PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
11705117-2	2001	It appears that 5-HT2A, 5-HT2C, and sigma 2 receptors are involved in mediating the stimulus effects of ibogaine.	Ibogaine	104-112	5-hydroxytryptamine receptor 2A	Homo sapiens	16-22
11705117-2	2001	It appears that 5-HT2A, 5-HT2C, and sigma 2 receptors are involved in mediating the stimulus effects of ibogaine.	Ibogaine	104-112	5-hydroxytryptamine receptor 2C	Homo sapiens	24-30
11705117-5	2001	Ibogaine"s hallucinogenic effects may be explained by its interactions with 5-HT2A and 5-HT2C receptors, while its putative antiaddictive properties may result from its interactions with sigma 2 and opiate receptors.	Ibogaine	0-8	5-hydroxytryptamine receptor 2A	Homo sapiens	76-82
11705117-5	2001	Ibogaine"s hallucinogenic effects may be explained by its interactions with 5-HT2A and 5-HT2C receptors, while its putative antiaddictive properties may result from its interactions with sigma 2 and opiate receptors.	Ibogaine	0-8	5-hydroxytryptamine receptor 2C	Homo sapiens	87-93
10911925-11	2000	Ibogaine and its metabolite noribogaine have low microM affinities for kappa and mu opioid receptors, NMDA receptors, 5HT-3 receptors, sigma-2 sites, sodium channels and the serotonin transporter.	Ibogaine	0-8	solute carrier family 6 member 4	Rattus norvegicus	174-195
11085338-6	2000	The majority of ibogaine biotransformation proceeds via CYP2D6, including the O-demethylation of ibogaine to 12-hydroxyibogamine (noribogaine).	Ibogaine	16-24	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	56-62
10640697-0	1999	Acute ibogaine injection induces expression of the immediate early genes, egr-1 and c-fos, in mouse brain.	Ibogaine	6-14	early growth response 1	Mus musculus	74-79
10640697-0	1999	Acute ibogaine injection induces expression of the immediate early genes, egr-1 and c-fos, in mouse brain.	Ibogaine	6-14	FBJ osteosarcoma oncogene	Mus musculus	84-89
10640697-3	1999	A single injection of IBO produced a significant increase of egr-1 messenger RNA induction in nucleus accumbens (NAc), caudate-putamen (CPu), frontal cortex (FCx), septum, dentate gyrus (DG) and CA3 region of hippocampus, whereas c-fos gene was induced in CPu, FCx, DG, septum and CA1 region of hippocampus.	Ibogaine	22-25	early growth response 1	Mus musculus	61-66
10640697-3	1999	A single injection of IBO produced a significant increase of egr-1 messenger RNA induction in nucleus accumbens (NAc), caudate-putamen (CPu), frontal cortex (FCx), septum, dentate gyrus (DG) and CA3 region of hippocampus, whereas c-fos gene was induced in CPu, FCx, DG, septum and CA1 region of hippocampus.	Ibogaine	22-25	carbonic anhydrase 3	Mus musculus	195-198
10640697-3	1999	A single injection of IBO produced a significant increase of egr-1 messenger RNA induction in nucleus accumbens (NAc), caudate-putamen (CPu), frontal cortex (FCx), septum, dentate gyrus (DG) and CA3 region of hippocampus, whereas c-fos gene was induced in CPu, FCx, DG, septum and CA1 region of hippocampus.	Ibogaine	22-25	FBJ osteosarcoma oncogene	Mus musculus	230-235
10640697-3	1999	A single injection of IBO produced a significant increase of egr-1 messenger RNA induction in nucleus accumbens (NAc), caudate-putamen (CPu), frontal cortex (FCx), septum, dentate gyrus (DG) and CA3 region of hippocampus, whereas c-fos gene was induced in CPu, FCx, DG, septum and CA1 region of hippocampus.	Ibogaine	22-25	carbonic anhydrase 1	Mus musculus	281-284
9804688-4	1998	In keeping with their structural similarity to ibogaine, all five compounds displayed weak to poor affinity for dopamine D1 and D2 receptors.	Ibogaine	47-55	dopamine receptor D1	Homo sapiens	112-140
10095030-3	1999	The ibogaine followed by methamphetamine injection showed no hyperthermia and decreased HSP-72 expression.	Ibogaine	4-12	heat shock protein 1A	Mus musculus	88-94
10095030-4	1999	These data indicate that pretreatment with ibogaine can completely block methamphetamine-induced hyperthermia and HSP-72 expression in the striatum.	Ibogaine	43-51	heat shock protein 1A	Mus musculus	114-120
10368872-4	1999	Significant ibogaine-appropriate responding was observed following treatment with the 5-HT2C agonists MK-212 (79.6%) and mCPP (76.4%).	Ibogaine	12-20	5-hydroxytryptamine receptor 2C	Rattus norvegicus	86-92
10368872-7	1999	This suggests that although ibogaine may act as an agonist at 5-HT2C receptors, this interaction is not essential to its discriminative cue.	Ibogaine	28-36	5-hydroxytryptamine receptor 2C	Rattus norvegicus	62-68
9862757-2	1999	The present study establishes the acute functional effects of bupropion, phencyclidine, and ibogaine on two human nAChR subtypes.	Ibogaine	92-100	cholinergic receptor nicotinic alpha 4 subunit	Homo sapiens	114-119
9698290-3	1998	In this report, evidence is presented that the O-demethylation of ibogaine observed in human hepatic microsomes is catalyzed primarily by the polymorphically expressed cytochrome P-4502D6 (CYP2D6).	Ibogaine	66-74	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	189-195
9685673-2	1998	Ibogaine and noribogaine were shown to have affinity for the serotonin transporter, and inhibition of serotonin reuptake has been proposed to be involved in their anti-addictive actions.	Ibogaine	0-8	solute carrier family 6 member 4	Rattus norvegicus	61-82
9685673-9	1998	These and other data suggest that (1) the serotonergic system may not be an essential factor in the anti-addictive actions of these drugs; (2) ibogaine (or an unidentified metabolite) may release serotonin as well as inhibit its reuptake; (3) stimulation of the ascending serotonergic system may mediate ibogaine"s hallucinogenic effect; and (4) 18-MC probably has no affinity for the serotonin transporter, and is unlikely to be a hallucinogen.	Ibogaine	143-151	solute carrier family 6 member 4	Rattus norvegicus	385-406
9698290-11	1998	Thus, it is concluded that ibogaine O-demethylase is catalyzed by CYP2D6 and that this isoform is the predominant enzyme of ibogaine O-demethylation in humans.	Ibogaine	27-35	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	66-72
8959035-2	1996	We examined whether acute and chronic administration of IBG to male and female rats results in gliosis as determined by quantification of the astroglial intermediate filament protein, glial fibrillary acidic protein (GFAP).	Ibogaine	56-59	glial fibrillary acidic protein	Rattus norvegicus	184-215
9668681-13	1998	It remains to be determined whether the signaling involving PKC is important in the antiaddictive properties of ibogaine.	Ibogaine	112-120	protein kinase C, gamma	Rattus norvegicus	60-63
29090806-13	1998	It remains to be determined whether the signaling involving PKC is important in the antiaddictive properties of ibogaine.	Ibogaine	112-120	protein kinase C, gamma	Rattus norvegicus	60-63
9476990-0	1998	Behavioral and biochemical evidence for a nonessential 5-HT2A component of the ibogaine-induced discriminative stimulus.	Ibogaine	79-87	5-hydroxytryptamine receptor 2A	Rattus norvegicus	55-61
9476990-3	1998	This intermediate generalization was completely blocked by pretreatment with the 5-HT2A antagonist pirenpirone, suggesting that the ibogaine-like effects of these agents are mediated by the 5-HT2A receptor.	Ibogaine	132-140	5-hydroxytryptamine receptor 2A	Rattus norvegicus	81-87
9476990-3	1998	This intermediate generalization was completely blocked by pretreatment with the 5-HT2A antagonist pirenpirone, suggesting that the ibogaine-like effects of these agents are mediated by the 5-HT2A receptor.	Ibogaine	132-140	5-hydroxytryptamine receptor 2A	Rattus norvegicus	190-196
9476990-6	1998	Micromolar 5-HT2A affinity was observed with ibogaine (92.5 microM), 12-hydroxyibogamine (34.5 microM), and harmaline (42.5 microM).	Ibogaine	45-53	5-hydroxytryptamine receptor 2A	Rattus norvegicus	11-17
9476990-8	1998	The results of these studies suggest that although ibogaine may produce some of its effects via interactions with 5-HT2A receptors, these do not appear to be essential to the ibogaine-induced discriminative stimulus.	Ibogaine	51-59	5-hydroxytryptamine receptor 2A	Rattus norvegicus	114-120
8959035-2	1996	We examined whether acute and chronic administration of IBG to male and female rats results in gliosis as determined by quantification of the astroglial intermediate filament protein, glial fibrillary acidic protein (GFAP).	Ibogaine	56-59	glial fibrillary acidic protein	Rattus norvegicus	217-221
8959035-3	1996	After acute administration of IBG, rats of both sexes showed dose-related increases in GFAP that were not confined to the cerebellar vermis.	Ibogaine	30-33	glial fibrillary acidic protein	Rattus norvegicus	87-91
8959035-5	1996	In hippocampus, the cytoskeletal proteins, neurofilament 68 (NF-68) and beta-tubulin were increased in females treated chronically with IBG, findings consistent with a damage-induced sprouting response.	Ibogaine	136-139	neurofilament light chain	Rattus norvegicus	43-59
8959035-5	1996	In hippocampus, the cytoskeletal proteins, neurofilament 68 (NF-68) and beta-tubulin were increased in females treated chronically with IBG, findings consistent with a damage-induced sprouting response.	Ibogaine	136-139	neurofilament light chain	Rattus norvegicus	61-66
7898613-7	1994	The long-lasting effect of ibogaine on serotonergic functioning, in particular, its blocking of the 5HT1B agonist-mediated increase in dopamine efflux, may have significance in the mediation of its anti-addictive properties.	Ibogaine	27-35	5-hydroxytryptamine receptor 1B	Rattus norvegicus	100-105
8880938-5	1996	Both ibogaine and 12-OH ibogamine demonstrated the highest potency values at the cocaine recognition site on the 5-HT transporter.	Ibogaine	5-13	solute carrier family 6 member 4	Rattus norvegicus	113-129
7596224-3	1995	We report here that 12-hydroxyibogamine, a primary metabolite of ibogaine, displays high affinity for the 5-HT transporter and elevates extracellular 5-HT.	Ibogaine	65-73	solute carrier family 6 member 4	Homo sapiens	106-122
6310434-0	1983	Cholecystokinin octapeptide (CCK-8), ceruletide and analogues of ceruletide: effects on tremors induced by oxotremorine, harmine and ibogaine.	Ibogaine	133-141	cholecystokinin	Mus musculus	0-15
34829663-3	2021	Single dose of ibogaine (10 mg/L i.e., 28.8 mumol/L) was applied to isolated rat uterus (spontaneous and Ca2+-stimulated) and contractility and antioxidant enzymes activity were monitored during 4 h. Ibogaine increased amplitude and frequency of spontaneous active uteri immediately after addition that was prevented by propranolol (beta1 and beta2 adrenoceptors selective antagonists) and glibenclamide (KATP sensitive channels inhibitor; only frequency) pre-treatment.	Ibogaine	200-208	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	333-338
34829663-3	2021	Single dose of ibogaine (10 mg/L i.e., 28.8 mumol/L) was applied to isolated rat uterus (spontaneous and Ca2+-stimulated) and contractility and antioxidant enzymes activity were monitored during 4 h. Ibogaine increased amplitude and frequency of spontaneous active uteri immediately after addition that was prevented by propranolol (beta1 and beta2 adrenoceptors selective antagonists) and glibenclamide (KATP sensitive channels inhibitor; only frequency) pre-treatment.	Ibogaine	200-208	UDP glucuronosyltransferase 1 family, polypeptide A7C	Rattus norvegicus	343-348
34829663-5	2021	In both types of active uterus, ibogaine induced a decrease in SOD1 and an increase in CAT activity after 2 h. In Ca2+-stimulated uterus, there was also a decrease of SOD2 activity after 2 h. After 4 h, SOD1 activity returned to the baseline level, but GSH-Px activity increased.	Ibogaine	32-40	superoxide dismutase 1	Rattus norvegicus	63-67
34829663-5	2021	In both types of active uterus, ibogaine induced a decrease in SOD1 and an increase in CAT activity after 2 h. In Ca2+-stimulated uterus, there was also a decrease of SOD2 activity after 2 h. After 4 h, SOD1 activity returned to the baseline level, but GSH-Px activity increased.	Ibogaine	32-40	catalase	Rattus norvegicus	87-90
34829663-5	2021	In both types of active uterus, ibogaine induced a decrease in SOD1 and an increase in CAT activity after 2 h. In Ca2+-stimulated uterus, there was also a decrease of SOD2 activity after 2 h. After 4 h, SOD1 activity returned to the baseline level, but GSH-Px activity increased.	Ibogaine	32-40	superoxide dismutase 2	Rattus norvegicus	167-171
34829663-5	2021	In both types of active uterus, ibogaine induced a decrease in SOD1 and an increase in CAT activity after 2 h. In Ca2+-stimulated uterus, there was also a decrease of SOD2 activity after 2 h. After 4 h, SOD1 activity returned to the baseline level, but GSH-Px activity increased.	Ibogaine	32-40	superoxide dismutase 1	Rattus norvegicus	203-207
35114149-2	2022	The cryo-EM structures of SERT bound to ibogaine and the physiological substrate serotonin resolved in different states provided a glimpse of functional conformations at atomistic resolution.	Ibogaine	40-48	solute carrier family 6 member 4	Homo sapiens	26-30
1475306-9	1992	The present data suggest the involvement of 5-HT2 receptor activity, and the possibility of a 5-HT1A contribution, in the stimulus properties of ibogaine.	Ibogaine	145-153	5-hydroxytryptamine receptor 1A	Rattus norvegicus	94-100
35614973-7	2022	Previous work has identified two DAT pharmacological chaperones with moderate potency and efficacy: bupropion and ibogaine.	Ibogaine	114-122	solute carrier family 6 member 3	Homo sapiens	33-36
32330007-4	2020	We have recently reported that the acute ibogaine administration induced a long-term increase of brain-derived neurotrophic factor mRNA levels in the rat prefrontal cortex, which led us to hypothesize that ibogaine may elicit antidepressant-like effects in rats.	Ibogaine	41-49	brain-derived neurotrophic factor	Rattus norvegicus	97-130
33860180-3	2021	Ibogaine and its active metabolite noribogaine correct folding defects in the dopamine transporter (DAT), but they rescue only a very limited number of folding-deficient DAT mutant proteins, which give rise to infantile Parkinsonism and dystonia.	Ibogaine	0-8	solute carrier family 6 member 3	Homo sapiens	78-98
33860180-3	2021	Ibogaine and its active metabolite noribogaine correct folding defects in the dopamine transporter (DAT), but they rescue only a very limited number of folding-deficient DAT mutant proteins, which give rise to infantile Parkinsonism and dystonia.	Ibogaine	0-8	solute carrier family 6 member 3	Homo sapiens	100-103
32330007-4	2020	We have recently reported that the acute ibogaine administration induced a long-term increase of brain-derived neurotrophic factor mRNA levels in the rat prefrontal cortex, which led us to hypothesize that ibogaine may elicit antidepressant-like effects in rats.	Ibogaine	206-214	brain-derived neurotrophic factor	Rattus norvegicus	97-130
29086036-6	2018	Ibogaine and its metabolite noribogaine also rescue several disease-relevant mutants of DAT.	Ibogaine	0-8	solute carrier family 6 member 3	Homo sapiens	88-91
30890941-0	2019	Ibogaine Administration Modifies GDNF and BDNF Expression in Brain Regions Involved in Mesocorticolimbic and Nigral Dopaminergic Circuits.	Ibogaine	0-8	glial cell derived neurotrophic factor	Rattus norvegicus	33-37
30890941-0	2019	Ibogaine Administration Modifies GDNF and BDNF Expression in Brain Regions Involved in Mesocorticolimbic and Nigral Dopaminergic Circuits.	Ibogaine	0-8	brain-derived neurotrophic factor	Rattus norvegicus	42-46
30890941-2	2019	Recent work has suggested that ibogaine effects on alcohol self-administration in rats are related to the release of Glial cell Derived Neurotrophic Factor (GDNF) in the Ventral Tegmental Area (VTA), a mesencephalic region which hosts the soma of dopaminergic neurons.	Ibogaine	31-39	glial cell derived neurotrophic factor	Rattus norvegicus	117-155
30890941-2	2019	Recent work has suggested that ibogaine effects on alcohol self-administration in rats are related to the release of Glial cell Derived Neurotrophic Factor (GDNF) in the Ventral Tegmental Area (VTA), a mesencephalic region which hosts the soma of dopaminergic neurons.	Ibogaine	31-39	glial cell derived neurotrophic factor	Rattus norvegicus	157-161
30890941-3	2019	Although previous reports have shown ibogaine"s ability to induce GDNF expression in rat midbrain, there are no studies addressing its effect on the expression of GDNF and other neurotrophic factors (NFs) such as Brain Derived Neurotrophic Factor (BDNF) or Nerve Growth Factor (NGF) in distinct brain regions containing dopaminergic neurons.	Ibogaine	37-45	glial cell derived neurotrophic factor	Rattus norvegicus	66-70
31829932-10	2019	Finally, we show how ibogaine could exert its anti-addictive properties through a completely different neurotrophic factor than other psychedelic drugs, the glial cell line-derived neurotrophic factor (GDNF).	Ibogaine	21-29	glial cell derived neurotrophic factor	Homo sapiens	157-200
31829932-10	2019	Finally, we show how ibogaine could exert its anti-addictive properties through a completely different neurotrophic factor than other psychedelic drugs, the glial cell line-derived neurotrophic factor (GDNF).	Ibogaine	21-29	glial cell derived neurotrophic factor	Homo sapiens	202-206
31019304-0	2019	Serotonin transporter-ibogaine complexes illuminate mechanisms of inhibition and transport.	Ibogaine	22-30	solute carrier family 6 member 4	Homo sapiens	0-21
31019304-7	2019	To elucidate structure-based mechanisms for transport in SERT we investigated its complexes with ibogaine, a hallucinogenic natural product with psychoactive and anti-addictive properties13,14.	Ibogaine	97-105	solute carrier family 6 member 4	Homo sapiens	57-61
31019304-9	2019	Here we report cryo-electron microscopy structures of SERT-ibogaine complexes captured in outward-open, occluded and inward-open conformations.	Ibogaine	59-67	solute carrier family 6 member 4	Homo sapiens	54-58
30976000-4	2019	Our results reveal significant changes in dynamics in regions TM1, EL3, EL4, and TM12 upon binding co-transported ions (Na+/K+) and ligand-mediated changes in TM1, EL3 and EL4 upon binding 5-HT, the drugs S-citalopram, cocaine and ibogaine.	Ibogaine	231-239	spectrin beta, erythrocytic	Homo sapiens	67-70
30976000-4	2019	Our results reveal significant changes in dynamics in regions TM1, EL3, EL4, and TM12 upon binding co-transported ions (Na+/K+) and ligand-mediated changes in TM1, EL3 and EL4 upon binding 5-HT, the drugs S-citalopram, cocaine and ibogaine.	Ibogaine	231-239	spectrin beta, erythrocytic	Homo sapiens	164-167
27555326-5	2016	Bupropion and ibogaine increased wild type DAT protein levels and also promoted maturation of the endoplasmic reticulum (ER)-retained DAT mutant K590A.	Ibogaine	14-22	solute carrier family 6 member 3	Homo sapiens	43-46
28405636-4	2016	The folding trajectory of DAT itself is not understood, though many insights have been gained from studies of folding-deficient mutants of the closely related serotonin transporter (SERT); i.e. their functional rescue by pharmacochaperoning with (nor)ibogaine or heat-shock protein inhibitors.	Ibogaine	251-259	solute carrier family 6 member 3	Homo sapiens	26-29
28405636-4	2016	The folding trajectory of DAT itself is not understood, though many insights have been gained from studies of folding-deficient mutants of the closely related serotonin transporter (SERT); i.e. their functional rescue by pharmacochaperoning with (nor)ibogaine or heat-shock protein inhibitors.	Ibogaine	251-259	solute carrier family 6 member 4	Homo sapiens	159-180
28405636-4	2016	The folding trajectory of DAT itself is not understood, though many insights have been gained from studies of folding-deficient mutants of the closely related serotonin transporter (SERT); i.e. their functional rescue by pharmacochaperoning with (nor)ibogaine or heat-shock protein inhibitors.	Ibogaine	251-259	solute carrier family 6 member 4	Homo sapiens	182-186
27555326-4	2016	After screening a set of known DAT ligands for their ability to increase DAT surface expression, we found that bupropion and ibogaine increased DAT surface expression, whereas others, including cocaine and methylphenidate, had no effect.	Ibogaine	125-133	solute carrier family 6 member 3	Homo sapiens	31-34
27555326-5	2016	Bupropion and ibogaine increased wild type DAT protein levels and also promoted maturation of the endoplasmic reticulum (ER)-retained DAT mutant K590A.	Ibogaine	14-22	solute carrier family 6 member 3	Homo sapiens	134-137
27555326-4	2016	After screening a set of known DAT ligands for their ability to increase DAT surface expression, we found that bupropion and ibogaine increased DAT surface expression, whereas others, including cocaine and methylphenidate, had no effect.	Ibogaine	125-133	solute carrier family 6 member 3	Homo sapiens	73-76
27555326-7	2016	Furthermore, knockdown of coat protein complex II (COPII) component SEC24D, which is important in the ER export of wild type DAT, also blocked the rescue effects of bupropion and ibogaine.	Ibogaine	179-187	SEC24 homolog D, COPII coat complex component	Homo sapiens	68-74
27555326-4	2016	After screening a set of known DAT ligands for their ability to increase DAT surface expression, we found that bupropion and ibogaine increased DAT surface expression, whereas others, including cocaine and methylphenidate, had no effect.	Ibogaine	125-133	solute carrier family 6 member 3	Homo sapiens	73-76
27555326-7	2016	Furthermore, knockdown of coat protein complex II (COPII) component SEC24D, which is important in the ER export of wild type DAT, also blocked the rescue effects of bupropion and ibogaine.	Ibogaine	179-187	solute carrier family 6 member 3	Homo sapiens	125-128
27555326-8	2016	These data suggest that bupropion and ibogaine promote maturation of DAT by acting as pharmacological chaperones in the ER.	Ibogaine	38-46	solute carrier family 6 member 3	Homo sapiens	69-72
26807959-9	2016	PHARMACOKINETICS AND PHARMACODYNAMICS: Ibogaine is metabolized mainly by CYP2D6 to the primary metabolite noribogaine (10-hydroxyibogamine).	Ibogaine	39-47	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	73-79
27140629-5	2016	Using membranes from HeLa cells expressing SERT and intact rat basophilic leukemia cells, we show that agents such as Na(+) and cocaine that stabilize outward-open conformations of SERT decreased phosphorylation and agents that stabilize inward-open conformations (e.g., 5-HT, ibogaine) increased phosphorylation.	Ibogaine	277-285	solute carrier family 6 member 4	Rattus norvegicus	181-185
27734823-7	2016	After oral application, 80% of ibogaine is subjected to the Odemethylation into noribogaine; main catalyzing enzyme is cytochrome CYP2D6.	Ibogaine	31-39	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	130-136
26517751-4	2016	Glial cell line-derived neurotrophic factor (GDNF), in particular, has been implicated in marked reduction of alcohol consumption in rodent addiction models, and the natural product ibogaine, a substance used traditionally in ritualistic ceremonies, has been suggested to increase the synthesis and release of GDNF in the dopaminergic system in rats.	Ibogaine	182-190	glial cell derived neurotrophic factor	Rattus norvegicus	310-314
26807959-13	2016	Furthermore, ibogaine has been shown to interact with the acetylcholine, serotonin and dopamine systems; it alters the expression of several proteins including substance P, brain-derived neurotrophic factor (BDNF), c-fos and egr-1.	Ibogaine	13-21	tachykinin precursor 1	Homo sapiens	160-171
26807959-17	2016	CARDIOTOXICITY: Ether-a-go-go-related gene (hERG) potassium channels in the heart might play a crucial role in ibogaine"s cardiotoxicity, as hERG channels are vital in the repolarization phase of cardiac action potentials and blockade by ibogaine delays this repolarization, resulting in QT (time interval between the start of the Q wave and the end of the T wave in the electrical cycle of the heart) interval prolongation and, subsequently, in arrhythmias and sudden cardiac arrest.	Ibogaine	111-119	ETS transcription factor ERG	Homo sapiens	44-48
26807959-17	2016	CARDIOTOXICITY: Ether-a-go-go-related gene (hERG) potassium channels in the heart might play a crucial role in ibogaine"s cardiotoxicity, as hERG channels are vital in the repolarization phase of cardiac action potentials and blockade by ibogaine delays this repolarization, resulting in QT (time interval between the start of the Q wave and the end of the T wave in the electrical cycle of the heart) interval prolongation and, subsequently, in arrhythmias and sudden cardiac arrest.	Ibogaine	111-119	ETS transcription factor ERG	Homo sapiens	141-145
26807959-17	2016	CARDIOTOXICITY: Ether-a-go-go-related gene (hERG) potassium channels in the heart might play a crucial role in ibogaine"s cardiotoxicity, as hERG channels are vital in the repolarization phase of cardiac action potentials and blockade by ibogaine delays this repolarization, resulting in QT (time interval between the start of the Q wave and the end of the T wave in the electrical cycle of the heart) interval prolongation and, subsequently, in arrhythmias and sudden cardiac arrest.	Ibogaine	238-246	ETS transcription factor ERG	Homo sapiens	44-48
26807959-17	2016	CARDIOTOXICITY: Ether-a-go-go-related gene (hERG) potassium channels in the heart might play a crucial role in ibogaine"s cardiotoxicity, as hERG channels are vital in the repolarization phase of cardiac action potentials and blockade by ibogaine delays this repolarization, resulting in QT (time interval between the start of the Q wave and the end of the T wave in the electrical cycle of the heart) interval prolongation and, subsequently, in arrhythmias and sudden cardiac arrest.	Ibogaine	238-246	ETS transcription factor ERG	Homo sapiens	141-145
26807959-21	2016	TOXICITY FROM DRUG-DRUG INTERACTION: Polymorphism in the CYP2D6 enzyme can influence blood concentrations of both ibogaine and its primary metabolite, which may have implications when a patient is taking other medication that is subject to significant CYP2D6 metabolism.	Ibogaine	114-122	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	57-63
26807959-21	2016	TOXICITY FROM DRUG-DRUG INTERACTION: Polymorphism in the CYP2D6 enzyme can influence blood concentrations of both ibogaine and its primary metabolite, which may have implications when a patient is taking other medication that is subject to significant CYP2D6 metabolism.	Ibogaine	114-122	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	252-258
26807959-13	2016	Furthermore, ibogaine has been shown to interact with the acetylcholine, serotonin and dopamine systems; it alters the expression of several proteins including substance P, brain-derived neurotrophic factor (BDNF), c-fos and egr-1.	Ibogaine	13-21	brain derived neurotrophic factor	Homo sapiens	173-206
26807959-13	2016	Furthermore, ibogaine has been shown to interact with the acetylcholine, serotonin and dopamine systems; it alters the expression of several proteins including substance P, brain-derived neurotrophic factor (BDNF), c-fos and egr-1.	Ibogaine	13-21	brain derived neurotrophic factor	Homo sapiens	208-212
26807959-13	2016	Furthermore, ibogaine has been shown to interact with the acetylcholine, serotonin and dopamine systems; it alters the expression of several proteins including substance P, brain-derived neurotrophic factor (BDNF), c-fos and egr-1.	Ibogaine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	215-220
26807959-13	2016	Furthermore, ibogaine has been shown to interact with the acetylcholine, serotonin and dopamine systems; it alters the expression of several proteins including substance P, brain-derived neurotrophic factor (BDNF), c-fos and egr-1.	Ibogaine	13-21	early growth response 1	Homo sapiens	225-230
25651476-0	2015	Influence of CYP2D6 activity on the pharmacokinetics and pharmacodynamics of a single 20 mg dose of ibogaine in healthy volunteers.	Ibogaine	100-108	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	13-19
25651476-1	2015	Conversion of ibogaine to its active metabolite noribogaine appears to be mediated primarily by CYP2D6.	Ibogaine	14-22	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	96-102
25651476-8	2015	CYP2D6 phenotype was robustly correlated with ibogaine AUC0-t (r = 0.82) and Cmax (r = 0.77).	Ibogaine	46-54	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-6
25651476-11	2015	The doubling of exposure to active moiety in subjects with reduced CYP2D6 activity suggests it may be prudent to genotype patients awaiting ibogaine treatment, and to at least halve the intended dose of ibogaine in CYP2D6 poor metabolizers.	Ibogaine	203-211	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	67-73
25651476-11	2015	The doubling of exposure to active moiety in subjects with reduced CYP2D6 activity suggests it may be prudent to genotype patients awaiting ibogaine treatment, and to at least halve the intended dose of ibogaine in CYP2D6 poor metabolizers.	Ibogaine	203-211	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	215-221
25660330-12	2015	Ibogaine also increased SOD1 activity in erythrocytes at both doses applied here.	Ibogaine	0-8	superoxide dismutase 1	Homo sapiens	24-28
25660330-13	2015	Treatment with 20 muM also elevated GR activity after in vitro incubation at 37 C. Electrophoretic profiles revealed that incubation with ibogaine mitigates H2O2 mediated suppression of SOD1 activity.	Ibogaine	138-146	latexin	Homo sapiens	18-21
25660330-13	2015	Treatment with 20 muM also elevated GR activity after in vitro incubation at 37 C. Electrophoretic profiles revealed that incubation with ibogaine mitigates H2O2 mediated suppression of SOD1 activity.	Ibogaine	138-146	glutathione-disulfide reductase	Homo sapiens	36-38
25660330-13	2015	Treatment with 20 muM also elevated GR activity after in vitro incubation at 37 C. Electrophoretic profiles revealed that incubation with ibogaine mitigates H2O2 mediated suppression of SOD1 activity.	Ibogaine	138-146	superoxide dismutase 1	Homo sapiens	186-190
23707769-3	2013	We have recently reported that ibogaine inhibits human ERG (hERG) potassium channels at concentrations similar to the drugs affinity for several of its known brain targets.	Ibogaine	31-39	ETS transcription factor ERG	Homo sapiens	55-58
22458604-0	2014	Anti-addiction drug ibogaine inhibits hERG channels: a cardiac arrhythmia risk.	Ibogaine	20-28	ETS transcription factor ERG	Homo sapiens	38-42
24307198-0	2014	Mechanism of hERG channel block by the psychoactive indole alkaloid ibogaine.	Ibogaine	68-76	ETS transcription factor ERG	Homo sapiens	13-17
24307198-3	2014	Therefore, we studied in detail the interaction of ibogaine with hERG channels heterologously expressed in mammalian kidney tsA-201 cells.	Ibogaine	51-59	ETS transcription factor ERG	Homo sapiens	65-69
24307198-4	2014	Currents through hERG channels were blocked regardless of whether ibogaine was applied via the extracellular or intracellular solution.	Ibogaine	66-74	ETS transcription factor ERG	Homo sapiens	17-21
24307198-10	2014	Mutations in the binding site reported for other hERG channel blockers (Y652A and F656A) reduced the potency of ibogaine, whereas an inactivation-deficient double mutant (G628C/S631C) was as sensitive as wild-type channels.	Ibogaine	112-120	ETS transcription factor ERG	Homo sapiens	49-53
24307198-12	2014	Experimental current traces were fit to a kinetic model of hERG channel gating, revealing preferential binding of ibogaine to the open and inactivated state.	Ibogaine	114-122	ETS transcription factor ERG	Homo sapiens	59-63
24307198-13	2014	Taken together, these findings show that ibogaine blocks hERG channels from the cytosolic side either in its charged form alone or in company with its uncharged form and alters the currents by changing the relative contribution of channel states over time.	Ibogaine	41-49	ETS transcription factor ERG	Homo sapiens	57-61
23707769-3	2013	We have recently reported that ibogaine inhibits human ERG (hERG) potassium channels at concentrations similar to the drugs affinity for several of its known brain targets.	Ibogaine	31-39	ETS transcription factor ERG	Homo sapiens	60-64
23707769-6	2013	We confirmed that heterologously expressed hERG currents are reduced by ibogaine in low micromolar concentrations.	Ibogaine	72-80	ETS transcription factor ERG	Homo sapiens	43-47
23706649-7	2013	Inhibitor binding assays showed that both of the thermostabilised SERT mutants bound [(125)I]RTI55 (beta-CIT) with affinity similar to that of the wild-type transporter, although cocaine bound with increased affinity (17- to 56-fold) whilst ibogaine, imipramine and paroxetine all bound with lower affinity (up to 90-fold).	Ibogaine	241-249	solute carrier family 6 member 4	Homo sapiens	66-70
24204784-6	2013	RESULTS AND SIGNIFICANCE: In rat thalamic membranes ibogaine, noribogaine and 18-MC were MOR antagonists with functional Ke values ranging from 3 uM (ibogaine) to 13 uM (noribogaine and 18MC).	Ibogaine	52-60	opioid receptor mu 1	Homo sapiens	89-92
23776432-1	2013	The competitive inhibitor cocaine and the non-competitive inhibitor ibogaine induce different conformational states of the human serotonin transporter.	Ibogaine	68-76	solute carrier family 6 member 4	Homo sapiens	129-150
23776432-2	2013	It has been shown from accessibility experiments that cocaine mainly induces an outward-facing conformation, while the non-competitive inhibitor ibogaine, and its active metabolite noribogaine, have been proposed to induce an inward-facing conformation of the human serotonin transporter similar to what has been observed for the endogenous substrate, serotonin.	Ibogaine	145-153	solute carrier family 6 member 4	Homo sapiens	266-287
20889976-9	2010	SERT-RI(607,608)AA and SERT-RII(607-609)AAA were partially rescued by treatment of cells with the nonspecific chemical chaperone DMSO or the specific pharmacochaperone ibogaine (which binds to the inward facing conformation of SERT) but not by other classes of ligands (inhibitors, substrates, amphetamines).	Ibogaine	168-176	solute carrier family 6 member 4	Homo sapiens	0-4
22451652-1	2012	Ibogaine, a hallucinogenic alkaloid proposed as a treatment for opiate withdrawal, has been shown to inhibit serotonin transporter (SERT) noncompetitively, in contrast to all other known inhibitors, which are competitive with substrate.	Ibogaine	0-8	solute carrier family 6 member 4	Homo sapiens	109-130
22451652-1	2012	Ibogaine, a hallucinogenic alkaloid proposed as a treatment for opiate withdrawal, has been shown to inhibit serotonin transporter (SERT) noncompetitively, in contrast to all other known inhibitors, which are competitive with substrate.	Ibogaine	0-8	solute carrier family 6 member 4	Homo sapiens	132-136
22451652-2	2012	Ibogaine binding to SERT increases accessibility in the permeation pathway connecting the substrate-binding site with the cytoplasm.	Ibogaine	0-8	solute carrier family 6 member 4	Homo sapiens	20-24
22451652-3	2012	Because of the structural similarity between ibogaine and serotonin, it had been suggested that ibogaine binds to the substrate site of SERT.	Ibogaine	45-53	solute carrier family 6 member 4	Homo sapiens	136-140
22451652-3	2012	Because of the structural similarity between ibogaine and serotonin, it had been suggested that ibogaine binds to the substrate site of SERT.	Ibogaine	96-104	solute carrier family 6 member 4	Homo sapiens	136-140
22451652-5	2012	Ibogaine noncompetitively inhibited transport by both SERT and the homologous dopamine transporter (DAT).	Ibogaine	0-8	solute carrier family 6 member 4	Homo sapiens	54-58
22451652-5	2012	Ibogaine noncompetitively inhibited transport by both SERT and the homologous dopamine transporter (DAT).	Ibogaine	0-8	solute carrier family 6 member 3	Homo sapiens	78-98
22451652-5	2012	Ibogaine noncompetitively inhibited transport by both SERT and the homologous dopamine transporter (DAT).	Ibogaine	0-8	solute carrier family 6 member 3	Homo sapiens	100-103
22451652-6	2012	Ibogaine blocked substrate-induced currents also in DAT and increased accessibility of the DAT cytoplasmic permeation pathway.	Ibogaine	0-8	solute carrier family 6 member 3	Homo sapiens	52-55
22451652-6	2012	Ibogaine blocked substrate-induced currents also in DAT and increased accessibility of the DAT cytoplasmic permeation pathway.	Ibogaine	0-8	solute carrier family 6 member 3	Homo sapiens	91-94
22451652-7	2012	When present on the cell exterior, ibogaine inhibited SERT substrate-induced currents, but not when it was introduced into the cytoplasm through the patch electrode.	Ibogaine	35-43	solute carrier family 6 member 4	Homo sapiens	54-58
22451652-9	2012	The kinetics of inhibitor binding and dissociation, as determined by their effect on SERT currents, indicated that ibogaine does not inhibit by forming a long-lived complex with SERT, but rather binds directly to the transporter in an inward-open conformation.	Ibogaine	115-123	solute carrier family 6 member 4	Homo sapiens	85-89
22451652-9	2012	The kinetics of inhibitor binding and dissociation, as determined by their effect on SERT currents, indicated that ibogaine does not inhibit by forming a long-lived complex with SERT, but rather binds directly to the transporter in an inward-open conformation.	Ibogaine	115-123	solute carrier family 6 member 4	Homo sapiens	178-182
22200647-3	2012	The question of whether ibogaine inhibits acetylcholinesterase (AChE) is of pharmacological and toxicological significance.	Ibogaine	24-32	acetylcholinesterase (Cartwright blood group)	Homo sapiens	42-62
22200647-3	2012	The question of whether ibogaine inhibits acetylcholinesterase (AChE) is of pharmacological and toxicological significance.	Ibogaine	24-32	acetylcholinesterase (Cartwright blood group)	Homo sapiens	64-68
22200647-5	2012	RESULTS: Ibogaine inhibited AChE with an IC(50) of 520+-40 muM.	Ibogaine	9-17	acetylcholinesterase (Cartwright blood group)	Homo sapiens	28-32
22200647-6	2012	CONCLUSIONS: Ibogaine"s inhibition of AChE is physiologically negligible, and does not appear to account for observations of functional effects in animals and humans that might otherwise suggest the possible involvement of pathways linked to muscarinic acetylcholine transmission.	Ibogaine	13-21	acetylcholinesterase (Cartwright blood group)	Homo sapiens	38-42
20889976-9	2010	SERT-RI(607,608)AA and SERT-RII(607-609)AAA were partially rescued by treatment of cells with the nonspecific chemical chaperone DMSO or the specific pharmacochaperone ibogaine (which binds to the inward facing conformation of SERT) but not by other classes of ligands (inhibitors, substrates, amphetamines).	Ibogaine	168-176	solute carrier family 6 member 4	Homo sapiens	23-27
20889976-9	2010	SERT-RI(607,608)AA and SERT-RII(607-609)AAA were partially rescued by treatment of cells with the nonspecific chemical chaperone DMSO or the specific pharmacochaperone ibogaine (which binds to the inward facing conformation of SERT) but not by other classes of ligands (inhibitors, substrates, amphetamines).	Ibogaine	168-176	solute carrier family 6 member 4	Homo sapiens	23-27
19887017-5	2010	Human P-gp was significantly inhibited in a concentration-dependent manner by norbuprenorphine>buprenorphine>methadone>ibogaine and THC.	Ibogaine	128-136	ATP binding cassette subfamily B member 1	Homo sapiens	6-10
21040239-3	2010	Previously, we reported that the desirable actions of ibogaine to reduce self-administration of, and relapse to, alcohol consumption are mediated via the upregulation of the expression of the glial cell line-derived neurotrophic factor (GDNF) in the midbrain ventral tegmental area (VTA), and the consequent activation of the GDNF pathway.	Ibogaine	54-62	glial cell derived neurotrophic factor	Homo sapiens	192-235
21040239-3	2010	Previously, we reported that the desirable actions of ibogaine to reduce self-administration of, and relapse to, alcohol consumption are mediated via the upregulation of the expression of the glial cell line-derived neurotrophic factor (GDNF) in the midbrain ventral tegmental area (VTA), and the consequent activation of the GDNF pathway.	Ibogaine	54-62	glial cell derived neurotrophic factor	Homo sapiens	237-241
21040239-3	2010	Previously, we reported that the desirable actions of ibogaine to reduce self-administration of, and relapse to, alcohol consumption are mediated via the upregulation of the expression of the glial cell line-derived neurotrophic factor (GDNF) in the midbrain ventral tegmental area (VTA), and the consequent activation of the GDNF pathway.	Ibogaine	54-62	glial cell derived neurotrophic factor	Homo sapiens	326-330
21040239-6	2010	We used SH-SY5Y cells as a cell culture model and found that noribogaine, like ibogaine, but not 18-MC, induces a robust increase in GDNF mRNA levels.	Ibogaine	64-72	glial cell derived neurotrophic factor	Homo sapiens	133-137
19887017-6	2010	Similarly, BCRP was inhibited by buprenorphine>norbuprenorphine>ibogaine and THC.	Ibogaine	70-78	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	11-15
19492342-4	2009	We measured the interactions of [(99m)Tc(CO)(3)-ibogaine](+) and (99m)Tc-tricarbonyl with the main BBB efflux transporters P-gp and BCRP in vitro and in vivo.	Ibogaine	48-56	phosphoglycolate phosphatase	Mus musculus	123-127
19492342-4	2009	We measured the interactions of [(99m)Tc(CO)(3)-ibogaine](+) and (99m)Tc-tricarbonyl with the main BBB efflux transporters P-gp and BCRP in vitro and in vivo.	Ibogaine	48-56	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	132-136
15659598-0	2005	Glial cell line-derived neurotrophic factor mediates the desirable actions of the anti-addiction drug ibogaine against alcohol consumption.	Ibogaine	102-110	glial cell derived neurotrophic factor	Homo sapiens	0-43
18541917-1	2008	Previously, we demonstrated that the action of the natural alkaloid, ibogaine, to reduce alcohol (ethanol) consumption is mediated by the glial cell line-derived neurotrophic factor (GDNF) in the ventral tegmental area (VTA).	Ibogaine	69-77	glial cell derived neurotrophic factor	Rattus norvegicus	138-181
18541917-1	2008	Previously, we demonstrated that the action of the natural alkaloid, ibogaine, to reduce alcohol (ethanol) consumption is mediated by the glial cell line-derived neurotrophic factor (GDNF) in the ventral tegmental area (VTA).	Ibogaine	69-77	glial cell derived neurotrophic factor	Rattus norvegicus	183-187
17698848-1	2007	Ibogaine, a hallucinogenic alkaloid with purported anti-addiction properties, inhibited serotonin transporter (SERT) noncompetitively by decreasing V(max) with little change in the K(m) for serotonin (5-HT).	Ibogaine	0-8	solute carrier family 6 member 4	Homo sapiens	88-109
17698848-1	2007	Ibogaine, a hallucinogenic alkaloid with purported anti-addiction properties, inhibited serotonin transporter (SERT) noncompetitively by decreasing V(max) with little change in the K(m) for serotonin (5-HT).	Ibogaine	0-8	solute carrier family 6 member 4	Homo sapiens	111-115
17698848-2	2007	Ibogaine also inhibited binding to SERT of the cocaine analog 2beta-2-carbomethoxy-3-(4-[(125)I]iodophenyl)tropane.	Ibogaine	0-8	solute carrier family 6 member 4	Homo sapiens	35-39
17698848-4	2007	Ibogaine increased the reactivity of cysteine residues positioned in the proposed cytoplasmic permeation pathway of SERT but not at nearby positions out of that pathway.	Ibogaine	0-8	solute carrier family 6 member 4	Homo sapiens	116-120
17698848-6	2007	These results are consistent with the proposal that ibogaine binds to and stabilizes the state of SERT from which 5-HT dissociates to the cytoplasm, in contrast with cocaine, which stabilizes the state that binds extracellular 5-HT.	Ibogaine	52-60	solute carrier family 6 member 4	Homo sapiens	98-102
17023388-0	2006	Autoregulation of glial cell line-derived neurotrophic factor expression: implications for the long-lasting actions of the anti-addiction drug, Ibogaine.	Ibogaine	144-152	glial cell derived neurotrophic factor	Homo sapiens	18-61
17023388-1	2006	We recently showed that the up-regulation of the glial cell line-derived neurotrophic factor (GDNF) pathway in the midbrain, is the molecular mechanism by which the putative anti-addiction drug Ibogaine mediates its desirable action of reducing alcohol consumption.	Ibogaine	194-202	glial cell derived neurotrophic factor	Homo sapiens	49-92
17023388-1	2006	We recently showed that the up-regulation of the glial cell line-derived neurotrophic factor (GDNF) pathway in the midbrain, is the molecular mechanism by which the putative anti-addiction drug Ibogaine mediates its desirable action of reducing alcohol consumption.	Ibogaine	194-202	glial cell derived neurotrophic factor	Homo sapiens	94-98
17023388-3	2006	Here we determine whether, and how, Ibogaine exerts its long-lasting actions on GDNF expression and signaling.	Ibogaine	36-44	glial cell derived neurotrophic factor	Homo sapiens	80-84
17023388-4	2006	Using the dopaminergic-like SHSY5Y cell line as a culture model, we observed that short-term Ibogaine exposure results in a sustained increase in GDNF expression that is mediated via the induction of a long-lasting autoregulatory cycle by which GDNF positively regulates its own expression.	Ibogaine	93-101	glial cell derived neurotrophic factor	Homo sapiens	146-150
17023388-4	2006	Using the dopaminergic-like SHSY5Y cell line as a culture model, we observed that short-term Ibogaine exposure results in a sustained increase in GDNF expression that is mediated via the induction of a long-lasting autoregulatory cycle by which GDNF positively regulates its own expression.	Ibogaine	93-101	glial cell derived neurotrophic factor	Homo sapiens	245-249
17023388-5	2006	We show that the initial exposure of cells to Ibogaine or GDNF results in an increase in GDNF mRNA, leading to protein expression and to the corresponding activation of the GDNF signaling pathway.	Ibogaine	46-54	glial cell derived neurotrophic factor	Homo sapiens	89-93
17023388-5	2006	We show that the initial exposure of cells to Ibogaine or GDNF results in an increase in GDNF mRNA, leading to protein expression and to the corresponding activation of the GDNF signaling pathway.	Ibogaine	46-54	glial cell derived neurotrophic factor	Homo sapiens	89-93
15659598-8	2005	Microinjection of ibogaine into the ventral tegmental area (VTA), but not the substantia nigra, reduced self-administration of ethanol, and systemic administration of ibogaine increased the expression of glial cell line-derived neurotrophic factor (GDNF) in a midbrain region that includes the VTA.	Ibogaine	18-26	glial cell derived neurotrophic factor	Homo sapiens	204-247
15659598-8	2005	Microinjection of ibogaine into the ventral tegmental area (VTA), but not the substantia nigra, reduced self-administration of ethanol, and systemic administration of ibogaine increased the expression of glial cell line-derived neurotrophic factor (GDNF) in a midbrain region that includes the VTA.	Ibogaine	18-26	glial cell derived neurotrophic factor	Homo sapiens	249-253
15659598-8	2005	Microinjection of ibogaine into the ventral tegmental area (VTA), but not the substantia nigra, reduced self-administration of ethanol, and systemic administration of ibogaine increased the expression of glial cell line-derived neurotrophic factor (GDNF) in a midbrain region that includes the VTA.	Ibogaine	167-175	glial cell derived neurotrophic factor	Homo sapiens	204-247
15659598-8	2005	Microinjection of ibogaine into the ventral tegmental area (VTA), but not the substantia nigra, reduced self-administration of ethanol, and systemic administration of ibogaine increased the expression of glial cell line-derived neurotrophic factor (GDNF) in a midbrain region that includes the VTA.	Ibogaine	167-175	glial cell derived neurotrophic factor	Homo sapiens	249-253
15659598-9	2005	In dopaminergic neuron-like SHSY5Y cells, ibogaine treatment upregulated the GDNF pathway as indicated by increases in phosphorylation of the GDNF receptor, Ret, and the downstream kinase, ERK1 (extracellular signal-regulated kinase 1).	Ibogaine	42-50	glial cell derived neurotrophic factor	Homo sapiens	77-81
15659598-9	2005	In dopaminergic neuron-like SHSY5Y cells, ibogaine treatment upregulated the GDNF pathway as indicated by increases in phosphorylation of the GDNF receptor, Ret, and the downstream kinase, ERK1 (extracellular signal-regulated kinase 1).	Ibogaine	42-50	glial cell derived neurotrophic factor	Homo sapiens	142-146
15659598-9	2005	In dopaminergic neuron-like SHSY5Y cells, ibogaine treatment upregulated the GDNF pathway as indicated by increases in phosphorylation of the GDNF receptor, Ret, and the downstream kinase, ERK1 (extracellular signal-regulated kinase 1).	Ibogaine	42-50	ret proto-oncogene	Homo sapiens	157-160
15659598-9	2005	In dopaminergic neuron-like SHSY5Y cells, ibogaine treatment upregulated the GDNF pathway as indicated by increases in phosphorylation of the GDNF receptor, Ret, and the downstream kinase, ERK1 (extracellular signal-regulated kinase 1).	Ibogaine	42-50	mitogen-activated protein kinase 3	Homo sapiens	189-193
15659598-9	2005	In dopaminergic neuron-like SHSY5Y cells, ibogaine treatment upregulated the GDNF pathway as indicated by increases in phosphorylation of the GDNF receptor, Ret, and the downstream kinase, ERK1 (extracellular signal-regulated kinase 1).	Ibogaine	42-50	mitogen-activated protein kinase 3	Homo sapiens	195-234
15659598-10	2005	Finally, the ibogaine-mediated decrease in ethanol self-administration was mimicked by intra-VTA microinjection of GDNF and was reduced by intra-VTA delivery of anti-GDNF neutralizing antibodies.	Ibogaine	13-21	glial cell derived neurotrophic factor	Homo sapiens	115-119
15659598-10	2005	Finally, the ibogaine-mediated decrease in ethanol self-administration was mimicked by intra-VTA microinjection of GDNF and was reduced by intra-VTA delivery of anti-GDNF neutralizing antibodies.	Ibogaine	13-21	glial cell derived neurotrophic factor	Homo sapiens	166-170
15659598-11	2005	Together, these results suggest that GDNF in the VTA mediates the action of ibogaine on ethanol consumption.	Ibogaine	76-84	glial cell derived neurotrophic factor	Homo sapiens	37-41
15659598-12	2005	These findings highlight the importance of GDNF as a new target for drug development for alcoholism that may mimic the effect of ibogaine against alcohol consumption but avoid the negative side effects.	Ibogaine	129-137	glial cell derived neurotrophic factor	Homo sapiens	43-47
12019193-0	2002	Metabolism of 18-methoxycoronaridine, an ibogaine analog, to 18-hydroxycoronaridine by genetically variable CYP2C19.	Ibogaine	41-49	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	108-115