependent amodiaquine N-deethylation by CYB5 and this was confirmed by genetic CYB5 single- and POR/CYB5 double-knockout.	Amodiaquine	144-155	cytochrome b5 type A	Homo sapiens	34-38
33441761-6	2021	Further studies on cytochrome b5 (CYB5), an alternative NADH-dependent electron donor indicated particularly strong support of CYP2C8-dependent amodiaquine N-deethylation by CYB5 and this was confirmed by genetic CYB5 single- and POR/CYB5 double-knockout.	Amodiaquine	144-155	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	127-133
33441761-6	2021	Further studies on cytochrome b5 (CYB5), an alternative NADH-dependent electron donor indicated particularly strong support of CYP2C8-dependent amodiaquine N-deethylation by CYB5 and this was confirmed by genetic CYB5 single- and POR/CYB5 double-knockout.	Amodiaquine	144-155	cytochrome b5 type A	Homo sapiens	174-178
33441761-6	2021	Further studies on cytochrome b5 (CYB5), an alternative NADH-dependent electron donor indicated particularly strong support of CYP2C8-dependent amodiaquine N-deethylation by CYB5 and this was confirmed by genetic CYB5 single- and POR/CYB5 double-knockout.	Amodiaquine	144-155	cytochrome b5 type A	Homo sapiens	174-178
33441761-6	2021	Further studies on cytochrome b5 (CYB5), an alternative NADH-dependent electron donor indicated particularly strong support of CYP2C8-dependent amodiaquine N-deethylation by CYB5 and this was confirmed by genetic CYB5 single- and POR/CYB5 double-knockout.	Amodiaquine	144-155	cytochrome p450 oxidoreductase	Homo sapiens	230-233
33441761-6	2021	Further studies on cytochrome b5 (CYB5), an alternative NADH-dependent electron donor indicated particularly strong support of CYP2C8-dependent amodiaquine N-deethylation by CYB5 and this was confirmed by genetic CYB5 single- and POR/CYB5 double-knockout.	Amodiaquine	144-155	cytochrome b5 type A	Homo sapiens	174-178
33289551-4	2020	Protein NMR structural footprinting data show that amodiaquine, chloroquine, and cytosporone B bind the Nurr1 LBD; ligands that do not bind include C-DIM12, celastrol, camptothecin, IP7e, isoalantolactone, ethyl 2-[2,3,4-trimethoxy-6-(1-octanoyl)phenyl]acetate (TMPA), and three high-throughput screening hit derivatives.	Amodiaquine	51-62	nuclear receptor subfamily 4 group A member 2	Homo sapiens	104-109
33507465-0	2021	The orphan nuclear receptor Nurr1 agonist amodiaquine mediates neuroprotective effects in 6-OHDA Parkinson"s disease animal model by enhancing the phosphorylation of P38 mitogen-activated kinase but not PI3K/AKT signaling pathway.	Amodiaquine	42-53	nuclear receptor subfamily 4, group A, member 2	Mus musculus	28-33
33507465-0	2021	The orphan nuclear receptor Nurr1 agonist amodiaquine mediates neuroprotective effects in 6-OHDA Parkinson"s disease animal model by enhancing the phosphorylation of P38 mitogen-activated kinase but not PI3K/AKT signaling pathway.	Amodiaquine	42-53	thymoma viral proto-oncogene 1	Mus musculus	208-211
33507465-2	2021	In an attempt to corroborate the treatment-modifying disease that would replicate the effect of Nurr1, it has been found that amodiaquine and Nurr1 had the same chemical scaffolding, indicating a crucial structure-activity relationship.	Amodiaquine	126-137	nuclear receptor subfamily 4, group A, member 2	Mus musculus	96-101
33507465-3	2021	Interestingly, amodiaquine stimulate the transcriptional function of Nurr1 by physical interaction with its ligand-binding domain (LBD).	Amodiaquine	15-26	nuclear receptor subfamily 4, group A, member 2	Mus musculus	69-74
33507465-4	2021	However, the signaling route by which Nurr1 is activated by amodiaquine to cause the protective effect remains to be elucidated.	Amodiaquine	60-71	nuclear receptor subfamily 4, group A, member 2	Mus musculus	38-43
33507465-5	2021	We first demonstrated that amodiaquine treatment ameliorated behavioural deficits in 6-OHDA Parkinson"s disease mouse model, and it promoted dopaminergic neurons protection signified by Tyrosine hydroxylase (TH) and dopamine transporter (DAT) mRNA; Tyrosine hydroxylase (TH) protein expression level and the immunoreactivity in the substantia nigra compacta.	Amodiaquine	27-38	tyrosine hydroxylase	Mus musculus	186-206
33507465-5	2021	We first demonstrated that amodiaquine treatment ameliorated behavioural deficits in 6-OHDA Parkinson"s disease mouse model, and it promoted dopaminergic neurons protection signified by Tyrosine hydroxylase (TH) and dopamine transporter (DAT) mRNA; Tyrosine hydroxylase (TH) protein expression level and the immunoreactivity in the substantia nigra compacta.	Amodiaquine	27-38	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	216-236
33507465-5	2021	We first demonstrated that amodiaquine treatment ameliorated behavioural deficits in 6-OHDA Parkinson"s disease mouse model, and it promoted dopaminergic neurons protection signified by Tyrosine hydroxylase (TH) and dopamine transporter (DAT) mRNA; Tyrosine hydroxylase (TH) protein expression level and the immunoreactivity in the substantia nigra compacta.	Amodiaquine	27-38	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	238-241
33507465-5	2021	We first demonstrated that amodiaquine treatment ameliorated behavioural deficits in 6-OHDA Parkinson"s disease mouse model, and it promoted dopaminergic neurons protection signified by Tyrosine hydroxylase (TH) and dopamine transporter (DAT) mRNA; Tyrosine hydroxylase (TH) protein expression level and the immunoreactivity in the substantia nigra compacta.	Amodiaquine	27-38	tyrosine hydroxylase	Mus musculus	249-269
33507465-6	2021	Subsequently, we used inhibitors to ascertain the effect of amodiaquine on Akt and P38 Mapk as crucial signaling pathways for neuroprotection.	Amodiaquine	60-71	thymoma viral proto-oncogene 1	Mus musculus	75-78
33507465-6	2021	Subsequently, we used inhibitors to ascertain the effect of amodiaquine on Akt and P38 Mapk as crucial signaling pathways for neuroprotection.	Amodiaquine	60-71	mitogen-activated protein kinase 14	Mus musculus	83-91
33507465-8	2021	Western blot analysis confirmed that the phosphorylated Akt decreased significantly in the amodiaquine group compared to the control group.	Amodiaquine	91-102	thymoma viral proto-oncogene 1	Mus musculus	56-59
33570383-8	2021	A subset of these potent RXR agonists can synergize with a presumed Nurr1 ligand and antimalarial drug (amodiaquine) to further enhance Nurr1/NBREs-directed transcription.	Amodiaquine	104-115	retinoid X receptor alpha	Homo sapiens	25-28
33570383-8	2021	A subset of these potent RXR agonists can synergize with a presumed Nurr1 ligand and antimalarial drug (amodiaquine) to further enhance Nurr1/NBREs-directed transcription.	Amodiaquine	104-115	nuclear receptor subfamily 4 group A member 2	Homo sapiens	136-141
33475021-5	2021	In our study, the antimalarial compounds have been screened and docked against SARS-CoV-2-RdRp (PDB ID: 7BTF), and it was observed that the antimalarials chloroquine, hydroxychloroquine, and amodiaquine exhibit good affinity.	Amodiaquine	191-202	ORF1a polyprotein;ORF1ab polyprotein	Severe acute respiratory syndrome coronavirus 2	90-94
33209048-2	2020	Amodiaquine, which is mainly bio-transformed by CYP2C8, is known to be associated with adverse events of different severity.	Amodiaquine	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	48-54
32924342-3	2020	We designed this study to explore the therapeutic potential of chloroquine (CQ) and amodiaquine (AQ) for inhibiting mitochondrial Nox4 and diabetic tubular injury.	Amodiaquine	84-95	NADPH oxidase 4	Mus musculus	130-134
32924342-3	2020	We designed this study to explore the therapeutic potential of chloroquine (CQ) and amodiaquine (AQ) for inhibiting mitochondrial Nox4 and diabetic tubular injury.	Amodiaquine	97-99	NADPH oxidase 4	Mus musculus	130-134
32924342-7	2020	RESULTS: CQ and AQ inhibited mitochondrial Nox4 and increased mitochondrial mass in hRPTCs under high-glucose conditions.	Amodiaquine	16-18	NADPH oxidase 4	Mus musculus	43-47
32924342-9	2020	Notably, CQ and AQ treatment diminished Nox4 activation and ER stress in the kidneys of STZ-induced diabetic mice.	Amodiaquine	16-18	NADPH oxidase 4	Mus musculus	40-44
32924342-11	2020	CONCLUSION: We substantiated the protective actions of CQ and AQ in diabetic tubulopathy associated with reduced mitochondrial Nox4 activation and ER stress alleviation.	Amodiaquine	62-64	NADPH oxidase 4	Mus musculus	127-131
32291412-10	2020	Finally, through virtual screening, we identified amodiaquine as a potential inhibitor targeting the Fyn/CD147 axis.	Amodiaquine	50-61	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	101-104
32600728-11	2020	AQ"s autophagy inhibition ability significantly increased (increased LC3B-II levels) with nanoparticle encapsulation, along with moderate improvement in apoptosis induction (Caspase-3 levels).	Amodiaquine	0-2	caspase 3	Homo sapiens	174-183
32291412-10	2020	Finally, through virtual screening, we identified amodiaquine as a potential inhibitor targeting the Fyn/CD147 axis.	Amodiaquine	50-61	basigin (Ok blood group)	Homo sapiens	105-110
32291412-11	2020	Amodiaquine treatment dramatically inhibited the phosphorylation of CD147 by Fyn, thus attenuating melanoma cell growth and invasion in vitro and in vivo, suggesting that amodiaquine is a promising inhibitor for melanoma treatment.	Amodiaquine	0-11	basigin (Ok blood group)	Homo sapiens	68-73
32291412-11	2020	Amodiaquine treatment dramatically inhibited the phosphorylation of CD147 by Fyn, thus attenuating melanoma cell growth and invasion in vitro and in vivo, suggesting that amodiaquine is a promising inhibitor for melanoma treatment.	Amodiaquine	0-11	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	77-80
32291412-11	2020	Amodiaquine treatment dramatically inhibited the phosphorylation of CD147 by Fyn, thus attenuating melanoma cell growth and invasion in vitro and in vivo, suggesting that amodiaquine is a promising inhibitor for melanoma treatment.	Amodiaquine	171-182	basigin (Ok blood group)	Homo sapiens	68-73
32291412-11	2020	Amodiaquine treatment dramatically inhibited the phosphorylation of CD147 by Fyn, thus attenuating melanoma cell growth and invasion in vitro and in vivo, suggesting that amodiaquine is a promising inhibitor for melanoma treatment.	Amodiaquine	171-182	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	77-80
31642009-0	2020	Influence of MAMA decoction, an Herbal Antimalarial, on the Pharmacokinetics of Amodiaquine in Mice.	Amodiaquine	80-91	lectin, galactoside-binding, soluble, 3 binding protein	Mus musculus	13-17
32238479-3	2020	In a second cohort, rats received the Nurr1 agonist amodiaquine (AQ) together with L-DOPA or ropinirole.	Amodiaquine	52-63	nuclear receptor subfamily 4, group A, member 2	Rattus norvegicus	38-43
32238479-3	2020	In a second cohort, rats received the Nurr1 agonist amodiaquine (AQ) together with L-DOPA or ropinirole.	Amodiaquine	65-67	nuclear receptor subfamily 4, group A, member 2	Rattus norvegicus	38-43
32238479-7	2020	Nurr1 agonism with AQ exacerbated LID in F344 rats.	Amodiaquine	19-21	nuclear receptor subfamily 4, group A, member 2	Rattus norvegicus	0-5
31285544-0	2020	The antimalarial drug amodiaquine stabilizes p53 through ribosome biogenesis stress, independently of its autophagy-inhibitory activity.	Amodiaquine	22-33	tumor protein p53	Homo sapiens	45-48
31285544-3	2020	Amodiaquine triggers degradation of the catalytic subunit of RNA polymerase I (Pol I), with ensuing RPL5/RPL11-dependent stabilization of p53.	Amodiaquine	0-11	DNA polymerase iota	Homo sapiens	79-84
31285544-3	2020	Amodiaquine triggers degradation of the catalytic subunit of RNA polymerase I (Pol I), with ensuing RPL5/RPL11-dependent stabilization of p53.	Amodiaquine	0-11	ribosomal protein L5	Homo sapiens	100-104
31285544-3	2020	Amodiaquine triggers degradation of the catalytic subunit of RNA polymerase I (Pol I), with ensuing RPL5/RPL11-dependent stabilization of p53.	Amodiaquine	0-11	ribosomal protein L11	Homo sapiens	105-110
31285544-3	2020	Amodiaquine triggers degradation of the catalytic subunit of RNA polymerase I (Pol I), with ensuing RPL5/RPL11-dependent stabilization of p53.	Amodiaquine	0-11	tumor protein p53	Homo sapiens	138-141
31285544-5	2020	RNAseq analysis revealed mechanistic similarities of amodiaquine with BMH-21, the first-in-class Pol I inhibitor, and with chloroquine, the antimalarial analog of amodiaquine, with well-established autophagy-inhibitory activity.	Amodiaquine	53-64	DNA polymerase iota	Homo sapiens	97-102
31629065-6	2020	Metabolic studies using microsomes obtained from HepG2 cell lines overexpressing human CYPs demonstrated that CYP1A1, 2C8, and 3A4 were the major enzymes that metabolized ADQ to NADQ and that CYP1A2, 1B1, 2C19, and 3A5 also metabolized ADQ, but to a lesser extent.	Amodiaquine	171-174	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	110-116
31629065-6	2020	Metabolic studies using microsomes obtained from HepG2 cell lines overexpressing human CYPs demonstrated that CYP1A1, 2C8, and 3A4 were the major enzymes that metabolized ADQ to NADQ and that CYP1A2, 1B1, 2C19, and 3A5 also metabolized ADQ, but to a lesser extent.	Amodiaquine	171-174	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	192-198
31629065-6	2020	Metabolic studies using microsomes obtained from HepG2 cell lines overexpressing human CYPs demonstrated that CYP1A1, 2C8, and 3A4 were the major enzymes that metabolized ADQ to NADQ and that CYP1A2, 1B1, 2C19, and 3A5 also metabolized ADQ, but to a lesser extent.	Amodiaquine	179-182	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	110-116
31629065-7	2020	The cytotoxicity of ADQ was increased in CYP2C8 and 3A4 overexpressing HepG2 cells compared to HepG2/CYP vector cells, confirming that NADQ was more toxic than ADQ.	Amodiaquine	20-23	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	41-55
31629065-7	2020	The cytotoxicity of ADQ was increased in CYP2C8 and 3A4 overexpressing HepG2 cells compared to HepG2/CYP vector cells, confirming that NADQ was more toxic than ADQ.	Amodiaquine	20-23	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	41-44
31629065-7	2020	The cytotoxicity of ADQ was increased in CYP2C8 and 3A4 overexpressing HepG2 cells compared to HepG2/CYP vector cells, confirming that NADQ was more toxic than ADQ.	Amodiaquine	136-139	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	41-55
31629065-8	2020	Moreover, treatment of CYP2C8 and 3A4 overexpressing HepG2 cells with ADQ increased the phosphorylation of JNK, ERK1/2, and p38, but not the expression of Bcl-2 family proteins.	Amodiaquine	70-73	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	23-37
31629065-8	2020	Moreover, treatment of CYP2C8 and 3A4 overexpressing HepG2 cells with ADQ increased the phosphorylation of JNK, ERK1/2, and p38, but not the expression of Bcl-2 family proteins.	Amodiaquine	70-73	mitogen-activated protein kinase 8	Homo sapiens	107-110
31629065-8	2020	Moreover, treatment of CYP2C8 and 3A4 overexpressing HepG2 cells with ADQ increased the phosphorylation of JNK, ERK1/2, and p38, but not the expression of Bcl-2 family proteins.	Amodiaquine	70-73	mitogen-activated protein kinase 3	Homo sapiens	112-118
31629065-8	2020	Moreover, treatment of CYP2C8 and 3A4 overexpressing HepG2 cells with ADQ increased the phosphorylation of JNK, ERK1/2, and p38, but not the expression of Bcl-2 family proteins.	Amodiaquine	70-73	mitogen-activated protein kinase 1	Homo sapiens	124-127
30709838-4	2019	Inactivation of CYP2C8 by amiodarone (100 muM), clopidogrel acyl-beta-d-glucuronide (100 muM), gemfibrozil 1-O-beta-glucuronide (100 muM), and phenelzine (100 muM) was investigated in HLMs and three recombinant human CYP2C8 preparations (Supersomes, Bactosomes, and EasyCYP Bactosomes) using amodiaquine N-deethylation as the marker reaction.	Amodiaquine	292-303	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	16-22
31861329-6	2019	In addition, AQ treatment increased the expression of cell proliferation markers MCM5 and PCNA, and transcription factor E2F1.	Amodiaquine	13-15	E2F transcription factor 1	Mus musculus	121-125
31861329-7	2019	Furthermore, pharmacological stimulation of Nurr1 by AQ increased the expression levels of positive cell cycle regulators such as cyclin A and cyclin-dependent kinases (CDK) 2.	Amodiaquine	53-55	nuclear receptor subfamily 4, group A, member 2	Mus musculus	44-49
31861329-7	2019	Furthermore, pharmacological stimulation of Nurr1 by AQ increased the expression levels of positive cell cycle regulators such as cyclin A and cyclin-dependent kinases (CDK) 2.	Amodiaquine	53-55	cyclin A2	Mus musculus	130-138
31861329-7	2019	Furthermore, pharmacological stimulation of Nurr1 by AQ increased the expression levels of positive cell cycle regulators such as cyclin A and cyclin-dependent kinases (CDK) 2.	Amodiaquine	53-55	cyclin-dependent kinase 2	Mus musculus	143-175
31861329-8	2019	In contrast, levels of CDK inhibitors p27KIP1 and p57KIP2 were reduced upon treatment with AQ.	Amodiaquine	91-93	cyclin-dependent kinase 2	Mus musculus	23-26
31861329-8	2019	In contrast, levels of CDK inhibitors p27KIP1 and p57KIP2 were reduced upon treatment with AQ.	Amodiaquine	91-93	cyclin-dependent kinase inhibitor 1B	Mus musculus	38-45
31861329-8	2019	In contrast, levels of CDK inhibitors p27KIP1 and p57KIP2 were reduced upon treatment with AQ.	Amodiaquine	91-93	cyclin-dependent kinase inhibitor 1C (P57)	Mus musculus	50-57
31861329-9	2019	Similar to the in vitro results, RT-qPCR analysis of AQ-administered mice brains revealed an increase in the levels of markers of cell cycle progression, PCNA, MCM5, and Cdc25a.	Amodiaquine	53-55	proliferating cell nuclear antigen	Mus musculus	154-158
31861329-9	2019	Similar to the in vitro results, RT-qPCR analysis of AQ-administered mice brains revealed an increase in the levels of markers of cell cycle progression, PCNA, MCM5, and Cdc25a.	Amodiaquine	53-55	minichromosome maintenance complex component 5	Mus musculus	160-164
31861329-9	2019	Similar to the in vitro results, RT-qPCR analysis of AQ-administered mice brains revealed an increase in the levels of markers of cell cycle progression, PCNA, MCM5, and Cdc25a.	Amodiaquine	53-55	cell division cycle 25A	Mus musculus	170-176
31861329-10	2019	Finally, AQ administration resulted in decreased p27KIP1 and increased CDK2 levels in the dentate gyrus of the mouse hippocampus, as quantified immunohistochemically.	Amodiaquine	9-11	cyclin-dependent kinase inhibitor 1B	Mus musculus	49-56
31861329-10	2019	Finally, AQ administration resulted in decreased p27KIP1 and increased CDK2 levels in the dentate gyrus of the mouse hippocampus, as quantified immunohistochemically.	Amodiaquine	9-11	cyclin-dependent kinase 2	Mus musculus	71-75
31861329-11	2019	Our results demonstrate that the pharmacological stimulation of Nurr1 in adult hNSCs by AQ promotes the cell cycle by modulating cell cycle-related molecules.	Amodiaquine	88-90	nuclear receptor subfamily 4, group A, member 2	Mus musculus	64-69
31102570-5	2019	In contrast, CQ and AQ were significantly less potent than the bis-indole derivatives and, for some of the NR4A2-regulated genes, CQ and AQ were inactive as inducers.	Amodiaquine	137-139	nuclear receptor subfamily 4 group A member 2	Homo sapiens	107-112
30825859-0	2019	A Nurr1 agonist amodiaquine attenuates inflammatory events and neurological deficits in a mouse model of intracerebral hemorrhage.	Amodiaquine	16-27	nuclear receptor subfamily 4, group A, member 2	Mus musculus	2-7
30825859-3	2019	Daily administration of a Nurr1 agonist amodiaquine (40 mg/kg, i.p.)	Amodiaquine	40-51	nuclear receptor subfamily 4, group A, member 2	Mus musculus	26-31
30825859-5	2019	Amodiaquine also suppressed ICH-induced mRNA expression of IL-1beta, CCL2 and CXCL2, and ameliorated motor dysfunction of mice.	Amodiaquine	0-11	interleukin 1 beta	Mus musculus	59-67
30825859-5	2019	Amodiaquine also suppressed ICH-induced mRNA expression of IL-1beta, CCL2 and CXCL2, and ameliorated motor dysfunction of mice.	Amodiaquine	0-11	chemokine (C-C motif) ligand 2	Mus musculus	69-73
30825859-5	2019	Amodiaquine also suppressed ICH-induced mRNA expression of IL-1beta, CCL2 and CXCL2, and ameliorated motor dysfunction of mice.	Amodiaquine	0-11	chemokine (C-X-C motif) ligand 2	Mus musculus	78-83
31861329-2	2019	We previously demonstrated that the pharmacological stimulation of Nurr1 by amodiaquine (AQ) promotes spatial memory by enhancing adult hippocampal neurogenesis.	Amodiaquine	76-87	nuclear receptor subfamily 4, group A, member 2	Mus musculus	67-72
31861329-2	2019	We previously demonstrated that the pharmacological stimulation of Nurr1 by amodiaquine (AQ) promotes spatial memory by enhancing adult hippocampal neurogenesis.	Amodiaquine	89-91	nuclear receptor subfamily 4, group A, member 2	Mus musculus	67-72
31861329-6	2019	In addition, AQ treatment increased the expression of cell proliferation markers MCM5 and PCNA, and transcription factor E2F1.	Amodiaquine	13-15	minichromosome maintenance complex component 5	Mus musculus	81-85
31861329-6	2019	In addition, AQ treatment increased the expression of cell proliferation markers MCM5 and PCNA, and transcription factor E2F1.	Amodiaquine	13-15	proliferating cell nuclear antigen	Mus musculus	90-94
30663942-0	2019	Involvement of CCL2/CCR2 macrophage recruitment in amodiaquine-induced liver injury.	Amodiaquine	51-62	chemokine (C-C motif) ligand 2	Mus musculus	15-19
30663942-0	2019	Involvement of CCL2/CCR2 macrophage recruitment in amodiaquine-induced liver injury.	Amodiaquine	51-62	chemokine (C-C motif) receptor 2	Mus musculus	20-24
30663942-5	2019	Specifically, amodiaquine (AQ), which is known to cause IDILI in humans, causes mild liver injury in wild-type C57BL/6 mice that resolves despite continued AQ treatment, but it causes more severe liver injury that does not resolve in PD-1-/- mice co-treated with anti-CTLA-4 to impair immune tolerance.	Amodiaquine	14-25	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	268-274
30663942-5	2019	Specifically, amodiaquine (AQ), which is known to cause IDILI in humans, causes mild liver injury in wild-type C57BL/6 mice that resolves despite continued AQ treatment, but it causes more severe liver injury that does not resolve in PD-1-/- mice co-treated with anti-CTLA-4 to impair immune tolerance.	Amodiaquine	27-29	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	268-274
30663942-6	2019	CCR2-/- mice treated with AQ were not protected from the expected AQ-induced liver injury seen in wild-type C57BL/6 mice.	Amodiaquine	26-28	chemokine (C-C motif) receptor 2	Mus musculus	0-4
30663942-7	2019	In contrast, anti-CCL2 antibodies attenuated the liver injury caused by AQ in the impaired immune tolerance model.	Amodiaquine	72-74	chemokine (C-C motif) ligand 2	Mus musculus	18-22
31078747-3	2019	Individuals carrying the CYP2C8*2 c.805A > T (CYP2C8*2; rs11572103) allele have impaired amodiaquine metabolism, increased risk of amodiaquine-related adverse events, and may promote the selection of drug-resistant parasite strains.	Amodiaquine	92-103	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	25-31
31078747-3	2019	Individuals carrying the CYP2C8*2 c.805A > T (CYP2C8*2; rs11572103) allele have impaired amodiaquine metabolism, increased risk of amodiaquine-related adverse events, and may promote the selection of drug-resistant parasite strains.	Amodiaquine	92-103	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	49-55
31078747-3	2019	Individuals carrying the CYP2C8*2 c.805A > T (CYP2C8*2; rs11572103) allele have impaired amodiaquine metabolism, increased risk of amodiaquine-related adverse events, and may promote the selection of drug-resistant parasite strains.	Amodiaquine	134-145	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	25-31
31078747-3	2019	Individuals carrying the CYP2C8*2 c.805A > T (CYP2C8*2; rs11572103) allele have impaired amodiaquine metabolism, increased risk of amodiaquine-related adverse events, and may promote the selection of drug-resistant parasite strains.	Amodiaquine	134-145	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	49-55
31078747-10	2019	CONCLUSIONS: This study gives the first description of CYP2C8*2 allele distribution in the Republic of Congo and highlights the potential risk of amodiaquine-related adverse events.	Amodiaquine	146-157	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	55-61
30208056-8	2018	The prototypical 4-aminoquinoline, amodiaquine was found to be a selective, non-competitive APJ antagonist that inhibited apelin signaling in a concentration-dependent manner.	Amodiaquine	35-46	apelin receptor	Homo sapiens	92-95
30976185-3	2019	The effect of pterostilbene on cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT) enzyme activities were studied using the enzyme-selective substrates amodiaquine (CYP2C8), midazolam (CYP3A4), estradiol (UGT1A1), serotonin (UGT1A6) and mycophenolic acid (UGT1A8/9/10).	Amodiaquine	160-171	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	31-46
30976185-3	2019	The effect of pterostilbene on cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT) enzyme activities were studied using the enzyme-selective substrates amodiaquine (CYP2C8), midazolam (CYP3A4), estradiol (UGT1A1), serotonin (UGT1A6) and mycophenolic acid (UGT1A8/9/10).	Amodiaquine	160-171	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	48-51
30976185-3	2019	The effect of pterostilbene on cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT) enzyme activities were studied using the enzyme-selective substrates amodiaquine (CYP2C8), midazolam (CYP3A4), estradiol (UGT1A1), serotonin (UGT1A6) and mycophenolic acid (UGT1A8/9/10).	Amodiaquine	160-171	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	57-84
30976185-3	2019	The effect of pterostilbene on cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT) enzyme activities were studied using the enzyme-selective substrates amodiaquine (CYP2C8), midazolam (CYP3A4), estradiol (UGT1A1), serotonin (UGT1A6) and mycophenolic acid (UGT1A8/9/10).	Amodiaquine	160-171	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	86-89
30976185-3	2019	The effect of pterostilbene on cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT) enzyme activities were studied using the enzyme-selective substrates amodiaquine (CYP2C8), midazolam (CYP3A4), estradiol (UGT1A1), serotonin (UGT1A6) and mycophenolic acid (UGT1A8/9/10).	Amodiaquine	160-171	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	173-179
30515963-8	2019	Importantly, 5XFAD mice treated with amodiaquine, a highly selective synthetic Nurr1 agonist, showed robust reduction in typical AD features including deposition of Abeta plaques, neuronal loss, microgliosis, and impairment of adult hippocampal neurogenesis, leading to significant improvement of cognitive impairment.	Amodiaquine	37-48	nuclear receptor subfamily 4, group A, member 2	Mus musculus	79-84
30208056-8	2018	The prototypical 4-aminoquinoline, amodiaquine was found to be a selective, non-competitive APJ antagonist that inhibited apelin signaling in a concentration-dependent manner.	Amodiaquine	35-46	apelin	Homo sapiens	122-128
30208056-9	2018	Additionally, amodiaquine suppressed both apelin-and VGEF-induced endothelial tube formation.	Amodiaquine	14-25	apelin	Homo sapiens	42-48
29943426-6	2018	This P450 was identified by screening of actinobacterial strains for amodiaquine and ritonavir metabolizing activities, followed by genome sequencing and expression of the annotated S. platensis P450s in Escherichia coli.	Amodiaquine	69-80	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	5-9
30206341-3	2018	By examining gene-edited parasites, we report that the ability of the wide-spread Dd2 PfCRT isoform to mediate chloroquine and amodiaquine resistance is substantially reduced by the addition of the PfCRT L272F mutation, which arose under blasticidin selection.	Amodiaquine	127-138	aldo-keto reductase family 1 member C2	Homo sapiens	82-85
29516607-7	2018	CONCLUSION: Our findings suggest that amodiaquine exerts beneficial effects on glucose and lipid metabolism by concurrent activation of PPARalpha/gamma.	Amodiaquine	38-49	peroxisome proliferator activated receptor alpha	Mus musculus	136-145
29938495-2	2018	We have previously shown that modulating the immune system by impairing programmed cell death protein (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) signaling, both receptors involved in immune tolerance, was capable of producing an animal model of amodiaquine (AQ) IDILI with characteristics very similar to IDILI in humans.	Amodiaquine	266-277	spermatogenesis associated 2	Homo sapiens	103-107
29938495-2	2018	We have previously shown that modulating the immune system by impairing programmed cell death protein (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) signaling, both receptors involved in immune tolerance, was capable of producing an animal model of amodiaquine (AQ) IDILI with characteristics very similar to IDILI in humans.	Amodiaquine	266-277	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	113-156
29938495-2	2018	We have previously shown that modulating the immune system by impairing programmed cell death protein (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) signaling, both receptors involved in immune tolerance, was capable of producing an animal model of amodiaquine (AQ) IDILI with characteristics very similar to IDILI in humans.	Amodiaquine	266-277	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	158-164
29938495-2	2018	We have previously shown that modulating the immune system by impairing programmed cell death protein (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) signaling, both receptors involved in immune tolerance, was capable of producing an animal model of amodiaquine (AQ) IDILI with characteristics very similar to IDILI in humans.	Amodiaquine	279-281	spermatogenesis associated 2	Homo sapiens	103-107
29938495-2	2018	We have previously shown that modulating the immune system by impairing programmed cell death protein (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) signaling, both receptors involved in immune tolerance, was capable of producing an animal model of amodiaquine (AQ) IDILI with characteristics very similar to IDILI in humans.	Amodiaquine	279-281	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	113-156
29938495-2	2018	We have previously shown that modulating the immune system by impairing programmed cell death protein (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) signaling, both receptors involved in immune tolerance, was capable of producing an animal model of amodiaquine (AQ) IDILI with characteristics very similar to IDILI in humans.	Amodiaquine	279-281	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	158-164
29938495-6	2018	Addition of anti-LAG3 or anti-TGF-beta antibodies produced a small increase ALT in AQ-treated wild-type mice.	Amodiaquine	83-85	lymphocyte-activation gene 3	Mus musculus	17-21
29938495-6	2018	Addition of anti-LAG3 or anti-TGF-beta antibodies produced a small increase ALT in AQ-treated wild-type mice.	Amodiaquine	83-85	transforming growth factor, beta 1	Mus musculus	30-38
29938495-6	2018	Addition of anti-LAG3 or anti-TGF-beta antibodies produced a small increase ALT in AQ-treated wild-type mice.	Amodiaquine	83-85	glutamic pyruvic transaminase, soluble	Mus musculus	76-79
29938495-7	2018	There was a significant increase in ALT in PD-1-/- mice co-treated with anti-LAG3 or anti-TGF-beta relative to AQ-treated wild-type mice.	Amodiaquine	111-113	glutamic pyruvic transaminase, soluble	Mus musculus	36-39
29938495-7	2018	There was a significant increase in ALT in PD-1-/- mice co-treated with anti-LAG3 or anti-TGF-beta relative to AQ-treated wild-type mice.	Amodiaquine	111-113	programmed cell death 1	Mus musculus	43-47
29938495-7	2018	There was a significant increase in ALT in PD-1-/- mice co-treated with anti-LAG3 or anti-TGF-beta relative to AQ-treated wild-type mice.	Amodiaquine	111-113	lymphocyte-activation gene 3	Mus musculus	77-81
29938495-7	2018	There was a significant increase in ALT in PD-1-/- mice co-treated with anti-LAG3 or anti-TGF-beta relative to AQ-treated wild-type mice.	Amodiaquine	111-113	transforming growth factor, beta 1	Mus musculus	90-98
29663414-1	2018	Amodiaquine (AQ) and pioglitazone (PGZ) are both metabolized by CYP2C8, an enzyme also inhibited by PGZ.	Amodiaquine	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	64-70
29663414-1	2018	Amodiaquine (AQ) and pioglitazone (PGZ) are both metabolized by CYP2C8, an enzyme also inhibited by PGZ.	Amodiaquine	13-15	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	64-70
29516607-2	2018	We aimed to demonstrate that amodiaquine, an antimalarial agent, has potential as a PPARalpha/gamma dual agonist with low risk of adverse effects.	Amodiaquine	29-40	peroxisome proliferator activated receptor alpha	Mus musculus	84-93
29516607-3	2018	METHODS: We screened a Prestwick library (Prestwick Chemical; Illkirch, France) to identify novel PPARalpha/gamma dual agonists and selected amodiaquine (4-[(7-chloroquinolin-4-yl)amino]-2-[(diethylamino)methyl]phenol), which activated both PPAR-alpha & -gamma, for further investigation.	Amodiaquine	154-217	peroxisome proliferator activated receptor alpha	Mus musculus	241-251
29516607-5	2018	RESULTS: Amodiaquine selectively activated the transcriptional activities of PPARalpha/gamma and enhanced both fatty acid oxidation and glucose uptake without altering insulin secretion in vitro.	Amodiaquine	9-20	peroxisome proliferator activated receptor alpha	Mus musculus	77-86
29514826-9	2018	The formation of M14 was inhibited by amodiaquine (an HNMT inhibitor) and DCMB, providing additional evidence that both HNMT and TMT catalyzed M14 formation.	Amodiaquine	38-49	histamine N-methyltransferase	Homo sapiens	54-58
29884802-5	2018	Treatment with CQ or AQ abolished high-glucose-induced phospho-AMPK and phosph-PGC1alpha down-regulation in HKC8 cells.	Amodiaquine	21-23	PPARG coactivator 1 alpha	Homo sapiens	79-88
29514826-9	2018	The formation of M14 was inhibited by amodiaquine (an HNMT inhibitor) and DCMB, providing additional evidence that both HNMT and TMT catalyzed M14 formation.	Amodiaquine	38-49	histamine N-methyltransferase	Homo sapiens	120-124
29720942-0	2018	Glutathione S-Transferase P1 Protects Against Amodiaquine Quinoneimines-Induced Cytotoxicity but Does Not Prevent Activation of Endoplasmic Reticulum Stress in HepG2 Cells.	Amodiaquine	46-57	glutathione S-transferase pi 1	Homo sapiens	0-28
29720942-2	2018	Glutathione conjugation protects against AQ-induced toxicity and GSTP1 is able to conjugate its quinoneimine metabolites AQ-QI and DEA-QI with glutathione.	Amodiaquine	41-43	glutathione S-transferase pi 1	Homo sapiens	65-70
29720942-2	2018	Glutathione conjugation protects against AQ-induced toxicity and GSTP1 is able to conjugate its quinoneimine metabolites AQ-QI and DEA-QI with glutathione.	Amodiaquine	121-123	glutathione S-transferase pi 1	Homo sapiens	65-70
29281794-5	2018	Using recombinant NQO1, we showed that low nM concentrations of NQO1 are sufficient to reduce synthetic amodiaquine and carbamazepine quinone-like metabolites in vitro.	Amodiaquine	104-115	NAD(P)H quinone dehydrogenase 1	Homo sapiens	18-22
29281794-5	2018	Using recombinant NQO1, we showed that low nM concentrations of NQO1 are sufficient to reduce synthetic amodiaquine and carbamazepine quinone-like metabolites in vitro.	Amodiaquine	104-115	NAD(P)H quinone dehydrogenase 1	Homo sapiens	64-68
29281794-7	2018	NQO2 catalyzed the reduction of quinone-like metabolites derived from acetaminophen, clozapine, 4"-hydroxydiclofenac, mefenamic acid, amodiaquine, and carbamazepine.	Amodiaquine	134-145	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	0-4
29087505-1	2018	We have developed an animal model of amodiaquine-induced liver injury that has characteristics very similar to idiosyncratic drug-induced liver injury (IDILI) in humans by impairing immune tolerance using a PD1-/- mouse and cotreatment with anti-CTLA-4.	Amodiaquine	37-48	programmed cell death 1	Homo sapiens	207-210
29087505-1	2018	We have developed an animal model of amodiaquine-induced liver injury that has characteristics very similar to idiosyncratic drug-induced liver injury (IDILI) in humans by impairing immune tolerance using a PD1-/- mouse and cotreatment with anti-CTLA-4.	Amodiaquine	37-48	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	246-252
29208963-0	2017	Enhanced CD25+Foxp3+ regulatory T cell development by amodiaquine through activation of nuclear receptor 4A.	Amodiaquine	54-65	interleukin 2 receptor subunit alpha	Homo sapiens	9-13
29208963-0	2017	Enhanced CD25+Foxp3+ regulatory T cell development by amodiaquine through activation of nuclear receptor 4A.	Amodiaquine	54-65	forkhead box P3	Homo sapiens	14-19
29208963-5	2017	Despite the anti-proliferative activity of AQ, AQ only moderately decreased iTreg cell proliferation but substantially increased IL-2 production by iTreg cells.	Amodiaquine	47-49	interleukin 2	Homo sapiens	129-133
29208963-6	2017	Furthermore, AQ dose-dependently increased iTreg cell development and significantly upregulated iTreg cell markers including CD25.	Amodiaquine	13-15	interleukin 2 receptor subunit alpha	Homo sapiens	125-129
29208963-7	2017	Interestingly, CD25 expression was decreased at later stages of iTreg cell development but was sustained in the presence of AQ, which was independent of IL-2 signaling pathway.	Amodiaquine	124-126	interleukin 2 receptor subunit alpha	Homo sapiens	15-19
29208963-8	2017	AQ directly increased CD25 gene transcription by enhancing the DNA-binding and transcriptional activity of nuclear receptor 4 A.	Amodiaquine	0-2	interleukin 2 receptor subunit alpha	Homo sapiens	22-26
28900272-0	2017	From malaria to cancer: Computational drug repositioning of amodiaquine using PLIP interaction patterns.	Amodiaquine	60-71	protein tyrosine phosphatase mitochondrial 1	Homo sapiens	78-82
29061131-8	2017	RESULTS: Amodiaquine, proguanil, pyrimethamine and quinine were the most potent inhibitors of 4-(4-(dimethylamino)styryl)-N-methylpyridinium iodide (ASP) transport, a known substrate of OCT1/2, resulting in half maximal inhibitory concentrations (IC50) of 11, 13, 1.6, and 3.4 microM, respectively.	Amodiaquine	9-20	solute carrier family 22 member 1	Homo sapiens	186-190
28934153-8	2017	Selaginellin and selaginellin M had high inhibitory potential for CYP2C8-mediated amodiaquine O-demethylation with IC50 values of 0.5 and 0.9 muM, respectively.	Amodiaquine	82-93	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	66-72
28070879-5	2017	Adverse effects of amodiaquine were more common in patients with decreased CYP2C8 metabolism.	Amodiaquine	19-30	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	75-81
28900272-5	2017	These patterns characterise BVDU"s interaction with its target s. Using PLIP we performed an in silico screen of all structural data currently available and identified the FDA approved malaria drug amodiaquine as a promising repositioning candidate.	Amodiaquine	198-209	protein tyrosine phosphatase mitochondrial 1	Homo sapiens	72-76
28900272-6	2017	We validated our prediction by showing that amodiaquine suppresses chemoresistance in a multiple myeloma cancer cell line by inhibiting the chaperone function of the cancer target Hsp27.	Amodiaquine	44-55	heat shock protein family B (small) member 1	Homo sapiens	180-185
28525267-11	2017	This is presumably because the myeloperoxidase in THP-1 cells can bioactivate amodiaquine to a reactive metabolite.	Amodiaquine	78-89	myeloperoxidase	Homo sapiens	31-46
27788475-4	2016	We then examined the effect of Nurr1 activation on adult hippocampal NPCs using amodiaquine (AQ), an anti-malarial drug that was recently discovered to be a Nurr1 agonist.	Amodiaquine	80-91	nuclear receptor subfamily 4, group A, member 2	Mus musculus	157-162
28484907-5	2017	MAM-2201 exhibited mechanism-based inhibition of CYP2C8-catalyzed amodiaquine N-de-ethylation with K i and k inact values of 1.0 microM and 0.0738 min-1, respectively.	Amodiaquine	66-77	sarcoglycan gamma	Homo sapiens	0-3
28484907-5	2017	MAM-2201 exhibited mechanism-based inhibition of CYP2C8-catalyzed amodiaquine N-de-ethylation with K i and k inact values of 1.0 microM and 0.0738 min-1, respectively.	Amodiaquine	66-77	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	49-55
28179134-3	2017	The results demonstrate that most of the unsaturated fatty acids showed marked inhibition towards CYP2C8 mediated amodiaquine N-deethylation followed by inhibition of CYP2C9 and CYP2B6 mediated activities.	Amodiaquine	114-125	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	98-104
28478157-0	2017	Human glutathione S-transferases- and NAD(P)H:quinone oxidoreductase 1-catalyzed inactivation of reactive quinoneimines of amodiaquine and N-desethylamodiaquine: Possible implications for susceptibility to amodiaquine-induced liver toxicity.	Amodiaquine	123-134	glutathione S-transferase kappa 1	Homo sapiens	6-32
28478157-0	2017	Human glutathione S-transferases- and NAD(P)H:quinone oxidoreductase 1-catalyzed inactivation of reactive quinoneimines of amodiaquine and N-desethylamodiaquine: Possible implications for susceptibility to amodiaquine-induced liver toxicity.	Amodiaquine	149-160	glutathione S-transferase kappa 1	Homo sapiens	6-32
28478157-3	2017	Oxidative bioactivation to protein-reactive quinonimines (QIs) by hepatic cytochrome P450s and myeloperoxidase (MPO) have been suggested to be important mechanisms underlying AQ idiosyncratic toxicity.	Amodiaquine	175-177	myeloperoxidase	Homo sapiens	95-110
28478157-3	2017	Oxidative bioactivation to protein-reactive quinonimines (QIs) by hepatic cytochrome P450s and myeloperoxidase (MPO) have been suggested to be important mechanisms underlying AQ idiosyncratic toxicity.	Amodiaquine	175-177	myeloperoxidase	Homo sapiens	112-115
28478157-5	2017	In the present study, the activities of 15 recombinant human GSTs and NQO1 in the inactivation of reactive QIs of AQ and its pharmacological active metabolite, N-desethylamodiaquine (DEAQ) were investigated.	Amodiaquine	114-116	glutathione S-transferase kappa 1	Homo sapiens	61-65
28478157-5	2017	In the present study, the activities of 15 recombinant human GSTs and NQO1 in the inactivation of reactive QIs of AQ and its pharmacological active metabolite, N-desethylamodiaquine (DEAQ) were investigated.	Amodiaquine	114-116	NAD(P)H quinone dehydrogenase 1	Homo sapiens	70-74
28478157-6	2017	The results showed that GSTP1-1, GSTA4-4, GSTM4-4, GSTM2-2 and GSTA2-2 (activity in decreasing order) were active isoforms in catalyzing GSH conjugation of reactive QIs of AQ and DEAQ.	Amodiaquine	172-174	glutathione S-transferase pi 1	Homo sapiens	24-31
28478157-6	2017	The results showed that GSTP1-1, GSTA4-4, GSTM4-4, GSTM2-2 and GSTA2-2 (activity in decreasing order) were active isoforms in catalyzing GSH conjugation of reactive QIs of AQ and DEAQ.	Amodiaquine	172-174	glutathione S-transferase alpha 4	Homo sapiens	33-40
28478157-6	2017	The results showed that GSTP1-1, GSTA4-4, GSTM4-4, GSTM2-2 and GSTA2-2 (activity in decreasing order) were active isoforms in catalyzing GSH conjugation of reactive QIs of AQ and DEAQ.	Amodiaquine	172-174	glutathione S-transferase mu 4	Homo sapiens	42-49
28478157-6	2017	The results showed that GSTP1-1, GSTA4-4, GSTM4-4, GSTM2-2 and GSTA2-2 (activity in decreasing order) were active isoforms in catalyzing GSH conjugation of reactive QIs of AQ and DEAQ.	Amodiaquine	172-174	glutathione S-transferase mu 2	Homo sapiens	51-58
28478157-6	2017	The results showed that GSTP1-1, GSTA4-4, GSTM4-4, GSTM2-2 and GSTA2-2 (activity in decreasing order) were active isoforms in catalyzing GSH conjugation of reactive QIs of AQ and DEAQ.	Amodiaquine	172-174	glutathione S-transferase alpha 2	Homo sapiens	63-70
27718269-0	2017	Characterization of human cytochrome P450 mediated bioactivation of amodiaquine and its major metabolite N-desethylamodiaquine.	Amodiaquine	68-79	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	26-41
27718269-1	2017	AIMS: Oxidative bioactivation of amodiaquine (AQ) by cytochrome P450s to a reactive quinoneimine is considered as an important mechanism underlying its idiosyncratic hepatotoxicity.	Amodiaquine	33-44	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	53-68
27718269-1	2017	AIMS: Oxidative bioactivation of amodiaquine (AQ) by cytochrome P450s to a reactive quinoneimine is considered as an important mechanism underlying its idiosyncratic hepatotoxicity.	Amodiaquine	46-48	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	53-68
27718269-7	2017	For AQ bioactivation, enzyme kinetical parameters were Km , 11.5 +- 2.0 mumol l-1 , Vmax , 59.2 +- 3.2 pmol min-1  mg-1 and CLint , 5.15 mul min-1  mg-1 .	Amodiaquine	4-6	CD59 molecule (CD59 blood group)	Homo sapiens	108-119
27718269-7	2017	For AQ bioactivation, enzyme kinetical parameters were Km , 11.5 +- 2.0 mumol l-1 , Vmax , 59.2 +- 3.2 pmol min-1  mg-1 and CLint , 5.15 mul min-1  mg-1 .	Amodiaquine	4-6	CD59 molecule (CD59 blood group)	Homo sapiens	141-152
27718269-11	2017	High expression of CYP3A4, CYP2C8, CYP2C9, and CYP2D6 may be risk factors for hepatotoxicity caused by AQ-therapy.	Amodiaquine	103-105	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	27-33
27718269-11	2017	High expression of CYP3A4, CYP2C8, CYP2C9, and CYP2D6 may be risk factors for hepatotoxicity caused by AQ-therapy.	Amodiaquine	103-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
27718269-11	2017	High expression of CYP3A4, CYP2C8, CYP2C9, and CYP2D6 may be risk factors for hepatotoxicity caused by AQ-therapy.	Amodiaquine	103-105	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	47-53
27788475-6	2016	AQ-treated NPCs showed increased levels of phosphorylation of Akt and ERK1/2 whereas AQ-treated Nurr1 siRNA-transfected NPCs showed no changes in those levels.	Amodiaquine	0-2	thymoma viral proto-oncogene 1	Mus musculus	62-65
27788475-6	2016	AQ-treated NPCs showed increased levels of phosphorylation of Akt and ERK1/2 whereas AQ-treated Nurr1 siRNA-transfected NPCs showed no changes in those levels.	Amodiaquine	0-2	mitogen-activated protein kinase 3	Mus musculus	70-76
27788475-6	2016	AQ-treated NPCs showed increased levels of phosphorylation of Akt and ERK1/2 whereas AQ-treated Nurr1 siRNA-transfected NPCs showed no changes in those levels.	Amodiaquine	85-87	nuclear receptor subfamily 4, group A, member 2	Mus musculus	96-101
26581561-4	2016	Amodiaquine, montelukast, quercetin and rosiglitazone, known as substrates or competitive inhibitors of human CYP2C8, were metabolically depleted by recombinant monkey CYP2C8 at relatively high rates.	Amodiaquine	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	110-116
27695271-0	2016	Inhibition of Human Cytochrome P450 2c8-catalyzed Amodiaquine N-desethylation: Effect of Five Traditionally and Commonly Used Herbs.	Amodiaquine	50-61	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	20-39
27057621-3	2016	OBJECTIVE: The study was designed to investigate the possible enhancement of the antimalarial potency as well as possible herb-drug interaction resulting from concurrent administration of MAMA decoction with amodiaquine (AQ).	Amodiaquine	208-219	lectin, galactoside-binding, soluble, 3 binding protein	Mus musculus	188-192
27057621-3	2016	OBJECTIVE: The study was designed to investigate the possible enhancement of the antimalarial potency as well as possible herb-drug interaction resulting from concurrent administration of MAMA decoction with amodiaquine (AQ).	Amodiaquine	221-223	lectin, galactoside-binding, soluble, 3 binding protein	Mus musculus	188-192
26581561-4	2016	Amodiaquine, montelukast, quercetin and rosiglitazone, known as substrates or competitive inhibitors of human CYP2C8, were metabolically depleted by recombinant monkey CYP2C8 at relatively high rates.	Amodiaquine	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	168-174
26581561-5	2016	Taken together with our reported findings of the slow eliminations of amodiaquine and montelukast by monkey CYP2C9, CYP2C19 and CYP2C76, the present results suggest that these at least four chemicals may be good marker substrates for monkey CYP2C8.	Amodiaquine	70-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
26581561-5	2016	Taken together with our reported findings of the slow eliminations of amodiaquine and montelukast by monkey CYP2C9, CYP2C19 and CYP2C76, the present results suggest that these at least four chemicals may be good marker substrates for monkey CYP2C8.	Amodiaquine	70-81	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	116-123
26581561-5	2016	Taken together with our reported findings of the slow eliminations of amodiaquine and montelukast by monkey CYP2C9, CYP2C19 and CYP2C76, the present results suggest that these at least four chemicals may be good marker substrates for monkey CYP2C8.	Amodiaquine	70-81	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	241-247
27128896-3	2016	Aschantin potently inhibited CYP2C8-mediated amodiaquine N-de-ethylation, CYP2C9-mediated diclofenac 4"-hydroxylation, CYP2C19-mediated [S]-mephenytoin 4"-hydroxylation, and CYP3A4-mediated midazolam 1"-hydroxylation, with Ki values of 10.2, 3.7, 5.8, and 12.6 microM, respectively.	Amodiaquine	45-56	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	29-35
27109480-7	2016	Both CQ and AQ elevated the transcription level of p21 though the activation of p53, but also blocked p21 protein degradation in the presence of cycloheximide, causing p21 protein accumulation mainly in the nucleus.	Amodiaquine	12-14	tumor protein p53	Homo sapiens	80-83
27109480-7	2016	Both CQ and AQ elevated the transcription level of p21 though the activation of p53, but also blocked p21 protein degradation in the presence of cycloheximide, causing p21 protein accumulation mainly in the nucleus.	Amodiaquine	12-14	cyclin dependent kinase inhibitor 1A	Homo sapiens	102-105
27109480-7	2016	Both CQ and AQ elevated the transcription level of p21 though the activation of p53, but also blocked p21 protein degradation in the presence of cycloheximide, causing p21 protein accumulation mainly in the nucleus.	Amodiaquine	12-14	cyclin dependent kinase inhibitor 1A	Homo sapiens	102-105
27109480-8	2016	Sustained treatment of developing T cells with either CQ or AQ suppressed IFN-gamma production in a dose dependent manner and potently inhibited the differentiation of IFN-gamma-producing Th1 cells.	Amodiaquine	60-62	interferon gamma	Homo sapiens	74-83
27109480-8	2016	Sustained treatment of developing T cells with either CQ or AQ suppressed IFN-gamma production in a dose dependent manner and potently inhibited the differentiation of IFN-gamma-producing Th1 cells.	Amodiaquine	60-62	interferon gamma	Homo sapiens	168-177
27109480-9	2016	These results demonstrate that CQ and AQ increase the expression level of p21 and inhibit T cell proliferation and the development of IFN-gamma-producing Th1 cells, thereby revealing beneficial roles in treating a wide range of chronic inflammatory diseases mediated by inflammatory T cells.	Amodiaquine	38-40	cyclin dependent kinase inhibitor 1A	Homo sapiens	74-77
27109480-9	2016	These results demonstrate that CQ and AQ increase the expression level of p21 and inhibit T cell proliferation and the development of IFN-gamma-producing Th1 cells, thereby revealing beneficial roles in treating a wide range of chronic inflammatory diseases mediated by inflammatory T cells.	Amodiaquine	38-40	interferon gamma	Homo sapiens	134-143
27109480-0	2016	Anti-inflammatory activity of chloroquine and amodiaquine through p21-mediated suppression of T cell proliferation and Th1 cell differentiation.	Amodiaquine	46-57	cyclin dependent kinase inhibitor 1A	Homo sapiens	66-69
27109480-6	2016	Interestingly, the cyclin-dependent kinase inhibitor p21 was significantly and dose-dependently increased by CQ, and more potently by AQ, while other cell cycle regulators were unchanged.	Amodiaquine	134-136	cyclin dependent kinase inhibitor 1A	Homo sapiens	53-56
27109480-7	2016	Both CQ and AQ elevated the transcription level of p21 though the activation of p53, but also blocked p21 protein degradation in the presence of cycloheximide, causing p21 protein accumulation mainly in the nucleus.	Amodiaquine	12-14	cyclin dependent kinase inhibitor 1A	Homo sapiens	51-54
26647924-7	2016	Interestingly, AQ-induced damage of spermatogenesis recovered over time, based on the survival of promyelocytic leukemia zinc-finger (PLZF)-positive, undifferentiated spermatogonia.	Amodiaquine	15-17	zinc finger and BTB domain containing 16	Rattus norvegicus	98-132
27045516-12	2016	An upregulation of P-gp was observed when artemisone and dihydroartemisinin were co-incubated with mefloquine and amodiaquine.	Amodiaquine	114-125	ATP binding cassette subfamily B member 1	Homo sapiens	19-23
26851641-3	2016	Recently, reactivation of OP-inhibited AChE by the antimalarial drug amodiaquine was reported.	Amodiaquine	69-80	acetylcholinesterase (Cartwright blood group)	Homo sapiens	39-43
26851641-5	2016	Thereby, reversible inhibition of human cholinesterases by amodiaquine (AChE >> BChE) was observed.	Amodiaquine	59-70	acetylcholinesterase (Cartwright blood group)	Homo sapiens	72-76
26851641-5	2016	Thereby, reversible inhibition of human cholinesterases by amodiaquine (AChE >> BChE) was observed.	Amodiaquine	59-70	butyrylcholinesterase	Homo sapiens	86-90
26851641-6	2016	Additionally, a mixed competitive-non-competitive inhibition type of amodiaquine with human AChE was determined.	Amodiaquine	69-80	acetylcholinesterase (Cartwright blood group)	Homo sapiens	92-96
26851641-8	2016	Amodiaquine, being a potent, reversible AChE inhibitor, was tested for its potential benefit as a pretreatment to prevent complete irreversible AChE inhibition by the nerve agent soman.	Amodiaquine	0-11	acetylcholinesterase (Cartwright blood group)	Homo sapiens	40-44
26851641-8	2016	Amodiaquine, being a potent, reversible AChE inhibitor, was tested for its potential benefit as a pretreatment to prevent complete irreversible AChE inhibition by the nerve agent soman.	Amodiaquine	0-11	acetylcholinesterase (Cartwright blood group)	Homo sapiens	144-148
26851641-9	2016	Hereby, amodiaquine failed to prevent phosphonylation and resulted only in a slight increase of AChE activity after removal of amodiaquine and soman.	Amodiaquine	8-19	acetylcholinesterase (Cartwright blood group)	Homo sapiens	96-100
26851641-9	2016	Hereby, amodiaquine failed to prevent phosphonylation and resulted only in a slight increase of AChE activity after removal of amodiaquine and soman.	Amodiaquine	127-138	acetylcholinesterase (Cartwright blood group)	Homo sapiens	96-100
26851641-10	2016	At present the molecular mechanism of amodiaquine-induced reactivation of OP-inhibited AChE is not known, nevertheless amodiaquine could be considered as a template for the design of more potent non-oxime reactivators.	Amodiaquine	38-49	acetylcholinesterase (Cartwright blood group)	Homo sapiens	87-91
26647924-7	2016	Interestingly, AQ-induced damage of spermatogenesis recovered over time, based on the survival of promyelocytic leukemia zinc-finger (PLZF)-positive, undifferentiated spermatogonia.	Amodiaquine	15-17	zinc finger and BTB domain containing 16	Rattus norvegicus	134-138
26641046-4	2015	Tissue was pretreated with or without aminoguanidine and amodiaquine to block the histamine-degrading enzymes diamine oxidase (DAO) and histamine -methyltransferase (HMT), respectively.	Amodiaquine	57-68	amine oxidase copper containing 1	Sus scrofa	110-125
26721703-3	2016	CYP2C8 substrate drugs include amodiaquine, cerivastatin, dasabuvir, enzalutamide, imatinib, loperamide, montelukast, paclitaxel, pioglitazone, repaglinide, and rosiglitazone, and the number is increasing.	Amodiaquine	31-42	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	0-6
26641046-4	2015	Tissue was pretreated with or without aminoguanidine and amodiaquine to block the histamine-degrading enzymes diamine oxidase (DAO) and histamine -methyltransferase (HMT), respectively.	Amodiaquine	57-68	amine oxidase copper containing 1	Sus scrofa	127-130
26124091-6	2015	In particular, we found that two antimalarial drugs, amodiaquine and chloroquine stimulate the transcriptional function of Nurr1 through physical interaction with its ligand binding domain (LBD).	Amodiaquine	53-64	nuclear receptor subfamily 4, group A, member 2	Rattus norvegicus	123-128
26310922-4	2015	We show that a clinically used antimalarial drug, Amodiaquine, discovered by this strategy, protects host cells against infection by multiple toxins and viruses by inhibiting host cathepsin B.	Amodiaquine	50-61	cathepsin B	Homo sapiens	180-191
26154582-0	2015	The Role of CD8 T Cells in Amodiaquine-Induced Liver Injury in PD1-/- Mice Cotreated with Anti-CTLA-4.	Amodiaquine	27-38	CD8a molecule	Homo sapiens	12-15
26154582-0	2015	The Role of CD8 T Cells in Amodiaquine-Induced Liver Injury in PD1-/- Mice Cotreated with Anti-CTLA-4.	Amodiaquine	27-38	programmed cell death 1	Mus musculus	63-66
26154582-4	2015	Recently our laboratory reported a model of amodiaquine (AQ)-induced IDILI using PD1-/- mice and an anti-CTLA4 antibody.	Amodiaquine	44-55	programmed cell death 1	Mus musculus	81-84
26154582-4	2015	Recently our laboratory reported a model of amodiaquine (AQ)-induced IDILI using PD1-/- mice and an anti-CTLA4 antibody.	Amodiaquine	44-55	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	105-110
26154582-4	2015	Recently our laboratory reported a model of amodiaquine (AQ)-induced IDILI using PD1-/- mice and an anti-CTLA4 antibody.	Amodiaquine	57-59	programmed cell death 1	Mus musculus	81-84
26154582-4	2015	Recently our laboratory reported a model of amodiaquine (AQ)-induced IDILI using PD1-/- mice and an anti-CTLA4 antibody.	Amodiaquine	57-59	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	105-110
26154582-8	2015	Mice treated with AQ and anti-CTLA4 had a significant increase in percentage of hepatic CD4, CD8, Th17, and Treg cells after 10 weeks of AQ treatment, as well as significantly decreased NK cells.	Amodiaquine	18-20	CD4 antigen	Mus musculus	88-91
26154582-8	2015	Mice treated with AQ and anti-CTLA4 had a significant increase in percentage of hepatic CD4, CD8, Th17, and Treg cells after 10 weeks of AQ treatment, as well as significantly decreased NK cells.	Amodiaquine	18-20	CD8a molecule	Homo sapiens	93-96
26154582-8	2015	Mice treated with AQ and anti-CTLA4 had a significant increase in percentage of hepatic CD4, CD8, Th17, and Treg cells after 10 weeks of AQ treatment, as well as significantly decreased NK cells.	Amodiaquine	137-139	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	30-35
26154582-10	2015	We found that depletion of CD8 T cells protected mice from AQ-induced liver injury in this model, which strongly suggests that they are responsible for the liver damage.	Amodiaquine	59-61	CD8a molecule	Homo sapiens	27-30
25959621-3	2015	The changes on G-6-Pase activity and liver glucose output induced by 5-CQA were also investigated.	Amodiaquine	71-74	glucose-6-phosphatase catalytic subunit 1	Homo sapiens	15-23
25046026-10	2015	Treatment of Rag1(-/-) mice with AQ resulted in higher ALT activities than C57BL/6 mice, which suggested that the adaptive immune response was responsible for immune tolerance.	Amodiaquine	33-35	recombination activating 1	Mus musculus	13-17
25046026-10	2015	Treatment of Rag1(-/-) mice with AQ resulted in higher ALT activities than C57BL/6 mice, which suggested that the adaptive immune response was responsible for immune tolerance.	Amodiaquine	33-35	glutamic pyruvic transaminase, soluble	Mus musculus	55-58
25046026-11	2015	In contrast, depletion of NK cells significantly attenuated the increase in ALT, which implied a role for NK cells in mild AQ-induced IDILI.	Amodiaquine	123-125	glutamic pyruvic transaminase, soluble	Mus musculus	76-79
24588327-0	2014	Involvement of myeloperoxidase and NADPH oxidase in the covalent binding of amodiaquine and clozapine to neutrophils: implications for drug-induced agranulocytosis.	Amodiaquine	76-87	myeloperoxidase	Mus musculus	15-30
24713129-3	2014	Amodiaquine N-deethylation and midazolam 1"-hydroxylation were used as marker reactions for CYP2C8 and CYP3A activity, respectively.	Amodiaquine	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	92-98
24713129-3	2014	Amodiaquine N-deethylation and midazolam 1"-hydroxylation were used as marker reactions for CYP2C8 and CYP3A activity, respectively.	Amodiaquine	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	103-108
25283142-5	2015	In this study we found that AQ treatment of Cbl-b(-/-) and PD-1(-/-) mice, which have impaired immune tolerance, resulted in a slightly greater injury.	Amodiaquine	28-30	Casitas B-lineage lymphoma b	Mus musculus	44-49
25283142-6	2015	Cotreatment of C57BL/6 with AQ and anti-CTLA4 also resulted in a greater increase in ALT than treatment with AQ alone; however, these mice also had an increase in T regulatory (Treg) cells and T helper cells expressing PD-1 and CTLA4.	Amodiaquine	28-30	glutamic pyruvic transaminase, soluble	Mus musculus	85-88
25283142-6	2015	Cotreatment of C57BL/6 with AQ and anti-CTLA4 also resulted in a greater increase in ALT than treatment with AQ alone; however, these mice also had an increase in T regulatory (Treg) cells and T helper cells expressing PD-1 and CTLA4.	Amodiaquine	28-30	cytotoxic T-lymphocyte protein 4	Sus scrofa	228-233
25283142-6	2015	Cotreatment of C57BL/6 with AQ and anti-CTLA4 also resulted in a greater increase in ALT than treatment with AQ alone; however, these mice also had an increase in T regulatory (Treg) cells and T helper cells expressing PD-1 and CTLA4.	Amodiaquine	109-111	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	40-45
25283142-8	2015	Cotreatment of PD-1(-/-) mice with anti-CTLA4 antibody and AQ resulted in the greatest increase in ALT (200-300 U/L), and necroinflammatory responses characterized by portal infiltration of lymphocytes with interface hepatitis.	Amodiaquine	59-61	glutamic pyruvic transaminase, soluble	Mus musculus	99-102
25283142-10	2015	In addition, the ALT activity in PD-1(-/-) mice cotreated with anti-CTLA4 antibody and AQ did not return to normal, as it had in other mice.	Amodiaquine	87-89	glutamic pyruvic transaminase, soluble	Mus musculus	17-20
25388906-9	2014	CONCLUSION: Independent association of SNPs in IL22 and IL-4 with clearance of amodiaquine- and sulphadoxine/pyrimethamine-resistant parasites did not reach statistical significance, but may suggest that not all drug-resistant mutants are adversely affected by the same immune-mediated mechanisms of clearance.	Amodiaquine	79-90	interleukin 22	Homo sapiens	47-51
25388906-9	2014	CONCLUSION: Independent association of SNPs in IL22 and IL-4 with clearance of amodiaquine- and sulphadoxine/pyrimethamine-resistant parasites did not reach statistical significance, but may suggest that not all drug-resistant mutants are adversely affected by the same immune-mediated mechanisms of clearance.	Amodiaquine	79-90	interleukin 4	Homo sapiens	56-60
24588327-2	2014	Previous studies have shown that both AQ and CLZ are oxidized to reactive intermediates in vitro by activated neutrophils or by the combination of hydrogen peroxide and myeloperoxidase (MPO).	Amodiaquine	38-40	myeloperoxidase	Mus musculus	169-184
24588327-2	2014	Previous studies have shown that both AQ and CLZ are oxidized to reactive intermediates in vitro by activated neutrophils or by the combination of hydrogen peroxide and myeloperoxidase (MPO).	Amodiaquine	38-40	myeloperoxidase	Mus musculus	186-189
24588327-5	2014	In this study, we found that the binding of both AQ and CLZ to neutrophils from MPO knockout mice ex vivo decreased approximately 2-fold compared to neutrophils from wild-type mice, whereas binding to activated neutrophils from gp91 knockout (NADPH oxidase null) mice decreased 6-7-fold.	Amodiaquine	49-51	myeloperoxidase	Mus musculus	80-83
24588327-5	2014	In this study, we found that the binding of both AQ and CLZ to neutrophils from MPO knockout mice ex vivo decreased approximately 2-fold compared to neutrophils from wild-type mice, whereas binding to activated neutrophils from gp91 knockout (NADPH oxidase null) mice decreased 6-7-fold.	Amodiaquine	49-51	paired Ig-like receptor B	Mus musculus	228-232
24588327-6	2014	When the AQ studies were performed in vivo, again the binding was decreased in MPO knockout mice to about 50% of the binding in wild-type mice; however, covalent binding was significant in the absence of MPO.	Amodiaquine	9-11	myeloperoxidase	Mus musculus	79-82
24113242-5	2013	Monitoring an established set of protein markers (LAMP1, LC3-II, SQSTM1) and cell ultrastructural changes detected by electron microscopy, we observed that AQ treatment caused autophagic-lysosomal blockade in malignant A375 melanoma cells, a finding substantiated by detection of rapid inactivation of lysosomal cathepsins (CTSB, CTSL, CTSD).	Amodiaquine	156-158	lysosomal associated membrane protein 1	Homo sapiens	50-55
24910237-3	2014	The metabolic pathways examined were the CYP1A2-catalyzed tacrine 1-hydroxylation, CYP2B6-catalyzed bupropion hydroxylation, CYP2C8-catalyzed amodiaquine N-deethylation, CYP2C9- catalyzed diclofenac 4"-hydroxylation, CYP2D6-catalyzed dextromethorphan O-demethylation, and CYP3A4-catalyzed midazolam 1"-hydroxylation.	Amodiaquine	142-153	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	125-131
24113242-5	2013	Monitoring an established set of protein markers (LAMP1, LC3-II, SQSTM1) and cell ultrastructural changes detected by electron microscopy, we observed that AQ treatment caused autophagic-lysosomal blockade in malignant A375 melanoma cells, a finding substantiated by detection of rapid inactivation of lysosomal cathepsins (CTSB, CTSL, CTSD).	Amodiaquine	156-158	sequestosome 1	Homo sapiens	65-71
24113242-5	2013	Monitoring an established set of protein markers (LAMP1, LC3-II, SQSTM1) and cell ultrastructural changes detected by electron microscopy, we observed that AQ treatment caused autophagic-lysosomal blockade in malignant A375 melanoma cells, a finding substantiated by detection of rapid inactivation of lysosomal cathepsins (CTSB, CTSL, CTSD).	Amodiaquine	156-158	cathepsin B	Homo sapiens	324-328
24113242-5	2013	Monitoring an established set of protein markers (LAMP1, LC3-II, SQSTM1) and cell ultrastructural changes detected by electron microscopy, we observed that AQ treatment caused autophagic-lysosomal blockade in malignant A375 melanoma cells, a finding substantiated by detection of rapid inactivation of lysosomal cathepsins (CTSB, CTSL, CTSD).	Amodiaquine	156-158	cathepsin L	Homo sapiens	330-334
24113242-5	2013	Monitoring an established set of protein markers (LAMP1, LC3-II, SQSTM1) and cell ultrastructural changes detected by electron microscopy, we observed that AQ treatment caused autophagic-lysosomal blockade in malignant A375 melanoma cells, a finding substantiated by detection of rapid inactivation of lysosomal cathepsins (CTSB, CTSL, CTSD).	Amodiaquine	156-158	cathepsin D	Homo sapiens	336-340
24113242-7	2013	AQ displayed potent antiproliferative effects, and gene expression array analysis revealed changes at the mRNA (CDKN1A, E2F1) and protein level (TP53, CDKN1A, CCND1, phospho-RB1 [Ser 780]/[Ser 807/811], E2F1) consistent with the observed proliferative blockade in S-phase.	Amodiaquine	0-2	E2F transcription factor 1	Homo sapiens	203-207
23204183-0	2013	CYP2C8 status of patients with malaria influences selection of Plasmodium falciparum pfmdr1 alleles after amodiaquine-artesunate treatment.	Amodiaquine	106-117	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	0-6
24591743-5	2013	This article deals with the development of a 2D QSAR model based on the inhibitory potential of gemfibrozil, its analogues and corresponding glucuronide conjugates in inhibiting the CYP2C8-catalysed amodiaquine N-deethylation.	Amodiaquine	199-210	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	182-188
22014153-3	2012	EXPERIMENTAL APPROACH: Amodiaquine N-deethylation and midazolam 1"-hydroxylation were used as marker reactions for CYP2C8 and CYP3A4/5 activity.	Amodiaquine	23-34	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	115-121
22658498-0	2012	Investigation of the interaction between amodiaquine and human serum albumin by fluorescence spectroscopy and molecular modeling.	Amodiaquine	41-52	albumin	Homo sapiens	63-76
22658498-1	2012	The interaction of amodiaquine (AQ) with human serum albumin (HSA) has been studied by fluorescence spectroscopy.	Amodiaquine	19-30	albumin	Homo sapiens	47-60
22658498-1	2012	The interaction of amodiaquine (AQ) with human serum albumin (HSA) has been studied by fluorescence spectroscopy.	Amodiaquine	32-34	albumin	Homo sapiens	47-60
22531455-2	2012	CYP2C8 enzyme is involved in the metabolism of the anti-malarials amodiaquine and chloroquine.	Amodiaquine	66-77	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	0-6
22014153-3	2012	EXPERIMENTAL APPROACH: Amodiaquine N-deethylation and midazolam 1"-hydroxylation were used as marker reactions for CYP2C8 and CYP3A4/5 activity.	Amodiaquine	23-34	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	126-132
21726541-3	2011	In this study, the contribution of the redox partners cytochrome P450 reductase (CPR) and cytochrome b5 to the substrate dependent activity of CYP2C8.3 (R139K, K399R) was investigated in human liver microsomes (HLMs) and Escherichia coli expressed recombinant CYP2C8 proteins using amodiaquine, paclitaxel, rosiglitazone and cerivastatin as probe substrates.	Amodiaquine	282-293	cytochrome p450 oxidoreductase	Homo sapiens	54-79
22003869-1	2012	CONTEXT: Artesunate (AS) and amodiaquine (AQ) are two prodrugs widely used as antimalarial agents and are metabolized by the CYP P450 2A6 (CYP 2A6) and CYP P450 2C8 (CYP 2C8) enzymes, respectively.	Amodiaquine	29-40	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	125-137
22003869-1	2012	CONTEXT: Artesunate (AS) and amodiaquine (AQ) are two prodrugs widely used as antimalarial agents and are metabolized by the CYP P450 2A6 (CYP 2A6) and CYP P450 2C8 (CYP 2C8) enzymes, respectively.	Amodiaquine	29-40	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	139-146
22003869-1	2012	CONTEXT: Artesunate (AS) and amodiaquine (AQ) are two prodrugs widely used as antimalarial agents and are metabolized by the CYP P450 2A6 (CYP 2A6) and CYP P450 2C8 (CYP 2C8) enzymes, respectively.	Amodiaquine	29-40	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	152-164
22003869-1	2012	CONTEXT: Artesunate (AS) and amodiaquine (AQ) are two prodrugs widely used as antimalarial agents and are metabolized by the CYP P450 2A6 (CYP 2A6) and CYP P450 2C8 (CYP 2C8) enzymes, respectively.	Amodiaquine	29-40	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	166-173
22003869-1	2012	CONTEXT: Artesunate (AS) and amodiaquine (AQ) are two prodrugs widely used as antimalarial agents and are metabolized by the CYP P450 2A6 (CYP 2A6) and CYP P450 2C8 (CYP 2C8) enzymes, respectively.	Amodiaquine	42-44	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	125-137
22003869-1	2012	CONTEXT: Artesunate (AS) and amodiaquine (AQ) are two prodrugs widely used as antimalarial agents and are metabolized by the CYP P450 2A6 (CYP 2A6) and CYP P450 2C8 (CYP 2C8) enzymes, respectively.	Amodiaquine	42-44	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	139-146
22003869-1	2012	CONTEXT: Artesunate (AS) and amodiaquine (AQ) are two prodrugs widely used as antimalarial agents and are metabolized by the CYP P450 2A6 (CYP 2A6) and CYP P450 2C8 (CYP 2C8) enzymes, respectively.	Amodiaquine	42-44	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	152-164
22003869-1	2012	CONTEXT: Artesunate (AS) and amodiaquine (AQ) are two prodrugs widely used as antimalarial agents and are metabolized by the CYP P450 2A6 (CYP 2A6) and CYP P450 2C8 (CYP 2C8) enzymes, respectively.	Amodiaquine	42-44	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	166-173
22122444-11	2011	IPT in children with artesunate (AS + SP), amodiaquine (AQ) + SPQ or SP alone is a cost effective and safe intervention for reducing the burden of malaria in children in areas with markedly seasonal malaria transmission.	Amodiaquine	43-54	tRNA isopentenyltransferase 1	Homo sapiens	0-3
22122444-11	2011	IPT in children with artesunate (AS + SP), amodiaquine (AQ) + SPQ or SP alone is a cost effective and safe intervention for reducing the burden of malaria in children in areas with markedly seasonal malaria transmission.	Amodiaquine	56-58	tRNA isopentenyltransferase 1	Homo sapiens	0-3
21726541-3	2011	In this study, the contribution of the redox partners cytochrome P450 reductase (CPR) and cytochrome b5 to the substrate dependent activity of CYP2C8.3 (R139K, K399R) was investigated in human liver microsomes (HLMs) and Escherichia coli expressed recombinant CYP2C8 proteins using amodiaquine, paclitaxel, rosiglitazone and cerivastatin as probe substrates.	Amodiaquine	282-293	cytochrome p450 oxidoreductase	Homo sapiens	81-84
21726541-3	2011	In this study, the contribution of the redox partners cytochrome P450 reductase (CPR) and cytochrome b5 to the substrate dependent activity of CYP2C8.3 (R139K, K399R) was investigated in human liver microsomes (HLMs) and Escherichia coli expressed recombinant CYP2C8 proteins using amodiaquine, paclitaxel, rosiglitazone and cerivastatin as probe substrates.	Amodiaquine	282-293	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	143-149
21726541-7	2011	In HLMs, carriers of the CYP2C8*1/*3 genotype were as active as CYP2C8*1/*1 towards the CYP2C8 specific reaction amodiaquine N-deethylation.	Amodiaquine	113-124	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	25-31
21726541-7	2011	In HLMs, carriers of the CYP2C8*1/*3 genotype were as active as CYP2C8*1/*1 towards the CYP2C8 specific reaction amodiaquine N-deethylation.	Amodiaquine	113-124	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	64-70
21726541-7	2011	In HLMs, carriers of the CYP2C8*1/*3 genotype were as active as CYP2C8*1/*1 towards the CYP2C8 specific reaction amodiaquine N-deethylation.	Amodiaquine	113-124	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	64-70
20382755-5	2010	Both dog CYP2A13 and CYP2A25 exhibited little or no catalytic activity toward other common cytochrome P450 probe substrates, including bupropion, amodiaquine, diclofenac, S-mephenytoin, bufuralol, dextromethorphan, midazolam, and testosterone.	Amodiaquine	146-157	cytochrome P450 family 2 subfamily A polypeptide 13	Canis lupus familiaris	9-16
21529379-5	2011	RESULTS: The combination therapy of AQ and SP results in more pronounced hepatotoxicity as revealed by elevated level of serum ALT, AST with respect to their individual drug exposure regimen.	Amodiaquine	36-38	glutamic pyruvic transaminase, soluble	Mus musculus	127-130
21529379-5	2011	RESULTS: The combination therapy of AQ and SP results in more pronounced hepatotoxicity as revealed by elevated level of serum ALT, AST with respect to their individual drug exposure regimen.	Amodiaquine	36-38	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	132-135
21597194-1	2011	Chlorogenic acid (CQA) is one of the major polyphenols in apple and a good substrate for the polyphenol oxidase (PPO) in apple.	Amodiaquine	18-21	polyphenol oxidase, chloroplastic	Malus domestica	93-111
21597194-1	2011	Chlorogenic acid (CQA) is one of the major polyphenols in apple and a good substrate for the polyphenol oxidase (PPO) in apple.	Amodiaquine	18-21	polyphenol oxidase, chloroplastic	Malus domestica	113-116
21597194-5	2011	Although catechins and CQA were oxidized by PPO, some catechins seemed to be non-enzymatically oxidized by CQA quinone.	Amodiaquine	23-26	polyphenol oxidase, chloroplastic	Malus domestica	44-47
20877236-5	2010	Eupatilin and jaceosidin were also found to moderately inhibit CYP2C19-catalyzed [S]-mephenytoin 4"-hydroxylation, CYP2D6-catalyzed bufuralol 1"-hydroxylation, and CYP2C8-catalyzed amodiaquine N-deethylation.	Amodiaquine	181-192	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	63-70
20382755-5	2010	Both dog CYP2A13 and CYP2A25 exhibited little or no catalytic activity toward other common cytochrome P450 probe substrates, including bupropion, amodiaquine, diclofenac, S-mephenytoin, bufuralol, dextromethorphan, midazolam, and testosterone.	Amodiaquine	146-157	cytochrome P450, family 2, subfamily A, polypeptide 7	Canis lupus familiaris	21-28
20212335-10	2010	CONCLUSION: The research provides the evidence that mutations present in dhfr and mdr1 86 has a significant effect on the type of treatment following SP and AQ chemotherapy.	Amodiaquine	157-159	ATP binding cassette subfamily B member 1	Homo sapiens	82-86