PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
31292387-0	2019	Extreme Elevation of the Prothrombin Time-International Normalized Ratio due to a Probable Interaction between Warfarin and Flutamide.	Flutamide	124-133	coagulation factor II, thrombin	Homo sapiens	25-36
31292387-5	2019	The prothrombin time-international normalized ratio was extremely elevated after starting flutamide to treat progression of prostate cancer.	Flutamide	90-99	coagulation factor II, thrombin	Homo sapiens	4-15
31455381-0	2019	Influence of androgenic blockade with flutamide on pain behaviour and expression of the genes that encode the NaV1.7 and NaV1.8 voltage-dependent sodium channels in a rat model of postoperative pain.	Flutamide	38-47	sodium voltage-gated channel alpha subunit 9	Rattus norvegicus	110-116
31378101-6	2019	Vehicle or flutamide (8 mg/kg/day; subcutaneous), an AR antagonist, was administered at 11.5 months of age for 2 weeks followed by measurement of blood pressure.	Flutamide	11-20	androgen receptor	Rattus norvegicus	53-55
31059691-4	2019	In this study, we used dihydrotestosterone (DHT) and an antagonist of the mammalian androgen receptor (flutamide) to examine the impact of androgens on sex determination in the snapping turtle.	Flutamide	103-112	androgen receptor	Homo sapiens	84-101
31480771-4	2019	Adding the antiandrogen flutamide with the stress hormone corticosterone can additively decrease BDNF mRNA in mouse hippocampus mHippoE-14 cells, which can then be reversed via down-regulating the miR-204-5p expression.	Flutamide	24-33	brain derived neurotrophic factor	Mus musculus	97-101
31544355-9	2019	In intact males, flutamide, an androgen receptor inhibitor, had similar effects to castration.	Flutamide	17-26	androgen receptor	Mus musculus	31-48
31544355-10	2019	Bronchoalveolar lavage concentrations of several cytokines were reduced by either castration or flutamide treatment, but only IL-1alpha was reduced by both castration and flutamide.	Flutamide	171-180	interleukin 1 alpha	Mus musculus	126-135
31455381-0	2019	Influence of androgenic blockade with flutamide on pain behaviour and expression of the genes that encode the NaV1.7 and NaV1.8 voltage-dependent sodium channels in a rat model of postoperative pain.	Flutamide	38-47	sodium voltage-gated channel alpha subunit 10	Rattus norvegicus	121-127
31132720-5	2019	In preantral follicles, the upregulation of GDF9 mRNA and protein expression was found in pigs that were neonatally exposed to TP or FLU, while administration of TP or ICI resulted in upregulation of BMP15.	Flutamide	133-136	growth differentiation factor 9	Sus scrofa	44-48
31132720-6	2019	TGFBR1 and BMPR2 mRNA and protein expression were upregulated in preantral follicles of adult pigs that were neonatally exposed to TP or FLU, while administration of TP or ICI resulted in upregulation of BMPR1B.	Flutamide	137-140	transforming growth factor beta receptor 1	Sus scrofa	0-6
31132720-6	2019	TGFBR1 and BMPR2 mRNA and protein expression were upregulated in preantral follicles of adult pigs that were neonatally exposed to TP or FLU, while administration of TP or ICI resulted in upregulation of BMPR1B.	Flutamide	137-140	bone morphogenetic protein receptor type 2	Sus scrofa	11-16
31132720-8	2019	In addition, treatment with FLU upregulated BMPR1B and BMPR2 mRNA and protein expression, while downregulated the expression of TGFBR1.	Flutamide	28-31	bone morphogenetic protein receptor type 1B	Sus scrofa	44-50
31132720-8	2019	In addition, treatment with FLU upregulated BMPR1B and BMPR2 mRNA and protein expression, while downregulated the expression of TGFBR1.	Flutamide	28-31	bone morphogenetic protein receptor type 2	Sus scrofa	55-60
31132720-8	2019	In addition, treatment with FLU upregulated BMPR1B and BMPR2 mRNA and protein expression, while downregulated the expression of TGFBR1.	Flutamide	28-31	transforming growth factor beta receptor 1	Sus scrofa	128-134
31048005-5	2019	The effects of zGnih on testosterone and SPD/SPZ production was blocked in the presence of androgen receptor antagonist, flutamide (FLU).	Flutamide	121-130	androgen receptor	Danio rerio	91-108
31048005-5	2019	The effects of zGnih on testosterone and SPD/SPZ production was blocked in the presence of androgen receptor antagonist, flutamide (FLU).	Flutamide	132-135	androgen receptor	Danio rerio	91-108
31262916-0	2019	Flutamide as an Alternative Anti-androgen Agent and Predictor of the Efficacy of Novel Androgen Receptor-targeted Agents.	Flutamide	0-9	androgen receptor	Homo sapiens	87-104
31262916-1	2019	BACKGROUND/AIM: There are few reports that verify the relationship between the therapeutic effects of flutamide and novel androgen receptor-targeted agents.	Flutamide	102-111	androgen receptor	Homo sapiens	122-139
31262916-2	2019	We aimed to evaluate the benefits of flutamide as an alternative anti-androgen agent and its effects on the efficacy of novel androgen receptor-targeted agents.	Flutamide	37-46	androgen receptor	Homo sapiens	126-143
31262916-5	2019	RESULTS: Patients who responded well to flutamide (Flutamide effective) following initial maximum androgen blockade (MAB) showed significantly higher changes in serum PSA levels (p=0.039) and PSA-progression-free survival (PFS) rate (p=0.016) following enzalutamide therapy compared to those who did not respond well to flutamide.	Flutamide	40-49	kallikrein related peptidase 3	Homo sapiens	167-170
31262916-5	2019	RESULTS: Patients who responded well to flutamide (Flutamide effective) following initial maximum androgen blockade (MAB) showed significantly higher changes in serum PSA levels (p=0.039) and PSA-progression-free survival (PFS) rate (p=0.016) following enzalutamide therapy compared to those who did not respond well to flutamide.	Flutamide	40-49	kallikrein related peptidase 3	Homo sapiens	192-195
31262916-5	2019	RESULTS: Patients who responded well to flutamide (Flutamide effective) following initial maximum androgen blockade (MAB) showed significantly higher changes in serum PSA levels (p=0.039) and PSA-progression-free survival (PFS) rate (p=0.016) following enzalutamide therapy compared to those who did not respond well to flutamide.	Flutamide	51-60	kallikrein related peptidase 3	Homo sapiens	167-170
31262916-5	2019	RESULTS: Patients who responded well to flutamide (Flutamide effective) following initial maximum androgen blockade (MAB) showed significantly higher changes in serum PSA levels (p=0.039) and PSA-progression-free survival (PFS) rate (p=0.016) following enzalutamide therapy compared to those who did not respond well to flutamide.	Flutamide	51-60	kallikrein related peptidase 3	Homo sapiens	192-195
31262916-6	2019	Multivariate analysis showed that the factor of Flutamide effective was significantly associated with a good PSA-PFS rate following enzalutamide therapy (HR=7.36, 95%CI=1.4-38.71, p=0.018).	Flutamide	48-57	kallikrein related peptidase 3	Homo sapiens	109-112
31262916-7	2019	CONCLUSION: Patients showing good response to flutamide following initial MAB may achieve a satisfactory PSA-PFS rate with subsequent enzalutamide therapy.	Flutamide	46-55	kallikrein related peptidase 3	Homo sapiens	105-108
31150416-5	2019	In this model, we observed the effect of hyperandrogenemia and flutamide on the decidualization, angiogenesis and uNK cells by methods of immunohistochemistry, quantitative PCR, western blotting and Dolichos biflorus agglutinin (DBA) lectin staining.	Flutamide	63-72	unkempt family zinc finger	Mus musculus	114-117
30849180-4	2019	EXPERIMENTAL APPROACH: The androgen receptor antagonist, flutamide, was administered to presymptomatic SOD1G93A mice as a slow-release subcutaneous implant (5 mg day-1 ).	Flutamide	57-66	androgen receptor	Mus musculus	27-44
30849180-8	2019	Flutamide treatment accelerated disease onset and locomotor dysfunction in male SOD1G93A mice, but not female mice, without affecting survival.	Flutamide	0-9	superoxide dismutase 1, soluble	Mus musculus	80-84
30849180-9	2019	Analysis of hindlimb muscles revealed exacerbation of myofibre atrophy in male SOD1G93A mice treated with flutamide, although motor neuron pathology was not affected.	Flutamide	106-115	superoxide dismutase 1, soluble	Mus musculus	79-83
30741370-1	2019	BACKGROUND: Alternative anti-androgen therapy (AAT) with flutamide after combined androgen blockade (CAB) therapy with bicalutamide for metastatic prostate cancer is common.	Flutamide	57-66	serpin family A member 1	Homo sapiens	47-50
30741370-13	2019	CONCLUSIONS: AAT with subsequent flutamide after CAB therapy with bicalutamide may be suitable for some CRPC patients.	Flutamide	33-42	serpin family A member 1	Homo sapiens	13-16
30951142-9	2019	VCAM1 mRNA and protein were higher in PCOS-derived theca cells compared with control theca and reduced markedly by the AR antagonist flutamide.	Flutamide	133-142	vascular cell adhesion molecule 1	Mus musculus	0-5
31018175-10	2019	Indeed, mice with implanted flutamide exhibited exacerbated AAA formation and aortic F4/80, Il-1b and Il-6 expression were significantly increased.	Flutamide	28-37	adhesion G protein-coupled receptor E1	Mus musculus	85-90
31018175-10	2019	Indeed, mice with implanted flutamide exhibited exacerbated AAA formation and aortic F4/80, Il-1b and Il-6 expression were significantly increased.	Flutamide	28-37	interleukin 1 beta	Mus musculus	92-97
31018175-10	2019	Indeed, mice with implanted flutamide exhibited exacerbated AAA formation and aortic F4/80, Il-1b and Il-6 expression were significantly increased.	Flutamide	28-37	interleukin 6	Mus musculus	102-106
31150416-8	2019	CONCLUSION: Flutamide treatment can efficiently ameliorate the hyperandrogenemia-induced the disorders in aspects of decidualization, angiogenesis and uNK cells, which further improve the poor endometrial receptivity in PCOS patients.	Flutamide	12-21	unk zinc finger	Homo sapiens	151-154
30971225-10	2019	The expected results of this study will be that enzalutamide is superior to flutamide in terms of PSA response.	Flutamide	76-85	kallikrein related peptidase 3	Homo sapiens	98-101
30653980-7	2019	To test this hypothesis, intact males were infused with the androgen receptor antagonist flutamide into the DH after object training.	Flutamide	89-98	androgen receptor	Mus musculus	60-77
30423122-7	2019	Pretreatment with flutamide, as well as knockdown of androgen receptor, decreased testosterone-induced DR5 and CHOP expression, as well as apoptosis.	Flutamide	18-27	TNF receptor superfamily member 10b	Homo sapiens	103-106
30580448-6	2019	DHEA-induced PCOS rats had a decreased level of IFN-gamma compared with the control rats, which was restored partly in flutamide (an androgen receptor antagonist)-treated rats.	Flutamide	119-128	interferon gamma	Rattus norvegicus	48-57
30580448-6	2019	DHEA-induced PCOS rats had a decreased level of IFN-gamma compared with the control rats, which was restored partly in flutamide (an androgen receptor antagonist)-treated rats.	Flutamide	119-128	androgen receptor	Rattus norvegicus	133-150
30580448-8	2019	Using the ovarian granulosa cells (KGN), we demonstrated that DHEA downregulated the expression and secretion of IFN-gamma in dose- and time-dependent manners, which could be restored to some extent by treating with flutamide.	Flutamide	216-225	interferon gamma	Homo sapiens	113-122
30580448-11	2019	Taken together, these results showed that DHEA inhibited the proliferation and promoted the apoptosis of ovarian granulosa cells through downregulating the expression of IFN-gamma which could be restored by flutamide, and IFN-gamma may serve as a potential inflammatory biomarker for PCOS detection.	Flutamide	207-216	interferon gamma	Homo sapiens	170-179
30778332-7	2019	This induction was blocked with flutamide, an antagonist of AR.	Flutamide	32-41	androgen receptor	Homo sapiens	60-62
29574659-10	2019	The androgen receptor antagonist flutamide markedly suppressed the neuroprotection of finasteride in the cerebral cortex, but not in the striatum, suggesting the androgen receptor-dependent mechanism of the finasteride-induced neuroprotection in the cerebral cortex.	Flutamide	33-42	androgen receptor	Rattus norvegicus	4-21
29574659-10	2019	The androgen receptor antagonist flutamide markedly suppressed the neuroprotection of finasteride in the cerebral cortex, but not in the striatum, suggesting the androgen receptor-dependent mechanism of the finasteride-induced neuroprotection in the cerebral cortex.	Flutamide	33-42	androgen receptor	Rattus norvegicus	162-179
30671954-4	2019	Moreover, we cultured luteal cells from middle phase CL and treated them with different concentrations of DHT (10-10 -10 -6  M) and the AR antagonist flutamide (10 -5  M), to evaluate whether DHT is involved in the regulation of progesterone (P4) secretion and progesterone nuclear receptor (PGR) expression and whether these effects are regulated by the AR pathway.	Flutamide	150-159	androgen receptor	Ovis aries	136-138
31096217-6	2019	To block the action of AR, we pretreated C2C12 myotubes with flutamide.	Flutamide	61-70	androgen receptor	Mus musculus	23-25
31096217-11	2019	Of interest, we found that myostatin was clearly inhibited by EPS, and its inhibition was significantly abrogated when AR was blocked by flutamide.	Flutamide	137-146	myostatin	Mus musculus	27-36
31096217-11	2019	Of interest, we found that myostatin was clearly inhibited by EPS, and its inhibition was significantly abrogated when AR was blocked by flutamide.	Flutamide	137-146	androgen receptor	Mus musculus	119-121
31096217-13	2019	C/EBPdelta expression was decreased by EPS, and this decrease was negated by flutamide.	Flutamide	77-86	CCAAT/enhancer binding protein (C/EBP), delta	Mus musculus	0-10
31096217-14	2019	IL-6 and phospho-STAT3 (pSTAT3) expression, the downstream pathway of myostatin, were decreased by EPS and this was also reversed by flutamide.	Flutamide	133-142	interleukin 6	Mus musculus	0-4
31096217-14	2019	IL-6 and phospho-STAT3 (pSTAT3) expression, the downstream pathway of myostatin, were decreased by EPS and this was also reversed by flutamide.	Flutamide	133-142	signal transducer and activator of transcription 3	Mus musculus	17-22
31096217-14	2019	IL-6 and phospho-STAT3 (pSTAT3) expression, the downstream pathway of myostatin, were decreased by EPS and this was also reversed by flutamide.	Flutamide	133-142	myostatin	Mus musculus	70-79
30153063-2	2019	Metformin is commonly used to treat insulin resistance-glucose intolerance, and flutamide, an androgen receptor (AR) antagonist, is used to target hyperandrogenemia and dyslipidemia.	Flutamide	80-89	androgen receptor	Homo sapiens	94-111
30153063-2	2019	Metformin is commonly used to treat insulin resistance-glucose intolerance, and flutamide, an androgen receptor (AR) antagonist, is used to target hyperandrogenemia and dyslipidemia.	Flutamide	80-89	androgen receptor	Homo sapiens	113-115
30153063-6	2019	Metformin was shown to improve fasting insulin and HOMA-IR, whereas flutamide and combination treatment were shown to reduce plasma triglycerides, ApoB48, and ApoB100, and this was associated with decreased intestinal secretion of ApoB48/triglyceride.	Flutamide	68-77	apolipoprotein B	Homo sapiens	147-153
30153063-6	2019	Metformin was shown to improve fasting insulin and HOMA-IR, whereas flutamide and combination treatment were shown to reduce plasma triglycerides, ApoB48, and ApoB100, and this was associated with decreased intestinal secretion of ApoB48/triglyceride.	Flutamide	68-77	apolipoprotein B	Homo sapiens	159-166
30153063-6	2019	Metformin was shown to improve fasting insulin and HOMA-IR, whereas flutamide and combination treatment were shown to reduce plasma triglycerides, ApoB48, and ApoB100, and this was associated with decreased intestinal secretion of ApoB48/triglyceride.	Flutamide	68-77	apolipoprotein B	Homo sapiens	231-237
30153063-9	2019	Metformin-flutamide treatment upregulated hepatic and intestinal insulin signaling, including insulin receptor, MAPK1, and AKT2.	Flutamide	10-19	insulin	Homo sapiens	65-72
30153063-9	2019	Metformin-flutamide treatment upregulated hepatic and intestinal insulin signaling, including insulin receptor, MAPK1, and AKT2.	Flutamide	10-19	insulin	Homo sapiens	94-101
30153063-9	2019	Metformin-flutamide treatment upregulated hepatic and intestinal insulin signaling, including insulin receptor, MAPK1, and AKT2.	Flutamide	10-19	mitogen-activated protein kinase 1	Homo sapiens	112-117
30153063-9	2019	Metformin-flutamide treatment upregulated hepatic and intestinal insulin signaling, including insulin receptor, MAPK1, and AKT2.	Flutamide	10-19	AKT serine/threonine kinase 2	Homo sapiens	123-127
30423122-7	2019	Pretreatment with flutamide, as well as knockdown of androgen receptor, decreased testosterone-induced DR5 and CHOP expression, as well as apoptosis.	Flutamide	18-27	DNA damage inducible transcript 3	Homo sapiens	111-115
30257382-0	2018	Endoglin inhibition by sodium acetate and flutamide ameliorates cardiac defective G6PD-dependent antioxidant defense in gestational testosterone-exposed rats.	Flutamide	42-51	endoglin	Rattus norvegicus	0-8
30367827-5	2018	We found that clonazepam, flunitrazepam, flutamide, nilutamide, nimesulide, and nimetazepam were substantially reduced by recombinant AOX1 and HLC, whereas azelnidipine, nifedipine, and nimodipine were slightly reduced and metronidazole and tolcapone were not reduced.	Flutamide	41-50	aldehyde oxidase 1	Homo sapiens	134-138
30257382-0	2018	Endoglin inhibition by sodium acetate and flutamide ameliorates cardiac defective G6PD-dependent antioxidant defense in gestational testosterone-exposed rats.	Flutamide	42-51	glucose-6-phosphate dehydrogenase	Rattus norvegicus	82-86
30257382-4	2018	We also hypothesized that sodium acetate (SAc) or androgen receptor blocker, flutamide (Flu) would ameliorate these effects through endoglin inhibition.	Flutamide	77-86	endoglin	Rattus norvegicus	132-140
30257382-4	2018	We also hypothesized that sodium acetate (SAc) or androgen receptor blocker, flutamide (Flu) would ameliorate these effects through endoglin inhibition.	Flutamide	88-91	endoglin	Rattus norvegicus	132-140
30257382-10	2018	Besides, the findings also suggest that the inhibitory effect of SAc or Flu on endoglin attenuates UA production and enhances the G6PD-dependent anti-oxidant barrier, thereby implying that endoglin may be a potentially novel therapeutic intervention for cardiac dysfunction particularly in pregnancy.	Flutamide	72-75	endoglin	Rattus norvegicus	79-87
30257382-10	2018	Besides, the findings also suggest that the inhibitory effect of SAc or Flu on endoglin attenuates UA production and enhances the G6PD-dependent anti-oxidant barrier, thereby implying that endoglin may be a potentially novel therapeutic intervention for cardiac dysfunction particularly in pregnancy.	Flutamide	72-75	glucose-6-phosphate dehydrogenase	Rattus norvegicus	130-134
30257382-10	2018	Besides, the findings also suggest that the inhibitory effect of SAc or Flu on endoglin attenuates UA production and enhances the G6PD-dependent anti-oxidant barrier, thereby implying that endoglin may be a potentially novel therapeutic intervention for cardiac dysfunction particularly in pregnancy.	Flutamide	72-75	endoglin	Rattus norvegicus	189-197
29730201-7	2018	Flutamide, nilutamide and bicalutamide, which were designed to target the androgen receptor, were developed primarily for use in combination with castration to provide combined androgen blockade.	Flutamide	0-9	androgen receptor	Homo sapiens	74-91
30400755-0	2018	MicroRNA-23b and microRNA-27b plus flutamide treatment enhances apoptosis rate and decreases CCNG1 expression in a castration-resistant prostate cancer cell line.	Flutamide	35-44	cyclin G1	Homo sapiens	93-98
30400755-13	2018	We postulated that microRNAs-23b/-27b sensitize the PC-3 cell line and that after the addition of flutamide in the apoptosis assay, we would observe synergism in the treatments between miR and flutamide.	Flutamide	98-107	membrane associated ring-CH-type finger 8	Homo sapiens	185-188
30228001-2	2018	However, AR antagonists in clinical use, such as flutamide (3a) and bicalutamide (4), encounter resistance after several years of hormone therapy, predominantly due to mutations of AR.	Flutamide	49-58	androgen receptor	Homo sapiens	9-11
30228001-2	2018	However, AR antagonists in clinical use, such as flutamide (3a) and bicalutamide (4), encounter resistance after several years of hormone therapy, predominantly due to mutations of AR.	Flutamide	49-58	androgen receptor	Homo sapiens	181-183
29958919-4	2018	Based on the results from in vivo and in vitro studies in the rat, we propose that flutamide affects the expression of junction proteins and junction complex structure not only by inhibiting androgen receptor activity, but equally important by modulating protein kinase-dependent signaling in testicular cells.	Flutamide	83-92	androgen receptor	Rattus norvegicus	191-208
29940312-7	2018	For instance, a decrease in the relative frequency of closed areas (mainly composed of saccules/alveoli) < 1000 mum2 and an increase for those > 2500 mum2 were observed after flutamide administration.	Flutamide	181-190	trafficking protein particle complex 1	Mus musculus	115-119
29940312-7	2018	For instance, a decrease in the relative frequency of closed areas (mainly composed of saccules/alveoli) < 1000 mum2 and an increase for those > 2500 mum2 were observed after flutamide administration.	Flutamide	181-190	trafficking protein particle complex 1	Mus musculus	156-160
30180954-3	2018	We aimed to characterize the expression of PEDF in the male reproductive tract of Wistar rats by using RT-PCR, western blot and immunostaining and also evaluate the effect of flutamide in PEDF expression.	Flutamide	175-184	serpin family F member 1	Rattus norvegicus	188-192
30180954-5	2018	Under the effect of flutamide PEDF expression decreased, recovering by suppressing the antiandrogen.	Flutamide	20-29	serpin family F member 1	Rattus norvegicus	30-34
30057686-0	2018	Flutamide Induces Hepatic Cell Death and Mitochondrial Dysfunction via Inhibition of Nrf2-Mediated Heme Oxygenase-1.	Flutamide	0-9	NFE2 like bZIP transcription factor 2	Homo sapiens	85-89
29882189-0	2018	Flutamide-Loaded Zein Nanocapsule Hydrogel, a Promising Dermal Delivery System for Pilosebaceous Unit Disorders.	Flutamide	0-9	zein	Zea mays	17-21
29606031-10	2018	Intriguingly, the level of apoptosis marker FAS, Cytochrome C and caspase-3 increased in Flu-induced and DEHP-induced groups.	Flutamide	89-92	caspase 3	Rattus norvegicus	66-75
29606031-12	2018	Significant decrease of autophagy gene (LC3-II and p62) expression is found in Flu-induced rats testes.	Flutamide	79-82	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	51-54
29882189-3	2018	In this study, zein-based nanocapsules (ZNCs) were exploited for the first time as dermal delivery carriers for flutamide (FLT), an antiandrogen used for the management of pilosebasceous unit disorders.	Flutamide	112-121	zein	Zea mays	15-19
30057686-0	2018	Flutamide Induces Hepatic Cell Death and Mitochondrial Dysfunction via Inhibition of Nrf2-Mediated Heme Oxygenase-1.	Flutamide	0-9	heme oxygenase 1	Homo sapiens	99-115
30057686-4	2018	This study was designed to delineate the role of Nrf2/HO-1 in flutamide-induced hepatic cell injury.	Flutamide	62-71	NFE2 like bZIP transcription factor 2	Homo sapiens	49-53
30057686-4	2018	This study was designed to delineate the role of Nrf2/HO-1 in flutamide-induced hepatic cell injury.	Flutamide	62-71	heme oxygenase 1	Homo sapiens	54-58
30057686-6	2018	The protein expression of Nrf2 and HO-1 was induced by flutamide at 12.5 muM but was downregulated by higher concentrations of flutamide.	Flutamide	55-64	NFE2 like bZIP transcription factor 2	Homo sapiens	26-30
30057686-6	2018	The protein expression of Nrf2 and HO-1 was induced by flutamide at 12.5 muM but was downregulated by higher concentrations of flutamide.	Flutamide	55-64	heme oxygenase 1	Homo sapiens	35-39
30057686-6	2018	The protein expression of Nrf2 and HO-1 was induced by flutamide at 12.5 muM but was downregulated by higher concentrations of flutamide.	Flutamide	127-136	NFE2 like bZIP transcription factor 2	Homo sapiens	26-30
30057686-6	2018	The protein expression of Nrf2 and HO-1 was induced by flutamide at 12.5 muM but was downregulated by higher concentrations of flutamide.	Flutamide	127-136	heme oxygenase 1	Homo sapiens	35-39
30057686-7	2018	Silencing either Nrf2 or HO-1 was found to aggravate flutamide-induced hydrogen peroxide accumulation and mitochondrial dysfunction as well as inhibition of the Nrf2 pathway.	Flutamide	53-62	NFE2 like bZIP transcription factor 2	Homo sapiens	17-21
30057686-7	2018	Silencing either Nrf2 or HO-1 was found to aggravate flutamide-induced hydrogen peroxide accumulation and mitochondrial dysfunction as well as inhibition of the Nrf2 pathway.	Flutamide	53-62	heme oxygenase 1	Homo sapiens	25-29
30057686-8	2018	Moreover, preinduction of HO-1 by Copp significantly attenuated flutamide-induced oxidative stress and mitochondrial dysfunction, while inhibition of HO-1 by Snpp aggravated these deleterious effects.	Flutamide	64-73	heme oxygenase 1	Homo sapiens	26-30
30057686-9	2018	These findings suggest that flutamide-induced hepatic cell death and mitochondrial dysfunction is assoicated with inhibition of Nrf2-mediated HO-1.	Flutamide	28-37	NFE2 like bZIP transcription factor 2	Homo sapiens	128-132
30057686-9	2018	These findings suggest that flutamide-induced hepatic cell death and mitochondrial dysfunction is assoicated with inhibition of Nrf2-mediated HO-1.	Flutamide	28-37	heme oxygenase 1	Homo sapiens	142-146
30057686-10	2018	Pharmacologic intervention of Nrf2/HO-1 may provide a promising therapeutic approach in flutamide-induced liver injury.	Flutamide	88-97	NFE2 like bZIP transcription factor 2	Homo sapiens	30-34
30057686-10	2018	Pharmacologic intervention of Nrf2/HO-1 may provide a promising therapeutic approach in flutamide-induced liver injury.	Flutamide	88-97	heme oxygenase 1	Homo sapiens	35-39
29596656-0	2018	On the Issue of the Derivation of Permitted Daily Exposure for the Androgen Receptor Antagonist Flutamide.	Flutamide	96-105	androgen receptor	Homo sapiens	67-84
29904069-6	2018	Flutamide exposure resulted in masculinisation of the nuptial pad and elevated mRNA levels of dmrt1, cyp17, amh and foxl2 in brains (metamorphs).	Flutamide	0-9	doublesex and mab-3 related transcription factor 1	Xenopus tropicalis	94-99
29904069-6	2018	Flutamide exposure resulted in masculinisation of the nuptial pad and elevated mRNA levels of dmrt1, cyp17, amh and foxl2 in brains (metamorphs).	Flutamide	0-9	anti-Mullerian hormone	Xenopus tropicalis	108-111
29904069-6	2018	Flutamide exposure resulted in masculinisation of the nuptial pad and elevated mRNA levels of dmrt1, cyp17, amh and foxl2 in brains (metamorphs).	Flutamide	0-9	forkhead box L2	Xenopus tropicalis	116-121
28776866-5	2018	Prenatal AR inhibition using the antagonist flutamide decreased adult male alcohol consumption.	Flutamide	44-53	androgen receptor	Homo sapiens	9-11
29843816-4	2018	The response to flutamide therapy was defined as any decrease in prostate-specific antigen compared to baseline prostate-specific antigen.	Flutamide	16-25	kallikrein related peptidase 3	Homo sapiens	65-90
29843816-4	2018	The response to flutamide therapy was defined as any decrease in prostate-specific antigen compared to baseline prostate-specific antigen.	Flutamide	16-25	kallikrein related peptidase 3	Homo sapiens	112-137
29843816-5	2018	Among the abiraterone-treated patients, those for whom flutamide after bicalutamide was effective showed significantly lower prostate-specific antigen changes than those for whom it was ineffective (P = 0.0175).	Flutamide	55-64	kallikrein related peptidase 3	Homo sapiens	125-150
29843816-6	2018	Prostate-specific antigen-progression-free survival was significantly higher in the abiraterone patients when flutamide was effective than in the patients when it was ineffective (P = 0.027).	Flutamide	110-119	kallikrein related peptidase 3	Homo sapiens	0-25
28822783-9	2017	Results from multilayer experiments demonstrate that hsa-miR-132-5p suppresses the expression of CYP1A2 and that this suppression is able to decrease the extent of an adverse drug-drug interaction involving lansoprazole and flutamide.	Flutamide	224-233	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	97-103
29421708-2	2018	Among all identified hCEs, human carboxylesterase 2 (hCE2) plays crucial roles in the metabolic activation of ester drugs including irinotecan and flutamide.	Flutamide	147-156	carboxylesterase 2	Homo sapiens	33-51
29421708-2	2018	Among all identified hCEs, human carboxylesterase 2 (hCE2) plays crucial roles in the metabolic activation of ester drugs including irinotecan and flutamide.	Flutamide	147-156	carboxylesterase 2	Homo sapiens	53-57
29471436-5	2018	C57BL/6 female mice were subcutaneously implanted with LET or placebo control and subsequently treated with the nonsteroidal AR antagonist flutamide or vehicle control.	Flutamide	139-148	androgen receptor	Mus musculus	125-127
29471436-6	2018	Flutamide treatment in LET females reversed elevated T levels and restored ovarian expression of Cyp17a1 (critical for androgen synthesis) to normal levels.	Flutamide	0-9	cytochrome P450, family 17, subfamily a, polypeptide 1	Mus musculus	97-104
29471436-7	2018	Pituitary expression of Lhb was decreased in LET females that received flutamide treatment, with no changes in expression of Fshb or Gnrhr.	Flutamide	71-80	luteinizing hormone beta	Mus musculus	24-27
28942551-7	2018	Treatment with flutamide showed to partially reverse insulin resistance.	Flutamide	15-24	insulin	Homo sapiens	53-60
29354784-5	2017	Expression of all Cx isoforms examined, except Cx31, was significantly increased by the treatment of a low-dose Flu (500 mug/kg BW).	Flutamide	112-115	LOC100128922	Homo sapiens	18-20
29545336-8	2018	Treatment of male mice with the pharmacological AR antagonist flutamide reduced monocyte recruitment in mice.	Flutamide	62-71	androgen receptor	Mus musculus	48-50
29229868-5	2018	The correlation between androgen receptor (AR) expression and liver recruited inflammatory cells was investigated by treatment with the AR antagonist flutamide.	Flutamide	150-159	androgen receptor	Homo sapiens	24-41
29229868-5	2018	The correlation between androgen receptor (AR) expression and liver recruited inflammatory cells was investigated by treatment with the AR antagonist flutamide.	Flutamide	150-159	androgen receptor	Homo sapiens	43-45
29229868-5	2018	The correlation between androgen receptor (AR) expression and liver recruited inflammatory cells was investigated by treatment with the AR antagonist flutamide.	Flutamide	150-159	androgen receptor	Homo sapiens	136-138
29247133-5	2018	As determined by xCELLigence system, DHT augmented (~2 folds) the migration of MSC toward cardiac tissue slices (at 12 h), and this effect was blocked by flutamide, an androgen receptor (AR) antagonist.	Flutamide	154-163	androgen receptor	Homo sapiens	168-185
29247133-5	2018	As determined by xCELLigence system, DHT augmented (~2 folds) the migration of MSC toward cardiac tissue slices (at 12 h), and this effect was blocked by flutamide, an androgen receptor (AR) antagonist.	Flutamide	154-163	androgen receptor	Homo sapiens	187-189
29354784-0	2017	Aberrant Expression of Cx Isoforms in the Adult Caput Epididymis exposed to Estradiol Benzoate or Flutamide at the Weaning.	Flutamide	98-107	LOC100128922	Homo sapiens	23-25
29354784-2	2017	The effect of a single subcutaneous treatment of estradiol benzoate (EB) or flutamide (Flu) at the weaning age on the expression of Cx isoforms in the adult caput epididymis was evaluated in this research.	Flutamide	76-85	LOC100128922	Homo sapiens	132-134
29354784-2	2017	The effect of a single subcutaneous treatment of estradiol benzoate (EB) or flutamide (Flu) at the weaning age on the expression of Cx isoforms in the adult caput epididymis was evaluated in this research.	Flutamide	87-90	LOC100128922	Homo sapiens	132-134
29354784-5	2017	Expression of all Cx isoforms examined, except Cx31, was significantly increased by the treatment of a low-dose Flu (500 mug/kg BW).	Flutamide	112-115	gap junction protein beta 3	Homo sapiens	47-51
29354784-6	2017	However, the treatment of a high-dose Flu (5 mg/kg BW) led significant expressional suppression of Cx30.3, Cx31, Cx31.1, Cx32, Cx40, Cx43, and Cx45 but an increase of Cx37 transcript level.	Flutamide	38-41	gap junction protein beta 4	Homo sapiens	99-105
29354784-6	2017	However, the treatment of a high-dose Flu (5 mg/kg BW) led significant expressional suppression of Cx30.3, Cx31, Cx31.1, Cx32, Cx40, Cx43, and Cx45 but an increase of Cx37 transcript level.	Flutamide	38-41	gap junction protein beta 3	Homo sapiens	107-111
28901488-4	2017	All cells were divided into four groups, as follows: Control group, testosterone group, androgen receptor antagonist-flutamide group and flutamide + testosterone group.	Flutamide	117-126	androgen receptor	Mus musculus	88-105
29354784-6	2017	However, the treatment of a high-dose Flu (5 mg/kg BW) led significant expressional suppression of Cx30.3, Cx31, Cx31.1, Cx32, Cx40, Cx43, and Cx45 but an increase of Cx37 transcript level.	Flutamide	38-41	gap junction protein beta 5	Homo sapiens	113-119
29354784-6	2017	However, the treatment of a high-dose Flu (5 mg/kg BW) led significant expressional suppression of Cx30.3, Cx31, Cx31.1, Cx32, Cx40, Cx43, and Cx45 but an increase of Cx37 transcript level.	Flutamide	38-41	gap junction protein beta 1	Homo sapiens	121-125
29354784-6	2017	However, the treatment of a high-dose Flu (5 mg/kg BW) led significant expressional suppression of Cx30.3, Cx31, Cx31.1, Cx32, Cx40, Cx43, and Cx45 but an increase of Cx37 transcript level.	Flutamide	38-41	gap junction protein alpha 5	Homo sapiens	127-131
29354784-6	2017	However, the treatment of a high-dose Flu (5 mg/kg BW) led significant expressional suppression of Cx30.3, Cx31, Cx31.1, Cx32, Cx40, Cx43, and Cx45 but an increase of Cx37 transcript level.	Flutamide	38-41	gap junction protein alpha 1	Homo sapiens	133-137
29354784-6	2017	However, the treatment of a high-dose Flu (5 mg/kg BW) led significant expressional suppression of Cx30.3, Cx31, Cx31.1, Cx32, Cx40, Cx43, and Cx45 but an increase of Cx37 transcript level.	Flutamide	38-41	gap junction protein gamma 1	Homo sapiens	143-147
29354784-6	2017	However, the treatment of a high-dose Flu (5 mg/kg BW) led significant expressional suppression of Cx30.3, Cx31, Cx31.1, Cx32, Cx40, Cx43, and Cx45 but an increase of Cx37 transcript level.	Flutamide	38-41	gap junction protein alpha 4	Homo sapiens	167-171
29354784-7	2017	With the comparison of previous findings, the expression of Cx isoforms in the adult epididymis after the exposure to EB or Flu is likely differentially regulated in regional-specific and/or exposed postnatal age-specific manner.	Flutamide	124-127	LOC100128922	Homo sapiens	60-62
27055586-0	2017	The effects of pH, temperature and protein concentration on the in vitro binding of flutamide to human serum albumin.	Flutamide	84-93	albumin	Homo sapiens	103-116
28901488-13	2017	In TICs, testosterone and flutamide inhibited the mRNA expression levels of FOXO1 and glucose-6-phosphatase enzyme, and promoted the expression of PCK1.	Flutamide	26-35	forkhead box O1	Mus musculus	76-81
28901488-13	2017	In TICs, testosterone and flutamide inhibited the mRNA expression levels of FOXO1 and glucose-6-phosphatase enzyme, and promoted the expression of PCK1.	Flutamide	26-35	glucose-6-phosphatase, catalytic	Mus musculus	86-107
28901488-5	2017	Flutamide was used in the present study as it blocks the effects of the androgen receptor.	Flutamide	0-9	androgen receptor	Mus musculus	72-89
28901488-13	2017	In TICs, testosterone and flutamide inhibited the mRNA expression levels of FOXO1 and glucose-6-phosphatase enzyme, and promoted the expression of PCK1.	Flutamide	26-35	phosphoenolpyruvate carboxykinase 1, cytosolic	Mus musculus	147-151
28891417-11	2017	Although flutamide treatment alone did not affect PR expression, flutamide diminished androgen-induced upregulation of PR in both endometrial explants and Ishikawa cells.	Flutamide	65-74	progesterone receptor	Homo sapiens	119-121
28666357-0	2017	Permitted Daily Exposure of the Androgen Receptor Antagonist Flutamide.	Flutamide	61-70	androgen receptor	Homo sapiens	32-49
28666357-1	2017	This report aims to determine the permitted daily exposure (PDE) of flutamide, an androgen receptor blocker, as directed by guideline EMA/CHMP/CVPM/SWP/169430/2012 that came into effect on June 2015.	Flutamide	68-77	androgen receptor	Homo sapiens	82-99
28530711-5	2017	The combination of these drugs modulates the stability of the androgen receptor (AR) and resensitizes AR-mutant prostate cancer cells to flutamide.	Flutamide	137-146	androgen receptor	Homo sapiens	102-104
28832499-1	2017	Hydroxyflutamide (HF), an active metabolite of the first generation antiandrogen flutamide, was used in clinic to treat prostate cancer targeting androgen receptor (AR).	Flutamide	7-16	androgen receptor	Homo sapiens	146-163
28832499-1	2017	Hydroxyflutamide (HF), an active metabolite of the first generation antiandrogen flutamide, was used in clinic to treat prostate cancer targeting androgen receptor (AR).	Flutamide	7-16	androgen receptor	Homo sapiens	165-167
29163791-4	2017	Trophoblastic cell invasion was assessed using transwell assays; BeWo cells were treated with testosterone and an androgen receptor (AR) inhibitor (flutamide) to elucidate the invasion mechanism.	Flutamide	148-157	androgen receptor	Homo sapiens	133-135
28176351-9	2017	The increase in Cx43 expression induced by Cd was presumably mediated by the androgen receptor, because it was abolished upon treatment with the androgen receptor antagonist, flutamide.	Flutamide	175-184	gap junction protein alpha 1	Homo sapiens	16-20
28176351-9	2017	The increase in Cx43 expression induced by Cd was presumably mediated by the androgen receptor, because it was abolished upon treatment with the androgen receptor antagonist, flutamide.	Flutamide	175-184	androgen receptor	Homo sapiens	77-94
28176351-9	2017	The increase in Cx43 expression induced by Cd was presumably mediated by the androgen receptor, because it was abolished upon treatment with the androgen receptor antagonist, flutamide.	Flutamide	175-184	androgen receptor	Homo sapiens	145-162
28459113-4	2017	There is also evidence that some AhR-active pharmaceuticals, including tranilast, flutamide, hydroxytamoxifen and omeprazole or their derivatives, may be effective AhR-dependent anticancer agents for single or combination cancer chemotherapies for treatment of breast and pancreatic cancers.	Flutamide	82-91	aryl hydrocarbon receptor	Homo sapiens	33-36
28697876-2	2017	Flutamide is a potent selective non-steroidal androgen receptor competitive antagonist that has been used in human beings as an anti-androgenic drug.	Flutamide	0-9	androgen receptor	Homo sapiens	46-63
28213303-5	2017	The different regulation of vtg1 expression in the liver in response to DES and FLU further confirmed the different modes of action of these drugs.	Flutamide	80-83	vitellogenin 1	Danio rerio	28-32
27967242-11	2017	The DHT-induced hepatocyte insulin resistance was reversed by the androgen-receptor antagonist, flutamide.	Flutamide	96-105	insulin	Homo sapiens	27-34
28405241-7	2017	The results showed that only this macrocyclic derivative exerts changes on perfusion pressure and vascular resistance translated as the positive inotropic effect, and this effect was blocked with flutamide; these data indicate that the positive inotropic activity induced by this macrocyclic derivative was via androgen receptor activation.	Flutamide	196-205	androgen receptor	Rattus norvegicus	311-328
28459113-4	2017	There is also evidence that some AhR-active pharmaceuticals, including tranilast, flutamide, hydroxytamoxifen and omeprazole or their derivatives, may be effective AhR-dependent anticancer agents for single or combination cancer chemotherapies for treatment of breast and pancreatic cancers.	Flutamide	82-91	aryl hydrocarbon receptor	Homo sapiens	164-167
28274354-6	2017	Androgen receptor blockers include spironolactone, cyproterone acetate, chlormadinone, and flutamide; adrenal androgen production blockers include glucocorticoids; and ovarian production blockers include gonadotropin-releasing agonists and oral contraceptives.	Flutamide	91-100	androgen receptor	Homo sapiens	0-17
28854419-9	2017	Blocking of AR by flutamide eliminated the stimulation effect of testosterone on kinase phosphorylation.	Flutamide	18-27	androgen receptor	Mus musculus	12-14
27765882-7	2016	In females, increasing androgen levels decreased AT2R mRNA and protein expression and this was attenuated by androgen receptor blocker flutamide.	Flutamide	135-144	angiotensin II receptor, type 2	Rattus norvegicus	49-53
28994098-8	2017	RESULTS: Flutamide treatment caused changes in both HIF-1a and VEGFA mRNA levels only in the placentas of the 90 dpc group.	Flutamide	9-18	hypoxia inducible factor 1 subunit alpha	Sus scrofa	52-58
28994098-8	2017	RESULTS: Flutamide treatment caused changes in both HIF-1a and VEGFA mRNA levels only in the placentas of the 90 dpc group.	Flutamide	9-18	vascular endothelial growth factor A	Sus scrofa	63-68
28994098-9	2017	Relative optical density analysis showed decreased HIF-1a and increased VEGFA protein expression in the placentas obtained from flutamide-treated 108 dpc group while no differences were observed in the 90 dpc group.	Flutamide	128-137	hypoxia inducible factor 1 subunit alpha	Sus scrofa	51-57
28994098-9	2017	Relative optical density analysis showed decreased HIF-1a and increased VEGFA protein expression in the placentas obtained from flutamide-treated 108 dpc group while no differences were observed in the 90 dpc group.	Flutamide	128-137	vascular endothelial growth factor A	Sus scrofa	72-77
27461546-3	2017	METHODS: A pharmacological approach was used to assess the ability of the androgen receptor antagonist flutamide, the estrogen receptor antagonist ICI 182 780 and the 5-alpha reductase inhibitor dutasteride to block the protective effect of testosterone, evaluated through the behavioral response induced by a TMJ injection of 0.5% formalin.	Flutamide	103-112	androgen receptor	Rattus norvegicus	74-91
28144639-6	2016	Expression of all Cx isoforms, except Cx45, was significantly increased by a low-dose Flu treatment.	Flutamide	86-89	gap junction protein, gamma 1	Rattus norvegicus	38-42
27866534-4	2016	The effect was partly reversed by the androgen receptor (AR) blocker flutamide (87.6%, P=0.004).	Flutamide	69-78	androgen receptor	Mus musculus	38-55
27866534-4	2016	The effect was partly reversed by the androgen receptor (AR) blocker flutamide (87.6%, P=0.004).	Flutamide	69-78	androgen receptor	Mus musculus	57-59
27511110-0	2016	Risk of false positive results to SARM S-4 in case of therapeutic use of antineoplastic/antiandrogen drug containing flutamide: a case study.	Flutamide	117-126	sterile alpha and TIR motif containing 1	Homo sapiens	34-38
27130232-9	2016	The decrease in tPA was blocked by the addition of flutamide (101.3% +- 16% of control), a classic nonsteroidal androgen receptor blocker.	Flutamide	51-60	chromosome 20 open reading frame 181	Homo sapiens	16-19
27130232-9	2016	The decrease in tPA was blocked by the addition of flutamide (101.3% +- 16% of control), a classic nonsteroidal androgen receptor blocker.	Flutamide	51-60	androgen receptor	Homo sapiens	112-129
28195074-12	2016	Likewise, the mRNA and protein levels of Lamp1 were elevated in both flutamide-treated groups.	Flutamide	69-78	lysosomal associated membrane protein 1	Sus scrofa	41-46
28195074-15	2016	Beclin 1/Bcl-2 complexes were less abundant following flutamide treatment in both flutamide-exposed groups.	Flutamide	54-63	beclin 1	Sus scrofa	0-8
28195074-15	2016	Beclin 1/Bcl-2 complexes were less abundant following flutamide treatment in both flutamide-exposed groups.	Flutamide	54-63	apoptosis regulator Bcl-2	Sus scrofa	9-14
28195074-15	2016	Beclin 1/Bcl-2 complexes were less abundant following flutamide treatment in both flutamide-exposed groups.	Flutamide	82-91	beclin 1	Sus scrofa	0-8
28195074-15	2016	Beclin 1/Bcl-2 complexes were less abundant following flutamide treatment in both flutamide-exposed groups.	Flutamide	82-91	apoptosis regulator Bcl-2	Sus scrofa	9-14
27569425-0	2016	The antiandrogen flutamide is a novel aryl hydrocarbon receptor ligand that disrupts bile acid homeostasis in mice through induction of Abcc4.	Flutamide	17-26	aryl-hydrocarbon receptor	Mus musculus	38-63
27569425-0	2016	The antiandrogen flutamide is a novel aryl hydrocarbon receptor ligand that disrupts bile acid homeostasis in mice through induction of Abcc4.	Flutamide	17-26	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	136-141
27569425-4	2016	Expression of the AhR gene battery was markedly increased in livers of wild-type mice Ahr+/+ treated with FLU, while no change was noted in Ahr-/- mice.	Flutamide	106-109	aryl-hydrocarbon receptor	Mus musculus	18-21
27569425-4	2016	Expression of the AhR gene battery was markedly increased in livers of wild-type mice Ahr+/+ treated with FLU, while no change was noted in Ahr-/- mice.	Flutamide	106-109	aryl-hydrocarbon receptor	Mus musculus	86-89
27569425-5	2016	Messenger RNAs encoded by AhR target genes were induced in primary mouse hepatocytes cultured with FLU, which confirmed the in vivo results.	Flutamide	99-102	aryl-hydrocarbon receptor	Mus musculus	26-29
27569425-6	2016	Ligand-docking analysis further predicted that FLU is an AhR agonist ligand which was confirmed by luciferase reporter gene assays.	Flutamide	47-50	aryl-hydrocarbon receptor	Mus musculus	57-60
27569425-7	2016	Multivariate data analysis showed that bile acids were responsible for the separation of vehicle- and FLU-treated Ahr+/+ mice, while there was no separation in Ahr-/- mice.	Flutamide	102-105	aryl-hydrocarbon receptor	Mus musculus	114-117
27569425-9	2016	These findings provide new insights into the mechanism of liver injury caused by FLU treatment involving activation of AhR and the alterations of bile acid homeostasis, which could guide clinical application.	Flutamide	81-84	aryl-hydrocarbon receptor	Mus musculus	119-122
27667110-2	2016	Methods: We established the cryptorchidism model by flutamide and took normal testis as normal group.The testicular tissue samples were collected on 15 days, 45 days, and 90 days after birth respectively.The expression of ALDH1A1 in rat cryptorchidism and normal testis were investigated by real-time PCR, Western blot and immunohistochemisty intissue microarray.	Flutamide	52-61	aldehyde dehydrogenase 1 family, member A1	Rattus norvegicus	222-229
27676332-5	2016	However, testosterone was down-regulated with a significant decrease of Cx43 in flutamide group.	Flutamide	80-89	gap junction protein, alpha 1	Rattus norvegicus	72-76
27543746-7	2016	Administration of the anti-androgen drug, Flutamide, during prenatal T treatment, prevented the reduction in IRbeta colocalization in AgRP, but not in KNDy neurons, suggesting that these effects are programmed by androgenic and oestrogenic actions, respectively.	Flutamide	42-51	agouti related neuropeptide	Homo sapiens	134-138
27413113-1	2016	The androgen receptor antagonist, flutamide, is strongly associated with idiosyncratic drug-induced liver injury (DILI).	Flutamide	34-43	androgen receptor	Homo sapiens	4-21
27320211-10	2016	Finally, we showed that flutamide, a specific AR antagonist, prevents complete Freund"s adjuvant (CFA)-induced upregulation of MOR mRNA in TG, and that flutamide dose-dependently blocks the efficacy of DAMGO, a specific MOR agonist, on CFA-induced mechanical hypersensitivity.	Flutamide	24-33	androgen receptor	Rattus norvegicus	46-48
27320211-10	2016	Finally, we showed that flutamide, a specific AR antagonist, prevents complete Freund"s adjuvant (CFA)-induced upregulation of MOR mRNA in TG, and that flutamide dose-dependently blocks the efficacy of DAMGO, a specific MOR agonist, on CFA-induced mechanical hypersensitivity.	Flutamide	24-33	opioid receptor mu 1	Homo sapiens	127-130
27320211-10	2016	Finally, we showed that flutamide, a specific AR antagonist, prevents complete Freund"s adjuvant (CFA)-induced upregulation of MOR mRNA in TG, and that flutamide dose-dependently blocks the efficacy of DAMGO, a specific MOR agonist, on CFA-induced mechanical hypersensitivity.	Flutamide	24-33	opioid receptor mu 1	Homo sapiens	220-223
27320211-10	2016	Finally, we showed that flutamide, a specific AR antagonist, prevents complete Freund"s adjuvant (CFA)-induced upregulation of MOR mRNA in TG, and that flutamide dose-dependently blocks the efficacy of DAMGO, a specific MOR agonist, on CFA-induced mechanical hypersensitivity.	Flutamide	152-161	androgen receptor	Rattus norvegicus	46-48
27320211-10	2016	Finally, we showed that flutamide, a specific AR antagonist, prevents complete Freund"s adjuvant (CFA)-induced upregulation of MOR mRNA in TG, and that flutamide dose-dependently blocks the efficacy of DAMGO, a specific MOR agonist, on CFA-induced mechanical hypersensitivity.	Flutamide	152-161	opioid receptor mu 1	Homo sapiens	127-130
27320211-10	2016	Finally, we showed that flutamide, a specific AR antagonist, prevents complete Freund"s adjuvant (CFA)-induced upregulation of MOR mRNA in TG, and that flutamide dose-dependently blocks the efficacy of DAMGO, a specific MOR agonist, on CFA-induced mechanical hypersensitivity.	Flutamide	152-161	opioid receptor mu 1	Homo sapiens	220-223
27553527-4	2016	Abrogation of androgen receptor (AR) activity by co-treatment with flutamide abolished testosterone-induced SMP30 expression in the kidney as well as in the NRK52E cells.	Flutamide	67-76	androgen receptor	Rattus norvegicus	14-31
27796005-8	2016	A low-dose flutamide induced increases of Cx31, Cx31.1, Cx32, and Cx43 expression but a decrease of Cx37 expression.	Flutamide	11-20	gap junction protein, beta 3	Rattus norvegicus	42-46
27796005-8	2016	A low-dose flutamide induced increases of Cx31, Cx31.1, Cx32, and Cx43 expression but a decrease of Cx37 expression.	Flutamide	11-20	gap junction protein, beta 5	Rattus norvegicus	48-54
27796005-8	2016	A low-dose flutamide induced increases of Cx31, Cx31.1, Cx32, and Cx43 expression but a decrease of Cx37 expression.	Flutamide	11-20	gap junction protein, beta 1	Rattus norvegicus	56-60
27796005-8	2016	A low-dose flutamide induced increases of Cx31, Cx31.1, Cx32, and Cx43 expression but a decrease of Cx37 expression.	Flutamide	11-20	gap junction protein, alpha 1	Rattus norvegicus	66-70
27796005-8	2016	A low-dose flutamide induced increases of Cx31, Cx31.1, Cx32, and Cx43 expression but a decrease of Cx37 expression.	Flutamide	11-20	gap junction protein, alpha 4	Rattus norvegicus	100-104
27553527-4	2016	Abrogation of androgen receptor (AR) activity by co-treatment with flutamide abolished testosterone-induced SMP30 expression in the kidney as well as in the NRK52E cells.	Flutamide	67-76	androgen receptor	Rattus norvegicus	33-35
27553527-4	2016	Abrogation of androgen receptor (AR) activity by co-treatment with flutamide abolished testosterone-induced SMP30 expression in the kidney as well as in the NRK52E cells.	Flutamide	67-76	regucalcin	Rattus norvegicus	108-113
27413634-11	2016	Co-treatment with flutamide or finasteride resulted in the levels of alpha, beta and gamma-ENaC proteins and mRNAs in kidneys to decrease.	Flutamide	18-27	sodium channel epithelial 1 subunit gamma	Rattus norvegicus	85-95
26566264-7	2016	E2 and T significantly reduced secretion of BDNF; effects prevented by estrogen and androgen receptor inhibitor, ICI 182,780 (1 muM), and flutamide (10 muM), respectively.	Flutamide	138-147	brain derived neurotrophic factor	Homo sapiens	44-48
26566264-7	2016	E2 and T significantly reduced secretion of BDNF; effects prevented by estrogen and androgen receptor inhibitor, ICI 182,780 (1 muM), and flutamide (10 muM), respectively.	Flutamide	138-147	latexin	Homo sapiens	152-155
27283984-4	2016	Here, we found that treatment of mice bearing LNCaP-derived xenograft tumors with cytotoxic (docetaxel) and anti-androgen (flutamide) compounds enriched for cells that express TROP2, a putative TIC marker.	Flutamide	123-132	tropomyosin 2, beta	Mus musculus	176-181
27283984-6	2016	TROP2 down-regulation in these cells reduced their ability to recur after treatment with docetaxel, in the presence or absence of flutamide.	Flutamide	130-139	tumor associated calcium signal transducer 2	Homo sapiens	0-5
27113045-9	2016	Furthermore, the increase in medullary angiotensin type 1 receptor mRNA expression was abolished in flutamide-treated growth-restricted relative to untreated counterparts and controls; cortical angiotensin-converting enzyme mRNA expression was reduced in flutamide-treated growth-restricted versus untreated counterparts.	Flutamide	255-264	angiotensin I converting enzyme	Rattus norvegicus	194-223
26538344-10	2016	Importantly, flutamide alone reduced IGF-IR mRNA in both cell types across time points, with an observed reduction in activity of ERK and Akt, suggesting that IGF-IR was transcriptionally regulated by AR.	Flutamide	13-22	thymoma viral proto-oncogene 1	Mus musculus	138-141
27178578-1	2016	Our previous study in male rats demonstrated that bilateral administration of flutamide, an androgen receptor (AR) antagonist, into the posterodorsal medial amygdala (MePD) increased the time sniffing male odors to as high as that sniffing estrous odors, eliminating the preference for estrous odors over male odors.	Flutamide	78-87	androgen receptor	Rattus norvegicus	92-109
27178578-1	2016	Our previous study in male rats demonstrated that bilateral administration of flutamide, an androgen receptor (AR) antagonist, into the posterodorsal medial amygdala (MePD) increased the time sniffing male odors to as high as that sniffing estrous odors, eliminating the preference for estrous odors over male odors.	Flutamide	78-87	androgen receptor	Rattus norvegicus	111-113
26817611-10	2016	Cytokine arrays of aortic tissue revealed decreased levels of proinflammatory cytokines interleukin (IL)-alpha, IL-6, and IL-17 in flutamide-treated and AR(-/-) groups compared with controls.	Flutamide	131-140	interleukin 6	Mus musculus	112-116
26817611-10	2016	Cytokine arrays of aortic tissue revealed decreased levels of proinflammatory cytokines interleukin (IL)-alpha, IL-6, and IL-17 in flutamide-treated and AR(-/-) groups compared with controls.	Flutamide	131-140	interleukin 17A	Mus musculus	122-127
27053365-4	2016	Insulin-stimulated phospho (p)-AKT was evaluated in control and prenatal T-, prenatal T plus postnatal flutamide-, and prenatal T plus postnatal rosiglitazone-treated females at 3 yr of age.	Flutamide	103-112	LOC105613195	Ovis aries	0-7
27239218-5	2016	RESULTS: Here we demonstrated the ability of the anti-androgen molecule, flutamide, to counteract the stimulatory effects of DHEA on RACK1 and GRbeta expression, and cytokine production.	Flutamide	73-82	receptor for activated C kinase 1	Homo sapiens	133-138
27239218-6	2016	In both THP-1 cells and human peripheral blood mononuclear cells (PBMC), flutamide blocked the effects of DHEA, suggesting a role of the AR in these effects.	Flutamide	73-82	androgen receptor	Homo sapiens	137-139
27123292-5	2016	Following the introduction of alternative anti-androgen therapy with flutamide, PSA decline was observed in 185 patients (68.0%), including 103 (37.9%) who achieved a PSA reduction of >50%; however, the PSA level continued to elevate in the remaining 87 (32.0%).	Flutamide	69-78	kallikrein related peptidase 3	Homo sapiens	80-83
27072650-12	2016	Administration of flutamide during days 12-15 of pregnancy resulted in non-significant increase in igfbp5 expression, however, combination of flutamide+AI treatments caused increased protein expression.	Flutamide	18-27	insulin-like growth factor binding protein 5	Rattus norvegicus	99-105
26965862-1	2016	The clinically used androgen receptor (AR) antagonists (bicalutamide, flutamide and nilutamide) bind with low affinity to AR and can induce escape mechanisms.	Flutamide	70-79	androgen receptor	Homo sapiens	20-37
26965862-1	2016	The clinically used androgen receptor (AR) antagonists (bicalutamide, flutamide and nilutamide) bind with low affinity to AR and can induce escape mechanisms.	Flutamide	70-79	androgen receptor	Homo sapiens	39-41
26965862-1	2016	The clinically used androgen receptor (AR) antagonists (bicalutamide, flutamide and nilutamide) bind with low affinity to AR and can induce escape mechanisms.	Flutamide	70-79	androgen receptor	Homo sapiens	122-124
27036707-0	2016	Flutamide induces alterations in the cell-cell junction ultrastructure and reduces the expression of Cx43 at the blood-testis barrier with no disturbance in the rat seminiferous tubule morphology.	Flutamide	0-9	gap junction protein, alpha 1	Rattus norvegicus	101-105
27482363-0	2016	Androgen receptor blockade using flutamide skewed sex ratio of litters in mice.	Flutamide	33-42	androgen receptor	Mus musculus	0-17
27482363-2	2016	The present study was conducted to elucidate the role of androgen receptor in this regard by blockade of androgen receptor using flutamide in female mice.	Flutamide	129-138	androgen receptor	Mus musculus	57-74
27482363-2	2016	The present study was conducted to elucidate the role of androgen receptor in this regard by blockade of androgen receptor using flutamide in female mice.	Flutamide	129-138	androgen receptor	Mus musculus	105-122
27482363-10	2016	In addition, the blockade of androgen receptor using flutamide appeared to enhance litter size.	Flutamide	53-62	androgen receptor	Mus musculus	29-46
27036707-12	2016	On the other hand, Cx43 expression in the interstitial tissue of flutamide-treated rats increased (p < 0.01), which could be associated with Leydig cell hypertrophy.	Flutamide	65-74	gap junction protein, alpha 1	Rattus norvegicus	19-23
27036707-14	2016	CONCLUSIONS: Short-term treatment with flutamide applied to adult rats exerts its primary effect on the basal ES, coexisting junctional complexes and their constituent proteins Cx43 and ZO-1, without any apparent morphological alterations in the seminiferous epithelium.	Flutamide	39-48	gap junction protein, alpha 1	Rattus norvegicus	177-181
27023109-0	2016	Knocking Down TMPRSS2-ERG Fusion Oncogene by siRNA Could be an Alternative Treatment to Flutamide.	Flutamide	88-97	transmembrane serine protease 2	Homo sapiens	14-21
27023109-0	2016	Knocking Down TMPRSS2-ERG Fusion Oncogene by siRNA Could be an Alternative Treatment to Flutamide.	Flutamide	88-97	ETS transcription factor ERG	Homo sapiens	22-25
27023109-4	2016	Therefore, concomitant or subsequent association of FLU to siRNA TMPRSS2-ERG was performed in VCaP cells and in SCID mice bearing xenografted VCaP tumors.	Flutamide	52-55	transmembrane serine protease 2	Homo sapiens	65-72
27023109-4	2016	Therefore, concomitant or subsequent association of FLU to siRNA TMPRSS2-ERG was performed in VCaP cells and in SCID mice bearing xenografted VCaP tumors.	Flutamide	52-55	ETS transcription factor ERG	Homo sapiens	73-76
27023109-7	2016	The association of siRNA TMPRSS2-ERG-squalene nanoparticles with flutamide displayed similar tumor growth inhibition as mice treated with siRNA TMPRSS2-ERG-squalene nanoparticles alone and was paralleled with modification of expression of ERG, androgen receptor, and cleaved-caspase-3.	Flutamide	65-74	transmembrane protease, serine 2	Mus musculus	25-32
27023109-7	2016	The association of siRNA TMPRSS2-ERG-squalene nanoparticles with flutamide displayed similar tumor growth inhibition as mice treated with siRNA TMPRSS2-ERG-squalene nanoparticles alone and was paralleled with modification of expression of ERG, androgen receptor, and cleaved-caspase-3.	Flutamide	65-74	ETS transcription factor	Mus musculus	33-36
27023109-7	2016	The association of siRNA TMPRSS2-ERG-squalene nanoparticles with flutamide displayed similar tumor growth inhibition as mice treated with siRNA TMPRSS2-ERG-squalene nanoparticles alone and was paralleled with modification of expression of ERG, androgen receptor, and cleaved-caspase-3.	Flutamide	65-74	androgen receptor	Mus musculus	244-261
26437446-1	2016	We investigated the effects of 2-hydroxyflutamide (HF), an active metabolite of the anti-androgen flutamide, on the activation of the phosphoinositide-3 kinase/protein kinase B (PI3K/Akt) in rat Sertoli cells.	Flutamide	40-49	AKT serine/threonine kinase 1	Rattus norvegicus	183-186
26437446-10	2016	Moreover, using testes of flutamide-treated rats for 7 days, we demonstrated that the anti-androgen can modulate the protein kinase-dependent pathways in long term by enhancing Akt and ERK1/2 protein expression (p<0.05).	Flutamide	26-35	AKT serine/threonine kinase 1	Rattus norvegicus	177-180
26437446-10	2016	Moreover, using testes of flutamide-treated rats for 7 days, we demonstrated that the anti-androgen can modulate the protein kinase-dependent pathways in long term by enhancing Akt and ERK1/2 protein expression (p<0.05).	Flutamide	26-35	mitogen activated protein kinase 3	Rattus norvegicus	185-191
26650569-4	2016	This study tested whether 1) in utero cotreatment of prenatally T-treated sheep with androgen antagonist (flutamide) or insulin sensitizer (rosiglitazone) prevents juvenile insulin resistance and adult changes in adipocyte size; and 2) visceral adiposity and insulin sensitivity are both unaltered during early adulthood, confirming the predicted developmental trajectory in this animal model.	Flutamide	106-115	LOC105613195	Ovis aries	173-180
26495828-5	2016	The TR and AR antagonistic potencies in the Yangtze River watershed were highlighted, with equivalents greater than the lowest observable effect concentration (LOEC) of dibutyl phthalate and flutamide, respectively.	Flutamide	191-200	androgen receptor	Homo sapiens	11-13
26650569-4	2016	This study tested whether 1) in utero cotreatment of prenatally T-treated sheep with androgen antagonist (flutamide) or insulin sensitizer (rosiglitazone) prevents juvenile insulin resistance and adult changes in adipocyte size; and 2) visceral adiposity and insulin sensitivity are both unaltered during early adulthood, confirming the predicted developmental trajectory in this animal model.	Flutamide	106-115	LOC105613195	Ovis aries	173-180
26817618-8	2016	Addition of flutamide significantly reduced secretion of IGFBP1 and prolactin and altered the expression of endometrial receptivity markers.	Flutamide	12-21	insulin like growth factor binding protein 1	Homo sapiens	57-63
26661749-0	2016	Effect of Prenatal and Neonatal Anti-Androgen Flutamide Treatment on Aquaporin 5 Expression in the Adult Porcine Ovary.	Flutamide	46-55	aquaporin 5	Sus scrofa	69-80
26661749-4	2016	Therefore, this study was performed to determine whether gestational or neonatal exposure to the anti-androgen flutamide influences androgen-dependent AQP5 expression in pre-antral and large antral follicles of adult pigs.	Flutamide	111-120	aquaporin 5	Sus scrofa	151-155
26661749-7	2016	In pre-antral follicles, AQP5 mRNA and protein levels were both downregulated following maternal (p < 0.01 and p < 0.01, respectively) and neonatal (p < 0.01 and p < 0.01, respectively) flutamide exposure.	Flutamide	198-207	aquaporin 5	Sus scrofa	25-29
26661749-9	2016	Immunohistochemistry showed decreased intensity of AQP5 immunoreaction in pre-antral (p < 0.01) and large antral (p < 0.001) follicles following flutamide treatment.	Flutamide	151-160	aquaporin 5	Sus scrofa	51-55
26661749-10	2016	Moreover, radioimmunological analysis revealed that changes observed in AQP5 expression corresponded with diminished follicular androgens production after both maternal (p < 0.05 and p < 0.05, respectively) and neonatal (p < 0.05 and p < 0.01, respectively) flutamide administration.	Flutamide	270-279	aquaporin 5	Sus scrofa	72-76
26817618-8	2016	Addition of flutamide significantly reduced secretion of IGFBP1 and prolactin and altered the expression of endometrial receptivity markers.	Flutamide	12-21	prolactin	Homo sapiens	68-77
26759714-8	2016	RESULTS: Treatment of neonates with flutamide on postnatal days 0 and 1 attenuated the spinal GRP system during adulthood.	Flutamide	36-45	gastrin releasing peptide	Rattus norvegicus	94-97
27493956-1	2016	We determined whether prostate specific antigen (PSA) would decrease with immediate antiandrogen switching from bicalutamide (BCL) to flutamide (FLT) in patients receiving combined androgen blockade for advanced prostate cancer.	Flutamide	134-143	kallikrein related peptidase 3	Homo sapiens	22-47
26722046-8	2016	In addition, MCS-C3-mediated apoptotic induction, and up-regulation of p21(CIP1) were almost completely blocked by the treatment of androgen-responsive LNCaP cells with flutamide, an androgen receptor (AR) antagonist.	Flutamide	169-178	cyclin dependent kinase inhibitor 1A	Homo sapiens	71-74
26722046-8	2016	In addition, MCS-C3-mediated apoptotic induction, and up-regulation of p21(CIP1) were almost completely blocked by the treatment of androgen-responsive LNCaP cells with flutamide, an androgen receptor (AR) antagonist.	Flutamide	169-178	cyclin dependent kinase inhibitor 1A	Homo sapiens	75-79
26722046-8	2016	In addition, MCS-C3-mediated apoptotic induction, and up-regulation of p21(CIP1) were almost completely blocked by the treatment of androgen-responsive LNCaP cells with flutamide, an androgen receptor (AR) antagonist.	Flutamide	169-178	androgen receptor	Homo sapiens	202-204
27493956-1	2016	We determined whether prostate specific antigen (PSA) would decrease with immediate antiandrogen switching from bicalutamide (BCL) to flutamide (FLT) in patients receiving combined androgen blockade for advanced prostate cancer.	Flutamide	134-143	kallikrein related peptidase 3	Homo sapiens	49-52
27493956-1	2016	We determined whether prostate specific antigen (PSA) would decrease with immediate antiandrogen switching from bicalutamide (BCL) to flutamide (FLT) in patients receiving combined androgen blockade for advanced prostate cancer.	Flutamide	145-148	kallikrein related peptidase 3	Homo sapiens	22-47
27493956-1	2016	We determined whether prostate specific antigen (PSA) would decrease with immediate antiandrogen switching from bicalutamide (BCL) to flutamide (FLT) in patients receiving combined androgen blockade for advanced prostate cancer.	Flutamide	145-148	kallikrein related peptidase 3	Homo sapiens	49-52
26154267-9	2016	CONCLUSION: It was concluded Flutamide-loaded SLN formulation can be used as a promising colloidal drug carriers for topical administration of Flutamide in the treatment of androgenic alopecia.	Flutamide	29-38	sarcolipin	Rattus norvegicus	46-49
26154267-9	2016	CONCLUSION: It was concluded Flutamide-loaded SLN formulation can be used as a promising colloidal drug carriers for topical administration of Flutamide in the treatment of androgenic alopecia.	Flutamide	143-152	sarcolipin	Rattus norvegicus	46-49
26393301-5	2015	Confirming a direct androgen receptor-mediated effect on sclerostin production, flutamide coincubation and silencing of androgen receptor gene in osteocytes abolished the DHT effects.	Flutamide	80-89	androgen receptor	Homo sapiens	20-37
25867062-0	2015	Anti-androgen flutamide suppresses hepatocellular carcinoma cell proliferation via the aryl hydrocarbon receptor mediated induction of transforming growth factor-beta1.	Flutamide	14-23	aryl hydrocarbon receptor	Homo sapiens	87-112
25867062-0	2015	Anti-androgen flutamide suppresses hepatocellular carcinoma cell proliferation via the aryl hydrocarbon receptor mediated induction of transforming growth factor-beta1.	Flutamide	14-23	transforming growth factor beta 1	Homo sapiens	135-167
25867062-3	2015	We conducted a chemical library screen to identify nontoxic AhR ligands with anti-cancer effects and discovered flutamide (Eulexin) as a putative AhR ligand.	Flutamide	112-121	aryl hydrocarbon receptor	Homo sapiens	146-149
25867062-3	2015	We conducted a chemical library screen to identify nontoxic AhR ligands with anti-cancer effects and discovered flutamide (Eulexin) as a putative AhR ligand.	Flutamide	123-130	aryl hydrocarbon receptor	Homo sapiens	146-149
25867062-4	2015	Flutamide is an androgen receptor (AR) antagonist approved by the United States Food and Drug Administration for the treatment of prostate cancer.	Flutamide	0-9	androgen receptor	Homo sapiens	16-33
25867062-4	2015	Flutamide is an androgen receptor (AR) antagonist approved by the United States Food and Drug Administration for the treatment of prostate cancer.	Flutamide	0-9	androgen receptor	Homo sapiens	35-37
25867062-5	2015	We found that flutamide inhibited the growth of several cancer cell lines independent of AR status, and that suppression of AhR expression reversed the anti-proliferative effects of flutamide.	Flutamide	182-191	aryl hydrocarbon receptor	Homo sapiens	124-127
25867062-6	2015	We investigated the AhR-dependent mechanism of action of flutamide in human hepatocellular carcinoma cells and identified that transforming growth factor-beta1 (TGF-beta1) is induced by flutamide in an AhR-dependent manner.	Flutamide	57-66	aryl hydrocarbon receptor	Homo sapiens	20-23
25867062-6	2015	We investigated the AhR-dependent mechanism of action of flutamide in human hepatocellular carcinoma cells and identified that transforming growth factor-beta1 (TGF-beta1) is induced by flutamide in an AhR-dependent manner.	Flutamide	57-66	transforming growth factor beta 1	Homo sapiens	127-159
25867062-6	2015	We investigated the AhR-dependent mechanism of action of flutamide in human hepatocellular carcinoma cells and identified that transforming growth factor-beta1 (TGF-beta1) is induced by flutamide in an AhR-dependent manner.	Flutamide	57-66	transforming growth factor beta 1	Homo sapiens	161-170
25867062-6	2015	We investigated the AhR-dependent mechanism of action of flutamide in human hepatocellular carcinoma cells and identified that transforming growth factor-beta1 (TGF-beta1) is induced by flutamide in an AhR-dependent manner.	Flutamide	57-66	aryl hydrocarbon receptor	Homo sapiens	202-205
25867062-6	2015	We investigated the AhR-dependent mechanism of action of flutamide in human hepatocellular carcinoma cells and identified that transforming growth factor-beta1 (TGF-beta1) is induced by flutamide in an AhR-dependent manner.	Flutamide	186-195	aryl hydrocarbon receptor	Homo sapiens	20-23
25867062-6	2015	We investigated the AhR-dependent mechanism of action of flutamide in human hepatocellular carcinoma cells and identified that transforming growth factor-beta1 (TGF-beta1) is induced by flutamide in an AhR-dependent manner.	Flutamide	186-195	transforming growth factor beta 1	Homo sapiens	127-159
25867062-6	2015	We investigated the AhR-dependent mechanism of action of flutamide in human hepatocellular carcinoma cells and identified that transforming growth factor-beta1 (TGF-beta1) is induced by flutamide in an AhR-dependent manner.	Flutamide	186-195	transforming growth factor beta 1	Homo sapiens	161-170
25867062-6	2015	We investigated the AhR-dependent mechanism of action of flutamide in human hepatocellular carcinoma cells and identified that transforming growth factor-beta1 (TGF-beta1) is induced by flutamide in an AhR-dependent manner.	Flutamide	186-195	aryl hydrocarbon receptor	Homo sapiens	202-205
25867062-8	2015	We also determined that TGF-beta1 induction is required for the AhR-dependent growth inhibitory effects of flutamide.	Flutamide	107-116	transforming growth factor beta 1	Homo sapiens	24-33
25867062-8	2015	We also determined that TGF-beta1 induction is required for the AhR-dependent growth inhibitory effects of flutamide.	Flutamide	107-116	aryl hydrocarbon receptor	Homo sapiens	64-67
25867062-9	2015	Therefore, flutamide may be effective in AhR-positive cancers that are sensitive to TGF-beta1 signaling, such as hepatocellular carcinoma.	Flutamide	11-20	aryl hydrocarbon receptor	Homo sapiens	41-44
25867062-9	2015	Therefore, flutamide may be effective in AhR-positive cancers that are sensitive to TGF-beta1 signaling, such as hepatocellular carcinoma.	Flutamide	11-20	transforming growth factor beta 1	Homo sapiens	84-93
26450018-4	2015	The impact of hormone deprivation was tested through both orchiectomy and chemical blockage of androgen receptor using flutamide (FLU).	Flutamide	119-128	androgen receptor	Rattus norvegicus	95-112
26450018-11	2015	IL-1beta production was increased only in the gingival tissue of OCX animals, whereas FLU-treated animals presented a decreased expression of IL-6.	Flutamide	86-89	interleukin 6	Rattus norvegicus	142-146
26450018-12	2015	Testosterone reduced the osteoclast formation in a dose-dependent manner, and significantly impacted the production of TNF-alpha; FLU partially reversed these actions.	Flutamide	130-133	tumor necrosis factor	Rattus norvegicus	119-128
26973973-9	2015	Exposure to 500 mg of Flu/kg BW induced an increase of Cx37 expression but significant decreases of Cxs43 and 45 mRNA levels.	Flutamide	22-25	gap junction protein, alpha 4	Rattus norvegicus	55-59
26973973-10	2015	Expression of Cx37 was increased by a treatment of 5 mg of Flu/kg BW, while transcript levels of Cxs26, 30.3, 31, 31.1, 32, and 43 were significantly decreased by same treatment.	Flutamide	59-62	gap junction protein, alpha 4	Rattus norvegicus	14-18
26265743-0	2015	A Screen of Approved Drugs Identifies the Androgen Receptor Antagonist Flutamide and Its Pharmacologically Active Metabolite 2-Hydroxy-Flutamide as Heterotropic Activators of Cytochrome P450 3A In Vitro and In Vivo.	Flutamide	71-80	androgen receptor	Homo sapiens	42-59
26578781-4	2015	PNA offspring displayed anxiety-like behavior in the elevated plus maze, which was reversed by flutamide [androgen receptor (AR) blocker] and tamoxifen [selective estrogen receptor (ER) modulator].	Flutamide	95-104	androgen receptor	Rattus norvegicus	106-123
26578781-4	2015	PNA offspring displayed anxiety-like behavior in the elevated plus maze, which was reversed by flutamide [androgen receptor (AR) blocker] and tamoxifen [selective estrogen receptor (ER) modulator].	Flutamide	95-104	androgen receptor	Rattus norvegicus	125-127
26759534-8	2015	Addition of 0.2microM flutamide, a testosterone receptor blocker to the incubation mixture restored the synthesis of maspin by 60.64 %.	Flutamide	22-31	serpin family B member 5	Homo sapiens	117-123
26484580-4	2015	GCNF expression decreased in mice testis upon flutamide (androgen receptor antagonist) treatment, indicating the presence of an androgen/GCNF network to direct GRTH expression in GC.	Flutamide	46-55	nuclear receptor subfamily 6, group A, member 1	Mus musculus	0-4
26484580-4	2015	GCNF expression decreased in mice testis upon flutamide (androgen receptor antagonist) treatment, indicating the presence of an androgen/GCNF network to direct GRTH expression in GC.	Flutamide	46-55	nuclear receptor subfamily 6, group A, member 1	Mus musculus	137-141
26484580-4	2015	GCNF expression decreased in mice testis upon flutamide (androgen receptor antagonist) treatment, indicating the presence of an androgen/GCNF network to direct GRTH expression in GC.	Flutamide	46-55	DEAD box helicase 25	Mus musculus	160-164
26484580-5	2015	Binding studies and chromatin immunoprecipitation demonstrated specific association of GCNF to a consensus half-site (-5270/-5252) of the GRTH gene in both round spermatids and spermatocytes, which was abolished by flutamide treatment in round spermatids.	Flutamide	215-224	nuclear receptor subfamily 6, group A, member 1	Mus musculus	87-91
26484580-5	2015	Binding studies and chromatin immunoprecipitation demonstrated specific association of GCNF to a consensus half-site (-5270/-5252) of the GRTH gene in both round spermatids and spermatocytes, which was abolished by flutamide treatment in round spermatids.	Flutamide	215-224	DEAD box helicase 25	Mus musculus	138-142
26484580-6	2015	Moreover, flutamide treatment of wild-type mice caused selective reduction of GCNF and GRTH in round spermatids.	Flutamide	10-19	nuclear receptor subfamily 6, group A, member 1	Mus musculus	78-82
26484580-6	2015	Moreover, flutamide treatment of wild-type mice caused selective reduction of GCNF and GRTH in round spermatids.	Flutamide	10-19	DEAD box helicase 25	Mus musculus	87-91
26484580-8	2015	Exposure of tubules to flutamide caused decrease in GCNF and GFP expression, whereas androgen exposure induced significant increase.	Flutamide	23-32	nuclear receptor subfamily 6, group A, member 1	Mus musculus	52-56
26493607-3	2015	Treatment with flutamide, an androgen receptor (AR) antagonist, during the perinatal period inhibits development of malespecific brain structure and function, suggesting that androgen signaling via AR also influences brain masculinization.	Flutamide	15-24	androgen receptor	Rattus norvegicus	29-46
26493607-3	2015	Treatment with flutamide, an androgen receptor (AR) antagonist, during the perinatal period inhibits development of malespecific brain structure and function, suggesting that androgen signaling via AR also influences brain masculinization.	Flutamide	15-24	androgen receptor	Rattus norvegicus	48-50
26493607-3	2015	Treatment with flutamide, an androgen receptor (AR) antagonist, during the perinatal period inhibits development of malespecific brain structure and function, suggesting that androgen signaling via AR also influences brain masculinization.	Flutamide	15-24	androgen receptor	Rattus norvegicus	198-200
25976454-0	2015	Flutamide alters beta-catenin expression and distribution, and its interactions with E-cadherin in the porcine corpus luteum of mid- and late pregnancy.	Flutamide	0-9	catenin beta 1	Sus scrofa	17-29
25976454-0	2015	Flutamide alters beta-catenin expression and distribution, and its interactions with E-cadherin in the porcine corpus luteum of mid- and late pregnancy.	Flutamide	0-9	cadherin 1	Sus scrofa	85-95
25976454-1	2015	This study examined whether flutamide-induced androgen deficiency during mid- and late pregnancy in pigs affected luteal expression of adherens junction protein, beta-catenin, and its interactions with E-cadherin.	Flutamide	28-37	catenin beta 1	Sus scrofa	162-174
25976454-1	2015	This study examined whether flutamide-induced androgen deficiency during mid- and late pregnancy in pigs affected luteal expression of adherens junction protein, beta-catenin, and its interactions with E-cadherin.	Flutamide	28-37	cadherin 1	Sus scrofa	202-212
25976454-7	2015	To determine whether flutamide disturbs beta-catenin/E-cadherin mutual interactions, coimmunoprecipitation using anti-beta-catenin antibody was performed.	Flutamide	21-30	catenin beta 1	Sus scrofa	40-52
25976454-7	2015	To determine whether flutamide disturbs beta-catenin/E-cadherin mutual interactions, coimmunoprecipitation using anti-beta-catenin antibody was performed.	Flutamide	21-30	cadherin 1	Sus scrofa	53-63
25976454-9	2015	Flutamide exposure led to decreased beta-catenin mRNA expression in all examined groups (p<0.001 or p<0.01), but protein level was lower only in the GD90F and GD108F groups (p<0.05).	Flutamide	0-9	catenin beta 1	Sus scrofa	36-48
25976454-10	2015	E-cadherin mRNA (p<0.05 or p<0.01) and protein (p<0.05) levels were up-regulated in all flutamide-treated groups when compared to controls.	Flutamide	97-106	cadherin 1	Sus scrofa	0-10
26265743-3	2015	Results of this screen revealed that the prescribed androgen receptor antagonist flutamide activated the intrinsic midazolam hydroxylase activity of CYP3A in human hepatic microsomes (66%), rat and human hepatocytes (36 and 160%, respectively), and in vivo in male Sprague-Dawley rats (>2-fold, combined area under the curve of primary rat in vivo midazolam metabolites).	Flutamide	81-90	androgen receptor	Homo sapiens	52-69
26265743-3	2015	Results of this screen revealed that the prescribed androgen receptor antagonist flutamide activated the intrinsic midazolam hydroxylase activity of CYP3A in human hepatic microsomes (66%), rat and human hepatocytes (36 and 160%, respectively), and in vivo in male Sprague-Dawley rats (>2-fold, combined area under the curve of primary rat in vivo midazolam metabolites).	Flutamide	81-90	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	149-154
26265743-5	2015	Importantly, both flutamide and 2-hydroxy-flutamide demonstrated a pronounced increase in the CYP3A-mediated metabolism of commonly paired medications, nifedipine (antihypertensive) and amiodarone (antiarrhythmic), in multispecies hepatocytes (100% over baseline).	Flutamide	18-27	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	94-99
26164127-1	2015	Human arylacetamide deacetylase (AADAC) is an esterase responsible for the hydrolysis of some drugs, including flutamide, indiplon, phenacetin, and rifamycins.	Flutamide	111-120	arylacetamide deacetylase	Homo sapiens	6-31
26164127-1	2015	Human arylacetamide deacetylase (AADAC) is an esterase responsible for the hydrolysis of some drugs, including flutamide, indiplon, phenacetin, and rifamycins.	Flutamide	111-120	arylacetamide deacetylase	Homo sapiens	33-38
26032259-5	2015	Testosterone (5-100 nM, 24-48 h) was provided into the media and androgen receptor (AR) blocked by flutamide (100 nM).	Flutamide	99-108	androgen receptor	Rattus norvegicus	65-82
26332122-7	2015	Examination of efficacy of MJC13 in conditions that reflect aspects castrate resistant prostate cancer (CRPC) reveals that it inhibits flutamide activation of an AR mutant (ART877A) that emerges during flutamide withdrawal syndrome, but displays greatly restricted gene-specific activity in 22Rv1 cells that express a constitutively active truncated AR and is inactive against glucocorticoid receptor (GR), which can co-opt androgen-dependent signaling networks in CRPC.	Flutamide	202-211	androgen receptor	Homo sapiens	162-164
26332122-7	2015	Examination of efficacy of MJC13 in conditions that reflect aspects castrate resistant prostate cancer (CRPC) reveals that it inhibits flutamide activation of an AR mutant (ART877A) that emerges during flutamide withdrawal syndrome, but displays greatly restricted gene-specific activity in 22Rv1 cells that express a constitutively active truncated AR and is inactive against glucocorticoid receptor (GR), which can co-opt androgen-dependent signaling networks in CRPC.	Flutamide	202-211	androgen receptor	Homo sapiens	173-175
26024831-1	2015	The study aims to compare serial changes in prostate-specific antigen (PSA), testosterone, dehydroepiandrosterone (DHEA), and androstenedione in patients treated with either of the antiandrogen agents, bicalutamide or flutamide, using a randomized controlled study.	Flutamide	218-227	kallikrein related peptidase 3	Homo sapiens	44-76
26199450-7	2015	The inhibitory effect of testosterone was abolished by androgen receptor antagonist, flutamide.	Flutamide	85-94	androgen receptor	Homo sapiens	55-72
26217181-7	2015	Androgen receptor (AR) inhibition with 20 muM flutamide but not aromatase inhibition with 10 muM letrozole reduced basal and T-induced neurosphere growth in females, while only concurrent inhibition of AR and aromatase produced the same effect in males.	Flutamide	46-55	androgen receptor	Mus musculus	0-17
26217181-7	2015	Androgen receptor (AR) inhibition with 20 muM flutamide but not aromatase inhibition with 10 muM letrozole reduced basal and T-induced neurosphere growth in females, while only concurrent inhibition of AR and aromatase produced the same effect in males.	Flutamide	46-55	androgen receptor	Mus musculus	19-21
26032259-5	2015	Testosterone (5-100 nM, 24-48 h) was provided into the media and androgen receptor (AR) blocked by flutamide (100 nM).	Flutamide	99-108	androgen receptor	Rattus norvegicus	84-86
26032259-9	2015	The hormonal effects were abolished by either AR blocker flutamide or NF-kappaB-knockdown.	Flutamide	57-66	androgen receptor	Rattus norvegicus	46-48
25862351-10	2015	A small experiment on mice (three per group) showed that Mate1 knockout mice had an elevated serum concentration of 4-nitro-3-(trifluoromethyl)phenylamine, a major metabolite of flutamide, 2 h after administration of the drug, suggesting that Mate1 could affect the pharmacokinetics of flutamide.	Flutamide	178-187	solute carrier family 47, member 1	Mus musculus	57-62
25598450-5	2015	RESULTS: Leydig cell-conditioned media dose-dependently stimulated expression of transcription factor Foxp3 and secretion of IL-10 in splenic CD4+ T cells, an effect abolished by addition of the anti-androgen flutamide.	Flutamide	209-218	forkhead box P3	Homo sapiens	102-107
25598450-5	2015	RESULTS: Leydig cell-conditioned media dose-dependently stimulated expression of transcription factor Foxp3 and secretion of IL-10 in splenic CD4+ T cells, an effect abolished by addition of the anti-androgen flutamide.	Flutamide	209-218	interleukin 10	Homo sapiens	125-130
25598450-5	2015	RESULTS: Leydig cell-conditioned media dose-dependently stimulated expression of transcription factor Foxp3 and secretion of IL-10 in splenic CD4+ T cells, an effect abolished by addition of the anti-androgen flutamide.	Flutamide	209-218	CD4 molecule	Homo sapiens	142-145
25159107-4	2015	Young adult ovariectomized rats were given either androstenedione, androstenedione plus the aromatase inhibitor anastrozole to block conversion to estrone, androstenedione plus the androgen receptor blocker flutamide to block androgen receptor activity, or vehicle treatment, and were then administered a battery of learning and memory maze tasks.	Flutamide	207-216	androgen receptor	Rattus norvegicus	181-198
25862351-10	2015	A small experiment on mice (three per group) showed that Mate1 knockout mice had an elevated serum concentration of 4-nitro-3-(trifluoromethyl)phenylamine, a major metabolite of flutamide, 2 h after administration of the drug, suggesting that Mate1 could affect the pharmacokinetics of flutamide.	Flutamide	286-295	solute carrier family 47, member 1	Mus musculus	57-62
25715734-1	2015	Arylacetamide deacetylase (AADAC), a microsomal serine esterase, hydrolyzes drugs, such as flutamide, phenacetin and rifampicin.	Flutamide	91-100	arylacetamide deacetylase	Homo sapiens	0-25
27004263-7	2015	Treatments of Flu caused significant decreases of expression of all examined Cx isoforms, except Cx37 and Cx43 shown no expressional change with high-dose Flu treatment.	Flutamide	14-17	gap junction protein, alpha 1	Rattus norvegicus	106-110
25715734-1	2015	Arylacetamide deacetylase (AADAC), a microsomal serine esterase, hydrolyzes drugs, such as flutamide, phenacetin and rifampicin.	Flutamide	91-100	arylacetamide deacetylase	Homo sapiens	27-32
25920548-9	2015	To explore further the possible role of miRNAs in the AR pathway, LNCaP cell line was treated with 5alpha-dihydrotestosterone and flutamide showing alteration in miRNAs expression, especially miR-34a, which was significantly underexpressed after treatment with high doses of 5alpha-dihydrotestosterone.	Flutamide	130-139	androgen receptor	Homo sapiens	54-56
25920548-9	2015	To explore further the possible role of miRNAs in the AR pathway, LNCaP cell line was treated with 5alpha-dihydrotestosterone and flutamide showing alteration in miRNAs expression, especially miR-34a, which was significantly underexpressed after treatment with high doses of 5alpha-dihydrotestosterone.	Flutamide	130-139	microRNA 34a	Homo sapiens	192-199
25873562-0	2015	Flutamide alters the distribution of c-Src and affects the N-cadherin-beta-catenin complex in the seminiferous epithelium of adult rat.	Flutamide	0-9	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	37-42
25873562-0	2015	Flutamide alters the distribution of c-Src and affects the N-cadherin-beta-catenin complex in the seminiferous epithelium of adult rat.	Flutamide	0-9	cadherin 2	Rattus norvegicus	59-69
25873562-0	2015	Flutamide alters the distribution of c-Src and affects the N-cadherin-beta-catenin complex in the seminiferous epithelium of adult rat.	Flutamide	0-9	catenin beta 1	Rattus norvegicus	70-82
25873562-1	2015	This study was undertaken to explore interactions between c-Src kinase and the N-cadherin-beta-catenin complex in seminiferous tubules of flutamide-treated rats.	Flutamide	138-147	C-terminal Src kinase	Rattus norvegicus	58-70
25873562-1	2015	This study was undertaken to explore interactions between c-Src kinase and the N-cadherin-beta-catenin complex in seminiferous tubules of flutamide-treated rats.	Flutamide	138-147	cadherin 2	Rattus norvegicus	79-89
25873562-1	2015	This study was undertaken to explore interactions between c-Src kinase and the N-cadherin-beta-catenin complex in seminiferous tubules of flutamide-treated rats.	Flutamide	138-147	catenin beta 1	Rattus norvegicus	90-102
25873562-5	2015	Real-time RT-PCR and western blot analyses revealed upregulation of N-cadherin at the mRNA and protein level after flutamide exposure (p < 0.05), whereas no changes in beta-catenin and c-Src expression were observed.	Flutamide	115-124	cadherin 2	Rattus norvegicus	68-78
25873562-5	2015	Real-time RT-PCR and western blot analyses revealed upregulation of N-cadherin at the mRNA and protein level after flutamide exposure (p < 0.05), whereas no changes in beta-catenin and c-Src expression were observed.	Flutamide	115-124	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	188-193
25873562-7	2015	As we used an exposure regime which avoided germ cell loss, it is likely that changes in the N-cadherin-beta-catenin complex are a primary effect of androgen signaling disruption by flutamide.	Flutamide	182-191	cadherin 2	Rattus norvegicus	93-103
25873562-7	2015	As we used an exposure regime which avoided germ cell loss, it is likely that changes in the N-cadherin-beta-catenin complex are a primary effect of androgen signaling disruption by flutamide.	Flutamide	182-191	catenin beta 1	Rattus norvegicus	104-116
25873562-9	2015	As detected by immunofluorescence and coimmunoprecipitation, flutamide promoted disassembly of the N-cadherin-ss-catenin complex, induced N-cadherin to dissociate from c-Src at the BTB site, and altered interactions between the cell junction proteins and/or c-Src.	Flutamide	61-70	cadherin 2	Rattus norvegicus	99-109
25873562-9	2015	As detected by immunofluorescence and coimmunoprecipitation, flutamide promoted disassembly of the N-cadherin-ss-catenin complex, induced N-cadherin to dissociate from c-Src at the BTB site, and altered interactions between the cell junction proteins and/or c-Src.	Flutamide	61-70	cadherin 2	Rattus norvegicus	138-148
25873562-9	2015	As detected by immunofluorescence and coimmunoprecipitation, flutamide promoted disassembly of the N-cadherin-ss-catenin complex, induced N-cadherin to dissociate from c-Src at the BTB site, and altered interactions between the cell junction proteins and/or c-Src.	Flutamide	61-70	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	168-173
25873562-9	2015	As detected by immunofluorescence and coimmunoprecipitation, flutamide promoted disassembly of the N-cadherin-ss-catenin complex, induced N-cadherin to dissociate from c-Src at the BTB site, and altered interactions between the cell junction proteins and/or c-Src.	Flutamide	61-70	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	258-263
25873562-11	2015	Overall, for the first time we have shown that flutamide alters the distribution of c-Src and affects N-cadherin-beta-catenin interactions at the BTB.	Flutamide	47-56	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	84-89
25873562-11	2015	Overall, for the first time we have shown that flutamide alters the distribution of c-Src and affects N-cadherin-beta-catenin interactions at the BTB.	Flutamide	47-56	cadherin 2	Rattus norvegicus	102-112
25873562-11	2015	Overall, for the first time we have shown that flutamide alters the distribution of c-Src and affects N-cadherin-beta-catenin interactions at the BTB.	Flutamide	47-56	catenin beta 1	Rattus norvegicus	113-125
25550341-8	2015	Vascular Agtr1/Agtr2 ratio was significantly higher in protein-restricted offspring, an effect that was reversed by flutamide.	Flutamide	116-125	angiotensin II receptor, type 1a	Rattus norvegicus	9-14
25949209-8	2015	Increased levels of Cx30.3 and Cx40 transcripts were observed with a low-dose Flu (500 mug/kg body weight) treatment.	Flutamide	78-81	gap junction protein, beta 6	Rattus norvegicus	20-24
25949209-8	2015	Increased levels of Cx30.3 and Cx40 transcripts were observed with a low-dose Flu (500 mug/kg body weight) treatment.	Flutamide	78-81	gap junction protein, alpha 5	Rattus norvegicus	31-35
25949209-9	2015	Treatment of high-dose Flu (50 mg/kg body weight) led to expressional increases of Cx30.3, 40, and 43 genes.	Flutamide	23-26	gap junction protein, beta 6	Rattus norvegicus	83-87
25489059-7	2015	Treatment with androgen receptor antagonist flutamide (10 mg/kg, SC, BID for 10 days) significantly attenuated hypertension, PKCdelta expression, and the exaggerated vasoconstriction in prenatal testosterone-exposed rats.	Flutamide	44-53	androgen receptor	Rattus norvegicus	15-32
25489059-7	2015	Treatment with androgen receptor antagonist flutamide (10 mg/kg, SC, BID for 10 days) significantly attenuated hypertension, PKCdelta expression, and the exaggerated vasoconstriction in prenatal testosterone-exposed rats.	Flutamide	44-53	BH3 interacting domain death agonist	Rattus norvegicus	69-72
25552366-4	2015	In this work, we demonstrate that Stat5a/b sequesters antiandrogen-liganded (MDV3100, bicalutamide, flutamide) AR in prostate cancer cells and protects it against proteasomal degradation in prostate cancer.	Flutamide	100-109	signal transducer and activator of transcription 5A	Homo sapiens	34-40
25552366-4	2015	In this work, we demonstrate that Stat5a/b sequesters antiandrogen-liganded (MDV3100, bicalutamide, flutamide) AR in prostate cancer cells and protects it against proteasomal degradation in prostate cancer.	Flutamide	100-109	androgen receptor	Homo sapiens	111-113
25715793-3	2015	The experimental design employed littermate pairs of boars with one member assigned to receive a daily oral dose of flutamide, an androgen receptor antagonist, beginning at 1 wk of age and the littermate the canola oil vehicle.	Flutamide	116-125	androgen receptor	Homo sapiens	130-147
25789054-9	2015	In addition, by using a phosphoinositide 3-kinase (PI3K)-specific inhibitor and AR antagonists, such as flutamide and bicalutamide, it was also observed that upregulation of ARGs in response to OPNc-CM involves PI3K signaling and depends on the AR.	Flutamide	104-113	androgen receptor	Homo sapiens	80-82
25789054-9	2015	In addition, by using a phosphoinositide 3-kinase (PI3K)-specific inhibitor and AR antagonists, such as flutamide and bicalutamide, it was also observed that upregulation of ARGs in response to OPNc-CM involves PI3K signaling and depends on the AR.	Flutamide	104-113	androgen receptor	Homo sapiens	174-176
25852559-2	2015	Current clinically used antiandrogens such as flutamide, bicalutamide, and newly approved enzalutamide mainly target the hormone binding pocket (HBP) of AR.	Flutamide	46-55	heme binding protein 1	Homo sapiens	145-148
25852559-2	2015	Current clinically used antiandrogens such as flutamide, bicalutamide, and newly approved enzalutamide mainly target the hormone binding pocket (HBP) of AR.	Flutamide	46-55	androgen receptor	Homo sapiens	153-155
25550341-8	2015	Vascular Agtr1/Agtr2 ratio was significantly higher in protein-restricted offspring, an effect that was reversed by flutamide.	Flutamide	116-125	angiotensin II receptor, type 2	Rattus norvegicus	15-20
25550341-11	2015	Flutamide treatment reversed the enhanced contractile response to angiotensin II in protein-restricted offspring without significant effect in controls.	Flutamide	0-9	angiotensinogen	Rattus norvegicus	66-80
25550341-12	2015	Vascular reactivity to phenylephrine was similar between the control and protein-restricted offspring with and without flutamide treatment, suggesting that enhanced contractile response and flutamide"s reversal effect is specific to angiotensin II.	Flutamide	190-199	angiotensinogen	Rattus norvegicus	233-247
25949200-8	2014	Significant decreases of Cx31, 31.1, 32, 37, and 45 gene expression were detected with a treatment of 500 mug Flu/kg BW, while expression of Cx43 gene was significantly increased with a treatment of 500 mug Flu/kg BW.	Flutamide	110-113	gap junction protein, beta 3	Rattus norvegicus	25-29
25375036-7	2015	Flutamide treatment increased circulating testosterone yet also reduced seminal vesicle weight due to local antagonism of androgen receptor.	Flutamide	0-9	androgen receptor	Rattus norvegicus	122-139
26521872-4	2015	We found that flutamide, phenacetin, rifamycins (rifampicin, rifabutin, and rifapentine), and indiplon are hydrolyzed by arylacetamide deacetylase (AADAC), which is highly expressed in human liver and gastrointestinal tissues.	Flutamide	14-23	arylacetamide deacetylase	Homo sapiens	148-153
25163025-6	2014	Conversely, testosterone-induced klotho expression was attenuated in the presence of flutamide, an AR antagonist.	Flutamide	85-94	Klotho	Rattus norvegicus	33-39
25163025-6	2014	Conversely, testosterone-induced klotho expression was attenuated in the presence of flutamide, an AR antagonist.	Flutamide	85-94	androgen receptor	Rattus norvegicus	99-101
25216387-12	2014	These results suggest that androgen receptor mediates the effect of testosterone on oSDN masculinization, because this process was blocked by the androgen receptor antagonist flutamide in eugonadal males.	Flutamide	175-184	androgen receptor	Ovis aries	27-44
25949200-8	2014	Significant decreases of Cx31, 31.1, 32, 37, and 45 gene expression were detected with a treatment of 500 mug Flu/kg BW, while expression of Cx43 gene was significantly increased with a treatment of 500 mug Flu/kg BW.	Flutamide	207-210	gap junction protein, alpha 1	Rattus norvegicus	141-145
25216387-12	2014	These results suggest that androgen receptor mediates the effect of testosterone on oSDN masculinization, because this process was blocked by the androgen receptor antagonist flutamide in eugonadal males.	Flutamide	175-184	androgen receptor	Ovis aries	146-163
25949200-9	2014	A treatment of 50 mg Flu/kg BW led to significant increases of Cx30.3, 32, 37, 40, and 43 gene expression.	Flutamide	21-24	gap junction protein, beta 6	Rattus norvegicus	63-67
25130562-5	2014	Brain morphological studies revealed that prenatal flutamide decreased the number of MAP2 (a microtubule-associated protein type 2, present almost exclusively in dendrites) immunoreactive neuronal processes in all evaluated brain areas, both in prepubertal and adult offspring, suggesting that prenatal androgen disruption induces long-term reductions of the dendritic arborization of several brain structures, affecting the normal connectivity between areas.	Flutamide	51-60	microtubule-associated protein 2	Rattus norvegicus	85-89
25130562-5	2014	Brain morphological studies revealed that prenatal flutamide decreased the number of MAP2 (a microtubule-associated protein type 2, present almost exclusively in dendrites) immunoreactive neuronal processes in all evaluated brain areas, both in prepubertal and adult offspring, suggesting that prenatal androgen disruption induces long-term reductions of the dendritic arborization of several brain structures, affecting the normal connectivity between areas.	Flutamide	51-60	microtubule-associated protein 2	Rattus norvegicus	93-130
25473629-10	2014	In addition, the fasting insulin was significantly greater in metformin group and flutamide group in comparison to metformin+flutamide and placebo groups after treatment (p<0.05).	Flutamide	82-91	insulin	Homo sapiens	25-32
25473629-10	2014	In addition, the fasting insulin was significantly greater in metformin group and flutamide group in comparison to metformin+flutamide and placebo groups after treatment (p<0.05).	Flutamide	125-134	insulin	Homo sapiens	25-32
25473629-11	2014	Within groups, insulin level showed significant changes (before and after treatment) in metformin+flutamide group and LDL reduction was significant in flutamide group before and after treatment.	Flutamide	98-107	insulin	Homo sapiens	15-22
24865629-0	2014	Connexin 43 expression in Sprague-Dawley rat seminiferous epithelium after in utero exposure to flutamide.	Flutamide	96-105	gap junction protein, alpha 1	Rattus norvegicus	0-11
24865629-1	2014	This study explored the expression of connexin 43 (Cx43) in the testes of prepubertal Sprague-Dawley (SD) rats following in utero flutamide (Flu) exposure.	Flutamide	130-139	gap junction protein, alpha 1	Rattus norvegicus	38-49
24929096-0	2014	Integration of pharmacokinetic and NRF2 system biology models to describe reactive oxygen species production and subsequent glutathione depletion in liver microfluidic biochips after flutamide exposure.	Flutamide	183-192	NFE2 like bZIP transcription factor 2	Rattus norvegicus	35-39
24865629-1	2014	This study explored the expression of connexin 43 (Cx43) in the testes of prepubertal Sprague-Dawley (SD) rats following in utero flutamide (Flu) exposure.	Flutamide	130-139	gap junction protein, alpha 1	Rattus norvegicus	51-55
24929096-2	2014	We coupled an in vitro pharmacokinetic (PK) model of flutamide to a system biology model of its reactive oxygen species (ROS) production and scavenging by the Nrf2 regulated glutathione production.	Flutamide	53-62	NFE2 like bZIP transcription factor 2	Rattus norvegicus	159-163
24865629-1	2014	This study explored the expression of connexin 43 (Cx43) in the testes of prepubertal Sprague-Dawley (SD) rats following in utero flutamide (Flu) exposure.	Flutamide	141-144	gap junction protein, alpha 1	Rattus norvegicus	38-49
24865629-1	2014	This study explored the expression of connexin 43 (Cx43) in the testes of prepubertal Sprague-Dawley (SD) rats following in utero flutamide (Flu) exposure.	Flutamide	141-144	gap junction protein, alpha 1	Rattus norvegicus	51-55
24865629-6	2014	Following Flu-exposure, Cx43 was observed between Sertoli cells in the seminiferous tubules.	Flutamide	10-13	gap junction protein, alpha 1	Rattus norvegicus	24-28
24865629-8	2014	Western blotting showed that Cx43 was expressed at significantly lower levels in Flu-exposed testes than controls on PD20 (p < 0.001).	Flutamide	81-84	gap junction protein, alpha 1	Rattus norvegicus	29-33
24865629-9	2014	On PD20, levels of Cx43 mRNA in undescended Flu-exposed testes were significantly lower than in controls (p < 0.05) and descended Flu-exposed testes (p < 0.01).	Flutamide	44-47	gap junction protein, alpha 1	Rattus norvegicus	19-23
24865629-9	2014	On PD20, levels of Cx43 mRNA in undescended Flu-exposed testes were significantly lower than in controls (p < 0.05) and descended Flu-exposed testes (p < 0.01).	Flutamide	133-136	gap junction protein, alpha 1	Rattus norvegicus	19-23
24865629-10	2014	After Flu-exposure in the rat embryonic period, Cx43 mRNA and protein expression were downregulated, and its distribution in the seminiferous tubules was abnormal.	Flutamide	6-9	gap junction protein, alpha 1	Rattus norvegicus	48-52
24799026-7	2014	Treatment of ER stress inhibitor or flutamide (AR inhibitor) could inhibit testosterone-induced cell apoptosis and CHOP expression.	Flutamide	36-45	DNA-damage inducible transcript 3	Rattus norvegicus	115-119
24742193-5	2014	In this study, we asked whether the nonsteroidal AR antagonist flutamide, delivered via a time-release pellet, could reverse or prevent androgen-dependent AR toxicity in three different mouse models of SBMA: the AR97Q transgenic (Tg) model, a knock-in (KI) model, and a myogenic Tg model.	Flutamide	63-72	androgen receptor	Mus musculus	49-51
24742193-6	2014	We find that flutamide protects mice from androgen-dependent AR toxicity in all three SBMA models, preventing or reversing motor dysfunction in the Tg models and significantly extending the life span in KI males.	Flutamide	13-22	androgen receptor	Homo sapiens	86-90
24742193-7	2014	Given that flutamide effectively protects against androgen-dependent disease in three different mouse models of SBMA, our data are proof of principle that AR antagonists have therapeutic potential for treating SBMA in humans and support the notion that toxicity caused by polyQ-expanded AR uses at least some of the same mechanisms as normal AR before diverging to produce disease and muscle atrophy.	Flutamide	11-20	androgen receptor	Homo sapiens	112-116
24742193-7	2014	Given that flutamide effectively protects against androgen-dependent disease in three different mouse models of SBMA, our data are proof of principle that AR antagonists have therapeutic potential for treating SBMA in humans and support the notion that toxicity caused by polyQ-expanded AR uses at least some of the same mechanisms as normal AR before diverging to produce disease and muscle atrophy.	Flutamide	11-20	androgen receptor	Mus musculus	155-157
24950779-5	2014	Flutamide decreased the levels, notably, of CSF-1 and ErbB4 in ovarian stroma (P <= 0.0006) and ovarian endosalpingiosis (P <= 0.01), ErbB4 in ovarian epithelium (P = 0.006), and CSF-1R in ovarian endosalpingiosis (P = 0.009).	Flutamide	0-9	colony stimulating factor 1	Homo sapiens	44-49
24950779-5	2014	Flutamide decreased the levels, notably, of CSF-1 and ErbB4 in ovarian stroma (P <= 0.0006) and ovarian endosalpingiosis (P <= 0.01), ErbB4 in ovarian epithelium (P = 0.006), and CSF-1R in ovarian endosalpingiosis (P = 0.009).	Flutamide	0-9	erb-b2 receptor tyrosine kinase 4	Homo sapiens	54-59
24950779-5	2014	Flutamide decreased the levels, notably, of CSF-1 and ErbB4 in ovarian stroma (P <= 0.0006) and ovarian endosalpingiosis (P <= 0.01), ErbB4 in ovarian epithelium (P = 0.006), and CSF-1R in ovarian endosalpingiosis (P = 0.009).	Flutamide	0-9	erb-b2 receptor tyrosine kinase 4	Homo sapiens	140-145
24950779-5	2014	Flutamide decreased the levels, notably, of CSF-1 and ErbB4 in ovarian stroma (P <= 0.0006) and ovarian endosalpingiosis (P <= 0.01), ErbB4 in ovarian epithelium (P = 0.006), and CSF-1R in ovarian endosalpingiosis (P = 0.009).	Flutamide	0-9	colony stimulating factor 1 receptor	Homo sapiens	185-191
24950779-8	2014	Thus, our data suggest that a short 6-week exposure of flutamide reversed elevated levels of CSF-1 and ErbB4 (both of which we had previously found correlated with high risk status).	Flutamide	55-64	colony stimulating factor 1	Homo sapiens	93-98
24950779-8	2014	Thus, our data suggest that a short 6-week exposure of flutamide reversed elevated levels of CSF-1 and ErbB4 (both of which we had previously found correlated with high risk status).	Flutamide	55-64	erb-b2 receptor tyrosine kinase 4	Homo sapiens	103-108
24950779-9	2014	CSF-1 and ErbB4 in ovarian stroma led to a model with high predictive value for flutamide sensitivity.	Flutamide	80-89	colony stimulating factor 1	Homo sapiens	0-5
24950779-9	2014	CSF-1 and ErbB4 in ovarian stroma led to a model with high predictive value for flutamide sensitivity.	Flutamide	80-89	erb-b2 receptor tyrosine kinase 4	Homo sapiens	10-15
24950779-10	2014	The effect of flutamide on marker expression in ovarian endosalpingiosis, previously associated with BRCA carrier status, suggests that ovarian endosalpingiosis may be a latent precursor to pelvic serous cancers.	Flutamide	14-23	BRCA1 DNA repair associated	Homo sapiens	101-105
24737412-0	2014	KLF9, a transcription factor induced in flutamide-caused cell apoptosis, inhibits AKT activation and suppresses tumor growth of prostate cancer cells.	Flutamide	40-49	Kruppel like factor 9	Homo sapiens	0-4
24737412-6	2014	RESULTS: KLF9 was induced in a time-dependent manner in flutamide-caused apoptosis, and knockdown of KLF9 significantly decreased flutamide-induced growth inhibition and apoptosis in LNCaP cells.	Flutamide	130-139	Kruppel like factor 9	Homo sapiens	101-105
24737412-6	2014	RESULTS: KLF9 was induced in a time-dependent manner in flutamide-caused apoptosis, and knockdown of KLF9 significantly decreased flutamide-induced growth inhibition and apoptosis in LNCaP cells.	Flutamide	56-65	Kruppel like factor 9	Homo sapiens	9-13
24353261-3	2014	In this study we tested whether early postnatal and prepubertal exposure to anti-androgen flutamide altered the expression of adherens junction genes encoding E-cadherin (CDH1) and beta-catenin (CTNNB1) in adult pig epididymis and prostate.	Flutamide	90-99	catenin beta 1	Sus scrofa	181-193
24429677-8	2014	Furthermore, exposure to flutamide during late pregnancy downregulated steroidogenic enzymes (CYP11A1 and HSD3B) in pigs.	Flutamide	25-34	cytochrome P450 family 11 subfamily A member 1	Sus scrofa	94-101
24429677-8	2014	Furthermore, exposure to flutamide during late pregnancy downregulated steroidogenic enzymes (CYP11A1 and HSD3B) in pigs.	Flutamide	25-34	3 beta-hydroxysteroid dehydrogenase/Delta 5-->4-isomerase	Sus scrofa	106-111
25031707-6	2014	Although no variation in PC3 cells was identified, Egr1 responded to dihydrotestosterone and flutamide in the androgen receptor (AR)-transfected PC3 cells.	Flutamide	93-102	early growth response 1	Homo sapiens	51-55
25031707-6	2014	Although no variation in PC3 cells was identified, Egr1 responded to dihydrotestosterone and flutamide in the androgen receptor (AR)-transfected PC3 cells.	Flutamide	93-102	androgen receptor	Homo sapiens	110-127
25031707-6	2014	Although no variation in PC3 cells was identified, Egr1 responded to dihydrotestosterone and flutamide in the androgen receptor (AR)-transfected PC3 cells.	Flutamide	93-102	androgen receptor	Homo sapiens	129-131
24512496-8	2014	TNFalpha release in the fasting state was also measured in cultured MNCs exposed to androgens with or without flutamide preincubation.	Flutamide	110-119	tumor necrosis factor	Homo sapiens	0-8
24512496-12	2014	Preincubation with flutamide reduced the TNFalpha response by >= 60% across all T concentrations.	Flutamide	19-28	tumor necrosis factor	Homo sapiens	41-49
24615730-10	2014	T and PRL acted synergistically to increase NO production, which was abolished only when receptor antagonists flutamide and Delta1-9-G129R-hPRL were used together.	Flutamide	110-119	prolactin	Homo sapiens	6-9
24464802-7	2014	In a panel of 24 individual HLM samples, the indiplon hydrolase activities were significantly correlated with the hydrolase activities of flutamide, phenacetin, and rifampicin, which are known AADAC substrates.	Flutamide	138-147	oxysterol binding protein 2	Homo sapiens	28-31
24464802-7	2014	In a panel of 24 individual HLM samples, the indiplon hydrolase activities were significantly correlated with the hydrolase activities of flutamide, phenacetin, and rifampicin, which are known AADAC substrates.	Flutamide	138-147	arylacetamide deacetylase	Homo sapiens	193-198
24353261-0	2014	Postnatal exposure to flutamide affects CDH1 and CTNNB1 gene expression in adult pig epididymis and prostate and alters metabolism of testosterone.	Flutamide	22-31	cadherin 1	Sus scrofa	40-44
24353261-0	2014	Postnatal exposure to flutamide affects CDH1 and CTNNB1 gene expression in adult pig epididymis and prostate and alters metabolism of testosterone.	Flutamide	22-31	catenin beta 1	Sus scrofa	49-55
24353261-3	2014	In this study we tested whether early postnatal and prepubertal exposure to anti-androgen flutamide altered the expression of adherens junction genes encoding E-cadherin (CDH1) and beta-catenin (CTNNB1) in adult pig epididymis and prostate.	Flutamide	90-99	cadherin 1	Sus scrofa	159-169
24353261-3	2014	In this study we tested whether early postnatal and prepubertal exposure to anti-androgen flutamide altered the expression of adherens junction genes encoding E-cadherin (CDH1) and beta-catenin (CTNNB1) in adult pig epididymis and prostate.	Flutamide	90-99	catenin beta 1	Sus scrofa	195-201
24353261-3	2014	In this study we tested whether early postnatal and prepubertal exposure to anti-androgen flutamide altered the expression of adherens junction genes encoding E-cadherin (CDH1) and beta-catenin (CTNNB1) in adult pig epididymis and prostate.	Flutamide	90-99	cadherin 1	Sus scrofa	171-175
24353261-8	2014	In response to flutamide, CDH1 and CTNNB1 expressions were down-regulated along the epididymis, mostly in PD2 group (p < 0.001, p < 0.01).	Flutamide	15-24	cadherin 1	Sus scrofa	26-30
24353261-8	2014	In response to flutamide, CDH1 and CTNNB1 expressions were down-regulated along the epididymis, mostly in PD2 group (p < 0.001, p < 0.01).	Flutamide	15-24	catenin beta 1	Sus scrofa	35-41
24353261-9	2014	In the prostate, CDH1 mRNA and protein expressions were significantly down-regulated (p < 0.01), whereas CTNNB1 mRNA was slightly up-regulated in both flutamide-treated groups.	Flutamide	154-163	catenin beta 1	Sus scrofa	108-114
24353261-13	2014	Overall, flutamide administration resulted in suppression of androgen action in the epididymis and prostate leading to deregulation of CDH1 and CTNNB1 gene expressions which is probably caused by the alterations in the expression of ST5AR2 and CYP19A1 in both reproductive organs.	Flutamide	9-18	cadherin 1	Sus scrofa	135-139
24353261-13	2014	Overall, flutamide administration resulted in suppression of androgen action in the epididymis and prostate leading to deregulation of CDH1 and CTNNB1 gene expressions which is probably caused by the alterations in the expression of ST5AR2 and CYP19A1 in both reproductive organs.	Flutamide	9-18	catenin beta 1	Sus scrofa	144-150
24353261-13	2014	Overall, flutamide administration resulted in suppression of androgen action in the epididymis and prostate leading to deregulation of CDH1 and CTNNB1 gene expressions which is probably caused by the alterations in the expression of ST5AR2 and CYP19A1 in both reproductive organs.	Flutamide	9-18	steroid 5 alpha-reductase 2	Sus scrofa	233-239
24353261-13	2014	Overall, flutamide administration resulted in suppression of androgen action in the epididymis and prostate leading to deregulation of CDH1 and CTNNB1 gene expressions which is probably caused by the alterations in the expression of ST5AR2 and CYP19A1 in both reproductive organs.	Flutamide	9-18	cytochrome P450 family 19 subfamily A member 1	Sus scrofa	244-251
23340667-7	2013	Androgen receptor appears to mediate this effect as its antagonist flutamide reduced the dendritic spines of normal adult rats while causing a mild feedback surge of serum testosterone.	Flutamide	67-76	androgen receptor	Rattus norvegicus	0-17
23885104-5	2014	Phase-contrast image analysis demonstrated that DHT increases the shape index of decidualizing cells, which was reversed upon cotreatment with the AR antagonist flutamide.	Flutamide	161-170	androgen receptor	Homo sapiens	147-149
24125761-1	2014	Human arylacetamide deacetylase (AADAC) can hydrolyze clinical drugs such as flutamide, phenacetin, and rifamycins.	Flutamide	77-86	arylacetamide deacetylase	Homo sapiens	6-31
24125761-1	2014	Human arylacetamide deacetylase (AADAC) can hydrolyze clinical drugs such as flutamide, phenacetin, and rifamycins.	Flutamide	77-86	arylacetamide deacetylase	Homo sapiens	33-38
24055403-5	2013	The cytokine-induced upregulation was prevented by the pretreatment with flutamide, a specific antagonist for AR, but not by ICI 182,780, a specific antagonist for estrogen receptor, suggesting that the effects of testosterone are not mediated by estradiol, a testosterone metabolite.	Flutamide	73-82	androgen receptor	Rattus norvegicus	110-112
24248458-6	2014	Development of papillary processes concomitant with the induction of Bmp7 and Lef1 in the distal bone nodules by exposure to methyltestosterone was significantly suppressed by an antiandrogen, flutamide, in female medaka.	Flutamide	193-202	lymphoid enhancer-binding factor 1	Oryzias latipes	78-82
24303814-0	2014	Flutamide influences placental aldo-keto reductase family 1 member C1 (AKR1C1) expression in pigs.	Flutamide	0-9	aldo-keto reductase family 1 member C1	Sus scrofa	31-69
24303814-0	2014	Flutamide influences placental aldo-keto reductase family 1 member C1 (AKR1C1) expression in pigs.	Flutamide	0-9	aldo-keto reductase family 1 member C1	Sus scrofa	71-77
24303814-3	2014	The aim of the study was to determine whether the anti-androgen flutamide administered during late pregnancy (83-89 days of gestation) or before parturition (101-107 days of gestation) influences AKR1C1 expression in the porcine placenta.	Flutamide	64-73	aldo-keto reductase family 1 member C1	Sus scrofa	196-202
24303814-6	2014	Flutamide significantly increased AKR1C1 mRNA (p = 0.008) and protein (p = 0.019) expression only during the pre-parturient period in pigs.	Flutamide	0-9	aldo-keto reductase family 1 member C1	Sus scrofa	34-40
24103231-2	2014	The chemical name of 2-methyl-N-[4-nitro-3-(trifluoromethyl)phenyl]-propanamide is usually called as Flutamide (In the present study it is abbreviated as FLT) and is an important and efficacious drug in the treatment of anti-cancer resistant.	Flutamide	21-79	fms related receptor tyrosine kinase 1	Homo sapiens	154-157
24103231-2	2014	The chemical name of 2-methyl-N-[4-nitro-3-(trifluoromethyl)phenyl]-propanamide is usually called as Flutamide (In the present study it is abbreviated as FLT) and is an important and efficacious drug in the treatment of anti-cancer resistant.	Flutamide	101-110	fms related receptor tyrosine kinase 1	Homo sapiens	154-157
25011927-10	2014	Moreover, treatment of HepG2 cells with the androgen receptor antagonist flutamide in presence of endogenous ligands in the medium significantly down-regulated AHSG mRNA expression and fetuin-A protein abundance.	Flutamide	73-82	alpha 2-HS glycoprotein	Homo sapiens	160-164
25011927-10	2014	Moreover, treatment of HepG2 cells with the androgen receptor antagonist flutamide in presence of endogenous ligands in the medium significantly down-regulated AHSG mRNA expression and fetuin-A protein abundance.	Flutamide	73-82	alpha 2-HS glycoprotein	Homo sapiens	185-193
25916165-0	2014	Influence of the antiandrogen flutamide on connexin 43 (Cx43) gene and protein expression in the porcine placenta and uterus during pregnancy.	Flutamide	30-39	gap junction protein alpha 1	Sus scrofa	43-54
25916165-0	2014	Influence of the antiandrogen flutamide on connexin 43 (Cx43) gene and protein expression in the porcine placenta and uterus during pregnancy.	Flutamide	30-39	gap junction protein alpha 1	Sus scrofa	56-60
25916165-7	2014	Flutamide treatment caused fluctuations in Cx43 expression especially before parturition.	Flutamide	0-9	gap junction protein alpha 1	Sus scrofa	43-47
23869618-7	2013	These responses were blocked by the androgen receptor antagonist, flutamide (10 muM); the sarcoplasmic reticulum ATPase pump inhibitor, thapsigargin (1 muM); the inositol trisphosphate receptor inhibitor, 2-aminoethyldiphenyl borate (50 muM) and the PLC inhibitor, U-73122 (1 muM).	Flutamide	66-75	latexin	Homo sapiens	80-83
24341087-0	2013	[Expression of insulin-like factor 3 in the testis of flutamide-induced cryptorchidism mice and its significance].	Flutamide	54-63	insulin-like 3	Mus musculus	15-36
24341087-1	2013	OBJECTIVE: To study the changes in the mRNA expression of insulin-like factor 3 (INSL-3) in the testis of mouse models of flutamide-induced cryptorchidism.	Flutamide	122-131	insulin-like 3	Mus musculus	58-79
24341087-1	2013	OBJECTIVE: To study the changes in the mRNA expression of insulin-like factor 3 (INSL-3) in the testis of mouse models of flutamide-induced cryptorchidism.	Flutamide	122-131	insulin-like 3	Mus musculus	81-87
24341087-5	2013	The expression of INSL-3 mRNA was reduced with the increased dose of flutamide, not significantly changed in groups B and C (P > 0.05) but remarkably decreased in D and E as compared with A (P < 0.05).	Flutamide	69-78	insulin-like 3	Mus musculus	18-24
24341087-6	2013	CONCLUSION: Administration of flutamide to pregnant mice can induce unilateral cryptorchidism at 150 and 300 mg/kg and bilateral cryptorchidism at 500 and 700 mg/kg in their male offspring, which may be related with its reducing effect on the expression of INSL-3 in the testis of the mice.	Flutamide	30-39	insulin-like 3	Mus musculus	257-263
23895735-4	2013	Ten of 13 samples of source water exhibited detectable AR antagonistic potencies with AR antagonist equivalents (Ant-AR-EQs) ranging from <15.3 (detection limit) to 140 mug flutamide/L.	Flutamide	176-185	androgen receptor	Homo sapiens	55-57
23546600-11	2013	Androgen receptor antagonist, flutamide treatment prevents GFP/GRTH expression in Tg lines, demonstrating in vivo direct and indirect effects of endogenous androgen on LCs and GCs, respectively.	Flutamide	30-39	DEAD box helicase 25	Mus musculus	63-67
23801677-6	2013	Our data showed that DHT alone decreased UCN1 levels, which were attenuated in the presence of the androgen receptor (AR) antagonist flutamide.	Flutamide	133-142	androgen receptor	Homo sapiens	99-116
23801677-6	2013	Our data showed that DHT alone decreased UCN1 levels, which were attenuated in the presence of the androgen receptor (AR) antagonist flutamide.	Flutamide	133-142	androgen receptor	Homo sapiens	118-120
23759306-6	2013	AR knockdown by RNAi or treatment with flutamide (an AR antagonist) in SCs inhibited the recovery of BTB-associated protein expression after 43 C heat treatment for 30 min.	Flutamide	39-48	androgen receptor	Mus musculus	0-2
23546600-11	2013	Androgen receptor antagonist, flutamide treatment prevents GFP/GRTH expression in Tg lines, demonstrating in vivo direct and indirect effects of endogenous androgen on LCs and GCs, respectively.	Flutamide	30-39	androgen receptor	Mus musculus	0-17
23782943-6	2013	In experiment 2, we injected the AR antagonist, flutamide, into castrated male rats and compared neurogenesis levels in the dentate gyrus of DHT and oil-treated controls.	Flutamide	48-57	androgen receptor	Rattus norvegicus	33-35
23415714-6	2013	DHT treatment induced the expression of the genes for cyclooxyganase-2 (Cox-2 or prostaglandin endoperoxidase synthase 2) and the epidermal growth factor-like factor, amphiregulin (Areg), in the ovary, whereas their hCG-induced expression was suppressed by the AR antagonist flutamide.	Flutamide	275-284	amphiregulin	Mus musculus	167-179
23571006-10	2013	However, the ovaries from animals treated with flutamide on GD108 showed increased Cx43 expression.	Flutamide	47-56	gap junction protein alpha 1	Sus scrofa	83-87
23571006-11	2013	The changes of Cx43 and beta-catenin expression after prenatal flutamide treatment were confirmed at the mRNA level.	Flutamide	63-72	gap junction protein alpha 1	Sus scrofa	15-19
23571006-11	2013	The changes of Cx43 and beta-catenin expression after prenatal flutamide treatment were confirmed at the mRNA level.	Flutamide	63-72	catenin beta 1	Sus scrofa	24-36
23438977-16	2013	FTA is associated with increased VEGF levels, both in serum and vitreous.	Flutamide	0-3	vascular endothelial growth factor A	Homo sapiens	33-37
23571006-0	2013	In utero exposure to the anti-androgen flutamide influences connexin 43 and beta-catenin expression in porcine fetal gonads.	Flutamide	39-48	gap junction protein alpha 1	Sus scrofa	60-71
23571006-0	2013	In utero exposure to the anti-androgen flutamide influences connexin 43 and beta-catenin expression in porcine fetal gonads.	Flutamide	39-48	catenin beta 1	Sus scrofa	76-88
23571006-9	2013	Immunohistochemistry showed decreased Cx43 and beta-catenin expression in fetal gonads from flutamide-treated pigs compared with respective controls.	Flutamide	92-101	gap junction protein alpha 1	Sus scrofa	38-42
23571006-9	2013	Immunohistochemistry showed decreased Cx43 and beta-catenin expression in fetal gonads from flutamide-treated pigs compared with respective controls.	Flutamide	92-101	catenin beta 1	Sus scrofa	47-59
22843567-3	2013	We investigated the metabolic response of HepG2/C3a cells exposed to flutamide, an anticancer prodrug, and hydroxyflutamide (HF), its active metabolite, in a microfluidic biochip.	Flutamide	69-78	complement C3	Homo sapiens	48-51
22951468-1	2013	The aim of this study was to determine the immunolocalization and expression of the androgen receptor (AR) in the pig placenta and umbilical cord during pregnancy following exposure to flutamide, a non-steroidal antiandrogen, at its various stages.	Flutamide	185-194	androgen receptor	Sus scrofa	84-101
22951468-1	2013	The aim of this study was to determine the immunolocalization and expression of the androgen receptor (AR) in the pig placenta and umbilical cord during pregnancy following exposure to flutamide, a non-steroidal antiandrogen, at its various stages.	Flutamide	185-194	androgen receptor	Sus scrofa	103-105
22951468-10	2013	Flutamide could impact on the levels of the AR protein in the reproductive tracts during pregnancy in sows.	Flutamide	0-9	androgen receptor	Sus scrofa	44-46
23399021-12	2013	Ectopic expression of AR in hepatocytes suppressed hepcidin transcription; this effect was blocked dose-dependently by AR antagonist flutamide.	Flutamide	133-142	androgen receptor	Mus musculus	22-24
23399021-12	2013	Ectopic expression of AR in hepatocytes suppressed hepcidin transcription; this effect was blocked dose-dependently by AR antagonist flutamide.	Flutamide	133-142	hepcidin antimicrobial peptide	Mus musculus	51-59
23399021-12	2013	Ectopic expression of AR in hepatocytes suppressed hepcidin transcription; this effect was blocked dose-dependently by AR antagonist flutamide.	Flutamide	133-142	androgen receptor	Mus musculus	119-121
24002408-7	2013	Antiandrogens can be competitive antagonists of the androgen receptor (spironolactone, cyproterone acetate, flutamide) or inhibitors of 5-alpha reductase, which decrease the conversion of testosterone to the more potent androgen 5-alpha dihydrotestosterone (finasteride).	Flutamide	108-117	androgen receptor	Homo sapiens	52-69
23135684-0	2013	Androgen deprivation by flutamide modulates uPAR, MMP-9 expressions, lipid profile, and oxidative stress: amelioration by daidzein.	Flutamide	24-33	plasminogen activator, urokinase receptor	Homo sapiens	44-48
23135684-0	2013	Androgen deprivation by flutamide modulates uPAR, MMP-9 expressions, lipid profile, and oxidative stress: amelioration by daidzein.	Flutamide	24-33	matrix metallopeptidase 9	Homo sapiens	50-55
23043943-0	2012	Elevated level of 17beta-estradiol is associated with overexpression of FSHR, CYP19A1, and CTNNB1 genes in porcine ovarian follicles after prenatal and neonatal flutamide exposure.	Flutamide	161-170	follicle stimulating hormone receptor	Sus scrofa	72-76
22533969-3	2012	2012 John Wiley & Sons A/S Background and Objective:  In our previous study, we found that flutamide [an androgen receptor (AR) antagonist] inhibited the up-regulation of collagen induced by interleukin (IL)-1beta and/or nifedipine in gingival fibroblasts.	Flutamide	95-104	androgen receptor	Homo sapiens	109-126
22533969-3	2012	2012 John Wiley & Sons A/S Background and Objective:  In our previous study, we found that flutamide [an androgen receptor (AR) antagonist] inhibited the up-regulation of collagen induced by interleukin (IL)-1beta and/or nifedipine in gingival fibroblasts.	Flutamide	95-104	androgen receptor	Homo sapiens	128-130
22533969-3	2012	2012 John Wiley & Sons A/S Background and Objective:  In our previous study, we found that flutamide [an androgen receptor (AR) antagonist] inhibited the up-regulation of collagen induced by interleukin (IL)-1beta and/or nifedipine in gingival fibroblasts.	Flutamide	95-104	interleukin 1 beta	Homo sapiens	195-217
22935919-0	2012	Expression changes and regulation of AR and IGF-1 in PC3 prostate cancer cells treated with sexual hormones and flutamide.	Flutamide	112-121	insulin like growth factor 1	Homo sapiens	44-49
22935919-1	2012	The study aims to investigate the changes and regulation of androgen receptor and insulin-like growth factor-1 in the PC3 prostate cells treated with 5alpha-dihydrotestosterone, estrone, and flutamide.	Flutamide	191-200	androgen receptor	Homo sapiens	60-77
22935919-1	2012	The study aims to investigate the changes and regulation of androgen receptor and insulin-like growth factor-1 in the PC3 prostate cells treated with 5alpha-dihydrotestosterone, estrone, and flutamide.	Flutamide	191-200	proprotein convertase subtilisin/kexin type 1	Homo sapiens	118-121
22935919-2	2012	The PC3 cells were cultured and treated with 5alpha-dihydrotestosterone, estrone, and flutamide.	Flutamide	86-95	proprotein convertase subtilisin/kexin type 1	Homo sapiens	4-7
23043943-0	2012	Elevated level of 17beta-estradiol is associated with overexpression of FSHR, CYP19A1, and CTNNB1 genes in porcine ovarian follicles after prenatal and neonatal flutamide exposure.	Flutamide	161-170	cytochrome P450 family 19 subfamily A member 1	Sus scrofa	78-85
23043943-0	2012	Elevated level of 17beta-estradiol is associated with overexpression of FSHR, CYP19A1, and CTNNB1 genes in porcine ovarian follicles after prenatal and neonatal flutamide exposure.	Flutamide	161-170	catenin beta 1	Sus scrofa	91-97
23043943-8	2012	Real-time polymerase chain reaction analysis revealed significant upregulation of FSHR, CYP19A1, and CTNNB1 at the mRNA level after maternal (P < 0.001, P < 0.01, P < 0.05, respectively) and neonatal (P < 0.001, P < 0.001, P < 0.01, respectively) flutamide exposure.	Flutamide	265-274	follicle stimulating hormone receptor	Sus scrofa	82-86
23043943-8	2012	Real-time polymerase chain reaction analysis revealed significant upregulation of FSHR, CYP19A1, and CTNNB1 at the mRNA level after maternal (P < 0.001, P < 0.01, P < 0.05, respectively) and neonatal (P < 0.001, P < 0.001, P < 0.01, respectively) flutamide exposure.	Flutamide	265-274	cytochrome P450 family 19 subfamily A member 1	Sus scrofa	88-95
23043943-8	2012	Real-time polymerase chain reaction analysis revealed significant upregulation of FSHR, CYP19A1, and CTNNB1 at the mRNA level after maternal (P < 0.001, P < 0.01, P < 0.05, respectively) and neonatal (P < 0.001, P < 0.001, P < 0.01, respectively) flutamide exposure.	Flutamide	265-274	catenin beta 1	Sus scrofa	101-107
23043943-9	2012	The expression of FSHR protein was higher (P < 0.01) only after neonatal exposure to flutamide, whereas CYP19A1 and CTNNB1 proteins were upregulated in response to both prenatal (P < 0.01) and neonatal (P < 0.001) flutamide administration.	Flutamide	88-97	follicle stimulating hormone receptor	Sus scrofa	18-22
23043943-9	2012	The expression of FSHR protein was higher (P < 0.01) only after neonatal exposure to flutamide, whereas CYP19A1 and CTNNB1 proteins were upregulated in response to both prenatal (P < 0.01) and neonatal (P < 0.001) flutamide administration.	Flutamide	223-232	follicle stimulating hormone receptor	Sus scrofa	18-22
23130941-8	2012	DHT-treated LNCaP cells induced a significant upregulation of PCA3 expression, which was reversed by flutamide.	Flutamide	101-110	prostate cancer associated 3	Homo sapiens	62-66
22728893-6	2012	The hormonal effect was completely blocked by an androgen receptor antagonist (flutamide); meanwhile it wasn"t modified by the presence of an estrogen receptor antagonist (ICI182780).The possibility of intracellular estradiol synthesis was ruled out when no differences were found in estradiol measurements performed in culture incubation medium from control and testosterone treated cells.	Flutamide	79-88	androgen receptor	Rattus norvegicus	49-66
23023563-1	2012	Previously available androgen receptor (AR) antagonists (bicalutamide, flutamide, and nilutamide) have limited activity against AR in prostate cancers that relapse after castration [castration resistant prostate cancer (CRPC)].	Flutamide	71-80	androgen receptor	Homo sapiens	21-38
23023563-1	2012	Previously available androgen receptor (AR) antagonists (bicalutamide, flutamide, and nilutamide) have limited activity against AR in prostate cancers that relapse after castration [castration resistant prostate cancer (CRPC)].	Flutamide	71-80	androgen receptor	Homo sapiens	40-42
21735453-0	2012	Involvement of Th2 cytokines in the mouse model of flutamide-induced acute liver injury.	Flutamide	51-60	heart and neural crest derivatives expressed 2	Mus musculus	15-18
21735453-6	2012	The biomarker for oxidative stress was not changed, but Th2-dominant immune-related factors, such as interleukin (IL)-4, IL-5, STAT6 and GATA-binding protein (GATA)-3, were induced in flutamide-administered mice.	Flutamide	184-193	heart and neural crest derivatives expressed 2	Mus musculus	56-59
21735453-6	2012	The biomarker for oxidative stress was not changed, but Th2-dominant immune-related factors, such as interleukin (IL)-4, IL-5, STAT6 and GATA-binding protein (GATA)-3, were induced in flutamide-administered mice.	Flutamide	184-193	GATA binding protein 3	Mus musculus	137-166
21735453-10	2012	Coadministration of DK-PGD2 and flutamide resulted in a significant increase in alanine aminotransferase and a remarkable increase of macrophage inflammatory protein-2.	Flutamide	32-41	chemokine (C-X-C motif) ligand 2	Mus musculus	134-167
21735453-11	2012	In conclusion, we demonstrated that flutamide-induced acute liver injury is mediated by Th2-dominant immune responses in mice.	Flutamide	36-45	heart and neural crest derivatives expressed 2	Mus musculus	88-91
22879383-1	2012	Leflunomide, flutamide, nimodipine, mexiletine, sulindac, tranilast, 4-hydroxytamoxifen, and omeprazole are pharmaceuticals previously characterized as aryl hydrocarbon receptor (AHR) agonists in various cell lines and animal models.	Flutamide	13-22	aryl hydrocarbon receptor	Homo sapiens	152-177
22180287-13	2012	CONCLUSIONS: The use of the finasteride/flutamide combination is feasible, and results in PSA declines of >=80% in 96% of patients with serologic progression after definitive local therapy.	Flutamide	40-49	kallikrein related peptidase 3	Homo sapiens	90-93
22807478-9	2012	Moreover, the increase of doublecortin or 5"-bromo-2"deoxyuridine/NeuN-positive cells in ORX rats was blocked by s.c. flutamide, an AR antagonist.	Flutamide	118-127	doublecortin	Rattus norvegicus	26-38
22807478-9	2012	Moreover, the increase of doublecortin or 5"-bromo-2"deoxyuridine/NeuN-positive cells in ORX rats was blocked by s.c. flutamide, an AR antagonist.	Flutamide	118-127	RNA binding fox-1 homolog 3	Rattus norvegicus	66-70
22807478-9	2012	Moreover, the increase of doublecortin or 5"-bromo-2"deoxyuridine/NeuN-positive cells in ORX rats was blocked by s.c. flutamide, an AR antagonist.	Flutamide	118-127	androgen receptor	Rattus norvegicus	132-134
22402471-6	2012	In addition, the animals received the AR antagonist flutamide or placebo, respectively.	Flutamide	52-61	androgen receptor	Rattus norvegicus	38-40
21876548-7	2012	Addition of the androgen receptor antagonist Flutamide (1 muM) to the media reversed the negative effect of testosterone and DHT by returning AMPK phosphorylation levels to those of basal.	Flutamide	45-54	latexin	Homo sapiens	58-61
22546276-6	2012	Testosterone and flutamide (as an androgen receptor blocker) were applied once, intramuscularly, at a dose of 5mg/kg.	Flutamide	17-26	androgen receptor	Rattus norvegicus	34-51
22546276-15	2012	This effect of increased testosterone was mediated via the androgen receptor as flutamide blocked the anxiolytic effect of exogenous testosterone.	Flutamide	80-89	androgen receptor	Rattus norvegicus	59-76
22402471-13	2012	Flutamide by itself exerts influence over aldosterone in the absence of gonadal steroid replacement suggesting AR involvement in renal sodium handling.	Flutamide	0-9	androgen receptor	Rattus norvegicus	111-113
22415931-1	2012	Human arylacetamide deacetylase (AADAC) is responsible for the hydrolysis of clinically used drugs such as flutamide, phenacetin, and rifamycins.	Flutamide	107-116	arylacetamide deacetylase	Homo sapiens	6-31
22415931-1	2012	Human arylacetamide deacetylase (AADAC) is responsible for the hydrolysis of clinically used drugs such as flutamide, phenacetin, and rifamycins.	Flutamide	107-116	arylacetamide deacetylase	Homo sapiens	33-38
22446520-0	2012	Contributions of arylacetamide deacetylase and carboxylesterase 2 to flutamide hydrolysis in human liver.	Flutamide	69-78	arylacetamide deacetylase	Homo sapiens	17-42
22415931-8	2012	COS7 cells expressing AADAC.1 (wild-type) exhibited flutamide, phenacetin, and rifampicin hydrolase activities with intrinsic clearance (CLint) values of 1.31 +- 0.06, 1.00 +- 0.02, and 0.39 +- 0.02 mul x min(-1) x unit(-1), respectively.	Flutamide	52-61	arylacetamide deacetylase	Homo sapiens	22-27
22446520-0	2012	Contributions of arylacetamide deacetylase and carboxylesterase 2 to flutamide hydrolysis in human liver.	Flutamide	69-78	carboxylesterase 2	Homo sapiens	47-65
22566500-7	2012	Flutamide (androgen receptor antagonist) and actinomycin D (gene transcription inhibitor) diminished ROS production (60 minutes).	Flutamide	0-9	androgen receptor	Rattus norvegicus	11-28
22446520-7	2012	In the present study, we found that recombinant carboxylesterase (CES) 2 could hydrolyze flutamide at low concentrations of flutamide.	Flutamide	89-98	carboxylesterase 2	Homo sapiens	66-72
22446520-7	2012	In the present study, we found that recombinant carboxylesterase (CES) 2 could hydrolyze flutamide at low concentrations of flutamide.	Flutamide	124-133	carboxylesterase 2	Homo sapiens	66-72
22446520-8	2012	In the inhibition assay, the flutamide hydrolase activities at a flutamide concentration of 5 muM in human liver and jejunum microsomes were strongly inhibited by a selective CES2 inhibitor, 10 muM loperamide, with the residual activities of 22.9 +- 3.5 and 18.6 +- 0.7%, respectively.	Flutamide	29-38	latexin	Homo sapiens	94-97
22446520-8	2012	In the inhibition assay, the flutamide hydrolase activities at a flutamide concentration of 5 muM in human liver and jejunum microsomes were strongly inhibited by a selective CES2 inhibitor, 10 muM loperamide, with the residual activities of 22.9 +- 3.5 and 18.6 +- 0.7%, respectively.	Flutamide	29-38	carboxylesterase 2	Homo sapiens	175-179
22446520-8	2012	In the inhibition assay, the flutamide hydrolase activities at a flutamide concentration of 5 muM in human liver and jejunum microsomes were strongly inhibited by a selective CES2 inhibitor, 10 muM loperamide, with the residual activities of 22.9 +- 3.5 and 18.6 +- 0.7%, respectively.	Flutamide	29-38	latexin	Homo sapiens	194-197
22446520-9	2012	These results suggest that CES2 is also involved in the flutamide hydrolysis in human tissues.	Flutamide	56-65	carboxylesterase 2	Homo sapiens	27-31
22446520-10	2012	Using six individual human livers, the contributions of AADAC and CES2 to flutamide hydrolysis were estimated by using the relative activity factor.	Flutamide	74-83	arylacetamide deacetylase	Homo sapiens	56-61
22446520-10	2012	Using six individual human livers, the contributions of AADAC and CES2 to flutamide hydrolysis were estimated by using the relative activity factor.	Flutamide	74-83	carboxylesterase 2	Homo sapiens	66-70
22446520-11	2012	The relative contribution of CES2 was approximately 75 to 99% at the concentration of 5 muM flutamide.	Flutamide	92-101	carboxylesterase 2	Homo sapiens	29-33
22446520-11	2012	The relative contribution of CES2 was approximately 75 to 99% at the concentration of 5 muM flutamide.	Flutamide	92-101	latexin	Homo sapiens	88-91
22446520-12	2012	In contrast, the relative contribution of AADAC increased in parallel with the concentration of flutamide.	Flutamide	96-105	arylacetamide deacetylase	Homo sapiens	42-47
22446520-13	2012	Thus, CES2, rather than AADAC, largely contributed to the flutamide hydrolysis in clinical therapeutics.	Flutamide	58-67	carboxylesterase 2	Homo sapiens	6-10
22566500-9	2012	Flutamide, actinomycin D, and cycloheximide (protein synthesis inhibitor) diminished testosterone effects on p47phox.	Flutamide	0-9	neutrophil cytosolic factor 1	Rattus norvegicus	109-116
22525094-10	2012	The percentage of apoptotic granulosa cells detected using TUNEL assay significantly decreased (p<0.01) after flutamide administration, that paralleled with down-regulation (p<0.01) of caspase-3 protein expression.	Flutamide	113-122	caspase 3	Sus scrofa	191-200
21812788-4	2012	Therefore, the purpose of this study was to analyse whether foetal and neonatal exposure to flutamide affects the expression and distribution of ZO-1, occludin, beta-catenin, and N-cadherin in testes of adult pigs.	Flutamide	92-101	zonula occludens 1	Sus scrofa	145-149
21812788-4	2012	Therefore, the purpose of this study was to analyse whether foetal and neonatal exposure to flutamide affects the expression and distribution of ZO-1, occludin, beta-catenin, and N-cadherin in testes of adult pigs.	Flutamide	92-101	occludin	Sus scrofa	151-159
21812788-4	2012	Therefore, the purpose of this study was to analyse whether foetal and neonatal exposure to flutamide affects the expression and distribution of ZO-1, occludin, beta-catenin, and N-cadherin in testes of adult pigs.	Flutamide	92-101	catenin beta 1	Sus scrofa	161-173
21812788-7	2012	In the testes of all flutamide-exposed boars, expressions of ZO-1, N-cadherin and beta-catenin were significantly decreased at mRNA and protein level, whereas expression of occludin was unchanged when compared with the controls.	Flutamide	21-30	zonula occludens 1	Sus scrofa	61-65
21812788-7	2012	In the testes of all flutamide-exposed boars, expressions of ZO-1, N-cadherin and beta-catenin were significantly decreased at mRNA and protein level, whereas expression of occludin was unchanged when compared with the controls.	Flutamide	21-30	catenin beta 1	Sus scrofa	82-94
21812788-7	2012	In the testes of all flutamide-exposed boars, expressions of ZO-1, N-cadherin and beta-catenin were significantly decreased at mRNA and protein level, whereas expression of occludin was unchanged when compared with the controls.	Flutamide	21-30	occludin	Sus scrofa	173-181
21812788-10	2012	Taken together, these results demonstrate that blockade of androgen action by flutamide during both gestational and neonatal periods affects the expression of ZO-1, N-cadherin and beta-catenin in adult pig testes.	Flutamide	78-87	zonula occludens 1	Sus scrofa	159-163
21812788-10	2012	Taken together, these results demonstrate that blockade of androgen action by flutamide during both gestational and neonatal periods affects the expression of ZO-1, N-cadherin and beta-catenin in adult pig testes.	Flutamide	78-87	catenin beta 1	Sus scrofa	180-192
22177695-1	2012	In this study, flutamide, an androgen receptor antagonist, was used as a tool to better understand the role of androgen receptor signaling and androgen signaling disruption during fetal and neonatal periods on porcine Leydig cell development and function.	Flutamide	15-24	androgen receptor	Sus scrofa	29-46
22405892-3	2012	In this paper, we showed that the expression of seladin-1 was significantly increased by testosterone at all concentrations tested at the protein and mRNA levels in C6 cells, the selective AR antagonist flutamide obviously inhibited the effect in a concentration-dependent manner.	Flutamide	203-212	24-dehydrocholesterol reductase	Mus musculus	48-57
22207054-1	2012	Human arylacetamide deacetylase (AADAC) is a major esterase responsible for the hydrolysis of clinical drugs such as flutamide, phenacetin, and rifampicin.	Flutamide	117-126	arylacetamide deacetylase	Homo sapiens	6-31
22207054-1	2012	Human arylacetamide deacetylase (AADAC) is a major esterase responsible for the hydrolysis of clinical drugs such as flutamide, phenacetin, and rifampicin.	Flutamide	117-126	arylacetamide deacetylase	Homo sapiens	33-38
22177695-1	2012	In this study, flutamide, an androgen receptor antagonist, was used as a tool to better understand the role of androgen receptor signaling and androgen signaling disruption during fetal and neonatal periods on porcine Leydig cell development and function.	Flutamide	15-24	androgen receptor	Sus scrofa	111-128
22813719-5	2012	Arylacetamide deacetylase (AADAC) is involved in the hydrolysis of flutamide, phenacetin, and rifamycins.	Flutamide	67-76	arylacetamide deacetylase	Homo sapiens	0-25
22309306-6	2012	SGK1-SD-enhanced cell motility was inhibited by activation of membrane androgen-binding sites (mAR) via testosterone-conjugates in both cell lines, whereas intracellular androgen receptor (iAR)-silencing and flutamide treatment revealed that these effects were clearly independent of the interaction of SGK1 with the classical androgen receptors (iAR).	Flutamide	208-217	serum/glucocorticoid regulated kinase 1	Homo sapiens	0-4
22234368-10	2012	Pretreatment with the androgen receptor (AR) inhibitor flutamide, but not the estrogen receptor inhibitor fulvestrant, abolished these effects.	Flutamide	55-64	androgen receptor	Rattus norvegicus	22-39
22234368-10	2012	Pretreatment with the androgen receptor (AR) inhibitor flutamide, but not the estrogen receptor inhibitor fulvestrant, abolished these effects.	Flutamide	55-64	androgen receptor	Rattus norvegicus	41-43
22076107-2	2012	Some CYP1A inducers are known to exert hepatocellular tumor-promoting activities in rodents, and reactive oxygen species (ROS) produced by CYP1A1 induction via a metabolism of FLU is probably involved in the liver tumor promotion.	Flutamide	176-179	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	139-145
22076107-7	2012	Immunohistochemically, the number and area of glutathione S-transferase placental form (GST-P)-positive foci significantly increased in the liver of rats given 0.2% FLU as compared with the control.	Flutamide	165-168	glutathione S-transferase pi 1	Rattus norvegicus	46-93
22076107-10	2012	The results of microarray and real-time RT-PCR revealed that phase 1 drug-metabolizing enzymes such as CYP1A1, Ugt1a61 and Nqo1 and phase II drug-metabolizing enzymes such as Yc2, Akr1b7, Akr1b8, Akr1b10, Aldh1a1, Gpx2 and Me1 were up-regulated in rats treated with FLU.	Flutamide	266-269	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	103-109
22076107-10	2012	The results of microarray and real-time RT-PCR revealed that phase 1 drug-metabolizing enzymes such as CYP1A1, Ugt1a61 and Nqo1 and phase II drug-metabolizing enzymes such as Yc2, Akr1b7, Akr1b8, Akr1b10, Aldh1a1, Gpx2 and Me1 were up-regulated in rats treated with FLU.	Flutamide	266-269	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	123-127
22076107-10	2012	The results of microarray and real-time RT-PCR revealed that phase 1 drug-metabolizing enzymes such as CYP1A1, Ugt1a61 and Nqo1 and phase II drug-metabolizing enzymes such as Yc2, Akr1b7, Akr1b8, Akr1b10, Aldh1a1, Gpx2 and Me1 were up-regulated in rats treated with FLU.	Flutamide	266-269	aldo-keto reductase family 1, member B7	Rattus norvegicus	180-186
22076107-11	2012	In addition, the MAPK pathway family-related genes such as Prkcalpha, Mek1, Rafb, Myc, Mek2, Raf1 and Egfr were also up-regulated in FLU-treated groups.	Flutamide	133-136	mitogen activated protein kinase kinase 1	Rattus norvegicus	70-74
22076107-11	2012	In addition, the MAPK pathway family-related genes such as Prkcalpha, Mek1, Rafb, Myc, Mek2, Raf1 and Egfr were also up-regulated in FLU-treated groups.	Flutamide	133-136	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	82-85
22076107-11	2012	In addition, the MAPK pathway family-related genes such as Prkcalpha, Mek1, Rafb, Myc, Mek2, Raf1 and Egfr were also up-regulated in FLU-treated groups.	Flutamide	133-136	mitogen activated protein kinase kinase 2	Rattus norvegicus	87-91
22076107-11	2012	In addition, the MAPK pathway family-related genes such as Prkcalpha, Mek1, Rafb, Myc, Mek2, Raf1 and Egfr were also up-regulated in FLU-treated groups.	Flutamide	133-136	Raf-1 proto-oncogene, serine/threonine kinase	Rattus norvegicus	93-97
22076107-11	2012	In addition, the MAPK pathway family-related genes such as Prkcalpha, Mek1, Rafb, Myc, Mek2, Raf1 and Egfr were also up-regulated in FLU-treated groups.	Flutamide	133-136	epidermal growth factor receptor	Rattus norvegicus	102-106
22219300-6	2012	Simultaneous treatment with testosterone, H(2)O(2), and the androgen receptor (AR) antagonist, flutamide, reduces the effects of the hormone, pointing to a possible participation of the AR in the antiapoptotic effect.	Flutamide	95-104	androgen receptor	Mus musculus	60-77
22219300-6	2012	Simultaneous treatment with testosterone, H(2)O(2), and the androgen receptor (AR) antagonist, flutamide, reduces the effects of the hormone, pointing to a possible participation of the AR in the antiapoptotic effect.	Flutamide	95-104	androgen receptor	Mus musculus	79-81
22219300-6	2012	Simultaneous treatment with testosterone, H(2)O(2), and the androgen receptor (AR) antagonist, flutamide, reduces the effects of the hormone, pointing to a possible participation of the AR in the antiapoptotic effect.	Flutamide	95-104	androgen receptor	Mus musculus	186-188
22813719-6	2012	AADAC is associated with adverse drug reactions because the hydrolytic metabolites of flutamide and phenacetin appear to be associated with hepatotoxicity and nephrotoxicity/hematotoxicity, respectively.	Flutamide	86-95	arylacetamide deacetylase	Homo sapiens	0-5
22813719-5	2012	Arylacetamide deacetylase (AADAC) is involved in the hydrolysis of flutamide, phenacetin, and rifamycins.	Flutamide	67-76	arylacetamide deacetylase	Homo sapiens	27-32
22661176-1	2012	BACKGROUND: It has previously been speculated that the androgen receptor antagonist flutamide produces behavioral effects that are not mediated by androgen receptors.	Flutamide	84-93	androgen receptor	Rattus norvegicus	55-72
22428303-0	2012	Prenatal exposure to antiandrogen flutamide affects androgen receptor (AR) expression in postnatal ovarian development in pig.	Flutamide	34-43	androgen receptor	Sus scrofa	52-69
22428303-0	2012	Prenatal exposure to antiandrogen flutamide affects androgen receptor (AR) expression in postnatal ovarian development in pig.	Flutamide	34-43	androgen receptor	Sus scrofa	71-73
22428303-7	2012	In adult animals, the immunoexpression of AR slightly decreased in antral follicles independently on the day of flutamide treatment.	Flutamide	112-121	androgen receptor	Sus scrofa	42-44
22276587-5	2012	Daily topical application of androgen receptor antagonist, flutamide, resulted in improved gap closure similar to orchiectomized controls and faster than orchidectomized mice treated with topical testosterone.	Flutamide	59-68	androgen receptor	Mus musculus	29-46
23284699-6	2012	In T-treated zebra finches, the anti-androgen flutamide blunted PV and IGF-I expression.	Flutamide	46-55	LOC108643395	Manacus vitellinus	71-76
21457361-0	2011	Differential expression of connexin 43 in adult pig testes during normal spermatogenic cycle and after flutamide treatment.	Flutamide	103-112	gap junction protein alpha 1	Sus scrofa	27-38
22009729-6	2011	Flutamide prevented the T-induced decrease in Cyp11a1 mRNA at d 90 but not the Cyp19 and 5alpha-reductase increase in d 65 ovaries.	Flutamide	0-9	cytochrome P450 family 11 subfamily A member 1	Homo sapiens	46-53
21748440-4	2011	MATERIAL AND METHODS: Prostate cancer cells were continuously treated with competitive androgen receptor inhibitor hydroxyflutamide for 1.5 years, which yielded an flutamide-insensitive LNCaP subline, LNCaP-flu, as confirmed by MTT assays, flow cytometry, and electron microscopy.	Flutamide	122-131	androgen receptor	Homo sapiens	87-104
21903763-14	2011	Testosterone increased 17beta-HSD3 expression and proliferation in NRICC that was blocked by flutamide and antitestosterone antibody.	Flutamide	93-102	hydroxysteroid (17-beta) dehydrogenase 3	Rattus norvegicus	23-34
21457361-2	2011	Thus, we asked whether androgen withdrawal caused by prenatal (GD20, GD80) or neonatal (PD2) exposure to an anti-androgen flutamide alters Cx43 gene expression and may induce delayed effects on morphology and function of adult pig testes.	Flutamide	122-131	gap junction protein alpha 1	Sus scrofa	139-143
21457361-9	2011	Significantly, lower Cx43 expression was found when flutamide was administered neonatally, which has coincided with severe disruption of spermatogenesis.	Flutamide	52-61	gap junction protein alpha 1	Sus scrofa	21-25
21457361-10	2011	Our data suggest that neonatal exposure to flutamide induces long-term effects on the spermatogenic capacity of the pig testis through alterations of Cx43-mediated intercellular communication and permanent alteration of both Sertoli and Leydig cell functions.	Flutamide	43-52	gap junction protein alpha 1	Sus scrofa	150-154
21965742-0	2011	Combination of resveratrol and antiandrogen flutamide has synergistic effect on androgen receptor inhibition in prostate cancer cells.	Flutamide	44-53	androgen receptor	Homo sapiens	80-97
21965742-8	2011	The combination of resveratrol with flutamide had a synergistic effect on down-regulation of AR.	Flutamide	36-45	androgen receptor	Homo sapiens	93-95
21203749-7	2011	In parallel, I3C, FLU, and BNF markedly increased mRNA levels of Cyp1a1 (50-, 23-, 299-fold) and antioxidant/detoxifying enzymes such as Gpx2 and Nqo1 as shown by real-time reverse transcription-polymerase chain reaction analysis.	Flutamide	18-21	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	65-71
21846805-5	2011	In contrast, inhibition of AR signaling with flutamide from midpuberty had no effect on the mammary gland, but flutamide treatment from 12-21 wk increased ductal branching (P = 0.004) and proliferation (P = 0.03) of breast epithelial cells.	Flutamide	45-54	androgen receptor	Mus musculus	27-29
21839661-6	2011	The non-steroidal androgen-receptor antagonist flutamide reversed DHT-induced inhibition of CGRP release.	Flutamide	47-56	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	92-96
20598360-0	2011	Immunohistochemical studies on the proliferative marker Ki-67 and estrogen receptor alpha (ERalpha) in the uterus of neonatal and immature pigs following exposure to flutamide.	Flutamide	166-175	estrogen receptor 1	Sus scrofa	66-89
20598360-0	2011	Immunohistochemical studies on the proliferative marker Ki-67 and estrogen receptor alpha (ERalpha) in the uterus of neonatal and immature pigs following exposure to flutamide.	Flutamide	166-175	estrogen receptor 1	Sus scrofa	91-98
20598360-3	2011	Therefore, the objective of the study was to determine whether the effects of maternal or neonatal administration of the anti-androgen, flutamide, could entail changes in the presence of ERalpha and proliferation of uterine cells in neonatal and three-month-old pigs.	Flutamide	136-145	estrogen receptor 1	Sus scrofa	187-194
20598360-4	2011	Following prenatal flutamide exposure, morphological differences and the acceleration of uterus differentiation marked by ERalpha expression in epithelial crypts were observed in the neonatal piglets.	Flutamide	19-28	estrogen receptor 1	Sus scrofa	122-129
20598360-6	2011	The neonatal administration of flutamide caused a significant decrease in the proliferation of the surface epithelium and diminished intensity of ERalpha staining in the stromal cells of the uterus of three-month-old pigs, which paralleled decreased estrogen levels in these animals.	Flutamide	31-40	estrogen receptor 1	Sus scrofa	146-153
20598360-8	2011	Moreover, in three-month-old pigs, flutamide application during the neonatal period decreased surface epithelium proliferation and stromal ERalpha expression, which confirmed the importance of epithelial-stromal interactions in the adenogenesis.	Flutamide	35-44	estrogen receptor 1	Sus scrofa	139-146
21203749-7	2011	In parallel, I3C, FLU, and BNF markedly increased mRNA levels of Cyp1a1 (50-, 23-, 299-fold) and antioxidant/detoxifying enzymes such as Gpx2 and Nqo1 as shown by real-time reverse transcription-polymerase chain reaction analysis.	Flutamide	18-21	glutathione peroxidase 2	Rattus norvegicus	137-141
21203749-7	2011	In parallel, I3C, FLU, and BNF markedly increased mRNA levels of Cyp1a1 (50-, 23-, 299-fold) and antioxidant/detoxifying enzymes such as Gpx2 and Nqo1 as shown by real-time reverse transcription-polymerase chain reaction analysis.	Flutamide	18-21	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	146-150
22007488-0	2011	[The regulation of T3 on maldeveloped gonocyte (Go) and expression of NCAM in flutamide-induced cryptorchidism rat].	Flutamide	78-87	neural cell adhesion molecule 1	Rattus norvegicus	70-74
22007488-1	2011	OBJECTIVE: To investigate the regulation of T3 on the maldeveloped gonocytes (Go) and the expression of NCAM in Flutamide-induced cryptorchidism SD rat.	Flutamide	112-121	neural cell adhesion molecule 1	Rattus norvegicus	104-108
21457548-6	2011	METHODS: We examined a synergy between the AR inhibitor flutamide and the MEK inhibitor CI-1040 in the molecular apocrine cell lines MDA-MB-453, HCC-1954 and HCC-202 using MTT cell viability and annexin V apoptosis assays.	Flutamide	56-65	androgen receptor	Homo sapiens	43-45
21540358-5	2011	Moreover, the transfection of siRNA for nuclear factor erythroid 2-related factor 2 (Nrf2) to decrease the cellular expression level of Nrf2 exacerbated the cytotoxicity of some drugs (troglitazone, flutamide, acetaminophen, clozapine, terbinafine, and desipramine), suggesting that the genes regulated by Nrf2 are associated with the detoxification of the cytotoxicities mediated by CYP3A4.	Flutamide	199-208	NFE2 like bZIP transcription factor 2	Homo sapiens	40-83
21540358-5	2011	Moreover, the transfection of siRNA for nuclear factor erythroid 2-related factor 2 (Nrf2) to decrease the cellular expression level of Nrf2 exacerbated the cytotoxicity of some drugs (troglitazone, flutamide, acetaminophen, clozapine, terbinafine, and desipramine), suggesting that the genes regulated by Nrf2 are associated with the detoxification of the cytotoxicities mediated by CYP3A4.	Flutamide	199-208	NFE2 like bZIP transcription factor 2	Homo sapiens	85-89
21540358-5	2011	Moreover, the transfection of siRNA for nuclear factor erythroid 2-related factor 2 (Nrf2) to decrease the cellular expression level of Nrf2 exacerbated the cytotoxicity of some drugs (troglitazone, flutamide, acetaminophen, clozapine, terbinafine, and desipramine), suggesting that the genes regulated by Nrf2 are associated with the detoxification of the cytotoxicities mediated by CYP3A4.	Flutamide	199-208	NFE2 like bZIP transcription factor 2	Homo sapiens	136-140
21540358-5	2011	Moreover, the transfection of siRNA for nuclear factor erythroid 2-related factor 2 (Nrf2) to decrease the cellular expression level of Nrf2 exacerbated the cytotoxicity of some drugs (troglitazone, flutamide, acetaminophen, clozapine, terbinafine, and desipramine), suggesting that the genes regulated by Nrf2 are associated with the detoxification of the cytotoxicities mediated by CYP3A4.	Flutamide	199-208	NFE2 like bZIP transcription factor 2	Homo sapiens	136-140
21521268-9	2011	Co-incubation with flutamide blunted OCN production.	Flutamide	19-28	bone gamma-carboxyglutamate protein	Homo sapiens	37-40
20642491-0	2011	The expression of FSH receptor (FSHR) in the neonatal porcine ovary and its regulation by flutamide.	Flutamide	90-99	follicle stimulating hormone receptor	Sus scrofa	18-30
20642491-0	2011	The expression of FSH receptor (FSHR) in the neonatal porcine ovary and its regulation by flutamide.	Flutamide	90-99	follicle stimulating hormone receptor	Sus scrofa	32-36
20642491-4	2011	The FSHR mRNA expression was significantly decreased after flutamide administration.	Flutamide	59-68	follicle stimulating hormone receptor	Sus scrofa	4-8
20642491-6	2011	Immunohistochemistry showed the positive immunostaining for FSHR in the oocytes, granulosa cells of primary follicles and the surface epithelium of the ovaries from both control and flutamide-treated pigs.	Flutamide	182-191	follicle stimulating hormone receptor	Sus scrofa	60-64
20642491-10	2011	Furthermore, the regulation of FSHR mRNA and protein expression in neonatal porcine ovaries after maternal exposure to flutamide confirms that androgens play a crucial role in porcine folliculogenesis at the early stages.	Flutamide	119-128	follicle stimulating hormone receptor	Sus scrofa	31-35
21456065-10	2011	Administration of flutamide decreased SepP mRNA levels whereas dihydrotestosterone or synthetic androgens induced SepP expression, indicating the importance of androgens for SepP expression.	Flutamide	18-27	selenoprotein P	Mus musculus	38-42
21605098-0	2011	Treatment of female pattern hair loss with the androgen receptor antagonist flutamide.	Flutamide	76-85	androgen receptor	Homo sapiens	47-64
21605098-4	2011	We report a woman whose hair loss progressed while using spironolactone and topical minoxidil in combination, but reversed with flutamide, a potent androgen receptor antagonist.	Flutamide	128-137	androgen receptor	Homo sapiens	148-165
21485540-7	2011	Immunohistochemistry showed the expression of NCAM on the membrane of the remaining Gos, and RT-PCR revealed significantly up-regulated expression of NCAM mRNA in the Flu-induced testes on PD 10 and 20 as compared with the controls (P < 0.05).	Flutamide	167-170	neural cell adhesion molecule 1	Rattus norvegicus	150-154
21111724-11	2011	Flutamide (10 muM), unexpectedly, also strongly increased nuclear beta-catenin accumulation.	Flutamide	0-9	latexin	Homo sapiens	14-17
21281786-7	2011	EPHX2 mRNA correlated with AR in primary prostate cancers, and its inhibition in vitro reduced AR signaling and potentiated the effect of antiandrogen flutamide in cultured prostate cancer cells.	Flutamide	151-160	epoxide hydrolase 2	Homo sapiens	0-5
21342526-3	2011	Thus, a question arised whether prenatal or postnatal exposure to an anti-androgen flutamide alters the expression of gap junction protein - connexin43 (Cx43) and androgen receptor (AR) expression in the caput, corpus and cauda epididymis and leads to delayed effects on morphology and function of adult pig epididymis.	Flutamide	83-92	gap junction protein alpha 1	Sus scrofa	141-151
21342526-3	2011	Thus, a question arised whether prenatal or postnatal exposure to an anti-androgen flutamide alters the expression of gap junction protein - connexin43 (Cx43) and androgen receptor (AR) expression in the caput, corpus and cauda epididymis and leads to delayed effects on morphology and function of adult pig epididymis.	Flutamide	83-92	gap junction protein alpha 1	Sus scrofa	153-157
21342526-3	2011	Thus, a question arised whether prenatal or postnatal exposure to an anti-androgen flutamide alters the expression of gap junction protein - connexin43 (Cx43) and androgen receptor (AR) expression in the caput, corpus and cauda epididymis and leads to delayed effects on morphology and function of adult pig epididymis.	Flutamide	83-92	androgen receptor	Sus scrofa	163-180
21342526-3	2011	Thus, a question arised whether prenatal or postnatal exposure to an anti-androgen flutamide alters the expression of gap junction protein - connexin43 (Cx43) and androgen receptor (AR) expression in the caput, corpus and cauda epididymis and leads to delayed effects on morphology and function of adult pig epididymis.	Flutamide	83-92	androgen receptor	Sus scrofa	182-184
21342526-16	2011	CONCLUSIONS: The region-specific alterations in the epididymis morphology and scarce spermatic content within the lumina of the corpus and cauda indicate that flutamide can induce delayed effects on the epididymal function of the adult boar by decrease in AR protein levels that results in altered androgen signaling.	Flutamide	159-168	androgen receptor	Sus scrofa	256-258
21342526-17	2011	This may cause disturbances in androgen-dependent processes including Cx43 (de)regulation, however, we can not exclude the possibility that in response to flutamide decreased Cx43 expression may represent one mechanism responsible for functional disturbance of the boar epididymis.	Flutamide	155-164	gap junction protein alpha 1	Sus scrofa	175-179
21111724-11	2011	Flutamide (10 muM), unexpectedly, also strongly increased nuclear beta-catenin accumulation.	Flutamide	0-9	catenin beta 1	Homo sapiens	66-78
20955177-7	2011	Interestingly, B3 treatment efficiently enhanced the antagonist activity of flutamide through suppression of p300 HAT activity, demonstrating that relative p300 activity is critical for the antagonist action.	Flutamide	76-85	E1A binding protein p300	Homo sapiens	109-117
19853283-0	2011	Connexin 43 gene expression in male and female gonads of porcine offspring following in utero exposure to an anti-androgen, flutamide.	Flutamide	124-133	gap junction protein alpha 1	Sus scrofa	0-11
19853283-1	2011	The aim of this study was to show the effect of maternal exposure to flutamide on connexin 43 (Cx43) gene expression in testes and ovaries of 2-day-old piglets.	Flutamide	69-78	gap junction protein alpha 1	Sus scrofa	82-93
19853283-1	2011	The aim of this study was to show the effect of maternal exposure to flutamide on connexin 43 (Cx43) gene expression in testes and ovaries of 2-day-old piglets.	Flutamide	69-78	gap junction protein alpha 1	Sus scrofa	95-99
19853283-4	2011	Following flutamide exposure strong immunostaining for Cx43 was observed between testicular Leydig cells, between granulosa cells of primary follicles, and between interstitial cells surrounding clusters of oocyte nests in the ovarian cortex as in the respective controls.	Flutamide	10-19	gap junction protein alpha 1	Sus scrofa	55-59
19853283-7	2011	Screening for Cx43 expression revealed the presence of a transcript, both in control and in flutamide-treated pigs.	Flutamide	92-101	gap junction protein alpha 1	Sus scrofa	14-18
20955177-7	2011	Interestingly, B3 treatment efficiently enhanced the antagonist activity of flutamide through suppression of p300 HAT activity, demonstrating that relative p300 activity is critical for the antagonist action.	Flutamide	76-85	E1A binding protein p300	Homo sapiens	109-113
20689246-4	2011	METHODS: We tested whether the AR antagonist flutamide could block perinatal toxicity.	Flutamide	45-54	androgen receptor	Mus musculus	31-33
20961722-0	2011	Prenatal and neonatal exposure to the antiandrogen flutamide alters connexin 43 gene expression in adult porcine ovary.	Flutamide	51-60	gap junction protein alpha 1	Sus scrofa	68-79
20961722-8	2011	In preantral follicles, Cx43 mRNA was down-regulated (P < 0.01) following maternal and neonatal flutamide exposure.	Flutamide	99-108	gap junction protein alpha 1	Sus scrofa	24-28
20961722-9	2011	In large antral follicles, Cx43 mRNA was up-regulated (P < 0.01) after neonatal flutamide administration.	Flutamide	83-92	gap junction protein alpha 1	Sus scrofa	27-31
20961722-10	2011	Immunofluorescence showed that Cx43 expression decreased (P < 0.001) in preantral follicles and increased (P < 0.001) in large antral follicles following flutamide exposure.	Flutamide	160-169	gap junction protein alpha 1	Sus scrofa	31-35
20961722-11	2011	In luteal tissues, Cx43 and 3beta-HSD expression and progesterone concentration decreased (P < 0.01) after postnatal flutamide treatment.	Flutamide	120-129	gap junction protein alpha 1	Sus scrofa	19-37
20961722-13	2011	Moreover, alteration of Cx43 expression by the administration of flutamide during particular prenatal and neonatal time periods may affect porcine follicle development, as well as CL formation and function.	Flutamide	65-74	gap junction protein alpha 1	Sus scrofa	24-28
20961723-6	2011	Flutamide, a compound that prevents androgen binding to the androgen receptor, suppresses (P < 0.05) TBA-induced alterations in protein synthesis and degradation in fused BSC cultures, indicating the androgen receptor is involved.	Flutamide	0-9	androgen receptor	Bos taurus	60-77
20961723-6	2011	Flutamide, a compound that prevents androgen binding to the androgen receptor, suppresses (P < 0.05) TBA-induced alterations in protein synthesis and degradation in fused BSC cultures, indicating the androgen receptor is involved.	Flutamide	0-9	androgen receptor	Bos taurus	203-220
20709811-7	2010	Nigericin suppressed the androgen-dependent LNCaP cell growth even though the cells expressed a flutamide-resistant mutant AR.	Flutamide	96-105	androgen receptor	Homo sapiens	123-125
21731703-9	2011	Treatment with the androgen antagonist flutamide partially restored PSMA expression in androgen-treated VCaP cells.	Flutamide	39-48	folate hydrolase 1	Homo sapiens	68-72
20041327-7	2010	RESULTS: Our study showed that vincristine, tamoxifen, vinblastine, docetaxel, cyclophosphamide, flutamide, ifosfamide and paclitaxel activate PXR-mediated Pgp induction, and were additionally shown to affect the intracellular accumulation of the Pgp probe rhodamine 123.	Flutamide	97-106	nuclear receptor subfamily 1 group I member 2	Homo sapiens	143-146
20546829-2	2010	The aim of this study was to determine the effects of E(2) (17beta-estradiol) replacement, acyline (GnRH antagonist) and flutamide (anti-androgen) treatment on the ovarian phenotype of ArKO mice.	Flutamide	121-130	cytochrome P450, family 19, subfamily a, polypeptide 1	Mus musculus	185-189
20709035-5	2010	Finally, the androgen receptor antagonist flutamide inhibited the increase in neuronal damage and sensorimotor impairment observed in testosterone treated mice.	Flutamide	42-51	androgen receptor	Mus musculus	13-30
20682842-2	2010	We postulated that relatively greater LH responses to flutamide (brain-permeant antiandrogen) than bicalutamide (brain-impermeant antiandrogen) should reflect greater feedback via CNS than pituitary/peripheral androgen receptor-dependent pathways.	Flutamide	54-63	androgen receptor	Homo sapiens	210-227
20041327-7	2010	RESULTS: Our study showed that vincristine, tamoxifen, vinblastine, docetaxel, cyclophosphamide, flutamide, ifosfamide and paclitaxel activate PXR-mediated Pgp induction, and were additionally shown to affect the intracellular accumulation of the Pgp probe rhodamine 123.	Flutamide	97-106	ATP binding cassette subfamily B member 1	Homo sapiens	156-159
20041327-7	2010	RESULTS: Our study showed that vincristine, tamoxifen, vinblastine, docetaxel, cyclophosphamide, flutamide, ifosfamide and paclitaxel activate PXR-mediated Pgp induction, and were additionally shown to affect the intracellular accumulation of the Pgp probe rhodamine 123.	Flutamide	97-106	ATP binding cassette subfamily B member 1	Homo sapiens	247-250
20542992-14	2010	In addition, the phenacetin hydrolase activity by AADAC was activated by flutamide (5-fold) as well as that in HLM (4-fold), and the activity in HLM was potently inhibited by eserine, a strong inhibitor of AADAC.	Flutamide	73-82	arylacetamide deacetylase	Homo sapiens	50-55
20138181-4	2010	After one day hCG-stimulated frogs were treated via aqueous exposure over three days without and with FLU at concentrations of 10(-8) and 10(-6) M in comparison to untreated frogs.	Flutamide	102-105	glycoprotein hormones, alpha polypeptide	Homo sapiens	14-17
20539040-10	2010	Finally, we examined the effect of flutamide--an antiandrogen--on cortactin isoform profiles and phosphorylation status.	Flutamide	35-44	cortactin	Mus musculus	66-75
20539040-11	2010	The amount of tyrosine 466-phosphorylated p85 isoform of cortactin relative to the total amount of the p85 isoform of cortactin decreased after flutamide injection, whereas no change was detected with regard to the total amount of cortactin p85 isoform.	Flutamide	144-153	extracellular matrix protein 1	Mus musculus	42-45
20539040-11	2010	The amount of tyrosine 466-phosphorylated p85 isoform of cortactin relative to the total amount of the p85 isoform of cortactin decreased after flutamide injection, whereas no change was detected with regard to the total amount of cortactin p85 isoform.	Flutamide	144-153	cortactin	Mus musculus	118-127
20539040-11	2010	The amount of tyrosine 466-phosphorylated p85 isoform of cortactin relative to the total amount of the p85 isoform of cortactin decreased after flutamide injection, whereas no change was detected with regard to the total amount of cortactin p85 isoform.	Flutamide	144-153	cortactin	Mus musculus	118-127
20539040-11	2010	The amount of tyrosine 466-phosphorylated p85 isoform of cortactin relative to the total amount of the p85 isoform of cortactin decreased after flutamide injection, whereas no change was detected with regard to the total amount of cortactin p85 isoform.	Flutamide	144-153	cortactin	Mus musculus	57-66
20337887-0	2010	Flutamide inhibits nifedipine- and interleukin-1 beta-induced collagen overproduction in gingival fibroblasts.	Flutamide	0-9	interleukin 1 beta	Homo sapiens	35-53
20399256-9	2010	Compared to vehicle controls, flutamide treatment significantly decreased (1) the number of microtubule-associated protein-2+ (MAP-2) neurons in the CA1 region, (2) the number of MAP-2+ neurons in the dentate gyrus (DG) region of the hippocampus, and (3) the density of dendritic spines of pyramidal neurons in the CA1 region.	Flutamide	30-39	microtubule-associated protein 2	Rattus norvegicus	92-124
20399256-9	2010	Compared to vehicle controls, flutamide treatment significantly decreased (1) the number of microtubule-associated protein-2+ (MAP-2) neurons in the CA1 region, (2) the number of MAP-2+ neurons in the dentate gyrus (DG) region of the hippocampus, and (3) the density of dendritic spines of pyramidal neurons in the CA1 region.	Flutamide	30-39	microtubule-associated protein 2	Rattus norvegicus	127-132
20399256-9	2010	Compared to vehicle controls, flutamide treatment significantly decreased (1) the number of microtubule-associated protein-2+ (MAP-2) neurons in the CA1 region, (2) the number of MAP-2+ neurons in the dentate gyrus (DG) region of the hippocampus, and (3) the density of dendritic spines of pyramidal neurons in the CA1 region.	Flutamide	30-39	carbonic anhydrase 1	Rattus norvegicus	149-152
20399256-9	2010	Compared to vehicle controls, flutamide treatment significantly decreased (1) the number of microtubule-associated protein-2+ (MAP-2) neurons in the CA1 region, (2) the number of MAP-2+ neurons in the dentate gyrus (DG) region of the hippocampus, and (3) the density of dendritic spines of pyramidal neurons in the CA1 region.	Flutamide	30-39	microtubule-associated protein 2	Rattus norvegicus	179-184
20399256-9	2010	Compared to vehicle controls, flutamide treatment significantly decreased (1) the number of microtubule-associated protein-2+ (MAP-2) neurons in the CA1 region, (2) the number of MAP-2+ neurons in the dentate gyrus (DG) region of the hippocampus, and (3) the density of dendritic spines of pyramidal neurons in the CA1 region.	Flutamide	30-39	carbonic anhydrase 1	Rattus norvegicus	315-318
20430028-2	2010	Gonadally intact, sexually experienced male rats received bilateral administration of flutamide, an androgen receptor (AR) blocker, aimed at either the posterior dorsal part (MePD) or the anterior dorsal part (MeAD) of the MeA through inner cannulae inserted into the implanted guide cannulae.	Flutamide	86-95	androgen receptor	Rattus norvegicus	100-117
20430028-2	2010	Gonadally intact, sexually experienced male rats received bilateral administration of flutamide, an androgen receptor (AR) blocker, aimed at either the posterior dorsal part (MePD) or the anterior dorsal part (MeAD) of the MeA through inner cannulae inserted into the implanted guide cannulae.	Flutamide	86-95	androgen receptor	Rattus norvegicus	119-121
20337887-1	2010	BACKGROUND AND OBJECTIVE: To understand the role of the androgen receptor in gingival overgrowth, the effects of flutamide on interleukin-1 beta- and nifedipine-induced gene expression of connective tissue growth factor (CTGF/CCN2) and collagen production in gingival fibroblasts were examined.	Flutamide	113-122	interleukin 1 beta	Homo sapiens	126-144
20337887-8	2010	Flutamide, an androgen receptor antagonist, inhibited stimulation by nifedipine or interleukin-1 beta.	Flutamide	0-9	androgen receptor	Homo sapiens	14-31
20337887-8	2010	Flutamide, an androgen receptor antagonist, inhibited stimulation by nifedipine or interleukin-1 beta.	Flutamide	0-9	interleukin 1 beta	Homo sapiens	83-101
20392832-10	2010	The LGD-3303 increase in male preference was blocked by pretreatment with the androgen receptor antagonist flutamide.	Flutamide	107-116	androgen receptor	Rattus norvegicus	78-95
20641097-3	2010	The Cyr61 gene exhibited the highest response to FLU in rat fetal testis, and we suggested it a promising candidate gene for epispadias in humans, because its protein product promotes proliferation, migration, and adhesion of endothelial cells and fibroblasts.	Flutamide	49-52	cellular communication network factor 1	Rattus norvegicus	4-9
20338164-7	2010	We show, however, that 5-Aza treatment, which caused demethylation of the AR promoter, led to a significant increase in IGF1R mRNA levels, whereas addition of the AR inhibitor flutamide decreased the IGF1R mRNA levels to basal values measured prior to the 5-Aza treatment.	Flutamide	176-185	androgen receptor	Homo sapiens	163-165
20338164-7	2010	We show, however, that 5-Aza treatment, which caused demethylation of the AR promoter, led to a significant increase in IGF1R mRNA levels, whereas addition of the AR inhibitor flutamide decreased the IGF1R mRNA levels to basal values measured prior to the 5-Aza treatment.	Flutamide	176-185	insulin like growth factor 1 receptor	Homo sapiens	200-205
20108248-6	2010	Administration of the androgen receptor inhibitor Flutamide blocked the basal and hCG stimulated GFP expression in Leydig cells.	Flutamide	50-59	androgen receptor	Mus musculus	22-39
20485034-3	2010	The present study was designed to test the hypothesis that flutamide, an androgen receptor-blocking agent, would "rescue" a coronal suture destined to fuse and improve craniofacial growth in a familial rabbit model of craniosynostosis.	Flutamide	59-68	androgen receptor	Oryctolagus cuniculus	73-90
20485034-9	2010	Results suggest that androgen receptor-blocking using flutamide may only provide a transient rescue to suture fusion in this model.	Flutamide	54-63	androgen receptor	Oryctolagus cuniculus	21-38
20558338-0	2010	Effects of pre- and postnatal exposure to flutamide on connexin 43 expression in testes and ovaries of prepubertal pigs.	Flutamide	42-51	gap junction protein alpha 1	Sus scrofa	55-66
20558338-7	2010	Since we demonstrated changes in gonad morphology and in the expression of Cx43 at the level of protein of prepubertal boars and gilts, it seems possible that flutamide through blocking androgen action, causes delayed gonadal maturation in later postnatal life and, among other factors, may be involved in the regulation of Cx43 gene expression in pig gonads.	Flutamide	159-168	gap junction protein alpha 1	Sus scrofa	75-79
20558338-7	2010	Since we demonstrated changes in gonad morphology and in the expression of Cx43 at the level of protein of prepubertal boars and gilts, it seems possible that flutamide through blocking androgen action, causes delayed gonadal maturation in later postnatal life and, among other factors, may be involved in the regulation of Cx43 gene expression in pig gonads.	Flutamide	159-168	gap junction protein alpha 1	Sus scrofa	324-328
20132345-2	2010	It was found that additive effects on the same molecular target (the androgen receptor; AR) can be predicted for both mixtures of compounds with effect on the AR (flutamide, procymidone and vinclozolin) and of compounds with and without effects on the AR [finasteride, mono-(2-ethylhexyl) phthalate, prochloraz and vinclozolin].	Flutamide	163-172	androgen receptor	Homo sapiens	69-86
19787772-1	2010	Antiandrogen flutamide, an antagonist of the wild-type androgen receptor (AR), is used in the clinics for treating metastatic prostate cancer.	Flutamide	13-22	androgen receptor	Homo sapiens	55-72
20154177-5	2010	Organ and primary cell cultures of gubernacula showed that 5alpha-dihydrotestosterone (DHT) upregulated the expression of Rxfp2 which was abolished by the addition of an AR antagonist, flutamide.	Flutamide	185-194	relaxin/insulin-like family peptide receptor 2	Mus musculus	122-127
20154177-5	2010	Organ and primary cell cultures of gubernacula showed that 5alpha-dihydrotestosterone (DHT) upregulated the expression of Rxfp2 which was abolished by the addition of an AR antagonist, flutamide.	Flutamide	185-194	androgen receptor	Mus musculus	170-172
19948840-5	2010	In 25-day-old rats, quantification of the mean pixel intensity of immunofluorescence-stained sections showed a significant decrease in AQP9 staining in the apical membrane of epididymal principal cells after treatments with GNRHa, DES, or flutamide, compared to controls.	Flutamide	239-248	aquaporin 9	Rattus norvegicus	135-139
19948840-9	2010	Our data show that expression of AQP9 in the developing rat epididymis is downregulated by neonatal DES, GNRHa, EE, and flutamide, and that the effects mediated by estrogens can be prevented by testosterone administration.	Flutamide	120-129	aquaporin 9	Rattus norvegicus	33-37
21069171-1	2010	In our efforts to develop a novel class of SPECT imaging agents based on nonsteroidal androgen receptor (AR) antagonists, we have synthesized N-cyclopentadienyltricarbonyltechnetium-N-[4-nitro-3-trifluoromethyl-phenyl] carboxamide (NF(99m)Tc), an analog of the AR antagonist ligand flutamide.	Flutamide	282-291	androgen receptor	Rattus norvegicus	86-103
21069171-1	2010	In our efforts to develop a novel class of SPECT imaging agents based on nonsteroidal androgen receptor (AR) antagonists, we have synthesized N-cyclopentadienyltricarbonyltechnetium-N-[4-nitro-3-trifluoromethyl-phenyl] carboxamide (NF(99m)Tc), an analog of the AR antagonist ligand flutamide.	Flutamide	282-291	androgen receptor	Rattus norvegicus	105-107
19787772-1	2010	Antiandrogen flutamide, an antagonist of the wild-type androgen receptor (AR), is used in the clinics for treating metastatic prostate cancer.	Flutamide	13-22	androgen receptor	Homo sapiens	74-76
19787772-2	2010	However, the T877A mutated AR is paradoxically activated by hydroxyflutamide, an active form of flutamide.	Flutamide	67-76	androgen receptor	Homo sapiens	27-29
19790238-5	2010	The effect of flutamide (FLT) on the W741C mutant AR was examined with transactivation assays in vitro and with the oral administration of FLT to non-castrated mice harboring KUCaP-1 in vivo.	Flutamide	14-23	androgen receptor	Mus musculus	50-52
19790238-5	2010	The effect of flutamide (FLT) on the W741C mutant AR was examined with transactivation assays in vitro and with the oral administration of FLT to non-castrated mice harboring KUCaP-1 in vivo.	Flutamide	25-28	androgen receptor	Mus musculus	50-52
20096826-9	2010	Flutamide or Finasteride are "only" to be used under the guise of contraception as a "thirdline therapy" in cases of severe hirsutism, the presence of side effects or counter-indications to EPP, CPA 50mg/day or spironolactone (grade C).	Flutamide	0-9	carboxypeptidase A1	Homo sapiens	195-198
19901962-6	2010	This mechanism was remarkable in that its androgen dependence was apparently for nuclear translocation of AR; it was otherwise androgen independent, flutamide insensitive and tolerant to disruption of AR dimerization.	Flutamide	149-158	androgen receptor	Homo sapiens	201-203
19766145-5	2010	Since some reports indicate that ATD, in addition to inhibit aromatase, also may affect the binding of testosterone to the androgen receptor, the effect of the non-steroidal androgen receptor antagonist flutamide was investigated.	Flutamide	203-212	androgen receptor	Rattus norvegicus	174-191
19714448-0	2010	Up-regulation of circadian clock gene Period 2 in the prostate mesenchymal cells during flutamide-induced apoptosis.	Flutamide	88-97	period circadian regulator 2	Rattus norvegicus	38-46
19714448-6	2010	Conversely, flutamide (FL) up-regulated the amplitude of circadian Per2-dLuc oscillations in a dose-dependent manner, whereas T antagonized the action of FL.	Flutamide	12-21	period circadian regulator 2	Rattus norvegicus	67-71
19714448-6	2010	Conversely, flutamide (FL) up-regulated the amplitude of circadian Per2-dLuc oscillations in a dose-dependent manner, whereas T antagonized the action of FL.	Flutamide	23-25	period circadian regulator 2	Rattus norvegicus	67-71
19714448-7	2010	The PER2 protein was markedly accumulated by FL treatment and localized in both the nucleus and cytoplasm during the first peak period of circadian Per2-dLuc oscillations.	Flutamide	45-47	period circadian regulator 2	Rattus norvegicus	4-8
20043082-5	2010	Expression of hsp70-1 in LNCaP cells was downregulated by the anti-androgens bicalutamide (Bic), and flutamide (Flut), and a newly identified AR signaling antagonist DL3.	Flutamide	101-110	heat shock protein family A (Hsp70) member 1A	Homo sapiens	14-21
20043082-5	2010	Expression of hsp70-1 in LNCaP cells was downregulated by the anti-androgens bicalutamide (Bic), and flutamide (Flut), and a newly identified AR signaling antagonist DL3.	Flutamide	112-116	heat shock protein family A (Hsp70) member 1A	Homo sapiens	14-21
21338237-0	2010	Changes of androgen receptor and insulin-like growth factor-1 in LNCaP prostate cancer cells treated with sex hormones and flutamide.	Flutamide	123-132	androgen receptor	Homo sapiens	11-28
19660519-4	2010	Pretreatment with the androgen receptor antagonist flutamide prevented these effects suggesting an androgen receptor mediated mode of action.	Flutamide	51-60	androgen receptor	Rattus norvegicus	22-39
19660519-4	2010	Pretreatment with the androgen receptor antagonist flutamide prevented these effects suggesting an androgen receptor mediated mode of action.	Flutamide	51-60	androgen receptor	Rattus norvegicus	99-116
19660519-5	2010	However, flutamide alone stimulated the phosphorylation of both extracellular signal-regulated kinase 1 and 2.	Flutamide	9-18	mitogen activated protein kinase 3	Rattus norvegicus	64-109
20332615-3	2010	First, we show that combined treatment of male and female zebra finches (Estrildidae: Taeniopygia guttata) with the androgen receptor antagonist flutamide and the aromatase inhibitor 1,4,6-androstatriene-3,17-dione does not alter the expression of VT immunoreactivity within the BSTm; however, both hormonal treatment and social housing environment (same-sex versus mixed-sex) alter VT colocalization with the immediate early gene product Fos (a proxy marker of neural activation) in the BSTm.	Flutamide	145-154	androgen receptor	Taeniopygia guttata	116-133
20332615-3	2010	First, we show that combined treatment of male and female zebra finches (Estrildidae: Taeniopygia guttata) with the androgen receptor antagonist flutamide and the aromatase inhibitor 1,4,6-androstatriene-3,17-dione does not alter the expression of VT immunoreactivity within the BSTm; however, both hormonal treatment and social housing environment (same-sex versus mixed-sex) alter VT colocalization with the immediate early gene product Fos (a proxy marker of neural activation) in the BSTm.	Flutamide	145-154	proto-oncogene c-Fos	Taeniopygia guttata	439-442
21338237-0	2010	Changes of androgen receptor and insulin-like growth factor-1 in LNCaP prostate cancer cells treated with sex hormones and flutamide.	Flutamide	123-132	insulin like growth factor 1	Homo sapiens	33-61
21338237-3	2010	Low concentrations of DHT, estrone and flutamide increased the expression of AR and IGF-1, especially estrone, with concentration and time dependence.	Flutamide	39-48	androgen receptor	Homo sapiens	77-79
21338237-3	2010	Low concentrations of DHT, estrone and flutamide increased the expression of AR and IGF-1, especially estrone, with concentration and time dependence.	Flutamide	39-48	insulin like growth factor 1	Homo sapiens	84-89
21338237-4	2010	With DHT and flutamide, there was a significant alteration in AR expression (p<0.001).	Flutamide	13-22	androgen receptor	Homo sapiens	62-64
21338237-5	2010	The results indicated expression of AR and IGF-1 genes to be influenced by DHT, estrone and flutamide in LNCaP cells, regulated by multiple signal pathways.	Flutamide	92-101	androgen receptor	Homo sapiens	36-38
21338237-5	2010	The results indicated expression of AR and IGF-1 genes to be influenced by DHT, estrone and flutamide in LNCaP cells, regulated by multiple signal pathways.	Flutamide	92-101	insulin like growth factor 1	Homo sapiens	43-48
18839173-7	2009	RESULTS: Paclitaxel, erlotinib, tamoxifen, ifosfamide, flutamide and docetaxel are able to activate PXR, while only strong PXR activation leads to significant induction of CYP3A4 activity.	Flutamide	55-64	nuclear receptor subfamily 1 group I member 2	Homo sapiens	100-103
20954080-8	2010	In particular, the expression of androgen receptor (AR) and 5alpha-reductase type 2 in the proximal penis was markedly depressed following administration of DBP (700 mg/kg/d) or flutamide (25 mg/kg/d).	Flutamide	178-187	androgen receptor	Rattus norvegicus	33-50
20954080-8	2010	In particular, the expression of androgen receptor (AR) and 5alpha-reductase type 2 in the proximal penis was markedly depressed following administration of DBP (700 mg/kg/d) or flutamide (25 mg/kg/d).	Flutamide	178-187	androgen receptor	Rattus norvegicus	52-54
20954080-9	2010	The expression of sonic hedgehog (Shh) in the urethral epithelium of the proximal penis was significantly less in the DBP (700 mg/kg/d)- or flutamide (25 mg/kg/d)-treated groups.	Flutamide	140-149	sonic hedgehog signaling molecule	Rattus norvegicus	18-32
20954080-9	2010	The expression of sonic hedgehog (Shh) in the urethral epithelium of the proximal penis was significantly less in the DBP (700 mg/kg/d)- or flutamide (25 mg/kg/d)-treated groups.	Flutamide	140-149	sonic hedgehog signaling molecule	Rattus norvegicus	34-37
19635294-13	2009	Flutamide treatment increased apoptosis compared to controls, but only with CGRP (2.3% vs 7.3%, P < .001).	Flutamide	0-9	calcitonin-related polypeptide alpha	Rattus norvegicus	76-80
19635294-18	2009	Androgen is also involved in the pathway controlling apoptosis, as androgen blockade with flutamide inhibited the action of CGRP.	Flutamide	90-99	calcitonin-related polypeptide alpha	Rattus norvegicus	124-128
19442681-9	2009	Indeed, mitochondria isolated from flutamide-treated Sod2(+/-) mice exhibited decreased aconitase activity as compared to vehicle controls.	Flutamide	35-44	superoxide dismutase 2, mitochondrial	Mus musculus	53-57
19442681-10	2009	A transcriptomics analysis using MitoChips revealed that flutamide-treated Sod2(+/-) mice exhibited a selective decrease in the expression of all complexes I and III subunits encoded by mitochondrial DNA.	Flutamide	57-66	superoxide dismutase 2, mitochondrial	Mus musculus	75-79
19339378-0	2009	Human arylacetamide deacetylase is a principal enzyme in flutamide hydrolysis.	Flutamide	57-66	arylacetamide deacetylase	Homo sapiens	6-31
19339378-5	2009	In the present study, we found that human arylacetamide deacetylase (AADAC) efficiently hydrolyzed flutamide using recombinant AADAC expressed in COS7 cells.	Flutamide	99-108	arylacetamide deacetylase	Homo sapiens	42-67
19339378-5	2009	In the present study, we found that human arylacetamide deacetylase (AADAC) efficiently hydrolyzed flutamide using recombinant AADAC expressed in COS7 cells.	Flutamide	99-108	arylacetamide deacetylase	Homo sapiens	69-74
19339378-5	2009	In the present study, we found that human arylacetamide deacetylase (AADAC) efficiently hydrolyzed flutamide using recombinant AADAC expressed in COS7 cells.	Flutamide	99-108	arylacetamide deacetylase	Homo sapiens	127-132
19339378-6	2009	In contrast, carboxylesterase1 (CES1) and CES2, which are responsible for the hydrolysis of many drugs, could not hydrolyze flutamide.	Flutamide	124-133	carboxylesterase 2	Homo sapiens	42-46
19339378-11	2009	Moreover, human liver and jejunum microsomes showing AADAC expression could hydrolyze flutamide, but human pulmonary and renal microsomes, which do not express AADAC, showed slight activity.	Flutamide	86-95	arylacetamide deacetylase	Homo sapiens	53-58
19339378-13	2009	In conclusion, these results clearly showed that flutamide is exclusively hydrolyzed by AADAC.	Flutamide	49-58	arylacetamide deacetylase	Homo sapiens	88-93
19339378-14	2009	AADAC would be an important enzyme responsible for flutamide-induced hepatotoxicity.	Flutamide	51-60	arylacetamide deacetylase	Homo sapiens	0-5
19136390-7	2009	Next GnRH antagonist-treated rats were given exogenous testosterone and flutamide to stabilize ITT levels and block its action.	Flutamide	72-81	gonadotropin releasing hormone 1	Rattus norvegicus	5-9
19201527-3	2009	As was the case with LNCaP cells, when androgen receptor (AR) was introduced into AR-negative PC-3 cells, dihydrotestosterone inhibited while flutamide increased Id-1 expression.	Flutamide	142-151	androgen receptor	Homo sapiens	39-56
19201527-3	2009	As was the case with LNCaP cells, when androgen receptor (AR) was introduced into AR-negative PC-3 cells, dihydrotestosterone inhibited while flutamide increased Id-1 expression.	Flutamide	142-151	androgen receptor	Homo sapiens	58-60
19201527-3	2009	As was the case with LNCaP cells, when androgen receptor (AR) was introduced into AR-negative PC-3 cells, dihydrotestosterone inhibited while flutamide increased Id-1 expression.	Flutamide	142-151	androgen receptor	Homo sapiens	82-84
19201527-3	2009	As was the case with LNCaP cells, when androgen receptor (AR) was introduced into AR-negative PC-3 cells, dihydrotestosterone inhibited while flutamide increased Id-1 expression.	Flutamide	142-151	inhibitor of DNA binding 1, HLH protein	Homo sapiens	162-166
19605781-4	2009	Age at VO was examined in mice fed high-fat or low-fat diets from weaning and treated with the androgen receptor antagonist flutamide or vehicle (controls).	Flutamide	124-133	androgen receptor	Mus musculus	95-112
19239458-11	2009	CONCLUSIONS: Our analysis suggests the therapeutic value of low-dose flutamide alone or combined with finasteride as first-line agents in a possible graduated approach for treating PSA-only recurrent prostate cancer.	Flutamide	69-78	kallikrein related peptidase 3	Homo sapiens	181-184
19628067-7	2009	RESULTS: Castration or flutamide treatment significantly increased SOCS3 expression in male hearts after I/R.	Flutamide	23-32	suppressor of cytokine signaling 3	Homo sapiens	67-72
19347872-8	2009	In LNCaP cells, DHT down-regulated regucalcin expression, an effect inhibited by the presence of both flutamide and cyclohexamide, suggesting the involvement of androgen receptor and de novo protein synthesis.	Flutamide	102-111	regucalcin	Homo sapiens	35-45
19441848-4	2009	Unlike the activity of traditional androgen receptor antagonists, such as flutamide and bicalutamide, inhibition by these coactivator binding inhibitors is insurmountable by increased concentrations of androgen agonists and maintains effectiveness even on a mutant androgen receptor that is resistant to traditional antagonists.	Flutamide	74-83	androgen receptor	Homo sapiens	35-52
18839173-7	2009	RESULTS: Paclitaxel, erlotinib, tamoxifen, ifosfamide, flutamide and docetaxel are able to activate PXR, while only strong PXR activation leads to significant induction of CYP3A4 activity.	Flutamide	55-64	nuclear receptor subfamily 1 group I member 2	Homo sapiens	123-126
18839173-7	2009	RESULTS: Paclitaxel, erlotinib, tamoxifen, ifosfamide, flutamide and docetaxel are able to activate PXR, while only strong PXR activation leads to significant induction of CYP3A4 activity.	Flutamide	55-64	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	172-178
19304795-0	2009	Modulation of ovarian structure and abdominal obesity in curcumin- and flutamide-treated aging FSH-R haploinsufficient mice.	Flutamide	71-80	follicle stimulating hormone receptor	Mus musculus	95-100
19213837-8	2009	The specific androgen receptor antagonist flutamide suppressed GDF-9-induced preantral follicle growth in vitro.	Flutamide	42-51	growth differentiation factor 9	Rattus norvegicus	63-68
19304795-6	2009	Flutamide reduced p450c-17 (cyp-17 protein) enzyme expression in thecal/interstitial cells, whereas increased expression of 3beta-hydroxysteroid dehydrogenase in thecal cells and granulosa-lutein cells of big follicles was apparent in curcumin-treated ovaries.	Flutamide	0-9	cytochrome P450, family 17, subfamily a, polypeptide 1	Mus musculus	18-26
19304795-6	2009	Flutamide reduced p450c-17 (cyp-17 protein) enzyme expression in thecal/interstitial cells, whereas increased expression of 3beta-hydroxysteroid dehydrogenase in thecal cells and granulosa-lutein cells of big follicles was apparent in curcumin-treated ovaries.	Flutamide	0-9	cytochrome P450, family 17, subfamily a, polypeptide 1	Mus musculus	28-34
19366804-8	2009	Selection was evident for the promiscuous receptor AR-V716M, which dominated three metastases from one flutamide-treated patient.	Flutamide	103-112	androgen receptor	Homo sapiens	51-53
19002196-5	2009	Testosterone effects on infarct size were blocked by the androgen receptor (AR) antagonist flutamide and further confirmed in young versus middle-aged mice.	Flutamide	91-100	androgen receptor	Mus musculus	57-74
19389135-6	2009	RESULTS: Flutamide, but not hydroxyflutamide, successfully suppressed the transcription of all of the mutant androgen receptors examined in this study and also showed suppressive effects on PSA secretion by LNCaP cells treated with dihydrotestosterone.	Flutamide	9-18	kallikrein related peptidase 3	Homo sapiens	190-193
19444000-1	2009	Ca(2+) release from intracellular store sites via the ryanodine receptor (RyR) and hormonal regulation by flutamide, an androgen-receptor (AR) antagonist, on it were examined in vas deferens (VD) smooth muscle cells (SMCs).	Flutamide	106-115	androgen receptor	Rattus norvegicus	120-137
19444000-1	2009	Ca(2+) release from intracellular store sites via the ryanodine receptor (RyR) and hormonal regulation by flutamide, an androgen-receptor (AR) antagonist, on it were examined in vas deferens (VD) smooth muscle cells (SMCs).	Flutamide	106-115	androgen receptor	Rattus norvegicus	139-141
19444000-1	2009	Ca(2+) release from intracellular store sites via the ryanodine receptor (RyR) and hormonal regulation by flutamide, an androgen-receptor (AR) antagonist, on it were examined in vas deferens (VD) smooth muscle cells (SMCs).	Flutamide	106-115	arginine vasopressin	Rattus norvegicus	178-181
19444000-7	2009	Real-time PCR analyses revealed that the transcripts of ryanodine receptor (RyR) type 2 and type 3 (RyR2 and RyR3) were expressed in VD and markedly reduced in Flu.	Flutamide	160-163	ryanodine receptor 2	Rattus norvegicus	56-74
19444000-7	2009	Real-time PCR analyses revealed that the transcripts of ryanodine receptor (RyR) type 2 and type 3 (RyR2 and RyR3) were expressed in VD and markedly reduced in Flu.	Flutamide	160-163	ryanodine receptor 2	Rattus norvegicus	76-79
19444000-7	2009	Real-time PCR analyses revealed that the transcripts of ryanodine receptor (RyR) type 2 and type 3 (RyR2 and RyR3) were expressed in VD and markedly reduced in Flu.	Flutamide	160-163	ryanodine receptor 2	Rattus norvegicus	100-104
19444000-7	2009	Real-time PCR analyses revealed that the transcripts of ryanodine receptor (RyR) type 2 and type 3 (RyR2 and RyR3) were expressed in VD and markedly reduced in Flu.	Flutamide	160-163	ryanodine receptor 3	Rattus norvegicus	109-113
19444000-8	2009	The protein expression of total RyR was significantly reduced by flutamide treatment, but that of inositol 1,4,5-trisphosphate receptor (IP3R) was not affected.	Flutamide	65-74	ryanodine receptor 2	Rattus norvegicus	32-35
19444000-9	2009	It can be strongly suggested that long term block of AR by flutamide reduced the expression of RyR and its contribution to the contraction, but not those of IP3R in VDSMCs.	Flutamide	59-68	androgen receptor	Rattus norvegicus	53-55
19444000-9	2009	It can be strongly suggested that long term block of AR by flutamide reduced the expression of RyR and its contribution to the contraction, but not those of IP3R in VDSMCs.	Flutamide	59-68	ryanodine receptor 2	Rattus norvegicus	95-98
18607612-18	2009	The follow-up of patients receiving flutamide can be done by monitoring AST or ALT levels for hepatotoxicity.	Flutamide	36-45	solute carrier family 17 member 5	Homo sapiens	72-75
19002196-5	2009	Testosterone effects on infarct size were blocked by the androgen receptor (AR) antagonist flutamide and further confirmed in young versus middle-aged mice.	Flutamide	91-100	androgen receptor	Mus musculus	76-78
19117492-2	2009	A series of single photon emission computed tomography imaging agents (SPECT) utilizing the organometallic radioactive imaging species, fac-99mTc(OH(2))(3)(CO)(3)+, were prepared on the basis of the structure of Flutamide, a potent nonsteroidal antiandrogen prostate cancer drug.	Flutamide	212-221	FA complementation group C	Homo sapiens	136-139
18971393-8	2009	In support of this, the cellular response to doxorubicin, tamoxifen, imatinib, trichostatin A, and flutamide increased in the presence of the cathepsin L inhibitor.	Flutamide	99-108	cathepsin L	Mus musculus	142-153
19258714-6	2009	Bone growth was also unaffected when the AR was blocked by flutamide.	Flutamide	59-68	androgen receptor	Rattus norvegicus	41-43
19754423-5	2009	Typical CYP1A2 substrates generally contain planar ring that can fit the narrow and planar active site of the enzyme, such as propranolol, clozapine, guanabenz, flutamide, imatinib, thalidomide, carbamazepine, lidocaine, theophylline, tacrine, tizanidine, zolpidem, riluzole, zileuton, and leflunomide.	Flutamide	161-170	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	8-14
18535113-6	2008	Both proteins completely disappeared immediately after terminating heat treatment and began to recover after 6 h. Treatment of the monkey Sertoli cells with an AR antagonist, flutamide, could mimic the heat-induced changes in the expression of junction-associated molecules in Sertoli cells.	Flutamide	175-184	androgen receptor	Homo sapiens	160-162
20107586-9	2009	Biz-2 was found to be a specific ligand for the AR in that the natural ligand, DHT, and the anti-androgen, flutamide, displaced Biz-2 bound to AR and inhibited Biz-2-induced transcription and PSA secretion.	Flutamide	107-116	aminopeptidase puromycin sensitive	Homo sapiens	192-195
19258714-3	2009	METHODS: Metatarsal bones from female and male rat fetuses (day E20) were cultured for 14 days in the presence of oxandrolone, testosterone or the androgen receptor (AR) antagonist flutamide with/without insulin-like growth-factor-I (IGF-I) or charcoal-treated serum.	Flutamide	181-190	androgen receptor	Rattus norvegicus	166-168
18798265-9	2008	Additionally, HDACi and flutamide caused retention of AR in the cytoplasm, indicating blockage of androgen signaling.	Flutamide	24-33	androgen receptor	Homo sapiens	54-56
19548358-0	2008	Comparison of in vitro bioactivation of flutamide and its cyano analogue: evidence for reductive activation by human NADPH:cytochrome P450 reductase.	Flutamide	40-49	cytochrome p450 oxidoreductase	Homo sapiens	117-148
19548358-14	2008	In an attempt to identify enzymes involved in the nitroreduction of FLU, NADPH:cytochrome P450 reductase (CPR) was shown to reduce FLU to FLU-6 under both aerobic and anaerobic conditions.	Flutamide	68-71	cytochrome p450 oxidoreductase	Homo sapiens	73-104
19548358-14	2008	In an attempt to identify enzymes involved in the nitroreduction of FLU, NADPH:cytochrome P450 reductase (CPR) was shown to reduce FLU to FLU-6 under both aerobic and anaerobic conditions.	Flutamide	68-71	cytochrome p450 oxidoreductase	Homo sapiens	106-109
19548358-14	2008	In an attempt to identify enzymes involved in the nitroreduction of FLU, NADPH:cytochrome P450 reductase (CPR) was shown to reduce FLU to FLU-6 under both aerobic and anaerobic conditions.	Flutamide	131-134	cytochrome p450 oxidoreductase	Homo sapiens	73-104
19548358-14	2008	In an attempt to identify enzymes involved in the nitroreduction of FLU, NADPH:cytochrome P450 reductase (CPR) was shown to reduce FLU to FLU-6 under both aerobic and anaerobic conditions.	Flutamide	131-134	cytochrome p450 oxidoreductase	Homo sapiens	106-109
19548358-15	2008	Furthermore, the formation of FLU-G5-7 was completely blocked by the addition of a reversible CPR inhibitor, alpha-lipoic acid, to the incubations of FLU under aerobic conditions.	Flutamide	30-33	cytochrome p450 oxidoreductase	Homo sapiens	94-97
19548358-16	2008	In summary, these results clearly demonstrate that nitroreduction of FLU by CPR contributes to bioactivation and potentially to hepatotoxicity of FLU.	Flutamide	69-72	cytochrome p450 oxidoreductase	Homo sapiens	76-79
19548358-16	2008	In summary, these results clearly demonstrate that nitroreduction of FLU by CPR contributes to bioactivation and potentially to hepatotoxicity of FLU.	Flutamide	146-149	cytochrome p450 oxidoreductase	Homo sapiens	76-79
18706413-16	2008	Flutamide treatment prevented the effect of DHT on CRHR2 mRNA indicating that DHT"s effect on CRHR2 expression is AR-mediated.	Flutamide	0-9	corticotropin releasing hormone receptor 2	Rattus norvegicus	51-56
18706413-16	2008	Flutamide treatment prevented the effect of DHT on CRHR2 mRNA indicating that DHT"s effect on CRHR2 expression is AR-mediated.	Flutamide	0-9	corticotropin releasing hormone receptor 2	Rattus norvegicus	94-99
18543106-7	2008	In vitro, AR could mediate beta-cell apoptosis, and AR antagonist flutamide contributed to beta-cell proliferation.	Flutamide	66-75	androgen receptor	Mus musculus	52-54
18650055-4	2008	Flutamide completely suppressed TBA-stimulated IGF-I mRNA expression in BSC cultures.	Flutamide	0-9	IGFI	Bos taurus	47-52
18647599-6	2008	Sixteen of these were negative (89%), whereas two of these, flutamide and haloperidol showed 16-fold (RIF ratio 0.79) and 10-fold (RIF ratio 0.48) maximal induction, respectively in the reporter-gene system.	Flutamide	60-69	ras homolog family member F, filopodia associated	Homo sapiens	102-105
18647599-6	2008	Sixteen of these were negative (89%), whereas two of these, flutamide and haloperidol showed 16-fold (RIF ratio 0.79) and 10-fold (RIF ratio 0.48) maximal induction, respectively in the reporter-gene system.	Flutamide	60-69	ras homolog family member F, filopodia associated	Homo sapiens	131-134
18647599-7	2008	Flutamide and haloperidol were further demonstrated to cause CYP3A4 induction in human cryopreserved hepatocytes based on testosterone 6beta-hydroxylation activity.	Flutamide	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	61-67
18535130-7	2008	The results indicate that flutamide administration after trauma-hemorrhage reduced liver injury, which was associated with decreased levels of alpha-glutathione S-transferase, myeloperoxidase activity, nitrotyrosine formation, lipid peroxidation, and cytokines/chemokines (systemic, liver tissue, and intracellular cytokines/chemokines).	Flutamide	26-35	myeloperoxidase	Mus musculus	176-191
18330893-13	2008	However, the flutamide treatment abolished the inhibitory effects of DHT on the H2O2-induced increase in the levels of p38 MAPK, JNK/SAPK, and NF-kappaB phosphorylation.	Flutamide	13-22	mitogen-activated protein kinase 14	Mus musculus	119-127
18411402-9	2008	Studies using recombinant P450s suggested that the major P450 isozymes involved in the bioactivation of flutamide and its metabolites were CYP1A2, CYP3A4, and CYP2C19.	Flutamide	104-113	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	139-145
18411402-9	2008	Studies using recombinant P450s suggested that the major P450 isozymes involved in the bioactivation of flutamide and its metabolites were CYP1A2, CYP3A4, and CYP2C19.	Flutamide	104-113	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	147-153
18411402-9	2008	Studies using recombinant P450s suggested that the major P450 isozymes involved in the bioactivation of flutamide and its metabolites were CYP1A2, CYP3A4, and CYP2C19.	Flutamide	104-113	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	159-166
18330893-13	2008	However, the flutamide treatment abolished the inhibitory effects of DHT on the H2O2-induced increase in the levels of p38 MAPK, JNK/SAPK, and NF-kappaB phosphorylation.	Flutamide	13-22	mitogen-activated protein kinase 8	Mus musculus	129-137
18330893-13	2008	However, the flutamide treatment abolished the inhibitory effects of DHT on the H2O2-induced increase in the levels of p38 MAPK, JNK/SAPK, and NF-kappaB phosphorylation.	Flutamide	13-22	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	143-152
18485830-13	2008	Treatment of testosterone undecanoate reduced the levels of serum TNF alpha, IL 6, sICAM and MMP 2 in castrated rabbits, while the presence of flutamide increased the levels of serum TNF alpha, IL 6, sICAM and MMP 2 again.	Flutamide	143-152	tumor necrosis factor	Oryctolagus cuniculus	183-192
18485830-13	2008	Treatment of testosterone undecanoate reduced the levels of serum TNF alpha, IL 6, sICAM and MMP 2 in castrated rabbits, while the presence of flutamide increased the levels of serum TNF alpha, IL 6, sICAM and MMP 2 again.	Flutamide	143-152	interleukin-6	Oryctolagus cuniculus	194-198
18485830-13	2008	Treatment of testosterone undecanoate reduced the levels of serum TNF alpha, IL 6, sICAM and MMP 2 in castrated rabbits, while the presence of flutamide increased the levels of serum TNF alpha, IL 6, sICAM and MMP 2 again.	Flutamide	143-152	72 kDa type IV collagenase	Oryctolagus cuniculus	210-215
17957793-8	2008	Cox regression analysis demonstrated that HGPIN with increased PSCA mRNA expression after flutamide had an increased relative risk of 4.33 to develop subsequent cancer (95% confidence intervals: 2.48-7.36; p < 0.001).	Flutamide	90-99	prostate stem cell antigen	Homo sapiens	63-67
18535355-5	2008	While clusterin, PBPC1BS and methionine adenosyl transferase II alpha are regulated by both castration and flutamide, S100 RVP and A7 are regulated by castration alone.	Flutamide	107-116	PBPC1BS-like	Rattus norvegicus	17-24
18535355-5	2008	While clusterin, PBPC1BS and methionine adenosyl transferase II alpha are regulated by both castration and flutamide, S100 RVP and A7 are regulated by castration alone.	Flutamide	107-116	methionine adenosyltransferase 2A	Rattus norvegicus	29-69
18346198-9	2008	The DHT-mediated increase in NEP expression and decrease in Abeta levels were (i) not observed in rat pheochromocytoma cell 12 lacking AR and (ii) blocked in AR-expressing cells by the antagonists, cyproterone acetate and flutamide.	Flutamide	222-231	membrane metallo-endopeptidase	Rattus norvegicus	29-32
18516291-8	2008	Conversely, the growth stimulatory effect of heregulin can also be inhibited with flutamide, suggesting a cross-talk between the AR and ErbB2 pathways affecting cell proliferation.	Flutamide	82-91	androgen receptor	Homo sapiens	129-131
18516291-8	2008	Conversely, the growth stimulatory effect of heregulin can also be inhibited with flutamide, suggesting a cross-talk between the AR and ErbB2 pathways affecting cell proliferation.	Flutamide	82-91	erb-b2 receptor tyrosine kinase 2	Homo sapiens	136-141
18516291-9	2008	Importantly, there is a synergy with the combined use of flutamide and AG825 on cell proliferation and apoptosis, which indicates a therapeutic advantage in the combined blockage of AR and ErbB2 pathways.	Flutamide	57-66	androgen receptor	Homo sapiens	182-184
18516291-9	2008	Importantly, there is a synergy with the combined use of flutamide and AG825 on cell proliferation and apoptosis, which indicates a therapeutic advantage in the combined blockage of AR and ErbB2 pathways.	Flutamide	57-66	erb-b2 receptor tyrosine kinase 2	Homo sapiens	189-194
18302198-10	2008	Treatment with DHT down-regulated the expression of UGT2B15/B17 in LNCaP in a time and dose dependent manner and this down-regulation was competitively antagonized by flutamide and bicalutimide, suggesting a pathway mediated by AR.	Flutamide	167-176	UDP glucuronosyltransferase family 2 member B15	Homo sapiens	52-59
18302198-10	2008	Treatment with DHT down-regulated the expression of UGT2B15/B17 in LNCaP in a time and dose dependent manner and this down-regulation was competitively antagonized by flutamide and bicalutimide, suggesting a pathway mediated by AR.	Flutamide	167-176	NADH:ubiquinone oxidoreductase subunit B6	Homo sapiens	60-63
18302198-10	2008	Treatment with DHT down-regulated the expression of UGT2B15/B17 in LNCaP in a time and dose dependent manner and this down-regulation was competitively antagonized by flutamide and bicalutimide, suggesting a pathway mediated by AR.	Flutamide	167-176	androgen receptor	Homo sapiens	228-230
18366771-7	2008	In another experiment the androgen receptor was blocked using flutamide in the diet.	Flutamide	62-71	androgen receptor	Rattus norvegicus	26-43
17957793-10	2008	Flutamide can effectively and safely reduce PCa development and significantly suppress PSCA mRNA expression in men with isolated HGPIN, whereas the increased PSCA mRNA expression after therapy may be a clinically adverse predictor for cancer onset.	Flutamide	0-9	prostate stem cell antigen	Homo sapiens	87-91
17968466-5	2007	RESULTS: We have identified beta2-microglobulin, cytoplasmic FMR1 interacting protein 2 and pumilio 1 as flutamide induced and spermine binding protein and ribophorin II as flutamide repressed targets in the rat ventral prostate.	Flutamide	105-114	beta-2 microglobulin	Rattus norvegicus	28-87
17823853-8	2008	However, testosterone together with 17beta-estradiol (E2) increased BCRP protein and mRNA approximately twofold, and this induction was abolished by ICI-182,780 or the testosterone receptor (TR) antagonist flutamide or knock-down of ER alpha expression.	Flutamide	206-215	BCR pseudogene 1	Homo sapiens	68-72
18497080-5	2008	Herein, we have elucidated the effects of flutamide (a defined anti-androgen) and DHT on the expression of PSA and Zinc finger E-box Binding factor (ZEB-1).	Flutamide	42-51	kallikrein related peptidase 3	Homo sapiens	107-110
18497080-5	2008	Herein, we have elucidated the effects of flutamide (a defined anti-androgen) and DHT on the expression of PSA and Zinc finger E-box Binding factor (ZEB-1).	Flutamide	42-51	zinc finger E-box binding homeobox 1	Homo sapiens	149-154
18497080-9	2008	In the current study, the effects of 1 and 10 nM flutamide, in combination with 1 and 10 nM DHT, on expression of ZEB-1 and PSA, were investigated in 22Rv1, an androgen-responsive human PC cell line.	Flutamide	49-58	zinc finger E-box binding homeobox 1	Homo sapiens	114-119
18497080-9	2008	In the current study, the effects of 1 and 10 nM flutamide, in combination with 1 and 10 nM DHT, on expression of ZEB-1 and PSA, were investigated in 22Rv1, an androgen-responsive human PC cell line.	Flutamide	49-58	kallikrein related peptidase 3	Homo sapiens	124-127
17916626-7	2008	Addition of flutamide (1 microM) to T-treated EBs inhibited the T-induced proliferation of cardiomyocytes, confirming that, in this instance, androgens act via the classical AR-mediated genomic pathway.	Flutamide	12-21	androgen receptor	Mus musculus	174-176
17968466-5	2007	RESULTS: We have identified beta2-microglobulin, cytoplasmic FMR1 interacting protein 2 and pumilio 1 as flutamide induced and spermine binding protein and ribophorin II as flutamide repressed targets in the rat ventral prostate.	Flutamide	105-114	pumilio RNA-binding family member 1	Rattus norvegicus	92-101
17968466-6	2007	Although flutamide treatment caused an induction of pumilio 1 mRNA, castration had no effect.	Flutamide	9-18	pumilio RNA-binding family member 1	Rattus norvegicus	52-61
17395695-13	2007	5) Flutamide, a testosterone receptor blocker, cancelled the suppressive effects of testosterone on HSP72 expression.	Flutamide	3-12	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	100-105
17984247-1	2007	OBJECTIVE: Addition of androgen receptor (AR) blockade (flutamide) to insulin-sensitising therapy (metformin) may confer synergistic benefits in girls with hyperinsulinaemic androgen excess.	Flutamide	56-65	androgen receptor	Homo sapiens	23-40
17984247-1	2007	OBJECTIVE: Addition of androgen receptor (AR) blockade (flutamide) to insulin-sensitising therapy (metformin) may confer synergistic benefits in girls with hyperinsulinaemic androgen excess.	Flutamide	56-65	androgen receptor	Homo sapiens	42-44
17984247-2	2007	We hypothesised that girls with shorter AR gene CAG repeat alleles, and thus greater receptor sensitivity, might benefit more from the addition of low-dose flutamide.	Flutamide	156-165	androgen receptor	Homo sapiens	40-42
17984247-12	2007	However, only those girls with genetic markers of greater AR sensitivity may benefit from the addition of flutamide above metformin alone.	Flutamide	106-115	androgen receptor	Homo sapiens	58-60
17516554-7	2007	A dose- and time-dependent decrease of DG expression also occurred in human prostate cancer cells following treatment with the anti-androgen flutamide.	Flutamide	141-150	dystroglycan 1	Homo sapiens	39-41
17825336-11	2007	After PRP was pretreated with flutamide, H(2)O(2)-induced platelet aggregation increased in castrated rats again.	Flutamide	30-39	proline rich protein 2-like 1	Rattus norvegicus	6-9
17870249-11	2007	Following treatment of primary hippocampal neurons with DHT, SERCA2 mRNA was increased, an effect that was blocked in the presence of flutamide.	Flutamide	134-143	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2	Rattus norvegicus	61-67
17558187-5	2007	Flutamide, ketoconazole, diethylhexylphthalate, nonylphenol, octylphenol and diethylstilbesterol significantly decreased SGP-2 mRNA expression in testes at all doses studied, with the exception of 1 mg/kg/day flutamide (P<0.05).	Flutamide	0-9	clusterin	Rattus norvegicus	121-126
17558187-5	2007	Flutamide, ketoconazole, diethylhexylphthalate, nonylphenol, octylphenol and diethylstilbesterol significantly decreased SGP-2 mRNA expression in testes at all doses studied, with the exception of 1 mg/kg/day flutamide (P<0.05).	Flutamide	209-218	clusterin	Rattus norvegicus	121-126
17369855-10	2007	AR antagonists (FLU and valproate) inhibit the hepatoma formation.	Flutamide	16-19	androgen receptor	Homo sapiens	0-2
17299064-1	2007	CONTEXT AND OBJECTIVE: One of the treatments for hyperinsulinemic hyperandrogenism in nonobese women is combined androgen receptor blockade (with flutamide; Flu), insulin sensitization (with metformin; Met) plus an estroprogestagen contraceptive.	Flutamide	146-155	insulin	Homo sapiens	54-61
17617741-9	2007	Flutamide (Flu), an AR antagonist, completely abolished DHT-stimulated cell growth and the expression of IL-6 and IL-8.	Flutamide	0-9	androgen receptor	Homo sapiens	20-22
17617741-9	2007	Flutamide (Flu), an AR antagonist, completely abolished DHT-stimulated cell growth and the expression of IL-6 and IL-8.	Flutamide	0-9	interleukin 6	Homo sapiens	105-109
17617741-9	2007	Flutamide (Flu), an AR antagonist, completely abolished DHT-stimulated cell growth and the expression of IL-6 and IL-8.	Flutamide	0-9	C-X-C motif chemokine ligand 8	Homo sapiens	114-118
17617741-9	2007	Flutamide (Flu), an AR antagonist, completely abolished DHT-stimulated cell growth and the expression of IL-6 and IL-8.	Flutamide	0-3	androgen receptor	Homo sapiens	20-22
17617741-9	2007	Flutamide (Flu), an AR antagonist, completely abolished DHT-stimulated cell growth and the expression of IL-6 and IL-8.	Flutamide	0-3	interleukin 6	Homo sapiens	105-109
17617741-9	2007	Flutamide (Flu), an AR antagonist, completely abolished DHT-stimulated cell growth and the expression of IL-6 and IL-8.	Flutamide	0-3	C-X-C motif chemokine ligand 8	Homo sapiens	114-118
17617741-11	2007	In the absence of androgen, both cytokines enhanced AR expression and AR promoter activation, which was completely blocked by Flu.	Flutamide	126-129	androgen receptor	Homo sapiens	52-54
17617741-11	2007	In the absence of androgen, both cytokines enhanced AR expression and AR promoter activation, which was completely blocked by Flu.	Flutamide	126-129	androgen receptor	Homo sapiens	70-72
17398002-4	2007	Co-administering flutamide, an androgen receptor blocker, with estrogen impedes estrogen"s masculinizing effects on the song system, suggesting that androgens are required for masculine development.	Flutamide	17-26	androgen receptor	Taeniopygia guttata	31-48
17464437-4	2007	Furthermore, we have demonstrated that ANG II-induced hypertension in males is blocked by central infusions of the androgen receptor antagonist, flutamide, and by central infusions of the superoxide dismutase mimetic, tempol.	Flutamide	145-154	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	39-45
17347309-0	2007	Flutamide and cyproterone acetate exert agonist effects: induction of androgen receptor-dependent neuroprotection.	Flutamide	0-9	androgen receptor	Homo sapiens	70-87
17229994-6	2007	However, flutamide remarkably increased the level of 3beta-HSD mRNA in the testes (P<0.05).	Flutamide	9-18	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	53-62
17636171-9	2007	Addition of flutamide to T-stimulated cells caused a twofold decrease in both TER and claudin-11 mRNA expression, and resulted in the loss of both proteins from cell contacts.	Flutamide	12-21	claudin 11	Rattus norvegicus	86-96
17254854-8	2007	Pretreatment with the AR blocker, flutamide, partially inhibited the effect of EXE.	Flutamide	34-43	androgen receptor	Homo sapiens	22-24
17409513-0	2007	Involvement of bile salt export pump in flutamide-induced cholestatic hepatitis.	Flutamide	40-49	ATP binding cassette subfamily B member 11	Rattus norvegicus	15-36
17409513-3	2007	We examined the inhibitory effects of flutamide and its active metabolite, hydroxyflutamide, on the transport of taurocholic acid (TCA) by membrane vesicles derived from hBSEP-expressing Sf9 cells.	Flutamide	38-47	ATP binding cassette subfamily B member 11	Homo sapiens	170-175
17409513-9	2007	These results suggest that flutamide itself, but not its major metabolite, may cause cholestasis by inhibiting BSEP-mediated bile salt excretion.	Flutamide	27-36	ATP binding cassette subfamily B member 11	Rattus norvegicus	111-115
17303007-7	2007	R1881 increased the expression of NKX3.1, and the AR antagonist flutamide decreased the expression of NKX3.1 in LNCaP cells, while curcumin could inhibit androgen-AR mediated induction of NKX3.1 expression.	Flutamide	64-73	androgen receptor	Homo sapiens	50-52
17303007-4	2007	Curcumin-treated cells disposed to a designated amount of androgen analog R1881 and the androgen receptor (AR) antagonist flutamide, then the expression of NKX3.1 or the activity of the NKX3.1 promoter were investigated by Western blotting or reporter gene assay, respectively.	Flutamide	122-131	androgen receptor	Homo sapiens	107-109
17303007-7	2007	R1881 increased the expression of NKX3.1, and the AR antagonist flutamide decreased the expression of NKX3.1 in LNCaP cells, while curcumin could inhibit androgen-AR mediated induction of NKX3.1 expression.	Flutamide	64-73	NK3 homeobox 1	Homo sapiens	102-108
17303007-7	2007	R1881 increased the expression of NKX3.1, and the AR antagonist flutamide decreased the expression of NKX3.1 in LNCaP cells, while curcumin could inhibit androgen-AR mediated induction of NKX3.1 expression.	Flutamide	64-73	androgen receptor	Homo sapiens	163-165
17303007-7	2007	R1881 increased the expression of NKX3.1, and the AR antagonist flutamide decreased the expression of NKX3.1 in LNCaP cells, while curcumin could inhibit androgen-AR mediated induction of NKX3.1 expression.	Flutamide	64-73	NK3 homeobox 1	Homo sapiens	102-108
17451792-13	2007	However, presence of flutamide (3 microM) significantly increased platelet aggregation in PRP diluted with autologous PPP or Tyrode"s buffer.	Flutamide	21-30	proline rich protein 2-like 1	Rattus norvegicus	90-93
17245185-0	2007	Flutamide attenuates pro-inflammatory cytokine production and hepatic injury following trauma-hemorrhage via estrogen receptor-related pathway.	Flutamide	0-9	estrogen receptor 1	Rattus norvegicus	109-126
17245185-5	2007	To block estrogen receptor (ER), ER antagonist ICI 182,780 was administrated with flutamide.	Flutamide	82-91	estrogen receptor 1	Rattus norvegicus	33-35
17245185-11	2007	Moreover, the salutary effects of flutamide administration appear to be mediated at least in part via ER-related pathway.	Flutamide	34-43	estrogen receptor 1	Rattus norvegicus	102-104
17132155-7	2007	Although the function of testicular Gal-3 remains to be investigated, a potential role of Gal-3 in germ cell survival/regeneration is suggested based on its increased expression 1 month after a transient germ cell death process triggered by 10 days of treatment with the antiandrogen flutamide.	Flutamide	284-293	galectin 3	Homo sapiens	90-95
17189957-6	2007	Co-treatment with 10(-6) M flutamide blocked 5alpha-DHT inhibition of OPG protein expression in LNCaP-FGC cells.	Flutamide	27-36	TNF receptor superfamily member 11b	Homo sapiens	70-73
17268154-6	2007	Some of them exhibited the androgen antagonistic activities in LNCaP cells with mutated androgen receptor in which conventional antagonists such as flutamide and RU56187 were inactive.	Flutamide	148-157	androgen receptor	Homo sapiens	88-105
17210686-6	2007	Androgen up-regulation of NAT1 was prevented by the AR antagonist flutamide.	Flutamide	66-75	N-acetyltransferase 1	Homo sapiens	26-30
17210686-6	2007	Androgen up-regulation of NAT1 was prevented by the AR antagonist flutamide.	Flutamide	66-75	androgen receptor	Homo sapiens	52-54
17207634-8	2006	Anti-CD3 stimulation, administration of 17beta-estradiol and 17beta-estradiol+flutamide, but not the administration of flutamide alone resulted in a significant increased release of TNF-alpha, IL-6 and IFN-gamma compared to vehicle-treated animals.	Flutamide	78-87	tumor necrosis factor	Mus musculus	182-191
17207634-5	2006	Administration of 17beta-estradiol, flutamide and 17beta-estradiol+flutamide following trauma-hemorrhage resulted in a significant increase in the in vitro IL-6 release by splenic MPhi.	Flutamide	36-45	interleukin 6	Mus musculus	156-160
17207634-5	2006	Administration of 17beta-estradiol, flutamide and 17beta-estradiol+flutamide following trauma-hemorrhage resulted in a significant increase in the in vitro IL-6 release by splenic MPhi.	Flutamide	67-76	interleukin 6	Mus musculus	156-160
17207634-8	2006	Anti-CD3 stimulation, administration of 17beta-estradiol and 17beta-estradiol+flutamide, but not the administration of flutamide alone resulted in a significant increased release of TNF-alpha, IL-6 and IFN-gamma compared to vehicle-treated animals.	Flutamide	78-87	interleukin 6	Mus musculus	193-197
17207634-6	2006	The TNF-alpha productive capacity, however, was only restored by 17beta-estradiol and 17beta-estradiol+flutamide administration following trauma-hemorrhage.	Flutamide	103-112	tumor necrosis factor	Mus musculus	4-13
17207634-8	2006	Anti-CD3 stimulation, administration of 17beta-estradiol and 17beta-estradiol+flutamide, but not the administration of flutamide alone resulted in a significant increased release of TNF-alpha, IL-6 and IFN-gamma compared to vehicle-treated animals.	Flutamide	78-87	interferon gamma	Mus musculus	202-211
17207634-8	2006	Anti-CD3 stimulation, administration of 17beta-estradiol and 17beta-estradiol+flutamide, but not the administration of flutamide alone resulted in a significant increased release of TNF-alpha, IL-6 and IFN-gamma compared to vehicle-treated animals.	Flutamide	119-128	tumor necrosis factor	Mus musculus	182-191
17110800-16	2006	Flutamide-treated FZDR showed enhanced pressor response to U46619 (P = 0.024, ANOVA), ET-1, and angiotensin II (P < 0.03, ANOVA).	Flutamide	0-9	endothelin 1	Rattus norvegicus	86-110
17110800-17	2006	Surprisingly, the augmented systemic pressor action of U46619 and ET-1 was accompanied by a renal vasodilator action, with paradoxic RCF increases to U46619 (P < 0.003, ANOVA) and to ET-1 (P < 0.001, ANOVA) only in flutamide-treated FZDR.	Flutamide	221-230	endothelin 1	Rattus norvegicus	66-70
17110800-22	2006	Flutamide caused a paradoxic but specific increase in renal perfusion during ET-1 and TXA2 receptor activation, which could be renoprotective in females.	Flutamide	0-9	endothelin 1	Rattus norvegicus	77-81
16777378-0	2006	Anti-progestogenic effect of flutamide on uterine expression of calbindin-D9k mRNA and protein in immature mice.	Flutamide	29-38	S100 calcium binding protein G	Mus musculus	64-77
16777378-7	2006	P4-induced expression levels of CaBP-9k mRNA and protein were abolished by FLU, in part, suggesting that FLU is a partial antagonist of P4 in the regulation of uterine CaBP-9k in immature mice.	Flutamide	75-78	S100 calcium binding protein G	Mus musculus	168-175
16777378-7	2006	P4-induced expression levels of CaBP-9k mRNA and protein were abolished by FLU, in part, suggesting that FLU is a partial antagonist of P4 in the regulation of uterine CaBP-9k in immature mice.	Flutamide	105-108	S100 calcium binding protein G	Mus musculus	32-39
16777378-7	2006	P4-induced expression levels of CaBP-9k mRNA and protein were abolished by FLU, in part, suggesting that FLU is a partial antagonist of P4 in the regulation of uterine CaBP-9k in immature mice.	Flutamide	105-108	S100 calcium binding protein G	Mus musculus	168-175
16777378-11	2006	Treatment with FLU suppressed partially P4-induced CaBP-9k mRNA and protein until 24 h. Taken together, these results indicate that FLU has an anti-progestogenic activity and plays a role as a partial antagonist of P4 in the regulation of uterine CaBP-9k in immature mouse model.	Flutamide	15-18	S100 calcium binding protein G	Mus musculus	51-58
16777378-11	2006	Treatment with FLU suppressed partially P4-induced CaBP-9k mRNA and protein until 24 h. Taken together, these results indicate that FLU has an anti-progestogenic activity and plays a role as a partial antagonist of P4 in the regulation of uterine CaBP-9k in immature mouse model.	Flutamide	15-18	S100 calcium binding protein G	Mus musculus	247-254
16777378-11	2006	Treatment with FLU suppressed partially P4-induced CaBP-9k mRNA and protein until 24 h. Taken together, these results indicate that FLU has an anti-progestogenic activity and plays a role as a partial antagonist of P4 in the regulation of uterine CaBP-9k in immature mouse model.	Flutamide	132-135	S100 calcium binding protein G	Mus musculus	51-58
16777378-11	2006	Treatment with FLU suppressed partially P4-induced CaBP-9k mRNA and protein until 24 h. Taken together, these results indicate that FLU has an anti-progestogenic activity and plays a role as a partial antagonist of P4 in the regulation of uterine CaBP-9k in immature mouse model.	Flutamide	132-135	S100 calcium binding protein G	Mus musculus	247-254
17073576-8	2006	Finally, there may be mechanisms for all nitroaromatic drugs that do not involve bioactivation of the nitro group, e.g., AHR interactions with flutamide.	Flutamide	143-152	aryl hydrocarbon receptor	Homo sapiens	121-124
16911836-10	2006	In particular, the antiandrogenic activities of phenyl- and benzyl salicylate, benzophenone-1 and -2, and of 4-hydroxybenzophenone were higher than that of flutamide, a known hAR antagonist.	Flutamide	156-165	lymphatic vessel endothelial hyaluronan receptor 1	Homo sapiens	175-178
16611858-6	2006	The FLU gene response was comparable with classical AhR ligands across a signature AhR ligand gene set that included CYP1A1 and other members of the AhR gene battery.	Flutamide	4-7	aryl hydrocarbon receptor	Rattus norvegicus	83-86
16809447-2	2006	The present study used in utero exposure of pregnant rats to the androgen receptor antagonist flutamide (50 or 100 mg/kg) to explore possible mechanisms.	Flutamide	94-103	androgen receptor	Rattus norvegicus	65-82
16895975-5	2006	Administration of E2, flutamide, or E2 + flutamide following T-H resulted in a significant decrease in systemic TNF-alpha, IL-6, and MCP-1 concentrations under those conditions.	Flutamide	22-31	tumor necrosis factor	Mus musculus	112-121
16895975-5	2006	Administration of E2, flutamide, or E2 + flutamide following T-H resulted in a significant decrease in systemic TNF-alpha, IL-6, and MCP-1 concentrations under those conditions.	Flutamide	22-31	interleukin 6	Mus musculus	123-127
16895975-5	2006	Administration of E2, flutamide, or E2 + flutamide following T-H resulted in a significant decrease in systemic TNF-alpha, IL-6, and MCP-1 concentrations under those conditions.	Flutamide	22-31	mast cell protease 1	Mus musculus	133-138
16895975-5	2006	Administration of E2, flutamide, or E2 + flutamide following T-H resulted in a significant decrease in systemic TNF-alpha, IL-6, and MCP-1 concentrations under those conditions.	Flutamide	41-50	tumor necrosis factor	Mus musculus	112-121
16895975-5	2006	Administration of E2, flutamide, or E2 + flutamide following T-H resulted in a significant decrease in systemic TNF-alpha, IL-6, and MCP-1 concentrations under those conditions.	Flutamide	41-50	interleukin 6	Mus musculus	123-127
16895975-5	2006	Administration of E2, flutamide, or E2 + flutamide following T-H resulted in a significant decrease in systemic TNF-alpha, IL-6, and MCP-1 concentrations under those conditions.	Flutamide	41-50	mast cell protease 1	Mus musculus	133-138
16895975-6	2006	This was accompanied by significantly decreased in vitro TNF-alpha release by Kupffer cells after administration of E2, flutamide, or E2 + flutamide.	Flutamide	120-129	tumor necrosis factor	Mus musculus	57-66
16895975-6	2006	This was accompanied by significantly decreased in vitro TNF-alpha release by Kupffer cells after administration of E2, flutamide, or E2 + flutamide.	Flutamide	139-148	tumor necrosis factor	Mus musculus	57-66
16980238-2	2006	Based upon this observation, two important discoveries also made by our group are applied worlwide, namely the use of GnRH (gonadotropin -releasing hormone) agonists that completely block testicular androgen secretion, while, simultaneously, the androgens made locally in the prostate from DHEA are blocked in their access to the androgen receptor by a pure antiandrogen (flutamide, bicalutamide or nilutamide).	Flutamide	372-381	gonadotropin releasing hormone 1	Homo sapiens	118-122
16980238-2	2006	Based upon this observation, two important discoveries also made by our group are applied worlwide, namely the use of GnRH (gonadotropin -releasing hormone) agonists that completely block testicular androgen secretion, while, simultaneously, the androgens made locally in the prostate from DHEA are blocked in their access to the androgen receptor by a pure antiandrogen (flutamide, bicalutamide or nilutamide).	Flutamide	372-381	gonadotropin releasing hormone 1	Homo sapiens	124-155
16652386-4	2006	After proteomic comparison of these cells to those where flutamide functioned normally as an antagonist, we identified DJ-1, a positive regulator of AR.	Flutamide	57-66	Parkinsonism associated deglycase	Homo sapiens	119-123
16652386-5	2006	DJ-1 expression increased in HPE and LNCaP cells during flutamide treatment as a result of DJ-1 protein stabilization.	Flutamide	56-65	Parkinsonism associated deglycase	Homo sapiens	0-4
16652386-5	2006	DJ-1 expression increased in HPE and LNCaP cells during flutamide treatment as a result of DJ-1 protein stabilization.	Flutamide	56-65	Parkinsonism associated deglycase	Homo sapiens	91-95
16868063-10	2006	Moreover, after 12 months, flutamide improved more than placebo the menstrual pattern (P = 0.008), glucose-stimulated glucose levels (P = 0.041), insulin sensitivity (P < 0.001), and low-density lipoprotein cholesterol levels (P = 0.003), whereas metformin decreased glucose-stimulated insulin levels (P = 0.014).	Flutamide	27-36	insulin	Homo sapiens	146-153
16868063-10	2006	Moreover, after 12 months, flutamide improved more than placebo the menstrual pattern (P = 0.008), glucose-stimulated glucose levels (P = 0.041), insulin sensitivity (P < 0.001), and low-density lipoprotein cholesterol levels (P = 0.003), whereas metformin decreased glucose-stimulated insulin levels (P = 0.014).	Flutamide	27-36	insulin	Homo sapiens	289-296
16784849-2	2006	Compound 1b (relative binding affinity, RBA = 6.4) and 1h (RBA = 12.6) showed higher binding affinity than flutamide (RBA = 1), a potent AR antagonist.	Flutamide	107-116	androgen receptor	Homo sapiens	137-139
16756952-0	2006	Anti-estrogen ICI 182.780 and anti-androgen flutamide induce tyrosine phosphorylation of cortactin in the ectoplasmic specialization between the Sertoli cell and spermatids in the mouse testis.	Flutamide	44-53	cortactin	Mus musculus	89-98
16756952-2	2006	Also, expression of cortactin, an F-actin-binding protein, was decreased by the treatment of FLUT in mouse testis.	Flutamide	93-97	cortactin	Mus musculus	20-29
16756952-5	2006	These results suggest that the sex hormone antagonists", ICI and FLUT, induced actin depolymerization and tyrosine phosphorylation of cortactin in the mouse testis.	Flutamide	65-69	cortactin	Mus musculus	134-143
16763722-7	2006	Dihydrotestosterone (DHT) regulated PAR mRNA expression in LNCaP cells and the effect was inhibited by the AR antagonist, flutamide.	Flutamide	122-131	jumping translocation breakpoint	Homo sapiens	36-39
16763722-7	2006	Dihydrotestosterone (DHT) regulated PAR mRNA expression in LNCaP cells and the effect was inhibited by the AR antagonist, flutamide.	Flutamide	122-131	androgen receptor	Homo sapiens	37-39
16611858-6	2006	The FLU gene response was comparable with classical AhR ligands across a signature AhR ligand gene set that included CYP1A1 and other members of the AhR gene battery.	Flutamide	4-7	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	117-123
16611858-6	2006	The FLU gene response was comparable with classical AhR ligands across a signature AhR ligand gene set that included CYP1A1 and other members of the AhR gene battery.	Flutamide	4-7	aryl hydrocarbon receptor	Rattus norvegicus	83-86
16611858-8	2006	FLU had a sharp down-regulation of c-fos that was comparable with all the compounds except CPZ and CLO.	Flutamide	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
16239932-3	2006	EGFR-mediated increase in 3H-thymidine uptake was inhibited by FTA.	Flutamide	63-66	epidermal growth factor receptor	Homo sapiens	0-4
16611858-9	2006	FLU absorption, distribution, metabolism, and excretion (ADME) gene expression analysis revealed that FLU, as well as I3C and OME, induced CYP2B and CYP3A, distinguishing them from the classical AhR ligands.	Flutamide	102-105	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	149-154
16481087-0	2006	Flutamide depresses expression of cortactin in the ectoplasmic specialization between the Sertoli cells and spermatids in the mouse testis.	Flutamide	0-9	cortactin	Mus musculus	34-43
16481087-11	2006	To our knowledge, this study is the first to document the decrease of cortactin expression in the abnormal apical ES following treatment with FLUT.	Flutamide	142-146	cortactin	Mus musculus	70-79
16735550-3	2006	Groups of laying hens (n = 10-22) were treated with the androgen receptor antagonist, flutamide, at 8 h intervals for 24 h at doses of 0, 31.25, 62.5, 125 and 250 mg. All doses reduced egg laying (P < 0.001), with the highest dose being the most effective.	Flutamide	86-95	androgen receptor	Gallus gallus	56-73
16537657-14	2006	FLU-induced changes suggest the importance of androgen receptor-mediated regulation of testosterone synthesis in the postnatal rat testis.	Flutamide	0-3	androgen receptor	Rattus norvegicus	46-63
16368782-7	2006	Flutamide abolished the DHT-modulated increases in IGF-I and IGFBP-2, suggesting that the influences of DHT and T on these measures were androgen receptor mediated.	Flutamide	0-9	insulin like growth factor 1	Homo sapiens	51-56
16368782-7	2006	Flutamide abolished the DHT-modulated increases in IGF-I and IGFBP-2, suggesting that the influences of DHT and T on these measures were androgen receptor mediated.	Flutamide	0-9	insulin like growth factor binding protein 2	Homo sapiens	61-68
16642786-14	2006	Moreover, testosterone-induced neuroprotection likely entails a linkage with the androgen receptor as is suggested by the flutamide-induced inhibition of the hormone activity.	Flutamide	122-131	androgen receptor	Mus musculus	81-98
16373395-4	2006	Consistent with a role in both antagonist- and agonist-regulated transcription by AR, chromatin immunoprecipitation analysis revealed that both SMRT and N-CoR were recruited by AR to these genes in the presence of either flutamide or R1881.	Flutamide	221-230	nuclear receptor corepressor 2	Homo sapiens	144-148
16373395-4	2006	Consistent with a role in both antagonist- and agonist-regulated transcription by AR, chromatin immunoprecipitation analysis revealed that both SMRT and N-CoR were recruited by AR to these genes in the presence of either flutamide or R1881.	Flutamide	221-230	nuclear receptor corepressor 1	Homo sapiens	153-158
16373395-4	2006	Consistent with a role in both antagonist- and agonist-regulated transcription by AR, chromatin immunoprecipitation analysis revealed that both SMRT and N-CoR were recruited by AR to these genes in the presence of either flutamide or R1881.	Flutamide	221-230	androgen receptor	Homo sapiens	177-179
16239932-5	2006	The sub-Go population of GBM cells was increased from 4.5 to 13.8% (control) to over 45-53.6% in FTA-treated cells within 24 h. Furthermore, FTA also increased the activities of both caspase-3 and -9, and PARP cleavage.	Flutamide	97-100	poly(ADP-ribose) polymerase 1	Homo sapiens	205-209
16239932-5	2006	The sub-Go population of GBM cells was increased from 4.5 to 13.8% (control) to over 45-53.6% in FTA-treated cells within 24 h. Furthermore, FTA also increased the activities of both caspase-3 and -9, and PARP cleavage.	Flutamide	141-144	caspase 3	Homo sapiens	183-199
16239932-5	2006	The sub-Go population of GBM cells was increased from 4.5 to 13.8% (control) to over 45-53.6% in FTA-treated cells within 24 h. Furthermore, FTA also increased the activities of both caspase-3 and -9, and PARP cleavage.	Flutamide	141-144	poly(ADP-ribose) polymerase 1	Homo sapiens	205-209
16239932-6	2006	Treatment of GBMs with FTA before or after EGF addition to the cultures blocked phosphorylation of Akt and mitogen-activated protein kinases (MAPK).	Flutamide	23-26	AKT serine/threonine kinase 1	Homo sapiens	99-102
16410299-4	2006	In this study, using a glial cell model (C6 cells) that we found to express the AR, we identified that DHT increased the phosphorylation of both ERK and Akt, key effectors of the neuroprotection-associated MAPK and phosphoinositide 3-kinase signaling pathways, respectively, and ERK phosphorylation was blocked by the AR antagonist, flutamide.	Flutamide	333-342	androgen receptor	Homo sapiens	80-82
16410299-4	2006	In this study, using a glial cell model (C6 cells) that we found to express the AR, we identified that DHT increased the phosphorylation of both ERK and Akt, key effectors of the neuroprotection-associated MAPK and phosphoinositide 3-kinase signaling pathways, respectively, and ERK phosphorylation was blocked by the AR antagonist, flutamide.	Flutamide	333-342	mitogen-activated protein kinase 1	Homo sapiens	145-148
16239932-5	2006	The sub-Go population of GBM cells was increased from 4.5 to 13.8% (control) to over 45-53.6% in FTA-treated cells within 24 h. Furthermore, FTA also increased the activities of both caspase-3 and -9, and PARP cleavage.	Flutamide	97-100	caspase 3	Homo sapiens	183-199
16597033-1	2006	OBJECTIVE: To investigate the effect of dihydrotestosterone (DHT) on the gene transcriptions and expressions of Smad3 and Smad4 in androgen dependent prostate cancer cell line LNCaP, and whether this effect can be suppressed by the androgen receptor inhibitor flutamide.	Flutamide	260-269	SMAD family member 3	Homo sapiens	112-117
16520034-8	2006	Finally, enhanced levels of alpha- and beta-globin mRNAs at the pituitary were also demonstrated after neonatal administration of the anti-androgen flutamide.	Flutamide	148-157	hemoglobin alpha, adult chain 3	Rattus norvegicus	28-50
16480982-9	2006	Furthermore, co-treatment of flutamide with estradiol-17beta (E2) also restored the phenotype, suggesting androgen-AR signaling might activate aromatase expression that is necessary for estrogen synthesis.	Flutamide	29-38	androgen receptor	Gallus gallus	115-117
16699857-0	2006	Metabolism and hepatic toxicity of flutamide in cytochrome P450 1A2 knockout SV129 mice.	Flutamide	35-44	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	48-67
16699857-4	2006	METHODS: Flutamide was administered daily to CYP1A2 knockout mice and parental SV129 mice to compare pharmacokinetics and appearance of hepatic toxicity.	Flutamide	9-18	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	45-51
16699857-5	2006	RESULTS: In the CYP1A2 knockout mice, the plasma concentration of flutamide maintained at a high level and OH-flutamide stayed low; a higher amount of FLU-1, an alternative metabolite of flutamide, was detected in urine.	Flutamide	66-75	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	16-22
16699857-5	2006	RESULTS: In the CYP1A2 knockout mice, the plasma concentration of flutamide maintained at a high level and OH-flutamide stayed low; a higher amount of FLU-1, an alternative metabolite of flutamide, was detected in urine.	Flutamide	110-119	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	16-22
16699857-6	2006	Simple repetitive administration of 800 mg/kg of flutamide for 28 days to CYP1A2 knockout mice did not show abnormal elevation of plasma alanine aminotransferase (ALT).	Flutamide	49-58	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	74-80
16699857-7	2006	However, after the knockout mice were fed with an amino acid-deficient diet for 2 weeks, which reduced the glutathione (GSH) content to 27% of the initial, administration of 400 mg/kg of flutamide increased ALT to over 200 IU/l and histopathologically moderate hepatitis developed.	Flutamide	187-196	glutamic pyruvic transaminase, soluble	Mus musculus	207-210
16597033-7	2006	Flutamide inhibited the up-regulation of both Smad3 mRNA transcription and expression significantly (P <0.05).	Flutamide	0-9	SMAD family member 3	Homo sapiens	46-51
16597033-11	2006	Flutamide inhibited the suppressive effects of DHT on both Smad4 mRNA transcription and expression.	Flutamide	0-9	SMAD family member 4	Homo sapiens	59-64
16155096-9	2006	The flutamide-mediated restoration of cardiac function, the increases in aromatase activity and estrogen levels, ER-alpha, ER-beta, PGC-1, COX I, COX activity, and ATP contents were, however, abolished when ER antagonist ICI-182,780 was administrated along with flutamide.	Flutamide	4-13	estrogen receptor 1	Rattus norvegicus	113-121
16239318-0	2006	Discontinuous low-dose flutamide-metformin plus an oral or a transdermal contraceptive in patients with hyperinsulinaemic hyperandrogenism: normalizing effects on CRP, TNF-alpha and the neutrophil/lymphocyte ratio.	Flutamide	23-32	C-reactive protein	Homo sapiens	163-166
16330533-0	2006	Mechanism of the salutary effects of flutamide on intestinal myeloperoxidase activity following trauma-hemorrhage: up-regulation of estrogen receptor-{beta}-dependent HO-1.	Flutamide	37-46	myeloperoxidase	Rattus norvegicus	61-76
16330533-0	2006	Mechanism of the salutary effects of flutamide on intestinal myeloperoxidase activity following trauma-hemorrhage: up-regulation of estrogen receptor-{beta}-dependent HO-1.	Flutamide	37-46	estrogen receptor 2	Rattus norvegicus	132-155
16330533-0	2006	Mechanism of the salutary effects of flutamide on intestinal myeloperoxidase activity following trauma-hemorrhage: up-regulation of estrogen receptor-{beta}-dependent HO-1.	Flutamide	37-46	heme oxygenase 1	Rattus norvegicus	167-171
16330533-3	2006	We hypothesized that flutamide administration in males following T-H up-regulates HO-1 via an ER-dependent pathway and protects against intestinal injury.	Flutamide	21-30	heme oxygenase 1	Rattus norvegicus	82-86
16330533-9	2006	These parameters were improved significantly in the flutamide-treated rats subjected to T-H. Flutamide treatment increased intestinal HO-1 and ER-beta mRNA/protein levels as compared with vehicle-treated T-H rats.	Flutamide	52-61	heme oxygenase 1	Rattus norvegicus	134-138
16330533-9	2006	These parameters were improved significantly in the flutamide-treated rats subjected to T-H. Flutamide treatment increased intestinal HO-1 and ER-beta mRNA/protein levels as compared with vehicle-treated T-H rats.	Flutamide	52-61	estrogen receptor 2	Rattus norvegicus	143-150
16330533-9	2006	These parameters were improved significantly in the flutamide-treated rats subjected to T-H. Flutamide treatment increased intestinal HO-1 and ER-beta mRNA/protein levels as compared with vehicle-treated T-H rats.	Flutamide	93-102	heme oxygenase 1	Rattus norvegicus	134-138
16330533-9	2006	These parameters were improved significantly in the flutamide-treated rats subjected to T-H. Flutamide treatment increased intestinal HO-1 and ER-beta mRNA/protein levels as compared with vehicle-treated T-H rats.	Flutamide	93-102	estrogen receptor 2	Rattus norvegicus	143-150
16330533-11	2006	Thus, the salutary effects of flutamide administration on attenuation of intestinal injury following T-H are mediated via up-regulation of ER-beta-dependent HO-1 expression.	Flutamide	30-39	estrogen receptor 2	Rattus norvegicus	139-146
16330533-11	2006	Thus, the salutary effects of flutamide administration on attenuation of intestinal injury following T-H are mediated via up-regulation of ER-beta-dependent HO-1 expression.	Flutamide	30-39	heme oxygenase 1	Rattus norvegicus	157-161
16481260-11	2006	D0 flutamide pretreated cultured with CGRP showed no increase in cell proliferation compared with controls (16% vs 11%), but a small response was seen by D2 (19% vs 9%, P < .05).	Flutamide	3-12	calcitonin-related polypeptide alpha	Rattus norvegicus	38-42
16155096-9	2006	The flutamide-mediated restoration of cardiac function, the increases in aromatase activity and estrogen levels, ER-alpha, ER-beta, PGC-1, COX I, COX activity, and ATP contents were, however, abolished when ER antagonist ICI-182,780 was administrated along with flutamide.	Flutamide	4-13	estrogen receptor 2	Rattus norvegicus	123-130
16210366-9	2006	However, flutamide given in a similar treatment schedule did increase the TDI in GnRH-ant plus testosterone-treated rats.	Flutamide	9-18	gonadotropin releasing hormone 1	Rattus norvegicus	81-85
18528466-13	2006	We further demonstrated that MRP1 overexpression blocked the accumulation of flutamide and hydroxy-flutamide (the active metabolite) without affecting transport of dihydrotesterone, thereby blocking access of the anti-androgen but not the androgen to intracellular androgen receptors.	Flutamide	77-86	ATP binding cassette subfamily B member 1	Homo sapiens	29-33
16169144-2	2005	The assay displayed appropriate response to the known AR agonist 5alpha-dihydrotestosterone (DHT) and AR antagonist flutamide.	Flutamide	116-125	lymphatic vessel endothelial hyaluronan receptor 1	Homo sapiens	102-104
16169144-3	2005	DHT induced AR-mediated transcriptional activity in a concentration-dependent manner with median effective concentration (EC50) value of (3.90+/-1.43)x10(-10)M. Flutamide exhibited potent antiandrogenic activity with median inhibitory concentration (IC50) value of (1.02+/-0.35)x10(-7)M. Bisphenol A (BPA) and alkylphenols (APs) belong to the industrial chemicals that have received considerable attention due to high production and widespread usage.	Flutamide	161-170	lymphatic vessel endothelial hyaluronan receptor 1	Homo sapiens	12-14
16055512-9	2005	Moreover, E2 and flutamide normalized expression of cardiac PGC-1, NRF-2, Tfam, cytochrome-c oxidase subunit IV, and the mitochondrial DNA-encoded gene cytochrome-c oxidase subunit I and beta-ATP synthase, mitochondrial ATP, and cytochrome-c oxidase activity.	Flutamide	17-26	NFE2 like bZIP transcription factor 2	Rattus norvegicus	67-72
15981214-1	2005	We have hypothesized that some steroid derivatives bind to the androgen receptor (AR) with very low androgenic activity and therefore potentially function as better AR antagonists than clinically used antiandrogens, such as flutamide.	Flutamide	224-233	androgen receptor	Homo sapiens	63-80
15981214-1	2005	We have hypothesized that some steroid derivatives bind to the androgen receptor (AR) with very low androgenic activity and therefore potentially function as better AR antagonists than clinically used antiandrogens, such as flutamide.	Flutamide	224-233	androgen receptor	Homo sapiens	82-84
16498641-10	2006	In flutamide, linuron, and p,p"-DDE treatment groups, the expression of hemoglobin Y, beta-like embryonic chain (Hbb-y) was reduced.	Flutamide	3-12	hemoglobin subunit epsilon 1	Rattus norvegicus	72-111
16498641-10	2006	In flutamide, linuron, and p,p"-DDE treatment groups, the expression of hemoglobin Y, beta-like embryonic chain (Hbb-y) was reduced.	Flutamide	3-12	hemoglobin subunit epsilon 1	Rattus norvegicus	113-118
16267627-7	2005	At this moment, potential clinically relevant application of CYP450 pharmacogenetics for anticancer therapy may be found for CYP1A2 and flutamide, CYP2A6 and tegafur, CYP2B6 and cyclophosphamide, CYP2C8 and paclitaxel, CYP2D6 and tamoxifen, and CYP3A5.	Flutamide	136-145	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	196-202
16267627-7	2005	At this moment, potential clinically relevant application of CYP450 pharmacogenetics for anticancer therapy may be found for CYP1A2 and flutamide, CYP2A6 and tegafur, CYP2B6 and cyclophosphamide, CYP2C8 and paclitaxel, CYP2D6 and tamoxifen, and CYP3A5.	Flutamide	136-145	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	219-225
16267627-7	2005	At this moment, potential clinically relevant application of CYP450 pharmacogenetics for anticancer therapy may be found for CYP1A2 and flutamide, CYP2A6 and tegafur, CYP2B6 and cyclophosphamide, CYP2C8 and paclitaxel, CYP2D6 and tamoxifen, and CYP3A5.	Flutamide	136-145	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	245-251
16294275-14	2005	The effects of E2 and Te on osteoclast formation and bone resorption were completely antagonized by an E2 receptor (ER) antagonist, ICI 182,780, and an androgen receptor (AR) antagonist, flutamide, suggesting ER- and AR-mediated mechanisms, respectively, in these cultures.	Flutamide	187-196	cystatin 12, pseudogene	Homo sapiens	15-24
16294275-14	2005	The effects of E2 and Te on osteoclast formation and bone resorption were completely antagonized by an E2 receptor (ER) antagonist, ICI 182,780, and an androgen receptor (AR) antagonist, flutamide, suggesting ER- and AR-mediated mechanisms, respectively, in these cultures.	Flutamide	187-196	androgen receptor	Homo sapiens	152-169
16301331-2	2005	It is highly expressed in the testis, and because spermatogenesis is androgen dependent, we investigated the androgen dependency expression of Cbl through its testicular sub-localization and its expression levels in rats that were exposed to the antiandrogen flutamide or were hypophysectomized.	Flutamide	259-268	Cbl proto-oncogene	Rattus norvegicus	143-146
16301331-3	2005	We report the androgen dependency of Cbl as it localizes in pachytene spermatocytes during androgen-dependent stages, is down-regulated upon flutamide exposure, and is up-regulated with testosterone in hypophysectomized rats.	Flutamide	141-150	Cbl proto-oncogene	Rattus norvegicus	37-40
16301331-5	2005	As flutamide induces germ cell apoptosis, we investigate members of the Bcl-2 family upon flutamide exposure.	Flutamide	3-12	BCL2, apoptosis regulator	Rattus norvegicus	72-77
16301331-5	2005	As flutamide induces germ cell apoptosis, we investigate members of the Bcl-2 family upon flutamide exposure.	Flutamide	90-99	BCL2, apoptosis regulator	Rattus norvegicus	72-77
16054371-3	2005	Today, treatment of prostate cancer is done by inhibition of AR using antiandrogens such as flutamide (pro-drug of hydroxyflutamide), nilutamide, and bicalutamide.	Flutamide	92-101	androgen receptor	Homo sapiens	61-63
16225762-0	2005	Induction of liver cytochrome P450 1A2 expression by flutamide in rats.	Flutamide	53-62	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	19-38
16225762-1	2005	AIM: To investigate the modulation of liver cytochrome P450 1A2 (CYP1A2) expression by giving flutamide to adult rats.	Flutamide	94-103	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	44-63
16225762-1	2005	AIM: To investigate the modulation of liver cytochrome P450 1A2 (CYP1A2) expression by giving flutamide to adult rats.	Flutamide	94-103	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	65-71
16225762-6	2005	RESULTS: CYP1A2 mRNA levels after flutamide treatment at 100 mg/kg and 200 mg/kg were, respectively, 1.86 and 3.11-fold higher than those of the control.	Flutamide	34-43	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	9-15
16225762-9	2005	CONCLUSION: Giving rats flutamide induced liver CYP1A2 expression in a dose-dependent manner.	Flutamide	24-33	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	48-54
16315394-3	2005	Combined treatment with continuous release of acyline (3 mg/kg BW/day) with flutamide (in the form of sc pellets of 25 mg) resulted in almost the same level of suppression of spermatogenesis, as judged by testis weight and by germ cell apoptotic index, in 2 weeks as that reported for rats after treatment with 1.25 mg/kg BW Nal-Glu GnRH-A for the same time period.	Flutamide	76-85	gonadotropin releasing hormone 1	Rattus norvegicus	333-339
16315394-7	2005	In fact, treatment with a single high (20 mg/kg BW) dose of acyline combined with flutamide in mice achieved same or greater level of suppression, measured by germ cell counts at stages VII-VIII, in two weeks when compared with those reported after daily treatment with Nal-Glu GnRH-A for 4 weeks in rats.	Flutamide	82-91	gonadotropin releasing hormone 1	Rattus norvegicus	278-284
16055512-9	2005	Moreover, E2 and flutamide normalized expression of cardiac PGC-1, NRF-2, Tfam, cytochrome-c oxidase subunit IV, and the mitochondrial DNA-encoded gene cytochrome-c oxidase subunit I and beta-ATP synthase, mitochondrial ATP, and cytochrome-c oxidase activity.	Flutamide	17-26	transcription factor A, mitochondrial	Rattus norvegicus	74-78
16055512-9	2005	Moreover, E2 and flutamide normalized expression of cardiac PGC-1, NRF-2, Tfam, cytochrome-c oxidase subunit IV, and the mitochondrial DNA-encoded gene cytochrome-c oxidase subunit I and beta-ATP synthase, mitochondrial ATP, and cytochrome-c oxidase activity.	Flutamide	17-26	cytochrome c oxidase subunit 4i1	Rattus norvegicus	80-111
16037377-7	2005	We also compared expression of Insl3 and P450 side-chain cleavage enzyme in fetal testes from rats exposed in utero to DBP or flutamide (50 mg/kg.d).	Flutamide	126-135	insulin-like 3	Rattus norvegicus	31-36
16275987-0	2005	Imaging androgen receptor function during flutamide treatment in the LAPC9 xenograft model.	Flutamide	42-51	androgen receptor	Homo sapiens	8-25
16275987-2	2005	In this study, we test whether a novel androgen receptor-specific molecular imaging system is able to detect the action of the antiandrogen flutamide on androgen receptor function in xenograft models of prostate cancer.	Flutamide	140-149	androgen receptor	Homo sapiens	39-56
16275987-2	2005	In this study, we test whether a novel androgen receptor-specific molecular imaging system is able to detect the action of the antiandrogen flutamide on androgen receptor function in xenograft models of prostate cancer.	Flutamide	140-149	androgen receptor	Homo sapiens	153-170
16275987-6	2005	Analysis of androgen receptor and RNA polymerase II binding to the endogenous PSA gene by chromatin immunoprecipitation revealed that flutamide treatment and androgen withdrawal have different molecular mechanisms.	Flutamide	134-143	androgen receptor	Homo sapiens	12-29
16275987-6	2005	Analysis of androgen receptor and RNA polymerase II binding to the endogenous PSA gene by chromatin immunoprecipitation revealed that flutamide treatment and androgen withdrawal have different molecular mechanisms.	Flutamide	134-143	kallikrein related peptidase 3	Homo sapiens	78-81
16153201-1	2005	OBJECTIVE: To determine the prostate-specific antigen (PSA) response and time to PSA or radiographic progression in men with prostate cancer refractory to bicalutamide and/or flutamide therapy.	Flutamide	175-184	kallikrein related peptidase 3	Homo sapiens	28-59
16153202-10	2005	CONCLUSIONS: MAB using flutamide as second-line hormonal therapy can give a comparatively favourable PSA response with no severe side-effects; therefore, this therapy may be suitable for patients with HRPC after primary MAB using bicalutamide has failed, particularly in those with no bone metastases or whose disease has progressed for >1 year after first-line therapy.	Flutamide	23-32	kallikrein related peptidase 3	Homo sapiens	101-104
16417039-5	2005	Other means of interfering with androgen receptor function (e.g., by exposure to the pharmaceutical agent flutamide) lead to similar adverse health outcomes.	Flutamide	106-115	androgen receptor	Homo sapiens	32-49
16172422-9	2005	The induction by testosterone was completely blocked by adding the AR antagonist flutamide.	Flutamide	81-90	androgen receptor	Homo sapiens	67-69
16116338-9	2005	At doses of 0.1 and 1 microM, the vasodilator effects of DHEAS and testosterone were inhibited by the androgen receptor antagonist flutamide but not the estrogen receptor antagonist ICI 182,780.	Flutamide	131-140	sulfotransferase family 2A member 1	Homo sapiens	57-62
15795901-8	2005	Expression of organic anion transporter 3 (OAT3) mRNA in TR-BBB cells was induced by treatment with dihydrotestosterone (DHT), an AR ligand, and this induction was suppressed by flutamide.	Flutamide	178-187	solute carrier family 22 member 8	Rattus norvegicus	14-41
15795901-8	2005	Expression of organic anion transporter 3 (OAT3) mRNA in TR-BBB cells was induced by treatment with dihydrotestosterone (DHT), an AR ligand, and this induction was suppressed by flutamide.	Flutamide	178-187	solute carrier family 22 member 8	Rattus norvegicus	43-47
16116338-9	2005	At doses of 0.1 and 1 microM, the vasodilator effects of DHEAS and testosterone were inhibited by the androgen receptor antagonist flutamide but not the estrogen receptor antagonist ICI 182,780.	Flutamide	131-140	androgen receptor	Sus scrofa	102-119
15699175-8	2005	The effects of T4 in vivo and in vitro were reversed by the androgen receptor antagonist, flutamide, indicating that the regulatory effects of T4 were mediated through the androgen receptor.	Flutamide	90-99	androgen receptor	Mus musculus	60-77
16005950-4	2005	Pregnant females received daily injections of the androgen receptor antagonist flutamide from day 12 of pregnancy until pups were born.	Flutamide	79-88	androgen receptor	Rattus norvegicus	50-67
15659706-7	2005	Treatment of adult rats with flutamide induced stage-dependent cyclin D2 immunoexpression in Sertoli cells within 18 h, and confocal microscopy revealed that immunoexpression of AR and cyclin D2 were mutually exclusive within individual seminiferous tubules in these animals.	Flutamide	29-38	cyclin D2	Rattus norvegicus	63-72
15659706-7	2005	Treatment of adult rats with flutamide induced stage-dependent cyclin D2 immunoexpression in Sertoli cells within 18 h, and confocal microscopy revealed that immunoexpression of AR and cyclin D2 were mutually exclusive within individual seminiferous tubules in these animals.	Flutamide	29-38	androgen receptor	Rattus norvegicus	178-180
15659706-7	2005	Treatment of adult rats with flutamide induced stage-dependent cyclin D2 immunoexpression in Sertoli cells within 18 h, and confocal microscopy revealed that immunoexpression of AR and cyclin D2 were mutually exclusive within individual seminiferous tubules in these animals.	Flutamide	29-38	cyclin D2	Rattus norvegicus	185-194
15735703-15	2005	Our study indicates that upregulation of Survivin via IGF-1 signaling confers resistance to Flutamide in prostate cancer cells.	Flutamide	92-101	insulin like growth factor 1	Homo sapiens	54-59
15625243-7	2005	Furthermore, 3 h after LPS administration, both flutamide- and ATD-treated animals had markedly higher levels of corticotropin-releasing factor mRNA in the parvocellular paraventricular nucleus (PVN) and proopiomelanocortin mRNA in the adenohypophysis.	Flutamide	48-57	corticotropin releasing hormone	Rattus norvegicus	113-143
15499084-7	2005	Administration of estradiol or the testosterone receptor antagonist, flutamide, to male rats abrogated the increase in gut injury and the increased IL-6 and MIP-2 response observed after hypoxia plus acidosis.	Flutamide	69-78	interleukin 6	Rattus norvegicus	148-152
15499084-7	2005	Administration of estradiol or the testosterone receptor antagonist, flutamide, to male rats abrogated the increase in gut injury and the increased IL-6 and MIP-2 response observed after hypoxia plus acidosis.	Flutamide	69-78	C-X-C motif chemokine ligand 2	Rattus norvegicus	157-162
16281084-7	2005	RESULTS: After AR antagonist flutamide treatment, three hundred and twenty-six genes (3.93%) expressed differentially, 97 down-regulated and 219 up-regulated.	Flutamide	29-38	androgen receptor	Homo sapiens	15-17
16281084-10	2005	CONCLUSION: Flutamide treatment might up-regulate CDKN1A and BTG1 expression in prostate cancer cells.	Flutamide	12-21	cyclin dependent kinase inhibitor 1A	Homo sapiens	50-56
16281084-10	2005	CONCLUSION: Flutamide treatment might up-regulate CDKN1A and BTG1 expression in prostate cancer cells.	Flutamide	12-21	BTG anti-proliferation factor 1	Homo sapiens	61-65
16141658-10	2005	In flutamide dose groups, AR mRNA expression tended to be increased in the prostate gland and decreased in the hippocampus.	Flutamide	3-12	androgen receptor	Rattus norvegicus	26-28
16141658-11	2005	These results might suggest that exposure to flutamide in utero might affect controlling AR expression on a hormonal signal transduction system mediated by testosterone.	Flutamide	45-54	androgen receptor	Rattus norvegicus	89-91
16003321-1	2005	BACKGROUND: Although flutamide (FTM), an androgen-receptor antagonist, normalizes the depressed immune and cardiac function in males after trauma hemorrhage (T-H), the mechanism responsible for its salutary effects remains unknown.	Flutamide	21-30	androgen receptor	Rattus norvegicus	41-58
16003321-1	2005	BACKGROUND: Although flutamide (FTM), an androgen-receptor antagonist, normalizes the depressed immune and cardiac function in males after trauma hemorrhage (T-H), the mechanism responsible for its salutary effects remains unknown.	Flutamide	32-35	androgen receptor	Rattus norvegicus	41-58
15788718-1	2005	Previous studies have indicated that the androgen receptor antagonist, flutamide, can produce a suite of reproductive malformations in the male rat when orally administered daily on gestation days (GD) 12-21.	Flutamide	71-80	androgen receptor	Rattus norvegicus	41-58
15591150-1	2005	In the present study we investigated whether fetal exposure to flutamide affected messenger and protein levels of claudin-11, a key Sertoli cell factor in the establishment of the hemotesticular barrier, at the time of two key events of postnatal testis development: 1) before puberty (postnatal d 14) during the establishment of the hemotesticular barrier, and 2) at the adult age (postnatal d 90) at the time of full spermatogenesis.	Flutamide	63-72	claudin 11	Rattus norvegicus	114-124
15591150-2	2005	The data obtained show that claudin-11 expression was inhibited in prepubertal rat testes exposed in utero to 2 and 10 mg/kg x d flutamide.	Flutamide	129-138	claudin 11	Rattus norvegicus	28-38
15699175-8	2005	The effects of T4 in vivo and in vitro were reversed by the androgen receptor antagonist, flutamide, indicating that the regulatory effects of T4 were mediated through the androgen receptor.	Flutamide	90-99	androgen receptor	Mus musculus	172-189
15590119-7	2005	The antiandogenic drug flutamide, included as a positive control, caused down-regulation of PBP C3 mRNA and up-regulation of TRPM-2 mRNA levels.	Flutamide	23-32	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	125-131
15750944-11	2005	CONCLUSIONS: Flutamide, a competitive androgen receptor blocker, reduces gubernacular mitosis to basal levels until day 6, highlighting the importance of androgen receptor.	Flutamide	13-22	androgen receptor	Rattus norvegicus	38-55
15750944-11	2005	CONCLUSIONS: Flutamide, a competitive androgen receptor blocker, reduces gubernacular mitosis to basal levels until day 6, highlighting the importance of androgen receptor.	Flutamide	13-22	androgen receptor	Rattus norvegicus	154-171
15356085-6	2004	By comparison of 3-month changes between randomized subgroups, the addition of low-dose flutamide was found to have consistently (more) normalizing effects on low-density lipoprotein cholesterol, IL-6, and adiponectin, lean body mass, total and abdominal fat mass, and arterial flow in the ovaries.	Flutamide	88-97	interleukin 6	Homo sapiens	196-200
15661065-3	2005	His serum prostate-specific antigen level was reduced to below the normal range after a combination treatment of a luteinizing hormone-releasing hormone agonist and flutamide for prostate carcinoma.	Flutamide	165-174	kallikrein related peptidase 3	Homo sapiens	10-35
15178643-0	2004	Effects of dehydroepiandrosterone and flutamide on hippocampal CA1 spine synapse density in male and female rats: implications for the role of androgens in maintenance of hippocampal structure.	Flutamide	38-47	carbonic anhydrase 1	Rattus norvegicus	63-66
15178643-1	2004	The effects of androgens and the androgen antagonist, flutamide, on the density of dendritic spine synapses in the CA1 subfield of the hippocampus were studied in gonadectomized male and female rats.	Flutamide	54-63	carbonic anhydrase 1	Rattus norvegicus	115-118
15178643-4	2004	By contrast, flutamide alone (2 d; 5 mg/d, sc) increased CA1 spine synapse density by 66%, whereas in combination the effects of flutamide and DHEA were additive rather than inhibitory.	Flutamide	13-22	carbonic anhydrase 1	Rattus norvegicus	57-60
15178643-5	2004	Additive effects on CA1 synapse density were also observed in males using combinations of flutamide with 5alpha-dihydrotestosterone (2 d, 500 microg/d, sc).	Flutamide	90-99	carbonic anhydrase 1	Rattus norvegicus	20-23
15178643-8	2004	As in males, flutamide in females increased CA1 spine synapse formation and further augmented the response to DHEA.	Flutamide	13-22	carbonic anhydrase 1	Rattus norvegicus	44-47
15178643-9	2004	These results demonstrate that flutamide and DHEA have positive effects on hippocampal CA1 spine synapse density in both sexes.	Flutamide	31-40	carbonic anhydrase 1	Rattus norvegicus	87-90
15178644-6	2004	Castration, estrogen, and androgen receptor antagonist (flutamide) counteracted these effects.	Flutamide	56-65	androgen receptor	Rattus norvegicus	26-43
15597888-1	2004	In this study, we characterized the effects of flutamide, a model mammalian androgen receptor (AR) antagonist, on endocrine function in the fathead minnow (Pimephales promelas), a small fish species that is widely used for testing endocrine-disrupting chemicals (EDCs).	Flutamide	47-56	androgen receptor	Homo sapiens	95-97
15597888-3	2004	However, as is true in mammalian systems, a 2-hydroxylated metabolite of flutamide binds to the AR with a much higher affinity than the parent chemical.	Flutamide	73-82	androgen receptor	Homo sapiens	96-98
15698549-8	2004	Co-administration of flutamide, an AR antagonist, inhibited DHT-induced p70(s6k) phosphorylation.	Flutamide	21-30	ribosomal protein S6 kinase B1	Rattus norvegicus	72-79
15371226-2	2004	Cotreatment of male rats with 675 mg/kg carbendazim and 50 or 100 mg/kg flutamide, an androgen receptor antagonist, once daily for 28 d blocked decrease of testis weight induced by treatment with carbendazim alone.	Flutamide	72-81	androgen receptor	Rattus norvegicus	86-103
15525576-4	2004	Moreover, for the Bcl-2-related proteins that were expressed mainly in the germ cells, a decrease in the levels of anti-apoptotic peptides Bcl-w (60%, P=0.003) and Bcl-2 (90%, P=0.0001) was observed at 2 mg/kg per day flutamide and an increase in levels of the pro-apoptotic Bax (2.3-fold, P=0.0004) was detected at 10 mg/kg per day.	Flutamide	218-227	BCL2, apoptosis regulator	Rattus norvegicus	18-23
15525576-7	2004	Together, these results showed that the apoptosis observed in adult germ cells from rats exposed in utero to flutamide may result from a long-term alteration in the balance between pro- and anti-apoptotic Bcl-2-related molecules in favour of pro-apoptotic proteins.	Flutamide	109-118	BCL2, apoptosis regulator	Rattus norvegicus	205-210
15570896-6	2004	Castration and treatment with the androgen receptor antagonist, flutamide, reduced blood pressure, the renal production of 20-HETE, and P-450 4A protein levels in both strains.	Flutamide	64-73	androgen receptor	Rattus norvegicus	34-51
15356085-6	2004	By comparison of 3-month changes between randomized subgroups, the addition of low-dose flutamide was found to have consistently (more) normalizing effects on low-density lipoprotein cholesterol, IL-6, and adiponectin, lean body mass, total and abdominal fat mass, and arterial flow in the ovaries.	Flutamide	88-97	adiponectin, C1Q and collagen domain containing	Homo sapiens	206-217
15207917-5	2004	In vivo treatment with flutamide (i.e., an antagonist of AR) induces a decrease of the synthesis of this myelin protein in the sciatic nerve of intact male rats confirming a role for this steroid receptor.	Flutamide	23-32	androgen receptor	Rattus norvegicus	57-59
15215042-4	2004	Six goats received the AR antagonist flutamide (9 mg/kg sc) 8 h before and 4 h after steroid injection.	Flutamide	37-46	androgen receptor	Capra hircus	23-25
15190103-4	2004	The neuroprotective action of the hormones is mediated by receptors, because the estrogen receptor (ER) antagonist tamoxifen and the androgen receptor (AR) antagonist flutamide completely block the estrogen- and androgen-mediated neuroprotection, respectively.	Flutamide	167-176	androgen receptor	Homo sapiens	133-150
15190103-4	2004	The neuroprotective action of the hormones is mediated by receptors, because the estrogen receptor (ER) antagonist tamoxifen and the androgen receptor (AR) antagonist flutamide completely block the estrogen- and androgen-mediated neuroprotection, respectively.	Flutamide	167-176	androgen receptor	Homo sapiens	152-154
15223852-7	2004	Testosterone and PSA levels show a dose-dependent response to flutamide monotherapy.	Flutamide	62-71	kallikrein related peptidase 3	Homo sapiens	17-20
15086464-9	2004	In both types of cell lines pretreatment with the androgen receptor antagonist flutamide prevented the T-induced apoptosis.	Flutamide	79-88	androgen receptor	Homo sapiens	50-67
14991321-10	2004	However, flutamide and 3 nM activin A significantly decreased cell proliferation in the presence and absence of KGF.	Flutamide	9-18	fibroblast growth factor 7	Homo sapiens	112-115
15086464-12	2004	Also, T significantly increased the expression of Bax protein (P < 0.01 vs. control) (an effect which was blocked by flutamide), and decreased the expression of Bcl-2.	Flutamide	120-129	BCL2 associated X, apoptosis regulator	Homo sapiens	50-53
15061970-6	2004	Furthermore, androgen up-regulation of intracellular AR protein was partially inhibited (50%) by nonsteroidal androgen antagonist, flutamide.	Flutamide	131-140	androgen receptor	Rattus norvegicus	53-55
15154626-1	2004	We report the case of an 82-year-old male patient with a > 8-year history of prostate cancer (PrCa), who developed breast adenocarcinoma (BrCa) (Ki-67+ and negative for ER, PR, PSA and HER2/neu) after prolonged (approximately 7-year) anti-androgen (flutamide) monotherapy for locally advanced PrCa.	Flutamide	252-261	BRCA1 DNA repair associated	Homo sapiens	118-146
14978252-8	2004	Similarly, wild-type male mice treated with flutamide, an androgen antagonist, exhibit reduced renal CYP2J5 levels.	Flutamide	44-53	cytochrome P450, family 2, subfamily j, polypeptide 5	Mus musculus	101-107
14767349-2	2004	MATERIALS AND METHODS: We administered 7.5 mg flutamide daily, a blocker of androgen receptor, into the abdomen of naturally pregnant female Sprague-Dawley rats from gestational days 14 to 20 to produce a hypospadiac rat model.	Flutamide	46-55	androgen receptor	Rattus norvegicus	76-93
14978252-9	2004	Female estrogen receptor-alpha knockout (alphaERKO) mice, which are known to have elevated circulating testosterone levels, have significantly increased renal CYP2J5 expression compared with wild-type female mice, and these differences are abrogated by ovariectomy or treatment with flutamide.	Flutamide	283-292	estrogen receptor 1 (alpha)	Mus musculus	7-30
14978252-9	2004	Female estrogen receptor-alpha knockout (alphaERKO) mice, which are known to have elevated circulating testosterone levels, have significantly increased renal CYP2J5 expression compared with wild-type female mice, and these differences are abrogated by ovariectomy or treatment with flutamide.	Flutamide	283-292	cytochrome P450, family 2, subfamily j, polypeptide 5	Mus musculus	159-165
15094514-5	2004	Pretreatment with the androgen receptor antagonist flutamide had no effect on seizure protection by 3alpha-androstanediol.	Flutamide	51-60	androgen receptor	Mus musculus	22-39
15499829-0	2004	Effects of the antiandrogen flutamide on the expression of protein kinase C isoenzymes in LNCaP and PC3 human prostate cancer cells.	Flutamide	28-37	proline rich transmembrane protein 2	Homo sapiens	59-75
15499829-9	2004	In PC3 cells flutamide potentiated the expression of the four PKC isoenzymes in almost all conditions tested (FBS- and CSS-cultured cells).	Flutamide	13-22	proprotein convertase subtilisin/kexin type 1	Homo sapiens	3-6
15499829-9	2004	In PC3 cells flutamide potentiated the expression of the four PKC isoenzymes in almost all conditions tested (FBS- and CSS-cultured cells).	Flutamide	13-22	proline rich transmembrane protein 2	Homo sapiens	62-65
15499829-0	2004	Effects of the antiandrogen flutamide on the expression of protein kinase C isoenzymes in LNCaP and PC3 human prostate cancer cells.	Flutamide	28-37	proprotein convertase subtilisin/kexin type 1	Homo sapiens	100-103
15499829-10	2004	Such effect of flutamide in PC3 cells is independent of AR since no expression of AR was detected.	Flutamide	15-24	proprotein convertase subtilisin/kexin type 1	Homo sapiens	28-31
15499829-6	2004	Flutamide up-regulated the expression of alpha, beta1 and zeta, but not epsilon, PKC isoenzymes in CSS-LNCaP cells.	Flutamide	0-9	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	41-62
15499829-6	2004	Flutamide up-regulated the expression of alpha, beta1 and zeta, but not epsilon, PKC isoenzymes in CSS-LNCaP cells.	Flutamide	0-9	proline rich transmembrane protein 2	Homo sapiens	81-84
14746863-1	2004	In the present study, we investigated whether the growth hormone-releasing hormone (GH-RH) antagonist JV-1-38 could enhance the effects of androgen deprivation produced by the anti-androgen Flutamide and luteinising hormone-releasing hormone (LH-RH) agonist Decapeptyl in an experimental model of human androgen-sensitive MDA PCa 2b prostate carcinoma implanted subcutaneously (s.c.) into nude mice.	Flutamide	190-199	growth hormone releasing hormone	Homo sapiens	50-82
14592959-5	2004	In the further studies, either castration (at 10 wk of age) or flutamide, an androgen receptor antagonist, markedly attenuated cardiac hypertrophy and fibrosis in male GC-A KO mice without blood pressure change.	Flutamide	63-72	grancalcin	Mus musculus	168-172
14746863-1	2004	In the present study, we investigated whether the growth hormone-releasing hormone (GH-RH) antagonist JV-1-38 could enhance the effects of androgen deprivation produced by the anti-androgen Flutamide and luteinising hormone-releasing hormone (LH-RH) agonist Decapeptyl in an experimental model of human androgen-sensitive MDA PCa 2b prostate carcinoma implanted subcutaneously (s.c.) into nude mice.	Flutamide	190-199	growth hormone releasing hormone	Homo sapiens	84-89
14652627-2	2003	In fact, it appears that endogenous testosterone inhibits wound healing and promotes inflammation since castration of male mice or systemic treatment with the androgen receptor antagonist flutamide accelerates cutaneous wound healing and reduces the inflammatory response.	Flutamide	188-197	androgen receptor	Mus musculus	159-176
14760064-9	2004	Interestingly, antiandrogen flutamide could also induce maspin in both cell lines tested.	Flutamide	28-37	serpin family B member 5	Homo sapiens	56-62
14630719-4	2004	We show that, in addition to MIS, flutamide, an androgen receptor antagonist, enhanced StAR mRNA expression when added to cAMP-treated MA-10 cells, whereas dihydrotestosterone, a potent androgen receptor agonist, attenuated these responses.	Flutamide	34-43	steroidogenic acute regulatory protein	Mus musculus	87-91
14654246-5	2003	Dihydrotestosterone (10(-11)M ) resulted in a dose dependent increase in PMCA activity (1.5+/-0.1-fold increase compared to control) with 24h, but not 1 or 5h, of exposure, an effect that was blocked by the androgen receptor agonist flutamide.	Flutamide	233-242	ATPase plasma membrane Ca2+ transporting 1	Bos taurus	73-77
14635088-9	2003	In LNCaP prostate carcinoma cells, I3C treatment inhibited production of PSA, whereas combinations of I3C and the androgen antagonist flutamide more effectively inhibited DNA synthesis and PSA levels compared with either agent alone.	Flutamide	134-143	kallikrein related peptidase 3	Homo sapiens	189-192
14616448-1	2003	OBJECTIVE: To investigate the efficacy of low-dose flutamide (125 mg twice daily) in the treatment of prostate-specific antigen (PSA) recurrence after definitive treatment with radical retropubic prostatectomy (RRP), external-beam radiation therapy (RT), or cryotherapy.	Flutamide	51-60	kallikrein related peptidase 3	Homo sapiens	102-133
14616448-2	2003	PATIENTS AND METHODS: In this phase II prospective trial, patients who had a PSA recurrence after definitive treatment for prostate cancer were treated with flutamide.	Flutamide	157-166	kallikrein related peptidase 3	Homo sapiens	77-80
14616448-9	2003	CONCLUSIONS: The administration of low-dose flutamide (125 mg) was clinically effective in treating PSA recurrence after definitive treatments for prostate cancer, and was well tolerated.	Flutamide	44-53	kallikrein related peptidase 3	Homo sapiens	100-103
14624911-0	2003	Combination of low-dose flutamide and finasteride for PSA-only recurrent prostate cancer after primary therapy.	Flutamide	24-33	kallikrein related peptidase 3	Homo sapiens	54-57
14624911-1	2003	OBJECTIVES: To evaluate the efficacy and tolerability of combined finasteride and low-dose flutamide for prostate-specific antigen (PSA)-only recurrence after definitive therapy and to determine the predictors of recurrence-free survival.	Flutamide	91-100	kallikrein related peptidase 3	Homo sapiens	105-137
14624911-12	2003	CONCLUSIONS: The combination of finasteride and flutamide showed a moderate efficacy in patients with PSA-only recurrence after definitive therapy.	Flutamide	48-57	kallikrein related peptidase 3	Homo sapiens	102-105
12970085-0	2003	Interactions of androgens, green tea catechins and the antiandrogen flutamide with the external glucose-binding site of the human erythrocyte glucose transporter GLUT1.	Flutamide	68-77	solute carrier family 2 member 1	Homo sapiens	162-167
12943996-6	2003	The decrease in LDHA mRNA levels (to 64 +/- 9% of the control, P<0.05) was observed with the lowest dose (2 mg/kg per day) of flutamide tested.	Flutamide	129-138	lactate dehydrogenase A	Rattus norvegicus	16-20
12943996-10	2003	In the adult testis exposed in utero to flutamide, MCT1 (53 +/- 8%, P<0.02) and MCT2 (52 +/- 9%, P<0.02) mRNA levels were significantly reduced indicating that lactate transport to germ cells could be also altered.	Flutamide	40-49	solute carrier family 16 member 1	Rattus norvegicus	51-55
12749825-0	2003	Effects of flutamide in the rat testis on the expression of occludin, an integral member of the tight junctions.	Flutamide	11-20	occludin	Rattus norvegicus	60-68
12734186-7	2003	The increase in GRTH 43-kDa protein in Leydig cells caused by hCG treatment was prevented by the androgen receptor antagonist, flutamide.	Flutamide	127-136	DEAD-box helicase 25	Rattus norvegicus	16-20
12734186-7	2003	The increase in GRTH 43-kDa protein in Leydig cells caused by hCG treatment was prevented by the androgen receptor antagonist, flutamide.	Flutamide	127-136	chorionic gonadotropin subunit beta 5	Homo sapiens	62-65
12855613-11	2003	HIF-1 activation by DHT was blocked by LY294002, a potent inhibitor of the phosphatidylinositol 3"-kinase signaling pathway, whereas HIF-1 activation by EGF, as ligand, was not inhibited by flutamide.	Flutamide	190-199	hypoxia inducible factor 1 subunit alpha	Homo sapiens	0-5
12831835-8	2003	treatment of adult males with flutamide caused an increase in the levels of expression of hCYP1B1 in the adult females, as indicated by the antiandrogenic activity.	Flutamide	30-39	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	90-97
12802502-9	2003	Flutamide produces direct vasodilation by inducing release of NO from the endothelium and causes subsequent activation of soluble guanylyl cyclase in an active androgen receptor independent manner.	Flutamide	0-9	androgen receptor	Rattus norvegicus	160-177
12788862-0	2003	Low-dose flutamide-metformin therapy reverses insulin resistance and reduces fat mass in nonobese adolescents with ovarian hyperandrogenism.	Flutamide	9-18	insulin	Homo sapiens	46-53
12788862-10	2003	Flutamide-metformin treatment (n = 30) was followed within 3 months by marked decreases in hirsutism score and serum androgens, by a more than 50% increase in insulin sensitivity and by a less atherogenic lipid profile (all P < 0.0001).	Flutamide	0-9	insulin	Homo sapiens	159-166
12788862-12	2003	Baseline GH hypersecretion and elevated serum IGF-1 normalized after 6 months on flutamide-metformin.	Flutamide	81-90	insulin like growth factor 1	Homo sapiens	46-51
12788862-14	2003	In conclusion, in teenage girls with ovarian hyperandrogenism, low-dose combined flutamide-metformin therapy attenuated a spectrum of abnormalities, including insulin resistance and hyperlipidemia.	Flutamide	81-90	insulin	Homo sapiens	159-166
12952365-10	2003	After 30 days of flutamide administration, LH, T, fT, A and E2 increased; DHEAS decreased, while FSH, SHBG and PRL were unchanged; NOx rose significantly (18.7 +/- 1.7 microM/l; p < 0.05), and its percentage increase with respect to pre-treatment levels correlated with that of E2 (R = 0.77; p < 0.01).	Flutamide	17-26	sex hormone binding globulin	Homo sapiens	102-106
12750271-5	2003	There were significant differences between the wild-type and MRP1-overexpressing cells in efflux and accumulation of flutamide and hydroxyflutamide, its active metabolite.	Flutamide	117-126	MDM4 regulator of p53	Homo sapiens	61-65
12750271-7	2003	Treating the cells with leukotriene D4, a known MRP1 substrate, or VX-710, an MRP1 modulator, restored flutamide and hydroxyflutamide accumulation.	Flutamide	103-112	MDM4 regulator of p53	Homo sapiens	78-82
12750271-9	2003	In summary, these studies indicate that flutamide and hydroxyflutamide but not dihydrotestosterone are transported by MRP1 and that these findings may contribute to our understanding of resistance to hormone refractory prostate cancer.	Flutamide	40-49	MDM4 regulator of p53	Homo sapiens	118-122
12586762-4	2003	These inhibitory effects were readily reversed by androgen receptor antagonist flutamide.	Flutamide	79-88	androgen receptor	Homo sapiens	50-67
12855613-7	2003	The effect of DHT on HIF-1 was blocked by nonsteroidal antiandrogens, flutamide and bicalutamide.	Flutamide	70-79	hypoxia inducible factor 1 subunit alpha	Homo sapiens	21-26
12802502-0	2003	Androgen receptor independent cardiovascular action of the antiandrogen flutamide.	Flutamide	72-81	androgen receptor	Rattus norvegicus	0-17
12802502-1	2003	We have previously shown that flutamide (specific antagonist of the androgen receptor) has antihypertensive effects.	Flutamide	30-39	androgen receptor	Rattus norvegicus	68-85
12624004-6	2003	Flutamide treatment significantly reduced plasma renin concentrations and rat renin mRNA in kidney but not plasma angiotensinogen levels.	Flutamide	0-9	renin	Rattus norvegicus	49-54
12624004-6	2003	Flutamide treatment significantly reduced plasma renin concentrations and rat renin mRNA in kidney but not plasma angiotensinogen levels.	Flutamide	0-9	renin	Rattus norvegicus	78-83
12624004-2	2003	Female TGR(mREN2)27 rats harboring the mouse Ren-2 renin gene were treated with Flutamide (specific antagonist of the androgen receptor, 30 mg/kg per day) starting at 4 weeks of age.	Flutamide	80-89	androgen receptor	Mus musculus	118-135
12624004-8	2003	These results demonstrate that the androgen receptor antagonist Flutamide protects against hypertension and end-organ damage not only in male but also in female TGR(mREN2)27 rats.	Flutamide	64-73	androgen receptor	Rattus norvegicus	35-52
12538628-8	2003	Indeed, whereas cleaved active caspase-3 and -6 proteins were absent in control animals, they were detected in adult rat testes exposed in utero to flutamide.	Flutamide	148-157	caspase 3	Rattus norvegicus	31-47
12441355-7	2003	Overexpression of SMRT inhibits dihydrotestosterone-dependent transactivation by AR and further suppresses the antiandrogen flutamide-mediated inhibition of AR activity.	Flutamide	124-133	nuclear receptor corepressor 2	Homo sapiens	18-22
12441355-7	2003	Overexpression of SMRT inhibits dihydrotestosterone-dependent transactivation by AR and further suppresses the antiandrogen flutamide-mediated inhibition of AR activity.	Flutamide	124-133	androgen receptor	Homo sapiens	157-159
12538628-0	2003	Long-term apoptotic cell death process with increased expression and activation of caspase-3 and -6 in adult rat germ cells exposed in utero to flutamide.	Flutamide	144-153	caspase 3	Rattus norvegicus	83-99
12538628-10	2003	Indeed, although an increase in caspase-3 and -6 mRNA and procaspase-3 and -6 protein levels was observed in germ cells after 3 d of exposure to flutamide, 1-2 wk after the cessation of the antiandrogen exposure, the caspase mRNA and procaspase protein levels were back to control.	Flutamide	145-154	caspase 3	Rattus norvegicus	32-48
12538628-2	2003	By using adult rats exposed in utero to flutamide (0.4, 2, 10 mg/kg.d) as a model, we show that the hypospermatogenesis could be related to a chronic apoptotic cell death process associated with a long-term increase in caspase-3 and -6 expression and activation in germ cells.	Flutamide	40-49	caspase 3	Rattus norvegicus	219-235
12536355-7	2002	This abnormality is reversed by the androgen receptor antagonist flutamide, suggesting that elevated androgen levels may alter the sensitivity of the hypothalamic GnRH pulse generator to steroid inhibition and lead to enhanced LH secretion.	Flutamide	65-74	gonadotropin releasing hormone 1	Homo sapiens	163-167
12350225-8	2003	In HeLa cells and the human prostate cancer cells line DU-145, co-transfected with SRAP, the DHT-dependent transactivation activities of AR were not completely inhibited by the anti-androgen flutamide, but the transactivation activities still remained high even in the presence of 5 microM flutamide, suggesting that SRAP may play an important role in enhancing AR activity in prostate cancer.	Flutamide	191-200	steroid receptor RNA activator 1	Homo sapiens	83-87
12350225-8	2003	In HeLa cells and the human prostate cancer cells line DU-145, co-transfected with SRAP, the DHT-dependent transactivation activities of AR were not completely inhibited by the anti-androgen flutamide, but the transactivation activities still remained high even in the presence of 5 microM flutamide, suggesting that SRAP may play an important role in enhancing AR activity in prostate cancer.	Flutamide	290-299	steroid receptor RNA activator 1	Homo sapiens	83-87
12350225-8	2003	In HeLa cells and the human prostate cancer cells line DU-145, co-transfected with SRAP, the DHT-dependent transactivation activities of AR were not completely inhibited by the anti-androgen flutamide, but the transactivation activities still remained high even in the presence of 5 microM flutamide, suggesting that SRAP may play an important role in enhancing AR activity in prostate cancer.	Flutamide	290-299	androgen receptor	Homo sapiens	137-139
14614228-0	2003	Leptin levels increase during flutamide therapy in women with polycystic ovary syndrome.	Flutamide	30-39	leptin	Homo sapiens	0-6
14614228-1	2003	AIM: To evaluate the serum leptin levels and the effects of flutamide treatment on the leptin levels in women with polycystic ovary syndrome (PCOS).	Flutamide	60-69	leptin	Homo sapiens	87-93
14614228-5	2003	In the PCOS group, leptin levels and area under curve for leptin levels increased significantly after flutamide treatment.	Flutamide	102-111	leptin	Homo sapiens	19-25
14614228-5	2003	In the PCOS group, leptin levels and area under curve for leptin levels increased significantly after flutamide treatment.	Flutamide	102-111	leptin	Homo sapiens	58-64
14614228-7	2003	Flutamide treatment led to increased leptin levels and leptin responses to oral glucose tolerance tests in PCOS patients.	Flutamide	0-9	leptin	Homo sapiens	37-43
14614228-7	2003	Flutamide treatment led to increased leptin levels and leptin responses to oral glucose tolerance tests in PCOS patients.	Flutamide	0-9	leptin	Homo sapiens	55-61
12446607-11	2002	Reduced androgen receptor immunoexpression was also induced by combined treatment with DES (0.1 micro g) plus GnRHa or flutamide, whereas treatment with any of these compounds alone had no or only minor effects.	Flutamide	119-128	androgen receptor	Rattus norvegicus	8-25
12457868-8	2002	This effect is receptor mediated since it is blocked by the AR antagonist, flutamide.	Flutamide	75-84	androgen receptor	Oryctolagus cuniculus	60-62
12397037-4	2002	Male TGR(mREN2)27 rats were treated with the androgen receptor antagonist Flutamide starting at 4 wk of age.	Flutamide	74-83	androgen receptor	Rattus norvegicus	45-62
12239082-7	2002	Prenatal exposure to the aromatase inhibitor, 1,4,6-androstatriene-3,17-dione, significantly reduced PRir in the MPN and AVPv of fetal males, whereas the androgen receptor antagonist flutamide had no effect.	Flutamide	183-192	androgen receptor	Rattus norvegicus	154-171
12475182-4	2002	These effects were reverted by the androgen receptor antagonist flutamide, suggesting they are dependent, at least in part, on the androgen receptor.	Flutamide	64-73	androgen receptor	Homo sapiens	35-52
12475182-4	2002	These effects were reverted by the androgen receptor antagonist flutamide, suggesting they are dependent, at least in part, on the androgen receptor.	Flutamide	64-73	androgen receptor	Homo sapiens	131-148
12060533-0	2002	Cytotoxicity of flutamide and 2-hydroxyflutamide and their effects on CYP1A2 mRNA in primary rat hepatocytes.	Flutamide	16-25	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	70-76
12364982-7	2002	Treatment of normal rats with flutamide decreased the weight of the gland and increased the levels of AR mRNA.	Flutamide	30-39	androgen receptor	Rattus norvegicus	102-104
12231070-3	2002	Efforts to use AR antagonists, such as flutamide or bicalutamide, to enhance responses to primary androgen ablation therapy or to treat androgen-independent prostate cancer have been disappointing, which has diminished enthusiasm for more aggressive or alternative methods to block AR function.	Flutamide	39-48	androgen receptor	Homo sapiens	15-17
12567773-0	2002	[Sex-difference on flutamide metabolism in rat liver microsomal cytochrome P450 1A2].	Flutamide	19-28	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	64-83
12567773-1	2002	AIM: To assess the sex-difference on flutamide metabolism in rat liver microsomes useing rat cytochrome P450, 1A2, inhibitory monoclonal antibody.	Flutamide	37-46	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	93-113
12567773-12	2002	The formation of 2-hydroxyflutamide from flutamide was inhibited by CYP1A2 antibodies (1:400) in male and female rat liver microsome for 30 min of incubation time, but the inhibition of flutamide metabolism in female rat was stronger than that in male.	Flutamide	26-35	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	68-74
12567773-12	2002	The formation of 2-hydroxyflutamide from flutamide was inhibited by CYP1A2 antibodies (1:400) in male and female rat liver microsome for 30 min of incubation time, but the inhibition of flutamide metabolism in female rat was stronger than that in male.	Flutamide	41-50	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	68-74
12215373-7	2002	Measurements of PKC(alpha) activity were in agreement with the observations on protein expression and showed that flutamide (that is extensively used in the treatment of advanced prostate cancer) elicits some impairment in the mechanisms of translocation of this isoform from the cytosol to the membrane.	Flutamide	114-123	protein kinase C, alpha	Rattus norvegicus	16-25
12060533-1	2002	AIM: To compare the cytotoxicity of flutamide and its active metabolite 2-hydroxyflutamide and their effects on cytochrome P-450 1A2 mRNA in primary rat hepatocytes.	Flutamide	36-45	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	112-132
12060533-3	2002	The effect of flutamide and 2-flutamide on the CYP1A2 mRNA level was further analyzed by Northern blot.	Flutamide	14-23	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	47-53
12060533-5	2002	The increase of ALT and AST activity and the decrease of glutathione content were also noted at 10, 20, and 50 mg/L of flutamide and 50 mg/L of 2-hydroxyflutamide as compared with normal rat hepatocytes.	Flutamide	119-128	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	24-27
12060533-6	2002	Induction of CYP1A 2 mRNA were 2-, 5-, and 7.5-fold at 10, 20, and 50 mg/L of flutamide and 3.5-fold at 50 mg/L of 2-hydroxyflutamide.	Flutamide	78-87	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	13-20
12060533-7	2002	CONCLUSION: Cytotoxicity of flutamide and its effect on CYP1A2 mRNA were stronger than those of its active metabolite 2-hydroxyflutamide in primary rat hepatocytes.	Flutamide	28-37	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	56-62
12358558-10	2002	Androgen receptor blockers currently in use include spironolactone, cyproterone acetate, and flutamide.	Flutamide	93-102	androgen receptor	Homo sapiens	0-17
12021052-4	2002	In this study we show that the nonsteroidal antiandrogen flutamide, given to adult rats at a dose of 50 mg x kg(-1) x day(-1) for 2 wk via osmotic minipumps significantly decreased the amount of AQP9 in the epididymis.	Flutamide	57-66	aquaporin 9	Rattus norvegicus	195-199
12047400-0	2002	The regulation of HSL and LPL expression by DHT and flutamide in human subcutaneous adipose tissue.	Flutamide	52-61	lipase E, hormone sensitive type	Homo sapiens	18-21
12047400-0	2002	The regulation of HSL and LPL expression by DHT and flutamide in human subcutaneous adipose tissue.	Flutamide	52-61	lipoprotein lipase	Homo sapiens	26-29
12050266-6	2002	Compared with monotherapy, combined flutamide-metformin therapy resulted in greater improvements in insulin sensitivity, in testosterone, androstenedione, dehydroepiandrosterone sulfate, and triglyceride levels, and in low-density lipoprotein/high-density lipoprotein-cholesterol ratio (all P < 0.005).	Flutamide	36-45	insulin	Homo sapiens	100-107
11956667-1	2002	OBJECTIVE: We investigated how the conserved mutation (Y486D) changed the kinetic parameters of uridine diphosphate glucuronosyltransferase 1A1 and 1A6 (UGT1A1 and 1A6) for 2-amino-5-nitro-4-trifluoromethylphenol, which is a major metabolite of flutamide, a nonsteroidal antiandrogenic agent.	Flutamide	245-254	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	153-167
12038706-5	2002	Blocking effect of flutamide and tamoxifen on T + E2 (testosterone and 17beta-estradiol) short-terms treatment was demonstrated by the similar histological changes identified in the mammary glands of the T + E2 and drug treated rats to that of the age matched E2 and T controls, respectively.	Flutamide	19-28	dihydrolipoamide S-succinyltransferase	Rattus norvegicus	260-268
12038706-11	2002	Pituitary size and level of prolactin were higher in the T + E2 + flutamide group than the T + E2 group in both short-term and long-term treatments.	Flutamide	66-75	prolactin	Rattus norvegicus	28-37
12403346-5	2002	Furthermore, castration or androgen receptor blockade with flutamide after trauma and hemorrhage in male mice showed similar beneficial effects.	Flutamide	59-68	androgen receptor	Mus musculus	27-44
11231319-2	2001	Moreover, prenatal administration of the androgen receptor antagonist, flutamide, equalizes developmental rates in male and female fetuses.	Flutamide	71-80	androgen receptor	Mus musculus	41-58
12497002-1	2002	The caffeine test measures the activity of cytochrome p450 (CYP1A2) which is a major enzyme involved in the activation of flutamide.	Flutamide	122-131	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	60-66
12497002-11	2002	The results suggest that a decrease in CYP1A2 activity is involved in the onset of flutamide-induced hepatic injury, and that the caffeine test seems to provide a useful means of its prediction.	Flutamide	83-92	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	39-45
11748029-7	2001	Tamoxifen and flutamide induced PR and slightly upregulated ERalpha immunoexpression but had only a minor or no effect on AR expression and the stromal:epithelial ratio, though flutamide retarded normal development of the SVs.	Flutamide	14-23	progesterone receptor	Rattus norvegicus	32-34
11748029-7	2001	Tamoxifen and flutamide induced PR and slightly upregulated ERalpha immunoexpression but had only a minor or no effect on AR expression and the stromal:epithelial ratio, though flutamide retarded normal development of the SVs.	Flutamide	14-23	estrogen receptor 1	Rattus norvegicus	60-67
11415997-9	2001	Addition of flutamide to this combination reversed the T inhibition of GnRH antagonist stimulation of spermatogonial differentiation to a TDI of 57%.	Flutamide	12-21	gonadotropin releasing hormone 1	Mus musculus	71-75
11328857-12	2001	In addition, the antiandrogen flutamide blocked maximal TP-induced p27 degradation completely.	Flutamide	30-39	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	67-70
11322786-7	2001	In contrast, DHT-mediated enhancement of STAT3 activation was inhibited by flutamide, an AR antagonist.	Flutamide	75-84	signal transducer and activator of transcription 3	Homo sapiens	41-46
11322786-7	2001	In contrast, DHT-mediated enhancement of STAT3 activation was inhibited by flutamide, an AR antagonist.	Flutamide	75-84	androgen receptor	Homo sapiens	89-91
11934529-2	2002	Although similar effects are produced by the potent androgen receptor (AR) antagonist flutamide and are indicative of disruption of male sexual differentiation via an antiandrogenic mechanism, DBP is not an AR antagonist.	Flutamide	86-95	androgen receptor	Rattus norvegicus	71-73
11934529-10	2002	Fewer epididymal ducts and reduced AR staining in some ducts were evident with DBP treatment, whereas decreased overall AR staining was seen with flutamide in the presence of mild Leydig cell hyperplasia.	Flutamide	146-155	androgen receptor	Rattus norvegicus	120-122
11703615-8	2001	In contrast, flutamide and finasteride reduced glomerulosclerosis as well as the inflammatory cell infiltration associated with decreased TGF-beta, PDGF-A, and -B chain mRNA expression.	Flutamide	13-22	transforming growth factor beta 1	Homo sapiens	138-146
11703615-8	2001	In contrast, flutamide and finasteride reduced glomerulosclerosis as well as the inflammatory cell infiltration associated with decreased TGF-beta, PDGF-A, and -B chain mRNA expression.	Flutamide	13-22	platelet derived growth factor subunit A	Homo sapiens	148-162
11509743-8	2001	Conversely, in the ovary, induction of cathepsin B by E2 was reversed after cotreatment with HPTE, and ERbeta expression was induced similarly by HPTE and FLU but not by E2.	Flutamide	155-158	estrogen receptor 2 (beta)	Mus musculus	103-109
11354908-16	2001	Studies on liver enzymes performed outside the scope of the enhanced protocol showed that flutamide at 100 mg/kg generally induced hepatic enzyme activities, but decreased the activity of the sex-specific testosterone-dependent liver enzyme CYP2C11 in male rats.	Flutamide	90-99	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	241-248
11160641-5	2001	Four agents were competitive inhibitors of CYP1B1 activity: flutamide (K(i) = 1.0 microM), paclitaxel (K(i) = 31.6 microM), mitoxantrone (K(i) = 11.6 microM), and docetaxel (K(i) = 28.0 microM).	Flutamide	60-69	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	43-49
11172772-6	2001	The addition of the androgen receptor antagonist flutamide abolished the protective effect of testosterone, suggesting an androgen receptor-mediated mechanism.	Flutamide	49-58	androgen receptor	Rattus norvegicus	20-37
11172772-6	2001	The addition of the androgen receptor antagonist flutamide abolished the protective effect of testosterone, suggesting an androgen receptor-mediated mechanism.	Flutamide	49-58	androgen receptor	Rattus norvegicus	122-139
11706524-9	2001	CONCLUSION: These results clearly demonstrate that, in patients with prostatic cancer, the administration of FLU for 2 weeks prior to the first LH-RHa administration is effective in preventing PSA flare, as well as in inducing an early decline in PSA levels.	Flutamide	109-112	HCL2	Homo sapiens	147-150
11706524-9	2001	CONCLUSION: These results clearly demonstrate that, in patients with prostatic cancer, the administration of FLU for 2 weeks prior to the first LH-RHa administration is effective in preventing PSA flare, as well as in inducing an early decline in PSA levels.	Flutamide	109-112	kallikrein related peptidase 3	Homo sapiens	193-196
11706524-9	2001	CONCLUSION: These results clearly demonstrate that, in patients with prostatic cancer, the administration of FLU for 2 weeks prior to the first LH-RHa administration is effective in preventing PSA flare, as well as in inducing an early decline in PSA levels.	Flutamide	109-112	kallikrein related peptidase 3	Homo sapiens	247-250
11706524-0	2001	Inhibition of PSA flare in prostate cancer patients by administration of flutamide for 2 weeks before initiation of treatment with slow-releasing LH-RH agonist.	Flutamide	73-82	kallikrein related peptidase 3	Homo sapiens	14-17
11706524-1	2001	BACKGROUND: A prospective randomized study was designed to determine whether flutamide (FLU) administered before treatment with a luteinizing hormone-releasing hormone agonist (LH-RHa) prevented prostate-specific antigen (PSA) flare in prostate cancer patients.	Flutamide	77-86	HCL2	Homo sapiens	180-183
11706524-1	2001	BACKGROUND: A prospective randomized study was designed to determine whether flutamide (FLU) administered before treatment with a luteinizing hormone-releasing hormone agonist (LH-RHa) prevented prostate-specific antigen (PSA) flare in prostate cancer patients.	Flutamide	77-86	kallikrein related peptidase 3	Homo sapiens	195-226
11706524-1	2001	BACKGROUND: A prospective randomized study was designed to determine whether flutamide (FLU) administered before treatment with a luteinizing hormone-releasing hormone agonist (LH-RHa) prevented prostate-specific antigen (PSA) flare in prostate cancer patients.	Flutamide	88-91	kallikrein related peptidase 3	Homo sapiens	195-226
11706524-5	2001	RESULTS: Treatment with FLU prior to LH-RHa induced an early decline in PSA level.	Flutamide	24-27	kallikrein related peptidase 3	Homo sapiens	72-75
11706524-8	2001	However, the number of patients with PSA flare was significantly lower in patients with prior FLU administration than in those with LH-RHa alone.	Flutamide	94-97	kallikrein related peptidase 3	Homo sapiens	37-40
11160641-9	2001	Comparison of kinetic parameters (K(m), K(i), V(max)) for flutamide 2-hydroxylation by CYP1B1, CYP1A1, and CYP1A2 indicate that CYP1B1 could play a major role for flutamide biotransformation in tumors.	Flutamide	58-67	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	87-93
11160641-9	2001	Comparison of kinetic parameters (K(m), K(i), V(max)) for flutamide 2-hydroxylation by CYP1B1, CYP1A1, and CYP1A2 indicate that CYP1B1 could play a major role for flutamide biotransformation in tumors.	Flutamide	58-67	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	95-101
11160641-9	2001	Comparison of kinetic parameters (K(m), K(i), V(max)) for flutamide 2-hydroxylation by CYP1B1, CYP1A1, and CYP1A2 indicate that CYP1B1 could play a major role for flutamide biotransformation in tumors.	Flutamide	58-67	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	107-113
11160641-9	2001	Comparison of kinetic parameters (K(m), K(i), V(max)) for flutamide 2-hydroxylation by CYP1B1, CYP1A1, and CYP1A2 indicate that CYP1B1 could play a major role for flutamide biotransformation in tumors.	Flutamide	58-67	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	128-134
11095431-0	2000	Polycystic ovarian syndrome: evidence that flutamide restores sensitivity of the gonadotropin-releasing hormone pulse generator to inhibition by estradiol and progesterone.	Flutamide	43-52	gonadotropin releasing hormone 1	Homo sapiens	81-111
11160641-9	2001	Comparison of kinetic parameters (K(m), K(i), V(max)) for flutamide 2-hydroxylation by CYP1B1, CYP1A1, and CYP1A2 indicate that CYP1B1 could play a major role for flutamide biotransformation in tumors.	Flutamide	163-172	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	87-93
11160641-9	2001	Comparison of kinetic parameters (K(m), K(i), V(max)) for flutamide 2-hydroxylation by CYP1B1, CYP1A1, and CYP1A2 indicate that CYP1B1 could play a major role for flutamide biotransformation in tumors.	Flutamide	163-172	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	95-101
11160641-9	2001	Comparison of kinetic parameters (K(m), K(i), V(max)) for flutamide 2-hydroxylation by CYP1B1, CYP1A1, and CYP1A2 indicate that CYP1B1 could play a major role for flutamide biotransformation in tumors.	Flutamide	163-172	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	107-113
11160641-9	2001	Comparison of kinetic parameters (K(m), K(i), V(max)) for flutamide 2-hydroxylation by CYP1B1, CYP1A1, and CYP1A2 indicate that CYP1B1 could play a major role for flutamide biotransformation in tumors.	Flutamide	163-172	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	128-134
11133514-7	2001	Flutamide, an androgen receptor antagonist, dose dependently blocked transgene expression in males and blunted the induction caused by testosterone in females.	Flutamide	0-9	androgen receptor	Mus musculus	14-31
11340263-1	2001	Specific blockade of the androgen receptor by the nonsteroid antiandrogens flutamide and Casodex has proven to be a useful tool for studying androgens in vivo.	Flutamide	75-84	androgen receptor	Rattus norvegicus	25-42
11316974-0	2001	Optimal starting time for flutamide to prevent disease flare in prostate cancer patients treated with a gonadotropin-releasing hormone agonist.	Flutamide	26-35	gonadotropin releasing hormone 1	Homo sapiens	104-134
11316974-6	2001	Flutamide was initiated on the day of leuprorelin injection in group B, and at 1, 2 and 4 weeks before leuprorelin injection in groups C, D and E, respectively.	Flutamide	0-9	angiotensin II receptor type 1	Homo sapiens	38-89
11316974-9	2001	In patients who had been treated with flutamide in combination with leuprorelin, the mean PSA level did not exceed the pretreatment levels after leuprorelin administration.	Flutamide	38-47	kallikrein related peptidase 3	Homo sapiens	90-93
11316974-10	2001	The rate of decrease in PSA in the group receiving simultaneous administration of flutamide with leuprorelin showed a decline comparable to that during the period before leuprorelin administration in the flutamide pretreatment groups.	Flutamide	82-91	kallikrein related peptidase 3	Homo sapiens	24-27
11316974-10	2001	The rate of decrease in PSA in the group receiving simultaneous administration of flutamide with leuprorelin showed a decline comparable to that during the period before leuprorelin administration in the flutamide pretreatment groups.	Flutamide	204-213	kallikrein related peptidase 3	Homo sapiens	24-27
11282290-3	2000	Administration of flutamide concurrently with testosterone (75 microg/mouse) caused a potent decrease of ODC induction in a dose-dependent manner, suppressing the enzyme activity at the doses of 0.1 and 0.5 mg/mouse by about 88 and 95%, respectively.	Flutamide	18-27	ornithine decarboxylase, structural 1	Mus musculus	105-108
11162924-10	2000	Flutamide alone was as effective as DHT in decreasing E2 and Vg levels in males but did not significantly reverse DHT induced Vg decreases in either sex (P>0.05, F-test).	Flutamide	0-9	LOC100136735	Oncorhynchus mykiss	61-63
11114872-3	2000	Flutamide patients had higher PSA levels at diagnosis and shorter duration of treatment, which could bias the results against flutamide monotherapy.	Flutamide	0-9	aminopeptidase puromycin sensitive	Homo sapiens	30-33
11085345-11	2000	Cessation of flutamide for at least 4 weeks and, in the case of bicalutamide, even 8 weeks, is mandatory before antiandrogen withdrawal syndrome can be excluded as the cause of decreasing PSA values.	Flutamide	13-22	kallikrein related peptidase 3	Homo sapiens	188-191
11114872-3	2000	Flutamide patients had higher PSA levels at diagnosis and shorter duration of treatment, which could bias the results against flutamide monotherapy.	Flutamide	126-135	aminopeptidase puromycin sensitive	Homo sapiens	30-33
11114872-4	2000	Kaplan Meier analysis of PSA -- disease free survival showed significantly poorer outcome with flutamide monotherapy.	Flutamide	95-104	aminopeptidase puromycin sensitive	Homo sapiens	25-28
11049111-9	2000	Trauma-hemorrhage decreased IL-6 release by T lymphocytes and the release was restored to sham levels with flutamide pre-treatment.	Flutamide	107-116	interleukin 6	Mus musculus	28-32
11062382-8	2000	CONCLUSIONS: When combined with castration, 500 mg of flutamide appears to be equally effective in lowering serum PSA and is not significantly more toxic than conventional dosing.	Flutamide	54-63	kallikrein related peptidase 3	Homo sapiens	114-117
11049111-10	2000	Similarly, STAT3 expression was decreased in T lymphocytes following trauma-hemorrhage and the expression was restored by flutamide pre-treatment.	Flutamide	122-131	signal transducer and activator of transcription 3	Mus musculus	11-16
11095136-5	2000	The testosterone and prostate-specific antigen (PSA) levels in patients administered flutamide (Group II) increased significantly 3 days after the first dose of LH-RH analog, whereas no such increase was observed in patients administered CMA (Group I), indicating that CMA prevented the flare-up.	Flutamide	85-94	kallikrein related peptidase 3	Homo sapiens	21-52
11043816-4	2000	Confirmatory evidence has now come from a double-blind, placebo-controlled trial in patients with pancreatic cancer in which flutamide, the pure androgen receptor blocker, doubled survival duration over control patients.	Flutamide	125-134	androgen receptor	Homo sapiens	145-162
10945615-14	2000	Flutamide had the ability to suppress T antigen-driven carcinogenesis, resulting in a significant decrease in the incidence of prostate cancer and an increase in the latency period of prostate cancer in TRAMP mice.	Flutamide	0-9	tumor necrosis factor receptor superfamily, member 25	Mus musculus	203-208
10705202-8	2000	PSA at diagnosis and PSA at the start of flutamide use were significantly lower for patients with CR.	Flutamide	41-50	kallikrein related peptidase 3	Homo sapiens	21-24
10879806-3	2000	Flutamide, a non-steroid-blocking androgen receptor, was subcutaneously administered to 30-d-old male Wistar rats for 4 wk.	Flutamide	0-9	androgen receptor	Rattus norvegicus	34-51
10879806-5	2000	Flutamide administration decreased body weight gain, serum IGF-I levels, hepatic IGF-I mRNA, and GH receptor mRNA content.	Flutamide	0-9	insulin-like growth factor 1	Rattus norvegicus	59-64
10879806-5	2000	Flutamide administration decreased body weight gain, serum IGF-I levels, hepatic IGF-I mRNA, and GH receptor mRNA content.	Flutamide	0-9	insulin-like growth factor 1	Rattus norvegicus	81-86
10879806-5	2000	Flutamide administration decreased body weight gain, serum IGF-I levels, hepatic IGF-I mRNA, and GH receptor mRNA content.	Flutamide	0-9	growth hormone receptor	Rattus norvegicus	97-108
10897581-5	2000	However, after flutamide was discontinued all patients with liver damage recovered with normalization of AST and ALT levels.	Flutamide	15-24	solute carrier family 17 member 5	Homo sapiens	105-108
10822172-0	2000	Effect of flutamide-induced androgen-receptor blockade on adenylate cyclase activation through G-protein coupled receptors in rat prostate.	Flutamide	10-19	androgen receptor	Rattus norvegicus	28-45
10822172-1	2000	The effect of the antiandrogen flutamide on the prostatic vasoactive intestinal peptide (VIP) receptor/effector system was studied in rats.	Flutamide	31-40	vasoactive intestinal peptide	Rattus norvegicus	89-92
10822172-5	2000	The number of VIP receptors and the stimulatory effect of VIP on adenylate cyclase activity in prostatic membranes decreased in flutamide-treated rats.	Flutamide	128-137	vasoactive intestinal peptide	Rattus norvegicus	14-17
10822172-5	2000	The number of VIP receptors and the stimulatory effect of VIP on adenylate cyclase activity in prostatic membranes decreased in flutamide-treated rats.	Flutamide	128-137	vasoactive intestinal peptide	Rattus norvegicus	58-61
10822172-7	2000	Androgen-receptor blockade by flutamide also decreased the prostatic levels of alpha(s,) alpha(i1/2), and alpha(i3/0) G-protein subunits, as estimated by an immunological procedure.	Flutamide	30-39	androgen receptor	Rattus norvegicus	0-17
10822172-9	2000	Thus, androgen-receptor blockade by flutamide results in an important impairment of the components of the VIP receptor/effector system in rat prostate as well as in a modification of their coupling extent, which is presumably due to differences observed in plasma membrane fluidity.	Flutamide	36-45	androgen receptor	Rattus norvegicus	6-23
10822172-9	2000	Thus, androgen-receptor blockade by flutamide results in an important impairment of the components of the VIP receptor/effector system in rat prostate as well as in a modification of their coupling extent, which is presumably due to differences observed in plasma membrane fluidity.	Flutamide	36-45	vasoactive intestinal peptide	Rattus norvegicus	106-109
10637363-5	2000	All androgen-responsive genes are activated by androgen receptor (AR) bound to either T or DHT and it is believed that AR is more transcriptionally active when bound to DHT than T. The two classes of antiandrogens, presently available, are the steroidal derivatives, all of which possess mixed agonistic and antagonistic activities, and the pure non-steroidal antiandrogens of the class of flutamide and its derivatives.	Flutamide	390-399	androgen receptor	Homo sapiens	47-64
10637363-5	2000	All androgen-responsive genes are activated by androgen receptor (AR) bound to either T or DHT and it is believed that AR is more transcriptionally active when bound to DHT than T. The two classes of antiandrogens, presently available, are the steroidal derivatives, all of which possess mixed agonistic and antagonistic activities, and the pure non-steroidal antiandrogens of the class of flutamide and its derivatives.	Flutamide	390-399	androgen receptor	Homo sapiens	66-68
10637363-5	2000	All androgen-responsive genes are activated by androgen receptor (AR) bound to either T or DHT and it is believed that AR is more transcriptionally active when bound to DHT than T. The two classes of antiandrogens, presently available, are the steroidal derivatives, all of which possess mixed agonistic and antagonistic activities, and the pure non-steroidal antiandrogens of the class of flutamide and its derivatives.	Flutamide	390-399	androgen receptor	Homo sapiens	119-121
10910998-2	2000	Some, like flutamide, procymidone, or vinclozolin compete with androgens for the androgen receptor (AR), inhibit AR-DNA binding, and alter androgen-dependent gene expression in vivo and in vitro.	Flutamide	11-20	androgen receptor	Rattus norvegicus	81-98
10910998-2	2000	Some, like flutamide, procymidone, or vinclozolin compete with androgens for the androgen receptor (AR), inhibit AR-DNA binding, and alter androgen-dependent gene expression in vivo and in vitro.	Flutamide	11-20	androgen receptor	Rattus norvegicus	100-102
10910998-2	2000	Some, like flutamide, procymidone, or vinclozolin compete with androgens for the androgen receptor (AR), inhibit AR-DNA binding, and alter androgen-dependent gene expression in vivo and in vitro.	Flutamide	11-20	androgen receptor	Rattus norvegicus	113-115
10871298-10	2000	Flutamide, a nonsteroidal androgen receptor antagonist, stimulated the activity by up to 349%.	Flutamide	0-9	androgen receptor	Homo sapiens	26-43
10855693-1	2000	A yeast genetic screening was developed to isolate androgen receptor (AR) mutants with divergent transactivation characteristics in response to hydroxyflutamide (HF), an active metabolite of flutamide used for prostate cancer treatment.	Flutamide	151-160	androgen receptor	Homo sapiens	51-68
10705202-9	2000	However, the results of multivariate logistic regression analysis demonstrated that only the post-treatment nadir PSA level was significantly correlated with prognosis of flutamide use.	Flutamide	171-180	kallikrein related peptidase 3	Homo sapiens	114-117
10705202-10	2000	CONCLUSIONS: Flutamide use as second-line hormone therapy should be limited to cases in which first-line hormone therapy has been highly effective and for whom the post-treatment nadir PSA level was within normal limits, and other patients should undergo other therapies.	Flutamide	13-22	kallikrein related peptidase 3	Homo sapiens	185-188
10718485-6	1999	This over-expression of TGF-beta1 can be blocked by flutamide, indicating that testosterone may be responsible for the expression of TGF-beta1 in mammary glands.	Flutamide	52-61	transforming growth factor, beta 1	Rattus norvegicus	24-33
10653987-5	2000	We now show that several classes of steroid hormones, antiestrogens, and antiandrogens, as well as various arylalkylamine drugs, all potently inhibit (3)H-histamine binding to cytochrome P-450 (K(i) values: testosterone 0.28 microM, progesterone 0.56 microM, flutamide 1.7 microM, tamoxifen 9.0 microM).	Flutamide	259-268	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	176-192
10888271-4	2000	We have shown that polyamines, hormones (including estrogen, testosterone and progesterone), antihormones (including tamoxifen and flutamide) and various antidepressants and antihistamines, all inhibit histamine binding to P450; we have postulated that, through binding to the heme moiety, intracellular histamine regulates cell function by modulating the catalytic activity of P450 enzymes, an action that may be perturbed by endogenous and exogenous substances.	Flutamide	131-140	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	223-227
10888271-4	2000	We have shown that polyamines, hormones (including estrogen, testosterone and progesterone), antihormones (including tamoxifen and flutamide) and various antidepressants and antihistamines, all inhibit histamine binding to P450; we have postulated that, through binding to the heme moiety, intracellular histamine regulates cell function by modulating the catalytic activity of P450 enzymes, an action that may be perturbed by endogenous and exogenous substances.	Flutamide	131-140	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	378-382
10634368-10	2000	A 6-month course of antiandrogen treatments with spironolactone, flutamide, or finasteride determines a reduction of PSA levels in these subjects.	Flutamide	65-74	kallikrein related peptidase 3	Homo sapiens	117-120
10673793-2	1999	Presently there are two classes of androgen receptor antagonists: the so-called pure, non-steroidal antiandrogens which include flutamide, nilutamide and the more recent bicalutamide and the steroidal antiandrogens cyproterone acetate, megestrol acetate and WIN 49596.	Flutamide	128-137	androgen receptor	Homo sapiens	35-52
10718485-6	1999	This over-expression of TGF-beta1 can be blocked by flutamide, indicating that testosterone may be responsible for the expression of TGF-beta1 in mammary glands.	Flutamide	52-61	transforming growth factor, beta 1	Rattus norvegicus	133-142
10590174-14	1999	The results demonstrate that (a) the endogenous androgens T and DHT regulate AR differently, suggesting a potential cellular mechanism that may contribute to the difference in neural target gene sensitivity to these androgens; (b) up-regulation of AR occurs only in the presence of agonists; (c) the mechanism of action of FLU in the brain involves inhibition of AR protein up-regulation normally seen in response to androgen; and (d) FLU promotes AR nuclear translocation but not augmentation of cellular AR populations.	Flutamide	323-326	androgen receptor	Mus musculus	248-250
10659414-4	1999	In 2 patients, glutamic-oxaloacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT) elevated over 100 IU/L, and treatment with flutamide was discontinued.	Flutamide	138-147	glutamic--pyruvic transaminase	Homo sapiens	90-93
10590174-14	1999	The results demonstrate that (a) the endogenous androgens T and DHT regulate AR differently, suggesting a potential cellular mechanism that may contribute to the difference in neural target gene sensitivity to these androgens; (b) up-regulation of AR occurs only in the presence of agonists; (c) the mechanism of action of FLU in the brain involves inhibition of AR protein up-regulation normally seen in response to androgen; and (d) FLU promotes AR nuclear translocation but not augmentation of cellular AR populations.	Flutamide	435-438	androgen receptor	Mus musculus	248-250
10590174-13	1999	While immunohistochemical studies showed that FLU was able to promote nuclear translocation of AR, Western analysis revealed that FLU, in contrast to T and DHT, failed to maintain the integrity of AR.	Flutamide	46-49	androgen receptor	Mus musculus	95-97
10590174-14	1999	The results demonstrate that (a) the endogenous androgens T and DHT regulate AR differently, suggesting a potential cellular mechanism that may contribute to the difference in neural target gene sensitivity to these androgens; (b) up-regulation of AR occurs only in the presence of agonists; (c) the mechanism of action of FLU in the brain involves inhibition of AR protein up-regulation normally seen in response to androgen; and (d) FLU promotes AR nuclear translocation but not augmentation of cellular AR populations.	Flutamide	435-438	androgen receptor	Mus musculus	248-250
10590174-14	1999	The results demonstrate that (a) the endogenous androgens T and DHT regulate AR differently, suggesting a potential cellular mechanism that may contribute to the difference in neural target gene sensitivity to these androgens; (b) up-regulation of AR occurs only in the presence of agonists; (c) the mechanism of action of FLU in the brain involves inhibition of AR protein up-regulation normally seen in response to androgen; and (d) FLU promotes AR nuclear translocation but not augmentation of cellular AR populations.	Flutamide	323-326	androgen receptor	Mus musculus	248-250
10590174-14	1999	The results demonstrate that (a) the endogenous androgens T and DHT regulate AR differently, suggesting a potential cellular mechanism that may contribute to the difference in neural target gene sensitivity to these androgens; (b) up-regulation of AR occurs only in the presence of agonists; (c) the mechanism of action of FLU in the brain involves inhibition of AR protein up-regulation normally seen in response to androgen; and (d) FLU promotes AR nuclear translocation but not augmentation of cellular AR populations.	Flutamide	323-326	androgen receptor	Mus musculus	248-250
10590174-14	1999	The results demonstrate that (a) the endogenous androgens T and DHT regulate AR differently, suggesting a potential cellular mechanism that may contribute to the difference in neural target gene sensitivity to these androgens; (b) up-regulation of AR occurs only in the presence of agonists; (c) the mechanism of action of FLU in the brain involves inhibition of AR protein up-regulation normally seen in response to androgen; and (d) FLU promotes AR nuclear translocation but not augmentation of cellular AR populations.	Flutamide	323-326	androgen receptor	Mus musculus	248-250
10590174-14	1999	The results demonstrate that (a) the endogenous androgens T and DHT regulate AR differently, suggesting a potential cellular mechanism that may contribute to the difference in neural target gene sensitivity to these androgens; (b) up-regulation of AR occurs only in the presence of agonists; (c) the mechanism of action of FLU in the brain involves inhibition of AR protein up-regulation normally seen in response to androgen; and (d) FLU promotes AR nuclear translocation but not augmentation of cellular AR populations.	Flutamide	435-438	androgen receptor	Mus musculus	248-250
10590174-14	1999	The results demonstrate that (a) the endogenous androgens T and DHT regulate AR differently, suggesting a potential cellular mechanism that may contribute to the difference in neural target gene sensitivity to these androgens; (b) up-regulation of AR occurs only in the presence of agonists; (c) the mechanism of action of FLU in the brain involves inhibition of AR protein up-regulation normally seen in response to androgen; and (d) FLU promotes AR nuclear translocation but not augmentation of cellular AR populations.	Flutamide	435-438	androgen receptor	Mus musculus	248-250
10590181-4	1999	We found that although treatment with testosterone, dihydrotestosterone (DHT), or the androgen receptor antagonist flutamide (FL) failed to affect the number of these MNs during PCD, administration of DHT from E12 to E15 following axotomy on E12 significantly attenuated injury-induced MN death.	Flutamide	115-124	androgen receptor	Homo sapiens	86-103
10574247-9	1999	The anti-androgen flutamide and the delta5NCIs displaced 53% and 32-51% of R1881 bound to AR respectively.	Flutamide	18-27	androgen receptor	Homo sapiens	90-92
10506535-0	1999	Prenatal flutamide treatment eliminates the adult male rat"s dependency upon vasopressin when forming social-olfactory memories.	Flutamide	9-18	arginine vasopressin	Rattus norvegicus	77-88
10453797-2	1999	In this study, we examined the effects of treatment with flutamide, a synthetic, nonsteroidal, competitive antagonist of the androgen receptor, on OCD symptoms.	Flutamide	57-66	androgen receptor	Homo sapiens	125-142
10519615-12	1999	Flutamide was capable of significantly blunting fasting and OGTT-stimulated secretion of insulin only in women with IH.	Flutamide	0-9	insulin	Homo sapiens	89-96
10433226-10	1999	To further assess whether AR mRNA was autologously regulated, neonatal male rats were treated with the androgen receptor antagonist, flutamide.	Flutamide	133-142	androgen receptor	Rattus norvegicus	103-120
10453797-9	1999	CONCLUSION: The lack of response to treatment with flutamide, an androgen receptor antagonist, suggests that any effects of gonadal steroids to exacerbate OCD symptoms are more likely to be mediated through estrogen receptors or through mechanisms that do not involve classical intracellular androgen receptors.	Flutamide	51-60	androgen receptor	Homo sapiens	65-82
10432234-13	1999	Flutamide, an AR antagonist, also blocked the enhancement of luciferase activity induced by EGF and testosterone, further confirming the role of AR in the effect of EGF and testosterone.	Flutamide	0-9	androgen receptor	Mus musculus	14-16
10432234-13	1999	Flutamide, an AR antagonist, also blocked the enhancement of luciferase activity induced by EGF and testosterone, further confirming the role of AR in the effect of EGF and testosterone.	Flutamide	0-9	epidermal growth factor	Mus musculus	92-95
10432237-5	1999	The androgen antagonist flutamide elevated ERK to similar levels and DNA synthesis to levels half those seen with R1881; in addition, excess flutamide lowered R1881-stimulated DNA synthesis to levels seen with flutamide alone.	Flutamide	24-33	mitogen-activated protein kinase 1	Homo sapiens	43-46
10432234-13	1999	Flutamide, an AR antagonist, also blocked the enhancement of luciferase activity induced by EGF and testosterone, further confirming the role of AR in the effect of EGF and testosterone.	Flutamide	0-9	androgen receptor	Mus musculus	145-147
10432234-13	1999	Flutamide, an AR antagonist, also blocked the enhancement of luciferase activity induced by EGF and testosterone, further confirming the role of AR in the effect of EGF and testosterone.	Flutamide	0-9	epidermal growth factor	Mus musculus	165-168
10397515-3	1999	The aims of this in vitro study were to assess, in the presence or absence of testosterone (T) or dihydrotestosterone (DHT), the production of interleukin-6 (IL-6) by human gingival fibroblasts (hGF), and to evaluate the effects of flutamide (a common anti-androgen) in this system.	Flutamide	232-241	interleukin 6	Homo sapiens	158-162
10363963-2	1999	Mutations were found in 5 of 16 patients who received combined androgen blockade with the AR antagonist flutamide, and these mutant ARs were strongly stimulated by flutamide.	Flutamide	104-113	androgen receptor	Homo sapiens	90-92
10363963-2	1999	Mutations were found in 5 of 16 patients who received combined androgen blockade with the AR antagonist flutamide, and these mutant ARs were strongly stimulated by flutamide.	Flutamide	164-173	androgen receptor	Homo sapiens	90-92
10363963-4	1999	Patients with flutamide-stimulated AR mutations responded to subsequent treatment with bicalutamide, an AR antagonist that blocks the mutant ARs.	Flutamide	14-23	androgen receptor	Homo sapiens	35-37
10363963-4	1999	Patients with flutamide-stimulated AR mutations responded to subsequent treatment with bicalutamide, an AR antagonist that blocks the mutant ARs.	Flutamide	14-23	androgen receptor	Homo sapiens	104-106
10363963-5	1999	These findings demonstrate that AR mutations occur in response to strong selective pressure from flutamide treatment.	Flutamide	97-106	androgen receptor	Homo sapiens	32-34
10416835-2	1999	In this study the influence of progesterone, androgens, the anti-estrogen ICI 182780 and the anti-androgen Flutamid on thioredoxin expression, has been studied in the rat uterus.	Flutamide	107-115	thioredoxin 1	Rattus norvegicus	119-130
10416835-8	1999	In addition, the anti-androgen Flutamid attenuated the thioredoxin mRNA increase seen after 5alpha-dihydrotestosterone treatment alone.	Flutamide	31-39	thioredoxin 1	Rattus norvegicus	55-66
10416835-10	1999	The attenuation of the estrogen and androgen-induced increases of the thioredoxin mRNA with ICI 182780 and Flutamid, indicate that the effect is mediated via the estrogen receptor and androgen receptor respectively.	Flutamide	107-115	thioredoxin 1	Rattus norvegicus	70-81
10188194-2	1999	For example, in utero treatment with the androgen receptor (AR) antagonist, flutamide, produces ventral prostate agenesis and testicular nondescent, while in contrast, finasteride, an inhibitor of 5 alpha-dihydrotestosterone (DHT) synthesis, rarely, if ever, induces such malformations.	Flutamide	76-85	androgen receptor	Rattus norvegicus	41-58
10449935-14	1999	However, seroreversion of the FTA-Abs test was related to a low baseline CD4+ cell count (p = 0.	Flutamide	30-33	CD4 molecule	Homo sapiens	73-76
10851326-2	1999	In the 26 patients with stage T(2) disease who have received continuous CAB with an LHRH agonist and flutamide, progression of cancer, as evidenced by rising serum prostate specific antigen (PSA), was observed in only one patient receiving CAB, occurring after 7.3 years of continuous CAB treatment.	Flutamide	101-110	kallikrein related peptidase 3	Homo sapiens	164-189
10851326-2	1999	In the 26 patients with stage T(2) disease who have received continuous CAB with an LHRH agonist and flutamide, progression of cancer, as evidenced by rising serum prostate specific antigen (PSA), was observed in only one patient receiving CAB, occurring after 7.3 years of continuous CAB treatment.	Flutamide	101-110	kallikrein related peptidase 3	Homo sapiens	191-194
10188194-2	1999	For example, in utero treatment with the androgen receptor (AR) antagonist, flutamide, produces ventral prostate agenesis and testicular nondescent, while in contrast, finasteride, an inhibitor of 5 alpha-dihydrotestosterone (DHT) synthesis, rarely, if ever, induces such malformations.	Flutamide	76-85	androgen receptor	Rattus norvegicus	60-62
9761805-2	1998	In a previous trial, we found that adding the antiandrogen flutamide to leuprolide acetate (a synthetic gonadotropin-releasing hormone that results in medical ablation of testicular function) significantly improved survival as compared with that achieved with placebo plus leuprolide acetate.	Flutamide	59-68	gonadotropin releasing hormone 1	Homo sapiens	104-134
9750522-1	1998	The antiandrogen withdrawal syndrome was first reported in patients with prostate cancer who manifested disease progression after total androgen blockage therapy with medical or surgical castration and pure antiandrogen, flutamide; discontinuation of flutamide resulted in a decline in prostate specific antigen and, in some cases, with clinical response.	Flutamide	251-260	kallikrein related peptidase 3	Homo sapiens	286-311
9690699-6	1998	Changes in hormone levels during flutamide administration provided evidence for the existence of physiologic mechanisms that compensate for the blocking of the androgen receptor.	Flutamide	33-42	androgen receptor	Homo sapiens	160-177
9690699-7	1998	The therapeutic effects of flutamide are modest in magnitude and they seem to be short-lived, possibly because of physiologic compensation for androgen receptor blockade.	Flutamide	27-36	androgen receptor	Homo sapiens	143-160
9349746-5	1997	In the Flutamide group, DHT is not modified, T is increased (P = 0.045), and EGF is decreased in total tissue (P < 0.02) and in the periurethral zone (P < 0.01).	Flutamide	7-16	epidermal growth factor	Homo sapiens	77-80
9797851-0	1998	Effects of flutamide on pituitary and adrenal responsiveness to corticotrophin releasing factor (CRF).	Flutamide	11-20	corticotropin releasing hormone	Homo sapiens	64-95
9797851-1	1998	OBJECTIVE: Flutamide is a non-steroid antiandrogen that specifically blocks the androgen receptor.	Flutamide	11-20	androgen receptor	Homo sapiens	80-97
9797851-2	1998	We have investigated the effect of flutamide treatment on the adrenal androgen response to corticotrophin releasing factor (CRF) in eight patients with polycystic ovary syndrome (PCOS).	Flutamide	35-44	corticotropin releasing hormone	Homo sapiens	91-122
9797851-8	1998	RESULTS: Androstenedione (delta 4), DHEA-S, 17-hydroxy-progesterone, testosterone and free-testosterone showed significantly reduced responses after six months of flutamide therapy whereas ACTH and cortisol response were similar to those before treatment.	Flutamide	163-172	proopiomelanocortin	Homo sapiens	189-193
9634122-1	1998	Flutamide withdrawal syndrome is characterized by a decrease in prostate-specific antigen (PSA) after flutamide withdrawal in a subset of patients with progressing metastatic carcinoma of the prostate.	Flutamide	0-9	kallikrein related peptidase 3	Homo sapiens	64-95
9634122-3	1998	We describe a patient with androgen-independent prostate cancer in whom PSA continued to decrease for a period of 15 months after flutamide withdrawal.	Flutamide	130-139	kallikrein related peptidase 3	Homo sapiens	72-75
9695882-0	1998	Blockade of the in vitro effects of testosterone and erythropoietin on Cfu-E and Bfu-E proliferation by pretreatment of the donor rats with cyproterone and flutamide.	Flutamide	156-165	erythropoietin	Homo sapiens	53-67
9351907-0	1997	Metabolism of the antiandrogenic drug (Flutamide) by human CYP1A2.	Flutamide	39-48	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	59-65
9351907-3	1997	These studies show the principal role of CYP1A2 in the metabolism of flutamide to 2-hydroxyflutamide.	Flutamide	69-78	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	41-47
9351907-4	1997	A minor metabolite is formed during the metabolism of flutamide by CYP3A4 in the presence of an excess of added purified NADPH-P450 reductase.	Flutamide	54-63	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	67-73
9351907-6	1997	Other substrates of CYP1A2, such as phenacetin, imipramine, caffeine, and estradiol, are also inhibitors of flutamide metabolism by CYP1A2.	Flutamide	108-117	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	20-26
9351907-6	1997	Other substrates of CYP1A2, such as phenacetin, imipramine, caffeine, and estradiol, are also inhibitors of flutamide metabolism by CYP1A2.	Flutamide	108-117	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	132-138
9351907-9	1997	In assays performed using this cell line transfected with the cDNA for the androgen receptor, flutamide is a pure antagonist, and 2-hydroxyflutamide, while a more potent androgen receptor (AR) antagonist, activates the AR at higher concentrations.	Flutamide	94-103	androgen receptor	Homo sapiens	75-92
9351907-9	1997	In assays performed using this cell line transfected with the cDNA for the androgen receptor, flutamide is a pure antagonist, and 2-hydroxyflutamide, while a more potent androgen receptor (AR) antagonist, activates the AR at higher concentrations.	Flutamide	94-103	androgen receptor	Homo sapiens	189-191
9351907-9	1997	In assays performed using this cell line transfected with the cDNA for the androgen receptor, flutamide is a pure antagonist, and 2-hydroxyflutamide, while a more potent androgen receptor (AR) antagonist, activates the AR at higher concentrations.	Flutamide	94-103	androgen receptor	Homo sapiens	219-221
9349746-0	1997	Prevalent decrease of the EGF content in the periurethral zone of BPH tissue induced by treatment with finasteride or flutamide.	Flutamide	118-127	epidermal growth factor	Homo sapiens	26-29
9349746-1	1997	The aim of the present investigation is to verify whether treatment with Finasteride or Flutamide influences the regional distribution of testosterone (T), dihydrotestosterone (DHT), and epidermal growth factor (EGF) in benign prostatic hyperplasia (BPH) tissue.	Flutamide	88-97	epidermal growth factor	Homo sapiens	187-210
9349746-1	1997	The aim of the present investigation is to verify whether treatment with Finasteride or Flutamide influences the regional distribution of testosterone (T), dihydrotestosterone (DHT), and epidermal growth factor (EGF) in benign prostatic hyperplasia (BPH) tissue.	Flutamide	88-97	epidermal growth factor	Homo sapiens	212-215
9529007-7	1998	The possible control by androgens of gene expression of the two isozymes has been studied in brain tissues of animals exposed in utero to the androgen antagonist flutamide; the sex of the animals was determined by genetic sex screening of the SRY gene located on the Y-chromosome.	Flutamide	162-171	sex determining region Y	Rattus norvegicus	243-246
9695882-13	1998	Surprisingly, the effects of erythropoietin on erythroid colonies proliferation were also completely blocked by pretreatment with flutamide and partially blocked by pretreatment with cyproterone.	Flutamide	130-139	erythropoietin	Rattus norvegicus	29-43
9428696-7	1997	CRISP-1 and CRISP-3 RNA levels were significantly increased, and these effects were prevented by a concomitant treatment with the antiandrogen flutamide.	Flutamide	143-152	cysteine-rich secretory protein 1	Mus musculus	0-7
9428696-7	1997	CRISP-1 and CRISP-3 RNA levels were significantly increased, and these effects were prevented by a concomitant treatment with the antiandrogen flutamide.	Flutamide	143-152	cysteine-rich secretory protein 3	Mus musculus	12-19
9192502-2	1997	The effect of long-term androgen-receptor blockade with flutamide (500 mg daily in two divided doses for 12 months) on BMD was assessed too.	Flutamide	56-65	androgen receptor	Homo sapiens	24-41
9471771-5	1997	Eight (22.9%) of 35 patients showed a decline in PSA levels following flutamide withdrawal.	Flutamide	70-79	kallikrein related peptidase 3	Homo sapiens	49-52
9224356-0	1997	Re: Characterization of patients with androgen independent prostatic carcinoma whose serum prostate specific antigen decreased following flutamide withdrawal.	Flutamide	137-146	kallikrein related peptidase 3	Homo sapiens	91-116
9201706-5	1997	Densitometric analysis of the autoradiographic signal revealed a rise in the level of androgen receptor RNA following treatment of rats with estradiol benzoate and flutamide.	Flutamide	164-173	androgen receptor	Rattus norvegicus	86-103
9228827-7	1997	Moreover we found that Testosterone, DHT and EGF are mainly concentrated in the periurethral zone in human BPH and long term treatment with Finasteride and with Flutamide modify the distribution and concentration of these factors.	Flutamide	161-170	epidermal growth factor	Homo sapiens	45-48
9186348-4	1997	In terms of biological response 11 of 20 patients (55%) receiving prednisolone and 10 of 20 (50%) receiving flutamide exhibited prostate specific antigen (PSA) suppression.	Flutamide	108-117	kallikrein related peptidase 3	Homo sapiens	128-153
9186348-4	1997	In terms of biological response 11 of 20 patients (55%) receiving prednisolone and 10 of 20 (50%) receiving flutamide exhibited prostate specific antigen (PSA) suppression.	Flutamide	108-117	kallikrein related peptidase 3	Homo sapiens	155-158
9186348-5	1997	Average minimum PSA was 54 and 52% of the initial PSA in patients receiving prednisolone and flutamide, respectively.	Flutamide	93-102	kallikrein related peptidase 3	Homo sapiens	16-19
9515293-4	1997	Following these two strategies, we first studied the pulsatile gonadotrophin secretion in hyperandrogenic women, following flutamide administration, a specific androgen receptor blocker.	Flutamide	123-132	androgen receptor	Homo sapiens	160-177
9187700-15	1997	Mean percent decline in PSA value from baseline was 87.0 +/- 3.1% with flutamide alone and 94.0 +/- 1.9% with both flutamide and finasteride (P = 0.001).	Flutamide	71-80	kallikrein related peptidase 3	Homo sapiens	24-27
9187700-15	1997	Mean percent decline in PSA value from baseline was 87.0 +/- 3.1% with flutamide alone and 94.0 +/- 1.9% with both flutamide and finasteride (P = 0.001).	Flutamide	115-124	kallikrein related peptidase 3	Homo sapiens	24-27
9515293-5	1997	Flutamide treatment was followed by a decrease in LH pulse amplitude and mean LH concentrations, demonstrating that androgen receptor blockade reduces LH secretion in hyperandrogenic women.	Flutamide	0-9	androgen receptor	Homo sapiens	116-133
9112515-0	1997	Prostate specific antigen decreases after withdrawal of antiandrogen therapy with bicalutamide or flutamide in patients receiving combined androgen blockade.	Flutamide	98-107	kallikrein related peptidase 3	Homo sapiens	0-25
9158528-0	1997	Reduction of flutamide-induced alanine aminotransferase elevation after replacement by bicalutamide in a patient with N+ disease treated with maximal androgen blockade as a primary treatment.	Flutamide	13-22	glutamic--pyruvic transaminase	Homo sapiens	31-55
9112515-1	1997	PURPOSE: We determined whether decreases in prostate specific antigen (PSA) would occur after withdrawal of double-blinded antiandrogen therapy with flutamide or bicalutamide for clinical progression or increasing PSA concentration in patients receiving combined androgen blockade for advanced prostate cancer.	Flutamide	149-158	kallikrein related peptidase 3	Homo sapiens	44-69
9112515-1	1997	PURPOSE: We determined whether decreases in prostate specific antigen (PSA) would occur after withdrawal of double-blinded antiandrogen therapy with flutamide or bicalutamide for clinical progression or increasing PSA concentration in patients receiving combined androgen blockade for advanced prostate cancer.	Flutamide	149-158	kallikrein related peptidase 3	Homo sapiens	71-74
9112515-6	1997	PSA responses after withdrawal of flutamide therapy occurred within the first few days, whereas those after withdrawal of bicalutamide therapy occurred within 4 to 8 weeks.	Flutamide	34-43	kallikrein related peptidase 3	Homo sapiens	0-3
9112515-9	1997	CONCLUSIONS: For patients with stage D2 prostate cancer and disease progression or an increasing PSA concentration, withdrawal of antiandrogen therapy with bicalutamide or flutamide may result in a PSA response.	Flutamide	172-181	kallikrein related peptidase 3	Homo sapiens	97-100
9112515-9	1997	CONCLUSIONS: For patients with stage D2 prostate cancer and disease progression or an increasing PSA concentration, withdrawal of antiandrogen therapy with bicalutamide or flutamide may result in a PSA response.	Flutamide	172-181	kallikrein related peptidase 3	Homo sapiens	198-201
9112515-10	1997	The time to PSA response is longer with bicalutamide than with flutamide.	Flutamide	63-72	kallikrein related peptidase 3	Homo sapiens	12-15
9144890-2	1997	A "flutamide withdrawal syndrome" was first described by Kelly and Scher [15], who reported a decrease in serum prostate-specific antigen (PSA) levels after the removal of flutamide from the treatment regimen.	Flutamide	3-12	kallikrein related peptidase 3	Homo sapiens	112-143
9292316-12	1997	In a second study, hCG (1.25 IU/kg) was administered alone or in combination with the androgen receptor antagonist, flutamide (100 mg/kg sc daily), to withdraw androgenic effects at all stages of spermatogenesis.	Flutamide	116-125	androgen receptor	Rattus norvegicus	86-103
9049038-4	1997	Ornithine decarboxylase (ODC) activity was significantly decreased by flutamide, and to a lesser extent by casodex.	Flutamide	70-79	ornithine decarboxylase 1	Rattus norvegicus	0-23
9049038-4	1997	Ornithine decarboxylase (ODC) activity was significantly decreased by flutamide, and to a lesser extent by casodex.	Flutamide	70-79	ornithine decarboxylase 1	Rattus norvegicus	25-28
9007049-7	1997	Densitometry scans of Northern blots indicated that vinclozolin, p,p"-DDE, and flutamide each induced TRPM-2 mRNA and repressed C3 mRNA compared to vehicle-treated T-implanted controls.	Flutamide	79-88	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	102-108
9175723-8	1997	At lower concentrations of flutamide (i.e. 25 microM), there was a tendency toward increased release of myeloperoxidase, whereas at higher concentrations (i.e. 75-100 microM) flutamide inhibited degranulation in response to fmlp.	Flutamide	27-36	myeloperoxidase	Homo sapiens	104-119
9175723-9	1997	In coculture with hepatocytes, PMNs exposed to either flutamide, fmlp, or PMA alone caused a significant increase in release of alanine aminotransferase.	Flutamide	54-63	glutamic--pyruvic transaminase	Homo sapiens	128-152
9027406-8	1997	Moreover, morphogenetic effects depended on androgen receptor (AR) activation, since morphological changes were completely inhibited by flutamide.	Flutamide	136-145	androgen receptor	Mus musculus	44-61
9027406-8	1997	Moreover, morphogenetic effects depended on androgen receptor (AR) activation, since morphological changes were completely inhibited by flutamide.	Flutamide	136-145	androgen receptor	Mus musculus	63-65
9007049-5	1997	Vinclozolin, p,p"-DDE, and flutamide all induced a reciprocal decline in seminal vesicle (p < 0.01) and prostate (p < 0.01) weight as well as a reduction in immunohistochemical staining of AR in epididymal nuclei compared to vehicle-treated T-implanted controls.	Flutamide	27-36	androgen receptor	Rattus norvegicus	195-197
9170575-1	1996	BACKGROUND: In a recent study by the Casodex Combination Study Group, USA, patients in a flutamide (750 mg/day) plus LH-RH agonist group showed a high treatment failure rate, mainly due to flutamide-induced diarrhea and hepatotoxicity.	Flutamide	189-198	gonadotropin releasing hormone 1	Homo sapiens	117-122
8973674-3	1996	Flutamide (250 mg three times a day) was added after serum PSA levels stabilized.	Flutamide	0-9	kallikrein related peptidase 3	Homo sapiens	59-62
8973674-5	1996	Combined finasteride and flutamide resulted in a mean 91% reduction in serum PSA levels, with 85% of men achieving a nadir serum PSA level of less than 4.0 ng/mL and 46% achieving undetectable levels (0.2 ng/mL or less).	Flutamide	25-34	kallikrein related peptidase 3	Homo sapiens	77-80
8973674-5	1996	Combined finasteride and flutamide resulted in a mean 91% reduction in serum PSA levels, with 85% of men achieving a nadir serum PSA level of less than 4.0 ng/mL and 46% achieving undetectable levels (0.2 ng/mL or less).	Flutamide	25-34	kallikrein related peptidase 3	Homo sapiens	129-132
9170575-9	1996	One patient administered 250 mg of flutamide experienced diarrhea, while the serum GOT and/or GPT were elevated in 3 patients administered 250 mg of flutamide and 4 patients administered 375 mg of flutamide.	Flutamide	149-158	glutamic--pyruvic transaminase	Homo sapiens	94-97
9170575-9	1996	One patient administered 250 mg of flutamide experienced diarrhea, while the serum GOT and/or GPT were elevated in 3 patients administered 250 mg of flutamide and 4 patients administered 375 mg of flutamide.	Flutamide	149-158	glutamic--pyruvic transaminase	Homo sapiens	94-97
8709345-4	1996	MATERIALS AND METHODS: Estrogen receptor expression by stromal and glandular cells was studied by immunohistochemistry in prostatectomy specimens of 21 patient with prostate cancer, treated for 3 months with a luteinizing hormone-releasing hormone (LHRH) agonist and flutamide.	Flutamide	267-276	estrogen receptor 1	Homo sapiens	23-40
8912815-4	1996	Anti-AR, flutamide and cyproterone acetate blocked the Wolffian duct-stabilizing effect of EGF.	Flutamide	9-18	epidermal growth factor	Mus musculus	91-94
8823479-10	1996	Only two participants experienced a greater than 50% decrease in serum PSA, one of which may have been attributed to a flutamide withdrawal syndrome.	Flutamide	119-128	aminopeptidase puromycin sensitive	Homo sapiens	71-74
8702703-6	1996	Two potent anti-androgens, casodex and flutamide, can significantly reduce this activation, confirming that the ligand-independent pathway is an androgen receptor-mediated phenomenon.	Flutamide	39-48	androgen receptor	Homo sapiens	145-162
8616754-2	1996	This Phase 11 study was designed to investigate the clinical activity and toxicity of flutamide in the treatment of patients with advanced HCC.	Flutamide	86-95	HCC	Homo sapiens	139-142
8593821-10	1996	Similarly, an antiandrogen receptor, flutamide (100 mg/kg.day) exposure during days 13-17 of gestation inhibited male reproductive tract differentiation and resulted in inhibition of EGF-mRNA expression.	Flutamide	37-46	epidermal growth factor	Mus musculus	183-186
8558675-0	1996	Characterization of patients with androgen-independent prostatic carcinoma whose serum prostate specific antigen decreased following flutamide withdrawal.	Flutamide	133-142	kallikrein related peptidase 3	Homo sapiens	87-112
8558675-1	1996	PURPOSE: We confirmed the reported rate of prostate specific antigen (PSA) suppression after flutamide withdrawal in patients with metastatic prostatic carcinoma, increasing serum PSA and tumor progression following treatment with total androgen blockade (castration and flutamide).	Flutamide	93-102	kallikrein related peptidase 3	Homo sapiens	43-68
8558675-1	1996	PURPOSE: We confirmed the reported rate of prostate specific antigen (PSA) suppression after flutamide withdrawal in patients with metastatic prostatic carcinoma, increasing serum PSA and tumor progression following treatment with total androgen blockade (castration and flutamide).	Flutamide	93-102	kallikrein related peptidase 3	Homo sapiens	70-73
8558675-1	1996	PURPOSE: We confirmed the reported rate of prostate specific antigen (PSA) suppression after flutamide withdrawal in patients with metastatic prostatic carcinoma, increasing serum PSA and tumor progression following treatment with total androgen blockade (castration and flutamide).	Flutamide	93-102	kallikrein related peptidase 3	Homo sapiens	180-183
8558675-1	1996	PURPOSE: We confirmed the reported rate of prostate specific antigen (PSA) suppression after flutamide withdrawal in patients with metastatic prostatic carcinoma, increasing serum PSA and tumor progression following treatment with total androgen blockade (castration and flutamide).	Flutamide	271-280	kallikrein related peptidase 3	Homo sapiens	43-68
8558675-1	1996	PURPOSE: We confirmed the reported rate of prostate specific antigen (PSA) suppression after flutamide withdrawal in patients with metastatic prostatic carcinoma, increasing serum PSA and tumor progression following treatment with total androgen blockade (castration and flutamide).	Flutamide	271-280	kallikrein related peptidase 3	Homo sapiens	70-73
8558675-2	1996	The value of clinical variables in predicting the rate of PSA decrease after flutamide withdrawal was assessed and adrenal androgen metabolism was correlated with the rate of PSA suppression following flutamide withdrawal.	Flutamide	77-86	kallikrein related peptidase 3	Homo sapiens	58-61
8558675-2	1996	The value of clinical variables in predicting the rate of PSA decrease after flutamide withdrawal was assessed and adrenal androgen metabolism was correlated with the rate of PSA suppression following flutamide withdrawal.	Flutamide	201-210	kallikrein related peptidase 3	Homo sapiens	175-178
8558675-7	1996	RESULTS: Of 39 patients studied 11 (28.2%, 95% confidence internal 14 to 45%) had a PSA decrease (more than 50% from baseline) following flutamide withdrawal and they were treated with initial complete androgen blockade.	Flutamide	137-146	kallikrein related peptidase 3	Homo sapiens	84-87
8558675-10	1996	No statistical correlation between endocrine studies or serum bombesin secretion and PSA decrease was found, although patients with a PSA decrease after flutamide withdrawal tended to have a lower dehydroepiandrosterone concentration than those with PSA progression.	Flutamide	153-162	kallikrein related peptidase 3	Homo sapiens	134-137
8558675-10	1996	No statistical correlation between endocrine studies or serum bombesin secretion and PSA decrease was found, although patients with a PSA decrease after flutamide withdrawal tended to have a lower dehydroepiandrosterone concentration than those with PSA progression.	Flutamide	153-162	kallikrein related peptidase 3	Homo sapiens	134-137
8558675-12	1996	CONCLUSIONS: We confirmed the existence of the reported paradoxical PSA decrease in patients with androgen-independent carcinoma of the prostate, and that the delivery of simultaneous initial flutamide with castration predicts for PSA decrease.	Flutamide	192-201	kallikrein related peptidase 3	Homo sapiens	231-234
8977067-0	1996	Tolerability and safety of flutamide in monotherapy, with orchiectomy or with LHRH-a in advanced prostate cancer patients.	Flutamide	27-36	gonadotropin releasing hormone 1	Homo sapiens	78-82
8995493-9	1996	In addition, prostate-specific antigen (PSA)-defined responses were observed in six patients receiving therapy at 175 microg/ml, but these responses were confounded by cessation of therapy with flutamide during suramin treatment.	Flutamide	194-203	kallikrein related peptidase 3	Homo sapiens	13-45
21597702-9	1995	Our results suggested that flutamide reduces cytosolic androgen receptor levels and increases DNA synthesis.	Flutamide	27-36	androgen receptor	Mus musculus	55-72
8620419-2	1995	BACKGROUND: Flutamide withdrawal has been reported to be therapeutically efficacious for patients with hormone-refractory prostate cancer, with a reported prostate specific antigen (PSA) response rate of 29%.	Flutamide	12-21	kallikrein related peptidase 3	Homo sapiens	155-180
8620419-2	1995	BACKGROUND: Flutamide withdrawal has been reported to be therapeutically efficacious for patients with hormone-refractory prostate cancer, with a reported prostate specific antigen (PSA) response rate of 29%.	Flutamide	12-21	kallikrein related peptidase 3	Homo sapiens	182-185
7641903-0	1995	Flutamide in the treatment of hirsutism: long-term clinical effects, endocrine changes, and androgen receptor behavior.	Flutamide	0-9	androgen receptor	Homo sapiens	92-109
7641903-16	1995	Flutamide affects androgen receptor behavior during the menstrual cycle.	Flutamide	0-9	androgen receptor	Homo sapiens	18-35
7538237-6	1995	Patients in the flutamide plus LHRH-A group were 34% more likely to fail treatment over the given time period, as indicated by the hazard ratio of 0.749 (95% confidence interval, 0.61 to 0.92) for bicalutamide plus LHRH-A to flutamide plus LHRH-A.	Flutamide	16-25	gonadotropin releasing hormone 1	Homo sapiens	215-219
7538237-6	1995	Patients in the flutamide plus LHRH-A group were 34% more likely to fail treatment over the given time period, as indicated by the hazard ratio of 0.749 (95% confidence interval, 0.61 to 0.92) for bicalutamide plus LHRH-A to flutamide plus LHRH-A.	Flutamide	16-25	gonadotropin releasing hormone 1	Homo sapiens	215-219
7538237-6	1995	Patients in the flutamide plus LHRH-A group were 34% more likely to fail treatment over the given time period, as indicated by the hazard ratio of 0.749 (95% confidence interval, 0.61 to 0.92) for bicalutamide plus LHRH-A to flutamide plus LHRH-A.	Flutamide	225-234	gonadotropin releasing hormone 1	Homo sapiens	31-35
7535978-0	1995	Prostate specific antigen decline following the discontinuation of flutamide in patients with stage D2 prostate cancer.	Flutamide	67-76	kallikrein related peptidase 3	Homo sapiens	0-25
8560673-8	1996	Studies with the LNCaP cell line are particularly interesting, as these cells contain a mutated androgen receptor (codon 868, Thr-->Ala), which behaves idiosyncratically with other antiandrogens (cyproterone acetate and flutamide): both these antiandrogens act as agonists in this cell line and stimulate proliferation.	Flutamide	223-232	androgen receptor	Homo sapiens	96-113
8548942-1	1995	BACKGROUND AND OBJECTIVE: High doses of flutamide, which is the only antiandrogen that specifically blocks the androgen receptor, have recently been used with good clinical results in women with hirsutism.	Flutamide	40-49	androgen receptor	Homo sapiens	111-128
8674832-7	1995	Administration of the androgen antagonist flutamide during the same interval caused a reduction in density and frequency of androgen receptor positive cells in male fetuses.	Flutamide	42-51	androgen receptor	Rattus norvegicus	124-141
7628354-11	1995	Ribonuclease protection assay demonstrated a significant decrease in the AR mRNA content of the hippocampus in animals killed 4 days after castration or in intact rats after four daily injections of the AR antagonist, flutamide (15 mg/animal), compared to that in intact controls (P < 0.01).	Flutamide	218-227	androgen receptor	Rattus norvegicus	73-75
7628354-11	1995	Ribonuclease protection assay demonstrated a significant decrease in the AR mRNA content of the hippocampus in animals killed 4 days after castration or in intact rats after four daily injections of the AR antagonist, flutamide (15 mg/animal), compared to that in intact controls (P < 0.01).	Flutamide	218-227	androgen receptor	Rattus norvegicus	203-205
7541862-1	1995	PURPOSE: We assess the impact of deferred flutamide treatment on the serum prostate specific antigen (PSA) level in patients with localized or metastatic cancer.	Flutamide	42-51	kallikrein related peptidase 3	Homo sapiens	75-100
7541862-1	1995	PURPOSE: We assess the impact of deferred flutamide treatment on the serum prostate specific antigen (PSA) level in patients with localized or metastatic cancer.	Flutamide	42-51	kallikrein related peptidase 3	Homo sapiens	102-105
7541862-3	1995	RESULTS: Of 40 evaluable patients with localized cancer and 50 with metastatic cancer 32 (80%) and 27 (54%), respectively, had a PSA decrease of 50% or more of baseline during flutamide treatment (p = 0.014).	Flutamide	176-185	kallikrein related peptidase 3	Homo sapiens	129-132
7541862-4	1995	Among patients with localized cancer actuarial analysis of freedom from PSA elevation during flutamide treatment favored those with a 50% or greater PSA decrease (p = 0.006) but in patients with metastatic cancer the analysis revealed no significant difference.	Flutamide	93-102	kallikrein related peptidase 3	Homo sapiens	72-75
7541862-4	1995	Among patients with localized cancer actuarial analysis of freedom from PSA elevation during flutamide treatment favored those with a 50% or greater PSA decrease (p = 0.006) but in patients with metastatic cancer the analysis revealed no significant difference.	Flutamide	93-102	kallikrein related peptidase 3	Homo sapiens	149-152
7567789-6	1995	Different doses of flutamide (FLU) and OH-FLU tested on cultured IIB-MEL-J cells in the presence of serum inhibited significantly cell proliferation in a dose-dependent manner.	Flutamide	19-28	ATPase, class II, type 9B	Mus musculus	65-68
7567789-6	1995	Different doses of flutamide (FLU) and OH-FLU tested on cultured IIB-MEL-J cells in the presence of serum inhibited significantly cell proliferation in a dose-dependent manner.	Flutamide	30-33	ATPase, class II, type 9B	Mus musculus	65-68
7567789-9	1995	In addition, male nude mice transplanted with IIB-MEL-J tumor were treated with FLU when tumors were palpable.	Flutamide	80-83	ATPase, class II, type 9B	Mus musculus	46-49
7821714-7	1994	Administration of the androgen antagonist flutamide (100 mg/kg body weight per day) during the same interval caused a reduction in androgen receptor level in the urogenital sinus and tubercle of the male.	Flutamide	42-51	androgen receptor	Rattus norvegicus	131-148
7997435-6	1994	The growth of AR-transfectant cells was markedly inhibited in culture in the presence of testosterone, and the effect of testosterone was reduced by simultaneous addition of flutamide.	Flutamide	174-183	androgen receptor	Mus musculus	14-16
7915761-8	1994	This study shows that prenatal androgen blockade with flutamide inhibits masculinization of the GFN, with significant reduction of its CGRP content.	Flutamide	54-63	calcitonin-related polypeptide alpha	Rattus norvegicus	135-139
7912743-2	1994	This fact led us to investigate whether epidermal growth factor can reverse the undescended testes and epididymal abnormalities associated with time specific flutamide administration.	Flutamide	158-167	epidermal growth factor like 1	Rattus norvegicus	40-63
7912743-5	1994	We performed immunohistological studies to evaluate whether flutamide alters epidermal growth factor expression in the paratesticular tissues during the time of maximal androgenic activity.	Flutamide	60-69	epidermal growth factor like 1	Rattus norvegicus	77-100
8111715-3	1994	One of the most popular agents is leuprolide (with or without flutamide), an agonist of luteinizing hormone-releasing hormone (LH-RH).	Flutamide	62-71	gonadotropin releasing hormone 1	Homo sapiens	88-125
8195454-1	1994	We report here the first use in Tourette"s syndrome of the nonsteroidal androgen receptor blocking agent flutamide.	Flutamide	105-114	androgen receptor	Homo sapiens	72-89
8170836-0	1994	TRPM-2 gene expression in normal rat ventral prostate following castration and exposure to diethylstilbestrol, flutamide, MK-906 (finasteride), and coumarin.	Flutamide	111-120	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	0-6
8136296-2	1994	These compounds presented exceptionally high relative binding affinities (RBAs) for the rat androgen receptor (AR): up to 3 times that of testosterone (T) and 100 times the RBAs of non-steroidal antiandrogens such as flutamide, Casodex and Anandron.	Flutamide	217-226	androgen receptor	Rattus norvegicus	92-109
7510915-4	1994	CONCLUSIONS: The relationship between antiandrogen withdrawal and a change in PSA may be a general phenomenon, not unique to flutamide.	Flutamide	125-134	kallikrein related peptidase 3	Homo sapiens	78-81
7525090-5	1994	This effect could be antagonized by the simultaneous administration of an antiandrogen, flutamide, indicating that CK-8 is a new class of androgen-repressed genes whose regulation is presumably mediated by androgen receptor mechanisms.	Flutamide	88-97	keratin 8	Rattus norvegicus	115-119
8288699-7	1994	A specific androgen receptor blocker, flutamide, when added to cultures containing T, inhibited PRL production in a dose-dependent manner, but did not affect the production of PRL induced by P. These results indicate that in vitro PRL production by human ESC is induced not only by P, but also by androgens through specific receptors and further suggest that androgens play an important role in human endometrial differentiation.	Flutamide	38-47	prolactin	Homo sapiens	96-99
8136296-2	1994	These compounds presented exceptionally high relative binding affinities (RBAs) for the rat androgen receptor (AR): up to 3 times that of testosterone (T) and 100 times the RBAs of non-steroidal antiandrogens such as flutamide, Casodex and Anandron.	Flutamide	217-226	androgen receptor	Rattus norvegicus	111-113
7910394-1	1993	Effect of combination endocrine therapy (LHRH agonist and flutamide) on the expression and location of proliferating cell nuclear antigen (PCNA).	Flutamide	58-67	proliferating cell nuclear antigen	Homo sapiens	103-137
7991782-7	1994	The testicular feminization mouse with complete androgen resistance and the rat exposed prenatally to the antiandrogen flutamide have a deficiency of CGRP in the GFN.	Flutamide	119-128	calcitonin-related polypeptide alpha	Rattus norvegicus	150-154
8087144-10	1994	In addition to androgens, the natural activators of the AR, the LNCaP receptor is activated also by progestagenic and estrogenic steroids and by the nonsteroidal antiandrogen flutamide.	Flutamide	175-184	androgen receptor	Homo sapiens	56-58
7910394-1	1993	Effect of combination endocrine therapy (LHRH agonist and flutamide) on the expression and location of proliferating cell nuclear antigen (PCNA).	Flutamide	58-67	proliferating cell nuclear antigen	Homo sapiens	139-143
8100863-1	1993	The relationship among calcitonin gene-related peptide (CGRP), a neurotransmitter in the genitofemoral nerve, androgens and gubernacular development was studied using rats treated prenatally with the antiandrogen flutamide and the mutant cryptorchid TS rat.	Flutamide	213-222	calcitonin-related polypeptide alpha	Rattus norvegicus	23-54
8370128-16	1993	CONCLUSION: Flutamide, which interacts only with the androgen receptor, is effective for hirsutism, acne and seborrhoea, and does not disturb menstrual cyclicity or ovulation.	Flutamide	12-21	androgen receptor	Homo sapiens	53-70
7679759-3	1993	We report 3 representative cases receiving complete androgen blockade with either gonadotropin-releasing hormone or orchiectomy plus the antiandrogen flutamide, which demonstrated sustained declines in serum PSA levels after discontinuation of the antiandrogen.	Flutamide	150-159	kallikrein related peptidase 3	Homo sapiens	208-211
7688829-14	1993	The serum prolactin level decreased significantly in the flutamide group, but increased significantly in the CMA group.	Flutamide	57-66	prolactin	Homo sapiens	10-19
8331696-2	1993	Testosterone and luteinizing hormone (LH) levels in serum, testis or pituitary and the in vitro binding affinities of procymidone, flutamide and related compounds to the androgen receptor in prostate cytosol of rats and mice were examined.	Flutamide	131-140	androgen receptor	Rattus norvegicus	170-187
8496305-0	1993	Androgen receptor blockade with flutamide enhances growth hormone secretion in late pubertal males: evidence for independent actions of estrogen and androgen.	Flutamide	32-41	androgen receptor	Homo sapiens	0-17
8386241-3	1993	In contrast, flutamide was oxidatively transformed by cytochrome P-450 into reactive metabolite(s) that covalently bound to microsomal proteins.	Flutamide	13-22	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	54-70
8480329-15	1993	The IC50 data for competition to the androgen receptor suggest that linuron is approximately 3.5 times less potent than flutamide.	Flutamide	120-129	androgen receptor	Rattus norvegicus	37-54
7679759-6	1993	The results suggest that a trial of flutamide withdrawal is justified in an asymptomatic patient with an increasing PSA before treatment with more toxic therapies.	Flutamide	36-45	kallikrein related peptidase 3	Homo sapiens	116-119
8472853-7	1993	Administration of FLU or 4-MA independently caused 33% and 10% decreases, respectively, of PBP-C3 mRNA levels stimulated by delta 4-dione while the combination of both compounds further inhibited PBP-C3 mRNA levels to reach a 55% inhibition.	Flutamide	18-21	phosphatidylethanolamine binding protein 1	Rattus norvegicus	91-94
8386109-7	1993	Treatment with flutamide, EDS or castration significantly increased (p < 0.05) serum levels of LH, FSH and alpha-subunit, whereas serum gonadotrophin levels were decreased in the GnRH antagonist-treated group.	Flutamide	15-24	gonadotropin releasing hormone 1	Rattus norvegicus	182-186
8386109-9	1993	FSH-beta mRNA levels were increased in the castrated group and decreased in the GnRH antagonist group, but remained unchanged in the flutamide and EDS group.	Flutamide	133-142	follicle stimulating hormone subunit beta	Rattus norvegicus	0-8
8472853-7	1993	Administration of FLU or 4-MA independently caused 33% and 10% decreases, respectively, of PBP-C3 mRNA levels stimulated by delta 4-dione while the combination of both compounds further inhibited PBP-C3 mRNA levels to reach a 55% inhibition.	Flutamide	18-21	phosphatidylethanolamine binding protein 1	Rattus norvegicus	196-199
1458483-8	1992	Addition of exogenous testosterone with, or without, flutamide demonstrated that the increased bcl-2 mRNA resulted from androgen ablation.	Flutamide	53-62	BCL2 apoptosis regulator	Homo sapiens	95-100
1509913-4	1992	Decrease of PSA and PAP was also higher in the group given flutamide.	Flutamide	59-68	aminopeptidase puromycin sensitive	Homo sapiens	12-15
1324152-12	1992	At dosages of 100, 200, and 300 mg/kg.day flutamide, the vas deferens was absent unilaterally or bilaterally, with small remnants of epididymal head and tail present.	Flutamide	42-51	arginine vasopressin	Rattus norvegicus	57-60
1948117-6	1991	The level of prostate-specific antigen was reduced markedly following 6 months" treatment with flutamide.	Flutamide	95-104	kallikrein related peptidase 3	Homo sapiens	13-38
1347714-7	1992	DNA synthesis in the presence of EGF/insulin was reduced by the "pure" anti-androgen flutamide, but stimulated by the "pure" progestin promegestone.	Flutamide	85-94	epidermal growth factor like 1	Rattus norvegicus	33-36
1586971-1	1992	The human osteosarcoma cell line (OST-1-PF) can grow in protein-free Coon"s modified Ham"s F12 medium.	Flutamide	85-101	ribophorin I	Homo sapiens	34-39
1349790-1	1992	PURPOSE: The incidence of flutamide-related liver toxicity was studied in 1,091 consecutive patients treated for stage C or D prostate cancer with the antiandrogen flutamide and the luteinizing hormone-releasing factor (LHRH) agonist [D-Trp6, des-Gly-NH2(10)] LHRH ethylamide.	Flutamide	26-35	transient receptor potential cation channel subfamily C member 6	Homo sapiens	237-241
2043742-6	1991	Alpha fetoprotein (AFP), which binds estrogen and modulates immune responsiveness, was greater in serum from both groups of testosterone-treated dams, while flutamide treatment increased serum AFP only in NZB dams.	Flutamide	157-166	alpha fetoprotein	Mus musculus	193-196
1877268-6	1991	Moreover, clinical improvement and normalization of the methemoglobin level after the drug was discontinued is highly suggestive of flutamide-induced methemoglobinemia.	Flutamide	132-141	hemoglobin subunit gamma 2	Homo sapiens	56-69
1877268-7	1991	Due to its chemical structure derived from anilide, flutamide may be considered as a potential methemoglobin-inducing agent.	Flutamide	52-61	hemoglobin subunit gamma 2	Homo sapiens	95-108
1794008-6	1991	Thus, while there seems to be little doubt that flutamide prevents the initial disease flare caused by GnRH agonists, an improvement in remission rate and survival remains contentious.	Flutamide	48-57	gonadotropin releasing hormone 1	Homo sapiens	103-107
2144819-0	1990	Advanced prostatic cancer: clinical and hormonal response to flutamide in patients pretreated with LHRH analogue and cyproterone acetate.	Flutamide	61-70	gonadotropin releasing hormone 1	Homo sapiens	99-103
2201967-0	1990	Flutamide blocks the self-priming effect of luteinizing hormone-releasing hormone in pubertal male rats.	Flutamide	0-9	gonadotropin releasing hormone 1	Rattus norvegicus	44-81
2118203-6	1990	In the estrogen-primed ovariectomized immature rat, flutamide was found to suppress LH, FSH and PRL secretion.	Flutamide	52-61	prolactin	Rattus norvegicus	96-99
2118203-9	1990	The effect of flutamide in suppressing LH, FSH and PRL release was not through suppression of an adrenal steroid as shown by adrenalectomy or the use of RU486.	Flutamide	14-23	prolactin	Rattus norvegicus	51-54
2118203-12	1990	These studies demonstrate that in the ovariectomized estrogen-primed immature rat flutamide has potent neuroendocrine regulatory ability leading to suppression of LH, FSH and PRL release.	Flutamide	82-91	prolactin	Rattus norvegicus	175-178
2193461-3	1990	Clinical studies in prostate cancer patients have demonstrated efficacy with flutamide monotherapy in patients who had received no prior treatment, in untreated patients with combined androgen blockade concomitantly with a luteinizing hormone-releasing hormone (LHRH)-agonist, and in relapsed patients.	Flutamide	77-86	gonadotropin releasing hormone 1	Homo sapiens	262-266
2193461-5	1990	When given as monotherapy and in combination with an LHRH-agonist, flutamide is well tolerated.	Flutamide	67-76	gonadotropin releasing hormone 1	Homo sapiens	53-57
2081373-4	1990	Similarly, inactive renin decreased (p less than 0.01) from 0.50 GU/l (range 0.28-0.67 GU/l) to 0.30 GU/l (range 0.19-0.47 GU/l) during treatment with the anti-androgen flutamide (n = 10).	Flutamide	169-178	renin	Rattus norvegicus	20-25
2144819-1	1990	The aim of the present investigation was to establish whether in advanced prostatic carcinoma in relapse treated with LHRH analogues combined with cyproterone acetate (CPA), substitution of this antiandrogen with another compound such as flutamide (FLU) might lead to further subjective and objective improvement.	Flutamide	238-247	gonadotropin releasing hormone 1	Homo sapiens	118-122
1978301-6	1990	Elevated ASAT values were observed during treatment with flutamide and with LH-RH-agonist + flutamide.	Flutamide	57-66	ATP binding cassette subfamily B member 7	Homo sapiens	9-13
1978301-6	1990	Elevated ASAT values were observed during treatment with flutamide and with LH-RH-agonist + flutamide.	Flutamide	92-101	ATP binding cassette subfamily B member 7	Homo sapiens	9-13
33971475-5	2021	First, we administered flutamide, an AR antagonist, via intraperitoneal injections daily during the establishment of dominance relationships in male hamsters.	Flutamide	23-32	androgen receptor	Mesocricetus auratus	37-39
1693455-9	1990	In follow-up studies a marked decline in PSA values after transurethral resection or antiandrogen therapy (orchiectomy/Zoladex/ICI/flutamide, Essex).	Flutamide	131-140	kallikrein related peptidase 3	Homo sapiens	41-44
8070366-12	1994	Androgenic effects on hypothalamic AA and aromatase-IR cell numbers were dose-dependent and mediated via androgen receptor stimulation, since the observed effects were inhibited by the androgen-receptor antagonist flutamide.	Flutamide	214-223	androgen receptor	Mus musculus	105-122
20048160-7	2010	These effects of androgen were blocked by an AR antagonist, flutamide, but not by an estrogen receptor antagonist, ICI 182,780.	Flutamide	60-69	androgen receptor	Homo sapiens	45-47
20048160-9	2010	Dihydrotestosterone stimulated Gas6 promoter activity, and this effect was abrogated by flutamide and by AR siRNA.	Flutamide	88-97	growth arrest specific 6	Homo sapiens	31-35
34864206-7	2022	Meanwhile, DHT interfered with the TGF-beta signaling by reducing the expression of TGF-betaRI and TGF-betaRII and inhibiting the expression and phosphorylation of Smad2 and Smad3, while flutamide (androgen receptor inhibitor) inhibited these effects of DHT.	Flutamide	187-196	protransforming growth factor alpha	Canis lupus familiaris	35-43
34838638-9	2022	We further explored whether DHT regulates ALK-6 and BMPRII through the nuclear androgen receptor (AR) pathway and found that 10-6-M flutamide, a non-selective androgen inhibitor, partially relieved the inhibitory effect of 10-7-M DHT on ALK-6 and BMPRII expression.	Flutamide	132-141	bone morphogenetic protein receptor type-1B	Ovis aries	42-47
34838638-9	2022	We further explored whether DHT regulates ALK-6 and BMPRII through the nuclear androgen receptor (AR) pathway and found that 10-6-M flutamide, a non-selective androgen inhibitor, partially relieved the inhibitory effect of 10-7-M DHT on ALK-6 and BMPRII expression.	Flutamide	132-141	androgen receptor	Ovis aries	79-96
34838638-9	2022	We further explored whether DHT regulates ALK-6 and BMPRII through the nuclear androgen receptor (AR) pathway and found that 10-6-M flutamide, a non-selective androgen inhibitor, partially relieved the inhibitory effect of 10-7-M DHT on ALK-6 and BMPRII expression.	Flutamide	132-141	androgen receptor	Ovis aries	98-100
34838638-9	2022	We further explored whether DHT regulates ALK-6 and BMPRII through the nuclear androgen receptor (AR) pathway and found that 10-6-M flutamide, a non-selective androgen inhibitor, partially relieved the inhibitory effect of 10-7-M DHT on ALK-6 and BMPRII expression.	Flutamide	132-141	bone morphogenetic protein receptor type-1B	Ovis aries	237-242
34864206-7	2022	Meanwhile, DHT interfered with the TGF-beta signaling by reducing the expression of TGF-betaRI and TGF-betaRII and inhibiting the expression and phosphorylation of Smad2 and Smad3, while flutamide (androgen receptor inhibitor) inhibited these effects of DHT.	Flutamide	187-196	androgen receptor	Canis lupus familiaris	198-215
34800879-6	2022	Generally, both cell lines treated with the combination of Flutamide and ATO showed a decrease in expression of KLK2, angiogenesis genes (VEGFA and VEGFC), and apoptosis gene (Bcl2), and an increase in expression of E-cadherin and P53 genes; however, contradictory findings were found regarding SNAIL expression in LNCaP and PC3 cells.	Flutamide	59-68	kallikrein related peptidase 2	Homo sapiens	112-116
34800879-6	2022	Generally, both cell lines treated with the combination of Flutamide and ATO showed a decrease in expression of KLK2, angiogenesis genes (VEGFA and VEGFC), and apoptosis gene (Bcl2), and an increase in expression of E-cadherin and P53 genes; however, contradictory findings were found regarding SNAIL expression in LNCaP and PC3 cells.	Flutamide	59-68	vascular endothelial growth factor A	Homo sapiens	138-143
34800879-6	2022	Generally, both cell lines treated with the combination of Flutamide and ATO showed a decrease in expression of KLK2, angiogenesis genes (VEGFA and VEGFC), and apoptosis gene (Bcl2), and an increase in expression of E-cadherin and P53 genes; however, contradictory findings were found regarding SNAIL expression in LNCaP and PC3 cells.	Flutamide	59-68	vascular endothelial growth factor C	Homo sapiens	148-153
34800879-6	2022	Generally, both cell lines treated with the combination of Flutamide and ATO showed a decrease in expression of KLK2, angiogenesis genes (VEGFA and VEGFC), and apoptosis gene (Bcl2), and an increase in expression of E-cadherin and P53 genes; however, contradictory findings were found regarding SNAIL expression in LNCaP and PC3 cells.	Flutamide	59-68	BCL2 apoptosis regulator	Homo sapiens	176-180
34800879-6	2022	Generally, both cell lines treated with the combination of Flutamide and ATO showed a decrease in expression of KLK2, angiogenesis genes (VEGFA and VEGFC), and apoptosis gene (Bcl2), and an increase in expression of E-cadherin and P53 genes; however, contradictory findings were found regarding SNAIL expression in LNCaP and PC3 cells.	Flutamide	59-68	cadherin 1	Homo sapiens	216-226
34800879-6	2022	Generally, both cell lines treated with the combination of Flutamide and ATO showed a decrease in expression of KLK2, angiogenesis genes (VEGFA and VEGFC), and apoptosis gene (Bcl2), and an increase in expression of E-cadherin and P53 genes; however, contradictory findings were found regarding SNAIL expression in LNCaP and PC3 cells.	Flutamide	59-68	tumor protein p53	Homo sapiens	231-234
34800879-6	2022	Generally, both cell lines treated with the combination of Flutamide and ATO showed a decrease in expression of KLK2, angiogenesis genes (VEGFA and VEGFC), and apoptosis gene (Bcl2), and an increase in expression of E-cadherin and P53 genes; however, contradictory findings were found regarding SNAIL expression in LNCaP and PC3 cells.	Flutamide	59-68	snail family transcriptional repressor 1	Homo sapiens	295-300
34180022-4	2021	We found that AR blockage using flutamide largely attenuated the DHT and INS-induced maternal endocrine, metabolic, and fertility impairments in pregnant rats in association with suppressed induction of uterine AR protein abundance and androgen-regulated response protein and normalized expression of several endometrial receptivity and decidualization genes.	Flutamide	32-41	androgen receptor	Rattus norvegicus	14-16
34547381-6	2021	Moreover, we cultured EECs from the mid-pregnancy phase and the in vitro study showed that DHT dose-dependently increased COX-2 expression and PGF2a release, but AR antagonist (flutamide) inhibited the stimulating effect via DHT.	Flutamide	177-186	androgen receptor	Bos taurus	162-164
34090906-0	2021	Potentiation of flutamide-induced hepatotoxicity in mice by Xian-Ling-Gu-Bao through induction of CYP1A2.	Flutamide	16-25	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	98-104
34090906-4	2021	AIM OF THE STUDY: The present study was designed to investigate the hepatotoxicity in the context of the combined treatment of XLGB and FLU in a mouse model, and to determine whether the metabolic activation of FLU through induction of CYP1A2 plays a role in the increased hepatoxicity caused by the combination of XLGB and FLU.	Flutamide	211-214	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	236-242
34090906-4	2021	AIM OF THE STUDY: The present study was designed to investigate the hepatotoxicity in the context of the combined treatment of XLGB and FLU in a mouse model, and to determine whether the metabolic activation of FLU through induction of CYP1A2 plays a role in the increased hepatoxicity caused by the combination of XLGB and FLU.	Flutamide	324-327	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	236-242
34090906-10	2021	The urine samples were collected for the analysis of FLU-NAC conjugate by UPLC-Q-Orbitrap MS.	Flutamide	53-56	NLR family, pyrin domain containing 1A	Mus musculus	57-60
34090906-13	2021	FLU increased hepatic expression of Cyp1a2 mRNA that was further elevated in the liver of mice when administered with both FLU and XLGB.	Flutamide	0-3	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	36-42
34090906-13	2021	FLU increased hepatic expression of Cyp1a2 mRNA that was further elevated in the liver of mice when administered with both FLU and XLGB.	Flutamide	123-126	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	36-42
34090906-14	2021	Treatment of FLU resulted in an increase in the expression of Cyp3a11 mRNA that was negated when mice were co-treated with FLU and XLGB.	Flutamide	13-16	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	62-69
34090906-14	2021	Treatment of FLU resulted in an increase in the expression of Cyp3a11 mRNA that was negated when mice were co-treated with FLU and XLGB.	Flutamide	123-126	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	62-69
34090906-17	2021	Mass spectrometry analysis identified the presence of FLU reactive metabolite derived FLU-NAC conjugate in the urine of mice treated with FLU.	Flutamide	54-57	NLR family, pyrin domain containing 1A	Mus musculus	90-93
34090906-17	2021	Mass spectrometry analysis identified the presence of FLU reactive metabolite derived FLU-NAC conjugate in the urine of mice treated with FLU.	Flutamide	138-141	NLR family, pyrin domain containing 1A	Mus musculus	90-93
34090906-18	2021	Strikingly, about a two-fold increase of the FLU-NAC conjugate was detected when treated with both FLU and XLGB, indicating an elevated amount of toxic metabolite produced from FLU in the present of XLGB.	Flutamide	45-48	NLR family, pyrin domain containing 1A	Mus musculus	49-52
34090906-18	2021	Strikingly, about a two-fold increase of the FLU-NAC conjugate was detected when treated with both FLU and XLGB, indicating an elevated amount of toxic metabolite produced from FLU in the present of XLGB.	Flutamide	99-102	NLR family, pyrin domain containing 1A	Mus musculus	49-52
34090906-18	2021	Strikingly, about a two-fold increase of the FLU-NAC conjugate was detected when treated with both FLU and XLGB, indicating an elevated amount of toxic metabolite produced from FLU in the present of XLGB.	Flutamide	177-180	NLR family, pyrin domain containing 1A	Mus musculus	49-52
34090906-20	2021	This increased hepatoxicity was mediated through the induction of CYP1A2 activity which in turn enhanced bioactivation of FLU leading to over production of FLU-NAC conjugate and oxidative stress.	Flutamide	122-125	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	66-72
34090906-20	2021	This increased hepatoxicity was mediated through the induction of CYP1A2 activity which in turn enhanced bioactivation of FLU leading to over production of FLU-NAC conjugate and oxidative stress.	Flutamide	122-125	NLR family, pyrin domain containing 1A	Mus musculus	160-163
34090906-20	2021	This increased hepatoxicity was mediated through the induction of CYP1A2 activity which in turn enhanced bioactivation of FLU leading to over production of FLU-NAC conjugate and oxidative stress.	Flutamide	156-159	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	66-72
34090906-20	2021	This increased hepatoxicity was mediated through the induction of CYP1A2 activity which in turn enhanced bioactivation of FLU leading to over production of FLU-NAC conjugate and oxidative stress.	Flutamide	156-159	NLR family, pyrin domain containing 1A	Mus musculus	160-163
34954075-5	2022	We found that prenatal DEHP exposure in vivo caused a significant increase in Fshb specifically in males, while the anti-androgen flutamide caused significant increases in both Lhb and Fshb in males.	Flutamide	130-139	luteinizing hormone beta	Mus musculus	177-180
34954075-5	2022	We found that prenatal DEHP exposure in vivo caused a significant increase in Fshb specifically in males, while the anti-androgen flutamide caused significant increases in both Lhb and Fshb in males.	Flutamide	130-139	follicle stimulating hormone beta	Mus musculus	185-189
34844599-14	2021	Finally, Progesterone, Flutamide, Nimesulide, Methotrexate and Temozolomide were identified to target these hub genes and might be targeted therapies for Chronic chagasic cardiomyopathy.	Flutamide	23-32	ELAV like RNA binding protein 2	Homo sapiens	108-111
34703906-4	2021	We also found that KLF9 expression was induced in response to apoptosis caused by flutamide, and further addition of dihydrotestosterone antagonized the action of flutamide and significantly decreased KLF9 expression.	Flutamide	82-91	Kruppel like factor 9	Homo sapiens	19-23
34703906-4	2021	We also found that KLF9 expression was induced in response to apoptosis caused by flutamide, and further addition of dihydrotestosterone antagonized the action of flutamide and significantly decreased KLF9 expression.	Flutamide	82-91	Kruppel like factor 9	Homo sapiens	201-205
34703906-4	2021	We also found that KLF9 expression was induced in response to apoptosis caused by flutamide, and further addition of dihydrotestosterone antagonized the action of flutamide and significantly decreased KLF9 expression.	Flutamide	163-172	Kruppel like factor 9	Homo sapiens	19-23
34180022-4	2021	We found that AR blockage using flutamide largely attenuated the DHT and INS-induced maternal endocrine, metabolic, and fertility impairments in pregnant rats in association with suppressed induction of uterine AR protein abundance and androgen-regulated response protein and normalized expression of several endometrial receptivity and decidualization genes.	Flutamide	32-41	androgen receptor	Rattus norvegicus	211-213
34422798-6	2021	To determine if androgen-mediated PD-L1 downregulation was AR-dependent, we treated cells with flutamide, a selective AR antagonist, and prior to DHT treatment to pharmacologically inhibit AR-induced signaling.	Flutamide	95-104	androgen receptor	Homo sapiens	118-120
34621174-10	2021	Conversely, BPAF induced RACK1 up-regulation via androgen receptor (AR) activation, as confirmed by treatment with AR antagonist flutamide.	Flutamide	129-138	receptor for activated C kinase 1	Homo sapiens	25-30
34621174-10	2021	Conversely, BPAF induced RACK1 up-regulation via androgen receptor (AR) activation, as confirmed by treatment with AR antagonist flutamide.	Flutamide	129-138	androgen receptor	Homo sapiens	49-66
34621174-10	2021	Conversely, BPAF induced RACK1 up-regulation via androgen receptor (AR) activation, as confirmed by treatment with AR antagonist flutamide.	Flutamide	129-138	androgen receptor	Homo sapiens	68-70
34621174-10	2021	Conversely, BPAF induced RACK1 up-regulation via androgen receptor (AR) activation, as confirmed by treatment with AR antagonist flutamide.	Flutamide	129-138	androgen receptor	Homo sapiens	115-117
34177574-11	2021	The analysis of data from both databases revealed the 95% confidence interval lower limits of ROR for bicalutamide and flutamide to be > 1, and adverse event signals were detected following the use of either drug.	Flutamide	119-128	long intergenic non-protein coding RNA, regulator of reprogramming	Homo sapiens	94-97
34128827-3	2021	Early efforts to augment ADT by adding adrenal-targeting agents (aminoglutethimide, ketoconazole) or AR antagonists (flutamide, bicalutamide, nilutamide, cyproterone) failed to achieve overall survival (OS) benefits, although they did exhibit some evidence of limited clinical activity.	Flutamide	117-126	androgen receptor	Homo sapiens	101-103
34098820-3	2021	In this work, we examined the single-electron reduction of nilutamide, flutamide, its metabolites 2-hydroxyflutamide and 4-nitro-3-trifluorormethyl-phenylamine, and a topical antiandrogen (3-amino-2-hydroxy-2-methyl-N-(4-nitro-3-trifluoromethyl)-phenyl) propanamide by NADPH:cytochrome P-450 reductase and adrenodoxin reductase/adrenodoxin.	Flutamide	71-80	cytochrome p450 oxidoreductase	Mus musculus	269-301
35434067-4	2022	CASE SUMMARY: We present the rare case of a female patient aged 11 years and 9 mo with type A insulin resistance and an INSR heterozygous mutation (c.3614C>T), who was treated with a combination of pioglitazone and flutamide.	Flutamide	215-224	insulin receptor	Homo sapiens	120-124
35599686-10	2022	Moreover, the androgen receptor (AR) antagonist flutamide mimicked the effects of testosterone deficiency on PCSK9 and LDLR indicating the role of AR as a mediator in triggering attenuating liver cholesterol uptake in which testosterone instead of dihydrotestosterone (DHT) is the major functional form of androgen.	Flutamide	48-57	androgen receptor	Homo sapiens	14-31
35599686-10	2022	Moreover, the androgen receptor (AR) antagonist flutamide mimicked the effects of testosterone deficiency on PCSK9 and LDLR indicating the role of AR as a mediator in triggering attenuating liver cholesterol uptake in which testosterone instead of dihydrotestosterone (DHT) is the major functional form of androgen.	Flutamide	48-57	androgen receptor	Homo sapiens	33-35
35599686-10	2022	Moreover, the androgen receptor (AR) antagonist flutamide mimicked the effects of testosterone deficiency on PCSK9 and LDLR indicating the role of AR as a mediator in triggering attenuating liver cholesterol uptake in which testosterone instead of dihydrotestosterone (DHT) is the major functional form of androgen.	Flutamide	48-57	proprotein convertase subtilisin/kexin type 9	Homo sapiens	109-114
35599686-10	2022	Moreover, the androgen receptor (AR) antagonist flutamide mimicked the effects of testosterone deficiency on PCSK9 and LDLR indicating the role of AR as a mediator in triggering attenuating liver cholesterol uptake in which testosterone instead of dihydrotestosterone (DHT) is the major functional form of androgen.	Flutamide	48-57	low density lipoprotein receptor	Homo sapiens	119-123
35599686-10	2022	Moreover, the androgen receptor (AR) antagonist flutamide mimicked the effects of testosterone deficiency on PCSK9 and LDLR indicating the role of AR as a mediator in triggering attenuating liver cholesterol uptake in which testosterone instead of dihydrotestosterone (DHT) is the major functional form of androgen.	Flutamide	48-57	androgen receptor	Homo sapiens	147-149
35066972-6	2022	These effects of Testosterone and DHT were reversed in the presence of the androgen receptor antagonist, flutamide.	Flutamide	105-114	androgen receptor	Homo sapiens	75-92
35353765-10	2022	Administration of the androgen receptor antagonist flutamide (200mg pellets) throughout the eight-week training program blocked the exercise induced protection against muscle pain in both sexes.	Flutamide	51-60	androgen receptor	Mus musculus	22-39
35434067-6	2022	CONCLUSION: Pioglitazone attenuated insulin resistance in this patient with TAIRS, and flutamide ameliorated masculinization.	Flutamide	87-96	insulin	Homo sapiens	36-43
2670515-12	1989	In combination with an LHRH agonist flutamide may become a first-line agent for previously untreated patients with cancer of the prostate.	Flutamide	36-45	gonadotropin releasing hormone 1	Homo sapiens	23-27
35237237-10	2022	Furthermore, the inhibition effect of DHEA on follicle development and ovulation was ameliorated by flutamide, an androgen receptor (AR) antagonist, suggesting the involvement of AR signaling.	Flutamide	100-109	androgen receptor	Homo sapiens	114-131
35237237-10	2022	Furthermore, the inhibition effect of DHEA on follicle development and ovulation was ameliorated by flutamide, an androgen receptor (AR) antagonist, suggesting the involvement of AR signaling.	Flutamide	100-109	androgen receptor	Homo sapiens	133-135
35237237-10	2022	Furthermore, the inhibition effect of DHEA on follicle development and ovulation was ameliorated by flutamide, an androgen receptor (AR) antagonist, suggesting the involvement of AR signaling.	Flutamide	100-109	androgen receptor	Homo sapiens	179-181
2514815-2	1989	That DHT acts through interaction with the androgen receptor is supported by the finding that simultaneous treatment with the antiandrogen Flutamide completely prevents DHT action.	Flutamide	139-148	androgen receptor	Rattus norvegicus	43-60
34995681-6	2022	Finally, testosterone and dihydrotestosterone (DHT) decreased the expression of Ucp1, Pcg1a and Prdm16 in forskolin-stimulated beige adipocytes, an effect that was prevented by the antiandrogen flutamide.	Flutamide	194-203	uncoupling protein 1	Rattus norvegicus	80-84
34995681-6	2022	Finally, testosterone and dihydrotestosterone (DHT) decreased the expression of Ucp1, Pcg1a and Prdm16 in forskolin-stimulated beige adipocytes, an effect that was prevented by the antiandrogen flutamide.	Flutamide	194-203	PR/SET domain 16	Rattus norvegicus	96-102
35097225-0	2022	Nitroreduction of flutamide by Cunninghamella elegans NADPH: Cytochrome P450 reductase.	Flutamide	18-27	cytochrome p450 oxidoreductase	Homo sapiens	54-86
35097225-3	2022	Whole cell assays with the recombinant yeast demonstrated that the reductases converted the anticancer drug flutamide to the nitroreduced metabolite that was also produced from the same substrate when incubated with human NADPH: cytochrome P450 reductase.	Flutamide	108-117	cytochrome p450 oxidoreductase	Homo sapiens	222-254
2788775-6	1989	In comparison the antiandrogens were strong competitors of [3H]R1881 binding to the androgen receptor, the order of decreasing potency, determined from ID50 (mumol/l) values were CPA (0.073) greater than ICI 176344 (0.4) greater than anandron (0.63) greater than hydroxyflutamide (1) greater than flutamide (greater than 100).	Flutamide	270-279	androgen receptor	Homo sapiens	84-101
3283766-14	1988	Considering the excellent tolerance coupled with an objective response observed in 34.5% of the patients, the combination therapy with Flutamide and castration (surgical or LHRH agonist) appears to be the treatment of choice for prostate cancer patients in relapse after standard endocrine therapy.	Flutamide	135-144	gonadotropin releasing hormone 1	Homo sapiens	173-177
2528737-4	1989	The combination of "Zoladex" and flutamide produced an earlier response in tumour markers (TAP, PAP) only.	Flutamide	33-42	regenerating family member 3 alpha	Homo sapiens	96-99
3131115-10	1988	The reduction in uterine estrogen and progesterone receptor levels was also counteracted by the concomitant injection of flutamide, but not by enclomiphene.	Flutamide	121-130	progesterone receptor	Rattus norvegicus	38-59
3397935-5	1988	ODC activity was significantly decreased by flutamide treatment of intact rats, but even at the highest dose used (10 mg/day) only a 39% inhibition was observed.	Flutamide	44-53	ornithine decarboxylase 1	Rattus norvegicus	0-3
3397935-7	1988	In androgen-treated castrated rats, flutamide caused epididymal ODC to fall to undetectable values.	Flutamide	36-45	ornithine decarboxylase 1	Rattus norvegicus	64-67
3397935-8	1988	These results show that: (1) androgens are essential for the maintenance of ODC activity in the epididymis; (2) epididymal ODC activity is maximally stimulated by endogenous androgens, at least in the pubertal rat; (3) the apparent potency of flutamide is substantially lowered by an increase in epididymal androgens.	Flutamide	243-252	ornithine decarboxylase 1	Rattus norvegicus	123-126
3071951-5	1988	Nonsteroid antiandrogens such as anandron and flutamide inhibit the uptake of androgen by the prostate by an action that probably involves the androgen receptor.	Flutamide	46-55	androgen receptor	Homo sapiens	143-160
2476834-0	1989	Effect of 5 alpha-dihydrotestosterone and flutamide on the facilitation of lordosis by LHRH and naloxone in estrogen-primed female rats.	Flutamide	42-51	gonadotropin releasing hormone 1	Rattus norvegicus	87-91
2852689-0	1988	The effect of flutamide on basal and ACTH-stimulated plasma levels of adrenal androgens in patients with advanced prostate cancer.	Flutamide	14-23	proopiomelanocortin	Homo sapiens	37-41
2852689-4	1988	The response of cortisol delta 4-17OHP, delta 5-17OHP, A and DHEA to ACTH, as well as the ACTH-stimulated delta 5-17OHP/delta 4-17OHP, delta 5-17OHP/DHEA, delta 4-17OHP/A and DHEA/A ratios, were unchanged by flutamide treatment.	Flutamide	208-217	proopiomelanocortin	Homo sapiens	90-94
2852689-5	1988	These findings indicate that: a) Short-term flutamide administration enhances testicular steroidogenesis, via augmented LH pulse frequency; b) Adrenal steroidogenesis seems to be not affected by the drug, since ACTH-stimulated plasma levels of adrenal androgens and precursors/products ratios were unchanged.	Flutamide	44-53	proopiomelanocortin	Homo sapiens	211-215
2838689-2	1988	Treatment for 10 days with Flutamide (5 mg/rat, twice daily) caused a marked stimulation of plasma testosterone (T) associated with a significant increase in plasma gonadotropin concentrations and inhibited plasma PRL levels.	Flutamide	27-36	prolactin	Rattus norvegicus	214-217
3285484-12	1988	The largest and best study to date is the Southwest Oncology Group (SWOG) study, which did show a near-significant (P less than 0.065) difference between patients treated for 20 months with a luteinizing hormone-releasing hormone (LH-RH) plus flutamide compared with LH-RH alone.	Flutamide	243-252	gonadotropin releasing hormone 1	Homo sapiens	231-236
3286322-3	1988	Of major significance is the finding that the changes in serum T levels observed during the first 3 weeks of treatment, as well as the complete inhibition of the intratesticular concentration of sex steroids observed at the end of this period of treatment with the LHRH agonist were not affected by simultaneous administration of flutamide (125 mg per os every 8 h).	Flutamide	330-339	gonadotropin releasing hormone 1	Homo sapiens	265-269
2459682-3	1988	Cyproterone acetate (10 mg/day) and flutamide (15 mg/day), when administered to castrated rats receiving a maintenance dose of 5 alpha-dihydrotestosterone proprionate (250 micrograms/day), induce the expression of TRPM-2.	Flutamide	36-45	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	214-220
2459682-4	1988	Northern hybridization and dot blot analysis demonstrate that TRPM-2 steady-state levels reach a maximum on day 4 of treatment with cyproterone acetate (520 ppm) and on day 6 of treatment with flutamide (190 ppm).	Flutamide	193-202	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	62-68
3279409-0	1988	Plasma levels of hydroxy-flutamide in patients with prostatic cancer receiving the combined hormonal therapy: an LHRH agonist and flutamide.	Flutamide	25-34	gonadotropin releasing hormone 1	Homo sapiens	113-117
3227089-0	1988	Nipple development and pup-induced prolactin release in male rats treated prenatally with the antiandrogen flutamide.	Flutamide	107-116	prolactin	Rattus norvegicus	35-44
6323856-1	1983	Flutamide, an anti-androgen known to act through the androgen receptor, abolished the inhibitory action of testosterone on the induction of peroxidase in immature rat uteri without affecting inhibition produced by progesterone.	Flutamide	0-9	androgen receptor	Rattus norvegicus	53-70
3956856-0	1986	Characteristics of interaction of the antiandrogen flutamide with the androgen receptor in various target tissues.	Flutamide	51-60	androgen receptor	Rattus norvegicus	70-87
2990868-8	1985	The inhibitory effects of higher concentrations of 4-OHA on LH receptor expression were potentiated by keoxifene or flutamide.	Flutamide	116-125	luteinizing hormone/choriogonadotropin receptor	Rattus norvegicus	60-71
3964747-0	1985	Effect of a nonsteroidal antiandrogen, flutamide, on androgen receptor dynamics and ornithine decarboxylase gene expression in mouse kidney.	Flutamide	39-48	androgen receptor	Mus musculus	53-70
3964747-0	1985	Effect of a nonsteroidal antiandrogen, flutamide, on androgen receptor dynamics and ornithine decarboxylase gene expression in mouse kidney.	Flutamide	39-48	ornithine decarboxylase, structural 1	Mus musculus	84-107
3964747-1	1985	The mechanisms by which nonsteroidal antiandrogens such as flutamide (alpha, alpha, alpha-trifluoro-2-methyl-4"-nitro-m-propionotoluidide) influence androgen receptor distribution and androgen-regulated gene expression are poorly understood.	Flutamide	59-68	androgen receptor	Mus musculus	149-166
3964747-1	1985	The mechanisms by which nonsteroidal antiandrogens such as flutamide (alpha, alpha, alpha-trifluoro-2-methyl-4"-nitro-m-propionotoluidide) influence androgen receptor distribution and androgen-regulated gene expression are poorly understood.	Flutamide	70-137	androgen receptor	Mus musculus	149-166
3964747-2	1985	Therefore, we studied acute and long-term effects of flutamide, administered alone or in combination with testosterone, on androgen receptor dynamics in mouse kidney.	Flutamide	53-62	androgen receptor	Mus musculus	123-140
3964747-6	1985	When 5 mg flutamide was given concomitantly with a submaximal dose of testosterone (0.1 mg), nuclear androgen receptor concentration was similar to that achieved with flutamide alone; this inhibitory effect of the antiandrogen was reversed by a 10-fold higher dose of testosterone.	Flutamide	10-19	androgen receptor	Mus musculus	101-118
3964747-8	1985	In these animals, flutamide administration decreased nuclear androgen receptor concentration with an initial half-life of about 3.3 h. This half-life was similar to that after cycloheximide administration, but significantly longer than that measured (1.3 h) upon removal of the implant.	Flutamide	18-27	androgen receptor	Mus musculus	61-78
3964747-11	1985	However, flutamide (up to 650 micrograms/day) given concomitantly with testosterone (40 micrograms/day) almost completely abolished the testosterone-induced increase in ODC.	Flutamide	9-18	ornithine decarboxylase, structural 1	Mus musculus	169-172
3964747-12	1985	The changes in ODC-messenger RNA concentration, as measured by hybridization to a complementary DNA probe, paralleled those of the enzyme protein suggesting that flutamide action involves inhibition of transcription of androgen-regulated gene(s).	Flutamide	162-171	ornithine decarboxylase, structural 1	Mus musculus	15-18
3964747-13	1985	We conclude that 1) nuclear androgen receptor turnover in mouse kidney is a relatively rapid process and 2) nonsteroidal antiandrogens such as flutamide have an intrinsic ability to form	Flutamide	143-152	androgen receptor	Mus musculus	28-45
6662517-4	1983	Flutamide, an androgen-receptor blocker, prevented the inhibition of lordosis by testosterone in females, indicating that the interaction of testosterone or a metabolite with an androgen receptor may be an important feature of this inhibition.	Flutamide	0-9	androgen receptor	Rattus norvegicus	178-195
2444770-11	1987	Flutamide, the compound used as reference, is the only compound devoid of any androgenic action and is thus acting as a pure antiandrogen on both ventral prostate weight and prostatic ODC activity.	Flutamide	0-9	ornithine decarboxylase 1	Homo sapiens	184-187
3100871-14	1986	Patients already castrated received only Flutamide while, for those previously treated with DES, the estrogen was replaced by the LHRH agonist [D-Trp6]LHRH ethylamide in association with Flutamide.	Flutamide	187-196	gonadotropin releasing hormone 1	Homo sapiens	130-134
3100871-14	1986	Patients already castrated received only Flutamide while, for those previously treated with DES, the estrogen was replaced by the LHRH agonist [D-Trp6]LHRH ethylamide in association with Flutamide.	Flutamide	187-196	gonadotropin releasing hormone 1	Homo sapiens	151-155
2934579-0	1985	Combination therapy with flutamide and castration (LHRH agonist or orchiectomy) in advanced prostate cancer: a marked improvement in response and survival.	Flutamide	25-34	gonadotropin releasing hormone 1	Homo sapiens	51-55
6422951-4	1984	Flutamide or 9-B-D-arabinofuranosyladenine (Ara-A) proved ineffective per se in reducing tumor growth of the human DU-145 or of the R-3327-G strain, respectively, but increased the efficacy of DFMO against the DU-145 tumor had a high level of ODC which was reduced by DFMO of by Ara-A; the R-3327 tumor had a low level of ODC which was too low to be decreased by DFMO.	Flutamide	0-9	ornithine decarboxylase 1	Homo sapiens	243-246
6422951-4	1984	Flutamide or 9-B-D-arabinofuranosyladenine (Ara-A) proved ineffective per se in reducing tumor growth of the human DU-145 or of the R-3327-G strain, respectively, but increased the efficacy of DFMO against the DU-145 tumor had a high level of ODC which was reduced by DFMO of by Ara-A; the R-3327 tumor had a low level of ODC which was too low to be decreased by DFMO.	Flutamide	0-9	ornithine decarboxylase 1	Homo sapiens	322-325
33722734-8	2021	Flutamide was hydrolyzed by monkey CES2, not by AADAC.	Flutamide	0-9	carboxylesterase 2	Homo sapiens	35-39
7044470-5	1982	Only 0.05% of patients, in whom repeat tests confirmed a positive TPHA but a negative FTA-ABS result, benefited from a TPI test.	Flutamide	86-89	triosephosphate isomerase 1	Homo sapiens	119-122
263325-6	1978	This showed that flutamide increased the t1/2 (from 80 to 108 min) but decreased the distribution volume (from 17.8 to 13.8 liters) and the MCR (from 222 to 130 liters/24 h).	Flutamide	17-26	nuclear receptor subfamily 3 group C member 2	Homo sapiens	140-143
34042216-7	2021	Moreover, the deteriorated renal outcomes in LPS/tacrolimus-treated rats were reduced after castration or androgen receptor blockade by flutamide.	Flutamide	136-145	androgen receptor	Rattus norvegicus	106-123
33011575-4	2021	Twelve of the 18 samples exhibited androgen receptor (AR) antagonistic activities, with AR antagonistic equivalents ranging from 1.2 x 102 mug flutamide/g sludge to 1.8 x 104 mug flutamide/g sludge; however, no AR agonistic activity was detected in any of the tested samples.	Flutamide	143-152	androgen receptor	Homo sapiens	35-52
33382900-8	2021	The effects of DHT on IRF-7, p-NFkappaB p65, and IFN abundance were abolished by flutamide, an anti-androgen.	Flutamide	81-90	interferon regulatory factor 7	Homo sapiens	22-27
33382900-8	2021	The effects of DHT on IRF-7, p-NFkappaB p65, and IFN abundance were abolished by flutamide, an anti-androgen.	Flutamide	81-90	RELA proto-oncogene, NF-kB subunit	Homo sapiens	31-43
33672867-8	2021	Application of flutamide (AR-antagonist) in intact adolescent rats exhibited identical changes to those in orchiectomized rats.	Flutamide	15-24	androgen receptor	Rattus norvegicus	26-28
33355366-8	2021	Finally, the increase in PMCA4 protein levels induced by testosterone was prevented by pre-treatment with the AR antagonist flutamide.	Flutamide	124-133	ATPase, Ca++ transporting, plasma membrane 4	Mus musculus	25-30
33355366-8	2021	Finally, the increase in PMCA4 protein levels induced by testosterone was prevented by pre-treatment with the AR antagonist flutamide.	Flutamide	124-133	androgen receptor	Mus musculus	110-112
33559058-7	2021	These direct effects were blunted by flutamide, an AR antagonist.	Flutamide	37-46	androgen receptor	Homo sapiens	51-53
33613770-8	2021	The in vitro study indicated that testosterone promoted the proliferation of the AR-positive SKOV3 cell line, which could be blocked by flutamide, but not in the AR-negative A2780 cell line.	Flutamide	136-145	androgen receptor	Homo sapiens	81-83
33011575-4	2021	Twelve of the 18 samples exhibited androgen receptor (AR) antagonistic activities, with AR antagonistic equivalents ranging from 1.2 x 102 mug flutamide/g sludge to 1.8 x 104 mug flutamide/g sludge; however, no AR agonistic activity was detected in any of the tested samples.	Flutamide	143-152	androgen receptor	Homo sapiens	88-90
33011575-4	2021	Twelve of the 18 samples exhibited androgen receptor (AR) antagonistic activities, with AR antagonistic equivalents ranging from 1.2 x 102 mug flutamide/g sludge to 1.8 x 104 mug flutamide/g sludge; however, no AR agonistic activity was detected in any of the tested samples.	Flutamide	143-152	androgen receptor	Homo sapiens	88-90
33113443-7	2021	Both FLU and ICI increased DICER1 protein abundance in the luteal tissue.	Flutamide	5-8	dicer 1, ribonuclease III	Sus scrofa	27-33
33393733-3	2021	We evaluated this phenomenon by pretreating neonatal rats on postnatal days (PD) 1, 6, 13, or 20 with flutamide (a nonsteroidal androgen receptor antagonist) at a standard or a high dose (10 or 50 mg/kg) compared to vehicle control.	Flutamide	102-111	androgen receptor	Rattus norvegicus	128-145
32781251-11	2020	DHEA + FLU rats showed a smaller increase in the myometrial thickness, an increase in the uterine water content without AQP8 induction and a smaller decrease in collagen remodeling.	Flutamide	7-10	aquaporin 8	Rattus norvegicus	120-124
32662666-5	2020	It was found that flutamide activated maybe the Atg7-Atg3-Lc3 pathway through the UPR pathway, caused cells excessive autophagy and apoptosis, and inhibited the formation of penile and testicular blood vessels by activating UPR and affecting the messenger RNA level of vascular endothelial growth factor and hypoxia-inducible factor 1.	Flutamide	18-27	autophagy related 7	Mus musculus	48-52
32662666-5	2020	It was found that flutamide activated maybe the Atg7-Atg3-Lc3 pathway through the UPR pathway, caused cells excessive autophagy and apoptosis, and inhibited the formation of penile and testicular blood vessels by activating UPR and affecting the messenger RNA level of vascular endothelial growth factor and hypoxia-inducible factor 1.	Flutamide	18-27	autophagy related 3	Mus musculus	53-57
32662666-5	2020	It was found that flutamide activated maybe the Atg7-Atg3-Lc3 pathway through the UPR pathway, caused cells excessive autophagy and apoptosis, and inhibited the formation of penile and testicular blood vessels by activating UPR and affecting the messenger RNA level of vascular endothelial growth factor and hypoxia-inducible factor 1.	Flutamide	18-27	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	58-61
32916283-4	2020	We showed that conditional inducible H2A.Z deletion blocked memory-enhancing effects of androgen depletion (induced by gonadectomy), and of pharmacological inhibition of the androgen receptor with flutamide.	Flutamide	197-206	H2A.Z variant histone 1	Mus musculus	37-42
32916283-4	2020	We showed that conditional inducible H2A.Z deletion blocked memory-enhancing effects of androgen depletion (induced by gonadectomy), and of pharmacological inhibition of the androgen receptor with flutamide.	Flutamide	197-206	androgen receptor	Mus musculus	174-191
33059492-11	2020	In vitro smooth muscle cell studies revealed that dihydrotestosterone potentiates transforming growth factor beta-induced Erk/Smad activation and MMP-2 activity, which is reversed by flutamide treatment.	Flutamide	183-192	mitogen-activated protein kinase 1	Mus musculus	122-125
33059492-11	2020	In vitro smooth muscle cell studies revealed that dihydrotestosterone potentiates transforming growth factor beta-induced Erk/Smad activation and MMP-2 activity, which is reversed by flutamide treatment.	Flutamide	183-192	matrix metallopeptidase 2	Mus musculus	146-151
33059492-12	2020	Finally, in vivo flutamide treatment reduced aneurysm growth via p-Erk1/2 and p-Smad2 reduction in Fbn1C1039G/+ males.	Flutamide	17-26	mitogen-activated protein kinase 3	Mus musculus	67-73
33059492-12	2020	Finally, in vivo flutamide treatment reduced aneurysm growth via p-Erk1/2 and p-Smad2 reduction in Fbn1C1039G/+ males.	Flutamide	17-26	SMAD family member 2	Mus musculus	80-85
33059492-12	2020	Finally, in vivo flutamide treatment reduced aneurysm growth via p-Erk1/2 and p-Smad2 reduction in Fbn1C1039G/+ males.	Flutamide	17-26	fibrillin 1	Mus musculus	99-103
33059492-15	2020	As biological proof of concept, flutamide treatment attenuated aneurysm growth and p-Erk1/2 and p-Smad2 signaling in Fbn1C1039G/+ males.	Flutamide	32-41	mitogen-activated protein kinase 3	Mus musculus	85-91
33059492-15	2020	As biological proof of concept, flutamide treatment attenuated aneurysm growth and p-Erk1/2 and p-Smad2 signaling in Fbn1C1039G/+ males.	Flutamide	32-41	SMAD family member 2	Mus musculus	98-103
33059492-15	2020	As biological proof of concept, flutamide treatment attenuated aneurysm growth and p-Erk1/2 and p-Smad2 signaling in Fbn1C1039G/+ males.	Flutamide	32-41	fibrillin 1	Mus musculus	117-121
32930727-4	2020	METHODS: Flutamide, an androgen receptor antagonist, was administered to male rats on postnatal days 2, 4, and 6 before 6 h of isoflurane on postnatal day 7 (ntotal = 26).	Flutamide	9-18	androgen receptor	Rattus norvegicus	23-40
32930727-10	2020	Flutamide changed expression patterns of NKCC1 (mean density +- SD: control, 1.49 +- 0.69; flutamide, 0.47 +- 0.11; P < 0.001) and KCC2 (median density [25th percentile, 75th percentile]: control, 0.23 [0.13, 0.49]; flutamide, 1.47 [1.18,1.62]; P < 0.001).	Flutamide	0-9	solute carrier family 12 member 2	Rattus norvegicus	41-46
32930727-10	2020	Flutamide changed expression patterns of NKCC1 (mean density +- SD: control, 1.49 +- 0.69; flutamide, 0.47 +- 0.11; P < 0.001) and KCC2 (median density [25th percentile, 75th percentile]: control, 0.23 [0.13, 0.49]; flutamide, 1.47 [1.18,1.62]; P < 0.001).	Flutamide	0-9	solute carrier family 12 member 5	Rattus norvegicus	131-135
32930727-10	2020	Flutamide changed expression patterns of NKCC1 (mean density +- SD: control, 1.49 +- 0.69; flutamide, 0.47 +- 0.11; P < 0.001) and KCC2 (median density [25th percentile, 75th percentile]: control, 0.23 [0.13, 0.49]; flutamide, 1.47 [1.18,1.62]; P < 0.001).	Flutamide	91-100	solute carrier family 12 member 2	Rattus norvegicus	41-46
32247919-5	2020	Spiggin transcription was strongly inhibited by flutamide under both AS conditions.	Flutamide	48-57	spiggin	Gasterosteus aculeatus	0-7
32738380-6	2020	Administration of the anti-androgen FLU alone significantly upregulated Cyp11a1 and Cyp17a1 gene expression while administration of LIN and DIES alone did not alter significantly gene expression.	Flutamide	36-39	cytochrome P450, family 11, subfamily a, polypeptide 1	Rattus norvegicus	72-79
32738380-6	2020	Administration of the anti-androgen FLU alone significantly upregulated Cyp11a1 and Cyp17a1 gene expression while administration of LIN and DIES alone did not alter significantly gene expression.	Flutamide	36-39	cytochrome P450, family 17, subfamily a, polypeptide 1	Rattus norvegicus	84-91
32738380-8	2020	Deregulation of Cyp17a1 in rat pup testis, following administration of FLU alone or in mixtures to dams, was significantly correlated with the observed feminization endpoints in male pups.	Flutamide	71-74	cytochrome P450, family 17, subfamily a, polypeptide 1	Rattus norvegicus	16-23
32759847-1	2020	First-generation nonsteroidal androgen receptor (AR) antagonists, such as flutamide (2a) and bicalutamide (3), are effective for most prostate cancer patients, but resistance often appears after several years due to the mutation of AR.	Flutamide	74-83	androgen receptor	Homo sapiens	30-47
32759847-1	2020	First-generation nonsteroidal androgen receptor (AR) antagonists, such as flutamide (2a) and bicalutamide (3), are effective for most prostate cancer patients, but resistance often appears after several years due to the mutation of AR.	Flutamide	74-83	androgen receptor	Homo sapiens	49-51
32759847-1	2020	First-generation nonsteroidal androgen receptor (AR) antagonists, such as flutamide (2a) and bicalutamide (3), are effective for most prostate cancer patients, but resistance often appears after several years due to the mutation of AR.	Flutamide	74-83	androgen receptor	Homo sapiens	232-234
32247919-7	2020	In the liver, hypoxia inducible factor 1alpha was induced following exposure to both flutamide and linuron, however this was independent of the level of air saturation.	Flutamide	85-94	hypoxia inducible factor 1 subunit alpha a	Gasterosteus aculeatus	14-45
32645119-8	2020	The effects of testosterone on the contraction of immune cell numbers and activity were blocked by co-administration of the androgen receptor antagonist flutamide and mimicked by treatment with dihydrotestosterone, which was also able to reduce the severity of IAV in female mice.	Flutamide	153-162	androgen receptor	Homo sapiens	124-141
32724436-11	2020	In conclusion, abiraterone combined with flutamide has better curative effect and lower incidence of adverse reactions in patients with metastatic castration-resistant PCa (CRPC) than abiraterone alone, and can increase the expression levels of miR-493-5p and miR-195-5p in patient serum.	Flutamide	41-50	microRNA 195	Homo sapiens	260-267
32450298-8	2020	Furthermore, administration of the AR-antagonist flutamide in intact rats showed similar changes to those in OCX rats, suggesting that androgens affect the excitability of CA1 pyramidal neurons possibly by acting on the AR.	Flutamide	49-58	androgen receptor	Rattus norvegicus	35-37
32450298-8	2020	Furthermore, administration of the AR-antagonist flutamide in intact rats showed similar changes to those in OCX rats, suggesting that androgens affect the excitability of CA1 pyramidal neurons possibly by acting on the AR.	Flutamide	49-58	carbonic anhydrase 1	Rattus norvegicus	172-175
32450298-8	2020	Furthermore, administration of the AR-antagonist flutamide in intact rats showed similar changes to those in OCX rats, suggesting that androgens affect the excitability of CA1 pyramidal neurons possibly by acting on the AR.	Flutamide	49-58	androgen receptor	Rattus norvegicus	220-222
32509382-8	2020	In TNBC/HER2+ cell lines, CPD and EDD protein expression were upregulated by PRL or synthetic androgen methyltrienolone (R1881) at 3-6 h. PRL/R1881-induced CPD in TNBC and HER2+ cells increased intracellular NO production, which was abolished by PRLR antagonist  1-9-G129R-hPRL and AR antagonist flutamide.	Flutamide	296-305	erb-b2 receptor tyrosine kinase 2	Homo sapiens	8-12
32580404-9	2020	Additionally, changes in the expression of PLIN1 and TSPO, involved in the initial step of testosterone synthesis in Leydig cells, suggest that testicular cells represent a target of flutamide action.	Flutamide	183-192	perilipin 1	Rattus norvegicus	43-48
32580404-9	2020	Additionally, changes in the expression of PLIN1 and TSPO, involved in the initial step of testosterone synthesis in Leydig cells, suggest that testicular cells represent a target of flutamide action.	Flutamide	183-192	translocator protein	Rattus norvegicus	53-57
32580404-10	2020	Increase in the gene expression of PLIN1 and TSPO and higher total plasma cholesterol content indicates enhanced availability of cholesterol in Leydig cells as a result of androgen-mediated effects of flutamide.	Flutamide	201-210	perilipin 1	Rattus norvegicus	35-40
32580404-10	2020	Increase in the gene expression of PLIN1 and TSPO and higher total plasma cholesterol content indicates enhanced availability of cholesterol in Leydig cells as a result of androgen-mediated effects of flutamide.	Flutamide	201-210	translocator protein	Rattus norvegicus	45-49
32247620-8	2020	On the other hand, treatment with flutamide ameliorated GIN and megalin expression and functionality.	Flutamide	34-43	LDL receptor related protein 2	Rattus norvegicus	64-71
32387527-13	2020	In the testes of flutamide-treated animals, EpiT reduced AMH, and both T and EpiT replacement diminished AMHR2 mRNA expression also on pnd 14.	Flutamide	17-26	anti-Mullerian hormone	Rattus norvegicus	57-60
32387527-13	2020	In the testes of flutamide-treated animals, EpiT reduced AMH, and both T and EpiT replacement diminished AMHR2 mRNA expression also on pnd 14.	Flutamide	17-26	anti-Mullerian hormone receptor type 2	Rattus norvegicus	105-110
32387527-16	2020	An increase in connexin 43 expression was observed in animals treated with EpiT without flutamide, whereas in rats treated with flutamide, both hormones were ineffective to increase connexin 43 expression reduced by EDS.	Flutamide	88-97	gap junction protein, alpha 1	Rattus norvegicus	15-26
32580404-0	2020	Flutamide Alters the Expression of Chemerin, Apelin, and Vaspin and Their Respective Receptors in the Testes of Adult Rats.	Flutamide	0-9	retinoic acid receptor responder 2	Rattus norvegicus	35-43
32580404-0	2020	Flutamide Alters the Expression of Chemerin, Apelin, and Vaspin and Their Respective Receptors in the Testes of Adult Rats.	Flutamide	0-9	apelin	Rattus norvegicus	45-51
32580404-0	2020	Flutamide Alters the Expression of Chemerin, Apelin, and Vaspin and Their Respective Receptors in the Testes of Adult Rats.	Flutamide	0-9	serpin family A member 12	Rattus norvegicus	57-63
32580404-2	2020	Here, we studied the impact of short-term exposure to flutamide (an anti-androgen that blocks androgen receptors) on the expression of chemerin, apelin, vaspin and their receptors (CCRL2, CMKLR1, GPR1, APLNR, GRP78, respectively) in adult rat testes.	Flutamide	54-63	retinoic acid receptor responder 2	Rattus norvegicus	135-143
32580404-2	2020	Here, we studied the impact of short-term exposure to flutamide (an anti-androgen that blocks androgen receptors) on the expression of chemerin, apelin, vaspin and their receptors (CCRL2, CMKLR1, GPR1, APLNR, GRP78, respectively) in adult rat testes.	Flutamide	54-63	apelin	Rattus norvegicus	145-151
32580404-2	2020	Here, we studied the impact of short-term exposure to flutamide (an anti-androgen that blocks androgen receptors) on the expression of chemerin, apelin, vaspin and their receptors (CCRL2, CMKLR1, GPR1, APLNR, GRP78, respectively) in adult rat testes.	Flutamide	54-63	serpin family A member 12	Rattus norvegicus	153-159
32580404-2	2020	Here, we studied the impact of short-term exposure to flutamide (an anti-androgen that blocks androgen receptors) on the expression of chemerin, apelin, vaspin and their receptors (CCRL2, CMKLR1, GPR1, APLNR, GRP78, respectively) in adult rat testes.	Flutamide	54-63	C-C motif chemokine receptor like 2	Rattus norvegicus	181-186
32580404-2	2020	Here, we studied the impact of short-term exposure to flutamide (an anti-androgen that blocks androgen receptors) on the expression of chemerin, apelin, vaspin and their receptors (CCRL2, CMKLR1, GPR1, APLNR, GRP78, respectively) in adult rat testes.	Flutamide	54-63	apelin receptor	Rattus norvegicus	202-207
32580404-2	2020	Here, we studied the impact of short-term exposure to flutamide (an anti-androgen that blocks androgen receptors) on the expression of chemerin, apelin, vaspin and their receptors (CCRL2, CMKLR1, GPR1, APLNR, GRP78, respectively) in adult rat testes.	Flutamide	54-63	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	209-214
32580404-6	2020	The androgen-mediated effects observed post-flutamide treatment were found at the gonadal level as chemerin, apelin, and vaspin gene expression alterations at mRNA and protein levels were detected, whereas the cellular targets for these adipokines were recognised by localisation of respective receptors in testicular cells.	Flutamide	44-53	retinoic acid receptor responder 2	Rattus norvegicus	99-107
32580404-6	2020	The androgen-mediated effects observed post-flutamide treatment were found at the gonadal level as chemerin, apelin, and vaspin gene expression alterations at mRNA and protein levels were detected, whereas the cellular targets for these adipokines were recognised by localisation of respective receptors in testicular cells.	Flutamide	44-53	apelin	Rattus norvegicus	109-115
32580404-6	2020	The androgen-mediated effects observed post-flutamide treatment were found at the gonadal level as chemerin, apelin, and vaspin gene expression alterations at mRNA and protein levels were detected, whereas the cellular targets for these adipokines were recognised by localisation of respective receptors in testicular cells.	Flutamide	44-53	serpin family A member 12	Rattus norvegicus	121-127
32328699-5	2020	In addition, a role of androgen receptor (AR) in RACK1 transcription was also demonstrated by the ability of flutamide, a nonsteroidal antiandrogen, to completely prevent diethylstilbestrol-induced RACK1 transcriptional activity and protein expression.	Flutamide	109-118	androgen receptor	Homo sapiens	23-40
32328699-5	2020	In addition, a role of androgen receptor (AR) in RACK1 transcription was also demonstrated by the ability of flutamide, a nonsteroidal antiandrogen, to completely prevent diethylstilbestrol-induced RACK1 transcriptional activity and protein expression.	Flutamide	109-118	androgen receptor	Homo sapiens	42-44
32328699-5	2020	In addition, a role of androgen receptor (AR) in RACK1 transcription was also demonstrated by the ability of flutamide, a nonsteroidal antiandrogen, to completely prevent diethylstilbestrol-induced RACK1 transcriptional activity and protein expression.	Flutamide	109-118	receptor for activated C kinase 1	Homo sapiens	49-54
32328699-5	2020	In addition, a role of androgen receptor (AR) in RACK1 transcription was also demonstrated by the ability of flutamide, a nonsteroidal antiandrogen, to completely prevent diethylstilbestrol-induced RACK1 transcriptional activity and protein expression.	Flutamide	109-118	receptor for activated C kinase 1	Homo sapiens	198-203
32509382-8	2020	In TNBC/HER2+ cell lines, CPD and EDD protein expression were upregulated by PRL or synthetic androgen methyltrienolone (R1881) at 3-6 h. PRL/R1881-induced CPD in TNBC and HER2+ cells increased intracellular NO production, which was abolished by PRLR antagonist  1-9-G129R-hPRL and AR antagonist flutamide.	Flutamide	296-305	carboxypeptidase D	Homo sapiens	26-29
32509382-8	2020	In TNBC/HER2+ cell lines, CPD and EDD protein expression were upregulated by PRL or synthetic androgen methyltrienolone (R1881) at 3-6 h. PRL/R1881-induced CPD in TNBC and HER2+ cells increased intracellular NO production, which was abolished by PRLR antagonist  1-9-G129R-hPRL and AR antagonist flutamide.	Flutamide	296-305	ubiquitin protein ligase E3 component n-recognin 5	Homo sapiens	34-37
32509382-8	2020	In TNBC/HER2+ cell lines, CPD and EDD protein expression were upregulated by PRL or synthetic androgen methyltrienolone (R1881) at 3-6 h. PRL/R1881-induced CPD in TNBC and HER2+ cells increased intracellular NO production, which was abolished by PRLR antagonist  1-9-G129R-hPRL and AR antagonist flutamide.	Flutamide	296-305	prolactin	Homo sapiens	77-80
32509382-8	2020	In TNBC/HER2+ cell lines, CPD and EDD protein expression were upregulated by PRL or synthetic androgen methyltrienolone (R1881) at 3-6 h. PRL/R1881-induced CPD in TNBC and HER2+ cells increased intracellular NO production, which was abolished by PRLR antagonist  1-9-G129R-hPRL and AR antagonist flutamide.	Flutamide	296-305	prolactin	Homo sapiens	138-141
32509382-8	2020	In TNBC/HER2+ cell lines, CPD and EDD protein expression were upregulated by PRL or synthetic androgen methyltrienolone (R1881) at 3-6 h. PRL/R1881-induced CPD in TNBC and HER2+ cells increased intracellular NO production, which was abolished by PRLR antagonist  1-9-G129R-hPRL and AR antagonist flutamide.	Flutamide	296-305	carboxypeptidase D	Homo sapiens	156-159
31693854-10	2020	Caspase-3/7 activity was significantly increased by both flutamide and bicalutamide.	Flutamide	57-66	caspase 3	Homo sapiens	0-9
32256674-3	2020	So the main purpose of this study was using AR antagonist flutamide to demonstrate AR"s effect on training-induced muscle hypertrophy and its possible mechanism: IGF-1/IGF-1R- PI3K/Akt- mTOR pathway?	Flutamide	58-67	insulin like growth factor 1	Homo sapiens	162-167
32256674-3	2020	So the main purpose of this study was using AR antagonist flutamide to demonstrate AR"s effect on training-induced muscle hypertrophy and its possible mechanism: IGF-1/IGF-1R- PI3K/Akt- mTOR pathway?	Flutamide	58-67	insulin like growth factor 1 receptor	Homo sapiens	168-174
32256674-3	2020	So the main purpose of this study was using AR antagonist flutamide to demonstrate AR"s effect on training-induced muscle hypertrophy and its possible mechanism: IGF-1/IGF-1R- PI3K/Akt- mTOR pathway?	Flutamide	58-67	AKT serine/threonine kinase 1	Homo sapiens	181-184
32256674-3	2020	So the main purpose of this study was using AR antagonist flutamide to demonstrate AR"s effect on training-induced muscle hypertrophy and its possible mechanism: IGF-1/IGF-1R- PI3K/Akt- mTOR pathway?	Flutamide	58-67	mechanistic target of rapamycin kinase	Homo sapiens	186-190
32256674-5	2020	Flutamide was used to block AR in rats.	Flutamide	0-9	androgen receptor	Rattus norvegicus	28-30
32256674-10	2020	Results: (1) The training-induced rise in the relative muscle mass and the expression levels of AR were only found in the gastrocnemius of R rats and in the soleus of E rats (selective muscle hypertrophy), which were blocked by flutamide.	Flutamide	228-237	androgen receptor	Rattus norvegicus	96-98
32256674-12	2020	(3) The levels of IGF-1, IGF-1R and mTOR as well as the activities of PI3K and Akt were enhanced selectively (in the gastrocnemius of R rats and in the soleus of E rats), which were reduced by flutamide.	Flutamide	193-202	AKT serine/threonine kinase 1	Rattus norvegicus	79-82
32299422-3	2020	METHODS: Peripubertal (5-week-old) Wistar rats received injections of flutamide (50 mg/kg bw) daily for 7 days to reduce androgen receptor (AR) signaling or a single injection of ethanedimethane sulphonate (EDS; 75 mg/kg bw) to reduce testosterone production.	Flutamide	70-79	androgen receptor	Rattus norvegicus	121-138
32299422-3	2020	METHODS: Peripubertal (5-week-old) Wistar rats received injections of flutamide (50 mg/kg bw) daily for 7 days to reduce androgen receptor (AR) signaling or a single injection of ethanedimethane sulphonate (EDS; 75 mg/kg bw) to reduce testosterone production.	Flutamide	70-79	androgen receptor	Rattus norvegicus	140-142
32299422-8	2020	In contrast, DLL1, JAG1 and HES5 expressions increased in seminiferous epithelium of both flutamide and EDS-treated rats (p < 0.05, p < 0.01, p < 0.001).	Flutamide	90-99	delta like canonical Notch ligand 1	Rattus norvegicus	13-17
32299422-8	2020	In contrast, DLL1, JAG1 and HES5 expressions increased in seminiferous epithelium of both flutamide and EDS-treated rats (p < 0.05, p < 0.01, p < 0.001).	Flutamide	90-99	jagged canonical Notch ligand 1	Rattus norvegicus	19-23
32299422-8	2020	In contrast, DLL1, JAG1 and HES5 expressions increased in seminiferous epithelium of both flutamide and EDS-treated rats (p < 0.05, p < 0.01, p < 0.001).	Flutamide	90-99	hes family bHLH transcription factor 5	Rattus norvegicus	28-32
31875599-5	2020	FTA-NaOH-based polymerase chain reaction (PCR) yielded the best detection rate for both COI gene and p104 gene.	Flutamide	0-3	coI	Theileria parva	88-91
31564004-7	2020	The 3- (80.8% vs. 35.3%; p &lt; 0.001) and 6-month (73.1% vs. 31.4%; p &lt; 0.001) prostate-specific antigen response rates were higher in the enzalutamide than in the flutamide group.	Flutamide	168-177	kallikrein related peptidase 3	Homo sapiens	83-108
31948482-12	2020	Treatment with the androgen receptor antagonist flutamide reduced blood pressure and vascular hypertrophy in castrated Ang II-infused mice injected with 6beta-OHT.	Flutamide	48-57	androgen receptor	Mus musculus	19-36
31948482-12	2020	Treatment with the androgen receptor antagonist flutamide reduced blood pressure and vascular hypertrophy in castrated Ang II-infused mice injected with 6beta-OHT.	Flutamide	48-57	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	119-125
31676390-6	2020	The simultaneous treatment with testosterone and the androgen receptor antagonist, Flutamide, reduced these effects.	Flutamide	83-92	androgen receptor	Mus musculus	53-70
31861570-3	2019	TP and FLU decreased plasma AMH and FSH concentration.	Flutamide	7-10	muellerian-inhibiting factor	Sus scrofa	28-31
31861570-6	2019	In small antral follicles, OP upregulated ACVR1 and BMPR1A expression, while FLU increased BMPR1A mRNA.	Flutamide	77-80	BMPR1A	Sus scrofa	91-97
31861570-7	2019	FLU and ICI resulted in upregulation of AMHR2 expression.	Flutamide	0-3	anti-Mullerian hormone receptor type 2	Sus scrofa	40-45
31861570-8	2019	TP and FLU upregulated AMH expression, while it was downregulated in response to OP or ICI.	Flutamide	7-10	muellerian-inhibiting factor	Sus scrofa	23-26
31861570-9	2019	Moreover, OP and ICI resulted in downregulation of FSHR expression, while FLU decreased FSHR protein abundance.	Flutamide	74-77	follicle stimulating hormone receptor	Sus scrofa	88-92
31861570-5	2019	FLU upregulated AMHR2 expression, while OP increased FSHR mRNA.	Flutamide	0-3	anti-Mullerian hormone receptor type 2	Sus scrofa	16-21