PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
31480671-5	2019	Among the top 10 most probable inhibitors of TRPA1 with good blood brain barrier (BBB) permeability, desvenlafaxine, paliperidone, and febuxostat emerged as the most promising repurposable agents for treating MS. Molecular docking studies indicated that desvenlafaxine, paliperidone, and febuxostat are likely to induce allosteric TRPA1 channel inhibition.	Desvenlafaxine Succinate	101-115	transient receptor potential cation channel subfamily A member 1	Homo sapiens	45-50
31480671-5	2019	Among the top 10 most probable inhibitors of TRPA1 with good blood brain barrier (BBB) permeability, desvenlafaxine, paliperidone, and febuxostat emerged as the most promising repurposable agents for treating MS. Molecular docking studies indicated that desvenlafaxine, paliperidone, and febuxostat are likely to induce allosteric TRPA1 channel inhibition.	Desvenlafaxine Succinate	254-268	transient receptor potential cation channel subfamily A member 1	Homo sapiens	45-50
30838456-7	2019	Venlafaxine is metabolized to the active metabolite O-desmethylvenlafaxine (ODV; desvenlafaxine) by CYP2D6, and it therefore is subject to significant inter-individual variation in blood levels and response dependent on variations in CYP2D6 metabolism.	Desvenlafaxine Succinate	52-74	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	100-106
30838456-7	2019	Venlafaxine is metabolized to the active metabolite O-desmethylvenlafaxine (ODV; desvenlafaxine) by CYP2D6, and it therefore is subject to significant inter-individual variation in blood levels and response dependent on variations in CYP2D6 metabolism.	Desvenlafaxine Succinate	52-74	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	234-240
30838456-7	2019	Venlafaxine is metabolized to the active metabolite O-desmethylvenlafaxine (ODV; desvenlafaxine) by CYP2D6, and it therefore is subject to significant inter-individual variation in blood levels and response dependent on variations in CYP2D6 metabolism.	Desvenlafaxine Succinate	76-79	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	100-106
30838456-7	2019	Venlafaxine is metabolized to the active metabolite O-desmethylvenlafaxine (ODV; desvenlafaxine) by CYP2D6, and it therefore is subject to significant inter-individual variation in blood levels and response dependent on variations in CYP2D6 metabolism.	Desvenlafaxine Succinate	76-79	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	234-240
30838456-7	2019	Venlafaxine is metabolized to the active metabolite O-desmethylvenlafaxine (ODV; desvenlafaxine) by CYP2D6, and it therefore is subject to significant inter-individual variation in blood levels and response dependent on variations in CYP2D6 metabolism.	Desvenlafaxine Succinate	81-95	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	100-106
30838456-7	2019	Venlafaxine is metabolized to the active metabolite O-desmethylvenlafaxine (ODV; desvenlafaxine) by CYP2D6, and it therefore is subject to significant inter-individual variation in blood levels and response dependent on variations in CYP2D6 metabolism.	Desvenlafaxine Succinate	81-95	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	234-240
29732526-8	2018	Alpha-lipoic acid and DVS, alone or combined, reversed CORT effect on TST.	Desvenlafaxine Succinate	22-25	thiosulfate sulfurtransferase	Homo sapiens	70-73
28079059-8	2017	Changes in miR-1202 levels following desvenlafaxine treatment were negatively correlated with changes in activity in right precuneus within the default-mode network, and in connectivity between the posterior cingulate and the temporal and prefrontal cortices, and the precuneus.	Desvenlafaxine Succinate	37-51	microRNA 1202	Homo sapiens	11-19
29897361-3	2018	Venlafaxine and its metabolite O-desmethylvenlafaxine were the primary compounds (reaching up to 132.04 and 173.68 ng L-1 as well as 3.03 and 4.53 ng L-1 in wastewater and receiving water, respectively).	Desvenlafaxine Succinate	31-53	L1 cell adhesion molecule	Homo sapiens	118-121
29897361-3	2018	Venlafaxine and its metabolite O-desmethylvenlafaxine were the primary compounds (reaching up to 132.04 and 173.68 ng L-1 as well as 3.03 and 4.53 ng L-1 in wastewater and receiving water, respectively).	Desvenlafaxine Succinate	31-53	L1 cell adhesion molecule	Homo sapiens	150-153
28866861-10	2018	The findings might be the result of different degrees of CYP2C19 involvement, therefore the inhibition of CYP2C19 by both PPIs may lead to an increased metabolism via CYP2D6 to O-desmethylvenlafaxine.	Desvenlafaxine Succinate	177-199	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
28866861-10	2018	The findings might be the result of different degrees of CYP2C19 involvement, therefore the inhibition of CYP2C19 by both PPIs may lead to an increased metabolism via CYP2D6 to O-desmethylvenlafaxine.	Desvenlafaxine Succinate	177-199	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	106-113
28866861-10	2018	The findings might be the result of different degrees of CYP2C19 involvement, therefore the inhibition of CYP2C19 by both PPIs may lead to an increased metabolism via CYP2D6 to O-desmethylvenlafaxine.	Desvenlafaxine Succinate	177-199	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	167-173
26331791-3	2016	Venlafaxine (VLX) is an antidepressant metabolized mainly by CYP2D6 to O-desmethylvenlafaxine (ODV), CYP3A to N-desmethylvenlafaxine (NDV), and CYP2D6 and CYP3A to N,O-didesmethylvenlafaxine (DDV).	Desvenlafaxine Succinate	71-93	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	61-67
27696548-0	2017	Spectroscopic exploration and thermodynamic characterization of desvenlafaxine interacting with fluorescent bovine serum albumin.	Desvenlafaxine Succinate	64-78	albumin	Homo sapiens	115-128
27696548-1	2017	The mechanism of the interaction between bovine serum albumin (BSA) and desvenlafaxine was studied using fluorescence, ultraviolet absorption, 3-dimensional fluorescence spectroscopy, circular dichroism, synchronous fluorescence spectroscopy, cyclic voltametry, differential scanning calorimetry, and attenuated total reflection-Fourier transform infrared spectroscopic techniques under physiological condition at pH 7.4.	Desvenlafaxine Succinate	72-86	albumin	Homo sapiens	48-61
27328779-2	2016	In humans, venlafaxine is biotransformed for the most part by CYP2D6 and CYP2C19 isoenzymes to its major metabolite O-desmethylvenlafaxine (ODV), and in parallel to N-desmethylvenlafaxine (NDV) and N,O-didesmethylvenlafaxine (NODV) by several CYP isoenzymes, mainly including CYP3A4 and CYP2C19.	Desvenlafaxine Succinate	116-138	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	73-80
28465217-4	2017	This study evaluates the involvement of nine common antidepressants in the NLRP3-inflammasome complex (fluoxetine, paroxetine, mianserin, mirtazapine, venlafaxine, desvenlafaxine, amitriptyline, imipramine and agomelatine), both in in vitro THP-1 cells stimulated by ATP, and in a stress-induced depressive animal or MDD patients.	Desvenlafaxine Succinate	164-178	NLR family pyrin domain containing 3	Homo sapiens	75-80
28229443-5	2017	CONCLUSIONS: Although evidence of desvenlafaxine in neuropathic pain is scarce, it presents some interesting pharmacokinetic properties, as it is not substrate or have activity on P-glycoprotein, and have a metabolism which practically does not depend on cytochrome P450 system, which limits the risk of pharmacokinetic interactions and potential problems associated tolerability when administered with drugs that are CYP2D6 moderate or potent inhibitors or other substrates of this isoenzyme.	Desvenlafaxine Succinate	34-48	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	418-424
29123929-3	2017	VEN is metabolized mainly by CYP2D6 and to a minor extent by CYP2C19 to the major active metabolite O-desmethylvenlafaxine (ODV).	Desvenlafaxine Succinate	100-122	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	61-68
27023264-1	2016	No studies to date have evaluated SLC6A2 and SLC6A4 genetic polymorphisms influencing antidepressant response to desvenlafaxine.	Desvenlafaxine Succinate	113-127	solute carrier family 6 member 4	Homo sapiens	45-51
27023264-2	2016	We conducted an 8-week, open-label, prospective pilot study in 35 patients with major depressive disorder to assess the effects of genetic variations in SLC6A2 and SLC6A4 on both efficacy and side effect profile of desvenlafaxine.	Desvenlafaxine Succinate	215-229	solute carrier family 6 member 2	Homo sapiens	153-159
27023264-2	2016	We conducted an 8-week, open-label, prospective pilot study in 35 patients with major depressive disorder to assess the effects of genetic variations in SLC6A2 and SLC6A4 on both efficacy and side effect profile of desvenlafaxine.	Desvenlafaxine Succinate	215-229	solute carrier family 6 member 4	Homo sapiens	164-170
27023264-5	2016	While these results need to be interpreted cautiously, they provide preliminary support for the SLC6A4 HTTLPR polymorphism as potential modifier of desvenlafaxine efficacy.	Desvenlafaxine Succinate	148-162	solute carrier family 6 member 4	Homo sapiens	96-102
26331791-3	2016	Venlafaxine (VLX) is an antidepressant metabolized mainly by CYP2D6 to O-desmethylvenlafaxine (ODV), CYP3A to N-desmethylvenlafaxine (NDV), and CYP2D6 and CYP3A to N,O-didesmethylvenlafaxine (DDV).	Desvenlafaxine Succinate	95-98	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	61-67
23541126-5	2013	CYP2D6 poor metabolizer phenotype was defined as O-desmethylvenlafaxine to venlafaxine ratio < 1 based on published data.	Desvenlafaxine Succinate	49-71	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-6
26514447-0	2015	Comparison of efficacy, safety and brain derived neurotrophic factor (BDNF) levels in patients of major depressive disorder, treated with fluoxetine and desvenlafaxine.	Desvenlafaxine Succinate	153-167	brain derived neurotrophic factor	Homo sapiens	70-74
26514447-1	2015	This randomized, open label, prospective, observational study compared clinical efficacy, safety alongwith plasma BDNF levels in outpatients of depression treated with fluoxetine and desvenlafaxine.	Desvenlafaxine Succinate	183-197	brain derived neurotrophic factor	Homo sapiens	114-118
26514447-7	2015	The BDNF levels in the desvenlafaxine group were 760.5+-28.53pg/ml at the start of treatment which significantly (p<0.05) increased to 845.8+-32.82pg/ml at 12 weeks.	Desvenlafaxine Succinate	23-37	brain derived neurotrophic factor	Homo sapiens	4-8
26091569-6	2015	Desvenlafaxine in vivo dissolution from the IRF and ERF was predicted from in vitro solubility studies and biorelevant dissolution studies (using the USP3 dissolution apparatus), respectively.	Desvenlafaxine Succinate	0-14	ubiquitin specific peptidase 3	Homo sapiens	150-154
23897419-1	2013	Venlafaxine, and to a lesser extent desvenlafaxine, has previously been shown to induce the expression of the drug efflux transporters P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) in whole cells and alter the cellular permeability of a known drug efflux probe (rhodamine 123).	Desvenlafaxine Succinate	36-50	phosphoglycolate phosphatase	Mus musculus	135-149
23897419-1	2013	Venlafaxine, and to a lesser extent desvenlafaxine, has previously been shown to induce the expression of the drug efflux transporters P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) in whole cells and alter the cellular permeability of a known drug efflux probe (rhodamine 123).	Desvenlafaxine Succinate	36-50	phosphoglycolate phosphatase	Mus musculus	151-155
23897419-1	2013	Venlafaxine, and to a lesser extent desvenlafaxine, has previously been shown to induce the expression of the drug efflux transporters P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) in whole cells and alter the cellular permeability of a known drug efflux probe (rhodamine 123).	Desvenlafaxine Succinate	36-50	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	161-193
23897419-1	2013	Venlafaxine, and to a lesser extent desvenlafaxine, has previously been shown to induce the expression of the drug efflux transporters P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) in whole cells and alter the cellular permeability of a known drug efflux probe (rhodamine 123).	Desvenlafaxine Succinate	36-50	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	195-199
26350703-0	2015	Reversal of corticosterone-induced BDNF alterations by the natural antioxidant alpha-lipoic acid alone and combined with desvenlafaxine: Emphasis on the neurotrophic hypothesis of depression.	Desvenlafaxine Succinate	121-135	brain derived neurotrophic factor	Mus musculus	35-39
24096053-13	2014	Although median increase in BDNF was not significantly different between desvenlafaxine (13.7%) and placebo (5.7%) groups, the increase was significantly greater (33.4% vs 4.3%; P=0.003) in patients with more severe depression at baseline (HAM-D17>22) vs those with less severe depression (HAM-D17<=22).	Desvenlafaxine Succinate	73-87	brain derived neurotrophic factor	Homo sapiens	28-32
23897419-3	2013	P-gp and BCRP expression was significantly upregulated in the intestine, following a treatment with venlafaxine (2.6- and 6.7-fold, respectively) or desvenlafaxine (2.3- and 4.8-fold, respectively).	Desvenlafaxine Succinate	149-163	phosphoglycolate phosphatase	Mus musculus	0-4
23897419-3	2013	P-gp and BCRP expression was significantly upregulated in the intestine, following a treatment with venlafaxine (2.6- and 6.7-fold, respectively) or desvenlafaxine (2.3- and 4.8-fold, respectively).	Desvenlafaxine Succinate	149-163	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	9-13
21840145-1	2012	Venlafaxine (VEN) is an antidepressant drug mainly metabolized by the cytochrome P450 (CYP) enzyme CYP2D6 to the active metabolite O-desmethylvenlafaxine (ODV).	Desvenlafaxine Succinate	131-153	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	99-105
23221858-1	2013	The results of two single-center, two-period, open-label trials that evaluated the effects of multiple doses of desvenlafaxine on the pharmacokinetics of desipramine, a cytochrome P450 (CYP) 2D6 enzyme substrate, are presented.	Desvenlafaxine Succinate	112-126	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	169-194
21840145-1	2012	Venlafaxine (VEN) is an antidepressant drug mainly metabolized by the cytochrome P450 (CYP) enzyme CYP2D6 to the active metabolite O-desmethylvenlafaxine (ODV).	Desvenlafaxine Succinate	155-158	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	99-105
21119521-3	2011	In this study, we report on five patients who had a historical pattern suggestive of tolerance to other antidepressant drugs, whose genotyping test indicated that they were CYP2C19 rapid metabolizers, and who experienced "poop out" again when commenced on desvenlafaxine.	Desvenlafaxine Succinate	256-270	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	173-180
21925241-3	2011	TP1 was designed as a prodrug of desvenlafaxine.	Desvenlafaxine Succinate	33-47	transition protein 1	Homo sapiens	0-3
21925241-6	2011	TP1 (0.06 mmol/kg, orally) rapidly penetrated rat brain and hypothalamus, translated into desvenlafaxine within 1 h, and demonstrated higher bioavailability and better pharmacokinetic properties than desvenlafaxine succinate (DVS).	Desvenlafaxine Succinate	90-104	transition protein 1	Rattus norvegicus	0-3
21925241-6	2011	TP1 (0.06 mmol/kg, orally) rapidly penetrated rat brain and hypothalamus, translated into desvenlafaxine within 1 h, and demonstrated higher bioavailability and better pharmacokinetic properties than desvenlafaxine succinate (DVS).	Desvenlafaxine Succinate	226-229	transition protein 1	Rattus norvegicus	0-3
21446053-3	2011	The present study expanded upon these findings by examining the effect of venlafaxine and desvenlafaxine on the expression of both P-gp and the breast cancer resistance protein (BCRP) in human brain endothelial cells (HBMEC), an in vitro model of the blood-brain barrier (BBB).	Desvenlafaxine Succinate	90-104	ATP binding cassette subfamily B member 1	Homo sapiens	131-135
21446053-3	2011	The present study expanded upon these findings by examining the effect of venlafaxine and desvenlafaxine on the expression of both P-gp and the breast cancer resistance protein (BCRP) in human brain endothelial cells (HBMEC), an in vitro model of the blood-brain barrier (BBB).	Desvenlafaxine Succinate	90-104	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	144-176
21446053-3	2011	The present study expanded upon these findings by examining the effect of venlafaxine and desvenlafaxine on the expression of both P-gp and the breast cancer resistance protein (BCRP) in human brain endothelial cells (HBMEC), an in vitro model of the blood-brain barrier (BBB).	Desvenlafaxine Succinate	90-104	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	178-182
21099743-6	2011	The sum of venlafaxine plus ODV concentration showed the same pattern as venlafaxine concentrations with CYP2D6 and CYP2C19 genotypes with higher activity scores being associated with a lower venlafaxine plus ODV concentration (2D6 P = 0.01; 2C19 P < 0.001).	Desvenlafaxine Succinate	209-212	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	116-123
21099743-7	2011	Because allelic variants in both CYP2D6 and CYP2C19 influence the total concentration of the active compounds venlafaxine and ODV, both CYP2D6 and CYP2C19 genotypes should be considered when using pharmacogenomic information for venlafaxine dose alterations.	Desvenlafaxine Succinate	126-129	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	33-39
21099743-1	2011	This study examines the relationship between blood concentrations of venlafaxine and its active metabolite, O-desmethyl venlafaxine (ODV), and genetic variants of the cytochrome P450 enzymes CYP2D6 and CYP2C19 in human subjects.	Desvenlafaxine Succinate	108-131	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	191-197
21099743-1	2011	This study examines the relationship between blood concentrations of venlafaxine and its active metabolite, O-desmethyl venlafaxine (ODV), and genetic variants of the cytochrome P450 enzymes CYP2D6 and CYP2C19 in human subjects.	Desvenlafaxine Succinate	133-136	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	191-197
21099743-7	2011	Because allelic variants in both CYP2D6 and CYP2C19 influence the total concentration of the active compounds venlafaxine and ODV, both CYP2D6 and CYP2C19 genotypes should be considered when using pharmacogenomic information for venlafaxine dose alterations.	Desvenlafaxine Succinate	126-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	44-51
21099743-7	2011	Because allelic variants in both CYP2D6 and CYP2C19 influence the total concentration of the active compounds venlafaxine and ODV, both CYP2D6 and CYP2C19 genotypes should be considered when using pharmacogenomic information for venlafaxine dose alterations.	Desvenlafaxine Succinate	126-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	147-154
21067460-6	2010	Desvenlafaxine has clinically insignificant effects on the activity of CYP and P-gp.	Desvenlafaxine Succinate	0-14	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	71-74
20441720-1	2010	INTRODUCTION: Venlafaxine, a serotonin-norepinephrine reuptake inhibitor antidepressant, is metabolized primarily by the cytochrome P450 2D6 enzyme into O-desmethylvenlafaxine (ODV).	Desvenlafaxine Succinate	153-175	cytochrome P450 2D6	Homo sapiens	121-140
20441720-1	2010	INTRODUCTION: Venlafaxine, a serotonin-norepinephrine reuptake inhibitor antidepressant, is metabolized primarily by the cytochrome P450 2D6 enzyme into O-desmethylvenlafaxine (ODV).	Desvenlafaxine Succinate	177-180	cytochrome P450 2D6	Homo sapiens	121-140
19919295-21	2010	The metabolic profile of desvenlafaxine suggests a low risk of drug-drug interactions owing to minimal inhibitory effects on CYP2D6, lack of interaction with p-glycoprotein, and low protein binding.	Desvenlafaxine Succinate	25-39	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	125-131
20466523-6	2010	One to six hours post-dose, the brain concentrations of venlafaxine, O-desmethylvenlafaxine and N-desmethylvenlafaxine were 2-3, 2-6 and 3-12 times higher in abcb1ab (-/-) mice compared to abcb1ab (+/+) mice, respectively.	Desvenlafaxine Succinate	69-91	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	158-163
19919295-21	2010	The metabolic profile of desvenlafaxine suggests a low risk of drug-drug interactions owing to minimal inhibitory effects on CYP2D6, lack of interaction with p-glycoprotein, and low protein binding.	Desvenlafaxine Succinate	25-39	ATP binding cassette subfamily B member 1	Homo sapiens	158-172
19593180-4	2009	The current analysis evaluates the use of the O-desmethylvenlafaxine-venlafaxine ratio (ODV/VEN) after administration of VEN, a CYP2D6 substrate, for determining CYP2D6 metabolic phenotype in healthy adults receiving VEN.	Desvenlafaxine Succinate	46-68	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	128-134
21391412-2	2010	However, the influence of the serotonin and noradrenalin reuptake inhibitor (SNRI) venlafaxine and its metabolite O-desmethylvenlafaxine on the stimulated blood cell secretion of IFN-gamma has not been studied so far.	Desvenlafaxine Succinate	114-136	interferon gamma	Homo sapiens	179-188
20098230-2	2010	The desvenlafaxine/venlafaxine ratio, either after a single dose or at steady state, can be used to determine whether a patient is functionally (i.e., phenotypically) a CYP 2D6 extensive or poor metabolizer (EM or PM).	Desvenlafaxine Succinate	4-18	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	169-176
19593180-4	2009	The current analysis evaluates the use of the O-desmethylvenlafaxine-venlafaxine ratio (ODV/VEN) after administration of VEN, a CYP2D6 substrate, for determining CYP2D6 metabolic phenotype in healthy adults receiving VEN.	Desvenlafaxine Succinate	46-68	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	162-168
19593180-4	2009	The current analysis evaluates the use of the O-desmethylvenlafaxine-venlafaxine ratio (ODV/VEN) after administration of VEN, a CYP2D6 substrate, for determining CYP2D6 metabolic phenotype in healthy adults receiving VEN.	Desvenlafaxine Succinate	88-91	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	128-134
19593180-4	2009	The current analysis evaluates the use of the O-desmethylvenlafaxine-venlafaxine ratio (ODV/VEN) after administration of VEN, a CYP2D6 substrate, for determining CYP2D6 metabolic phenotype in healthy adults receiving VEN.	Desvenlafaxine Succinate	88-91	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	162-168
19557107-7	2009	Desvenlafaxine is excreted in urine, it is minimally metabolized via the CYP450 pathway, and is a weak inhibitor of CYP2D6.	Desvenlafaxine Succinate	0-14	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	116-122
19127490-3	2009	Unlike various other antidepressants including venlafaxine, desvenlafaxine is not metabolized by cytochrome p450 (CYP) enzyme pathways and is associated with minimal inhibition of CYP enzymes.	Desvenlafaxine Succinate	60-74	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	180-183
19629022-0	2009	Desvenlafaxine and venlafaxine exert minimal in vitro inhibition of human cytochrome P450 and P-glycoprotein activities.	Desvenlafaxine Succinate	0-14	ATP binding cassette subfamily B member 1	Homo sapiens	94-108
18809731-0	2008	An assessment of drug-drug interactions: the effect of desvenlafaxine and duloxetine on the pharmacokinetics of the CYP2D6 probe desipramine in healthy subjects.	Desvenlafaxine Succinate	55-69	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	116-122
19001559-0	2009	The effects of desvenlafaxine and paroxetine on the pharmacokinetics of the cytochrome P450 2D6 substrate desipramine in healthy adults.	Desvenlafaxine Succinate	15-29	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	76-95
19001559-1	2009	The potential for cytochrome P450 (CYP) 2D6 substrates to interact with desvenlafaxine (administered as desvenlafaxine succinate) and paroxetine was evaluated.	Desvenlafaxine Succinate	72-86	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	18-43
19001559-1	2009	The potential for cytochrome P450 (CYP) 2D6 substrates to interact with desvenlafaxine (administered as desvenlafaxine succinate) and paroxetine was evaluated.	Desvenlafaxine Succinate	104-128	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	18-43
19629022-6	2009	CONCLUSIONS: Considering in vitro and available clinical data, desvenlafaxine and venlafaxine appear to have low potential for pharmacokinetic drug-drug interactions via inhibiting the metabolic clearance of concomitant drugs that are substrates of various CYP enzymes, in particular CYP2D6.	Desvenlafaxine Succinate	63-77	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	257-260
19629022-6	2009	CONCLUSIONS: Considering in vitro and available clinical data, desvenlafaxine and venlafaxine appear to have low potential for pharmacokinetic drug-drug interactions via inhibiting the metabolic clearance of concomitant drugs that are substrates of various CYP enzymes, in particular CYP2D6.	Desvenlafaxine Succinate	63-77	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	284-290
18806899-4	2008	Desvenlafaxine has linear pharmacokinetics, low protein binding, a half-life of approximately 10 hours and is metabolized primarily via glucuronidation, and to a minor extent through CYP3A4.	Desvenlafaxine Succinate	0-14	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	183-189
19057238-0	2008	Effect of desvenlafaxine on the cytochrome P450 2D6 enzyme system.	Desvenlafaxine Succinate	10-24	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	32-51
19057238-3	2008	METHODS: Five studies assessing the interaction between desvenlafaxine and CYP2D6 are reviewed.	Desvenlafaxine Succinate	56-70	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	75-81
19057238-10	2008	CONCLUSIONS: Based on the findings presented here, desvenlafaxine is expected to have a low risk for variability in efficacy and safety/tolerability resulting from CYP2D6 polymorphisms or drug-drug interactions when coadministered with CYP2D6 substrates or inhibitors.	Desvenlafaxine Succinate	51-65	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	164-170
19057238-10	2008	CONCLUSIONS: Based on the findings presented here, desvenlafaxine is expected to have a low risk for variability in efficacy and safety/tolerability resulting from CYP2D6 polymorphisms or drug-drug interactions when coadministered with CYP2D6 substrates or inhibitors.	Desvenlafaxine Succinate	51-65	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	236-242
18698015-11	2008	The decreased potential of CYP2D6 activity with desvenlafaxine compared with the parent drug may be a potential advantage in patients on other medications metabolized via this enzymatic pathway.	Desvenlafaxine Succinate	48-62	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	27-33
17673606-0	2007	Desvenlafaxine succinate identifies novel antagonist binding determinants in the human norepinephrine transporter.	Desvenlafaxine Succinate	0-24	solute carrier family 6 member 2	Homo sapiens	87-113
17673606-1	2007	Desvenlafaxine succinate (DVS) is a recently introduced antagonist of the human norepinephrine and serotonin transporters (hNET and hSERT, respectively), currently in clinical development for use in the treatment of major depressive disorder and vasomotor symptoms associated with menopause.	Desvenlafaxine Succinate	0-24	solute carrier family 6 member 2	Homo sapiens	123-127
17673606-1	2007	Desvenlafaxine succinate (DVS) is a recently introduced antagonist of the human norepinephrine and serotonin transporters (hNET and hSERT, respectively), currently in clinical development for use in the treatment of major depressive disorder and vasomotor symptoms associated with menopause.	Desvenlafaxine Succinate	0-24	solute carrier family 6 member 4	Homo sapiens	132-137
17673606-1	2007	Desvenlafaxine succinate (DVS) is a recently introduced antagonist of the human norepinephrine and serotonin transporters (hNET and hSERT, respectively), currently in clinical development for use in the treatment of major depressive disorder and vasomotor symptoms associated with menopause.	Desvenlafaxine Succinate	26-29	solute carrier family 6 member 2	Homo sapiens	123-127
17673606-1	2007	Desvenlafaxine succinate (DVS) is a recently introduced antagonist of the human norepinephrine and serotonin transporters (hNET and hSERT, respectively), currently in clinical development for use in the treatment of major depressive disorder and vasomotor symptoms associated with menopause.	Desvenlafaxine Succinate	26-29	solute carrier family 6 member 4	Homo sapiens	132-137
16958828-2	2006	It is metabolized primarily by the highly polymorphic cytochrome P450 (CYP) enzyme CYP2D6 to yield a pharmacologically active metabolite, O-desmethylvenlafaxine (ODV), and to a lesser extent by CYP3A4, to yield N-desmethylvenlafaxine (NDV).	Desvenlafaxine Succinate	138-160	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	54-69
16958828-2	2006	It is metabolized primarily by the highly polymorphic cytochrome P450 (CYP) enzyme CYP2D6 to yield a pharmacologically active metabolite, O-desmethylvenlafaxine (ODV), and to a lesser extent by CYP3A4, to yield N-desmethylvenlafaxine (NDV).	Desvenlafaxine Succinate	138-160	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	71-74
16958828-2	2006	It is metabolized primarily by the highly polymorphic cytochrome P450 (CYP) enzyme CYP2D6 to yield a pharmacologically active metabolite, O-desmethylvenlafaxine (ODV), and to a lesser extent by CYP3A4, to yield N-desmethylvenlafaxine (NDV).	Desvenlafaxine Succinate	138-160	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	83-89
16958828-2	2006	It is metabolized primarily by the highly polymorphic cytochrome P450 (CYP) enzyme CYP2D6 to yield a pharmacologically active metabolite, O-desmethylvenlafaxine (ODV), and to a lesser extent by CYP3A4, to yield N-desmethylvenlafaxine (NDV).	Desvenlafaxine Succinate	162-165	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	54-69
16958828-2	2006	It is metabolized primarily by the highly polymorphic cytochrome P450 (CYP) enzyme CYP2D6 to yield a pharmacologically active metabolite, O-desmethylvenlafaxine (ODV), and to a lesser extent by CYP3A4, to yield N-desmethylvenlafaxine (NDV).	Desvenlafaxine Succinate	162-165	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	71-74
16958828-2	2006	It is metabolized primarily by the highly polymorphic cytochrome P450 (CYP) enzyme CYP2D6 to yield a pharmacologically active metabolite, O-desmethylvenlafaxine (ODV), and to a lesser extent by CYP3A4, to yield N-desmethylvenlafaxine (NDV).	Desvenlafaxine Succinate	162-165	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	83-89
16958828-2	2006	It is metabolized primarily by the highly polymorphic cytochrome P450 (CYP) enzyme CYP2D6 to yield a pharmacologically active metabolite, O-desmethylvenlafaxine (ODV), and to a lesser extent by CYP3A4, to yield N-desmethylvenlafaxine (NDV).	Desvenlafaxine Succinate	162-165	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	194-200
24930414-6	2003	Although there is insufficient evidence, a substantial inhibition of CYP 3A3/4 by venlafaxine could result in a meaningful increase in plasma levels of venlafaxine, O-desmethylvenlafaxine, alprazolam and diazepam, particularly in patients who are CYP 2D6 deficient.	Desvenlafaxine Succinate	165-187	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	69-76
16642541-3	2006	We investigated the relationship between the CYP2D6 polymorphism and steady-state plasma concentration of venlafaxine (VEN) and its primary metabolite o-desmethylvenlafaxine (ODV) in elderly participants receiving venlafaxine-XR for major depression in order to explore the contribution of pharmacogenetics to medication tolerability.	Desvenlafaxine Succinate	151-173	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	45-51
12649369-5	2003	All antidepressants tested except O-desmethylvenlafaxine showed Pgp inhibitory activity with sertraline, desmethylsertraline, and paroxetine being the most potent, comparable with the well known Pgp inhibitor quinidine.	Desvenlafaxine Succinate	34-56	ATP binding cassette subfamily B member 1	Homo sapiens	64-67
10192828-6	1999	Studies using expressed cytochromes showed that ODV was formed by CYP2C9, -2C19, and -2D6.	Desvenlafaxine Succinate	48-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
35363936-8	2022	Moreover, IHC analysis of maternal and fetal rat brains showed that groups treated with desvenlafaxine demonstrated a significant increase of NGF protein immunoreactivity compared with that in the controls.	Desvenlafaxine Succinate	88-102	nerve growth factor	Rattus norvegicus	142-145
34855082-3	2021	JNK inhibitor added to the liver homogenate containing antidepressant enhanced and accelerated the formation of the only pharmacologically active venlafaxine metabolite O-desmethylvenlafaxine in the cell suspension.	Desvenlafaxine Succinate	169-191	mitogen-activated protein kinase 8	Homo sapiens	0-3
34197885-7	2021	Children of DVs ages 2-3 had significantly worse dentition (13.9% vs. 4.8%, P = 0.03) and more EBP {least square means (lsmeans) 54.31 vs. 47.59, P = 0.02}.	Desvenlafaxine Succinate	12-15	EBP cholestenol delta-isomerase	Homo sapiens	95-98
34197885-9	2021	Among children 4-11, male children of DVs had significantly more TBP (lsmeans 70.68 vs. 57.34, P = 0.003), IBP (lsmeans 63.59 vs. 56.16, P = 0.002) and EBP (lsmeans 61.60 vs. 52.93, P = 0.03), but female children did not.	Desvenlafaxine Succinate	38-41	DEF6 guanine nucleotide exchange factor	Homo sapiens	107-110
34197885-9	2021	Among children 4-11, male children of DVs had significantly more TBP (lsmeans 70.68 vs. 57.34, P = 0.003), IBP (lsmeans 63.59 vs. 56.16, P = 0.002) and EBP (lsmeans 61.60 vs. 52.93, P = 0.03), but female children did not.	Desvenlafaxine Succinate	38-41	EBP cholestenol delta-isomerase	Homo sapiens	152-155
34197885-10	2021	For children ages 12-18, male children of DVs had more EBP (lsmeans 63.73 vs. 43.51, P = 0.008), while female children of DVs had fewer EBP (lsmeans 45.50 vs. 50.48, P = 0.02).	Desvenlafaxine Succinate	42-45	EBP cholestenol delta-isomerase	Homo sapiens	55-58
34197885-10	2021	For children ages 12-18, male children of DVs had more EBP (lsmeans 63.73 vs. 43.51, P = 0.008), while female children of DVs had fewer EBP (lsmeans 45.50 vs. 50.48, P = 0.02).	Desvenlafaxine Succinate	42-45	EBP cholestenol delta-isomerase	Homo sapiens	136-139
34197885-10	2021	For children ages 12-18, male children of DVs had more EBP (lsmeans 63.73 vs. 43.51, P = 0.008), while female children of DVs had fewer EBP (lsmeans 45.50 vs. 50.48, P = 0.02).	Desvenlafaxine Succinate	122-125	EBP cholestenol delta-isomerase	Homo sapiens	136-139
33204067-9	2020	Compared with that in the control group (without vonoprazan), the pharmacokinetic parameters of venlafaxine and its metabolite, O-desmethylvenlafaxine, were significantly increased in both 5 and 20 mg/kg vonoprazan groups, with an increase in MRO-desmethylvenlafaxine.	Desvenlafaxine Succinate	128-150	maestro	Rattus norvegicus	243-246
33325920-5	2021	Exploring a multidimensional parameter space spanning cell-adhesive ligand, seeding density, fiber alignment, and stiffness, we found that fibronectin-functionalized DVS matrices composed of highly aligned fibers with low stiffness optimally promoted the organization of functional iPSC-CM tissues.	Desvenlafaxine Succinate	166-169	fibronectin 1	Homo sapiens	139-150
31658948-7	2019	In addition, O-desmethyl venlafaxine formation was reduced as well in CYP2D1-null rats compared with that in WT rats.	Desvenlafaxine Succinate	13-36	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	70-76
32134850-9	2020	CONCLUSIONS: The combined CYP2D6/CYP2C19 phenotype has a significant impact on serum concentrations of venlafaxine and also on the active moiety of venlafaxine + ODV, than CYP2D6 alone.	Desvenlafaxine Succinate	162-165	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	26-32
32134850-9	2020	CONCLUSIONS: The combined CYP2D6/CYP2C19 phenotype has a significant impact on serum concentrations of venlafaxine and also on the active moiety of venlafaxine + ODV, than CYP2D6 alone.	Desvenlafaxine Succinate	162-165	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
32134850-9	2020	CONCLUSIONS: The combined CYP2D6/CYP2C19 phenotype has a significant impact on serum concentrations of venlafaxine and also on the active moiety of venlafaxine + ODV, than CYP2D6 alone.	Desvenlafaxine Succinate	162-165	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	172-178