PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
21045201-9	2011	Combining the results of these four enzyme phenotyping approaches, we demonstrated that CYP4F2 and possibly other enzymes of the CYP4F subfamily (e.g., CYP4F3B) are the major enzymes responsible for the omega-hydroxylation of fingolimod, the main elimination pathway of the drug in vivo.	Fingolimod Hydrochloride	226-236	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	88-94
21710707-12	2011	Fingolimod acts on sphingosine 1-phosphate receptors-1 (S1P1).	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Homo sapiens	19-60
20413685-9	2010	Using S1P receptor specific agonists and antagonists, we determined that fingolimod-induced effects on remyelination and astrogliosis were mediated primarily through S1P3 and S1P5, whereas enhanced microgliosis was mediated through S1P1 and S1P5.	Fingolimod Hydrochloride	73-83	sphingosine-1-phosphate receptor 3	Homo sapiens	166-170
20804717-9	2011	The method was applied to confirm FTY720 as the inhibitor of S1PL with an IC50 value of 52.4muM.	Fingolimod Hydrochloride	34-40	sphingosine-1-phosphate lyase 1	Homo sapiens	61-65
20570726-2	2010	We demonstrate here that FTY720 (Fingolimod) and (S)-FTY720 vinylphosphonate are novel inhibitors of SK1 catalytic activity and induce the proteasomal degradation of this enzyme in human pulmonary artery smooth muscle cells, MCF-7 breast cancer cells and androgen-independent LNCaP-AI prostate cancer cells.	Fingolimod Hydrochloride	25-31	sphingosine kinase 1	Homo sapiens	101-104
20570726-2	2010	We demonstrate here that FTY720 (Fingolimod) and (S)-FTY720 vinylphosphonate are novel inhibitors of SK1 catalytic activity and induce the proteasomal degradation of this enzyme in human pulmonary artery smooth muscle cells, MCF-7 breast cancer cells and androgen-independent LNCaP-AI prostate cancer cells.	Fingolimod Hydrochloride	33-43	sphingosine kinase 1	Homo sapiens	101-104
20403428-7	2010	The biological significance of 14-3-3 phosphorylation was demonstrated with a non-phosphorylatable 14-3-3zeta mutant which retarded apoptosis induced by sphingosine and FTY720.	Fingolimod Hydrochloride	169-175	tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein zeta	Homo sapiens	99-109
20506484-8	2010	In conclusion, our results suggest that FTY720 induces a significant increase of PTEN, which inhibits p-Akt and MDM2, and then increases the level of p53, thereby inducing G1 phase arrest and apoptosis.	Fingolimod Hydrochloride	40-46	phosphatase and tensin homolog	Mus musculus	81-85
20506484-8	2010	In conclusion, our results suggest that FTY720 induces a significant increase of PTEN, which inhibits p-Akt and MDM2, and then increases the level of p53, thereby inducing G1 phase arrest and apoptosis.	Fingolimod Hydrochloride	40-46	thymoma viral proto-oncogene 1	Mus musculus	104-107
20506484-8	2010	In conclusion, our results suggest that FTY720 induces a significant increase of PTEN, which inhibits p-Akt and MDM2, and then increases the level of p53, thereby inducing G1 phase arrest and apoptosis.	Fingolimod Hydrochloride	40-46	transformed mouse 3T3 cell double minute 2	Mus musculus	112-116
20506484-8	2010	In conclusion, our results suggest that FTY720 induces a significant increase of PTEN, which inhibits p-Akt and MDM2, and then increases the level of p53, thereby inducing G1 phase arrest and apoptosis.	Fingolimod Hydrochloride	40-46	transformation related protein 53, pseudogene	Mus musculus	150-153
21130737-6	2011	Both Desipramine and FTY720 treatment reduced ASMase without significant inhibition of other lysosomal hydrolases but most hydrolases showed increased secretion (up to a 50% increase) providing more evidence of lysosomal disruption by these drugs.	Fingolimod Hydrochloride	21-27	sphingomyelin phosphodiesterase 1	Homo sapiens	46-52
21280082-6	2011	Neuroprotection was accompanied by decreased inflammation, as fingolimod-treated mice had fewer activated neutrophils, microglia/macrophages, and intercellular adhesion molecule-1 (ICAM-1)-positive blood vessels.	Fingolimod Hydrochloride	62-72	intercellular adhesion molecule 1	Mus musculus	146-179
21280082-6	2011	Neuroprotection was accompanied by decreased inflammation, as fingolimod-treated mice had fewer activated neutrophils, microglia/macrophages, and intercellular adhesion molecule-1 (ICAM-1)-positive blood vessels.	Fingolimod Hydrochloride	62-72	intercellular adhesion molecule 1	Mus musculus	181-187
21280082-10	2011	Fingolimod did not protect primary neurons against glutamate excitotoxicity or hydrogen peroxide, but decreased ICAM-1 expression in brain endothelial cells stimulated by tumor necrosis factor alpha.	Fingolimod Hydrochloride	0-10	intercellular adhesion molecule 1	Mus musculus	112-118
21280082-10	2011	Fingolimod did not protect primary neurons against glutamate excitotoxicity or hydrogen peroxide, but decreased ICAM-1 expression in brain endothelial cells stimulated by tumor necrosis factor alpha.	Fingolimod Hydrochloride	0-10	tumor necrosis factor	Mus musculus	171-198
20826007-2	2011	The S1P agonist FTY720 decreased ERK phosphorylation and induced myosin light chain (MLC) II phosphorylation only in macrophages and DCs.	Fingolimod Hydrochloride	16-22	modulator of VRAC current 1	Homo sapiens	65-83
20826007-2	2011	The S1P agonist FTY720 decreased ERK phosphorylation and induced myosin light chain (MLC) II phosphorylation only in macrophages and DCs.	Fingolimod Hydrochloride	16-22	modulator of VRAC current 1	Homo sapiens	85-88
20959468-5	2010	In prostate cancer cell lines, FTY720 acted as a sphingosine kinase 1 (SphK1) inhibitor that induced prostate cancer cell apoptosis in a manner independent of sphingosine-1-phosphate receptors.	Fingolimod Hydrochloride	31-37	sphingosine kinase 1	Mus musculus	49-69
20959468-5	2010	In prostate cancer cell lines, FTY720 acted as a sphingosine kinase 1 (SphK1) inhibitor that induced prostate cancer cell apoptosis in a manner independent of sphingosine-1-phosphate receptors.	Fingolimod Hydrochloride	31-37	sphingosine kinase 1	Mus musculus	71-76
20610734-2	2010	Phosphorylation of FTY720 by sphingosine kinase 2 (SphK2) yields the active metabolite FTY720-phosphate (FTY-P), which induces lymphopenia through agonism of the sphingosine 1-phosphate receptor S1P(1) on endothelial cells and lymphocytes.	Fingolimod Hydrochloride	19-25	sphingosine kinase 2	Homo sapiens	29-49
20610734-2	2010	Phosphorylation of FTY720 by sphingosine kinase 2 (SphK2) yields the active metabolite FTY720-phosphate (FTY-P), which induces lymphopenia through agonism of the sphingosine 1-phosphate receptor S1P(1) on endothelial cells and lymphocytes.	Fingolimod Hydrochloride	19-25	sphingosine kinase 2	Homo sapiens	51-56
20600904-8	2010	Therefore, FTY720-induced apoptosis is initiated by the release of cytochrome c from mitochondria, resulting in the activation of caspases in rat thymocytes.	Fingolimod Hydrochloride	11-17	caspase 6	Rattus norvegicus	130-138
20413685-9	2010	Using S1P receptor specific agonists and antagonists, we determined that fingolimod-induced effects on remyelination and astrogliosis were mediated primarily through S1P3 and S1P5, whereas enhanced microgliosis was mediated through S1P1 and S1P5.	Fingolimod Hydrochloride	73-83	sphingosine-1-phosphate receptor 5	Homo sapiens	175-179
20413685-9	2010	Using S1P receptor specific agonists and antagonists, we determined that fingolimod-induced effects on remyelination and astrogliosis were mediated primarily through S1P3 and S1P5, whereas enhanced microgliosis was mediated through S1P1 and S1P5.	Fingolimod Hydrochloride	73-83	sphingosine-1-phosphate receptor 1	Homo sapiens	232-236
20413685-9	2010	Using S1P receptor specific agonists and antagonists, we determined that fingolimod-induced effects on remyelination and astrogliosis were mediated primarily through S1P3 and S1P5, whereas enhanced microgliosis was mediated through S1P1 and S1P5.	Fingolimod Hydrochloride	73-83	sphingosine-1-phosphate receptor 5	Homo sapiens	241-245
20497959-2	2010	Fingolimod (FTY720), the S1P receptor modulator, inhibits lymphocyte egress from SLO and decreases circulating lymphocytes; however, it also induces a significant decrease in the number of peripheral blood lymphocytes in alymphoplasia (aly/aly) mice lacking SLO.	Fingolimod Hydrochloride	0-10	Aly/REF export factor	Mus musculus	221-224
20460491-9	2010	Furthermore, concentrations of FTY720 that induced cytotoxicity led to decreased phospho-Akt in primary MCL cells and cell lines.	Fingolimod Hydrochloride	31-37	AKT serine/threonine kinase 1	Homo sapiens	89-92
20497959-2	2010	Fingolimod (FTY720), the S1P receptor modulator, inhibits lymphocyte egress from SLO and decreases circulating lymphocytes; however, it also induces a significant decrease in the number of peripheral blood lymphocytes in alymphoplasia (aly/aly) mice lacking SLO.	Fingolimod Hydrochloride	0-10	Aly/REF export factor	Mus musculus	236-239
20497959-2	2010	Fingolimod (FTY720), the S1P receptor modulator, inhibits lymphocyte egress from SLO and decreases circulating lymphocytes; however, it also induces a significant decrease in the number of peripheral blood lymphocytes in alymphoplasia (aly/aly) mice lacking SLO.	Fingolimod Hydrochloride	12-18	Aly/REF export factor	Mus musculus	221-224
20497959-2	2010	Fingolimod (FTY720), the S1P receptor modulator, inhibits lymphocyte egress from SLO and decreases circulating lymphocytes; however, it also induces a significant decrease in the number of peripheral blood lymphocytes in alymphoplasia (aly/aly) mice lacking SLO.	Fingolimod Hydrochloride	12-18	Aly/REF export factor	Mus musculus	236-239
20497959-3	2010	In this study, we demonstrated that the administration of FTY720 induced sequestration of mature lymphocytes, particularly T cells, into the bone marrow (BM) in aly/aly mice, implying that the reduction of circulating lymphocytes in these mice by FTY720 was due to inhibition of lymphocyte egress from the BM.	Fingolimod Hydrochloride	58-64	Aly/REF export factor	Mus musculus	161-164
20497959-3	2010	In this study, we demonstrated that the administration of FTY720 induced sequestration of mature lymphocytes, particularly T cells, into the bone marrow (BM) in aly/aly mice, implying that the reduction of circulating lymphocytes in these mice by FTY720 was due to inhibition of lymphocyte egress from the BM.	Fingolimod Hydrochloride	58-64	Aly/REF export factor	Mus musculus	165-168
20056921-7	2010	Instead, FTY720 stimulated the production of 27-hydroxycholesterol, an endogenous ligand of the liver X receptor, leading to liver X receptor-induced upregulation of ABCA1.	Fingolimod Hydrochloride	9-15	ATP binding cassette subfamily A member 1	Homo sapiens	166-171
21063113-6	2010	Within 48 hours exposure to FTY720 (10 muM) significantly increased annexin V-binding, decreased forward scatter and increased cytosolic Ca(2+) concentration but did not significantly modify ceramide formation.	Fingolimod Hydrochloride	28-34	latexin	Homo sapiens	39-42
20032465-8	2010	The PKC activator phorbol 12-myristate 13-acetate partially rescued FTY720-induced down-regulation of the S1P(1) receptor, linking PKC activation with S1P(1) receptor surface expression.	Fingolimod Hydrochloride	68-74	protein kinase C, gamma	Rattus norvegicus	4-7
20032465-8	2010	The PKC activator phorbol 12-myristate 13-acetate partially rescued FTY720-induced down-regulation of the S1P(1) receptor, linking PKC activation with S1P(1) receptor surface expression.	Fingolimod Hydrochloride	68-74	sphingosine-1-phosphate receptor 1	Rattus norvegicus	106-112
20032465-8	2010	The PKC activator phorbol 12-myristate 13-acetate partially rescued FTY720-induced down-regulation of the S1P(1) receptor, linking PKC activation with S1P(1) receptor surface expression.	Fingolimod Hydrochloride	68-74	protein kinase C, gamma	Rattus norvegicus	131-134
20032465-8	2010	The PKC activator phorbol 12-myristate 13-acetate partially rescued FTY720-induced down-regulation of the S1P(1) receptor, linking PKC activation with S1P(1) receptor surface expression.	Fingolimod Hydrochloride	68-74	sphingosine-1-phosphate receptor 1	Rattus norvegicus	151-157
19965812-4	2010	METHODS: Concurrent to VEGFR blockade in mice, S1P signaling augmentation was achieved via treatment with the S1P precursor sphingosine, S1P agonist FTY720, or S1P receptor-1 (S1PR1) agonist SEW2871.	Fingolimod Hydrochloride	149-155	sphingosine-1-phosphate receptor 1	Mus musculus	47-50
19119142-6	2009	In vitro kinetic studies revealed that FTY720 is a competitive inhibitor of ceramide synthase 2 toward dihydrosphingosine with an apparent K(i) of 2.15 microm.	Fingolimod Hydrochloride	39-45	ceramide synthase 2	Homo sapiens	76-95
19328962-2	2009	We showed that clinically relevant concentrations of FTY720 inhibited TNF-alpha-induced SMC proliferation and extracellular signal-regulated kinase (ERK) phosphorylation.	Fingolimod Hydrochloride	53-59	tumor necrosis factor	Homo sapiens	70-79
19328962-2	2009	We showed that clinically relevant concentrations of FTY720 inhibited TNF-alpha-induced SMC proliferation and extracellular signal-regulated kinase (ERK) phosphorylation.	Fingolimod Hydrochloride	53-59	mitogen-activated protein kinase 1	Homo sapiens	110-147
19328962-2	2009	We showed that clinically relevant concentrations of FTY720 inhibited TNF-alpha-induced SMC proliferation and extracellular signal-regulated kinase (ERK) phosphorylation.	Fingolimod Hydrochloride	53-59	mitogen-activated protein kinase 1	Homo sapiens	149-152
19814729-4	2009	The S1P mimetic FTY720-phosphate causes internalization and degradation of cell membrane-expressed S1P1, thereby antagonizing S1P action at the receptor.	Fingolimod Hydrochloride	16-22	sphingosine-1-phosphate receptor 1	Homo sapiens	99-103
19490468-0	2009	Expression of sphingosine kinase 2 in synovial fibroblasts of rheumatoid arthritis contributing to apoptosis by a sphingosine analogue, FTY720.	Fingolimod Hydrochloride	136-142	sphingosine kinase 2	Homo sapiens	14-34
19490468-6	2009	A sphingosine analogue, FTY720, which is activated by phosphorylation specifically by SPHK2, mediated apoptotic signaling of the cultured synovial fibroblasts.	Fingolimod Hydrochloride	24-30	sphingosine kinase 2	Homo sapiens	86-91
18638568-5	2008	We believe that the seminal event was the linking of the investigational drug, FTY720 (fingolimod), to S1P signaling.	Fingolimod Hydrochloride	79-85	membrane bound transcription factor peptidase, site 1	Homo sapiens	103-106
19118083-0	2009	Ketoconazole increases fingolimod blood levels in a drug interaction via CYP4F2 inhibition.	Fingolimod Hydrochloride	23-33	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	73-79
19118083-1	2009	The sphingosine-1-phosphate receptor modulator fingolimod is predominantly hydroxylated by cytochrome CYP4F2.	Fingolimod Hydrochloride	47-57	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	102-108
19118083-2	2009	In vitro experiments showed that ketoconazole significantly inhibited the oxidative metabolism of fingolimod by human liver microsomes and by recombinant CYP4F2.	Fingolimod Hydrochloride	98-108	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	154-160
18772343-9	2008	Fingolimod rescued human OLGs from serum and glucose deprivation-induced apoptosis, which was reversed with suramin co-treatment and mimicked using an S1P5 agonist.	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 5	Homo sapiens	151-155
18772343-10	2008	High doses of fingolimod induced an initial down-regulation of S1P5 mRNA levels relative to control (4 hours), subsequent up-regulation (2 days), and recurrent down-regulation (8 days).	Fingolimod Hydrochloride	14-24	sphingosine-1-phosphate receptor 5	Homo sapiens	63-67
18638568-5	2008	We believe that the seminal event was the linking of the investigational drug, FTY720 (fingolimod), to S1P signaling.	Fingolimod Hydrochloride	87-97	membrane bound transcription factor peptidase, site 1	Homo sapiens	103-106
18365684-1	2008	FTY720 is a derivative of ISP-1 (myriocin), a fungal metabolite of the Chinese herb Iscaria sinclarii, with agonistic effect for sphingosine-1-phosphate receptor.	Fingolimod Hydrochloride	0-6	protease, serine 28	Mus musculus	26-31
18507656-5	2008	RESULTS: Fingolimod administration alone yielded a heart rate nadir of 51 +/- 5 beats min(-1) at a median 4 h postdose with heart rate remaining depressed at 51-64 beats min(-1) over the rest of the day.	Fingolimod Hydrochloride	9-19	CD59 molecule (CD59 blood group)	Homo sapiens	86-92
18507656-6	2008	Concurrent administration of fingolimod and atropine yielded a nadir of 66 +/- 6 beats min(-1) resulting in an atropine: placebo ratio (90% confidence interval) of 1.30 (1.22, 1.36).	Fingolimod Hydrochloride	29-39	CD59 molecule (CD59 blood group)	Homo sapiens	87-93
18507656-7	2008	When atropine was administered at the time of the nadir, it was able to reverse the negative chronotropic effect of fingolimod from a heart rate of 56 +/- 9 beats min(-1) (placebo) to 64 +/- 8 beats min(-1) (atropine) resulting in an atropine: placebo ratio of 1.15 (1.04, 1.26).	Fingolimod Hydrochloride	116-126	CD59 molecule (CD59 blood group)	Homo sapiens	163-169
18507656-7	2008	When atropine was administered at the time of the nadir, it was able to reverse the negative chronotropic effect of fingolimod from a heart rate of 56 +/- 9 beats min(-1) (placebo) to 64 +/- 8 beats min(-1) (atropine) resulting in an atropine: placebo ratio of 1.15 (1.04, 1.26).	Fingolimod Hydrochloride	116-126	CD59 molecule (CD59 blood group)	Homo sapiens	199-205
18213449-5	2008	Remarkably, drugs such as forskolin, 1,9-dideoxy-forskolin and FTY720 which lead to PP2A activation effectively antagonize leukemogenesis in both in vitro and in vivo models of these cancers.	Fingolimod Hydrochloride	63-69	protein phosphatase 2 phosphatase activator	Homo sapiens	84-88
18494940-3	2008	Recently it was also shown that FTY720 can reduce prostaglandin synthesis through the direct inhibition of the cytosolic phospholipase A2 (cPLA2).	Fingolimod Hydrochloride	32-38	phospholipase A2 group IVA	Rattus norvegicus	111-137
18494940-3	2008	Recently it was also shown that FTY720 can reduce prostaglandin synthesis through the direct inhibition of the cytosolic phospholipase A2 (cPLA2).	Fingolimod Hydrochloride	32-38	phospholipase A2 group IVA	Rattus norvegicus	139-144
18281497-0	2008	FTY720 induces apoptosis in hepatocellular carcinoma cells through activation of protein kinase C delta signaling.	Fingolimod Hydrochloride	0-6	protein kinase C delta	Homo sapiens	81-103
18281497-7	2008	Equally important, pharmacologic inhibition or shRNA-mediated knockdown of PKC delta protected FTY720-treated Huh7 cells from caspase-3 activation.	Fingolimod Hydrochloride	95-101	protein kinase C delta	Homo sapiens	75-84
18281497-7	2008	Equally important, pharmacologic inhibition or shRNA-mediated knockdown of PKC delta protected FTY720-treated Huh7 cells from caspase-3 activation.	Fingolimod Hydrochloride	95-101	MIR7-3 host gene	Homo sapiens	110-114
18281497-7	2008	Equally important, pharmacologic inhibition or shRNA-mediated knockdown of PKC delta protected FTY720-treated Huh7 cells from caspase-3 activation.	Fingolimod Hydrochloride	95-101	caspase 3	Homo sapiens	126-135
18281497-10	2008	Blockade of ROS production by an NADPH oxidase inhibitor protected Huh7 cells from FTY720-induced PKC delta activation and caspase-3-dependent apoptosis.	Fingolimod Hydrochloride	83-89	MIR7-3 host gene	Homo sapiens	67-71
18281497-10	2008	Blockade of ROS production by an NADPH oxidase inhibitor protected Huh7 cells from FTY720-induced PKC delta activation and caspase-3-dependent apoptosis.	Fingolimod Hydrochloride	83-89	protein kinase C delta	Homo sapiens	98-107
18281497-10	2008	Blockade of ROS production by an NADPH oxidase inhibitor protected Huh7 cells from FTY720-induced PKC delta activation and caspase-3-dependent apoptosis.	Fingolimod Hydrochloride	83-89	caspase 3	Homo sapiens	123-132
18474015-4	2008	The sphingosine analogue, FTY720 (fingolimod), a high affinity agonist of sphingosine-1-phosphate type-1 receptor (S1P-1), acts primarily by sequestering lymphocytes within peripheral lymphoid organs rendering them incapable of migrating to the sites of inflammation.	Fingolimod Hydrochloride	26-32	sphingosine-1-phosphate receptor 1	Homo sapiens	74-113
18474015-4	2008	The sphingosine analogue, FTY720 (fingolimod), a high affinity agonist of sphingosine-1-phosphate type-1 receptor (S1P-1), acts primarily by sequestering lymphocytes within peripheral lymphoid organs rendering them incapable of migrating to the sites of inflammation.	Fingolimod Hydrochloride	26-32	sphingosine-1-phosphate receptor 1	Homo sapiens	115-120
18474015-4	2008	The sphingosine analogue, FTY720 (fingolimod), a high affinity agonist of sphingosine-1-phosphate type-1 receptor (S1P-1), acts primarily by sequestering lymphocytes within peripheral lymphoid organs rendering them incapable of migrating to the sites of inflammation.	Fingolimod Hydrochloride	34-44	sphingosine-1-phosphate receptor 1	Homo sapiens	74-113
18474015-4	2008	The sphingosine analogue, FTY720 (fingolimod), a high affinity agonist of sphingosine-1-phosphate type-1 receptor (S1P-1), acts primarily by sequestering lymphocytes within peripheral lymphoid organs rendering them incapable of migrating to the sites of inflammation.	Fingolimod Hydrochloride	34-44	sphingosine-1-phosphate receptor 1	Homo sapiens	115-120
17717597-3	2007	We assessed the therapeutic potential of the PP2A activator FTY720 (2-amino-2-[2-(4-octylphenyl)ethyl]-1,3-propanediol hydrochloride), an immunomodulator in Phase III trials for patients with multiple sclerosis or undergoing organ transplantation, in CML-BC and Ph1 ALL patient cells and in in vitro and in vivo models of these BCR/ABL+ leukemias.	Fingolimod Hydrochloride	68-132	protein phosphatase 2 phosphatase activator	Homo sapiens	45-49
17716652-13	2007	In conclusion, FTY720 is an effective compound in the treatment of collagen-induced arthritic rats and in reducing CD4(+) T cells in collagen-induced arthritic rats.	Fingolimod Hydrochloride	15-21	Cd4 molecule	Rattus norvegicus	115-118
17726159-2	2007	In vivo phosphorylation of FTY720 generates an agonist for G protein-coupled receptors for sphingosine-1-phosphate, a lipid mediator that plays a crucial role in the stimulation of OLG survival by neurotrophin-3 (NT-3).	Fingolimod Hydrochloride	27-33	neurotrophin 3	Homo sapiens	197-211
17726159-5	2007	Treatment of these cells with FTY720 causes activation of extracellular signal-regulated kinase 1/2 and Akt, accompanied by protection from apoptosis.	Fingolimod Hydrochloride	30-36	AKT serine/threonine kinase 1	Homo sapiens	58-107
17761943-0	2007	Sphingosine-1-phosphate analogue FTY720 causes lymphocyte redistribution and hypercholesterolemia in ApoE-deficient mice.	Fingolimod Hydrochloride	33-39	apolipoprotein E	Mus musculus	101-105
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	Fingolimod Hydrochloride	23-29	BCR activator of RhoGEF and GTPase	Homo sapiens	126-138
17717597-3	2007	We assessed the therapeutic potential of the PP2A activator FTY720 (2-amino-2-[2-(4-octylphenyl)ethyl]-1,3-propanediol hydrochloride), an immunomodulator in Phase III trials for patients with multiple sclerosis or undergoing organ transplantation, in CML-BC and Ph1 ALL patient cells and in in vitro and in vivo models of these BCR/ABL+ leukemias.	Fingolimod Hydrochloride	68-132	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	262-265
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	Fingolimod Hydrochloride	23-29	CD34 molecule	Homo sapiens	183-187
17242282-0	2007	FTY720, a synthetic sphingosine 1 phosphate analogue, inhibits development of atherosclerosis in low-density lipoprotein receptor-deficient mice.	Fingolimod Hydrochloride	0-6	low density lipoprotein receptor	Mus musculus	97-129
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	Fingolimod Hydrochloride	23-29	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	194-197
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	Fingolimod Hydrochloride	23-29	CD34 molecule	Homo sapiens	202-206
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	Fingolimod Hydrochloride	23-29	CD19 molecule	Homo sapiens	208-212
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	Fingolimod Hydrochloride	23-29	CD34 molecule	Homo sapiens	202-206
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	Fingolimod Hydrochloride	23-29	CD34 molecule	Homo sapiens	202-206
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	Fingolimod Hydrochloride	23-29	CD19 molecule	Homo sapiens	261-265
17595677-6	2007	Treatment of mice with blocking antibody to CD62L reduced appearance of cells in mesenteric lymph nodes; treatment with FTY720, a sphingosine 1-phosphate receptor agonist that blocks egress of T cells from lymph nodes, reduced appearance of cells in spleen.	Fingolimod Hydrochloride	120-126	selectin, lymphocyte	Mus musculus	44-49
17008548-0	2007	The immunosuppressant drug FTY720 inhibits cytosolic phospholipase A2 independently of sphingosine-1-phosphate receptors.	Fingolimod Hydrochloride	27-33	phospholipase A2 group IVA	Homo sapiens	43-69
17008548-7	2007	Remarkably, however, FTY720 drastically inhibited recombinant cPLA2alpha activity, whereas FTY720-phosphate, sphingosine, or S1P had no effect.	Fingolimod Hydrochloride	21-27	phospholipase A2 group IVA	Homo sapiens	62-72
17008548-8	2007	This study has uncovered a unique action of FTY720 as an inhibitor of cPLA2alpha and hence on production of all eicosanoids.	Fingolimod Hydrochloride	44-50	phospholipase A2 group IVA	Homo sapiens	70-80
17912702-0	2007	Dimethylsphingosine and FTY720 inhibit the SK1 form but activate the SK2 form of sphingosine kinase from rat heart.	Fingolimod Hydrochloride	24-30	sphingosine kinase 1	Rattus norvegicus	43-46
17200201-0	2007	Immunomodulator FTY720 induces myofibroblast differentiation via the lysophospholipid receptor S1P3 and Smad3 signaling.	Fingolimod Hydrochloride	16-22	sphingosine-1-phosphate receptor 3	Mus musculus	95-99
17200201-0	2007	Immunomodulator FTY720 induces myofibroblast differentiation via the lysophospholipid receptor S1P3 and Smad3 signaling.	Fingolimod Hydrochloride	16-22	SMAD family member 3	Mus musculus	104-109
17352219-8	2007	The molecular analysis revealed that FTY720-induced apoptosis was mediated by a Fas-independent, Bcl-associated signal transduction pathway, and that inhibition of extracellular signal-regulated kinase (ERK) activity was involved in its underlying mechanism of action.	Fingolimod Hydrochloride	37-43	mitogen-activated protein kinase 1	Homo sapiens	164-201
17352219-8	2007	The molecular analysis revealed that FTY720-induced apoptosis was mediated by a Fas-independent, Bcl-associated signal transduction pathway, and that inhibition of extracellular signal-regulated kinase (ERK) activity was involved in its underlying mechanism of action.	Fingolimod Hydrochloride	37-43	mitogen-activated protein kinase 1	Homo sapiens	203-206
17912702-0	2007	Dimethylsphingosine and FTY720 inhibit the SK1 form but activate the SK2 form of sphingosine kinase from rat heart.	Fingolimod Hydrochloride	24-30	potassium calcium-activated channel subfamily N member 2	Rattus norvegicus	69-72
16549044-10	2006	Thus, it is presumed that FTY720-induced lymphocyte sequestration is due to the inhibition of S1P/S1P1-dependent lymphocyte egress from secondary lymphoid tissues and thymus by its active metabolite (S)-FTY720-P.	Fingolimod Hydrochloride	26-32	sphingosine-1-phosphate receptor 1	Homo sapiens	98-102
16571654-4	2006	We now report that both FTY720 and sphingosine interact with CB1 but not CB2 cannabinoid receptors.	Fingolimod Hydrochloride	24-30	cannabinoid receptor 1 (brain)	Mus musculus	61-64
16571654-8	2006	FTY720 and sphingosine also inhibited activation of extracellular signal-regulated kinases 1 and 2 and Akt by WIN55,212-2 in intact Chinese hamster ovary (CHO) cells expressing CB1 receptors and attenuated WIN55,212-2-stimulated internalization of a fluorescence-tagged CB1 receptor in CHO cells.	Fingolimod Hydrochloride	0-6	cannabinoid receptor 1 (brain)	Mus musculus	177-180
16571654-8	2006	FTY720 and sphingosine also inhibited activation of extracellular signal-regulated kinases 1 and 2 and Akt by WIN55,212-2 in intact Chinese hamster ovary (CHO) cells expressing CB1 receptors and attenuated WIN55,212-2-stimulated internalization of a fluorescence-tagged CB1 receptor in CHO cells.	Fingolimod Hydrochloride	0-6	cannabinoid receptor 1 (brain)	Mus musculus	270-273
16571654-9	2006	Moreover, both FTY720 and sphingosine produced rightward shifts in the concentration-effect curves of cannabinoid agonists for G-protein activation, indicating that they act as competitive CB1 antagonists.	Fingolimod Hydrochloride	15-21	cannabinoid receptor 1 (brain)	Mus musculus	189-192
16403835-5	2006	FTY-720, a non-receptor-selective sphingosine analog, was given intraperitoneally to C57BL/6 mice, and animals were subjected to ischemia for 32 min followed by reperfusion for 24 h. Plasma creatinine, blood count, myeloperoxidase (MPO) activity, and renal histology were determined.	Fingolimod Hydrochloride	0-7	myeloperoxidase	Mus musculus	215-230
16403835-5	2006	FTY-720, a non-receptor-selective sphingosine analog, was given intraperitoneally to C57BL/6 mice, and animals were subjected to ischemia for 32 min followed by reperfusion for 24 h. Plasma creatinine, blood count, myeloperoxidase (MPO) activity, and renal histology were determined.	Fingolimod Hydrochloride	0-7	myeloperoxidase	Mus musculus	232-235
16403835-8	2006	MPO, leukocyte infiltration, vascular permeability, and peripheral blood lymphocyte counts were markedly decreased with FTY-720 treatment.	Fingolimod Hydrochloride	120-127	myeloperoxidase	Mus musculus	0-3
16403835-9	2006	The protective effect of FTY-720 was reversed with VPC-44116, a selective S1P1 receptor antagonist.	Fingolimod Hydrochloride	25-32	sphingosine-1-phosphate receptor 1	Mus musculus	74-78
16393960-4	2006	We showed that sphingosine 1-phosphate receptor-1 agonist FTY720 induces relocation of circulating memory CD4 T cells into secondary lymphoid organs.	Fingolimod Hydrochloride	58-64	sphingosine-1-phosphate receptor 1	Homo sapiens	15-49
16393960-4	2006	We showed that sphingosine 1-phosphate receptor-1 agonist FTY720 induces relocation of circulating memory CD4 T cells into secondary lymphoid organs.	Fingolimod Hydrochloride	58-64	CD4 molecule	Homo sapiens	106-109
16365393-1	2006	FTY720 is a high-affinity agonist at the sphingosine 1-phosphate receptor 1 that prevents lymphocyte egress from lymphoid tissue and prolongs allograft survival in several animal models of solid organ transplantation.	Fingolimod Hydrochloride	0-6	sphingosine-1-phosphate receptor 1	Homo sapiens	41-75
16093248-2	2005	The prototypical therapeutic agent, 2-alkyl-2-amino-1,3-propanediol (FTY720), stimulates S1P signaling pathways only after it is phosphorylated by one or more unknown kinases.	Fingolimod Hydrochloride	69-75	sphingosine-1-phosphate receptor 1	Mus musculus	89-92
16426494-6	2005	Similar therapeutic effect by FTY720 was obtained in myelin oligodendrocyte glycoprotein-induced EAE in C57BL/6 mice.	Fingolimod Hydrochloride	30-36	myelin oligodendrocyte glycoprotein	Mus musculus	53-88
16093248-5	2005	Although FTY720 was selectively activated in vivo by SPHK2, other S1P pro-drugs can be phosphorylated to cause lymphopenia through the action of additional sphingosine kinases.	Fingolimod Hydrochloride	9-15	sphingosine kinase 2	Mus musculus	53-58
16386642-1	2005	Phosphorylated FTY720 is an analog of Sphingosine 1 Phosphate (S1P) with immunosuppressive activity that negatively regulates the expression of S1P-Receptor 1.	Fingolimod Hydrochloride	15-21	sphingosine-1-phosphate receptor 1	Mus musculus	144-158
16118221-3	2005	Evidence suggests that FTY720-phosphate-induced activation of S1P1 is responsible for its mechanism of action.	Fingolimod Hydrochloride	23-29	sphingosine-1-phosphate receptor 1	Mus musculus	62-66
15814275-9	2005	Preoperative FTY 720 administration significantly decreased the number of CD4 positive cells and the percentage of interleukin 2 receptor (IL-2 R) positive cells infiltrating both spleen and allograft at the dose of 3 mg/kg/day or 5 mg/kg/day.	Fingolimod Hydrochloride	13-20	CD4 molecule	Homo sapiens	74-77
15802614-0	2005	Immunomodulator FTY720 Induces eNOS-dependent arterial vasodilatation via the lysophospholipid receptor S1P3.	Fingolimod Hydrochloride	16-22	sphingosine-1-phosphate receptor 3	Mus musculus	104-108
15814275-9	2005	Preoperative FTY 720 administration significantly decreased the number of CD4 positive cells and the percentage of interleukin 2 receptor (IL-2 R) positive cells infiltrating both spleen and allograft at the dose of 3 mg/kg/day or 5 mg/kg/day.	Fingolimod Hydrochloride	13-20	interleukin 2 receptor subunit alpha	Homo sapiens	115-137
15814275-9	2005	Preoperative FTY 720 administration significantly decreased the number of CD4 positive cells and the percentage of interleukin 2 receptor (IL-2 R) positive cells infiltrating both spleen and allograft at the dose of 3 mg/kg/day or 5 mg/kg/day.	Fingolimod Hydrochloride	13-20	interleukin 2 receptor subunit alpha	Homo sapiens	139-145
15458436-0	2004	Selective lymphocyte inhibition by FTY720 slows the progressive course of chronic anti-thy 1 glomerulosclerosis.	Fingolimod Hydrochloride	35-41	Thy-1 cell surface antigen	Rattus norvegicus	87-92
15297371-5	2004	FTY720 selectively induced cell apoptosis in hepatoma cell lines with overexpression of cleaved caspase-3 and caspase-9, but the same phenomena were not found in MIHA cells.	Fingolimod Hydrochloride	0-6	caspase 9	Homo sapiens	110-119
15297371-6	2004	FTY720 induced Akt dephosphorylation at Ser473 mediated by phosphoinositide 3-kinase (PI3-K) inhibition.	Fingolimod Hydrochloride	0-6	AKT serine/threonine kinase 1	Homo sapiens	15-18
15297371-6	2004	FTY720 induced Akt dephosphorylation at Ser473 mediated by phosphoinositide 3-kinase (PI3-K) inhibition.	Fingolimod Hydrochloride	0-6	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	59-84
15297371-10	2004	In conclusion, FTY720 is a novel anticancer agent that induces apoptosis of hepatoma cell lines both in vitro and in vivo through PI3-K-mediated Akt dephosphorylation in a p53-independent manner.	Fingolimod Hydrochloride	15-21	AKT serine/threonine kinase 1	Homo sapiens	145-148
15297371-10	2004	In conclusion, FTY720 is a novel anticancer agent that induces apoptosis of hepatoma cell lines both in vitro and in vivo through PI3-K-mediated Akt dephosphorylation in a p53-independent manner.	Fingolimod Hydrochloride	15-21	tumor protein p53	Homo sapiens	172-175
15458436-2	2004	To define the role of lymphocytes in this process, the novel lymphocyte-specific inhibitor FTY720 was administered to rats with anti-thy 1-induced chronic progressive glomerulosclerosis.	Fingolimod Hydrochloride	91-97	Thy-1 cell surface antigen	Rattus norvegicus	133-138
11857403-0	2002	Anticarcinogenic effect of FTY720 in human prostate carcinoma DU145 cells: modulation of mitogenic signaling, FAK, cell-cycle entry and apoptosis.	Fingolimod Hydrochloride	27-33	protein tyrosine kinase 2	Homo sapiens	110-113
14596938-5	2003	FTY720 inhibited phosphorylation of sphingosine catalyzed by SphK2 to a greater extent than it inhibits SphK1.	Fingolimod Hydrochloride	0-6	sphingosine kinase 2	Homo sapiens	61-66
14634137-0	2003	Inhibition of Th1- and Th2-mediated airway inflammation by the sphingosine 1-phosphate receptor agonist FTY720.	Fingolimod Hydrochloride	104-110	negative elongation factor complex member C/D, Th1l	Mus musculus	14-17
14634137-0	2003	Inhibition of Th1- and Th2-mediated airway inflammation by the sphingosine 1-phosphate receptor agonist FTY720.	Fingolimod Hydrochloride	104-110	heart and neural crest derivatives expressed 2	Mus musculus	23-26
14634137-6	2003	Similarly, FTY720 suppressed the Th2 cell-induced bronchoalveolar lavage fluid eosinophilia and the infiltration of T lymphocytes and eosinophils into the bronchial tissue.	Fingolimod Hydrochloride	11-17	heart and neural crest derivatives expressed 2	Mus musculus	33-36
14634137-8	2003	The inhibitory effect of FTY720 on airway inflammation, induction of bronchial hyperresponsiveness, and goblet cell hyperplasia could be confirmed in an actively Ag-sensitized murine asthma model, clearly indicating that Th2 cell-driven allergic diseases such as asthma could benefit from such treatment.	Fingolimod Hydrochloride	25-31	heart and neural crest derivatives expressed 2	Mus musculus	221-224
13129923-6	2003	Further SPHK superfamily members, namely ceramide kinase and a "SPHK-like" protein, failed to phosphorylate sphingosine and FTY720.	Fingolimod Hydrochloride	124-130	sphingosine kinase 1	Homo sapiens	8-12
12711631-17	2003	OA partially inhibited FTY720-induced caspase-3 activation.	Fingolimod Hydrochloride	23-29	caspase 3	Homo sapiens	38-47
12711631-22	2003	Overall, the results suggest that FTY720 activated PP2A or PP2A-like phosphatase and dephosphorylated Akt pathway factors resulting in the enhancement of apoptosis via mitochondria.	Fingolimod Hydrochloride	34-40	protein phosphatase 2 phosphatase activator	Homo sapiens	51-55
12711631-22	2003	Overall, the results suggest that FTY720 activated PP2A or PP2A-like phosphatase and dephosphorylated Akt pathway factors resulting in the enhancement of apoptosis via mitochondria.	Fingolimod Hydrochloride	34-40	protein phosphatase 2 phosphatase activator	Homo sapiens	59-63
12711631-22	2003	Overall, the results suggest that FTY720 activated PP2A or PP2A-like phosphatase and dephosphorylated Akt pathway factors resulting in the enhancement of apoptosis via mitochondria.	Fingolimod Hydrochloride	34-40	AKT serine/threonine kinase 1	Homo sapiens	102-105
11857403-3	2002	We previously reported that FTY720, a metabolite from Isaria sinclarii, is a unique antitumor agent for an androgen-independent prostate cancer cell line and requires caspase-3 activation in apoptosis.	Fingolimod Hydrochloride	28-34	caspase 3	Homo sapiens	167-176
11429058-4	2001	Moreover, FTY720 activates protein phosphatase (PP) 2A and affects anti-apoptotic intracellular signal transduction proteins to attenuate the anti-apoptotic effect.	Fingolimod Hydrochloride	10-16	protein phosphatase 2 phosphatase activator	Homo sapiens	27-54
11429058-7	2001	Simultaneously, retinoblastoma protein (pRB) was dephosphorylated, suggesting that dephosphorylation of pRB was related to FTY720-induced G0 / G1 cell cycle arrest.	Fingolimod Hydrochloride	123-129	RB transcriptional corepressor 1	Homo sapiens	40-43
11429058-7	2001	Simultaneously, retinoblastoma protein (pRB) was dephosphorylated, suggesting that dephosphorylation of pRB was related to FTY720-induced G0 / G1 cell cycle arrest.	Fingolimod Hydrochloride	123-129	RB transcriptional corepressor 1	Homo sapiens	104-107
10344723-2	1999	In this study we investigated whether FTY720 was able to induce apoptosis in an androgen-independent prostate cancer cell line, DU145, which is not only resistant to androgen-withdrawal-induced apoptosis but also Fas- and TNF-alpha-mediated apoptosis.	Fingolimod Hydrochloride	38-44	tumor necrosis factor	Homo sapiens	222-231
10975841-0	2000	Immunosuppressant FTY720 induces apoptosis by direct induction of permeability transition and release of cytochrome c from mitochondria.	Fingolimod Hydrochloride	18-24	cytochrome c, somatic	Homo sapiens	105-117
11181042-4	2001	Among the caspase family proteases, mainly caspase-6 was activated during the apoptosis by FTY720 but not etoposide.	Fingolimod Hydrochloride	91-97	caspase 6	Homo sapiens	10-17
11181042-4	2001	Among the caspase family proteases, mainly caspase-6 was activated during the apoptosis by FTY720 but not etoposide.	Fingolimod Hydrochloride	91-97	caspase 6	Homo sapiens	43-52
11181042-5	2001	In addition, FTY720 caused tyrosine dephosphorylation of FAK and did not activate a FAK-PI3-kinase survival pathway.	Fingolimod Hydrochloride	13-19	protein tyrosine kinase 2	Homo sapiens	57-60
11181042-7	2001	We assumed that FTY720 induced FAK dephosphorylation and cut off the FAK-PI3-kinase pathway resulting in the induction of apoptosis via caspase-6 activation in these glioma cells.	Fingolimod Hydrochloride	16-22	protein tyrosine kinase 2	Homo sapiens	31-34
11181042-7	2001	We assumed that FTY720 induced FAK dephosphorylation and cut off the FAK-PI3-kinase pathway resulting in the induction of apoptosis via caspase-6 activation in these glioma cells.	Fingolimod Hydrochloride	16-22	protein tyrosine kinase 2	Homo sapiens	69-72
11181042-7	2001	We assumed that FTY720 induced FAK dephosphorylation and cut off the FAK-PI3-kinase pathway resulting in the induction of apoptosis via caspase-6 activation in these glioma cells.	Fingolimod Hydrochloride	16-22	caspase 6	Homo sapiens	136-145
10344723-8	1999	Furthermore, FTY720-induced apoptosis was prevented by caspase-3 inhibitor.	Fingolimod Hydrochloride	13-19	caspase 3	Homo sapiens	55-64
34958115-4	2022	Previously, we have reported that the combination of epidermal growth factor receptor/HER2 inhibitor lapatinib and sphingosine analog fingolimod (FTY720) confers a significant cytostatic effect in lung cancer cells.	Fingolimod Hydrochloride	134-144	epidermal growth factor receptor	Homo sapiens	53-85
33971218-8	2021	Moreover, we observed that the immunomodulatory drug fingolimod attenuated LID without lessening the therapeutic efficacy of L-dopa and normalized p75NTR levels.	Fingolimod Hydrochloride	53-63	nerve growth factor receptor	Rattus norvegicus	147-153
34958115-4	2022	Previously, we have reported that the combination of epidermal growth factor receptor/HER2 inhibitor lapatinib and sphingosine analog fingolimod (FTY720) confers a significant cytostatic effect in lung cancer cells.	Fingolimod Hydrochloride	134-144	erb-b2 receptor tyrosine kinase 2	Homo sapiens	86-90
34958115-4	2022	Previously, we have reported that the combination of epidermal growth factor receptor/HER2 inhibitor lapatinib and sphingosine analog fingolimod (FTY720) confers a significant cytostatic effect in lung cancer cells.	Fingolimod Hydrochloride	146-152	epidermal growth factor receptor	Homo sapiens	53-85
34958115-4	2022	Previously, we have reported that the combination of epidermal growth factor receptor/HER2 inhibitor lapatinib and sphingosine analog fingolimod (FTY720) confers a significant cytostatic effect in lung cancer cells.	Fingolimod Hydrochloride	146-152	erb-b2 receptor tyrosine kinase 2	Homo sapiens	86-90
34774547-8	2022	Furthermore, the latter were enhanced by shRNA-PAK1 interference and mitigated by the PAK1 agonist FTY720.	Fingolimod Hydrochloride	99-105	p21 (RAC1) activated kinase 1	Rattus norvegicus	86-90
34949130-7	2022	This ranged from 18% for teriflunomide (aHR: 0.82; 95% CI: 0.67-1.00) to 44% for fingolimod (aHR: 0.56; 95% CI: 0.36-0.87).	Fingolimod Hydrochloride	81-91	aryl hydrocarbon receptor	Homo sapiens	93-96
34288557-6	2021	RESULTS: Overexpression of ORMDL3 enhanced IL-4, TNF-alpha, and MCP-1 expression after FcepsilonRI cross-linking, whereas the sphingosine-1-phosphate (S1P) agonist FTY720 suppressed this enhancement.	Fingolimod Hydrochloride	164-170	tumor necrosis factor	Rattus norvegicus	49-58
34288557-6	2021	RESULTS: Overexpression of ORMDL3 enhanced IL-4, TNF-alpha, and MCP-1 expression after FcepsilonRI cross-linking, whereas the sphingosine-1-phosphate (S1P) agonist FTY720 suppressed this enhancement.	Fingolimod Hydrochloride	164-170	C-C motif chemokine ligand 2	Rattus norvegicus	64-69
34549307-9	2021	Suppression of SPHK1 by small interfering RNA or FTY-720 significantly reversed the antiapoptotic effect.	Fingolimod Hydrochloride	49-56	sphingosine kinase 1	Homo sapiens	15-20
34603029-1	2021	This study aimed to investigate the interactions between fingolimod, a sphingosine 1-phosphate receptor (S1PR) agonist, and melanocortin receptors 1 and 5 (MCR1, MCR5).	Fingolimod Hydrochloride	57-67	sphingosine-1-phosphate receptor 1	Mus musculus	105-109
34638286-5	2021	We show that FTY720 and Acriflavine exhibit therapeutic activity in several different settings of HIF-2alpha inhibitor resistance.	Fingolimod Hydrochloride	13-19	endothelial PAS domain protein 1	Homo sapiens	98-108
34559972-1	2022	Fingolimod (FTY720) inhibits Ca2+-permeable, Mg2+-sensitive channels called transient receptor potential melastatin 7 (TRPM7), but its effects on Ca2+ paradox (CP)-induced myocardial damage have not been evaluated.	Fingolimod Hydrochloride	0-10	transient receptor potential cation channel, subfamily M, member 7	Rattus norvegicus	76-117
34559972-1	2022	Fingolimod (FTY720) inhibits Ca2+-permeable, Mg2+-sensitive channels called transient receptor potential melastatin 7 (TRPM7), but its effects on Ca2+ paradox (CP)-induced myocardial damage have not been evaluated.	Fingolimod Hydrochloride	0-10	transient receptor potential cation channel, subfamily M, member 7	Rattus norvegicus	119-124
34559972-1	2022	Fingolimod (FTY720) inhibits Ca2+-permeable, Mg2+-sensitive channels called transient receptor potential melastatin 7 (TRPM7), but its effects on Ca2+ paradox (CP)-induced myocardial damage have not been evaluated.	Fingolimod Hydrochloride	12-18	transient receptor potential cation channel, subfamily M, member 7	Rattus norvegicus	76-117
34559972-1	2022	Fingolimod (FTY720) inhibits Ca2+-permeable, Mg2+-sensitive channels called transient receptor potential melastatin 7 (TRPM7), but its effects on Ca2+ paradox (CP)-induced myocardial damage have not been evaluated.	Fingolimod Hydrochloride	12-18	transient receptor potential cation channel, subfamily M, member 7	Rattus norvegicus	119-124
34603029-7	2021	Diabetic animals treated with fingolimod showed a decrease of retinal vascular endothelial growth factor A (VEGFA) and vascular endothelial growth factor receptors 1 and 2 (VEGFR1 and VEGFR2), compared to diabetic control group.	Fingolimod Hydrochloride	30-40	vascular endothelial growth factor A	Mus musculus	70-106
34603029-7	2021	Diabetic animals treated with fingolimod showed a decrease of retinal vascular endothelial growth factor A (VEGFA) and vascular endothelial growth factor receptors 1 and 2 (VEGFR1 and VEGFR2), compared to diabetic control group.	Fingolimod Hydrochloride	30-40	vascular endothelial growth factor A	Mus musculus	108-113
34437865-6	2021	Moreover, p38 and AKT inhibitor significantly suppressed the NET formation by FTY720, whereas ERK inhibitor had no effect, suggesting that FTY720-induced NETs depended on the activation of p38 and AKT.	Fingolimod Hydrochloride	78-84	mitogen-activated protein kinase 14	Homo sapiens	10-13
34437865-6	2021	Moreover, p38 and AKT inhibitor significantly suppressed the NET formation by FTY720, whereas ERK inhibitor had no effect, suggesting that FTY720-induced NETs depended on the activation of p38 and AKT.	Fingolimod Hydrochloride	78-84	AKT serine/threonine kinase 1	Homo sapiens	18-21
34437865-6	2021	Moreover, p38 and AKT inhibitor significantly suppressed the NET formation by FTY720, whereas ERK inhibitor had no effect, suggesting that FTY720-induced NETs depended on the activation of p38 and AKT.	Fingolimod Hydrochloride	78-84	mitogen-activated protein kinase 14	Homo sapiens	189-192
34437865-6	2021	Moreover, p38 and AKT inhibitor significantly suppressed the NET formation by FTY720, whereas ERK inhibitor had no effect, suggesting that FTY720-induced NETs depended on the activation of p38 and AKT.	Fingolimod Hydrochloride	78-84	AKT serine/threonine kinase 1	Homo sapiens	197-200
34437865-6	2021	Moreover, p38 and AKT inhibitor significantly suppressed the NET formation by FTY720, whereas ERK inhibitor had no effect, suggesting that FTY720-induced NETs depended on the activation of p38 and AKT.	Fingolimod Hydrochloride	139-145	mitogen-activated protein kinase 14	Homo sapiens	10-13
34437865-6	2021	Moreover, p38 and AKT inhibitor significantly suppressed the NET formation by FTY720, whereas ERK inhibitor had no effect, suggesting that FTY720-induced NETs depended on the activation of p38 and AKT.	Fingolimod Hydrochloride	139-145	AKT serine/threonine kinase 1	Homo sapiens	18-21
34437865-6	2021	Moreover, p38 and AKT inhibitor significantly suppressed the NET formation by FTY720, whereas ERK inhibitor had no effect, suggesting that FTY720-induced NETs depended on the activation of p38 and AKT.	Fingolimod Hydrochloride	139-145	mitogen-activated protein kinase 14	Homo sapiens	189-192
34437865-6	2021	Moreover, p38 and AKT inhibitor significantly suppressed the NET formation by FTY720, whereas ERK inhibitor had no effect, suggesting that FTY720-induced NETs depended on the activation of p38 and AKT.	Fingolimod Hydrochloride	139-145	AKT serine/threonine kinase 1	Homo sapiens	197-200
34768523-4	2021	In this study, we hypothesized that high relative AURKA expression could predict sensitivity to FTY720-induced apoptosis in colorectal cancer (CRC).	Fingolimod Hydrochloride	96-102	aurora kinase A	Homo sapiens	50-55
34603029-7	2021	Diabetic animals treated with fingolimod showed a decrease of retinal vascular endothelial growth factor A (VEGFA) and vascular endothelial growth factor receptors 1 and 2 (VEGFR1 and VEGFR2), compared to diabetic control group.	Fingolimod Hydrochloride	30-40	FMS-like tyrosine kinase 1	Mus musculus	119-171
34603029-7	2021	Diabetic animals treated with fingolimod showed a decrease of retinal vascular endothelial growth factor A (VEGFA) and vascular endothelial growth factor receptors 1 and 2 (VEGFR1 and VEGFR2), compared to diabetic control group.	Fingolimod Hydrochloride	30-40	FMS-like tyrosine kinase 1	Mus musculus	173-179
34603029-7	2021	Diabetic animals treated with fingolimod showed a decrease of retinal vascular endothelial growth factor A (VEGFA) and vascular endothelial growth factor receptors 1 and 2 (VEGFR1 and VEGFR2), compared to diabetic control group.	Fingolimod Hydrochloride	30-40	kinase insert domain protein receptor	Mus musculus	184-190
34603029-8	2021	Fingolimod co-treatment with MC1R and MC5R selective antagonists significantly (p < 0.05) increased retinal VEGFR1, VEGFR2, and VEGFA levels compared to mice treated with fingolimod alone.	Fingolimod Hydrochloride	0-10	melanocortin 1 receptor	Mus musculus	29-33
34603029-8	2021	Fingolimod co-treatment with MC1R and MC5R selective antagonists significantly (p < 0.05) increased retinal VEGFR1, VEGFR2, and VEGFA levels compared to mice treated with fingolimod alone.	Fingolimod Hydrochloride	0-10	melanocortin 5 receptor	Mus musculus	38-42
34603029-8	2021	Fingolimod co-treatment with MC1R and MC5R selective antagonists significantly (p < 0.05) increased retinal VEGFR1, VEGFR2, and VEGFA levels compared to mice treated with fingolimod alone.	Fingolimod Hydrochloride	0-10	FMS-like tyrosine kinase 1	Mus musculus	108-114
34603029-1	2021	This study aimed to investigate the interactions between fingolimod, a sphingosine 1-phosphate receptor (S1PR) agonist, and melanocortin receptors 1 and 5 (MCR1, MCR5).	Fingolimod Hydrochloride	57-67	melanocortin 1 receptor	Mus musculus	124-154
34603029-8	2021	Fingolimod co-treatment with MC1R and MC5R selective antagonists significantly (p < 0.05) increased retinal VEGFR1, VEGFR2, and VEGFA levels compared to mice treated with fingolimod alone.	Fingolimod Hydrochloride	0-10	kinase insert domain protein receptor	Mus musculus	116-122
34603029-8	2021	Fingolimod co-treatment with MC1R and MC5R selective antagonists significantly (p < 0.05) increased retinal VEGFR1, VEGFR2, and VEGFA levels compared to mice treated with fingolimod alone.	Fingolimod Hydrochloride	0-10	vascular endothelial growth factor A	Mus musculus	128-133
34603029-8	2021	Fingolimod co-treatment with MC1R and MC5R selective antagonists significantly (p < 0.05) increased retinal VEGFR1, VEGFR2, and VEGFA levels compared to mice treated with fingolimod alone.	Fingolimod Hydrochloride	171-181	FMS-like tyrosine kinase 1	Mus musculus	108-114
34603029-8	2021	Fingolimod co-treatment with MC1R and MC5R selective antagonists significantly (p < 0.05) increased retinal VEGFR1, VEGFR2, and VEGFA levels compared to mice treated with fingolimod alone.	Fingolimod Hydrochloride	171-181	vascular endothelial growth factor A	Mus musculus	128-133
34603029-1	2021	This study aimed to investigate the interactions between fingolimod, a sphingosine 1-phosphate receptor (S1PR) agonist, and melanocortin receptors 1 and 5 (MCR1, MCR5).	Fingolimod Hydrochloride	57-67	melanocortin 1 receptor	Mus musculus	156-160
34603029-3	2021	We showed, by a molecular modeling approach, that fingolimod can bind with good-predicted affinity to MC1R and MC5R.	Fingolimod Hydrochloride	50-60	melanocortin 1 receptor	Mus musculus	102-106
34603029-9	2021	Diabetic animals treated with fingolimod plus Ex 26 (S1PR1 selective blocker) had VEGFR1, VEGFR2, and VEGFA levels between diabetic mice group and the group of diabetic mice treated with fingolimod alone.	Fingolimod Hydrochloride	30-40	sphingosine-1-phosphate receptor 1	Mus musculus	53-58
34603029-3	2021	We showed, by a molecular modeling approach, that fingolimod can bind with good-predicted affinity to MC1R and MC5R.	Fingolimod Hydrochloride	50-60	melanocortin 5 receptor	Mus musculus	111-115
34603029-9	2021	Diabetic animals treated with fingolimod plus Ex 26 (S1PR1 selective blocker) had VEGFR1, VEGFR2, and VEGFA levels between diabetic mice group and the group of diabetic mice treated with fingolimod alone.	Fingolimod Hydrochloride	30-40	FMS-like tyrosine kinase 1	Mus musculus	82-88
34603029-9	2021	Diabetic animals treated with fingolimod plus Ex 26 (S1PR1 selective blocker) had VEGFR1, VEGFR2, and VEGFA levels between diabetic mice group and the group of diabetic mice treated with fingolimod alone.	Fingolimod Hydrochloride	30-40	kinase insert domain protein receptor	Mus musculus	90-96
34603029-9	2021	Diabetic animals treated with fingolimod plus Ex 26 (S1PR1 selective blocker) had VEGFR1, VEGFR2, and VEGFA levels between diabetic mice group and the group of diabetic mice treated with fingolimod alone.	Fingolimod Hydrochloride	30-40	vascular endothelial growth factor A	Mus musculus	102-107
34480787-10	2022	Experiment 2: To examine whether fingolimod (lymphocytes inhibitor) enhances the action of tissue plasminogen activator (tPA) in eMCAO rats on cerebral angiographic reperfusion.	Fingolimod Hydrochloride	33-43	plasminogen activator, tissue type	Rattus norvegicus	91-119
34603029-9	2021	Diabetic animals treated with fingolimod plus Ex 26 (S1PR1 selective blocker) had VEGFR1, VEGFR2, and VEGFA levels between diabetic mice group and the group of diabetic mice treated with fingolimod alone.	Fingolimod Hydrochloride	187-197	sphingosine-1-phosphate receptor 1	Mus musculus	53-58
34603029-10	2021	This vascular protective effect of fingolimod, through activation of MC1R and MC5R, was evidenced also by fluorescein angiography in mice.	Fingolimod Hydrochloride	35-45	melanocortin 1 receptor	Mus musculus	69-73
34603029-10	2021	This vascular protective effect of fingolimod, through activation of MC1R and MC5R, was evidenced also by fluorescein angiography in mice.	Fingolimod Hydrochloride	35-45	melanocortin 5 receptor	Mus musculus	78-82
34603029-11	2021	Finally, molecular dynamic simulations showed a strong similarity between fingolimod and the MC1R agonist BMS-470539.	Fingolimod Hydrochloride	74-84	melanocortin 1 receptor	Mus musculus	93-97
34405859-4	2021	In this work we observed that fingolimod (FTY720), used as a medication for multiple sclerosis, induced coordinated expression of p62, P-Ser349 p62 and inhibitory TFEB form, phosphorylated on Serine 211 (P-Ser211 TFEB), in human synovial fibroblasts.	Fingolimod Hydrochloride	30-40	sequestosome 1	Homo sapiens	130-133
34405859-4	2021	In this work we observed that fingolimod (FTY720), used as a medication for multiple sclerosis, induced coordinated expression of p62, P-Ser349 p62 and inhibitory TFEB form, phosphorylated on Serine 211 (P-Ser211 TFEB), in human synovial fibroblasts.	Fingolimod Hydrochloride	30-40	transcription factor EB	Homo sapiens	163-167
34405859-4	2021	In this work we observed that fingolimod (FTY720), used as a medication for multiple sclerosis, induced coordinated expression of p62, P-Ser349 p62 and inhibitory TFEB form, phosphorylated on Serine 211 (P-Ser211 TFEB), in human synovial fibroblasts.	Fingolimod Hydrochloride	30-40	transcription factor EB	Homo sapiens	213-217
34405859-9	2021	Autophagy and VPS34 kinase inhibitor, autophinib, further increased FTY720-induced P-Ser349 p62 but inhibited concomitant expression of P-Ser211 TFEB.	Fingolimod Hydrochloride	68-74	phosphatidylinositol 3-kinase catalytic subunit type 3	Homo sapiens	14-19
34405859-9	2021	Autophagy and VPS34 kinase inhibitor, autophinib, further increased FTY720-induced P-Ser349 p62 but inhibited concomitant expression of P-Ser211 TFEB.	Fingolimod Hydrochloride	68-74	sequestosome 1	Homo sapiens	92-95
34504491-5	2021	To validate the obtained results, the gene expression of HBD, as the most remarkable DEG in the PBMCS of affected patients, was measured in the PBMCS of healthy donors, treatment-naive MS patients, and MS patients treated with GA, fingolimod, DMF, and IFNbeta-1alpha.	Fingolimod Hydrochloride	231-241	HBD	Homo sapiens	57-60
34504491-10	2021	Of interest, immunomodulatory therapies with fingolimod, DMF, and IFNbeta-1alpha have significantly decreased HBD expression.	Fingolimod Hydrochloride	45-55	HBD	Homo sapiens	110-113
34504491-12	2021	HBD is substantially up-regulated in treatment-naive MS patients, and immunomodulatory therapies with fingolimod, DMF, and IFNbeta-1alpha can remarkably down-regulate HBD expression.	Fingolimod Hydrochloride	102-112	HBD	Homo sapiens	0-3
34504491-12	2021	HBD is substantially up-regulated in treatment-naive MS patients, and immunomodulatory therapies with fingolimod, DMF, and IFNbeta-1alpha can remarkably down-regulate HBD expression.	Fingolimod Hydrochloride	102-112	HBD	Homo sapiens	167-170
34429366-7	2021	Although there was no difference in the frequencies of MCAM+ lymphocytes among the DMD-treated groups, fingolimod decreased the absolute number of MCAM+ lymphocytes.	Fingolimod Hydrochloride	103-113	melanoma cell adhesion molecule	Homo sapiens	147-151
34500564-3	2021	S1P1 modulators, such as fingolimod, disrupt this recycling by inducing persistent S1P1 internalization and receptor degradation, which results in blocked egress of T cells from the secondary lymphoid tissues.	Fingolimod Hydrochloride	25-35	sphingosine-1-phosphate receptor 1	Mus musculus	0-4
34500564-3	2021	S1P1 modulators, such as fingolimod, disrupt this recycling by inducing persistent S1P1 internalization and receptor degradation, which results in blocked egress of T cells from the secondary lymphoid tissues.	Fingolimod Hydrochloride	25-35	sphingosine-1-phosphate receptor 1	Mus musculus	83-87
34484174-9	2021	Reduced uptake of 99mTc-HYNIC-S1PR1mAb in SK-HEP-1 was observed in tumor-bearing nude mice pretreated with fingolimod, which binds competitively to the receptors, especially S1PR1.	Fingolimod Hydrochloride	107-117	sphingosine-1-phosphate receptor 1	Mus musculus	30-35
34484174-9	2021	Reduced uptake of 99mTc-HYNIC-S1PR1mAb in SK-HEP-1 was observed in tumor-bearing nude mice pretreated with fingolimod, which binds competitively to the receptors, especially S1PR1.	Fingolimod Hydrochloride	107-117	sphingosine-1-phosphate receptor 1	Mus musculus	174-179
34382511-4	2022	RB005 is a selective SK1 inhibitor and a structural analog of PP2A activator FTY720.	Fingolimod Hydrochloride	77-83	protein phosphatase 2 phosphatase activator	Homo sapiens	62-66
34502385-7	2021	Furthermore, the approved S1P receptor modulator FTY720, and its active form FTY720-phosphate, both exerted a similar effect on Epo expression as S1P.	Fingolimod Hydrochloride	49-55	sphingosine-1-phosphate receptor 1	Mus musculus	26-29
34502385-7	2021	Furthermore, the approved S1P receptor modulator FTY720, and its active form FTY720-phosphate, both exerted a similar effect on Epo expression as S1P.	Fingolimod Hydrochloride	49-55	erythropoietin	Mus musculus	128-131
34442365-0	2021	Regulation of CTLA-4 and PD-L1 Expression in Relapsing-Remitting Multiple Sclerosis Patients after Treatment with Fingolimod, IFNbeta-1alpha, Glatiramer Acetate, and Dimethyl Fumarate Drugs.	Fingolimod Hydrochloride	114-124	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	14-20
34442365-0	2021	Regulation of CTLA-4 and PD-L1 Expression in Relapsing-Remitting Multiple Sclerosis Patients after Treatment with Fingolimod, IFNbeta-1alpha, Glatiramer Acetate, and Dimethyl Fumarate Drugs.	Fingolimod Hydrochloride	114-124	CD274 molecule	Homo sapiens	25-30
34305524-0	2021	Age-Related Transcriptional Deregulation of Genes Coding Synaptic Proteins in Alzheimer"s Disease Murine Model: Potential Neuroprotective Effect of Fingolimod.	Fingolimod Hydrochloride	148-158	renin binding protein	Mus musculus	0-3
34340233-0	2022	CXCL13 Levels Indicate Treatment Responsiveness to Fingolimod in MS Patients.	Fingolimod Hydrochloride	51-61	C-X-C motif chemokine ligand 13	Homo sapiens	0-6
34271980-13	2021	One of these predicted combinations, fingolimod with a TAK1 inhibitor, was validated in an animal model of MS.	Fingolimod Hydrochloride	37-47	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	55-59
34337080-0	2021	Exosomes Derived from Nerve Stem Cells Loaded with FTY720 Promote the Recovery after Spinal Cord Injury in Rats by PTEN/AKT Signal Pathway.	Fingolimod Hydrochloride	51-57	phosphatase and tensin homolog	Rattus norvegicus	115-119
34337080-0	2021	Exosomes Derived from Nerve Stem Cells Loaded with FTY720 Promote the Recovery after Spinal Cord Injury in Rats by PTEN/AKT Signal Pathway.	Fingolimod Hydrochloride	51-57	AKT serine/threonine kinase 1	Rattus norvegicus	120-123
34662222-12	2021	Furthermore, FTY720 treatment up-regulated the expression level of M2 biomarker CD206, Arg-1, Fizz-1, which could be weakened by the STAT3 inhibitor.	Fingolimod Hydrochloride	13-19	mannose receptor, C type 1	Mus musculus	80-85
34177891-10	2021	FTY720 treatment in the absence of EAE resulted in overall downregulation of S1PR1 and S1PR3, while S1PR5 exhibited a dose-dependent upregulation.	Fingolimod Hydrochloride	0-6	sphingosine-1-phosphate receptor 1	Mus musculus	77-82
34177891-10	2021	FTY720 treatment in the absence of EAE resulted in overall downregulation of S1PR1 and S1PR3, while S1PR5 exhibited a dose-dependent upregulation.	Fingolimod Hydrochloride	0-6	sphingosine-1-phosphate receptor 3	Mus musculus	87-92
34122439-1	2021	Although fingolimod and interferon-beta are two mechanistically different multiple sclerosis (MS) treatments, they both induce B cell activating factor (BAFF) and shift the B cell pool towards a regulatory phenotype.	Fingolimod Hydrochloride	9-19	TNF superfamily member 13b	Homo sapiens	127-151
34122439-1	2021	Although fingolimod and interferon-beta are two mechanistically different multiple sclerosis (MS) treatments, they both induce B cell activating factor (BAFF) and shift the B cell pool towards a regulatory phenotype.	Fingolimod Hydrochloride	9-19	TNF superfamily member 13b	Homo sapiens	153-157
34122439-5	2021	Our flow experiments showed that interferon-beta and fingolimod induced BAFF protein and mRNA expression (P <= 3.15 x 10-4) without disproportional change in the antagonizing splice form.	Fingolimod Hydrochloride	53-63	TNF superfamily member 13b	Homo sapiens	72-76
34662222-12	2021	Furthermore, FTY720 treatment up-regulated the expression level of M2 biomarker CD206, Arg-1, Fizz-1, which could be weakened by the STAT3 inhibitor.	Fingolimod Hydrochloride	13-19	arginase, liver	Mus musculus	87-92
34662222-12	2021	Furthermore, FTY720 treatment up-regulated the expression level of M2 biomarker CD206, Arg-1, Fizz-1, which could be weakened by the STAT3 inhibitor.	Fingolimod Hydrochloride	13-19	resistin like alpha	Mus musculus	94-100
34662222-12	2021	Furthermore, FTY720 treatment up-regulated the expression level of M2 biomarker CD206, Arg-1, Fizz-1, which could be weakened by the STAT3 inhibitor.	Fingolimod Hydrochloride	13-19	signal transducer and activator of transcription 3	Mus musculus	133-138
35288472-5	2022	Whereas S-specific CD4 and CD8 T cell responses were largely compromised by fingolimod treatment, T cell responses were robustly generated in anti-CD20-treated MS patients, but with a reduced proportion of CD4+CXCR5+ circulating follicular Th cells.	Fingolimod Hydrochloride	76-86	CD4 molecule	Homo sapiens	19-22
35274449-0	2022	Fingolimod ameliorates acetic acid-induced ulcerative colitis: An insight into its modulatory impact on pro/anti-inflammatory cytokines and AKT/mTOR signalling.	Fingolimod Hydrochloride	0-10	AKT serine/threonine kinase 1	Rattus norvegicus	140-143
35274449-0	2022	Fingolimod ameliorates acetic acid-induced ulcerative colitis: An insight into its modulatory impact on pro/anti-inflammatory cytokines and AKT/mTOR signalling.	Fingolimod Hydrochloride	0-10	mechanistic target of rapamycin kinase	Rattus norvegicus	144-148
35302173-0	2022	FTY720 attenuates APAP-induced liver injury via the JAK2/STAT3 signaling pathway.	Fingolimod Hydrochloride	0-6	Janus kinase 2	Mus musculus	52-56
35302173-0	2022	FTY720 attenuates APAP-induced liver injury via the JAK2/STAT3 signaling pathway.	Fingolimod Hydrochloride	0-6	signal transducer and activator of transcription 3	Mus musculus	57-62
35302173-17	2022	Inhibition of JAK2/STAT3 signaling attenuated the protective, antioxidant effects of FTY720.	Fingolimod Hydrochloride	85-91	Janus kinase 2	Mus musculus	14-18
35302173-17	2022	Inhibition of JAK2/STAT3 signaling attenuated the protective, antioxidant effects of FTY720.	Fingolimod Hydrochloride	85-91	signal transducer and activator of transcription 3	Mus musculus	19-24
35499794-7	2022	Fingolimod treatment coordinated lncRNAs" role on Bdnf expression in glial cells and enhanced OPC myelination three times compared to control.	Fingolimod Hydrochloride	0-10	brain-derived neurotrophic factor	Rattus norvegicus	50-54
35239006-6	2022	Median anti-spike titre was lower in anti-CD20 antibodies and fingolimod-treated pwMS compared to those receiving other DMTs, and it correlated with anti-CD20 treatment duration (R - 0.93, p < 0.0001) and with age at vaccination in pwMS not receiving depletive treatments (R - 0.25, p = 0.028).	Fingolimod Hydrochloride	62-72	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	12-17
35613869-1	2022	Combination treatment using fingolimod (FTY720), an immunomodulator, and a pathogenic antigen prevents the progression of glucose-6-phosphate isomerase (GPI)325-339-induced arthritis.	Fingolimod Hydrochloride	28-38	glucose-6-phosphate isomerase	Homo sapiens	122-151
35613869-1	2022	Combination treatment using fingolimod (FTY720), an immunomodulator, and a pathogenic antigen prevents the progression of glucose-6-phosphate isomerase (GPI)325-339-induced arthritis.	Fingolimod Hydrochloride	40-46	glucose-6-phosphate isomerase	Homo sapiens	122-151
35605667-5	2022	Translating these studies into a clinically applicable approach, we show that the established immunomodulators fingolimod and teriflunomide significantly attenuate the neurodegenerative phenotype and improve gait performance in the SPG11 model, even when applied relatively late during disease progression.	Fingolimod Hydrochloride	111-121	SPG11, spatacsin vesicle trafficking associated	Mus musculus	232-237
35274449-1	2022	BACKGROUND: Because of the approved immunomodulatory activities of fingolimod, the current study aimed at studying the curative potential of fingolimod against experimentally induced ulcerative colitis (UC) via modulating pro/anti-inflammatory cytokines release and AKT/mTOR signalling.	Fingolimod Hydrochloride	141-151	AKT serine/threonine kinase 1	Rattus norvegicus	266-269
35274449-1	2022	BACKGROUND: Because of the approved immunomodulatory activities of fingolimod, the current study aimed at studying the curative potential of fingolimod against experimentally induced ulcerative colitis (UC) via modulating pro/anti-inflammatory cytokines release and AKT/mTOR signalling.	Fingolimod Hydrochloride	141-151	mechanistic target of rapamycin kinase	Rattus norvegicus	270-274
35274449-9	2022	Fingolimod also significantly decreased the expressions of pro-inflammatory cytokines interleukin-9 and T-helper 17 along with increasing the expression of anti-inflammatory interleukin-10 and transforming growth factor-beta compared to the UC group.	Fingolimod Hydrochloride	0-10	interleukin 9	Rattus norvegicus	86-99
35274449-9	2022	Fingolimod also significantly decreased the expressions of pro-inflammatory cytokines interleukin-9 and T-helper 17 along with increasing the expression of anti-inflammatory interleukin-10 and transforming growth factor-beta compared to the UC group.	Fingolimod Hydrochloride	0-10	interleukin 10	Rattus norvegicus	174-188
35274449-10	2022	In addition, fingolimod decreased the expressions of AKT and mTOR compared to the UC group.	Fingolimod Hydrochloride	13-23	AKT serine/threonine kinase 1	Rattus norvegicus	53-56
35274449-10	2022	In addition, fingolimod decreased the expressions of AKT and mTOR compared to the UC group.	Fingolimod Hydrochloride	13-23	mechanistic target of rapamycin kinase	Rattus norvegicus	61-65
35274449-11	2022	CONCLUSION: Fingolimod attenuated acetic acid-induced UC through its immunomodulatory effect by shifting the balance to favour anti-inflammatory cytokine production rather than pro-inflammatory cytokines and modulating the AKT/mTOR signalling.	Fingolimod Hydrochloride	12-22	AKT serine/threonine kinase 1	Rattus norvegicus	223-226
35274449-11	2022	CONCLUSION: Fingolimod attenuated acetic acid-induced UC through its immunomodulatory effect by shifting the balance to favour anti-inflammatory cytokine production rather than pro-inflammatory cytokines and modulating the AKT/mTOR signalling.	Fingolimod Hydrochloride	12-22	mechanistic target of rapamycin kinase	Rattus norvegicus	227-231
35288472-5	2022	Whereas S-specific CD4 and CD8 T cell responses were largely compromised by fingolimod treatment, T cell responses were robustly generated in anti-CD20-treated MS patients, but with a reduced proportion of CD4+CXCR5+ circulating follicular Th cells.	Fingolimod Hydrochloride	76-86	CD8a molecule	Homo sapiens	27-30
35288472-5	2022	Whereas S-specific CD4 and CD8 T cell responses were largely compromised by fingolimod treatment, T cell responses were robustly generated in anti-CD20-treated MS patients, but with a reduced proportion of CD4+CXCR5+ circulating follicular Th cells.	Fingolimod Hydrochloride	76-86	C-X-C motif chemokine receptor 5	Homo sapiens	210-215
35558966-9	2022	In addition, fingolimod treatment was found to blunt the pro-inflammatory phenotype of activated macrophages and decrease interleukin-17 (IL-17) secretion.	Fingolimod Hydrochloride	13-23	interleukin 17A	Mus musculus	122-136
35558966-9	2022	In addition, fingolimod treatment was found to blunt the pro-inflammatory phenotype of activated macrophages and decrease interleukin-17 (IL-17) secretion.	Fingolimod Hydrochloride	13-23	interleukin 17A	Mus musculus	138-143
35237148-13	2021	Results: In this study, we found that SPHK inhibitors (ABC294640 and FTY720) combined with ZA decreased the degree of inflammatory osteolysis in vivo.	Fingolimod Hydrochloride	69-75	sphingosine kinase 1	Homo sapiens	38-42
35020157-5	2022	Interferon beta (30.7%) was the most common pre-fingolimod treatment.	Fingolimod Hydrochloride	48-58	interferon beta 1	Homo sapiens	0-15
35197967-5	2022	Results: RRMS patients during fingolimod (FTY) and natalizumab (NTZ) treatment showed increased percentage of circulating CD8+GzmB+ T lymphocytes when compared to healthy volunteers.	Fingolimod Hydrochloride	30-40	CD8a molecule	Homo sapiens	122-125
35197967-5	2022	Results: RRMS patients during fingolimod (FTY) and natalizumab (NTZ) treatment showed increased percentage of circulating CD8+GzmB+ T lymphocytes when compared to healthy volunteers.	Fingolimod Hydrochloride	30-40	granzyme B	Homo sapiens	126-130
35216791-1	2022	Fingolimod treatment has been associated with opportunistic infections, most notably PML and cryptococcal meningitis.	Fingolimod Hydrochloride	0-10	PML nuclear body scaffold	Homo sapiens	85-88
35158767-3	2022	FTY720 (Fingolimod), which targets SphK1 and S1P1, prevented HIF-1alpha accumulation, and also inhibited cell proliferation in both normoxia and hypoxia unlike conventional chemotherapy.	Fingolimod Hydrochloride	8-18	sphingosine kinase 1	Homo sapiens	35-40
35158767-3	2022	FTY720 (Fingolimod), which targets SphK1 and S1P1, prevented HIF-1alpha accumulation, and also inhibited cell proliferation in both normoxia and hypoxia unlike conventional chemotherapy.	Fingolimod Hydrochloride	8-18	sphingosine-1-phosphate receptor 1	Homo sapiens	45-49
35158767-3	2022	FTY720 (Fingolimod), which targets SphK1 and S1P1, prevented HIF-1alpha accumulation, and also inhibited cell proliferation in both normoxia and hypoxia unlike conventional chemotherapy.	Fingolimod Hydrochloride	8-18	hypoxia inducible factor 1 subunit alpha	Homo sapiens	61-71
34051694-0	2021	Effect of fingolimod vs interferon treatment on OCT measurements and cognitive function in RRMS.	Fingolimod Hydrochloride	10-20	plexin A2	Homo sapiens	48-51
33932092-10	2021	Pharmacological activation of PP2A with FTY-720 markedly compromised the growth advantage induced by the SF3B1K700E mutation in vitro and in vivo.	Fingolimod Hydrochloride	40-47	protein phosphatase 2 phosphatase activator	Homo sapiens	30-34
34007158-0	2021	FTY720 Inhibits the Development of Collagen-Induced Arthritis in Mice by Suppressing the Recruitment of CD4+ T Lymphocytes.	Fingolimod Hydrochloride	0-6	CD4 antigen	Mus musculus	104-107
34007158-8	2021	Results: In vivo experiments showed that FTY720 inhibited the recruitment of CD4+ lymphocytes in the affected joints of CIA mice.	Fingolimod Hydrochloride	41-47	CD4 antigen	Mus musculus	77-80
34007158-9	2021	FTY720 reduced the secretion of IL-1beta, IL-6, and IL-8 from TNF-alpha-stimulated MH7A cells in a dose-dependent manner.	Fingolimod Hydrochloride	0-6	interleukin 1 alpha	Homo sapiens	32-40
34007158-9	2021	FTY720 reduced the secretion of IL-1beta, IL-6, and IL-8 from TNF-alpha-stimulated MH7A cells in a dose-dependent manner.	Fingolimod Hydrochloride	0-6	interleukin 6	Homo sapiens	42-46
34007158-9	2021	FTY720 reduced the secretion of IL-1beta, IL-6, and IL-8 from TNF-alpha-stimulated MH7A cells in a dose-dependent manner.	Fingolimod Hydrochloride	0-6	C-X-C motif chemokine ligand 8	Homo sapiens	52-56
34007158-9	2021	FTY720 reduced the secretion of IL-1beta, IL-6, and IL-8 from TNF-alpha-stimulated MH7A cells in a dose-dependent manner.	Fingolimod Hydrochloride	0-6	tumor necrosis factor	Homo sapiens	62-71
34007158-10	2021	FTY720 also inhibited TNF-alpha-induced phosphorylation of NF-kappaBp65 and IkappaBalpha, as well as NF-kappaBp65 nuclear translocation, in a dose- and time-dependent manner.	Fingolimod Hydrochloride	0-6	tumor necrosis factor	Homo sapiens	22-31
34007158-10	2021	FTY720 also inhibited TNF-alpha-induced phosphorylation of NF-kappaBp65 and IkappaBalpha, as well as NF-kappaBp65 nuclear translocation, in a dose- and time-dependent manner.	Fingolimod Hydrochloride	0-6	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	76-88
34007158-12	2021	Conclusion: Our findings demonstrated that oral administration of FTY720 exerted beneficial effects in CIA mice by inhibiting CD4+ T lymphocyte recruitment to the affected joints.	Fingolimod Hydrochloride	66-72	CD4 antigen	Mus musculus	126-129
34007158-13	2021	Our data also indicated that FTY720 inhibited TNF-alpha-induced inflammation by suppressing the AKT/PI3K/NF-kappaB pathway in MH7A cells.	Fingolimod Hydrochloride	29-35	tumor necrosis factor	Homo sapiens	46-55
34007158-13	2021	Our data also indicated that FTY720 inhibited TNF-alpha-induced inflammation by suppressing the AKT/PI3K/NF-kappaB pathway in MH7A cells.	Fingolimod Hydrochloride	29-35	AKT serine/threonine kinase 1	Homo sapiens	96-99
34007158-13	2021	Our data also indicated that FTY720 inhibited TNF-alpha-induced inflammation by suppressing the AKT/PI3K/NF-kappaB pathway in MH7A cells.	Fingolimod Hydrochloride	29-35	nuclear factor kappa B subunit 1	Homo sapiens	105-114
33046864-2	2021	Here, we show that, in mice with EAE, the accumulation and persistence in the lymph nodes and spleen of a systemically administered serum albumin (SA)-IL-4 fusion protein leads to higher efficacy in preventing disease development than the administration of wild-type IL-4 or of the clinically approved drug fingolimod.	Fingolimod Hydrochloride	307-317	albumin	Mus musculus	132-145
33046864-2	2021	Here, we show that, in mice with EAE, the accumulation and persistence in the lymph nodes and spleen of a systemically administered serum albumin (SA)-IL-4 fusion protein leads to higher efficacy in preventing disease development than the administration of wild-type IL-4 or of the clinically approved drug fingolimod.	Fingolimod Hydrochloride	307-317	interleukin 4	Mus musculus	151-155
33932092-10	2021	Pharmacological activation of PP2A with FTY-720 markedly compromised the growth advantage induced by the SF3B1K700E mutation in vitro and in vivo.	Fingolimod Hydrochloride	40-47	splicing factor 3b subunit 1	Homo sapiens	105-110
33342303-7	2021	De novo elevated alanine aminotransferase affected 13.2% (DMF), 12.4% (teriflunomide), and 30.0% (fingolimod) of users.	Fingolimod Hydrochloride	98-108	glutamic--pyruvic transaminase	Homo sapiens	17-41
33922540-4	2021	The results suggest that polymorphisms detected in the GSTP1, ITGA4, NQO1, AKT1, and GP6 genes, for treatment with natalizumab, ZMIZ1, for fingolimod and dimethyl fumarate, ADA, for cladribine, and NOX3, for dimethyl fumarate, may be used in the future as predictive markers of treatment response to new therapies in MS patients.	Fingolimod Hydrochloride	139-149	glutathione S-transferase pi 1	Homo sapiens	55-60
33922540-4	2021	The results suggest that polymorphisms detected in the GSTP1, ITGA4, NQO1, AKT1, and GP6 genes, for treatment with natalizumab, ZMIZ1, for fingolimod and dimethyl fumarate, ADA, for cladribine, and NOX3, for dimethyl fumarate, may be used in the future as predictive markers of treatment response to new therapies in MS patients.	Fingolimod Hydrochloride	139-149	integrin subunit alpha 4	Homo sapiens	62-67
33922540-4	2021	The results suggest that polymorphisms detected in the GSTP1, ITGA4, NQO1, AKT1, and GP6 genes, for treatment with natalizumab, ZMIZ1, for fingolimod and dimethyl fumarate, ADA, for cladribine, and NOX3, for dimethyl fumarate, may be used in the future as predictive markers of treatment response to new therapies in MS patients.	Fingolimod Hydrochloride	139-149	NAD(P)H quinone dehydrogenase 1	Homo sapiens	69-73
33922540-4	2021	The results suggest that polymorphisms detected in the GSTP1, ITGA4, NQO1, AKT1, and GP6 genes, for treatment with natalizumab, ZMIZ1, for fingolimod and dimethyl fumarate, ADA, for cladribine, and NOX3, for dimethyl fumarate, may be used in the future as predictive markers of treatment response to new therapies in MS patients.	Fingolimod Hydrochloride	139-149	AKT serine/threonine kinase 1	Homo sapiens	75-79
33922540-4	2021	The results suggest that polymorphisms detected in the GSTP1, ITGA4, NQO1, AKT1, and GP6 genes, for treatment with natalizumab, ZMIZ1, for fingolimod and dimethyl fumarate, ADA, for cladribine, and NOX3, for dimethyl fumarate, may be used in the future as predictive markers of treatment response to new therapies in MS patients.	Fingolimod Hydrochloride	139-149	glycoprotein VI platelet	Homo sapiens	85-88
33922540-4	2021	The results suggest that polymorphisms detected in the GSTP1, ITGA4, NQO1, AKT1, and GP6 genes, for treatment with natalizumab, ZMIZ1, for fingolimod and dimethyl fumarate, ADA, for cladribine, and NOX3, for dimethyl fumarate, may be used in the future as predictive markers of treatment response to new therapies in MS patients.	Fingolimod Hydrochloride	139-149	NADPH oxidase 3	Homo sapiens	198-202
33888401-9	2021	On day 6, the mRNA expression level of IL-17A was lower in the skin of fingolimod-treated mice than in that of PBS-treated mice, whereas it was higher in the inguinal lymph nodes of fingolimod-treated mice than in those of PBS-treated mice.	Fingolimod Hydrochloride	71-81	interleukin 17A	Mus musculus	39-45
33888401-9	2021	On day 6, the mRNA expression level of IL-17A was lower in the skin of fingolimod-treated mice than in that of PBS-treated mice, whereas it was higher in the inguinal lymph nodes of fingolimod-treated mice than in those of PBS-treated mice.	Fingolimod Hydrochloride	182-192	interleukin 17A	Mus musculus	39-45
33888401-10	2021	Flow cytometric analyses revealed that fingolimod reduced IL-17A-producing gammadelta T cells infiltrating into the skin, whereas it increased these cells in the inguinal lymph nodes.	Fingolimod Hydrochloride	39-49	interleukin 17A	Mus musculus	58-64
33888401-12	2021	CONCLUSION: Our results demonstrated that fingolimod showed effectiveness for IMQ-induced psoriasiform dermatitis by hindering the emigration of IL-17A-producing gammadelta T cells from the lymph nodes to the skin, and suggest that fingolimod is a promising candidate for the treatment of psoriasis.	Fingolimod Hydrochloride	42-52	interleukin 17A	Mus musculus	145-151
33504740-1	2021	An increase in the number of glucocorticoid-induced tumor necrosis factor receptor-family related gene/protein (GITR)+CD25- (or fork-head box protein 3: Foxp3-) CD4+ T cells, after treating a mouse model of arthritis with fingolimod (FTY720), and a pathogenic antigen may play a key role in the establishment of immune tolerance.	Fingolimod Hydrochloride	222-232	tumor necrosis factor receptor superfamily, member 18	Mus musculus	29-110
33504740-1	2021	An increase in the number of glucocorticoid-induced tumor necrosis factor receptor-family related gene/protein (GITR)+CD25- (or fork-head box protein 3: Foxp3-) CD4+ T cells, after treating a mouse model of arthritis with fingolimod (FTY720), and a pathogenic antigen may play a key role in the establishment of immune tolerance.	Fingolimod Hydrochloride	222-232	tumor necrosis factor receptor superfamily, member 18	Mus musculus	112-116
33504740-1	2021	An increase in the number of glucocorticoid-induced tumor necrosis factor receptor-family related gene/protein (GITR)+CD25- (or fork-head box protein 3: Foxp3-) CD4+ T cells, after treating a mouse model of arthritis with fingolimod (FTY720), and a pathogenic antigen may play a key role in the establishment of immune tolerance.	Fingolimod Hydrochloride	222-232	interleukin 2 receptor, alpha chain	Mus musculus	118-122
33568357-5	2021	PADs, including FTY720 and DT-061, enhanced FLT3 inhibitor growth suppression and apoptosis induction in FLT3-ITD-expressing cell lines and primary AML cells in vitro and MV4-11 growth suppression in vivo.	Fingolimod Hydrochloride	16-22	fms related receptor tyrosine kinase 3	Homo sapiens	44-48
33797705-1	2021	Fingolimod (Gilenya) received regulatory approval from the US FDA in 2010 as the first-in-class sphingosine 1-phosphate (S1P) receptor (S1PR) modulator and was the first oral disease-modifying therapy (DMT) used for the treatment of the relapsing forms of multiple sclerosis (MS).	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Homo sapiens	136-140
33797705-7	2021	Improved understanding of fingolimod"s mechanism of action has provided strategies for the development of the more selective second-generation S1PR modulators.	Fingolimod Hydrochloride	26-36	sphingosine-1-phosphate receptor 1	Homo sapiens	143-147
33797705-16	2021	This review covers the available data about the mechanisms of action, pharmacodynamics and kinetics, efficacy, safety, and tolerability of the various S1PR modulators for patients with relapsing-remitting, secondary progressive, and, for fingolimod, primary progressive MS.	Fingolimod Hydrochloride	238-248	sphingosine-1-phosphate receptor 1	Homo sapiens	151-155
33274566-7	2021	In our study, we find that FTY720 and curcumol have a significant inhibitory effect on K562 cells, K562/ADR cells, and CD34+ cells from CML patients.	Fingolimod Hydrochloride	27-33	CD34 molecule	Homo sapiens	119-123
33516800-6	2021	The results of open field, novel object recognition and elevated plus maze tasks showed that Fingolimod prevents hippocampal memory dysfunction and anxiety-like behavior in both male and female hypoxic groups, which was accompanied with decreased TNF-alpha level in hippocampus.	Fingolimod Hydrochloride	93-103	tumor necrosis factor	Rattus norvegicus	247-256
33460688-2	2021	FingolimodR (FTY720) is the first functional antagonist of S1P1 that has been approved for oral treatment of MS.	Fingolimod Hydrochloride	13-19	sphingosine-1-phosphate receptor 1	Mus musculus	59-63
33704423-6	2021	Interestingly, genetic deletion of TCRbeta or CD4, as well as the use of the immunosuppressive drug fingolimod, were able to reduce the CNS myeloid MHCII response to alpha-syn.	Fingolimod Hydrochloride	100-110	histocompatibility-2, MHC	Mus musculus	148-153
33704423-6	2021	Interestingly, genetic deletion of TCRbeta or CD4, as well as the use of the immunosuppressive drug fingolimod, were able to reduce the CNS myeloid MHCII response to alpha-syn.	Fingolimod Hydrochloride	100-110	synuclein, alpha	Mus musculus	166-175
32342246-0	2021	FTY720 Modulates Microglia Toward Anti-inflammatory Phenotype by Suppressing Autophagy via STAT1 Pathway.	Fingolimod Hydrochloride	0-6	signal transducer and activator of transcription 1	Homo sapiens	91-96
33568357-5	2021	PADs, including FTY720 and DT-061, enhanced FLT3 inhibitor growth suppression and apoptosis induction in FLT3-ITD-expressing cell lines and primary AML cells in vitro and MV4-11 growth suppression in vivo.	Fingolimod Hydrochloride	16-22	fms related receptor tyrosine kinase 3	Homo sapiens	105-109
33131698-0	2021	Fingolimod (FTY720) prevents chronic rejection of rodent cardiac allografts through inhibition of the RhoA pathway.	Fingolimod Hydrochloride	0-10	ras homolog family member A	Rattus norvegicus	102-106
33131698-0	2021	Fingolimod (FTY720) prevents chronic rejection of rodent cardiac allografts through inhibition of the RhoA pathway.	Fingolimod Hydrochloride	12-18	ras homolog family member A	Rattus norvegicus	102-106
33428887-6	2021	Fingolimod-mediated inhibition of 4-AP-induced glutamate release was also abolished by the sphingosine kinase inhibitor DMS, selective S1P1 receptor antagonist W146, Gi/o protein inhibitor pertussis toxin, and G protein betagamma subunit inhibitor gallein; however, it was unaffected by the adenylyl cyclase inhibitor SQ22536, protein kinase A inhibitor H89, and phospholipase C inhibitor U73122.	Fingolimod Hydrochloride	0-10	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	327-343
33597189-6	2021	Based on an analysis of individual treatments (interferon-beta, glatiramer acetate, fingolimod, and natalizumab), interferon-beta was associated with inferior RGC preservation, relative to the other drugs.	Fingolimod Hydrochloride	84-94	interferon beta 1	Homo sapiens	114-129
33691194-9	2021	These inhibitory effects were recapitulated by either siRNA-mediated TRPM7 knockdown or treatment with TRPM7 antagonist FTY-720.	Fingolimod Hydrochloride	120-127	transient receptor potential cation channel, subfamily M, member 7	Rattus norvegicus	103-108
33301355-2	2021	Sphingosine 1-phosphate (S1P) signaling coordinates vascular functions in other organs, and S1P receptor-1 (S1P1) modulators including fingolimod show promise for the treatment of ischemic and hemorrhagic stroke.	Fingolimod Hydrochloride	135-145	sphingosine-1-phosphate receptor 1	Mus musculus	92-106
33603005-1	2021	The Fingolimod Patient Support Program (F-PSP) is an interprofessional specialty pharmacy service designed to ensure responsible use of fingolimod by promoting patient safety and medication adherence.	Fingolimod Hydrochloride	4-14	persephin	Homo sapiens	42-45
33603005-1	2021	The Fingolimod Patient Support Program (F-PSP) is an interprofessional specialty pharmacy service designed to ensure responsible use of fingolimod by promoting patient safety and medication adherence.	Fingolimod Hydrochloride	136-146	persephin	Homo sapiens	42-45
33603005-11	2021	The F-PSP seems valuable for supporting individual patients (ensuring responsible use of fingolimod and inviting patients for shared-decision making) and public health (indirectly gathering real-world evidence).	Fingolimod Hydrochloride	89-99	persephin	Homo sapiens	6-9
33659007-2	2021	These patients developed relapses with anti-MOG antibody seroconversion after switching from fingolimod or steroid pulse therapy to DMF, which was associated with peripheral lymphocyte recovery.	Fingolimod Hydrochloride	93-103	myelin oligodendrocyte glycoprotein	Homo sapiens	44-47
33301355-2	2021	Sphingosine 1-phosphate (S1P) signaling coordinates vascular functions in other organs, and S1P receptor-1 (S1P1) modulators including fingolimod show promise for the treatment of ischemic and hemorrhagic stroke.	Fingolimod Hydrochloride	135-145	sphingosine-1-phosphate receptor 1	Mus musculus	108-112
33603656-1	2021	Background: The sphingosine-1-phosphate receptor (S1PR) modulator fingolimod (FTY720), which is commonly used as an immunomodulator in multiple sclerosis treatment, has recently been found to reduce pathological changes in the brain tissue of Alzheimer"s disease (AD) animal models, but this has yet to be verified in human brain tissue.	Fingolimod Hydrochloride	66-76	sphingosine-1-phosphate receptor 1	Homo sapiens	50-54
33530945-1	2021	BACKGROUND: Fingolimod is a S1P1 receptor modulator that prevents activated lymphocyte egress from lymphoid tissues causing lymphopenia, mainly affecting CD4+ T lymphocytes.	Fingolimod Hydrochloride	12-22	CD4 molecule	Homo sapiens	154-157
33603656-1	2021	Background: The sphingosine-1-phosphate receptor (S1PR) modulator fingolimod (FTY720), which is commonly used as an immunomodulator in multiple sclerosis treatment, has recently been found to reduce pathological changes in the brain tissue of Alzheimer"s disease (AD) animal models, but this has yet to be verified in human brain tissue.	Fingolimod Hydrochloride	78-84	sphingosine-1-phosphate receptor 1	Homo sapiens	50-54
33516262-12	2021	RESULTS: Fingolimod significantly increased the frequency of Tregs within the CD4+ T cell population in blood and spleen post-ischaemia in all three mouse cohorts compared to untreated ischemic mice.	Fingolimod Hydrochloride	9-19	CD4 antigen	Mus musculus	78-81
33516262-13	2021	The highest splenic Treg frequency in fingolimod-treated mice was observed in ApoE-/- mice (9.32 +- 1.73% vs. 7.8 +- 3.01% in young, 6.09 +- 1.64% in aged mice).	Fingolimod Hydrochloride	38-48	apolipoprotein E	Mus musculus	78-82
33516262-15	2021	Fingolimod significantly increased the number of FoxP3+ cells in the infarct core of all mice.	Fingolimod Hydrochloride	0-10	forkhead box P3	Mus musculus	49-54
33516262-17	2021	CONCLUSIONS: Fingolimod increases Treg frequency in spleen and blood post-ischaemia and enhances the number of FoxP3+ cells in the ischaemic brain.	Fingolimod Hydrochloride	13-23	forkhead box P3	Mus musculus	111-116
33007647-6	2020	Interestingly fingolimod led to a marked reduction of CD4+ and a significant increase in CD8+ cell numbers.	Fingolimod Hydrochloride	14-24	CD4 molecule	Homo sapiens	54-57
33573114-9	2021	Our data reveal that overexpression of APP and PS1 mutations in AD model mice disrupts t-LTP in an Abeta plaque distance-dependent manner, but cannot be improved by fingolimod (FTY720) that has been shown to rescue conventional LTP in CA1 of APP/PS1 mice.	Fingolimod Hydrochloride	177-183	presenilin 1	Mus musculus	47-50
33058911-0	2020	Fingolimod suppressed the chronic unpredictable mild stress-induced depressive-like behaviors via affecting microglial and NLRP3 inflammasome activation.	Fingolimod Hydrochloride	0-10	NLR family, pyrin domain containing 3	Rattus norvegicus	123-128
33058911-8	2020	Furthermore, FTY720 inhibited the microglial M1 polarization markers iNOS and CD16, and promoted the M2 markers Arg-1 and CD206.	Fingolimod Hydrochloride	13-19	nitric oxide synthase 2	Rattus norvegicus	69-73
33058911-8	2020	Furthermore, FTY720 inhibited the microglial M1 polarization markers iNOS and CD16, and promoted the M2 markers Arg-1 and CD206.	Fingolimod Hydrochloride	13-19	arginase 1	Rattus norvegicus	112-117
33473182-7	2021	We found that fingolimod administration significantly enhanced the gut barrier (evidenced by enhanced expression of tight junction proteins and reduced intestinal permeability), attenuated intestinal microbial dysbiosis (evidenced by the reduction of enteric pathogenic Proteobacteria clusters), as well as intestinal immune dysfunction (evidenced by inhibition of CD4+ cells activation, reduction of T helper type 1 cells and macrophages, and the expansion of regulatory T cells).	Fingolimod Hydrochloride	14-24	CD4 antigen	Mus musculus	365-368
33473182-8	2021	We further revealed that fingolimod administration suppressed the activation of CD4+ cells and the differentiation of T helper type 1 cells, promoted the expansion of regulatory T cells in the pancreas, which might contribute to the maintenance of pancreatic immune tolerance and the reduction of T1D incidence.	Fingolimod Hydrochloride	25-35	CD4 antigen	Mus musculus	80-83
33473182-9	2021	The protection might be due to fingolimod inhibiting the toll-like receptor 2/4/nuclear factor-kappaB/NOD-like receptor protein 3 inflammasome pathway in the colon.	Fingolimod Hydrochloride	31-41	toll-like receptor 2	Mus musculus	57-79
33315370-7	2021	We investigated fingolimod"s mechanism of action using a combination of computational studies, biophysical methods, and synthetic chemistry, showing that fingolimod bound to cTnC repels cTnISP via mainly electrostatic repulsion of its positively charged tail.	Fingolimod Hydrochloride	16-26	troponin C1, slow skeletal and cardiac type	Homo sapiens	174-178
33315370-7	2021	We investigated fingolimod"s mechanism of action using a combination of computational studies, biophysical methods, and synthetic chemistry, showing that fingolimod bound to cTnC repels cTnISP via mainly electrostatic repulsion of its positively charged tail.	Fingolimod Hydrochloride	154-164	troponin C1, slow skeletal and cardiac type	Homo sapiens	174-178
33007647-6	2020	Interestingly fingolimod led to a marked reduction of CD4+ and a significant increase in CD8+ cell numbers.	Fingolimod Hydrochloride	14-24	CD8a molecule	Homo sapiens	89-92
33007647-11	2020	CM CD4+ and CD8+ cells migrated across BBB more efficiently in fingolimod-treated patients.	Fingolimod Hydrochloride	63-73	CD4 molecule	Homo sapiens	3-6
33007647-11	2020	CM CD4+ and CD8+ cells migrated across BBB more efficiently in fingolimod-treated patients.	Fingolimod Hydrochloride	63-73	CD8a molecule	Homo sapiens	12-15
33007647-12	2020	We found that while fingolimod reduced the proportions of naive CD19+ B cells, it significantly increased the proportions of these cells which migrated.	Fingolimod Hydrochloride	20-30	CD19 molecule	Homo sapiens	64-68
33007647-13	2020	When B cells were further stratified based on CD24, CD27 and CD38 expression, the only effect of fingolimod was an enhancement of CD24hiCD27+ B cell migration, compared to untreated MS patients.	Fingolimod Hydrochloride	97-107	CD27 molecule	Homo sapiens	52-56
33007647-13	2020	When B cells were further stratified based on CD24, CD27 and CD38 expression, the only effect of fingolimod was an enhancement of CD24hiCD27+ B cell migration, compared to untreated MS patients.	Fingolimod Hydrochloride	97-107	CD38 molecule	Homo sapiens	61-65
33007647-13	2020	When B cells were further stratified based on CD24, CD27 and CD38 expression, the only effect of fingolimod was an enhancement of CD24hiCD27+ B cell migration, compared to untreated MS patients.	Fingolimod Hydrochloride	97-107	CD24 molecule	Homo sapiens	130-140
33007647-14	2020	The migratory capacities of CD8hi Natural Killer (NK), CD8dim NK and NK-T cells were also reduced by fingolimod.	Fingolimod Hydrochloride	101-111	CD8a molecule	Homo sapiens	28-31
33092620-9	2020	Our data identify S1PR1 antagonists as potential therapeutics to mitigate opioid-induced dependence and support repurposing the S1PR1 functional antagonist FTY720, which is FDA-approved for multiple sclerosis, as an opioid adjunct.	Fingolimod Hydrochloride	156-162	sphingosine-1-phosphate receptor 1	Mus musculus	18-23
33293462-5	2020	Deletion of Trpm7 and inhibition of TRPM7 channel activity by the FDA-approved drug FTY720 increased the sensitivity of T cells to the cytokine interleukin-2 (IL-2) through a positive feed-forward loop involving increased expression of the IL-2 receptor alpha-subunit and activation of the transcriptional regulator STAT5.	Fingolimod Hydrochloride	84-90	transient receptor potential cation channel, subfamily M, member 7	Mus musculus	36-41
33293462-5	2020	Deletion of Trpm7 and inhibition of TRPM7 channel activity by the FDA-approved drug FTY720 increased the sensitivity of T cells to the cytokine interleukin-2 (IL-2) through a positive feed-forward loop involving increased expression of the IL-2 receptor alpha-subunit and activation of the transcriptional regulator STAT5.	Fingolimod Hydrochloride	84-90	interleukin 2	Mus musculus	144-157
33293462-5	2020	Deletion of Trpm7 and inhibition of TRPM7 channel activity by the FDA-approved drug FTY720 increased the sensitivity of T cells to the cytokine interleukin-2 (IL-2) through a positive feed-forward loop involving increased expression of the IL-2 receptor alpha-subunit and activation of the transcriptional regulator STAT5.	Fingolimod Hydrochloride	84-90	interleukin 2	Mus musculus	159-163
33293462-5	2020	Deletion of Trpm7 and inhibition of TRPM7 channel activity by the FDA-approved drug FTY720 increased the sensitivity of T cells to the cytokine interleukin-2 (IL-2) through a positive feed-forward loop involving increased expression of the IL-2 receptor alpha-subunit and activation of the transcriptional regulator STAT5.	Fingolimod Hydrochloride	84-90	signal transducer and activator of transcription 5A	Mus musculus	316-321
33272956-0	2021	Combination of teriflunomide and interferon as follow-up therapy after fingolimod-associated PML.	Fingolimod Hydrochloride	71-81	PML nuclear body scaffold	Homo sapiens	93-96
33035646-4	2020	Here we present a structural rationale, based on homology modelling and ligand docking, to account for the capacity of SK2, but not SK1, to efficiently process the pharmacologically active substances, fingolimod (FTY720) and safingol, as substrates.	Fingolimod Hydrochloride	201-211	potassium calcium-activated channel subfamily N member 2	Homo sapiens	119-122
33035646-4	2020	Here we present a structural rationale, based on homology modelling and ligand docking, to account for the capacity of SK2, but not SK1, to efficiently process the pharmacologically active substances, fingolimod (FTY720) and safingol, as substrates.	Fingolimod Hydrochloride	213-219	potassium calcium-activated channel subfamily N member 2	Homo sapiens	119-122
33035646-6	2020	Our analysis accounts for the contrasting behaviour of fingolimod and safingol as non-turnover inhibitors of SK1, but substrates for SK2, and the observed stereoselectivity for phosphorylation of the pro-S hydroxymethyl group of fingolimod to generate (S)-FTY720-P in vivo.	Fingolimod Hydrochloride	55-65	sphingosine kinase 1	Homo sapiens	109-112
33035646-7	2020	We also rationalise why methylation of the pro-R hydroxymethyl of FTY720 switches the behaviour of the resulting compound, (R)-FTY720 methyl ether (ROMe), to SK2-selective inhibition.	Fingolimod Hydrochloride	66-72	potassium calcium-activated channel subfamily N member 2	Homo sapiens	158-161
33255764-8	2020	Immunohistochemical analysis with markers of microgliosis (ionized calcium-binding adapter molecule 1; Iba1) and astrogliosis (glial fibrillary acid protein; GFAP) revealed that our fingolimod treatment regime strongly down regulated neuroinflammation in the hippocampus and neocortex of this AD model.	Fingolimod Hydrochloride	182-192	allograft inflammatory factor 1	Mus musculus	59-101
33255764-8	2020	Immunohistochemical analysis with markers of microgliosis (ionized calcium-binding adapter molecule 1; Iba1) and astrogliosis (glial fibrillary acid protein; GFAP) revealed that our fingolimod treatment regime strongly down regulated neuroinflammation in the hippocampus and neocortex of this AD model.	Fingolimod Hydrochloride	182-192	induction of brown adipocytes 1	Mus musculus	103-107
33255764-10	2020	Our results suggest that fingolimod, when applied after onset of disease symptoms in an APP/PS1 mouse model, rescues synaptic pathology that is believed to underlie memory deficits in AD mice, and that this beneficial effect is mediated via anti-neuroinflammatory actions of the drug on microglia and astrocytes.	Fingolimod Hydrochloride	25-35	presenilin 1	Mus musculus	92-95
33189062-0	2020	Correlation between IL-31 and sCD40L plasma levels in Fingolimod-treated patients with Relapsing-Remitting Multiple Sclerosis (RRMS).	Fingolimod Hydrochloride	54-64	interleukin 31	Homo sapiens	20-25
33189062-3	2020	In this longitudinal study, we aim to quantify the concentration of plasma cytokines of MS patients treated with Fingolimod alone or after Glatiramer Acetate (GA) or Interferon-beta (IFN-beta), in order to compeer both treatments and describes if it is possible to use them as biomarkers.	Fingolimod Hydrochloride	113-123	interferon beta 1	Homo sapiens	166-181
33189062-3	2020	In this longitudinal study, we aim to quantify the concentration of plasma cytokines of MS patients treated with Fingolimod alone or after Glatiramer Acetate (GA) or Interferon-beta (IFN-beta), in order to compeer both treatments and describes if it is possible to use them as biomarkers.	Fingolimod Hydrochloride	113-123	IFN1@	Homo sapiens	183-191
33189062-10	2020	However, the treatment with GA or IFN-beta on Group 1 showed a tendency to increase the number of relapses after 6 months of follow-up, which decrease when the therapy was changed to Fingolimod.	Fingolimod Hydrochloride	183-193	IFN1@	Homo sapiens	34-42
33189062-12	2020	CONCLUSIONS: Our study describes the existence of two promising plasmatic biomarkers (IL-31 and sCD40L), which reduced plasmatic levels in RRMS patients followed the treatment time of Fingolimod, despite that more studies are needed to prove their efficiency.	Fingolimod Hydrochloride	184-194	interleukin 31	Homo sapiens	86-91
33069748-5	2020	Results revealed that PP2A activity was significantly diminished in inflamed cells but the surprising observation was the cell viability of only 35.99% upon FTY720 treatment in inflamed cells lacking basal PP2A activity.	Fingolimod Hydrochloride	157-163	protein phosphatase 2 phosphatase activator	Homo sapiens	206-210
33207629-7	2020	Interestingly, cathepsin inhibitors (E64D and pepstatin A) and ectopic expression of heat shock protein 70 (HSP70), which is an endogenous inhibitor of LMP, markedly inhibited FTY720-induced cell death.	Fingolimod Hydrochloride	176-182	heat shock protein family A (Hsp70) member 4	Homo sapiens	85-106
33207629-7	2020	Interestingly, cathepsin inhibitors (E64D and pepstatin A) and ectopic expression of heat shock protein 70 (HSP70), which is an endogenous inhibitor of LMP, markedly inhibited FTY720-induced cell death.	Fingolimod Hydrochloride	176-182	heat shock protein family A (Hsp70) member 4	Homo sapiens	108-113
32871475-0	2020	A new lipophilic amino alcohol, chemically similar to compound FTY720, attenuates the pathogenesis of experimental autoimmune encephalomyelitis by PI3K/Akt pathway inhibition.	Fingolimod Hydrochloride	63-69	thymoma viral proto-oncogene 1	Mus musculus	152-155
33092620-9	2020	Our data identify S1PR1 antagonists as potential therapeutics to mitigate opioid-induced dependence and support repurposing the S1PR1 functional antagonist FTY720, which is FDA-approved for multiple sclerosis, as an opioid adjunct.	Fingolimod Hydrochloride	156-162	sphingosine-1-phosphate receptor 1	Mus musculus	128-133
32745802-2	2020	Fingolimod reduced the CD56bright NK cell subset.	Fingolimod Hydrochloride	0-10	neural cell adhesion molecule 1	Homo sapiens	23-27
32745802-5	2020	Molecular signature of the CD56dim NK cells from fingolimod-treated MS patients was closely associated to those from healthy subjects.	Fingolimod Hydrochloride	49-59	neural cell adhesion molecule 1	Homo sapiens	27-31
32848587-7	2020	Results: Fingolimod treatment reduced the number of infiltrated inflammatory cells and lowered the mRNA level of Tnfalpha.	Fingolimod Hydrochloride	9-19	tumor necrosis factor	Mus musculus	113-121
33010954-5	2020	Functional sphingosine-1-phosphate (S1P) receptor 1 (S1PR1) antagonists, such as FTY720/fingolimod, used clinically for non-pain conditions, are emerging as non-narcotic analgesics, supporting the repurposing of fingolimod for chronic pain treatment and energizing drug discovery focused on S1P signaling.	Fingolimod Hydrochloride	81-87	sphingosine-1-phosphate receptor 1	Homo sapiens	36-51
33010954-5	2020	Functional sphingosine-1-phosphate (S1P) receptor 1 (S1PR1) antagonists, such as FTY720/fingolimod, used clinically for non-pain conditions, are emerging as non-narcotic analgesics, supporting the repurposing of fingolimod for chronic pain treatment and energizing drug discovery focused on S1P signaling.	Fingolimod Hydrochloride	81-87	sphingosine-1-phosphate receptor 1	Homo sapiens	53-58
33010954-5	2020	Functional sphingosine-1-phosphate (S1P) receptor 1 (S1PR1) antagonists, such as FTY720/fingolimod, used clinically for non-pain conditions, are emerging as non-narcotic analgesics, supporting the repurposing of fingolimod for chronic pain treatment and energizing drug discovery focused on S1P signaling.	Fingolimod Hydrochloride	88-98	sphingosine-1-phosphate receptor 1	Homo sapiens	36-51
33010954-5	2020	Functional sphingosine-1-phosphate (S1P) receptor 1 (S1PR1) antagonists, such as FTY720/fingolimod, used clinically for non-pain conditions, are emerging as non-narcotic analgesics, supporting the repurposing of fingolimod for chronic pain treatment and energizing drug discovery focused on S1P signaling.	Fingolimod Hydrochloride	88-98	sphingosine-1-phosphate receptor 1	Homo sapiens	53-58
33010954-5	2020	Functional sphingosine-1-phosphate (S1P) receptor 1 (S1PR1) antagonists, such as FTY720/fingolimod, used clinically for non-pain conditions, are emerging as non-narcotic analgesics, supporting the repurposing of fingolimod for chronic pain treatment and energizing drug discovery focused on S1P signaling.	Fingolimod Hydrochloride	212-222	sphingosine-1-phosphate receptor 1	Homo sapiens	36-51
33010954-5	2020	Functional sphingosine-1-phosphate (S1P) receptor 1 (S1PR1) antagonists, such as FTY720/fingolimod, used clinically for non-pain conditions, are emerging as non-narcotic analgesics, supporting the repurposing of fingolimod for chronic pain treatment and energizing drug discovery focused on S1P signaling.	Fingolimod Hydrochloride	212-222	sphingosine-1-phosphate receptor 1	Homo sapiens	53-58
32673690-13	2020	ELISA kit results showed that fingolimod could down-regulate IL-6 and TNF-alpha and up-regulate IL-10 and TGF-beta1 in serum.	Fingolimod Hydrochloride	30-40	interleukin 6	Mus musculus	61-65
32673690-13	2020	ELISA kit results showed that fingolimod could down-regulate IL-6 and TNF-alpha and up-regulate IL-10 and TGF-beta1 in serum.	Fingolimod Hydrochloride	30-40	tumor necrosis factor	Mus musculus	70-79
32673690-13	2020	ELISA kit results showed that fingolimod could down-regulate IL-6 and TNF-alpha and up-regulate IL-10 and TGF-beta1 in serum.	Fingolimod Hydrochloride	30-40	interleukin 10	Mus musculus	96-101
32673690-13	2020	ELISA kit results showed that fingolimod could down-regulate IL-6 and TNF-alpha and up-regulate IL-10 and TGF-beta1 in serum.	Fingolimod Hydrochloride	30-40	transforming growth factor, beta 1	Mus musculus	106-115
32899717-0	2020	Morpholino Analogues of Fingolimod as Novel and Selective S1P1 Ligands with In Vivo Efficacy in a Mouse Model of Experimental Antigen-Induced Encephalomyelitis.	Fingolimod Hydrochloride	24-34	sphingosine-1-phosphate receptor 1	Mus musculus	58-62
32899717-3	2020	A new therapeutic paradigm for the treatment of MS was introduced in 2010 through the sphingosine 1-phosphate (S1P) analogue fingolimod (FTY720, Gilenya ), which acts as a functional S1P1 antagonist on T lymphocytes to deplete these cells from the blood.	Fingolimod Hydrochloride	125-135	sphingosine-1-phosphate receptor 1	Mus musculus	183-187
32899717-3	2020	A new therapeutic paradigm for the treatment of MS was introduced in 2010 through the sphingosine 1-phosphate (S1P) analogue fingolimod (FTY720, Gilenya ), which acts as a functional S1P1 antagonist on T lymphocytes to deplete these cells from the blood.	Fingolimod Hydrochloride	137-143	sphingosine-1-phosphate receptor 1	Mus musculus	183-187
32696271-6	2020	Fingolimod has shown neuroprotective effects in different animal models of neurodegenerative diseases, summarized here, correlating with increased brain-derived neurotrophic factor and improved disease phenotype (cognition and/or motor abilities).	Fingolimod Hydrochloride	0-10	brain derived neurotrophic factor	Homo sapiens	147-180
32696271-8	2020	Furthermore, fingolimod treatment exhibited additional effects for specific neurodegenerative disorders, such as reduction of amyloid-beta production, and antiepileptogenic properties.	Fingolimod Hydrochloride	13-23	amyloid beta precursor protein	Homo sapiens	126-138
32301840-9	2020	Our data support investigating S1PR1 antagonists as a clinical approach to mitigate opioid-induced adverse effects and repurposing the functional S1PR1 antagonist FTY720, which is FDA-approved for multiple sclerosis, as an opioid adjunct.	Fingolimod Hydrochloride	163-169	sphingosine-1-phosphate receptor 1	Mus musculus	146-151
32848587-9	2020	However, fingolimod significantly aggravated brain edema and reduced the expression levels of tight junction proteins ZO-1 and Occludin.	Fingolimod Hydrochloride	9-19	tight junction protein 1	Mus musculus	118-122
32848587-9	2020	However, fingolimod significantly aggravated brain edema and reduced the expression levels of tight junction proteins ZO-1 and Occludin.	Fingolimod Hydrochloride	9-19	occludin	Mus musculus	127-135
32402923-7	2020	Administration of FTY720, an inhibitory agonist of sphingosine 1-phosphate receptor 1 that stabilizes TJ permeability, increased the myeloid cell proportion in milk.	Fingolimod Hydrochloride	18-24	sphingosine-1-phosphate receptor 1	Mus musculus	51-85
32618344-0	2020	Retraction: Fingolimod inhibits proliferation and epithelial- mesenchymal transition in sacral chordoma by inactivating IL-6/STAT3 signaling.	Fingolimod Hydrochloride	12-22	interleukin 6	Homo sapiens	120-124
32618344-0	2020	Retraction: Fingolimod inhibits proliferation and epithelial- mesenchymal transition in sacral chordoma by inactivating IL-6/STAT3 signaling.	Fingolimod Hydrochloride	12-22	signal transducer and activator of transcription 3	Homo sapiens	125-130
32646493-0	2020	Two susceptible HLA-DRB1 alleles for multiple sclerosis differentially regulate anti-JC virus antibody serostatus along with fingolimod.	Fingolimod Hydrochloride	125-135	major histocompatibility complex, class II, DR beta 1	Homo sapiens	16-24
32646493-3	2020	The strongest susceptibility human leukocyte antigen (HLA) class II alleles for MS are distinct between races (DRB1*15:01 for Caucasians and DRB1*04:05 and DRB1*15:01 for Japanese); therefore, we investigated whether HLA class II alleles modulate anti-JCV antibody serostatus in Japanese MS patients with and without fingolimod.	Fingolimod Hydrochloride	317-327	major histocompatibility complex, class II, DR beta 1	Homo sapiens	54-57
32646493-3	2020	The strongest susceptibility human leukocyte antigen (HLA) class II alleles for MS are distinct between races (DRB1*15:01 for Caucasians and DRB1*04:05 and DRB1*15:01 for Japanese); therefore, we investigated whether HLA class II alleles modulate anti-JCV antibody serostatus in Japanese MS patients with and without fingolimod.	Fingolimod Hydrochloride	317-327	major histocompatibility complex, class II, DR beta 1	Homo sapiens	111-115
32579203-0	2020	Expression of Concern: Fingolimod inhibits proliferation and epithelial-mesenchymal transition in sacral chordoma by inactivating IL-6/STAT3 signaling.	Fingolimod Hydrochloride	23-33	interleukin 6	Homo sapiens	130-134
32579203-0	2020	Expression of Concern: Fingolimod inhibits proliferation and epithelial-mesenchymal transition in sacral chordoma by inactivating IL-6/STAT3 signaling.	Fingolimod Hydrochloride	23-33	signal transducer and activator of transcription 3	Homo sapiens	135-140
32670281-2	2020	Sphingosine 1-phosphate (S1P) modulates immunity through binding to its receptors (S1P1-5), and protection from kidney IRI occurs in mice treated with S1PR agonist, FTY720 (FTY).	Fingolimod Hydrochloride	165-171	sphingosine-1-phosphate receptor 1	Mus musculus	83-89
32670281-2	2020	Sphingosine 1-phosphate (S1P) modulates immunity through binding to its receptors (S1P1-5), and protection from kidney IRI occurs in mice treated with S1PR agonist, FTY720 (FTY).	Fingolimod Hydrochloride	165-171	sphingosine-1-phosphate receptor 1	Mus musculus	151-155
32457139-8	2020	Treatment with natalizumab and fingolimod showed different compartmental changes in protein levels of CSF and peripheral blood, respectively, including many disease-associated markers (e.g., IL12B, CD5) showing potential application for both diagnosing disease and monitoring treatment efficacy.	Fingolimod Hydrochloride	31-41	interleukin 12B	Homo sapiens	191-196
32655793-8	2020	Moreover, fingolimod suppressed the secretion of pro-inflammatory or inflammatory cytokines IL-17A, IL-6, and INF-gamma, but did not noticeably alter the secretion of immunosuppressive cytokines TGF-beta1 and IL-4.	Fingolimod Hydrochloride	10-20	interleukin 17A	Homo sapiens	92-98
32655793-8	2020	Moreover, fingolimod suppressed the secretion of pro-inflammatory or inflammatory cytokines IL-17A, IL-6, and INF-gamma, but did not noticeably alter the secretion of immunosuppressive cytokines TGF-beta1 and IL-4.	Fingolimod Hydrochloride	10-20	interleukin 6	Homo sapiens	100-104
32714497-0	2020	Effects of fingolimod treatments on alanine transaminase and aspartate transaminase levels in patients with multiple sclerosis.	Fingolimod Hydrochloride	11-21	solute carrier family 17 member 5	Homo sapiens	61-83
32714497-19	2020	In addition, previous studies have cited a return to normal ALT and AST levels after cessation of fingolimod, suggesting its effects are temporary and not severely damaged in the usual patient.	Fingolimod Hydrochloride	98-108	solute carrier family 17 member 5	Homo sapiens	68-71
32457139-8	2020	Treatment with natalizumab and fingolimod showed different compartmental changes in protein levels of CSF and peripheral blood, respectively, including many disease-associated markers (e.g., IL12B, CD5) showing potential application for both diagnosing disease and monitoring treatment efficacy.	Fingolimod Hydrochloride	31-41	CD5 molecule	Homo sapiens	198-201
32404429-8	2020	Patients with insufficient control of clinical or MRI disease activity under treatment with interferon beta-1a/b or glatiramer acetate who switched to fingolimod (n = 18) showed a reduction of sNfL levels from 16.5 to 10.0 pg/mL 6 +- 2 months after switch (CI [0.481, 0.701], p < 0.001).	Fingolimod Hydrochloride	151-161	serpin family A member 1	Homo sapiens	103-112
32356173-8	2020	Fingolimod (FTY720), a modulator of sphingosine-1-phosphate receptors countered the AbetaPP-dependent upregulation of hippocampal ceramide synthase CERS2 at 3 months.	Fingolimod Hydrochloride	0-10	ceramide synthase 2	Homo sapiens	148-153
32356173-8	2020	Fingolimod (FTY720), a modulator of sphingosine-1-phosphate receptors countered the AbetaPP-dependent upregulation of hippocampal ceramide synthase CERS2 at 3 months.	Fingolimod Hydrochloride	12-18	ceramide synthase 2	Homo sapiens	148-153
32356173-11	2020	FTY720 counteracted the AbetaPP-linked reduction of sphingomyelin synthases SGMS1/2 (at 12 and 6 months, respectively) and led to elevation of sphingomyelinase SMPD2 (at 6 and 12 months).	Fingolimod Hydrochloride	0-6	sphingomyelin synthase 1	Homo sapiens	76-83
32356173-11	2020	FTY720 counteracted the AbetaPP-linked reduction of sphingomyelin synthases SGMS1/2 (at 12 and 6 months, respectively) and led to elevation of sphingomyelinase SMPD2 (at 6 and 12 months).	Fingolimod Hydrochloride	0-6	sphingomyelin phosphodiesterase 2	Homo sapiens	160-165
32122996-10	2020	Fingolimod (FTY720) treatment of Y. enterocolitica-infected mice reduced the CD11b- subset of migratory DCs in RLN of TNFRp55-/- mice and significantly suppressed the severity of ReA in these mice.	Fingolimod Hydrochloride	0-10	integrin alpha M	Mus musculus	77-82
32414131-6	2020	The number of CD56bright NK cells increases upon treatment with interferon-beta, alemtuzumab, dimethyl fumarate, after autologous hematopoietic stem cell transplantation, and is higher in those who respond to fingolimod.	Fingolimod Hydrochloride	209-219	neural cell adhesion molecule 1	Homo sapiens	14-18
32414131-6	2020	The number of CD56bright NK cells increases upon treatment with interferon-beta, alemtuzumab, dimethyl fumarate, after autologous hematopoietic stem cell transplantation, and is higher in those who respond to fingolimod.	Fingolimod Hydrochloride	209-219	interferon beta 1	Homo sapiens	64-79
32132224-7	2020	Fingolimod reduced the annualised rate of formation of new/newly enlarging T2 lesions (52.6%, p<0.001), number of Gd+ T1 lesions per scan (66.0%, p<0.001), annualised rate of new T1 hypointense lesions (62.8%, p<0.001) and CUA lesions per scan (60.7%, p<0.001) versus IFN beta-1a at EOS.	Fingolimod Hydrochloride	0-10	transmembrane protein 165	Homo sapiens	114-120
32132224-7	2020	Fingolimod reduced the annualised rate of formation of new/newly enlarging T2 lesions (52.6%, p<0.001), number of Gd+ T1 lesions per scan (66.0%, p<0.001), annualised rate of new T1 hypointense lesions (62.8%, p<0.001) and CUA lesions per scan (60.7%, p<0.001) versus IFN beta-1a at EOS.	Fingolimod Hydrochloride	0-10	IFN1@	Homo sapiens	268-276
32349283-0	2020	Fingolimod Modulates Dendritic Architecture in a BDNF-Dependent Manner.	Fingolimod Hydrochloride	0-10	brain derived neurotrophic factor	Mus musculus	49-53
32349283-3	2020	Among the different therapeutic strategies developed to improve endogenous BDNF levels is the administration of the BDNF-inducing drug Fingolimod, an agonist of the sphingosine-1-phosphate receptor.	Fingolimod Hydrochloride	135-145	brain derived neurotrophic factor	Mus musculus	75-79
32349283-3	2020	Among the different therapeutic strategies developed to improve endogenous BDNF levels is the administration of the BDNF-inducing drug Fingolimod, an agonist of the sphingosine-1-phosphate receptor.	Fingolimod Hydrochloride	135-145	brain derived neurotrophic factor	Mus musculus	116-120
32349283-5	2020	However, the cellular mechanisms through which Fingolimod mediates its BDNF-dependent therapeutic effects remain unclear.	Fingolimod Hydrochloride	47-57	brain derived neurotrophic factor	Mus musculus	71-75
32349283-7	2020	Moreover, the application of Fingolimod upregulates the expression of activity-related proteins c-Fos and pERK1/2 in these cells.	Fingolimod Hydrochloride	29-39	FBJ osteosarcoma oncogene	Mus musculus	96-101
32349283-8	2020	Importantly, we show that BDNF release is required for these actions of Fingolimod.	Fingolimod Hydrochloride	72-82	brain derived neurotrophic factor	Mus musculus	26-30
32349283-11	2020	Our study provides insights into understanding the BDNF-dependent therapeutic actions of Fingolimod.	Fingolimod Hydrochloride	89-99	brain derived neurotrophic factor	Mus musculus	51-55
32331328-4	2020	Then, we analyzed proliferation, migration and VEGF-A expression in three melanoma cell lines and found out that both natalizumab and fingolimod inhibited tumor cell proliferation but promoted or blocked cell migration depending on the cell line examined.	Fingolimod Hydrochloride	134-144	vascular endothelial growth factor A	Homo sapiens	47-53
32331328-5	2020	VEGF-A secretion was augmented in one melanoma cell line only after fingolimod treatment.	Fingolimod Hydrochloride	68-78	vascular endothelial growth factor A	Homo sapiens	0-6
32127495-4	2020	Twitcher mice, both male and female, carrying a natural mutation in the galc gene were given fingolimod via drinking water (1 mg/kg/d).	Fingolimod Hydrochloride	93-103	galactosylceramidase	Mus musculus	72-76
32122996-10	2020	Fingolimod (FTY720) treatment of Y. enterocolitica-infected mice reduced the CD11b- subset of migratory DCs in RLN of TNFRp55-/- mice and significantly suppressed the severity of ReA in these mice.	Fingolimod Hydrochloride	0-10	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	118-125
32122996-10	2020	Fingolimod (FTY720) treatment of Y. enterocolitica-infected mice reduced the CD11b- subset of migratory DCs in RLN of TNFRp55-/- mice and significantly suppressed the severity of ReA in these mice.	Fingolimod Hydrochloride	12-18	integrin alpha M	Mus musculus	77-82
32122996-10	2020	Fingolimod (FTY720) treatment of Y. enterocolitica-infected mice reduced the CD11b- subset of migratory DCs in RLN of TNFRp55-/- mice and significantly suppressed the severity of ReA in these mice.	Fingolimod Hydrochloride	12-18	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	118-125
32034063-2	2020	It is well established that fingolimod, a modulator of the sphingosine-1-phosphate pathway, restrains the egress of CCR7+ lymphocytes from lymphatic tissues into the blood, thus resulting in reduced lymphocyte counts in peripheral blood.	Fingolimod Hydrochloride	28-38	C-C motif chemokine receptor 7	Homo sapiens	116-120
31751571-6	2020	Our prior studies using the parent compound FTY720, a food and drug administration (FDA) approved immunosuppressive for multiple sclerosis, reveal that FTY720 protects parkinsonian mice by increasing BDNF.	Fingolimod Hydrochloride	44-50	brain derived neurotrophic factor	Mus musculus	200-204
32034063-7	2020	The circulating T follicular regulatory cell subset and CXCR5+ CD8+ T cell frequencies were also strongly and disproportionally decreased after fingolimod treatment.	Fingolimod Hydrochloride	144-154	C-X-C motif chemokine receptor 5	Homo sapiens	56-61
32034063-7	2020	The circulating T follicular regulatory cell subset and CXCR5+ CD8+ T cell frequencies were also strongly and disproportionally decreased after fingolimod treatment.	Fingolimod Hydrochloride	144-154	CD8a molecule	Homo sapiens	63-66
32104183-9	2020	FTY720 (a MITF inhibitor), RP67580 (NK1R inhibitor), or both inhibited the migration and proliferation of c-Kit+ cells increased by SP and blocked the upregulation of c-Kit, GATA4, and MITF.	Fingolimod Hydrochloride	0-6	melanocyte inducing transcription factor	Rattus norvegicus	10-14
32104183-9	2020	FTY720 (a MITF inhibitor), RP67580 (NK1R inhibitor), or both inhibited the migration and proliferation of c-Kit+ cells increased by SP and blocked the upregulation of c-Kit, GATA4, and MITF.	Fingolimod Hydrochloride	0-6	GATA binding protein 4	Rattus norvegicus	174-179
32104183-9	2020	FTY720 (a MITF inhibitor), RP67580 (NK1R inhibitor), or both inhibited the migration and proliferation of c-Kit+ cells increased by SP and blocked the upregulation of c-Kit, GATA4, and MITF.	Fingolimod Hydrochloride	0-6	melanocyte inducing transcription factor	Rattus norvegicus	185-189
31069623-0	2019	FTY720 Inhibits MPP+-Induced Microglial Activation by Affecting NLRP3 Inflammasome Activation.	Fingolimod Hydrochloride	0-6	NLR family, pyrin domain containing 3	Mus musculus	64-69
31708456-3	2020	The pro-drug FTY720 (fingolimod, Gilenya) used to treat multiple sclerosis is phosphorylated in the body to a S1P mimic that binds to S1PRs, except S1PR2, and also acts as a functional antagonist of S1PR1.	Fingolimod Hydrochloride	13-19	sphingosine-1-phosphate receptor 2	Mus musculus	148-153
31708456-3	2020	The pro-drug FTY720 (fingolimod, Gilenya) used to treat multiple sclerosis is phosphorylated in the body to a S1P mimic that binds to S1PRs, except S1PR2, and also acts as a functional antagonist of S1PR1.	Fingolimod Hydrochloride	13-19	sphingosine-1-phosphate receptor 1	Mus musculus	199-204
31708456-3	2020	The pro-drug FTY720 (fingolimod, Gilenya) used to treat multiple sclerosis is phosphorylated in the body to a S1P mimic that binds to S1PRs, except S1PR2, and also acts as a functional antagonist of S1PR1.	Fingolimod Hydrochloride	21-31	sphingosine-1-phosphate receptor 2	Mus musculus	148-153
31708456-3	2020	The pro-drug FTY720 (fingolimod, Gilenya) used to treat multiple sclerosis is phosphorylated in the body to a S1P mimic that binds to S1PRs, except S1PR2, and also acts as a functional antagonist of S1PR1.	Fingolimod Hydrochloride	21-31	sphingosine-1-phosphate receptor 1	Mus musculus	199-204
31593801-5	2020	The PP2A activating drug FTY720 has potent anti-leukemic effects; nevertheless, FTY720 induces cardiotoxicity at the anti-neoplastic dose.	Fingolimod Hydrochloride	25-31	protein phosphatase 2 phosphatase activator	Homo sapiens	4-8
31593801-5	2020	The PP2A activating drug FTY720 has potent anti-leukemic effects; nevertheless, FTY720 induces cardiotoxicity at the anti-neoplastic dose.	Fingolimod Hydrochloride	80-86	protein phosphatase 2 phosphatase activator	Homo sapiens	4-8
32310049-8	2020	Emerging experimental findings suggest that Fingolimod treatment exerts disease- modifying anti-epileptic effects based on its anti-neuroinflammatory properties, potent neuroprotection, anti-gliotic effects, myelin protection, reduction of mTOR signaling pathway and activation of microglia and astrocytes.	Fingolimod Hydrochloride	44-54	mechanistic target of rapamycin kinase	Homo sapiens	240-244
31467033-1	2020	BACKGROUND: In PARADIGMS, a double-blind phase III trial in 215 paediatric patients with multiple sclerosis (MS) (10 to <18 years), fingolimod administered for up to 2 years significantly reduced the annualised relapse rate (ARR) and rate of new/newly enlarged T2 (n/neT2) lesions compared with interferon (IFN) beta-1a.	Fingolimod Hydrochloride	132-142	tetraspanin 12	Homo sapiens	267-271
31467033-5	2020	RESULTS: In the treatment-naive subpopulation, fingolimod reduced ARR and n/neT2 lesions by 85.8% and 53.4%, respectively versus INF beta-1a (both p<0.001), compared with 81.9% and 52.6% in the overall population.	Fingolimod Hydrochloride	47-57	tetraspanin 12	Homo sapiens	76-80
32259820-5	2020	However, Fingolimod, an S1P1 inhibitor, could reverse these Floralozone effects in experimental atherosclerotic rats.	Fingolimod Hydrochloride	9-19	sphingosine-1-phosphate receptor 1	Rattus norvegicus	24-28
31526917-1	2019	Fingolimod inhibits the egress of lymphocytes from lymphatic tissues and also directly affects their functions by modulation of the sphingosine-1-phosphate receptor 1 (S1P1).	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Homo sapiens	132-166
31526917-1	2019	Fingolimod inhibits the egress of lymphocytes from lymphatic tissues and also directly affects their functions by modulation of the sphingosine-1-phosphate receptor 1 (S1P1).	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Homo sapiens	168-172
31526917-5	2019	CCL2 (p = 0.039), and CCL5 (p = 0.001) levels were significantly higher in fingolimod-treated patients than healthy controls, whereas end-of-study serum levels of IL-6, IL-8, IL-17A, IL-22, IL-23, TNF-alpha, CXCL10, and CXCL13 were comparable to the baseline levels.	Fingolimod Hydrochloride	75-85	C-C motif chemokine ligand 2	Homo sapiens	0-4
31526917-5	2019	CCL2 (p = 0.039), and CCL5 (p = 0.001) levels were significantly higher in fingolimod-treated patients than healthy controls, whereas end-of-study serum levels of IL-6, IL-8, IL-17A, IL-22, IL-23, TNF-alpha, CXCL10, and CXCL13 were comparable to the baseline levels.	Fingolimod Hydrochloride	75-85	C-C motif chemokine ligand 5	Homo sapiens	22-26
31526917-5	2019	CCL2 (p = 0.039), and CCL5 (p = 0.001) levels were significantly higher in fingolimod-treated patients than healthy controls, whereas end-of-study serum levels of IL-6, IL-8, IL-17A, IL-22, IL-23, TNF-alpha, CXCL10, and CXCL13 were comparable to the baseline levels.	Fingolimod Hydrochloride	75-85	interleukin 6	Homo sapiens	163-167
31526917-5	2019	CCL2 (p = 0.039), and CCL5 (p = 0.001) levels were significantly higher in fingolimod-treated patients than healthy controls, whereas end-of-study serum levels of IL-6, IL-8, IL-17A, IL-22, IL-23, TNF-alpha, CXCL10, and CXCL13 were comparable to the baseline levels.	Fingolimod Hydrochloride	75-85	C-X-C motif chemokine ligand 8	Homo sapiens	169-173
31526917-5	2019	CCL2 (p = 0.039), and CCL5 (p = 0.001) levels were significantly higher in fingolimod-treated patients than healthy controls, whereas end-of-study serum levels of IL-6, IL-8, IL-17A, IL-22, IL-23, TNF-alpha, CXCL10, and CXCL13 were comparable to the baseline levels.	Fingolimod Hydrochloride	75-85	interleukin 22	Homo sapiens	183-188
31526917-5	2019	CCL2 (p = 0.039), and CCL5 (p = 0.001) levels were significantly higher in fingolimod-treated patients than healthy controls, whereas end-of-study serum levels of IL-6, IL-8, IL-17A, IL-22, IL-23, TNF-alpha, CXCL10, and CXCL13 were comparable to the baseline levels.	Fingolimod Hydrochloride	75-85	interleukin 23 subunit alpha	Homo sapiens	190-195
31526917-5	2019	CCL2 (p = 0.039), and CCL5 (p = 0.001) levels were significantly higher in fingolimod-treated patients than healthy controls, whereas end-of-study serum levels of IL-6, IL-8, IL-17A, IL-22, IL-23, TNF-alpha, CXCL10, and CXCL13 were comparable to the baseline levels.	Fingolimod Hydrochloride	75-85	tumor necrosis factor	Homo sapiens	197-206
31526917-5	2019	CCL2 (p = 0.039), and CCL5 (p = 0.001) levels were significantly higher in fingolimod-treated patients than healthy controls, whereas end-of-study serum levels of IL-6, IL-8, IL-17A, IL-22, IL-23, TNF-alpha, CXCL10, and CXCL13 were comparable to the baseline levels.	Fingolimod Hydrochloride	75-85	C-X-C motif chemokine ligand 10	Homo sapiens	208-214
31526917-5	2019	CCL2 (p = 0.039), and CCL5 (p = 0.001) levels were significantly higher in fingolimod-treated patients than healthy controls, whereas end-of-study serum levels of IL-6, IL-8, IL-17A, IL-22, IL-23, TNF-alpha, CXCL10, and CXCL13 were comparable to the baseline levels.	Fingolimod Hydrochloride	75-85	C-X-C motif chemokine ligand 13	Homo sapiens	220-226
31597715-7	2019	Lymphocyte sequestration with sphingosine-1-phosphate receptor 1 antagonist FTY720 specifically inhibited anti-MHC class II antibody production and abrogated macrophage infiltration into glomeruli.	Fingolimod Hydrochloride	76-82	sphingosine-1-phosphate receptor 1	Mus musculus	30-64
31228713-0	2019	Fingolimod reduces CXCR4-mediated B cell migration and induces regulatory B cells-mediated anti-inflammatory immune repertoire.	Fingolimod Hydrochloride	0-10	C-X-C motif chemokine receptor 4	Homo sapiens	19-24
31228713-1	2019	BACKGROUND: Fingolimod, an oral therapy for patients with relapsing Multiple Sclerosis (MS), traps CC chemokine receptor type 7 (CCR7)-expresssing lymphocytes within lymphoid tissues in the periphery, thereby supposedly reducing the infiltration of pathogenic cells into the central nervous system.	Fingolimod Hydrochloride	12-22	C-C motif chemokine receptor 7	Homo sapiens	99-127
31228713-1	2019	BACKGROUND: Fingolimod, an oral therapy for patients with relapsing Multiple Sclerosis (MS), traps CC chemokine receptor type 7 (CCR7)-expresssing lymphocytes within lymphoid tissues in the periphery, thereby supposedly reducing the infiltration of pathogenic cells into the central nervous system.	Fingolimod Hydrochloride	12-22	C-C motif chemokine receptor 7	Homo sapiens	129-133
31228713-12	2019	Fingolimod therapy reduced CXCR4 expression and B cell migration towards CXCL12.	Fingolimod Hydrochloride	0-10	C-X-C motif chemokine receptor 4	Homo sapiens	27-32
31228713-12	2019	Fingolimod therapy reduced CXCR4 expression and B cell migration towards CXCL12.	Fingolimod Hydrochloride	0-10	C-X-C motif chemokine ligand 12	Homo sapiens	73-79
31228713-14	2019	B cells from Fingolimod-treated patients induced a reduction in pro-inflammatory cytokines in T cells, while increased transforming growth factor beta (TGFbeta)+ B and T cells, and downregulated IL2-secretion from proliferative T cells.	Fingolimod Hydrochloride	13-23	tumor necrosis factor	Homo sapiens	119-150
31228713-14	2019	B cells from Fingolimod-treated patients induced a reduction in pro-inflammatory cytokines in T cells, while increased transforming growth factor beta (TGFbeta)+ B and T cells, and downregulated IL2-secretion from proliferative T cells.	Fingolimod Hydrochloride	13-23	transforming growth factor alpha	Homo sapiens	152-159
31228713-14	2019	B cells from Fingolimod-treated patients induced a reduction in pro-inflammatory cytokines in T cells, while increased transforming growth factor beta (TGFbeta)+ B and T cells, and downregulated IL2-secretion from proliferative T cells.	Fingolimod Hydrochloride	13-23	interleukin 2	Homo sapiens	195-198
31313064-5	2019	Recent in vitro and in vivo evidence indicate that fingolimod may suppress Abeta secretion and deposition, inhibit apoptosis and enhance brain-derived neurotrophic factor (BDNF) production.	Fingolimod Hydrochloride	51-61	amyloid beta precursor protein	Homo sapiens	75-80
31313064-5	2019	Recent in vitro and in vivo evidence indicate that fingolimod may suppress Abeta secretion and deposition, inhibit apoptosis and enhance brain-derived neurotrophic factor (BDNF) production.	Fingolimod Hydrochloride	51-61	brain derived neurotrophic factor	Homo sapiens	137-170
31313064-5	2019	Recent in vitro and in vivo evidence indicate that fingolimod may suppress Abeta secretion and deposition, inhibit apoptosis and enhance brain-derived neurotrophic factor (BDNF) production.	Fingolimod Hydrochloride	51-61	brain derived neurotrophic factor	Homo sapiens	172-176
30843214-0	2019	FTY720 alleviates coxsackievirus B3-induced myocarditis and inhibits viral replication through regulating sphingosine 1-phosphate receptors and AKT/caspase-3 pathways.	Fingolimod Hydrochloride	0-6	AKT serine/threonine kinase 1	Homo sapiens	144-147
30843214-0	2019	FTY720 alleviates coxsackievirus B3-induced myocarditis and inhibits viral replication through regulating sphingosine 1-phosphate receptors and AKT/caspase-3 pathways.	Fingolimod Hydrochloride	0-6	caspase 3	Homo sapiens	148-157
30802544-4	2019	The functional S1PR1 antagonist FTY720 blocked NLRP3 activation and IL-1beta production.	Fingolimod Hydrochloride	32-38	sphingosine-1-phosphate receptor 1	Mus musculus	15-20
30802544-4	2019	The functional S1PR1 antagonist FTY720 blocked NLRP3 activation and IL-1beta production.	Fingolimod Hydrochloride	32-38	NLR family, pyrin domain containing 3	Mus musculus	47-52
30802544-4	2019	The functional S1PR1 antagonist FTY720 blocked NLRP3 activation and IL-1beta production.	Fingolimod Hydrochloride	32-38	interleukin 1 beta	Mus musculus	68-76
31358793-5	2019	At 1 mg/kg/day, fingolimod decreased both peripheral blood lymphocyte counts and brain Abeta levels, but at the lowest dose tested (0.03 mg/kg/day), we detected improved memory, decreased activation of brain microglia and astrocytes, and restored hippocampal levels of GABA and glycerophosphocholine with no effect on circulating lymphocyte counts.	Fingolimod Hydrochloride	16-26	histocompatibility 2, class II antigen A, beta 1	Mus musculus	87-92
31129200-0	2019	FTY720 Improves Behavior, Increases Brain Derived Neurotrophic Factor Levels and Reduces alpha-Synuclein Pathology in Parkinsonian GM2+/- Mice.	Fingolimod Hydrochloride	0-6	brain derived neurotrophic factor	Mus musculus	36-69
31129200-0	2019	FTY720 Improves Behavior, Increases Brain Derived Neurotrophic Factor Levels and Reduces alpha-Synuclein Pathology in Parkinsonian GM2+/- Mice.	Fingolimod Hydrochloride	0-6	synuclein, alpha	Mus musculus	89-104
31129200-0	2019	FTY720 Improves Behavior, Increases Brain Derived Neurotrophic Factor Levels and Reduces alpha-Synuclein Pathology in Parkinsonian GM2+/- Mice.	Fingolimod Hydrochloride	0-6	cytochrome b5 domain containing 2	Mus musculus	131-134
31129200-9	2019	This allowed us to demonstrate improved motor and bladder function in GM2+/- mice treated with FTY720.	Fingolimod Hydrochloride	95-101	cytochrome b5 domain containing 2	Mus musculus	70-73
30623407-3	2019	It was disclosed that FTY-720 significantly stimulates Bcl2 overexpression.	Fingolimod Hydrochloride	22-29	BCL2 apoptosis regulator	Homo sapiens	55-59
30623407-6	2019	Besides, FTY-720 induced the overexpression of CACNA1C, nNOS gene, and nitric oxide production.	Fingolimod Hydrochloride	9-16	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	47-54
30623407-6	2019	Besides, FTY-720 induced the overexpression of CACNA1C, nNOS gene, and nitric oxide production.	Fingolimod Hydrochloride	9-16	nitric oxide synthase 1	Homo sapiens	56-60
31861585-0	2019	In Silico and In Vivo Analysis of IL37 in Multiple Sclerosis Reveals Its Probable Homeostatic Role on the Clinical Activity, Disability, and Treatment with Fingolimod.	Fingolimod Hydrochloride	156-166	interleukin 37	Homo sapiens	34-38
31861585-5	2019	In addition, the in vivo part of the study showed that IL37 was selectively augmented in the sera of MS patients during a relapse and that treatment with the high potency disease-modifying drug fingolimod significantly increased the frequency of patients with circulating blood levels of IL37 (6/9, 66%) as compared to patients receiving no treatment (n = 48) or platform therapy (n = 59) who had levels of IL37 below the limit of the sensitivity of the assay.	Fingolimod Hydrochloride	194-204	interleukin 37	Homo sapiens	55-59
31861585-5	2019	In addition, the in vivo part of the study showed that IL37 was selectively augmented in the sera of MS patients during a relapse and that treatment with the high potency disease-modifying drug fingolimod significantly increased the frequency of patients with circulating blood levels of IL37 (6/9, 66%) as compared to patients receiving no treatment (n = 48) or platform therapy (n = 59) who had levels of IL37 below the limit of the sensitivity of the assay.	Fingolimod Hydrochloride	194-204	interleukin 37	Homo sapiens	288-292
31861585-5	2019	In addition, the in vivo part of the study showed that IL37 was selectively augmented in the sera of MS patients during a relapse and that treatment with the high potency disease-modifying drug fingolimod significantly increased the frequency of patients with circulating blood levels of IL37 (6/9, 66%) as compared to patients receiving no treatment (n = 48) or platform therapy (n = 59) who had levels of IL37 below the limit of the sensitivity of the assay.	Fingolimod Hydrochloride	194-204	interleukin 37	Homo sapiens	288-292
31861585-6	2019	This finding therefore anticipates that fingolimod may at least partially exert its beneficial effects in MS by upregulating the production of IL37.	Fingolimod Hydrochloride	40-50	interleukin 37	Homo sapiens	143-147
30701416-0	2019	Fingolimod Suppresses the Proinflammatory Status of Interferon-gamma-Activated Cultured Rat Astrocytes.	Fingolimod Hydrochloride	0-10	interferon gamma	Rattus norvegicus	52-68
30701416-3	2019	We characterized the anti-inflammatory effects of fingolimod (FTY720), an established drug for MS, and its phosphorylated metabolite (FTY720-P) in IFN-gamma-activated cultured rat astrocytes.	Fingolimod Hydrochloride	50-60	interferon gamma	Rattus norvegicus	147-156
31237525-5	2019	Administration of fingolimod during disease onset completely prevented the formation of TSHR-stimulating autoantibodies.	Fingolimod Hydrochloride	18-28	thyroid stimulating hormone receptor	Mus musculus	88-92
31237525-11	2019	Fingolimod decreased elevated T cell levels and increased CD4+CD25+Foxp3+ regulatory T cell populations.	Fingolimod Hydrochloride	0-10	forkhead box P3	Mus musculus	67-72
31336697-6	2019	MSN@PDA loaded with doxorubicin (hydrophilic) and fingolimod (hydrophobic) was studied via a systematic in vitro approach (cellular internalization, intracellular drug distribution and cytotoxicity).	Fingolimod Hydrochloride	50-60	moesin	Homo sapiens	0-3
31336697-8	2019	Drug-loaded, copolymer-coated MSN@PDA showed effective cellular uptake, intracellular release and an amplified cytotoxic effect with both doxorubicin and fingolimod.	Fingolimod Hydrochloride	154-164	moesin	Homo sapiens	30-33
31069623-8	2019	FTY720 directly inhibited MPTP-induced microglial activation in the SNpc, suppressed the production of interleukin (IL)-6, IL-1beta, and tumor necrosis factor-alpha in BV-2 microglial cells treated with 1-methyl-4-phenylpyridinium (MPP+), and subsequently decreased apoptosis in SH-SY5Y neuroblastoma cells.	Fingolimod Hydrochloride	0-6	interleukin 6	Mus musculus	103-121
31069623-8	2019	FTY720 directly inhibited MPTP-induced microglial activation in the SNpc, suppressed the production of interleukin (IL)-6, IL-1beta, and tumor necrosis factor-alpha in BV-2 microglial cells treated with 1-methyl-4-phenylpyridinium (MPP+), and subsequently decreased apoptosis in SH-SY5Y neuroblastoma cells.	Fingolimod Hydrochloride	0-6	interleukin 1 alpha	Mus musculus	123-131
31069623-8	2019	FTY720 directly inhibited MPTP-induced microglial activation in the SNpc, suppressed the production of interleukin (IL)-6, IL-1beta, and tumor necrosis factor-alpha in BV-2 microglial cells treated with 1-methyl-4-phenylpyridinium (MPP+), and subsequently decreased apoptosis in SH-SY5Y neuroblastoma cells.	Fingolimod Hydrochloride	0-6	tumor necrosis factor	Mus musculus	137-164
31069623-9	2019	Moreover, in MPP+-treated BV-2 cells and primary microglia, FTY720 treatment significantly attenuated the increases in the phosphorylation of PI3K/AKT/GSK-3beta, reduced ROS generation and p65 activation, and also inhibited the activation of NLRP3 inflammasome and caspase-1.	Fingolimod Hydrochloride	60-66	thymoma viral proto-oncogene 1	Mus musculus	147-150
31069623-9	2019	Moreover, in MPP+-treated BV-2 cells and primary microglia, FTY720 treatment significantly attenuated the increases in the phosphorylation of PI3K/AKT/GSK-3beta, reduced ROS generation and p65 activation, and also inhibited the activation of NLRP3 inflammasome and caspase-1.	Fingolimod Hydrochloride	60-66	glycogen synthase kinase 3 alpha	Mus musculus	151-160
31069623-9	2019	Moreover, in MPP+-treated BV-2 cells and primary microglia, FTY720 treatment significantly attenuated the increases in the phosphorylation of PI3K/AKT/GSK-3beta, reduced ROS generation and p65 activation, and also inhibited the activation of NLRP3 inflammasome and caspase-1.	Fingolimod Hydrochloride	60-66	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	189-192
31069623-9	2019	Moreover, in MPP+-treated BV-2 cells and primary microglia, FTY720 treatment significantly attenuated the increases in the phosphorylation of PI3K/AKT/GSK-3beta, reduced ROS generation and p65 activation, and also inhibited the activation of NLRP3 inflammasome and caspase-1.	Fingolimod Hydrochloride	60-66	NLR family, pyrin domain containing 3	Mus musculus	242-247
31069623-9	2019	Moreover, in MPP+-treated BV-2 cells and primary microglia, FTY720 treatment significantly attenuated the increases in the phosphorylation of PI3K/AKT/GSK-3beta, reduced ROS generation and p65 activation, and also inhibited the activation of NLRP3 inflammasome and caspase-1.	Fingolimod Hydrochloride	60-66	caspase 1	Mus musculus	265-274
31069623-12	2019	Graphical Abstract FTY720 may reduce ROS production by inhibiting the PI3K/AKT/GSK-3beta signaling pathway, while at the same time reducing p65 phosphorylation, thus decreasing NLRP3 inflammasome activation through these two pathways, ultimately reducing microglia activation-induced neuronal damage.	Fingolimod Hydrochloride	19-25	thymoma viral proto-oncogene 1	Mus musculus	75-78
31069623-12	2019	Graphical Abstract FTY720 may reduce ROS production by inhibiting the PI3K/AKT/GSK-3beta signaling pathway, while at the same time reducing p65 phosphorylation, thus decreasing NLRP3 inflammasome activation through these two pathways, ultimately reducing microglia activation-induced neuronal damage.	Fingolimod Hydrochloride	19-25	glycogen synthase kinase 3 alpha	Mus musculus	79-88
31069623-12	2019	Graphical Abstract FTY720 may reduce ROS production by inhibiting the PI3K/AKT/GSK-3beta signaling pathway, while at the same time reducing p65 phosphorylation, thus decreasing NLRP3 inflammasome activation through these two pathways, ultimately reducing microglia activation-induced neuronal damage.	Fingolimod Hydrochloride	19-25	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	140-143
31069623-12	2019	Graphical Abstract FTY720 may reduce ROS production by inhibiting the PI3K/AKT/GSK-3beta signaling pathway, while at the same time reducing p65 phosphorylation, thus decreasing NLRP3 inflammasome activation through these two pathways, ultimately reducing microglia activation-induced neuronal damage.	Fingolimod Hydrochloride	19-25	NLR family, pyrin domain containing 3	Mus musculus	177-182
31059070-0	2019	Fingolimod sensitizes EGFR wild-type non-small cell lung cancer cells to lapatinib or sorafenib and induces cell cycle arrest.	Fingolimod Hydrochloride	0-10	epidermal growth factor receptor	Homo sapiens	22-26
31165772-9	2019	Fingolimod prevented lymphocyte infiltration, and attenuated the severity of HT in Rag2-/- mice but it was ineffective under thrombocytopenia.	Fingolimod Hydrochloride	0-10	recombination activating gene 2	Mus musculus	83-87
31214192-4	2019	FTY720 treatment could prevent ischemia-induced brain injury and neurological dysfunction, also decrease the levels of IL-1beta and TNF-alpha and promote M2 microglial polarization in rats.	Fingolimod Hydrochloride	0-6	interleukin 1 alpha	Rattus norvegicus	119-127
31214192-4	2019	FTY720 treatment could prevent ischemia-induced brain injury and neurological dysfunction, also decrease the levels of IL-1beta and TNF-alpha and promote M2 microglial polarization in rats.	Fingolimod Hydrochloride	0-6	tumor necrosis factor	Rattus norvegicus	132-141
31214192-7	2019	The sphingosine kinase 1/2 (SphK1/2) or the Sphk2 inhibitor could prevent the M1 to M2 phenotype shift improved by FTY720, but the Sphk1 inhibitor failed to affect the roles of FTY720.	Fingolimod Hydrochloride	115-121	sphingosine kinase 1	Rattus norvegicus	4-26
31214192-7	2019	The sphingosine kinase 1/2 (SphK1/2) or the Sphk2 inhibitor could prevent the M1 to M2 phenotype shift improved by FTY720, but the Sphk1 inhibitor failed to affect the roles of FTY720.	Fingolimod Hydrochloride	115-121	sphingosine kinase 1	Rattus norvegicus	28-35
31214192-7	2019	The sphingosine kinase 1/2 (SphK1/2) or the Sphk2 inhibitor could prevent the M1 to M2 phenotype shift improved by FTY720, but the Sphk1 inhibitor failed to affect the roles of FTY720.	Fingolimod Hydrochloride	115-121	sphingosine kinase 2	Rattus norvegicus	44-49
31165772-10	2019	Fingolimod prevented beta-catenin degradation but not Evans blue extravasation.	Fingolimod Hydrochloride	0-10	catenin (cadherin associated protein), beta 1	Mus musculus	21-33
30898076-1	2019	The immunosuppressive activity of myriocin (ISP-1), a lead compound of fingolimod (FTY720), is derived from its 2-amino-1,3-propandiol structure.	Fingolimod Hydrochloride	71-81	protease, serine 28	Mus musculus	44-49
30377924-9	2019	Meanwhile, fingolimod hydrochloride (FTY720, 1 microM), a PAK-1 activator, increased cell viability and inhibited hypertrophy induced by methoxetamine in H9c2 cells.	Fingolimod Hydrochloride	11-35	p21 (RAC1) activated kinase 1	Rattus norvegicus	58-63
30377924-9	2019	Meanwhile, fingolimod hydrochloride (FTY720, 1 microM), a PAK-1 activator, increased cell viability and inhibited hypertrophy induced by methoxetamine in H9c2 cells.	Fingolimod Hydrochloride	37-43	p21 (RAC1) activated kinase 1	Rattus norvegicus	58-63
30898076-1	2019	The immunosuppressive activity of myriocin (ISP-1), a lead compound of fingolimod (FTY720), is derived from its 2-amino-1,3-propandiol structure.	Fingolimod Hydrochloride	83-89	protease, serine 28	Mus musculus	44-49
30917007-2	2019	Targeting SET with a sphingolipid analog drug fingolimod (FTY720) or ceramide leads to the reactivation of tumor suppressor PP2A.	Fingolimod Hydrochloride	46-56	protein phosphatase 2 phosphatase activator	Homo sapiens	124-128
30917007-2	2019	Targeting SET with a sphingolipid analog drug fingolimod (FTY720) or ceramide leads to the reactivation of tumor suppressor PP2A.	Fingolimod Hydrochloride	58-64	protein phosphatase 2 phosphatase activator	Homo sapiens	124-128
30784773-4	2019	High ANGPTL6 levels associated with slow disease progression and good response to fingolimod treatment and low ANGPTL4 associated with poor response to natalizumab treatment.	Fingolimod Hydrochloride	82-92	angiopoietin like 6	Homo sapiens	5-12
30963819-8	2019	Furthermore, an in vivo study demonstrated that blocking S1PR1 by FTY720 administration could reduce the incidence and severity of thyroiditis and goiter in SAT mice in a time-dependent manner.	Fingolimod Hydrochloride	66-72	sphingosine-1-phosphate receptor 1	Mus musculus	57-62
30963819-9	2019	The proportions of STAT3-related and inflammation-related cell subtypes, such as T helper 1, T helper 17, and follicular T helper cells, were elevated in the SAT group when compared to the control group, and these cell subtypes decreased after FTY720 administration.	Fingolimod Hydrochloride	244-250	signal transducer and activator of transcription 3	Mus musculus	19-24
30963819-10	2019	Furthermore, the downstream inflammatory cytokines of STAT3 were also downregulated after FTY720 administration.	Fingolimod Hydrochloride	90-96	signal transducer and activator of transcription 3	Mus musculus	54-59
29985084-5	2019	The adjusted odds ratio of PML for each drug was as follows; natalizumab 115.72 (95% CI; 83.83, 159.74), fingolimod 4.98 (3.64, 6.81) followed by dimethyl fumarate 1.77 (1.2, 2.62) and rituximab 3.22 (1.07, 9.72).	Fingolimod Hydrochloride	105-115	PML nuclear body scaffold	Homo sapiens	27-30
29985084-8	2019	CONCLUSION: The reporting proportion of PML was relatively higher in natalizumab followed by fingolimod, dimethyl fumarate and rituximab.	Fingolimod Hydrochloride	93-103	PML nuclear body scaffold	Homo sapiens	40-43
31123291-0	2019	Sphingosine Kinase 2 Phosphorylation of FTY720 is Unnecessary for Prevention of Light-Induced Retinal Damage.	Fingolimod Hydrochloride	40-46	sphingosine kinase 2	Mus musculus	0-20
31123291-6	2019	Additionally, FTY720 treatment protected Sphk2 KO retinas from light-induced damage despite significant retardation of FTY720 phosphorylation in Sphk2 KO mice.	Fingolimod Hydrochloride	14-20	sphingosine kinase 2	Mus musculus	41-46
31123291-6	2019	Additionally, FTY720 treatment protected Sphk2 KO retinas from light-induced damage despite significant retardation of FTY720 phosphorylation in Sphk2 KO mice.	Fingolimod Hydrochloride	14-20	sphingosine kinase 2	Mus musculus	145-150
30784773-5	2019	Therefore, we propose high ANGPTL4 and 6 levels as markers for positive response to MS treatments either natalizumab or fingolimod respectively.	Fingolimod Hydrochloride	120-130	angiopoietin like 4	Homo sapiens	27-34
30825874-9	2019	Therapeutic FTY720 treatment reversed electrophysiological and histological anomalies, suggesting that myelinated fibers were subsequently preserved, it inhibited macrophage and IL-17+ cell infiltration in PNS, and it significantly reduced circulating pro-inflammatory cytokines.	Fingolimod Hydrochloride	12-18	interleukin 17A	Rattus norvegicus	178-183
30565812-3	2019	Recently, it has been demonstrated that Fingolimod increases the expression of transcription factor NR4A2 in murine brain.	Fingolimod Hydrochloride	40-50	nuclear receptor subfamily 4, group A, member 2	Mus musculus	100-105
30565812-10	2019	Patients treated with Fingolimod for >2 years were characterized by higher levels of NR4A2 compared with the T0 group, approaching those of HCs.	Fingolimod Hydrochloride	22-32	nuclear receptor subfamily 4 group A member 2	Homo sapiens	85-90
30565812-12	2019	CONCLUSIONS: Involvement of the NR4A family in the pathogenesis of multiple sclerosis and a role of Fingolimod in the recovery from NR4A2 deficit can be hypothesized based on our data.	Fingolimod Hydrochloride	100-110	nuclear receptor subfamily 4 group A member 2	Homo sapiens	132-137
30785748-2	2019	In comparison to fingolimod (1), a full agonist of S1P1 currently marketed for the treatment of relapse remitting multiple sclerosis (RRMS), 2 offers several potential advantages having demonstrated improved safety multiples in preclinical evaluations against undesired pulmonary and cardiovascular effects.	Fingolimod Hydrochloride	17-27	sphingosine-1-phosphate receptor 1	Homo sapiens	51-55
30484906-5	2019	Fingolimod (FTY720), a S1P receptor 1 (S1PR1) functional antagonist and FDA approved drug for relapsing-remitting multiple sclerosis, partially blunted Abeta42-induced pro-inflammatory cytokine generation, suggesting that Spns2 promotes microglia pro-inflammatory activation through S1P-signaling.	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Mus musculus	23-37
30484906-5	2019	Fingolimod (FTY720), a S1P receptor 1 (S1PR1) functional antagonist and FDA approved drug for relapsing-remitting multiple sclerosis, partially blunted Abeta42-induced pro-inflammatory cytokine generation, suggesting that Spns2 promotes microglia pro-inflammatory activation through S1P-signaling.	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Mus musculus	39-44
30484906-5	2019	Fingolimod (FTY720), a S1P receptor 1 (S1PR1) functional antagonist and FDA approved drug for relapsing-remitting multiple sclerosis, partially blunted Abeta42-induced pro-inflammatory cytokine generation, suggesting that Spns2 promotes microglia pro-inflammatory activation through S1P-signaling.	Fingolimod Hydrochloride	0-10	spinster homolog 2	Mus musculus	222-227
30484906-5	2019	Fingolimod (FTY720), a S1P receptor 1 (S1PR1) functional antagonist and FDA approved drug for relapsing-remitting multiple sclerosis, partially blunted Abeta42-induced pro-inflammatory cytokine generation, suggesting that Spns2 promotes microglia pro-inflammatory activation through S1P-signaling.	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Mus musculus	23-26
30484906-5	2019	Fingolimod (FTY720), a S1P receptor 1 (S1PR1) functional antagonist and FDA approved drug for relapsing-remitting multiple sclerosis, partially blunted Abeta42-induced pro-inflammatory cytokine generation, suggesting that Spns2 promotes microglia pro-inflammatory activation through S1P-signaling.	Fingolimod Hydrochloride	12-18	sphingosine-1-phosphate receptor 1	Mus musculus	23-37
30484906-5	2019	Fingolimod (FTY720), a S1P receptor 1 (S1PR1) functional antagonist and FDA approved drug for relapsing-remitting multiple sclerosis, partially blunted Abeta42-induced pro-inflammatory cytokine generation, suggesting that Spns2 promotes microglia pro-inflammatory activation through S1P-signaling.	Fingolimod Hydrochloride	12-18	sphingosine-1-phosphate receptor 1	Mus musculus	39-44
30484906-5	2019	Fingolimod (FTY720), a S1P receptor 1 (S1PR1) functional antagonist and FDA approved drug for relapsing-remitting multiple sclerosis, partially blunted Abeta42-induced pro-inflammatory cytokine generation, suggesting that Spns2 promotes microglia pro-inflammatory activation through S1P-signaling.	Fingolimod Hydrochloride	12-18	spinster homolog 2	Mus musculus	222-227
30484906-5	2019	Fingolimod (FTY720), a S1P receptor 1 (S1PR1) functional antagonist and FDA approved drug for relapsing-remitting multiple sclerosis, partially blunted Abeta42-induced pro-inflammatory cytokine generation, suggesting that Spns2 promotes microglia pro-inflammatory activation through S1P-signaling.	Fingolimod Hydrochloride	12-18	sphingosine-1-phosphate receptor 1	Mus musculus	23-26
30828332-7	2019	Comparison of peripheral blood ILC numbers between fingolimod-receiving and treatment-free MS patients revealed that, in vivo, ILCs respond to fingolimod, an S1PR1 agonist, resulting in ILC-penia in circulation.	Fingolimod Hydrochloride	51-61	sphingosine-1-phosphate receptor 1	Homo sapiens	158-163
30828332-7	2019	Comparison of peripheral blood ILC numbers between fingolimod-receiving and treatment-free MS patients revealed that, in vivo, ILCs respond to fingolimod, an S1PR1 agonist, resulting in ILC-penia in circulation.	Fingolimod Hydrochloride	143-153	sphingosine-1-phosphate receptor 1	Homo sapiens	158-163
30828332-9	2019	Importantly, ex vivo exposure of ILC3 and ILC1 to fingolimod or SEW2871, another S1PR1 antagonist, reduced production of ILC3- and ILC1- associated cytokines GM-CSF, IL-22, IL-17, and IFN-gamma, respectively.	Fingolimod Hydrochloride	50-60	sphingosine-1-phosphate receptor 1	Homo sapiens	81-86
30828332-9	2019	Importantly, ex vivo exposure of ILC3 and ILC1 to fingolimod or SEW2871, another S1PR1 antagonist, reduced production of ILC3- and ILC1- associated cytokines GM-CSF, IL-22, IL-17, and IFN-gamma, respectively.	Fingolimod Hydrochloride	50-60	colony stimulating factor 2	Homo sapiens	158-164
30828332-9	2019	Importantly, ex vivo exposure of ILC3 and ILC1 to fingolimod or SEW2871, another S1PR1 antagonist, reduced production of ILC3- and ILC1- associated cytokines GM-CSF, IL-22, IL-17, and IFN-gamma, respectively.	Fingolimod Hydrochloride	50-60	interleukin 22	Homo sapiens	166-171
30828332-9	2019	Importantly, ex vivo exposure of ILC3 and ILC1 to fingolimod or SEW2871, another S1PR1 antagonist, reduced production of ILC3- and ILC1- associated cytokines GM-CSF, IL-22, IL-17, and IFN-gamma, respectively.	Fingolimod Hydrochloride	50-60	interleukin 17A	Homo sapiens	173-178
30828332-9	2019	Importantly, ex vivo exposure of ILC3 and ILC1 to fingolimod or SEW2871, another S1PR1 antagonist, reduced production of ILC3- and ILC1- associated cytokines GM-CSF, IL-22, IL-17, and IFN-gamma, respectively.	Fingolimod Hydrochloride	50-60	interferon gamma	Homo sapiens	184-193
29804232-7	2019	Moreover, we confirmed the contribution of the proper balance of BDNF/TrkB/p75NTR on HD pathology by a pharmacological approach using fingolimod.	Fingolimod Hydrochloride	134-144	brain derived neurotrophic factor	Mus musculus	65-69
29804232-7	2019	Moreover, we confirmed the contribution of the proper balance of BDNF/TrkB/p75NTR on HD pathology by a pharmacological approach using fingolimod.	Fingolimod Hydrochloride	134-144	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	70-74
29804232-7	2019	Moreover, we confirmed the contribution of the proper balance of BDNF/TrkB/p75NTR on HD pathology by a pharmacological approach using fingolimod.	Fingolimod Hydrochloride	134-144	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	75-81
29804232-8	2019	We observed that chronic infusion of fingolimod normalizes p75NTR levels, which is likely to improve motor coordination and striatal neuropathology in HD transgenic mice.	Fingolimod Hydrochloride	37-47	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	59-65
30550889-14	2019	SIGNIFICANCE: Our results indicated that FTY720 inhibited PSC activation by promoting cell apoptosis and inhibiting PSC autophagy by suppressing AMPK and activating the mTOR pathway.	Fingolimod Hydrochloride	41-47	mechanistic target of rapamycin kinase	Rattus norvegicus	169-173
30644981-13	2019	Conclusions and Relevance: Among patients with relapsing-remitting MS, initial treatment with fingolimod, alemtuzumab, or natalizumab was associated with a lower risk of conversion to secondary progressive MS vs initial treatment with glatiramer acetate or interferon beta.	Fingolimod Hydrochloride	94-104	interferon beta 1	Homo sapiens	257-272
30388910-0	2019	Fingolimod augments Pemetrexed killing of non-small cell lung cancer and overcomes resistance to ERBB inhibition.	Fingolimod Hydrochloride	0-10	epidermal growth factor receptor	Homo sapiens	97-101
30388910-8	2019	Autophagy protein 5 (ATG5) knock down afforded greater protection against the combination of pemetrexed with fingolimod.	Fingolimod Hydrochloride	109-119	autophagy related 5	Homo sapiens	0-19
30388910-8	2019	Autophagy protein 5 (ATG5) knock down afforded greater protection against the combination of pemetrexed with fingolimod.	Fingolimod Hydrochloride	109-119	autophagy related 5	Homo sapiens	21-25
30388910-9	2019	Treatment of cells with the mTOR inhibitor everolimus markedly enhanced the lethality of pemetrexed plus fingolimod combination.	Fingolimod Hydrochloride	105-115	mechanistic target of rapamycin kinase	Homo sapiens	28-32
30122421-4	2019	Besides decreasing the cell numbers in peripheral blood and sera levels of pro-inflammatory cytokines, Fingolimod inhibited the expression of Th1 and Th17 cytokines on CD4+ T cells and increased the expression of exhaustion markers.	Fingolimod Hydrochloride	103-113	CD4 molecule	Homo sapiens	168-171
30852478-6	2019	24 hours after oral administration of Fingolimod (0.5 mg), the circulating blood CD4 + T, CD8 + T, CD19 + B and CD56 + natural killer cells of the patients in the combined treatment group decreased steadily to varying degrees.	Fingolimod Hydrochloride	38-48	CD4 molecule	Homo sapiens	81-84
30852478-6	2019	24 hours after oral administration of Fingolimod (0.5 mg), the circulating blood CD4 + T, CD8 + T, CD19 + B and CD56 + natural killer cells of the patients in the combined treatment group decreased steadily to varying degrees.	Fingolimod Hydrochloride	38-48	CD8a molecule	Homo sapiens	90-93
30852478-6	2019	24 hours after oral administration of Fingolimod (0.5 mg), the circulating blood CD4 + T, CD8 + T, CD19 + B and CD56 + natural killer cells of the patients in the combined treatment group decreased steadily to varying degrees.	Fingolimod Hydrochloride	38-48	CD19 molecule	Homo sapiens	99-103
30852478-6	2019	24 hours after oral administration of Fingolimod (0.5 mg), the circulating blood CD4 + T, CD8 + T, CD19 + B and CD56 + natural killer cells of the patients in the combined treatment group decreased steadily to varying degrees.	Fingolimod Hydrochloride	38-48	neural cell adhesion molecule 1	Homo sapiens	112-116
31399186-3	2019	Fingolimod, whose active metabolite, fingolimod phosphate, acts as a nonselective S1P-receptor agonist, exerts its immunomodulatory effect, at least in part, by regulating lymphocyte trafficking via downregulation of S1P1 expression on lymphocytes.	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Rattus norvegicus	217-221
30007065-0	2018	Primary cutaneous CD30+ anaplastic large-cell lymphoma associated with fingolimod.	Fingolimod Hydrochloride	71-81	TNF receptor superfamily member 8	Homo sapiens	18-22
30122421-3	2019	Here we examined the in vivo effects of Fingolimod in modulating the phenotype and function of T cell and Foxp3 regulatory T cell populations in patients with multiple sclerosis under Fingolimod treatment.	Fingolimod Hydrochloride	40-50	forkhead box P3	Homo sapiens	106-111
30205205-0	2018	Rapamycin and fingolimod modulate Treg/Th17 cells in experimental autoimmune encephalomyelitis by regulating the Akt-mTOR and MAPK/ERK pathways.	Fingolimod Hydrochloride	14-24	thymoma viral proto-oncogene 1	Mus musculus	113-116
30152864-16	2018	We did find an increase of BDNF protein after a single injection of fingolimod 0.1 or 1.0 mg/kg, but not after multiple injections, indicating that the BDNF response to fingolimod is unsustainable over time.	Fingolimod Hydrochloride	68-78	brain derived neurotrophic factor	Mus musculus	27-31
30152864-16	2018	We did find an increase of BDNF protein after a single injection of fingolimod 0.1 or 1.0 mg/kg, but not after multiple injections, indicating that the BDNF response to fingolimod is unsustainable over time.	Fingolimod Hydrochloride	169-179	brain derived neurotrophic factor	Mus musculus	152-156
30320355-8	2018	Similar to WM-155 cells, the viability of R-SK-Mel cells was reduced and the expression of cleaved PARP was increased by the combination treatment with FTY720 and vemurafenib.	Fingolimod Hydrochloride	152-158	poly(ADP-ribose) polymerase 1	Homo sapiens	99-103
30005970-0	2018	Inhibition of RhoA and mTORC2/Rictor by Fingolimod (FTY720) induces p21-activated kinase 1, PAK-1 and amplifies podosomes in mouse peritoneal macrophages.	Fingolimod Hydrochloride	40-50	ras homolog family member A	Mus musculus	14-18
30005970-0	2018	Inhibition of RhoA and mTORC2/Rictor by Fingolimod (FTY720) induces p21-activated kinase 1, PAK-1 and amplifies podosomes in mouse peritoneal macrophages.	Fingolimod Hydrochloride	40-50	CREB regulated transcription coactivator 2	Mus musculus	23-29
30005970-0	2018	Inhibition of RhoA and mTORC2/Rictor by Fingolimod (FTY720) induces p21-activated kinase 1, PAK-1 and amplifies podosomes in mouse peritoneal macrophages.	Fingolimod Hydrochloride	40-50	RPTOR independent companion of MTOR, complex 2	Mus musculus	30-36
30005970-0	2018	Inhibition of RhoA and mTORC2/Rictor by Fingolimod (FTY720) induces p21-activated kinase 1, PAK-1 and amplifies podosomes in mouse peritoneal macrophages.	Fingolimod Hydrochloride	40-50	p21 (RAC1) activated kinase 1	Mus musculus	68-90
30005970-0	2018	Inhibition of RhoA and mTORC2/Rictor by Fingolimod (FTY720) induces p21-activated kinase 1, PAK-1 and amplifies podosomes in mouse peritoneal macrophages.	Fingolimod Hydrochloride	40-50	p21 (RAC1) activated kinase 1	Mus musculus	92-97
30005970-0	2018	Inhibition of RhoA and mTORC2/Rictor by Fingolimod (FTY720) induces p21-activated kinase 1, PAK-1 and amplifies podosomes in mouse peritoneal macrophages.	Fingolimod Hydrochloride	52-58	ras homolog family member A	Mus musculus	14-18
30005970-0	2018	Inhibition of RhoA and mTORC2/Rictor by Fingolimod (FTY720) induces p21-activated kinase 1, PAK-1 and amplifies podosomes in mouse peritoneal macrophages.	Fingolimod Hydrochloride	52-58	CREB regulated transcription coactivator 2	Mus musculus	23-29
30005970-0	2018	Inhibition of RhoA and mTORC2/Rictor by Fingolimod (FTY720) induces p21-activated kinase 1, PAK-1 and amplifies podosomes in mouse peritoneal macrophages.	Fingolimod Hydrochloride	52-58	RPTOR independent companion of MTOR, complex 2	Mus musculus	30-36
30005970-0	2018	Inhibition of RhoA and mTORC2/Rictor by Fingolimod (FTY720) induces p21-activated kinase 1, PAK-1 and amplifies podosomes in mouse peritoneal macrophages.	Fingolimod Hydrochloride	52-58	p21 (RAC1) activated kinase 1	Mus musculus	68-90
30005970-0	2018	Inhibition of RhoA and mTORC2/Rictor by Fingolimod (FTY720) induces p21-activated kinase 1, PAK-1 and amplifies podosomes in mouse peritoneal macrophages.	Fingolimod Hydrochloride	52-58	p21 (RAC1) activated kinase 1	Mus musculus	92-97
30005970-5	2018	Here we showed that a fungus metabolite Fingolimod (FTY720, Gilenya), which is clinically approved for the treatment of multiple sclerosis, down-regulates Rictor, which is a signature molecule of mTORC2 and dictates its substrate (actin cytoskeleton) specificity, down-regulates RhoA, up-regulates PAK-1, and causes amplification of podosomes in mouse peritoneal macrophages.	Fingolimod Hydrochloride	40-50	RPTOR independent companion of MTOR, complex 2	Mus musculus	155-161
30005970-5	2018	Here we showed that a fungus metabolite Fingolimod (FTY720, Gilenya), which is clinically approved for the treatment of multiple sclerosis, down-regulates Rictor, which is a signature molecule of mTORC2 and dictates its substrate (actin cytoskeleton) specificity, down-regulates RhoA, up-regulates PAK-1, and causes amplification of podosomes in mouse peritoneal macrophages.	Fingolimod Hydrochloride	40-50	CREB regulated transcription coactivator 2	Mus musculus	196-202
30005970-5	2018	Here we showed that a fungus metabolite Fingolimod (FTY720, Gilenya), which is clinically approved for the treatment of multiple sclerosis, down-regulates Rictor, which is a signature molecule of mTORC2 and dictates its substrate (actin cytoskeleton) specificity, down-regulates RhoA, up-regulates PAK-1, and causes amplification of podosomes in mouse peritoneal macrophages.	Fingolimod Hydrochloride	40-50	ras homolog family member A	Mus musculus	279-283
30005970-5	2018	Here we showed that a fungus metabolite Fingolimod (FTY720, Gilenya), which is clinically approved for the treatment of multiple sclerosis, down-regulates Rictor, which is a signature molecule of mTORC2 and dictates its substrate (actin cytoskeleton) specificity, down-regulates RhoA, up-regulates PAK-1, and causes amplification of podosomes in mouse peritoneal macrophages.	Fingolimod Hydrochloride	40-50	p21 (RAC1) activated kinase 1	Mus musculus	298-303
30205205-0	2018	Rapamycin and fingolimod modulate Treg/Th17 cells in experimental autoimmune encephalomyelitis by regulating the Akt-mTOR and MAPK/ERK pathways.	Fingolimod Hydrochloride	14-24	mechanistic target of rapamycin kinase	Mus musculus	117-121
30205205-0	2018	Rapamycin and fingolimod modulate Treg/Th17 cells in experimental autoimmune encephalomyelitis by regulating the Akt-mTOR and MAPK/ERK pathways.	Fingolimod Hydrochloride	14-24	mitogen-activated protein kinase 1	Mus musculus	131-134
30319641-8	2018	Immunofluorescent staining demonstrated a dramatic lessening of brain T cell and macrophage infiltration, and a significant reduction in cortical leakage of serum albumin, in fingolimod treated mice.	Fingolimod Hydrochloride	175-185	albumin	Mus musculus	157-170
29974307-9	2018	Conversely, patients treated with fingolimod following IFN-beta did not have significant BVL.	Fingolimod Hydrochloride	34-44	interferon beta 1	Homo sapiens	55-63
30263146-8	2018	Results: CD62L+CD3+CD4+ expression was significantly decreased in patients treated with natalizumab (n = 26) and fingolimod (n = 20) and increased with dimethyl-fumarate (n = 15) compared to patients receiving interferon/glatiramer acetate (n = 90/30) or no disease-modifying therapies (n = 53) and controls (n = 51) (p&lt;0.001).	Fingolimod Hydrochloride	113-123	selectin L	Homo sapiens	9-14
30263146-8	2018	Results: CD62L+CD3+CD4+ expression was significantly decreased in patients treated with natalizumab (n = 26) and fingolimod (n = 20) and increased with dimethyl-fumarate (n = 15) compared to patients receiving interferon/glatiramer acetate (n = 90/30) or no disease-modifying therapies (n = 53) and controls (n = 51) (p&lt;0.001).	Fingolimod Hydrochloride	113-123	CD4 molecule	Homo sapiens	19-22
30026610-8	2018	FTY720 induced aberrant NFAT1, AP1 and NFkappaB activation which were associated with increased acetylation of histone (H3K9).	Fingolimod Hydrochloride	0-6	nuclear factor of activated T cells 2	Homo sapiens	24-29
30255127-6	2018	ieAstrocyte formation was reduced by either astrocyte-specific genetic removal of sphingosine 1-phosphate receptor 1 (S1P1) or pharmacological inhibition by fingolimod (FTY720), an FDA-approved MS medicine that can functionally antagonize S1P1.	Fingolimod Hydrochloride	157-167	sphingosine-1-phosphate receptor 1	Mus musculus	239-243
30255127-6	2018	ieAstrocyte formation was reduced by either astrocyte-specific genetic removal of sphingosine 1-phosphate receptor 1 (S1P1) or pharmacological inhibition by fingolimod (FTY720), an FDA-approved MS medicine that can functionally antagonize S1P1.	Fingolimod Hydrochloride	169-175	sphingosine-1-phosphate receptor 1	Mus musculus	239-243
29945931-1	2018	The immunomodulatory prodrug 2-amino-2-(2-[4-octylphenyl]ethyl)-1,3-propanediol (FTY720), which acts as an agonist for sphingosine-1-phosphate (S1P) receptors (S1PR) when phosphorylated, is proposed as a novel pain therapeutic.	Fingolimod Hydrochloride	81-87	sphingosine-1-phosphate receptor 1	Mus musculus	144-147
29945931-3	2018	FTY720 produced antinociception and antiallodynia, respectively, and these effects were dose-dependent and mimicked by the S1PR1-selective agonist CYM-5442.	Fingolimod Hydrochloride	0-6	sphingosine-1-phosphate receptor 1	Mus musculus	123-128
30537798-0	2018	Characterization of CD4+ and CD8+ T Cell Subsets and Interferon Regulatory Factor 4 (IRF4) in MS Patients Treated with Fingolimod (FTY-720): A Follow-up Study.	Fingolimod Hydrochloride	119-129	CD4 molecule	Homo sapiens	20-23
30537798-0	2018	Characterization of CD4+ and CD8+ T Cell Subsets and Interferon Regulatory Factor 4 (IRF4) in MS Patients Treated with Fingolimod (FTY-720): A Follow-up Study.	Fingolimod Hydrochloride	119-129	CD8a molecule	Homo sapiens	29-32
30537798-0	2018	Characterization of CD4+ and CD8+ T Cell Subsets and Interferon Regulatory Factor 4 (IRF4) in MS Patients Treated with Fingolimod (FTY-720): A Follow-up Study.	Fingolimod Hydrochloride	119-129	interferon regulatory factor 4	Homo sapiens	53-83
30537798-0	2018	Characterization of CD4+ and CD8+ T Cell Subsets and Interferon Regulatory Factor 4 (IRF4) in MS Patients Treated with Fingolimod (FTY-720): A Follow-up Study.	Fingolimod Hydrochloride	119-129	interferon regulatory factor 4	Homo sapiens	85-89
30537798-5	2018	In contrast, Fingolimod increased IL10+ CD4+ T cells.	Fingolimod Hydrochloride	13-23	interleukin 10	Homo sapiens	34-38
30537798-5	2018	In contrast, Fingolimod increased IL10+ CD4+ T cells.	Fingolimod Hydrochloride	13-23	CD4 molecule	Homo sapiens	40-43
30537798-6	2018	We also showed that IFN-gamma+IL17+ co-producing CD8+ T cells were reduced in patients under fingolimod therapy.	Fingolimod Hydrochloride	93-103	interferon gamma	Homo sapiens	20-29
30537798-6	2018	We also showed that IFN-gamma+IL17+ co-producing CD8+ T cells were reduced in patients under fingolimod therapy.	Fingolimod Hydrochloride	93-103	interleukin 17A	Homo sapiens	30-34
30537798-6	2018	We also showed that IFN-gamma+IL17+ co-producing CD8+ T cells were reduced in patients under fingolimod therapy.	Fingolimod Hydrochloride	93-103	CD8a molecule	Homo sapiens	49-52
30537798-7	2018	furthermore, Fingolimod could reduce the expression level of IRF4 in patients while IL6 was increased in the supernatant of cultured peripheral blood mononuclear cells.	Fingolimod Hydrochloride	13-23	interferon regulatory factor 4	Homo sapiens	61-65
30537798-8	2018	Our data showed that Fingolimod treatment alters CD4+ and CD8+ T cell subsets and reduces expression of IRF-4, which affects the proportion of pathogenic memory T cells in peripheral blood.	Fingolimod Hydrochloride	21-31	CD4 molecule	Homo sapiens	49-52
30537798-8	2018	Our data showed that Fingolimod treatment alters CD4+ and CD8+ T cell subsets and reduces expression of IRF-4, which affects the proportion of pathogenic memory T cells in peripheral blood.	Fingolimod Hydrochloride	21-31	CD8a molecule	Homo sapiens	58-61
30537798-8	2018	Our data showed that Fingolimod treatment alters CD4+ and CD8+ T cell subsets and reduces expression of IRF-4, which affects the proportion of pathogenic memory T cells in peripheral blood.	Fingolimod Hydrochloride	21-31	interferon regulatory factor 4	Homo sapiens	104-109
30127782-11	2018	CD4 T cell subset analysis revealed that circulating regulatory and effector T cells counts were similarly decreased after FTY720 treatment.	Fingolimod Hydrochloride	123-129	CD4 antigen	Mus musculus	0-3
29694732-6	2018	Coadministration of fingolimod at steady-state carbamazepine concentrations resulted in increased fingolimod CL/F by 67% through the induction of CYP3A4, a cytochrome with negligible involvement in fingolimod clearance in an uninduced state.	Fingolimod Hydrochloride	20-30	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	146-152
30112230-1	2018	During treatment with fingolimod, B cells are redistributed from blood to secondary lymphoid organs, where they are protected from the effect of anti-CD20 and other cell-depleting therapies.	Fingolimod Hydrochloride	22-32	keratin 20	Homo sapiens	150-154
30026610-8	2018	FTY720 induced aberrant NFAT1, AP1 and NFkappaB activation which were associated with increased acetylation of histone (H3K9).	Fingolimod Hydrochloride	0-6	FosB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	31-34
29986744-6	2018	Furthermore, the role of NO in mediating the expression of PP2A was further validated with Z-VAD-FMK (a caspase inhibitor), Carboxy-PTIO (a NO scavenger), okadaic acid (OA, a PP2A inhibitor) and FTY720 (a PP2A agonist) in JS-K treated cells.	Fingolimod Hydrochloride	195-201	protein phosphatase 2 phosphatase activator	Homo sapiens	59-63
29380527-0	2018	The Sphingosine 1-Phosphate Analogue FTY720 Alleviates Seizure-induced Overexpression of P-Glycoprotein in Rat Hippocampus.	Fingolimod Hydrochloride	37-43	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	89-103
29771310-9	2018	Fingolimod promotes cytokine homeostasis, down-regulates signaling within the PI3K/Akt and MAPK pathways and restores the lysosomal compartment in Mcoln1-/- astrocytes.	Fingolimod Hydrochloride	0-10	thymoma viral proto-oncogene 1	Mus musculus	83-86
29771310-9	2018	Fingolimod promotes cytokine homeostasis, down-regulates signaling within the PI3K/Akt and MAPK pathways and restores the lysosomal compartment in Mcoln1-/- astrocytes.	Fingolimod Hydrochloride	0-10	mucolipin 1	Mus musculus	147-153
29380527-3	2018	In this study, we tested the hypothesis that FTY720, a sphingosine 1-phosphate (S1P) analogue used for treating multiple sclerosis, modulates the up-regulation of P-gp and improves brain delivery of phenytoin (PHT) through S1P receptor 1 in the hippocampus of a pilocarpine-induced rat model of status epilepticus (SE).	Fingolimod Hydrochloride	45-51	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	163-167
29380527-3	2018	In this study, we tested the hypothesis that FTY720, a sphingosine 1-phosphate (S1P) analogue used for treating multiple sclerosis, modulates the up-regulation of P-gp and improves brain delivery of phenytoin (PHT) through S1P receptor 1 in the hippocampus of a pilocarpine-induced rat model of status epilepticus (SE).	Fingolimod Hydrochloride	45-51	sphingosine-1-phosphate receptor 1	Rattus norvegicus	223-237
28627962-8	2018	In patients starting fingolimod ( n = 243), mean NFL pg/mL ( SD) in plasma was reduced between baseline (20.4 (10.7)) and at 12 months (13.5 (7.3), p &lt; 3 x 10-6), and levels remained stable at 24 months (13.2 (6.2)).	Fingolimod Hydrochloride	21-31	neurofilament light chain	Homo sapiens	49-52
30083262-9	2018	FTY720 in combination with gemcitabine breached the mitochondrial membrane potential, altered the S1PR1-STAT3 loop, and inhibited epithelial to mesenchymal (EMT) transition.	Fingolimod Hydrochloride	0-6	sphingosine-1-phosphate receptor 1	Homo sapiens	98-103
29377379-7	2018	Applying a potent S1P-S1PR1 signaling modulator, Fingolimod (FTY720), in a Wistar rat apical periodontitis model effectively prevented bone lesions in vivo via downregulation of RANKL production, osteoclastogenesis, and bone resorption.	Fingolimod Hydrochloride	49-59	sphingosine-1-phosphate receptor 1	Rattus norvegicus	22-27
29377379-7	2018	Applying a potent S1P-S1PR1 signaling modulator, Fingolimod (FTY720), in a Wistar rat apical periodontitis model effectively prevented bone lesions in vivo via downregulation of RANKL production, osteoclastogenesis, and bone resorption.	Fingolimod Hydrochloride	49-59	TNF superfamily member 11	Rattus norvegicus	178-183
29377379-7	2018	Applying a potent S1P-S1PR1 signaling modulator, Fingolimod (FTY720), in a Wistar rat apical periodontitis model effectively prevented bone lesions in vivo via downregulation of RANKL production, osteoclastogenesis, and bone resorption.	Fingolimod Hydrochloride	61-67	sphingosine-1-phosphate receptor 1	Rattus norvegicus	22-27
29377379-7	2018	Applying a potent S1P-S1PR1 signaling modulator, Fingolimod (FTY720), in a Wistar rat apical periodontitis model effectively prevented bone lesions in vivo via downregulation of RANKL production, osteoclastogenesis, and bone resorption.	Fingolimod Hydrochloride	61-67	TNF superfamily member 11	Rattus norvegicus	178-183
29530550-0	2018	Fingolimod inhibits brain atrophy and promotes brain-derived neurotrophic factor in an animal model of multiple sclerosis.	Fingolimod Hydrochloride	0-10	brain derived neurotrophic factor	Mus musculus	47-80
29530550-6	2018	Fingolimod-dependent tissue preservation was associated with induction of BDNF specifically within the brain and co-localized with neuronal soma.	Fingolimod Hydrochloride	0-10	brain derived neurotrophic factor	Mus musculus	74-78
29530550-9	2018	Fingolimod-mediated BDNF increases within the CNS may contribute to limiting progressive tissue loss during chronic neuroinflammation.	Fingolimod Hydrochloride	0-10	brain derived neurotrophic factor	Mus musculus	20-24
29536648-0	2018	S1PR3 is essential for phosphorylated fingolimod to protect astrocytes against oxygen-glucose deprivation-induced neuroinflammation via inhibiting TLR2/4-NFkappaB signalling.	Fingolimod Hydrochloride	38-48	sphingosine-1-phosphate receptor 3	Homo sapiens	0-5
29481916-0	2018	Pramipexole and Fingolimod exert neuroprotection in a mouse model of Parkinson"s disease by activation of sphingosine kinase 1 and Akt kinase.	Fingolimod Hydrochloride	16-26	sphingosine kinase 1	Mus musculus	106-126
29854416-7	2018	Regardless of age, fingolimod-treated patients were more likely to achieve NEDA-3 versus placebo/IFN beta-1a, with strongest benefits in the youngest patients (all p &lt; 0.05).	Fingolimod Hydrochloride	19-29	interferon alpha 1	Homo sapiens	97-100
29548997-10	2018	Finally, FTY720 significantly inhibited activation of PI3K/Akt/GSK3beta/p65 signaling, which further reduced the expression levels of adhesion molecules in bEND.3 cells treated with B6.MRL-lpr mouse serum.	Fingolimod Hydrochloride	9-15	thymoma viral proto-oncogene 1	Mus musculus	59-62
29548997-10	2018	Finally, FTY720 significantly inhibited activation of PI3K/Akt/GSK3beta/p65 signaling, which further reduced the expression levels of adhesion molecules in bEND.3 cells treated with B6.MRL-lpr mouse serum.	Fingolimod Hydrochloride	9-15	glycogen synthase kinase 3 beta	Mus musculus	63-71
29548997-10	2018	Finally, FTY720 significantly inhibited activation of PI3K/Akt/GSK3beta/p65 signaling, which further reduced the expression levels of adhesion molecules in bEND.3 cells treated with B6.MRL-lpr mouse serum.	Fingolimod Hydrochloride	9-15	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	72-75
29521113-0	2018	Lateral switch to IFN beta-1a 44 mcg may be effective as escalation switch to fingolimod in selected persons with relapsing remitting multiple sclerosis: a real-world setting experience.	Fingolimod Hydrochloride	78-88	interferon beta 1	Homo sapiens	18-26
30083262-9	2018	FTY720 in combination with gemcitabine breached the mitochondrial membrane potential, altered the S1PR1-STAT3 loop, and inhibited epithelial to mesenchymal (EMT) transition.	Fingolimod Hydrochloride	0-6	signal transducer and activator of transcription 3	Homo sapiens	104-109
30083262-9	2018	FTY720 in combination with gemcitabine breached the mitochondrial membrane potential, altered the S1PR1-STAT3 loop, and inhibited epithelial to mesenchymal (EMT) transition.	Fingolimod Hydrochloride	0-6	IL2 inducible T cell kinase	Homo sapiens	157-160
29518148-0	2018	Beneficial effects of fingolimod in MS patients with high serum Sema4A levels.	Fingolimod Hydrochloride	22-32	semaphorin 4A	Homo sapiens	64-70
29618748-5	2018	We started fingolimod treatment when CD86-/- NOD mice showed signs of unilateral hind limb weakness and continued at a dose of 1 mg/kg/day for eight weeks.	Fingolimod Hydrochloride	11-21	CD86 antigen	Mus musculus	37-41
29623068-3	2018	Oncogenic IGFBP-3 signaling can be targeted by combination treatment with the S1P receptor modulator and SphK inhibitor, fingolimod, and the EGFR kinase inhibitor, gefitinib (F + G).	Fingolimod Hydrochloride	121-131	insulin-like growth factor binding protein 3	Mus musculus	10-17
29518148-3	2018	Thus, in this study we investigated whether fingolimod has beneficial effects on MS patients with high Sema4A levels.	Fingolimod Hydrochloride	44-54	semaphorin 4A	Homo sapiens	103-109
29518148-8	2018	Consistent with this observation, improvement in the disease severity of EAE mice receiving recombinant Sema4A-Fc was also observed after fingolimod treatment.	Fingolimod Hydrochloride	138-148	semaphorin 4A	Homo sapiens	104-110
29205338-0	2018	S1P receptor antagonists fingolimod and siponimod do not improve the outcome of experimental autoimmune myasthenia gravis mice after disease onset.	Fingolimod Hydrochloride	25-35	sphingosine-1-phosphate receptor 1	Mus musculus	0-3
29205338-3	2018	Functional sphingosine-1-phosphate (S1P) antagonists like fingolimod and siponimod (BAF312) are successfully used for the treatment of multiple sclerosis, and fingolimod was shown to prevent the development of myasthenic symptoms in experimental autoimmune myasthenia gravis (EAMG), the standard model of MG.	Fingolimod Hydrochloride	58-68	sphingosine-1-phosphate receptor 1	Mus musculus	36-39
29205338-3	2018	Functional sphingosine-1-phosphate (S1P) antagonists like fingolimod and siponimod (BAF312) are successfully used for the treatment of multiple sclerosis, and fingolimod was shown to prevent the development of myasthenic symptoms in experimental autoimmune myasthenia gravis (EAMG), the standard model of MG.	Fingolimod Hydrochloride	159-169	sphingosine-1-phosphate receptor 1	Mus musculus	36-39
29197515-0	2018	Fingolimod anti-inflammatory and neuroprotective effects modulation of RAGE axis in multiple sclerosis patients.	Fingolimod Hydrochloride	0-10	advanced glycosylation end-product specific receptor	Homo sapiens	71-75
29197515-1	2018	BACKGROUND: We investigated Fingolimod treatment effects on the RAGE (receptor for advanced glycation endproducts) axis in multiple sclerosis (MS) patients.	Fingolimod Hydrochloride	28-38	advanced glycosylation end-product specific receptor	Homo sapiens	64-68
29197515-1	2018	BACKGROUND: We investigated Fingolimod treatment effects on the RAGE (receptor for advanced glycation endproducts) axis in multiple sclerosis (MS) patients.	Fingolimod Hydrochloride	28-38	advanced glycosylation end-product specific receptor	Homo sapiens	70-113
29197515-2	2018	The primary outcome of the study was whether Fingolimod treatment increases serum levels of the soluble RAGE isoforms, sRAGE and esRAGE - both being considered putative endogenous inhibitors of RAGE signaling.	Fingolimod Hydrochloride	45-55	advanced glycosylation end-product specific receptor	Homo sapiens	104-108
29197515-2	2018	The primary outcome of the study was whether Fingolimod treatment increases serum levels of the soluble RAGE isoforms, sRAGE and esRAGE - both being considered putative endogenous inhibitors of RAGE signaling.	Fingolimod Hydrochloride	45-55	advanced glycosylation end-product specific receptor	Homo sapiens	120-124
29197515-6	2018	In addition, Fingolimod treatment reduced serum levels of HMGB1 by 71.6% (P = 0.02) and pentosidine serum levels by 41.3% (P = 0.12).	Fingolimod Hydrochloride	13-23	high mobility group box 1	Homo sapiens	58-63
29195114-4	2018	RESULT: Our patient developed CD30+ cutaneous large cell lymphoma two years after initiation of Fingolimod treatment and her symptoms regressed following the cessation of treatment.	Fingolimod Hydrochloride	96-106	TNF receptor superfamily member 8	Homo sapiens	30-34
30032136-14	2018	The metformin/FTY720 regimen markedly induced ROS generation; moreover, apoptosis, ER stress and inhibition of PI3K/AKT/ mTOR were attenuated by the ROS scavenger NAC.	Fingolimod Hydrochloride	14-20	AKT serine/threonine kinase 1	Homo sapiens	116-119
30032136-14	2018	The metformin/FTY720 regimen markedly induced ROS generation; moreover, apoptosis, ER stress and inhibition of PI3K/AKT/ mTOR were attenuated by the ROS scavenger NAC.	Fingolimod Hydrochloride	14-20	mechanistic target of rapamycin kinase	Homo sapiens	121-125
30032136-14	2018	The metformin/FTY720 regimen markedly induced ROS generation; moreover, apoptosis, ER stress and inhibition of PI3K/AKT/ mTOR were attenuated by the ROS scavenger NAC.	Fingolimod Hydrochloride	14-20	X-linked Kx blood group	Homo sapiens	163-166
29532286-9	2018	Fingolimod treatment is likely to increase serum JCVAb index, possibly leading to the development of PML.	Fingolimod Hydrochloride	0-10	PML nuclear body scaffold	Homo sapiens	101-104
29535596-10	2018	FTY720 induced PP2A activation would lead to dephosphorylation and activation of TTP and decreased production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-8.	Fingolimod Hydrochloride	0-6	zinc finger protein 36	Rattus norvegicus	81-84
29535596-10	2018	FTY720 induced PP2A activation would lead to dephosphorylation and activation of TTP and decreased production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-8.	Fingolimod Hydrochloride	0-6	tumor necrosis factor	Rattus norvegicus	113-146
29535596-10	2018	FTY720 induced PP2A activation would lead to dephosphorylation and activation of TTP and decreased production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-8.	Fingolimod Hydrochloride	0-6	interleukin 6	Rattus norvegicus	148-166
29497558-8	2018	Conclusions: Low baseline ALC and treatment history with any interferon-beta were risk factors for fingolimod-induced lymphopenia, possibly predicted from ALC on day 2.	Fingolimod Hydrochloride	99-109	interferon beta 1	Homo sapiens	61-76
29079163-0	2018	Fingolimod induces BAFF and expands circulating transitional B cells without activating memory B cells and plasma cells in multiple sclerosis.	Fingolimod Hydrochloride	0-10	TNF superfamily member 13b	Homo sapiens	19-23
29079163-3	2018	Compared with healthy controls and untreated MS patients, fingolimod-treated MS patients had significantly higher serum concentrations of BAFF, which positively correlated with the proportions and the absolute numbers of transitional B cells in blood.	Fingolimod Hydrochloride	58-68	TNF superfamily member 13b	Homo sapiens	138-142
29079163-4	2018	Despite the elevated concentrations of BAFF in fingolimod-treated MS patients, serum levels of soluble transmembrane activator and calcium-modulating cyclophilin ligand interactor, and B cell maturation antigen were not elevated.	Fingolimod Hydrochloride	47-57	TNF superfamily member 13b	Homo sapiens	39-43
29079163-5	2018	Our results show that fingolimod induces BAFF in the circulation and expands transitional B cells, but does not activate memory B cells or plasma cells in MS, which is favorable for the treatment of this disease.	Fingolimod Hydrochloride	22-32	TNF superfamily member 13b	Homo sapiens	41-45
29140922-0	2018	Fingolimod reduces neuropathic pain behaviors in a mouse model of multiple sclerosis by a sphingosine-1 phosphate receptor 1-dependent inhibition of central sensitization in the dorsal horn.	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Mus musculus	90-124
29140922-3	2018	We explored the analgesic potential of fingolimod (FTY720), an agonist and/or functional antagonist at the sphingosine-1-phosphate receptor 1 (S1PR1), because it reduces hyperalgesia in models of peripheral inflammatory and neuropathic pain.	Fingolimod Hydrochloride	39-49	sphingosine-1-phosphate receptor 1	Mus musculus	107-141
29140922-3	2018	We explored the analgesic potential of fingolimod (FTY720), an agonist and/or functional antagonist at the sphingosine-1-phosphate receptor 1 (S1PR1), because it reduces hyperalgesia in models of peripheral inflammatory and neuropathic pain.	Fingolimod Hydrochloride	39-49	sphingosine-1-phosphate receptor 1	Mus musculus	143-148
29140922-3	2018	We explored the analgesic potential of fingolimod (FTY720), an agonist and/or functional antagonist at the sphingosine-1-phosphate receptor 1 (S1PR1), because it reduces hyperalgesia in models of peripheral inflammatory and neuropathic pain.	Fingolimod Hydrochloride	51-57	sphingosine-1-phosphate receptor 1	Mus musculus	143-148
29140922-7	2018	Fingolimod also reduced cellular markers of central sensitization of neurons in the dorsal horn of the spinal cord: glutamate-evoked Ca signaling and stimulus-evoked phospho-extracellular signal-related kinase ERK (pERK) expression, as well as upregulation of astrocytes (GFAP) and macrophage/microglia (Iba1) immunoreactivity.	Fingolimod Hydrochloride	0-10	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	215-219
29140922-7	2018	Fingolimod also reduced cellular markers of central sensitization of neurons in the dorsal horn of the spinal cord: glutamate-evoked Ca signaling and stimulus-evoked phospho-extracellular signal-related kinase ERK (pERK) expression, as well as upregulation of astrocytes (GFAP) and macrophage/microglia (Iba1) immunoreactivity.	Fingolimod Hydrochloride	0-10	glial fibrillary acidic protein	Mus musculus	272-276
29140922-7	2018	Fingolimod also reduced cellular markers of central sensitization of neurons in the dorsal horn of the spinal cord: glutamate-evoked Ca signaling and stimulus-evoked phospho-extracellular signal-related kinase ERK (pERK) expression, as well as upregulation of astrocytes (GFAP) and macrophage/microglia (Iba1) immunoreactivity.	Fingolimod Hydrochloride	0-10	induction of brown adipocytes 1	Mus musculus	304-308
29140922-8	2018	The antihyperalgesic effects of fingolimod were prevented or reversed by the S1PR1 antagonist W146 (1 mg/kg daily, i.p.)	Fingolimod Hydrochloride	32-42	sphingosine-1-phosphate receptor 1	Mus musculus	77-82
29140922-11	2018	We conclude that fingolimod behaves as an S1PR1 agonist to reduce pain in multiple sclerosis by reversing central sensitization of spinal nociceptive neurons.	Fingolimod Hydrochloride	17-27	sphingosine-1-phosphate receptor 1	Mus musculus	42-47
29673751-0	2018	[Primary cutaneous CD30+ T-cell lymphoproliferation during treatment with fingolimod: Case report and literature review].	Fingolimod Hydrochloride	74-84	TNF receptor superfamily member 8	Homo sapiens	19-23
29673751-2	2018	We report a case of a primary cutaneous CD30+ T-cell lymphoproliferation occurring 6 months after initiation of fingolimod.	Fingolimod Hydrochloride	112-122	TNF receptor superfamily member 8	Homo sapiens	40-44
29673751-10	2018	We would also stress that these CD30+ lymphoproliferative disorders can disappear spontaneously, as in our case, even if treatment by fingolimod is continued.	Fingolimod Hydrochloride	134-144	TNF receptor superfamily member 8	Homo sapiens	32-36
28543283-4	2017	We assessed whether enhancing PP2A activity with fingolimod (FTY720) or 2-amino-4-(4-(heptyloxy) phenyl)-2-methylbutan-1-ol (AAL(S) ), or inhibiting proteasome activity with bortezomib (BORT), could suppress experimental AAD.	Fingolimod Hydrochloride	49-59	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	30-34
28543283-4	2017	We assessed whether enhancing PP2A activity with fingolimod (FTY720) or 2-amino-4-(4-(heptyloxy) phenyl)-2-methylbutan-1-ol (AAL(S) ), or inhibiting proteasome activity with bortezomib (BORT), could suppress experimental AAD.	Fingolimod Hydrochloride	61-67	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	30-34
29108879-8	2017	MS patients treated with fingolimod had higher LCN2 levels compared to those on natalizumab (r=0.25, p=0.03).	Fingolimod Hydrochloride	25-35	lipocalin 2	Homo sapiens	47-51
29214311-15	2017	The therapeutic mechanisms of fingolimod may be associated with inhibitory roles of "cytokines-MMPs/MAPKs" cycle in NOD mouse ocular surface tissues by mediating S1PRs in infiltrating leukocytes.	Fingolimod Hydrochloride	30-40	matrix metallopeptidase 2	Mus musculus	95-99
28620801-0	2017	FTY720 Attenuates Infection-Induced Enhancement of Abeta Accumulation in APP/PS1 Mice by Modulating Astrocytic Activation.	Fingolimod Hydrochloride	0-6	amyloid beta (A4) precursor protein	Mus musculus	51-56
28940479-10	2017	Application of the ceramide analogue C2 and the sphingosine-1-phosphate-receptor agonist Fingolimod (FTY720) up-regulated levels of IL-1beta and cleaved caspase-1 in wild-type microglia, whereas ASC-/- microglia were unaffected.	Fingolimod Hydrochloride	89-99	interleukin 1 beta	Homo sapiens	132-140
28940479-10	2017	Application of the ceramide analogue C2 and the sphingosine-1-phosphate-receptor agonist Fingolimod (FTY720) up-regulated levels of IL-1beta and cleaved caspase-1 in wild-type microglia, whereas ASC-/- microglia were unaffected.	Fingolimod Hydrochloride	89-99	caspase 1	Homo sapiens	153-162
28940479-10	2017	Application of the ceramide analogue C2 and the sphingosine-1-phosphate-receptor agonist Fingolimod (FTY720) up-regulated levels of IL-1beta and cleaved caspase-1 in wild-type microglia, whereas ASC-/- microglia were unaffected.	Fingolimod Hydrochloride	89-99	PYD and CARD domain containing	Homo sapiens	195-198
28620801-0	2017	FTY720 Attenuates Infection-Induced Enhancement of Abeta Accumulation in APP/PS1 Mice by Modulating Astrocytic Activation.	Fingolimod Hydrochloride	0-6	presenilin 1	Mus musculus	77-80
29186197-0	2017	Fingolimod suppresses neuronal autophagy through the mTOR/p70S6K pathway and alleviates ischemic brain damage in mice.	Fingolimod Hydrochloride	0-10	mechanistic target of rapamycin kinase	Mus musculus	53-57
27924525-13	2017	Fingolimod decreased infiltrated T lymphocytes and NK cells but increased the percentage of regulatory T (Treg) cells, and the concentration of IL-10 on the 3rd day after TBI.	Fingolimod Hydrochloride	0-10	interleukin 10	Mus musculus	144-149
29114096-0	2017	Fingolimod Protects Against Ischemic White Matter Damage by Modulating Microglia Toward M2 Polarization via STAT3 Pathway.	Fingolimod Hydrochloride	0-10	signal transducer and activator of transcription 3	Homo sapiens	108-113
28813646-9	2017	Finally, we showed that other well-known PP2A activators, including forskolin and FTY720, did not inhibit CIP2A and that their activities were not dependent on CIP2A.	Fingolimod Hydrochloride	82-88	protein phosphatase 2 phosphatase activator	Homo sapiens	41-45
29186197-0	2017	Fingolimod suppresses neuronal autophagy through the mTOR/p70S6K pathway and alleviates ischemic brain damage in mice.	Fingolimod Hydrochloride	0-10	ribosomal protein S6 kinase, polypeptide 1	Mus musculus	58-64
29299124-6	2017	FTY-720 rapidly inhibits TRPM7 channel activity, and inhibited TRPM7 kinase activity, modulates calcium signaling, induces a loss of mitochondrial membrane potential and opening of the mitochondrial permeability transition pore, and ultimately leads to cell death.	Fingolimod Hydrochloride	0-7	transient receptor potential cation channel subfamily M member 7	Homo sapiens	25-30
29299124-6	2017	FTY-720 rapidly inhibits TRPM7 channel activity, and inhibited TRPM7 kinase activity, modulates calcium signaling, induces a loss of mitochondrial membrane potential and opening of the mitochondrial permeability transition pore, and ultimately leads to cell death.	Fingolimod Hydrochloride	0-7	transient receptor potential cation channel subfamily M member 7	Homo sapiens	63-68
28716816-6	2017	We show in vitro and in human NB xenograft models that treatment with FTY720, an FDA-approved drug and antagonist of S1PR1, dramatically sensitizes drug-resistant cells to etoposide.	Fingolimod Hydrochloride	70-76	sphingosine-1-phosphate receptor 1	Homo sapiens	117-122
28653281-7	2017	Furthermore, a temporary reduction of mTOR signaling pathway activity, indicated by reduced phosphorylated mammalian target of rapamycin and phosphorylated p70S6k levels, and by increased phosphorylated Akt in WAG/Rij rats of 6 months of age accompanied the transitory antiepileptogenic effects of fingolimod.	Fingolimod Hydrochloride	298-308	mechanistic target of rapamycin kinase	Homo sapiens	38-42
29018225-2	2017	Although S1P1 agonist fingolimod is currently used for the treatment of multiple sclerosis (MS) little is known how S1P1 signaling regulates Th17 and Treg cell homeostasis.	Fingolimod Hydrochloride	22-32	sphingosine-1-phosphate receptor 1	Mus musculus	9-13
28695300-2	2017	Sphingosine-1-phosphate (S1P) receptor antagonist and sphingosine kinase 1 (SK1) inhibitor FTY720 (FTY) has promising anticancer properties, however, it causes systemic lymphopenia which impairs its use in cancer patients.	Fingolimod Hydrochloride	91-97	sphingosine kinase 1	Homo sapiens	76-79
28817212-11	2017	RESULTS: Maternal fingolimod treatment attenuated endotoxin-related fetal brain injury and led to lower immunoreactions for IL-6, caspase-3, and S100beta compared with endotoxin controls (P &lt; 0.0001 for all comparisons).	Fingolimod Hydrochloride	18-28	interleukin 6	Rattus norvegicus	124-128
28817212-11	2017	RESULTS: Maternal fingolimod treatment attenuated endotoxin-related fetal brain injury and led to lower immunoreactions for IL-6, caspase-3, and S100beta compared with endotoxin controls (P &lt; 0.0001 for all comparisons).	Fingolimod Hydrochloride	18-28	caspase 3	Rattus norvegicus	130-139
28817212-11	2017	RESULTS: Maternal fingolimod treatment attenuated endotoxin-related fetal brain injury and led to lower immunoreactions for IL-6, caspase-3, and S100beta compared with endotoxin controls (P &lt; 0.0001 for all comparisons).	Fingolimod Hydrochloride	18-28	S100 calcium binding protein B	Rattus norvegicus	145-153
28237728-9	2017	However, while TH1 cells responded consistently to viruses, TH1/TH17CM cells reacted strongly with John Cunningham virus in healthy subjects but responded instead to myelin-derived self-antigens in patients with MS. Fingolimod and natalizumab therapies efficiently targeted autoreactive TH1/TH17CM cells but also blocked virus-specific TH1 cells.	Fingolimod Hydrochloride	216-226	negative elongation factor complex member C/D	Homo sapiens	60-63
28695300-2	2017	Sphingosine-1-phosphate (S1P) receptor antagonist and sphingosine kinase 1 (SK1) inhibitor FTY720 (FTY) has promising anticancer properties, however, it causes systemic lymphopenia which impairs its use in cancer patients.	Fingolimod Hydrochloride	91-97	sphingosine kinase 1	Homo sapiens	54-74
27631876-0	2017	High-Resolution Expression Profiling of Peripheral Blood CD8+ Cells in Patients with Multiple Sclerosis Displays Fingolimod-Induced Immune Cell Redistribution.	Fingolimod Hydrochloride	113-123	CD8a molecule	Homo sapiens	57-60
27631876-10	2017	The fingolimod-induced transcriptome changes reflect a shift in the proportions of CD8+ T cell subsets, with CCR7- effector memory T cells being relatively increased in frequency in the blood of fingolimod-treated patients.	Fingolimod Hydrochloride	4-14	CD8a molecule	Homo sapiens	83-86
27631876-10	2017	The fingolimod-induced transcriptome changes reflect a shift in the proportions of CD8+ T cell subsets, with CCR7- effector memory T cells being relatively increased in frequency in the blood of fingolimod-treated patients.	Fingolimod Hydrochloride	4-14	C-C motif chemokine receptor 7	Homo sapiens	109-113
27631876-10	2017	The fingolimod-induced transcriptome changes reflect a shift in the proportions of CD8+ T cell subsets, with CCR7- effector memory T cells being relatively increased in frequency in the blood of fingolimod-treated patients.	Fingolimod Hydrochloride	195-205	CD8a molecule	Homo sapiens	83-86
27631876-10	2017	The fingolimod-induced transcriptome changes reflect a shift in the proportions of CD8+ T cell subsets, with CCR7- effector memory T cells being relatively increased in frequency in the blood of fingolimod-treated patients.	Fingolimod Hydrochloride	195-205	C-C motif chemokine receptor 7	Homo sapiens	109-113
28742634-1	2017	HYPOTHESIS: The potential of Fingolimod (FTY-720), a sphingosine-1-phosphate analogue, to revoke the changes in cochlear blood flow induced by tumor necrosis factor (TNF) was investigated.	Fingolimod Hydrochloride	41-48	tumor necrosis factor	Cavia porcellus	143-164
28742634-1	2017	HYPOTHESIS: The potential of Fingolimod (FTY-720), a sphingosine-1-phosphate analogue, to revoke the changes in cochlear blood flow induced by tumor necrosis factor (TNF) was investigated.	Fingolimod Hydrochloride	29-39	tumor necrosis factor	Cavia porcellus	143-164
28742634-1	2017	HYPOTHESIS: The potential of Fingolimod (FTY-720), a sphingosine-1-phosphate analogue, to revoke the changes in cochlear blood flow induced by tumor necrosis factor (TNF) was investigated.	Fingolimod Hydrochloride	29-39	tumor necrosis factor	Cavia porcellus	166-169
28506594-7	2017	Based on these findings, and because side effects were not detected, we suggest that clinically approved immune modulators such as fingolimod and teriflunomide may be suitable to attenuate progression of CLN1 and CLN3 disease and, possibly, other orphan diseases with pathogenically relevant neuroinflammation.	Fingolimod Hydrochloride	131-141	palmitoyl-protein thioesterase 1	Mus musculus	204-208
28237728-9	2017	However, while TH1 cells responded consistently to viruses, TH1/TH17CM cells reacted strongly with John Cunningham virus in healthy subjects but responded instead to myelin-derived self-antigens in patients with MS. Fingolimod and natalizumab therapies efficiently targeted autoreactive TH1/TH17CM cells but also blocked virus-specific TH1 cells.	Fingolimod Hydrochloride	216-226	negative elongation factor complex member C/D	Homo sapiens	60-63
28237728-9	2017	However, while TH1 cells responded consistently to viruses, TH1/TH17CM cells reacted strongly with John Cunningham virus in healthy subjects but responded instead to myelin-derived self-antigens in patients with MS. Fingolimod and natalizumab therapies efficiently targeted autoreactive TH1/TH17CM cells but also blocked virus-specific TH1 cells.	Fingolimod Hydrochloride	216-226	negative elongation factor complex member C/D	Homo sapiens	60-63
28778177-2	2017	This pre-clinical study investigated the combination of the EGFR inhibitor gefitinib with the sphingosine kinase (SphK) inhibitor FTY720 (Fingolimod), aiming to block tumorigenic signaling downstream of IGFBP-3, which is abundantly expressed in basal-like TNBC.	Fingolimod Hydrochloride	130-136	insulin-like growth factor binding protein 3	Mus musculus	203-210
28778177-2	2017	This pre-clinical study investigated the combination of the EGFR inhibitor gefitinib with the sphingosine kinase (SphK) inhibitor FTY720 (Fingolimod), aiming to block tumorigenic signaling downstream of IGFBP-3, which is abundantly expressed in basal-like TNBC.	Fingolimod Hydrochloride	138-148	insulin-like growth factor binding protein 3	Mus musculus	203-210
28742634-1	2017	HYPOTHESIS: The potential of Fingolimod (FTY-720), a sphingosine-1-phosphate analogue, to revoke the changes in cochlear blood flow induced by tumor necrosis factor (TNF) was investigated.	Fingolimod Hydrochloride	41-48	tumor necrosis factor	Cavia porcellus	166-169
28717222-4	2017	Mechanistic evidence suggests that FTY720-induced apoptosis was associated with its ability to inhibit Akt-NF-kappaB signaling, to facilitate the proteasomal degradation of the antiapoptotic protein Mcl-1, and to increase reactive oxygen species (ROS) generation.	Fingolimod Hydrochloride	35-41	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	199-204
28236206-14	2017	Furthermore, Fingolimod reduce glutamate-mediated intracortical excitability in relapsing-remitting MS. Glatiramer acetate -COPAXONE , an immunomodulator drug for MS, reverses TNF-alpha-induced alterations of striatal glutamate-mediated excitatory postsynaptic currents in EAE-afflicted mice.	Fingolimod Hydrochloride	13-23	tumor necrosis factor	Mus musculus	176-185
28218904-7	2017	Furthermore, we showed that FTY720 triggers MDSCs to release GM-CSF via S1P receptor 3 (S1pr3) through Rho kinase and extracellular signal-regulated kinase-dependent pathway.	Fingolimod Hydrochloride	28-34	colony stimulating factor 2	Homo sapiens	61-67
28218904-7	2017	Furthermore, we showed that FTY720 triggers MDSCs to release GM-CSF via S1P receptor 3 (S1pr3) through Rho kinase and extracellular signal-regulated kinase-dependent pathway.	Fingolimod Hydrochloride	28-34	sphingosine-1-phosphate receptor 3	Homo sapiens	72-86
28218904-7	2017	Furthermore, we showed that FTY720 triggers MDSCs to release GM-CSF via S1P receptor 3 (S1pr3) through Rho kinase and extracellular signal-regulated kinase-dependent pathway.	Fingolimod Hydrochloride	28-34	sphingosine-1-phosphate receptor 3	Homo sapiens	88-93
28577576-14	2017	Studies using S1P3 selective agonists/antagonists as well as Fingolimod (FTY720) confirmed that stimulation of S1P3 induces COX-2 expression in astrocytes.	Fingolimod Hydrochloride	73-79	sphingosine-1-phosphate receptor 3	Mus musculus	111-115
28577576-14	2017	Studies using S1P3 selective agonists/antagonists as well as Fingolimod (FTY720) confirmed that stimulation of S1P3 induces COX-2 expression in astrocytes.	Fingolimod Hydrochloride	73-79	prostaglandin-endoperoxide synthase 2	Mus musculus	124-129
27439747-6	2017	To increase BDNF, we use a novel strategy, repeated intraperitoneal injections of fingolimod (Gilenya).	Fingolimod Hydrochloride	82-92	brain derived neurotrophic factor	Mus musculus	12-16
28480040-8	2017	Together, FTY720-induced an enhanced response of artery contractility in aorta and in arterial pressure involving ERK activation, with an attenuation in basilarartery contractility.	Fingolimod Hydrochloride	10-16	Eph receptor B1	Rattus norvegicus	114-117
28082351-6	2017	Together, these findings suggest that FTY720 administration can ameliorate cholesterol and sphingolipid storage and trafficking defects in NPC1 mutant fibroblasts.	Fingolimod Hydrochloride	38-44	NPC intracellular cholesterol transporter 1	Homo sapiens	139-143
27812788-9	2017	The SF2/ASF reduction, parallel to JCV activation, during the second year of therapy with natalizumab, but not with fingolimod, may help explain the increased risk of PML after the second year of treatment with natalizumab, but not with fingolimod.	Fingolimod Hydrochloride	237-247	serine and arginine rich splicing factor 1	Homo sapiens	4-7
27812788-9	2017	The SF2/ASF reduction, parallel to JCV activation, during the second year of therapy with natalizumab, but not with fingolimod, may help explain the increased risk of PML after the second year of treatment with natalizumab, but not with fingolimod.	Fingolimod Hydrochloride	237-247	serine and arginine rich splicing factor 1	Homo sapiens	8-11
28356890-2	2017	Sphingosine-1-phosphate receptor (S1PR1) modulators have been approved for the management of MS. Phosphorylated fingolimod mimics endogenous sphingosine-1-phosphate (S1P), a bioactive lipid that regulates remyelination and cell injury.	Fingolimod Hydrochloride	112-122	sphingosine-1-phosphate receptor 1	Homo sapiens	34-39
28356890-4	2017	This study utilized the fingolimod and amiselimod scaffolds, together with their critical binding interactions for the S1PR1 Ligand Binding Pocket, as templates for the in silico de novo design of high efficiency binding Lipinski rule-compliant molecules.	Fingolimod Hydrochloride	24-34	sphingosine-1-phosphate receptor 1	Homo sapiens	119-124
28039158-3	2017	Therefore, we hypothesized that FTY720, an S1P antagonist, would ameliorate NASH by inhibiting proinflammatory monocyte chemotaxis.	Fingolimod Hydrochloride	32-38	sphingosine-1-phosphate receptor 1	Mus musculus	43-46
28063629-4	2017	MS therapies fingolimod and dimethyl fumarate altered blood ZMIZ1 gene expression compared to untreated MS.	Fingolimod Hydrochloride	13-23	zinc finger MIZ-type containing 1	Homo sapiens	60-65
28241801-12	2017	Further, the PP2A activator (FTY720) and the CAMKIIalpha inhibitor (KN93) could reverse the neuroprotective effect of propofol.	Fingolimod Hydrochloride	29-35	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	13-17
28231856-9	2017	CD83, CD150, and HLADR were all inhibited, but CD86 was upregulated in DCs after incubation in the presence of fingolimod.	Fingolimod Hydrochloride	111-121	CD86 molecule	Homo sapiens	47-51
28054340-0	2017	Fingolimod confers neuroprotection through activation of Rac1 after experimental germinal matrix hemorrhage in rat pups.	Fingolimod Hydrochloride	0-10	Rac family small GTPase 1	Rattus norvegicus	57-61
28155899-3	2017	Fingolimod modulates sphingosine-1-phosphate receptors, thereby preventing the egress of lymphocytes, especially CCR7-expressing CD8+ and CD4+ T cells, from lymphoid tissues.	Fingolimod Hydrochloride	0-10	C-C motif chemokine receptor 7	Homo sapiens	113-117
28082452-6	2017	T-cell egress from lymph nodes was found to be a critical initial step for the onset of hypertension as fingolimod, a S1P-receptor agonist sequestering lymphocytes in the lymph nodes and inducing lymphopenia, blunted BP responses to AngII.	Fingolimod Hydrochloride	104-114	sphingosine-1-phosphate receptor 1	Mus musculus	118-121
28082452-6	2017	T-cell egress from lymph nodes was found to be a critical initial step for the onset of hypertension as fingolimod, a S1P-receptor agonist sequestering lymphocytes in the lymph nodes and inducing lymphopenia, blunted BP responses to AngII.	Fingolimod Hydrochloride	104-114	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	233-238
28155899-3	2017	Fingolimod modulates sphingosine-1-phosphate receptors, thereby preventing the egress of lymphocytes, especially CCR7-expressing CD8+ and CD4+ T cells, from lymphoid tissues.	Fingolimod Hydrochloride	0-10	CD8a molecule	Homo sapiens	129-132
28155899-3	2017	Fingolimod modulates sphingosine-1-phosphate receptors, thereby preventing the egress of lymphocytes, especially CCR7-expressing CD8+ and CD4+ T cells, from lymphoid tissues.	Fingolimod Hydrochloride	0-10	CD4 molecule	Homo sapiens	138-141
28283109-4	2017	Fingolimod and dimethyl fumarate have also been unquestionably associated with a risk of PML in the MS population.	Fingolimod Hydrochloride	0-10	PML nuclear body scaffold	Homo sapiens	89-92
28035084-4	2017	Another unexpected finding that fingolimod (FTY720) modulates S1P receptors accelerated drug discovery in this field.	Fingolimod Hydrochloride	32-42	sphingosine-1-phosphate receptor 1	Mus musculus	62-65
28054340-10	2017	S1PR1 agonism showed similar protection, whereas S1PR or Rac1 inhibition abolished the protective effect of fingolimod.	Fingolimod Hydrochloride	108-118	Rac family small GTPase 1	Rattus norvegicus	57-61
28054340-11	2017	Fingolimod treatment improved functional and morphological outcomes after GMH, in part, by tempering acute post-hemorrhagic blood-brain barrier disruption via the activation of the S1PR1/Akt/Rac1 pathway.	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Rattus norvegicus	181-186
28054340-11	2017	Fingolimod treatment improved functional and morphological outcomes after GMH, in part, by tempering acute post-hemorrhagic blood-brain barrier disruption via the activation of the S1PR1/Akt/Rac1 pathway.	Fingolimod Hydrochloride	0-10	AKT serine/threonine kinase 1	Rattus norvegicus	187-190
28054340-11	2017	Fingolimod treatment improved functional and morphological outcomes after GMH, in part, by tempering acute post-hemorrhagic blood-brain barrier disruption via the activation of the S1PR1/Akt/Rac1 pathway.	Fingolimod Hydrochloride	0-10	Rac family small GTPase 1	Rattus norvegicus	191-195
28134307-4	2017	Using a combination of biochemical assays, live imaging and electrophysiology we demonstrate that FTY720 induces a rapid increase in GLUN2A-containing neuroprotective NMDARs on the surface of dendritic spines in cultured hippocampal neurons.	Fingolimod Hydrochloride	98-104	glutamate receptor, ionotropic, NMDA2A (epsilon 1)	Mus musculus	133-139
27802432-4	2017	Pretreatment with FTY720 (2.5 mg/kg) inhibited platelet aggregation induced by ADP, elongated the thrombin time and decreased the fibrinogen levels.	Fingolimod Hydrochloride	18-24	coagulation factor II	Rattus norvegicus	98-106
28035084-4	2017	Another unexpected finding that fingolimod (FTY720) modulates S1P receptors accelerated drug discovery in this field.	Fingolimod Hydrochloride	44-50	sphingosine-1-phosphate receptor 1	Mus musculus	62-65
27671228-2	2017	Emerging evidence shows that FTY720 protects against neural injury via modulation of the sphingosine-1-phosphate 1 receptor (S1PR1).	Fingolimod Hydrochloride	29-35	sphingosine-1-phosphate receptor 1	Mus musculus	125-130
27634580-7	2017	We found that FTY720 administration decreases cell death and glial activation in CA1 and CA3 regions of hippocampus.	Fingolimod Hydrochloride	14-20	carbonic anhydrase 1	Homo sapiens	81-84
27634580-7	2017	We found that FTY720 administration decreases cell death and glial activation in CA1 and CA3 regions of hippocampus.	Fingolimod Hydrochloride	14-20	carbonic anhydrase 3	Homo sapiens	89-92
27671228-6	2017	An S1PR1-selective antagonist, W146, blocked the neuroprotective effects of FTY720.	Fingolimod Hydrochloride	76-82	sphingosine-1-phosphate receptor 1	Mus musculus	3-8
27528608-0	2016	FTY720/Fingolimod Reduces Synucleinopathy and Improves Gut Motility in A53T Mice: CONTRIBUTIONS OF PRO-BRAIN-DERIVED NEUROTROPHIC FACTOR (PRO-BDNF) AND MATURE BDNF.	Fingolimod Hydrochloride	0-6	brain derived neurotrophic factor	Mus musculus	142-146
28003234-4	2016	Fingolimod has been found to inhibit metastatic melanoma growth in a mouse model that depends on vascular endothelial growth factor (VEGF)-induced angiogenesis for metastasis.	Fingolimod Hydrochloride	0-10	vascular endothelial growth factor A	Mus musculus	97-131
28003234-4	2016	Fingolimod has been found to inhibit metastatic melanoma growth in a mouse model that depends on vascular endothelial growth factor (VEGF)-induced angiogenesis for metastasis.	Fingolimod Hydrochloride	0-10	vascular endothelial growth factor A	Mus musculus	133-137
27681411-9	2016	Fingolimod hydrochloride (FTY720), a pak1 activator, inhibited astemizole-induced hypertrophy and cytotoxicity in H9c2 cells.	Fingolimod Hydrochloride	0-24	p21 (RAC1) activated kinase 1	Rattus norvegicus	37-41
27681411-9	2016	Fingolimod hydrochloride (FTY720), a pak1 activator, inhibited astemizole-induced hypertrophy and cytotoxicity in H9c2 cells.	Fingolimod Hydrochloride	26-32	p21 (RAC1) activated kinase 1	Rattus norvegicus	37-41
27683081-7	2016	DOP and FTY720 treatment significantly reduced levels of Evans blue leakage from blood into liver and lung, decreased hematocrit values, and lowered plasma levels of VEGF-A in septic mice.	Fingolimod Hydrochloride	8-14	vascular endothelial growth factor A	Mus musculus	166-172
27857690-0	2016	Interferon-Beta Increases Plasma Ceramides of Specific Chain Length in Multiple Sclerosis Patients, Unlike Fingolimod or Natalizumab.	Fingolimod Hydrochloride	107-117	interferon beta 1	Homo sapiens	0-15
27663260-3	2016	The therapeutic potential of targeting this system took center stage when it was demonstrated that the immune modulator, fingolimod (FTY720/Gilenya), exerts it lymphopenic effect by acting on S1P receptors, primarily on S1P receptor 1 (S1P1).	Fingolimod Hydrochloride	121-131	sphingosine-1-phosphate receptor 1	Homo sapiens	220-234
27663260-3	2016	The therapeutic potential of targeting this system took center stage when it was demonstrated that the immune modulator, fingolimod (FTY720/Gilenya), exerts it lymphopenic effect by acting on S1P receptors, primarily on S1P receptor 1 (S1P1).	Fingolimod Hydrochloride	121-131	sphingosine-1-phosphate receptor 1	Homo sapiens	236-240
27752051-2	2016	Fingolimod, a highly effective disease-modifying drug for MS, retains CCR7+ central memory T cells in which autoaggressive T cells putatively exist, in secondary lymphoid organs, although relapse may still occur in some patients.	Fingolimod Hydrochloride	0-10	C-C motif chemokine receptor 7	Homo sapiens	70-74
27752051-6	2016	Interestingly, T cells from fingolimod-treated patients exhibited interferon-gamma biased production, and more myelin basic protein-reactive cells was noted in CD56+ than in CD56- T cells.	Fingolimod Hydrochloride	28-38	interferon gamma	Homo sapiens	66-82
27752051-6	2016	Interestingly, T cells from fingolimod-treated patients exhibited interferon-gamma biased production, and more myelin basic protein-reactive cells was noted in CD56+ than in CD56- T cells.	Fingolimod Hydrochloride	28-38	myelin basic protein	Homo sapiens	111-131
27519818-8	2016	Repeated oral dosing of the S1PL inhibitor in telemeterized, conscious rats resulted in significant bradycardia within 48 hours of drug treatment, comparable in magnitude to the bradycardia induced by 3 mg/kg fingolimod.	Fingolimod Hydrochloride	209-219	sphingosine-1-phosphate lyase 1	Rattus norvegicus	28-32
27507852-0	2016	FTY720 (Fingolimod) Inhibits HIF1 and HIF2 Signaling, Promotes Vascular Remodeling, and Chemosensitizes in Renal Cell Carcinoma Animal Model.	Fingolimod Hydrochloride	0-6	hypoxia inducible factor 1 subunit alpha	Homo sapiens	29-33
27507852-0	2016	FTY720 (Fingolimod) Inhibits HIF1 and HIF2 Signaling, Promotes Vascular Remodeling, and Chemosensitizes in Renal Cell Carcinoma Animal Model.	Fingolimod Hydrochloride	8-18	hypoxia inducible factor 1 subunit alpha	Homo sapiens	29-33
27507852-4	2016	Here, we report that FTY720, an inhibitor of the S1P signaling pathway, inhibits both HIF1alpha and HIF2alpha accumulation in several human cancer cell lines.	Fingolimod Hydrochloride	21-27	hypoxia inducible factor 1 subunit alpha	Homo sapiens	86-95
27507852-4	2016	Here, we report that FTY720, an inhibitor of the S1P signaling pathway, inhibits both HIF1alpha and HIF2alpha accumulation in several human cancer cell lines.	Fingolimod Hydrochloride	21-27	endothelial PAS domain protein 1	Homo sapiens	100-109
27003946-5	2017	RESULTS: The levels of NFL, CXCL13, and CHI3L1 decreased ( p &lt; 0.05) after fingolimod treatment.	Fingolimod Hydrochloride	78-88	neurofilament light chain	Homo sapiens	23-26
27003946-5	2017	RESULTS: The levels of NFL, CXCL13, and CHI3L1 decreased ( p &lt; 0.05) after fingolimod treatment.	Fingolimod Hydrochloride	78-88	C-X-C motif chemokine ligand 13	Homo sapiens	28-34
27003946-5	2017	RESULTS: The levels of NFL, CXCL13, and CHI3L1 decreased ( p &lt; 0.05) after fingolimod treatment.	Fingolimod Hydrochloride	78-88	chitinase 3 like 1	Homo sapiens	40-46
27003946-8	2017	CONCLUSION: We found reduced inflammatory activity (CXCL13, CHI3L1, and CHIT1) and reduced axonal damage (NFL) in patients switching from first-line DMTs to fingolimod.	Fingolimod Hydrochloride	157-167	C-X-C motif chemokine ligand 13	Homo sapiens	52-58
27003946-8	2017	CONCLUSION: We found reduced inflammatory activity (CXCL13, CHI3L1, and CHIT1) and reduced axonal damage (NFL) in patients switching from first-line DMTs to fingolimod.	Fingolimod Hydrochloride	157-167	chitinase 3 like 1	Homo sapiens	60-66
27003946-8	2017	CONCLUSION: We found reduced inflammatory activity (CXCL13, CHI3L1, and CHIT1) and reduced axonal damage (NFL) in patients switching from first-line DMTs to fingolimod.	Fingolimod Hydrochloride	157-167	chitinase 1	Homo sapiens	72-77
27003946-8	2017	CONCLUSION: We found reduced inflammatory activity (CXCL13, CHI3L1, and CHIT1) and reduced axonal damage (NFL) in patients switching from first-line DMTs to fingolimod.	Fingolimod Hydrochloride	157-167	neurofilament light chain	Homo sapiens	106-109
27983657-5	2016	Intravitreal administration of antibodies raised against vascular endothelial growth factor A (VEGF-A) has not yet been used in the management of FAME, however, the excellent therapeutic response in our patient may justify the use of anti-VEGF-A agents in combination with cessation of fingolimod to achieve fast resolution of FAME and to prevent visual deficits, particularly in bilateral FAME.	Fingolimod Hydrochloride	286-296	vascular endothelial growth factor A	Homo sapiens	57-93
27983657-5	2016	Intravitreal administration of antibodies raised against vascular endothelial growth factor A (VEGF-A) has not yet been used in the management of FAME, however, the excellent therapeutic response in our patient may justify the use of anti-VEGF-A agents in combination with cessation of fingolimod to achieve fast resolution of FAME and to prevent visual deficits, particularly in bilateral FAME.	Fingolimod Hydrochloride	286-296	vascular endothelial growth factor A	Homo sapiens	95-101
27905921-9	2016	Prophylactic administration of FTY720, rosiglitazone or inhalation of nitric oxide (NO) during malaria disease in mice resulted in an increase in Ang-1, a decrease in Ang-2 and an increased survival.	Fingolimod Hydrochloride	31-37	angiopoietin 1	Mus musculus	146-151
27905921-9	2016	Prophylactic administration of FTY720, rosiglitazone or inhalation of nitric oxide (NO) during malaria disease in mice resulted in an increase in Ang-1, a decrease in Ang-2 and an increased survival.	Fingolimod Hydrochloride	31-37	angiogenin, ribonuclease A family, member 2	Mus musculus	167-172
26931477-5	2016	Fingolimod dramatically reduced tumour necrosis factor (TNF)-induced endothelial microparticle release in vitro.	Fingolimod Hydrochloride	0-10	tumor necrosis factor	Homo sapiens	32-54
26931477-5	2016	Fingolimod dramatically reduced tumour necrosis factor (TNF)-induced endothelial microparticle release in vitro.	Fingolimod Hydrochloride	0-10	tumor necrosis factor	Homo sapiens	56-59
27207455-0	2016	Development of a primary cutaneous CD30(+) anaplastic large-cell T-cell lymphoma during treatment of multiple sclerosis with fingolimod.	Fingolimod Hydrochloride	125-135	TNF receptor superfamily member 8	Homo sapiens	35-39
27207455-2	2016	OBJECTIVE: To report a case of primary cutaneous CD30(+) anaplastic large-cell T-cell lymphoma during treatment of multiple sclerosis (MS) with fingolimod.	Fingolimod Hydrochloride	144-154	TNF receptor superfamily member 8	Homo sapiens	49-53
27434365-0	2016	Tp-Te interval predicts heart rate reduction after fingolimod administration in patients with multiple sclerosis.	Fingolimod Hydrochloride	51-61	transmembrane phosphatase with tensin homology	Homo sapiens	0-5
27434365-12	2016	CONCLUSIONS: This study firstly demonstrates that prolonged Tp-Te interval may identify those MS patients treated with fingolimod at higher risk of having significant, asymptomatic HR reduction during clinical observation.	Fingolimod Hydrochloride	119-129	transmembrane phosphatase with tensin homology	Homo sapiens	60-65
27725128-0	2016	Effect of fingolimod treatment on circulating miR-15b, miR23a and miR-223 levels in patients with multiple sclerosis.	Fingolimod Hydrochloride	10-20	microRNA 15b	Homo sapiens	46-53
27725128-0	2016	Effect of fingolimod treatment on circulating miR-15b, miR23a and miR-223 levels in patients with multiple sclerosis.	Fingolimod Hydrochloride	10-20	microRNA 23a	Homo sapiens	55-61
27725128-0	2016	Effect of fingolimod treatment on circulating miR-15b, miR23a and miR-223 levels in patients with multiple sclerosis.	Fingolimod Hydrochloride	10-20	microRNA 223	Homo sapiens	66-73
27528608-0	2016	FTY720/Fingolimod Reduces Synucleinopathy and Improves Gut Motility in A53T Mice: CONTRIBUTIONS OF PRO-BRAIN-DERIVED NEUROTROPHIC FACTOR (PRO-BDNF) AND MATURE BDNF.	Fingolimod Hydrochloride	0-6	brain derived neurotrophic factor	Mus musculus	159-163
27528608-0	2016	FTY720/Fingolimod Reduces Synucleinopathy and Improves Gut Motility in A53T Mice: CONTRIBUTIONS OF PRO-BRAIN-DERIVED NEUROTROPHIC FACTOR (PRO-BDNF) AND MATURE BDNF.	Fingolimod Hydrochloride	7-17	brain derived neurotrophic factor	Mus musculus	142-146
27528608-0	2016	FTY720/Fingolimod Reduces Synucleinopathy and Improves Gut Motility in A53T Mice: CONTRIBUTIONS OF PRO-BRAIN-DERIVED NEUROTROPHIC FACTOR (PRO-BDNF) AND MATURE BDNF.	Fingolimod Hydrochloride	7-17	brain derived neurotrophic factor	Mus musculus	159-163
27556014-9	2016	Furthermore, drugs such as FTY-720 can activate PP2A isoforms directly.	Fingolimod Hydrochloride	27-34	protein phosphatase 2 phosphatase activator	Homo sapiens	48-52
27695399-8	2016	Lastly, we will review four new MS treatments which interrupt NF-kappaB pathways-fingolimod, teriflunomide, dimethyl fumarate (DMF) and laquinimod (LAQ)-and explain their mechanisms, and the possible strategy for MS treatments in the future.	Fingolimod Hydrochloride	81-91	nuclear factor kappa B subunit 1	Homo sapiens	62-71
27429358-9	2016	KEY RESULTS: FTY-720 promoted the proliferation of embryonic hippocampal NSCs probably via the activation of ERK signalling, Gi/o proteins and S1P1 receptors.	Fingolimod Hydrochloride	13-20	sphingosine-1-phosphate receptor 1	Mus musculus	143-147
26970935-3	2016	Fingolimod, an immunomodulating agent used in the treatment of relapsing-remitting multiple sclerosis, has also been suggested to impart a cardioprotective role in heart failure and arrhythmia via activation of P21-activated kinase-1 (Pak1).	Fingolimod Hydrochloride	0-10	p21 (RAC1) activated kinase 1	Homo sapiens	211-233
26970935-3	2016	Fingolimod, an immunomodulating agent used in the treatment of relapsing-remitting multiple sclerosis, has also been suggested to impart a cardioprotective role in heart failure and arrhythmia via activation of P21-activated kinase-1 (Pak1).	Fingolimod Hydrochloride	0-10	p21 (RAC1) activated kinase 1	Homo sapiens	235-239
26970935-5	2016	A molecular mechanism underlying a link between fingolimod use and glioblastoma development may involve activation of Pak1.	Fingolimod Hydrochloride	48-58	p21 (RAC1) activated kinase 1	Homo sapiens	118-122
27164718-0	2016	Fingolimod-associated PML in a patient with prior immunosuppression.	Fingolimod Hydrochloride	0-10	PML nuclear body scaffold	Homo sapiens	22-25
27412504-5	2016	Analyses performed in RRMS showed that fingolimod-induced disease remission is associated with a significant increase in Bregs, CD19+/BTLA+, and CD19+/BTLA+/IL-10+ B lymphocytes.	Fingolimod Hydrochloride	39-49	CD19 molecule	Homo sapiens	128-132
27412504-5	2016	Analyses performed in RRMS showed that fingolimod-induced disease remission is associated with a significant increase in Bregs, CD19+/BTLA+, and CD19+/BTLA+/IL-10+ B lymphocytes.	Fingolimod Hydrochloride	39-49	B and T lymphocyte associated	Homo sapiens	134-138
27412504-5	2016	Analyses performed in RRMS showed that fingolimod-induced disease remission is associated with a significant increase in Bregs, CD19+/BTLA+, and CD19+/BTLA+/IL-10+ B lymphocytes.	Fingolimod Hydrochloride	39-49	CD19 molecule	Homo sapiens	145-149
27412504-5	2016	Analyses performed in RRMS showed that fingolimod-induced disease remission is associated with a significant increase in Bregs, CD19+/BTLA+, and CD19+/BTLA+/IL-10+ B lymphocytes.	Fingolimod Hydrochloride	39-49	B and T lymphocyte associated	Homo sapiens	151-155
27412504-5	2016	Analyses performed in RRMS showed that fingolimod-induced disease remission is associated with a significant increase in Bregs, CD19+/BTLA+, and CD19+/BTLA+/IL-10+ B lymphocytes.	Fingolimod Hydrochloride	39-49	interleukin 24	Homo sapiens	157-165
26967515-2	2016	Fingolimod is a known PP2A activator that inhibits multiple signalling pathways and has been used extensively in patients with multiple sclerosis and other indications.	Fingolimod Hydrochloride	0-10	protein phosphatase 2 phosphatase activator	Homo sapiens	22-26
26967515-5	2016	A literature review was carried out to assess safety before the commencement of Phase I trials of the PP2A activator Fingolimod in AML.	Fingolimod Hydrochloride	117-127	protein phosphatase 2 phosphatase activator	Homo sapiens	102-106
27174529-3	2016	In addition, fingolimod-induced adverse effects could limit its use in patients with stroke because of interactions with other S1PR subtypes, particularly with S1PR3.	Fingolimod Hydrochloride	13-23	sphingosine-1-phosphate receptor 3	Homo sapiens	160-165
27699272-5	2016	Long-term treatment with FTY720 induced significant lymphopenia and suppressed Th17 response in the peripheral immune system via downregulating STAT3 phosphorylation in both WT and S1PR1(S5A) mice.	Fingolimod Hydrochloride	25-31	signal transducer and activator of transcription 3	Mus musculus	144-149
27699272-5	2016	Long-term treatment with FTY720 induced significant lymphopenia and suppressed Th17 response in the peripheral immune system via downregulating STAT3 phosphorylation in both WT and S1PR1(S5A) mice.	Fingolimod Hydrochloride	25-31	sphingosine-1-phosphate receptor 1	Mus musculus	181-186
27001955-7	2016	The present study reveals that when applied topically, fingolimod attenuates both immediate and late-phase responses to histamine with reduced extravasation of fluid, SK-1 activity, proinflammatory cytokine and chemokine production, and neutrophil influx and prevents ear swelling.	Fingolimod Hydrochloride	55-65	sphingosine kinase 1	Homo sapiens	167-171
27456702-7	2016	The beneficial effect of fingolimod administration was associated with a significant modulation of neuroinflammatory and protective genes (CD11b, Foxp3, iNOS, Il1beta, Il10, Arg1, and Bdnf) in motor cortex and spinal cord of animals.	Fingolimod Hydrochloride	25-35	integrin alpha M	Mus musculus	139-144
27456702-7	2016	The beneficial effect of fingolimod administration was associated with a significant modulation of neuroinflammatory and protective genes (CD11b, Foxp3, iNOS, Il1beta, Il10, Arg1, and Bdnf) in motor cortex and spinal cord of animals.	Fingolimod Hydrochloride	25-35	forkhead box P3	Mus musculus	146-151
27456702-7	2016	The beneficial effect of fingolimod administration was associated with a significant modulation of neuroinflammatory and protective genes (CD11b, Foxp3, iNOS, Il1beta, Il10, Arg1, and Bdnf) in motor cortex and spinal cord of animals.	Fingolimod Hydrochloride	25-35	nitric oxide synthase 2, inducible	Mus musculus	153-157
27456702-7	2016	The beneficial effect of fingolimod administration was associated with a significant modulation of neuroinflammatory and protective genes (CD11b, Foxp3, iNOS, Il1beta, Il10, Arg1, and Bdnf) in motor cortex and spinal cord of animals.	Fingolimod Hydrochloride	25-35	interleukin 1 alpha	Mus musculus	159-166
27456702-7	2016	The beneficial effect of fingolimod administration was associated with a significant modulation of neuroinflammatory and protective genes (CD11b, Foxp3, iNOS, Il1beta, Il10, Arg1, and Bdnf) in motor cortex and spinal cord of animals.	Fingolimod Hydrochloride	25-35	interleukin 10	Mus musculus	168-172
27456702-7	2016	The beneficial effect of fingolimod administration was associated with a significant modulation of neuroinflammatory and protective genes (CD11b, Foxp3, iNOS, Il1beta, Il10, Arg1, and Bdnf) in motor cortex and spinal cord of animals.	Fingolimod Hydrochloride	25-35	arginase, liver	Mus musculus	174-178
27456702-7	2016	The beneficial effect of fingolimod administration was associated with a significant modulation of neuroinflammatory and protective genes (CD11b, Foxp3, iNOS, Il1beta, Il10, Arg1, and Bdnf) in motor cortex and spinal cord of animals.	Fingolimod Hydrochloride	25-35	brain derived neurotrophic factor	Mus musculus	184-188
27283020-4	2016	Furthermore, fingolimod has been reported to reduce LPA synthesis via inhibition of the lysophospholipase autotaxin.	Fingolimod Hydrochloride	13-23	ectonucleotide pyrophosphatase/phosphodiesterase 2	Mus musculus	106-115
27277195-7	2016	Cardioprotective effects of FTY720 were abolished following administration of a S1P receptor 2 (S1P2) antagonist or a PI3K inhibitor.	Fingolimod Hydrochloride	28-34	sphingosine-1-phosphate receptor 2	Mus musculus	80-94
27277195-7	2016	Cardioprotective effects of FTY720 were abolished following administration of a S1P receptor 2 (S1P2) antagonist or a PI3K inhibitor.	Fingolimod Hydrochloride	28-34	sphingosine-1-phosphate receptor 2	Mus musculus	96-100
27621810-0	2016	Combination treatment with fingolimod and a pathogenic antigen prevents relapse of glucose-6-phosphate isomerase peptide-induced arthritis.	Fingolimod Hydrochloride	27-37	glucose-6-phosphate isomerase 1	Mus musculus	83-112
27621810-1	2016	INTRODUCTION: Combination treatment with fingolimod (FTY720) plus pathogenic antigen is thought to prevent glucose-6-phosphate isomerase (GPI)325-339-induced arthritis progression by effective induction of immune tolerance.	Fingolimod Hydrochloride	41-51	glucose-6-phosphate isomerase 1	Mus musculus	107-136
27621810-1	2016	INTRODUCTION: Combination treatment with fingolimod (FTY720) plus pathogenic antigen is thought to prevent glucose-6-phosphate isomerase (GPI)325-339-induced arthritis progression by effective induction of immune tolerance.	Fingolimod Hydrochloride	41-51	glucose-6-phosphate isomerase 1	Mus musculus	138-141
27055778-0	2016	Fingolimod therapy modulates circulating B cell composition, increases B regulatory subsets and production of IL-10 and TGFbeta in patients with Multiple Sclerosis.	Fingolimod Hydrochloride	0-10	interleukin 10	Homo sapiens	110-115
27055778-0	2016	Fingolimod therapy modulates circulating B cell composition, increases B regulatory subsets and production of IL-10 and TGFbeta in patients with Multiple Sclerosis.	Fingolimod Hydrochloride	0-10	transforming growth factor beta 1	Homo sapiens	120-127
27055778-3	2016	Fingolimod therapy increased the ratio of naive to memory cells, elevated the percentage of plasma cells and highly increased the proportion of transitional B cells as well as additional regulatory subsets, including: IL10(+), CD25(+) and CD5(+) B cells.	Fingolimod Hydrochloride	0-10	interleukin 10	Homo sapiens	218-222
27055778-3	2016	Fingolimod therapy increased the ratio of naive to memory cells, elevated the percentage of plasma cells and highly increased the proportion of transitional B cells as well as additional regulatory subsets, including: IL10(+), CD25(+) and CD5(+) B cells.	Fingolimod Hydrochloride	0-10	interleukin 2 receptor subunit alpha	Homo sapiens	227-231
27055778-5	2016	Furthermore, fingolimod therapy reduced ICAM-1(+) cells, suggesting a possible reduction in antigen-presenting capacity.	Fingolimod Hydrochloride	13-23	intercellular adhesion molecule 1	Homo sapiens	40-46
27055778-6	2016	Phosphorylated-fingolimod was shown in vitro to reduce S1PR1 RNA and protein, to slightly increase viability and to activate anti-apoptotic Bcl2 in transformed B cells of patients with MS.	Fingolimod Hydrochloride	15-25	sphingosine-1-phosphate receptor 1	Homo sapiens	55-60
27055778-6	2016	Phosphorylated-fingolimod was shown in vitro to reduce S1PR1 RNA and protein, to slightly increase viability and to activate anti-apoptotic Bcl2 in transformed B cells of patients with MS.	Fingolimod Hydrochloride	15-25	BCL2 apoptosis regulator	Homo sapiens	140-144
27083962-2	2016	FTY720, an agonist of the sphingosine-1-phosphate receptor 1 (S1PR1), inhibits apoptosis in ischemic stroke.	Fingolimod Hydrochloride	0-6	sphingosine-1-phosphate receptor 1	Rattus norvegicus	26-60
26111826-8	2016	After switching to fingolimod (M0-12 vs M13-EOS), patients initially treated with IFN had a 50% reduction in ARR (0.40 vs 0.20), reduced MRI activity and a lower rate of brain volume loss.	Fingolimod Hydrochloride	19-29	interferon alpha 1	Homo sapiens	82-85
26111826-9	2016	In a post hoc analysis, the proportion of IFN-switch patients with no evidence of disease activity increased by approximately 50% in the first year after switching to fingolimod treatment (44.3% to 66.0%).	Fingolimod Hydrochloride	167-177	interferon alpha 1	Homo sapiens	42-45
27083962-2	2016	FTY720, an agonist of the sphingosine-1-phosphate receptor 1 (S1PR1), inhibits apoptosis in ischemic stroke.	Fingolimod Hydrochloride	0-6	sphingosine-1-phosphate receptor 1	Rattus norvegicus	62-67
26826180-10	2016	Furthermore, fingolimod decreased interstitial fibrosis, cardiomyocyte hypertrophy, and chronic activation of Akt and extracellular receptor kinase 1/2 in the remote noninfarcted myocardium.	Fingolimod Hydrochloride	13-23	AKT serine/threonine kinase 1	Sus scrofa	110-113
27010095-1	2016	Fingolimod, a sphingosine-1-phosphate receptor modulator, inhibits the egress of CCR7-positive lymphocytes, including encephalitogenic lymphocytes, from lymph nodes and may sometimes cause lymphopenia.	Fingolimod Hydrochloride	0-10	C-C motif chemokine receptor 7	Homo sapiens	81-85
27117087-6	2016	Fingolimod also decreased GFAP staining and the number of activated microglia.	Fingolimod Hydrochloride	0-10	glial fibrillary acidic protein	Mus musculus	26-30
26683421-0	2016	Fingolimod targeting protein phosphatase 2A differently affects IL-33 induced IL-2 and IFN-gamma production in CD8(+) lymphocytes.	Fingolimod Hydrochloride	0-10	interleukin 33	Homo sapiens	64-69
26683421-0	2016	Fingolimod targeting protein phosphatase 2A differently affects IL-33 induced IL-2 and IFN-gamma production in CD8(+) lymphocytes.	Fingolimod Hydrochloride	0-10	interleukin 2	Homo sapiens	78-82
26683421-0	2016	Fingolimod targeting protein phosphatase 2A differently affects IL-33 induced IL-2 and IFN-gamma production in CD8(+) lymphocytes.	Fingolimod Hydrochloride	0-10	interferon gamma	Homo sapiens	87-96
26683421-0	2016	Fingolimod targeting protein phosphatase 2A differently affects IL-33 induced IL-2 and IFN-gamma production in CD8(+) lymphocytes.	Fingolimod Hydrochloride	0-10	CD8a molecule	Homo sapiens	111-114
26099903-7	2016	We found that FTY720 administration after TBI improved neurobehavioral function, alleviated brain edema, accompanied by modulation of apoptotic indicators such as Bcl-2, Bcl-xL, Bax, and cytochrome c. In experiment 2, ICR mice were also divided into four groups: sham group, TBI + vehicle group, TBI + FTY720 group, and TBI + FTY720 + inhibitors group.	Fingolimod Hydrochloride	14-20	B cell leukemia/lymphoma 2	Mus musculus	163-168
26719367-3	2016	Sphingosine kinases (Sphk1, Sphk2) phosphorylate FTY720 in vivo to form the bioactive metabolite FTY720-1-phosphate (FTY720-P).	Fingolimod Hydrochloride	49-55	sphingosine kinase 1	Mus musculus	21-26
26719367-3	2016	Sphingosine kinases (Sphk1, Sphk2) phosphorylate FTY720 in vivo to form the bioactive metabolite FTY720-1-phosphate (FTY720-P).	Fingolimod Hydrochloride	49-55	sphingosine kinase 2	Mus musculus	28-33
26719367-7	2016	Treatment of LM/Bc MEFs with FTY720 and a selective Sphk2 inhibitor, ABC294640, significantly reduces the amount of FTY720-P that accumulates in the nucleus.	Fingolimod Hydrochloride	29-35	sphingosine kinase 2	Mus musculus	52-57
26673009-6	2016	In addition, we further evaluated the effect of SphK1 antagonist fingolimod (FTY720) in ACC in vitro and in vivo, as a single agent or in combination with mitotane, and attempted to explore its anticarcinogenic mechanisms.	Fingolimod Hydrochloride	65-75	sphingosine kinase 1	Homo sapiens	48-53
26589326-8	2016	Administration of FTY720, a functional S1PR1 antagonist, obviously blocked cardiac SphK1/S1P/S1PR1 signaling, ameliorated chronic cardiac inflammation, and then improved cardiac remodeling and dysfunction in vivo post-MI.	Fingolimod Hydrochloride	18-24	sphingosine-1-phosphate receptor 1	Mus musculus	39-44
26589326-8	2016	Administration of FTY720, a functional S1PR1 antagonist, obviously blocked cardiac SphK1/S1P/S1PR1 signaling, ameliorated chronic cardiac inflammation, and then improved cardiac remodeling and dysfunction in vivo post-MI.	Fingolimod Hydrochloride	18-24	sphingosine kinase 1	Mus musculus	83-88
26589326-8	2016	Administration of FTY720, a functional S1PR1 antagonist, obviously blocked cardiac SphK1/S1P/S1PR1 signaling, ameliorated chronic cardiac inflammation, and then improved cardiac remodeling and dysfunction in vivo post-MI.	Fingolimod Hydrochloride	18-24	sphingosine-1-phosphate receptor 1	Mus musculus	39-42
26589326-8	2016	Administration of FTY720, a functional S1PR1 antagonist, obviously blocked cardiac SphK1/S1P/S1PR1 signaling, ameliorated chronic cardiac inflammation, and then improved cardiac remodeling and dysfunction in vivo post-MI.	Fingolimod Hydrochloride	18-24	sphingosine-1-phosphate receptor 1	Mus musculus	93-98
26099903-7	2016	We found that FTY720 administration after TBI improved neurobehavioral function, alleviated brain edema, accompanied by modulation of apoptotic indicators such as Bcl-2, Bcl-xL, Bax, and cytochrome c. In experiment 2, ICR mice were also divided into four groups: sham group, TBI + vehicle group, TBI + FTY720 group, and TBI + FTY720 + inhibitors group.	Fingolimod Hydrochloride	14-20	BCL2-like 1	Mus musculus	170-176
26099903-7	2016	We found that FTY720 administration after TBI improved neurobehavioral function, alleviated brain edema, accompanied by modulation of apoptotic indicators such as Bcl-2, Bcl-xL, Bax, and cytochrome c. In experiment 2, ICR mice were also divided into four groups: sham group, TBI + vehicle group, TBI + FTY720 group, and TBI + FTY720 + inhibitors group.	Fingolimod Hydrochloride	14-20	BCL2-associated X protein	Mus musculus	178-181
26099903-10	2016	In addition, the apoptosis inhibition effect of FTY720 was partly abrogated by the phosphatidylinositide 3-kinases (PI3K)/AKT pathway inhibitor LY294002 and autophagy inhibitor 3-methyladenine.	Fingolimod Hydrochloride	48-54	thymoma viral proto-oncogene 1	Mus musculus	122-125
26632437-0	2016	Fingolimod ameliorates the development of experimental autoimmune encephalomyelitis by inhibiting Akt-mTOR axis in mice.	Fingolimod Hydrochloride	0-10	thymoma viral proto-oncogene 1	Mus musculus	98-101
26632437-0	2016	Fingolimod ameliorates the development of experimental autoimmune encephalomyelitis by inhibiting Akt-mTOR axis in mice.	Fingolimod Hydrochloride	0-10	mechanistic target of rapamycin kinase	Mus musculus	102-106
26632437-8	2016	After treatment with fingolimod, these parameters were reversed, suggesting that fingolimod treatment inhibits the Akt-mTOR axis in EAE, which affects the differentiation and function of Th1 and Treg cells.	Fingolimod Hydrochloride	21-31	thymoma viral proto-oncogene 1	Mus musculus	115-118
26632437-8	2016	After treatment with fingolimod, these parameters were reversed, suggesting that fingolimod treatment inhibits the Akt-mTOR axis in EAE, which affects the differentiation and function of Th1 and Treg cells.	Fingolimod Hydrochloride	21-31	mechanistic target of rapamycin kinase	Mus musculus	119-123
26632437-8	2016	After treatment with fingolimod, these parameters were reversed, suggesting that fingolimod treatment inhibits the Akt-mTOR axis in EAE, which affects the differentiation and function of Th1 and Treg cells.	Fingolimod Hydrochloride	21-31	negative elongation factor complex member C/D, Th1l	Mus musculus	187-190
26632437-8	2016	After treatment with fingolimod, these parameters were reversed, suggesting that fingolimod treatment inhibits the Akt-mTOR axis in EAE, which affects the differentiation and function of Th1 and Treg cells.	Fingolimod Hydrochloride	81-91	thymoma viral proto-oncogene 1	Mus musculus	115-118
26632437-8	2016	After treatment with fingolimod, these parameters were reversed, suggesting that fingolimod treatment inhibits the Akt-mTOR axis in EAE, which affects the differentiation and function of Th1 and Treg cells.	Fingolimod Hydrochloride	81-91	mechanistic target of rapamycin kinase	Mus musculus	119-123
26632437-8	2016	After treatment with fingolimod, these parameters were reversed, suggesting that fingolimod treatment inhibits the Akt-mTOR axis in EAE, which affects the differentiation and function of Th1 and Treg cells.	Fingolimod Hydrochloride	81-91	negative elongation factor complex member C/D, Th1l	Mus musculus	187-190
26804601-6	2016	Fingolimod impairs migration of lymphocytes from lymph nodes and it is hypothesized that Fingolimod could alleviate and decrease disease burden of lymphoma as it sequesters malignant cells within involved lymph nodes and it decelerates progression of the disease, increases efficacy of other treatment options and it is synergistic with anti-VEGF medications, it is an anti-metastatic, anti-inflammatory, cytostatic/cytotoxic agent and it boosts function of immune system in deterioration of neoplastic cells.	Fingolimod Hydrochloride	0-10	vascular endothelial growth factor A	Homo sapiens	342-346
26219664-3	2016	OBJECTIVE: To describe a case of lymphomatoid papulosis, a CD30+ cutaneous lymphoproliferative disorder, in a patient taking fingolimod.	Fingolimod Hydrochloride	125-135	TNF receptor superfamily member 8	Homo sapiens	59-63
26714756-0	2015	Identification of a novel mechanism of action of fingolimod (FTY720) on human effector T cell function through TCF-1 upregulation.	Fingolimod Hydrochloride	49-59	transcription factor 7	Homo sapiens	111-116
26900439-6	2015	RESULTS: The mean level of Plts before initiation of fingolimod therapy (Plt1) among these MS patients was 256.53 +- 66.26.	Fingolimod Hydrochloride	53-63	major histocompatibility complex, class II, DP alpha 1	Homo sapiens	73-77
26109007-2	2015	We describe three cases (one male and two females) with neuroimaging features suggestive of BCS and heterogeneous symptoms, with benign long-term clinical course upon treatment with natalizumab and fingolimod.	Fingolimod Hydrochloride	198-208	BCS1 homolog, ubiquinol-cytochrome c reductase complex chaperone	Homo sapiens	92-95
25958190-7	2015	Interestingly, fingolimod protected vascular permeability as indicated by a decreased plasma level of MMP9 and the reduced rT1%.	Fingolimod Hydrochloride	15-25	matrix metallopeptidase 9	Homo sapiens	102-106
26795749-2	2015	It is thought that fingolimod modulates the immune response by activating sphingosine-1 phosphate receptor type 1 (S1P1) on lymphocytes following its in vivo phosphorylation.	Fingolimod Hydrochloride	19-29	sphingosine-1-phosphate receptor 1	Mus musculus	74-113
26795749-2	2015	It is thought that fingolimod modulates the immune response by activating sphingosine-1 phosphate receptor type 1 (S1P1) on lymphocytes following its in vivo phosphorylation.	Fingolimod Hydrochloride	19-29	sphingosine-1-phosphate receptor 1	Mus musculus	115-119
27853088-5	2016	This dissemination might be associated with fingolimod-induced CD4 lymphocytopenia.	Fingolimod Hydrochloride	44-54	CD4 molecule	Homo sapiens	63-66
25936777-8	2015	Interestingly however fingolimod, an immunosuppressive drug structurally related to sphingosine, used for the treatment of multiple sclerosis, is a powerful activator of Fam20C, both wild type and its pathogenic, loss of function, T268M mutant.	Fingolimod Hydrochloride	22-32	FAM20C golgi associated secretory pathway kinase	Homo sapiens	170-176
26587553-4	2015	RESULTS: We found that in vitro exposure of human monocytes to fingolimod inhibited LPS-induced CD25 and CD150 expression and tumor necrosis factor-alpha (TNF-alpha) secretion without altering immune cell survival.	Fingolimod Hydrochloride	63-73	interleukin 2 receptor subunit alpha	Homo sapiens	96-100
26587553-4	2015	RESULTS: We found that in vitro exposure of human monocytes to fingolimod inhibited LPS-induced CD25 and CD150 expression and tumor necrosis factor-alpha (TNF-alpha) secretion without altering immune cell survival.	Fingolimod Hydrochloride	63-73	signaling lymphocytic activation molecule family member 1	Homo sapiens	105-110
26587553-4	2015	RESULTS: We found that in vitro exposure of human monocytes to fingolimod inhibited LPS-induced CD25 and CD150 expression and tumor necrosis factor-alpha (TNF-alpha) secretion without altering immune cell survival.	Fingolimod Hydrochloride	63-73	tumor necrosis factor	Homo sapiens	126-153
26587553-4	2015	RESULTS: We found that in vitro exposure of human monocytes to fingolimod inhibited LPS-induced CD25 and CD150 expression and tumor necrosis factor-alpha (TNF-alpha) secretion without altering immune cell survival.	Fingolimod Hydrochloride	63-73	tumor necrosis factor	Homo sapiens	155-164
26587553-5	2015	Further, EAE treatment with fingolimod led to reduced amounts of TNF-alpha produced by myeloid cells in vivo in the spleen and CNS.	Fingolimod Hydrochloride	28-38	tumor necrosis factor	Homo sapiens	65-74
26130058-1	2015	Fingolimod affords protection from MS by sequestering lymphocytes in secondary lymphoid organs via down regulation of their sphingosine 1 phosphate receptor (S1P1).	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Homo sapiens	158-162
26130058-7	2015	Also, consistent with the ability of S1P1 to counteract polarization and function of T regulatory lymphocytes their number and suppression of effector T cells is reduced by fingolimod suspension.	Fingolimod Hydrochloride	173-183	sphingosine-1-phosphate receptor 1	Homo sapiens	37-41
26285786-5	2015	During an observation period of 6h peripheral blood depletion of CD56(bright) NK cells was observed 3 h after first dose of fingolimod, with 40-50% depletion after 6 h, while a decrease of the numbers of CD56(dim) NK cells did not reach the level of statistical significance.	Fingolimod Hydrochloride	124-134	neural cell adhesion molecule 1	Homo sapiens	65-69
25583847-9	2015	By reducing CCR7-expressing Tcon, fingolimod increased relative proportions of Treg.	Fingolimod Hydrochloride	34-44	C-C motif chemokine receptor 7	Homo sapiens	12-16
26516583-7	2015	Further studies in Huh7 revealed that combined treatment with FTY720 and sorafenib resulted in G1 arrest and enhanced cell death measured using flow cytometry analysis of cells labeled with propidium iodide (PI)/Annexin-V and PI and 4",6-diamidino-2-phenylindole-staining of nuclei.	Fingolimod Hydrochloride	62-68	MIR7-3 host gene	Homo sapiens	19-23
26516583-7	2015	Further studies in Huh7 revealed that combined treatment with FTY720 and sorafenib resulted in G1 arrest and enhanced cell death measured using flow cytometry analysis of cells labeled with propidium iodide (PI)/Annexin-V and PI and 4",6-diamidino-2-phenylindole-staining of nuclei.	Fingolimod Hydrochloride	62-68	annexin A5	Homo sapiens	212-221
26516583-9	2015	We also detected features of autophagy blockage, as the protein levels of LC3-II and p62 were affected by combined treatment with FTY720 and sorafenib.	Fingolimod Hydrochloride	130-136	nucleoporin 62	Homo sapiens	85-88
26063761-0	2015	Fingolimod (FTY720) enhances hippocampal synaptic plasticity and memory in Huntington"s disease by preventing p75NTR up-regulation and astrocyte-mediated inflammation.	Fingolimod Hydrochloride	0-10	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	110-116
26063761-0	2015	Fingolimod (FTY720) enhances hippocampal synaptic plasticity and memory in Huntington"s disease by preventing p75NTR up-regulation and astrocyte-mediated inflammation.	Fingolimod Hydrochloride	12-18	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	110-116
26063761-4	2015	Fingolimod (FTY720), a modulator of sphingosine-1 phosphate (S1P) receptors, has been shown to increase BDNF levels and to reduce astrogliosis, proving its potential to regulate trophic support and inflammatory response.	Fingolimod Hydrochloride	0-10	brain derived neurotrophic factor	Mus musculus	104-108
26063761-4	2015	Fingolimod (FTY720), a modulator of sphingosine-1 phosphate (S1P) receptors, has been shown to increase BDNF levels and to reduce astrogliosis, proving its potential to regulate trophic support and inflammatory response.	Fingolimod Hydrochloride	12-18	brain derived neurotrophic factor	Mus musculus	104-108
26063761-7	2015	Furthermore, FTY720 delivery prevented astrogliosis and over-activation of nuclear factor kappa beta (NF-kappaB) signaling in the R6/1 hippocampus, reducing tumor necrosis factor alpha (TNFalpha) and induced nitric oxide synthase (iNOS) levels.	Fingolimod Hydrochloride	13-19	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	102-111
26063761-7	2015	Furthermore, FTY720 delivery prevented astrogliosis and over-activation of nuclear factor kappa beta (NF-kappaB) signaling in the R6/1 hippocampus, reducing tumor necrosis factor alpha (TNFalpha) and induced nitric oxide synthase (iNOS) levels.	Fingolimod Hydrochloride	13-19	tumor necrosis factor	Mus musculus	157-184
26063761-7	2015	Furthermore, FTY720 delivery prevented astrogliosis and over-activation of nuclear factor kappa beta (NF-kappaB) signaling in the R6/1 hippocampus, reducing tumor necrosis factor alpha (TNFalpha) and induced nitric oxide synthase (iNOS) levels.	Fingolimod Hydrochloride	13-19	tumor necrosis factor	Mus musculus	186-194
26063761-7	2015	Furthermore, FTY720 delivery prevented astrogliosis and over-activation of nuclear factor kappa beta (NF-kappaB) signaling in the R6/1 hippocampus, reducing tumor necrosis factor alpha (TNFalpha) and induced nitric oxide synthase (iNOS) levels.	Fingolimod Hydrochloride	13-19	nitric oxide synthase 2, inducible	Mus musculus	231-235
25720064-1	2015	FTY720 (fingolimod) is, after its phosphorylation by sphingosine kinase (SPHK) 2, a potent, non-selective sphingosine-1-phosphate (S1P) receptor agonist.	Fingolimod Hydrochloride	0-6	sphingosine kinase 2	Mus musculus	53-80
26216939-4	2015	Fingolimod also induces typical apoptotic features, including rapid externalization of phosphatidylserine and activation of caspase-8.	Fingolimod Hydrochloride	0-10	caspase 8	Homo sapiens	124-133
26216939-6	2015	Furthermore, NADPH oxidase 1 inhibition with diphenyleneiodonium chloride protects neutrophils against fingolimod-mediated cell death.	Fingolimod Hydrochloride	103-113	NADPH oxidase 1	Homo sapiens	13-28
26197437-4	2015	Fingolimod, an immune modulatory drug whose structure is similar to S1P, has been approved for treatment in multiple sclerosis (MS): fingolimod reduces the rate of MS relapses by preventing leukocyte egress from the lymph nodes.	Fingolimod Hydrochloride	0-10	membrane bound transcription factor peptidase, site 1	Homo sapiens	68-71
26197437-4	2015	Fingolimod, an immune modulatory drug whose structure is similar to S1P, has been approved for treatment in multiple sclerosis (MS): fingolimod reduces the rate of MS relapses by preventing leukocyte egress from the lymph nodes.	Fingolimod Hydrochloride	133-143	membrane bound transcription factor peptidase, site 1	Homo sapiens	68-71
26197437-7	2015	When acting on astrocytes, fingolimod treatment induced the release of a factor, granulocyte macrophage colony-stimulating factor (GM-CSF) that reduced the effects of cytokines on endothelium.	Fingolimod Hydrochloride	27-37	colony stimulating factor 2	Homo sapiens	81-129
26197437-7	2015	When acting on astrocytes, fingolimod treatment induced the release of a factor, granulocyte macrophage colony-stimulating factor (GM-CSF) that reduced the effects of cytokines on endothelium.	Fingolimod Hydrochloride	27-37	colony stimulating factor 2	Homo sapiens	131-137
25720064-1	2015	FTY720 (fingolimod) is, after its phosphorylation by sphingosine kinase (SPHK) 2, a potent, non-selective sphingosine-1-phosphate (S1P) receptor agonist.	Fingolimod Hydrochloride	8-18	sphingosine kinase 2	Mus musculus	53-80
26171219-1	2015	Recent findings indicate that fingolimod, the first oral drug approved for the treatment of multiple sclerosis (MS), acts as a direct inhibitor of histone deacetylases (HDACs) and enhances the production of brain-derived neurotrophic factor (BDNF) in the CNS.	Fingolimod Hydrochloride	30-40	brain derived neurotrophic factor	Mus musculus	207-240
26171219-1	2015	Recent findings indicate that fingolimod, the first oral drug approved for the treatment of multiple sclerosis (MS), acts as a direct inhibitor of histone deacetylases (HDACs) and enhances the production of brain-derived neurotrophic factor (BDNF) in the CNS.	Fingolimod Hydrochloride	30-40	brain derived neurotrophic factor	Mus musculus	242-246
26023836-3	2015	We treated PC-3 and LNCaP cell lines with the PP2A activators forskolin and FTY720 alone or combined with the PP2A inhibitor okadaic acid.	Fingolimod Hydrochloride	76-82	protein phosphatase 2 phosphatase activator	Homo sapiens	46-50
26023836-5	2015	Interestingly, both forskolin and FTY720 dephosphorylated and activated PP2A, impairing proliferation and prostasphere formation and inducing changes in AKT and ERK phosphorylation.	Fingolimod Hydrochloride	34-40	protein phosphatase 2 phosphatase activator	Homo sapiens	72-76
26023836-5	2015	Interestingly, both forskolin and FTY720 dephosphorylated and activated PP2A, impairing proliferation and prostasphere formation and inducing changes in AKT and ERK phosphorylation.	Fingolimod Hydrochloride	34-40	AKT serine/threonine kinase 1	Homo sapiens	153-156
26023836-5	2015	Interestingly, both forskolin and FTY720 dephosphorylated and activated PP2A, impairing proliferation and prostasphere formation and inducing changes in AKT and ERK phosphorylation.	Fingolimod Hydrochloride	34-40	mitogen-activated protein kinase 1	Homo sapiens	161-164
26023836-7	2015	Treatment with okadaic acid impaired PP2A activation thus demonstrating the antitumoral PP2A-dependent mechanism of action of both forskolin and FTY720.	Fingolimod Hydrochloride	145-151	protein phosphatase 2 phosphatase activator	Homo sapiens	37-41
26023836-7	2015	Treatment with okadaic acid impaired PP2A activation thus demonstrating the antitumoral PP2A-dependent mechanism of action of both forskolin and FTY720.	Fingolimod Hydrochloride	145-151	protein phosphatase 2 phosphatase activator	Homo sapiens	88-92
25953296-13	2015	CONCLUSIONS: These data support a role for FTY720 as a neuroprotective agent against excitotoxin-induced neuronal death and as a negative modulator of neuroinflammation by targeting the p38 MAPK stress signalling pathway in microglia.	Fingolimod Hydrochloride	43-49	mitogen activated protein kinase 14	Rattus norvegicus	186-189
25880547-11	2015	Moreover, after a 1-h pretreatment with FTY720 (an agonist for S1PR1/R3/R4/R5), neither SEW2871 (S1PR1 selective agonist) nor S1P augmented the excitability.	Fingolimod Hydrochloride	40-46	sphingosine-1-phosphate receptor 1	Rattus norvegicus	63-68
25637283-8	2015	The drug FTY-720 (activator of PP2A) induced apoptosis of pancreatic cancer cells.	Fingolimod Hydrochloride	9-16	protein phosphatase 2 phosphatase activator	Homo sapiens	31-35
25680941-7	2015	The mechanistic premise underlying the therapeutic effect of Fingolimod, was that Fingolimod stimulates the sonic hedgehog (Shh) pathway, and this pathway promotes OPC differentiation.	Fingolimod Hydrochloride	61-71	sonic hedgehog	Mus musculus	108-122
25680941-7	2015	The mechanistic premise underlying the therapeutic effect of Fingolimod, was that Fingolimod stimulates the sonic hedgehog (Shh) pathway, and this pathway promotes OPC differentiation.	Fingolimod Hydrochloride	61-71	sonic hedgehog	Mus musculus	124-127
25680941-12	2015	EAE mice treated with Fingolimod exhibited substantially elevated levels of Shh, its receptor Smoothened and effector Gli1 in the white matter of the CNS.	Fingolimod Hydrochloride	22-32	sonic hedgehog	Mus musculus	76-79
25680941-12	2015	EAE mice treated with Fingolimod exhibited substantially elevated levels of Shh, its receptor Smoothened and effector Gli1 in the white matter of the CNS.	Fingolimod Hydrochloride	22-32	smoothened, frizzled class receptor	Mus musculus	94-104
25680941-12	2015	EAE mice treated with Fingolimod exhibited substantially elevated levels of Shh, its receptor Smoothened and effector Gli1 in the white matter of the CNS.	Fingolimod Hydrochloride	22-32	GLI-Kruppel family member GLI1	Mus musculus	118-122
25680941-13	2015	However, combination treatment of EAE mice with cyclopamine-Fingolimod decreased Fingolimod monotherapy elevated protein levels of Smoothened and Gli1, and abolished the effect of Fingolimod on OPC proliferation and differentiation, as well as on neurological function outcome.	Fingolimod Hydrochloride	60-70	smoothened, frizzled class receptor	Mus musculus	131-141
25680941-13	2015	However, combination treatment of EAE mice with cyclopamine-Fingolimod decreased Fingolimod monotherapy elevated protein levels of Smoothened and Gli1, and abolished the effect of Fingolimod on OPC proliferation and differentiation, as well as on neurological function outcome.	Fingolimod Hydrochloride	60-70	GLI-Kruppel family member GLI1	Mus musculus	146-150
25680941-15	2015	In addition, the Shh pathway likely contributes to the therapeutic effects of Fingolimod on OPCs.	Fingolimod Hydrochloride	78-88	sonic hedgehog	Mus musculus	17-20
25582213-2	2015	Interfering with the activation and recruitment of immune cells reduces disease activity in MS. We review the mechanism of action and treatment effects of natalizumab and fingolimod, which interfere with the recruitment of pathogenic immune cells in MS. Fingolimod blocks the egress of activated lymphocytes from lymph nodes by binding to the sphingosine-1-phosphate (S1P) receptor 1, but may also have effects on S1P receptor-expressing cells within the central nervous system (CNS).	Fingolimod Hydrochloride	171-181	sphingosine-1-phosphate receptor 1	Homo sapiens	343-383
25582213-2	2015	Interfering with the activation and recruitment of immune cells reduces disease activity in MS. We review the mechanism of action and treatment effects of natalizumab and fingolimod, which interfere with the recruitment of pathogenic immune cells in MS. Fingolimod blocks the egress of activated lymphocytes from lymph nodes by binding to the sphingosine-1-phosphate (S1P) receptor 1, but may also have effects on S1P receptor-expressing cells within the central nervous system (CNS).	Fingolimod Hydrochloride	254-264	sphingosine-1-phosphate receptor 1	Homo sapiens	343-383
25699237-7	2015	We review the mechanisms of functional PP2A activation by drugs such as fingolimod, forskolin, OP449, and perphenazine.	Fingolimod Hydrochloride	72-82	protein phosphatase 2 phosphatase activator	Homo sapiens	39-43
25546031-1	2015	OBJECTIVE: In patients suffering multiple sclerosis activity despite treatment with interferon beta or glatiramer acetate, clinicians often switch therapy to either natalizumab or fingolimod.	Fingolimod Hydrochloride	180-190	interferon beta 1	Homo sapiens	84-99
25400014-6	2015	FTY720 (1 or 5 mg/kg, i.p., 1 h after the last MA administration), a PP2A activator, significantly reversed the recovery in TH phosphorylation mediated by inhibition of PKCdelta after MA treatment.	Fingolimod Hydrochloride	0-6	protein phosphatase 2, regulatory subunit A, alpha	Mus musculus	69-73
25400014-6	2015	FTY720 (1 or 5 mg/kg, i.p., 1 h after the last MA administration), a PP2A activator, significantly reversed the recovery in TH phosphorylation mediated by inhibition of PKCdelta after MA treatment.	Fingolimod Hydrochloride	0-6	protein kinase C, delta	Mus musculus	169-177
25994913-0	2015	Functional Mechanism(s) of the Inhibition of Disease Progression by Combination Treatment with Fingolimod Plus Pathogenic Antigen in a Glucose-6-phosphate Isomerase Peptide-Induced Arthritis Mouse Model.	Fingolimod Hydrochloride	95-105	glucosamine-6-phosphate deaminase 1	Mus musculus	135-164
25239520-0	2014	Prominence of central sphingosine-1-phosphate receptor-1 in attenuating abeta-induced injury by fingolimod.	Fingolimod Hydrochloride	96-106	sphingosine-1-phosphate receptor 1	Homo sapiens	22-56
25803131-5	2015	Expression of activated forms of AKT, p70 S6K and mTOR or inhibition of JNK and p38 MAPK suppressed the interaction between FTY720 and pemetrexed.	Fingolimod Hydrochloride	124-130	mechanistic target of rapamycin kinase	Homo sapiens	50-54
25803131-5	2015	Expression of activated forms of AKT, p70 S6K and mTOR or inhibition of JNK and p38 MAPK suppressed the interaction between FTY720 and pemetrexed.	Fingolimod Hydrochloride	124-130	mitogen-activated protein kinase 8	Homo sapiens	72-75
26648781-2	2015	Mode of action of fingolimod is based on intense S1P1 receptor stimulation and "arresting" lymphocytes in lymphatic organs.	Fingolimod Hydrochloride	18-28	sphingosine-1-phosphate receptor 1	Homo sapiens	49-53
25239520-2	2014	The present work aims to answer whether central S1P receptor 1 (S1P1) plays significant role in the impact of fingolimod in AD.	Fingolimod Hydrochloride	110-120	sphingosine-1-phosphate receptor 1	Homo sapiens	48-62
25239520-2	2014	The present work aims to answer whether central S1P receptor 1 (S1P1) plays significant role in the impact of fingolimod in AD.	Fingolimod Hydrochloride	110-120	sphingosine-1-phosphate receptor 1	Homo sapiens	64-68
25207757-7	2014	The IL-33/ST2-TIR Th2-like response in ST2-EL4 cells was inhibited by fingolimod and analogues at varying degrees.	Fingolimod Hydrochloride	70-80	interleukin 33	Homo sapiens	4-9
25207757-10	2014	Interestingly, the effects of the parent compound fingolimod were modulated by the PP2A inhibitor okadaic acid, thus suggesting PP2A as relevant intracellular target.	Fingolimod Hydrochloride	50-60	protein phosphatase 2 phosphatase activator	Homo sapiens	83-87
25207757-10	2014	Interestingly, the effects of the parent compound fingolimod were modulated by the PP2A inhibitor okadaic acid, thus suggesting PP2A as relevant intracellular target.	Fingolimod Hydrochloride	50-60	protein phosphatase 2 phosphatase activator	Homo sapiens	128-132
25207757-12	2014	Moreover, differential effects of fingolimod versus its phosphorylated derivative on TLR-activated and antigen-dependent Th1 activation suggest PP2A as an additional target of fingolimod immune therapy.	Fingolimod Hydrochloride	34-44	negative elongation factor complex member C/D	Homo sapiens	121-124
25207757-12	2014	Moreover, differential effects of fingolimod versus its phosphorylated derivative on TLR-activated and antigen-dependent Th1 activation suggest PP2A as an additional target of fingolimod immune therapy.	Fingolimod Hydrochloride	34-44	protein phosphatase 2 phosphatase activator	Homo sapiens	144-148
25518386-3	2014	In lymph node, fingolimod acts as functional antagonist, leading to internalization of sphingosine-1-phosphate 1(S1P1) receptors of lymphocytes.	Fingolimod Hydrochloride	15-25	sphingosine-1-phosphate receptor 1	Homo sapiens	113-117
25223691-6	2014	Meanwhile, fingolimod significantly inhibited hERG current, which was not observed by siponimod.	Fingolimod Hydrochloride	11-21	ETS transcription factor ERG	Homo sapiens	46-50
24641481-9	2014	FTY720-P stimulated a higher level of beta-arrestin recruitment at S1P1Rs, 132% of the total recruited by S1P.	Fingolimod Hydrochloride	0-6	membrane bound transcription factor peptidase, site 1	Homo sapiens	67-70
25347187-2	2014	S1P1 is a major regulator of lymphocyte trafficking, and fingolimod, whose active metabolite fingolimod phosphate acts as a nonselective S1P receptor agonist, exerts its immunomodulatory effect, at least in part, by regulating the lymphocyte trafficking by inducing down regulation of lymphocyte S1P1.	Fingolimod Hydrochloride	57-67	sphingosine-1-phosphate receptor 1	Rattus norvegicus	296-300
25344679-9	2014	Western blot analysis showed that FTY720 induced cleavage of caspases 3, 8 and 9, and of PARP, in a dose-dependent manner, consistent with a substantial decrease in p-STAT3, Bcl-xL, Bcl-2, survivin, cyclin D1, cyclin E, N-cadherin, vimentin, VEGF and TWIST1.	Fingolimod Hydrochloride	34-40	caspase 3	Homo sapiens	61-80
24876766-9	2014	We also discuss new unexpected mechanisms of these drugs, such as the induction of brain-derived neurotrophic factor by fingolimod and the possibility that laquinimod and teriflunomide regulate the kynurenine pathway of tryptophan metabolism.	Fingolimod Hydrochloride	120-130	brain derived neurotrophic factor	Homo sapiens	83-116
25344679-9	2014	Western blot analysis showed that FTY720 induced cleavage of caspases 3, 8 and 9, and of PARP, in a dose-dependent manner, consistent with a substantial decrease in p-STAT3, Bcl-xL, Bcl-2, survivin, cyclin D1, cyclin E, N-cadherin, vimentin, VEGF and TWIST1.	Fingolimod Hydrochloride	34-40	collagen type XI alpha 2 chain	Homo sapiens	89-93
25344679-9	2014	Western blot analysis showed that FTY720 induced cleavage of caspases 3, 8 and 9, and of PARP, in a dose-dependent manner, consistent with a substantial decrease in p-STAT3, Bcl-xL, Bcl-2, survivin, cyclin D1, cyclin E, N-cadherin, vimentin, VEGF and TWIST1.	Fingolimod Hydrochloride	34-40	signal transducer and activator of transcription 3	Homo sapiens	167-172
25344679-9	2014	Western blot analysis showed that FTY720 induced cleavage of caspases 3, 8 and 9, and of PARP, in a dose-dependent manner, consistent with a substantial decrease in p-STAT3, Bcl-xL, Bcl-2, survivin, cyclin D1, cyclin E, N-cadherin, vimentin, VEGF and TWIST1.	Fingolimod Hydrochloride	34-40	BCL2 like 1	Homo sapiens	174-180
25344679-9	2014	Western blot analysis showed that FTY720 induced cleavage of caspases 3, 8 and 9, and of PARP, in a dose-dependent manner, consistent with a substantial decrease in p-STAT3, Bcl-xL, Bcl-2, survivin, cyclin D1, cyclin E, N-cadherin, vimentin, VEGF and TWIST1.	Fingolimod Hydrochloride	34-40	BCL2 apoptosis regulator	Homo sapiens	182-187
25344679-9	2014	Western blot analysis showed that FTY720 induced cleavage of caspases 3, 8 and 9, and of PARP, in a dose-dependent manner, consistent with a substantial decrease in p-STAT3, Bcl-xL, Bcl-2, survivin, cyclin D1, cyclin E, N-cadherin, vimentin, VEGF and TWIST1.	Fingolimod Hydrochloride	34-40	cyclin D1	Homo sapiens	199-208
25344679-9	2014	Western blot analysis showed that FTY720 induced cleavage of caspases 3, 8 and 9, and of PARP, in a dose-dependent manner, consistent with a substantial decrease in p-STAT3, Bcl-xL, Bcl-2, survivin, cyclin D1, cyclin E, N-cadherin, vimentin, VEGF and TWIST1.	Fingolimod Hydrochloride	34-40	cadherin 2	Homo sapiens	220-230
25344679-9	2014	Western blot analysis showed that FTY720 induced cleavage of caspases 3, 8 and 9, and of PARP, in a dose-dependent manner, consistent with a substantial decrease in p-STAT3, Bcl-xL, Bcl-2, survivin, cyclin D1, cyclin E, N-cadherin, vimentin, VEGF and TWIST1.	Fingolimod Hydrochloride	34-40	vimentin	Homo sapiens	232-240
25344679-9	2014	Western blot analysis showed that FTY720 induced cleavage of caspases 3, 8 and 9, and of PARP, in a dose-dependent manner, consistent with a substantial decrease in p-STAT3, Bcl-xL, Bcl-2, survivin, cyclin D1, cyclin E, N-cadherin, vimentin, VEGF and TWIST1.	Fingolimod Hydrochloride	34-40	vascular endothelial growth factor A	Homo sapiens	242-246
25344679-9	2014	Western blot analysis showed that FTY720 induced cleavage of caspases 3, 8 and 9, and of PARP, in a dose-dependent manner, consistent with a substantial decrease in p-STAT3, Bcl-xL, Bcl-2, survivin, cyclin D1, cyclin E, N-cadherin, vimentin, VEGF and TWIST1.	Fingolimod Hydrochloride	34-40	twist family bHLH transcription factor 1	Homo sapiens	251-257
25344679-11	2014	CONCLUSIONS: These results suggest that FTY720 induces a significant decrease in p-STAT3, which inhibits proliferation and EMT of CC cells, and then induces G1 phase arrest and apoptosis.	Fingolimod Hydrochloride	40-46	signal transducer and activator of transcription 3	Homo sapiens	83-88
25109763-8	2014	In addition, the combination of FTY720 and cisplatin reduced the protein expression of SK1 and the phosphorylation levels of phosphoinositide 3-kinase (PI3K), Akt and mTOR in the SK-Mel-28 cells; the expression of epidermal growth factor receptor (EGFR) was also markedly reduced.	Fingolimod Hydrochloride	32-38	sphingosine kinase 1	Homo sapiens	87-90
25109763-8	2014	In addition, the combination of FTY720 and cisplatin reduced the protein expression of SK1 and the phosphorylation levels of phosphoinositide 3-kinase (PI3K), Akt and mTOR in the SK-Mel-28 cells; the expression of epidermal growth factor receptor (EGFR) was also markedly reduced.	Fingolimod Hydrochloride	32-38	AKT serine/threonine kinase 1	Homo sapiens	159-162
25109763-8	2014	In addition, the combination of FTY720 and cisplatin reduced the protein expression of SK1 and the phosphorylation levels of phosphoinositide 3-kinase (PI3K), Akt and mTOR in the SK-Mel-28 cells; the expression of epidermal growth factor receptor (EGFR) was also markedly reduced.	Fingolimod Hydrochloride	32-38	mechanistic target of rapamycin kinase	Homo sapiens	167-171
25109763-8	2014	In addition, the combination of FTY720 and cisplatin reduced the protein expression of SK1 and the phosphorylation levels of phosphoinositide 3-kinase (PI3K), Akt and mTOR in the SK-Mel-28 cells; the expression of epidermal growth factor receptor (EGFR) was also markedly reduced.	Fingolimod Hydrochloride	32-38	epidermal growth factor receptor	Homo sapiens	214-246
25109763-8	2014	In addition, the combination of FTY720 and cisplatin reduced the protein expression of SK1 and the phosphorylation levels of phosphoinositide 3-kinase (PI3K), Akt and mTOR in the SK-Mel-28 cells; the expression of epidermal growth factor receptor (EGFR) was also markedly reduced.	Fingolimod Hydrochloride	32-38	epidermal growth factor receptor	Homo sapiens	248-252
24713151-0	2014	Fingolimod increases brain-derived neurotrophic factor levels and ameliorates amyloid beta-induced memory impairment.	Fingolimod Hydrochloride	0-10	brain derived neurotrophic factor	Homo sapiens	21-54
24713151-0	2014	Fingolimod increases brain-derived neurotrophic factor levels and ameliorates amyloid beta-induced memory impairment.	Fingolimod Hydrochloride	0-10	amyloid beta precursor protein	Homo sapiens	78-90
24713151-3	2014	We previously revealed that fingolimod, a new oral immunosuppressant used to treat multiple sclerosis, ameliorates oligomeric amyloid beta-induced neuronal damage via up-regulation of neuronal brain-derived neurotrophic factor (BDNF).	Fingolimod Hydrochloride	28-38	amyloid beta precursor protein	Homo sapiens	126-138
25309325-6	2014	The immunomodulator fingolimod is the prodrug of an S1P receptor agonist.	Fingolimod Hydrochloride	20-30	sphingosine-1-phosphate receptor 1	Mus musculus	52-55
25309325-11	2014	Indeed, a seminal study showed that the protective effect of fingolimod in experimental autoimmune encephalitis (EAE), a murine MS model, is lost in mice lacking the S1P1 receptor on astrocytes, arguing for a specific role of astrocytic S1P signaling in MS.	Fingolimod Hydrochloride	61-71	sphingosine-1-phosphate receptor 1	Mus musculus	166-169
25043204-8	2014	Importantly, fingolimod blocked the 2 activation events evoked in astrocytes by either S1P or inflammatory cytokines, resulting in inhibition of astrocyte-mediated neurodegeneration.	Fingolimod Hydrochloride	13-23	sphingosine-1-phosphate receptor 1	Mus musculus	87-90
25213591-3	2014	We have previously reviewed the use of  fingolimod for highly active relapsing-remitting MS1 and  teriflunomide for the management of relapsing-remitting MS in adults.2 Here, we review the evidence for  dimethyl fumarate (Tecfidera-Biogen Idec Ltd) for the treatment of adults with relapsing-remitting MS.	Fingolimod Hydrochloride	40-50	MS	Homo sapiens	89-92
24816681-1	2014	The CYP4F subfamily of enzymes has been identified recently to be involved in the metabolism of endogenous compounds (arachidonic acid and leukotriene B4), nutrients (vitamins K1 and E), and xenobiotics (pafuramidine and fingolimod).	Fingolimod Hydrochloride	221-231	keratin 1	Homo sapiens	176-184
24713151-3	2014	We previously revealed that fingolimod, a new oral immunosuppressant used to treat multiple sclerosis, ameliorates oligomeric amyloid beta-induced neuronal damage via up-regulation of neuronal brain-derived neurotrophic factor (BDNF).	Fingolimod Hydrochloride	28-38	brain derived neurotrophic factor	Homo sapiens	193-226
24713151-3	2014	We previously revealed that fingolimod, a new oral immunosuppressant used to treat multiple sclerosis, ameliorates oligomeric amyloid beta-induced neuronal damage via up-regulation of neuronal brain-derived neurotrophic factor (BDNF).	Fingolimod Hydrochloride	28-38	brain derived neurotrophic factor	Homo sapiens	228-232
24713151-4	2014	Here, we showed that oral administration of fingolimod ameliorated the impairment in object recognition memory and associative learning in mice injected with amyloid beta.	Fingolimod Hydrochloride	44-54	amyloid beta precursor protein	Homo sapiens	158-170
24911000-2	2014	The phosphorylated version of Fingolimod (pFTY720), an oral therapy for multiple sclerosis (MS), induces S1PR1 internalisation in T cells, subsequent insensitivity to S1P gradients and sequestering of these cells within lymphoid organs, thus limiting immune response.	Fingolimod Hydrochloride	30-40	sphingosine-1-phosphate receptor 1	Mus musculus	105-110
24657936-4	2014	Fingolimod (FTY720) is a novel sphingosine analog and a potent immunosuppressive drug that acts as a SphK1 antagonist, inhibits the growth, and induces apoptosis in different human cancer cell lines.	Fingolimod Hydrochloride	0-10	sphingosine kinase 1	Homo sapiens	101-106
24657936-4	2014	Fingolimod (FTY720) is a novel sphingosine analog and a potent immunosuppressive drug that acts as a SphK1 antagonist, inhibits the growth, and induces apoptosis in different human cancer cell lines.	Fingolimod Hydrochloride	12-18	sphingosine kinase 1	Homo sapiens	101-106
24740509-5	2014	Treatment with fingolimod (FTY720) during the late phase of disease revealed that retinal CD8(+) T cells were tissue resident.	Fingolimod Hydrochloride	15-25	CD8a molecule	Homo sapiens	90-93
24740509-5	2014	Treatment with fingolimod (FTY720) during the late phase of disease revealed that retinal CD8(+) T cells were tissue resident.	Fingolimod Hydrochloride	27-33	CD8a molecule	Homo sapiens	90-93
24239768-3	2014	In September 2010, fingolimod/FTY720 (Gilenya, Novartis) was approved as the first oral treatment for relapsing forms of MS. Fingolimod causes down-modulation of S1P1 receptors on lymphocytes which prevents the invasion of autoaggressive T cells into the CNS.	Fingolimod Hydrochloride	125-135	sphingosine-1-phosphate receptor 1	Homo sapiens	162-166
24680062-1	2014	Fingolimod (FTY720) is a multiple sclerosis (MS) therapeutic that upon phosphorylation causes the internalization of sphingosine-1-phosphate receptors (S1PR) and traps CCR7+ T-cells in lymph nodes but relatively spares CCR7-effector T-cells.	Fingolimod Hydrochloride	0-10	C-C motif chemokine receptor 7	Homo sapiens	168-172
24680062-1	2014	Fingolimod (FTY720) is a multiple sclerosis (MS) therapeutic that upon phosphorylation causes the internalization of sphingosine-1-phosphate receptors (S1PR) and traps CCR7+ T-cells in lymph nodes but relatively spares CCR7-effector T-cells.	Fingolimod Hydrochloride	0-10	C-C motif chemokine receptor 7	Homo sapiens	219-223
24680062-1	2014	Fingolimod (FTY720) is a multiple sclerosis (MS) therapeutic that upon phosphorylation causes the internalization of sphingosine-1-phosphate receptors (S1PR) and traps CCR7+ T-cells in lymph nodes but relatively spares CCR7-effector T-cells.	Fingolimod Hydrochloride	12-18	C-C motif chemokine receptor 7	Homo sapiens	168-172
24680062-1	2014	Fingolimod (FTY720) is a multiple sclerosis (MS) therapeutic that upon phosphorylation causes the internalization of sphingosine-1-phosphate receptors (S1PR) and traps CCR7+ T-cells in lymph nodes but relatively spares CCR7-effector T-cells.	Fingolimod Hydrochloride	12-18	C-C motif chemokine receptor 7	Homo sapiens	219-223
24507619-1	2014	Fingolimod has demonstrated efficacy in patients with multiple sclerosis (MS), and patients become gradually lymphopenic after a few days of treatment, with selective reductions in CD4+ subsets.	Fingolimod Hydrochloride	0-10	CD4 molecule	Homo sapiens	181-184
24301680-5	2014	The beneficial effect of FTY720 administration was associated with a significant strengthening of neuronal activity and connectivity and, with reduction of mutant huntingtin aggregates, and it was also paralleled by increased phosphorylation of mutant huntingtin at serine 13/16 residues that are predicted to attenuate protein toxicity.	Fingolimod Hydrochloride	25-31	huntingtin	Mus musculus	163-173
24301680-5	2014	The beneficial effect of FTY720 administration was associated with a significant strengthening of neuronal activity and connectivity and, with reduction of mutant huntingtin aggregates, and it was also paralleled by increased phosphorylation of mutant huntingtin at serine 13/16 residues that are predicted to attenuate protein toxicity.	Fingolimod Hydrochloride	25-31	huntingtin	Mus musculus	252-262
24343820-2	2014	Fingolimod hydrochloride (FTY720), an S1P1 functional antagonist, induced significant accumulation of CD62L(high)CD69(low) mature SP thymocytes in the thymic medulla.	Fingolimod Hydrochloride	0-24	sphingosine-1-phosphate receptor 1	Mus musculus	38-42
24343820-2	2014	Fingolimod hydrochloride (FTY720), an S1P1 functional antagonist, induced significant accumulation of CD62L(high)CD69(low) mature SP thymocytes in the thymic medulla.	Fingolimod Hydrochloride	0-24	selectin, lymphocyte	Mus musculus	102-107
24343820-2	2014	Fingolimod hydrochloride (FTY720), an S1P1 functional antagonist, induced significant accumulation of CD62L(high)CD69(low) mature SP thymocytes in the thymic medulla.	Fingolimod Hydrochloride	0-24	CD69 antigen	Mus musculus	113-117
24343820-2	2014	Fingolimod hydrochloride (FTY720), an S1P1 functional antagonist, induced significant accumulation of CD62L(high)CD69(low) mature SP thymocytes in the thymic medulla.	Fingolimod Hydrochloride	26-32	sphingosine-1-phosphate receptor 1	Mus musculus	38-42
24343820-2	2014	Fingolimod hydrochloride (FTY720), an S1P1 functional antagonist, induced significant accumulation of CD62L(high)CD69(low) mature SP thymocytes in the thymic medulla.	Fingolimod Hydrochloride	26-32	selectin, lymphocyte	Mus musculus	102-107
24343820-2	2014	Fingolimod hydrochloride (FTY720), an S1P1 functional antagonist, induced significant accumulation of CD62L(high)CD69(low) mature SP thymocytes in the thymic medulla.	Fingolimod Hydrochloride	26-32	CD69 antigen	Mus musculus	113-117
25876471-4	2014	RESULTS: Both fingolimod doses significantly reduced annualized relapse rate in patients that received prior interferon-beta or glatiramer acetate, discontinued prior disease-modifying therapy owing to unsatisfactory therapeutic effect, were treatment-naive, or had prior disease-modifying therapy duration of &gt;1-3 years (P&lt;=0.0301 for all comparisons vs placebo).	Fingolimod Hydrochloride	14-24	interferon beta 1	Homo sapiens	109-124
25876473-5	2014	RESULTS: Compared with interferon beta-1a intramuscular, fingolimod 0.5mg significantly reduced annualized relapse rate in patients who were treatment naive, received prior interferon-beta treatment, discontinued prior disease-modifying therapy for unsatisfactory therapeutic effect, or had prior disease-modifying therapy duration of &gt;=1 year (P&lt;=0.05, all comparisons).	Fingolimod Hydrochloride	57-67	interferon beta 1	Homo sapiens	173-188
25876473-7	2014	Significant reductions were also seen with fingolimod 1.25mg for treatment-naive and prior interferon-beta-treated patients.	Fingolimod Hydrochloride	43-53	interferon beta 1	Homo sapiens	91-106
23753531-12	2013	CONCLUSIONS: FTY-720 alleviates existing cardiac hypertrophy/fibrosis through mechanisms involving negative regulation of NFAT activity in cardiomyocytes and reduction of periostin expression allowing for a more homeostatic extracellular compartment milieu.	Fingolimod Hydrochloride	13-20	periostin	Homo sapiens	171-180
24335183-4	2014	Transduction of the renal carcinoma cell line ACHN or cervical cancer cell line HeLa with lentivirus expressing the oncogenic family member pp32r1 or a pp32r1Y140H functional mutant illustrated an enhanced resistance to FTY720 induced apoptosis.	Fingolimod Hydrochloride	220-226	acidic nuclear phosphoprotein 32 family member C	Homo sapiens	140-146
24335440-11	2014	FTY720 (S)-phosphonate maintains endothelial sphingosine 1-phosphate receptor 1 protein expression in contrast to greater than 50% reduction after incubation with sphingosine 1-phosphate, FTY720, or other sphingosine 1-phosphate receptor 1 agonists.	Fingolimod Hydrochloride	0-6	sphingosine-1-phosphate receptor 1	Mus musculus	45-79
24335440-13	2014	Intraperitoneal administration of FTY720 (S)-phosphonate every other day for 1 week in normal or bleomycin-injured mice maintains significantly higher lung sphingosine 1-phosphate receptor 1 expression compared with FTY720.	Fingolimod Hydrochloride	34-40	sphingosine-1-phosphate receptor 1	Mus musculus	156-190
24335440-15	2014	CONCLUSION: FTY720 (S)-phosphonate is a promising barrier-promoting agent that effectively maintains sphingosine 1-phosphate receptor 1 levels and improves outcomes in the bleomycin model of acute lung injury.	Fingolimod Hydrochloride	12-18	sphingosine-1-phosphate receptor 1	Mus musculus	101-135
24059944-8	2013	After adjusting for baseline differences, fingolimod was associated with a 52% reduction in the probability of having a relapse (odds ratio, 0.48; 95% confidence interval [CI], 0.28-0.84; p = 0.0097) and a 50% reduction in ARR (rate ratio, 0.50; 95% CI, 0.34-0.75; p = 0.0006) compared with IFN/GA.	Fingolimod Hydrochloride	42-52	interferon alpha 1	Homo sapiens	291-297
24139422-1	2013	BACKGROUND: Patients with multiple sclerosis (MS) whose disease activity is inadequately controlled with a platform therapy (interferon beta or glatiramer acetate [GA]) may switch to another platform therapy or escalate therapy to natalizumab or fingolimod, which were approved in the US in 2006 and 2010, respectively.	Fingolimod Hydrochloride	246-256	interferon beta 1	Homo sapiens	125-140
24475777-8	2014	Four patients were aquaporin-4 (AQP4) antibody-positive, three of whom showed rapid disease exacerbations within 10 days of fingolimod initiation.	Fingolimod Hydrochloride	124-134	aquaporin 4	Homo sapiens	19-30
24475777-8	2014	Four patients were aquaporin-4 (AQP4) antibody-positive, three of whom showed rapid disease exacerbations within 10 days of fingolimod initiation.	Fingolimod Hydrochloride	124-134	aquaporin 4	Homo sapiens	32-36
24029635-5	2013	METHODS: Transient middle cerebral artery occlusion (tMCAO) was induced in wild-type and lymphocyte-deficient Rag1(-/-) mice treated with FTY720 (1 mg/kg) or vehicle immediately before reperfusion.	Fingolimod Hydrochloride	138-144	recombination activating 1	Mus musculus	110-114
23435938-7	2013	Chronic daily administration of FTY720 (1 mg/kg, i.p., 14 days) significantly attenuated the Abeta(42)-induced learning and memory impairment and prevented the hippocampus neuronal damage as well as caspase-3 activation.	Fingolimod Hydrochloride	32-38	caspase 3	Rattus norvegicus	199-208
23738997-1	2013	Fingolimod 0.5 mg (Gilenya( ), Novartis Pharmaceuticals Corporation, FL, USA) is the first once-daily oral therapy approved for relapsing forms of multiple sclerosis (MS) in the USA and for rapidly evolving severe MS or highly active disease despite IFN-beta treatment in Europe.	Fingolimod Hydrochloride	0-10	interferon beta 1	Homo sapiens	250-258
24069553-5	2013	FTY720, an antagonist of S1PR1, abolished persistent NFkappaB/IL-6/STAT3 signaling and reduced the development and progression of colitis-associated cancer.	Fingolimod Hydrochloride	0-6	sphingosine-1-phosphate receptor 1	Homo sapiens	25-30
24069553-5	2013	FTY720, an antagonist of S1PR1, abolished persistent NFkappaB/IL-6/STAT3 signaling and reduced the development and progression of colitis-associated cancer.	Fingolimod Hydrochloride	0-6	nuclear factor kappa B subunit 1	Homo sapiens	53-61
24069553-5	2013	FTY720, an antagonist of S1PR1, abolished persistent NFkappaB/IL-6/STAT3 signaling and reduced the development and progression of colitis-associated cancer.	Fingolimod Hydrochloride	0-6	interleukin 6	Homo sapiens	62-66
24069553-5	2013	FTY720, an antagonist of S1PR1, abolished persistent NFkappaB/IL-6/STAT3 signaling and reduced the development and progression of colitis-associated cancer.	Fingolimod Hydrochloride	0-6	signal transducer and activator of transcription 3	Homo sapiens	67-72
23667698-2	2013	Sphingosine related compounds, FTY720 and KRP203 known as S1PR modulators, are phosphorylated by sphingosine kinase 2 (SphK2) to yield the active metabolites FTY720-P and KRP203-P, which work as functional antagonists for S1PRs.	Fingolimod Hydrochloride	31-37	sphingosine kinase 2	Mus musculus	97-117
23518370-4	2013	However, emerging evidence indicates that fingolimod has direct effects in the CNS in MS. For example, in the MS animal model of experimental autoimmune encephalomyelitis (EAE), fingolimod is highly efficacious in both a prophylactic and therapeutic setting, yet becomes ineffective in animals selectively deficient for S1P1 on astrocytes, despite maintained normal immunologic receptor expression and functions, and S1P-mediated immune activities.	Fingolimod Hydrochloride	42-52	sphingosine-1-phosphate receptor 1	Homo sapiens	320-324
23667698-2	2013	Sphingosine related compounds, FTY720 and KRP203 known as S1PR modulators, are phosphorylated by sphingosine kinase 2 (SphK2) to yield the active metabolites FTY720-P and KRP203-P, which work as functional antagonists for S1PRs.	Fingolimod Hydrochloride	31-37	sphingosine kinase 2	Mus musculus	119-124
23073075-1	2013	Fingolimod (FTY720), a novel drug approved for the treatment of relapsing-remitting multiple sclerosis, activates different sphingosine-1-phosphate receptor (S1PR) subtypes.	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Mus musculus	124-147
23261767-8	2013	Moreover, fingolimod treatment significantly reduced the expression of intercellular adhesion molecule-1 (ICAM-1), interferon-gamma (INF-gamma), and interleukin-17 (IL-17) in the mouse brain at 72 h post-cICH (p&lt;0.05 compared to vehicle).	Fingolimod Hydrochloride	10-20	intercellular adhesion molecule 1	Mus musculus	71-104
23261767-8	2013	Moreover, fingolimod treatment significantly reduced the expression of intercellular adhesion molecule-1 (ICAM-1), interferon-gamma (INF-gamma), and interleukin-17 (IL-17) in the mouse brain at 72 h post-cICH (p&lt;0.05 compared to vehicle).	Fingolimod Hydrochloride	10-20	intercellular adhesion molecule 1	Mus musculus	106-112
23261767-8	2013	Moreover, fingolimod treatment significantly reduced the expression of intercellular adhesion molecule-1 (ICAM-1), interferon-gamma (INF-gamma), and interleukin-17 (IL-17) in the mouse brain at 72 h post-cICH (p&lt;0.05 compared to vehicle).	Fingolimod Hydrochloride	10-20	interferon gamma	Mus musculus	115-131
23261767-8	2013	Moreover, fingolimod treatment significantly reduced the expression of intercellular adhesion molecule-1 (ICAM-1), interferon-gamma (INF-gamma), and interleukin-17 (IL-17) in the mouse brain at 72 h post-cICH (p&lt;0.05 compared to vehicle).	Fingolimod Hydrochloride	10-20	interferon gamma	Mus musculus	133-142
23261767-8	2013	Moreover, fingolimod treatment significantly reduced the expression of intercellular adhesion molecule-1 (ICAM-1), interferon-gamma (INF-gamma), and interleukin-17 (IL-17) in the mouse brain at 72 h post-cICH (p&lt;0.05 compared to vehicle).	Fingolimod Hydrochloride	10-20	interleukin 17A	Mus musculus	149-163
23261767-8	2013	Moreover, fingolimod treatment significantly reduced the expression of intercellular adhesion molecule-1 (ICAM-1), interferon-gamma (INF-gamma), and interleukin-17 (IL-17) in the mouse brain at 72 h post-cICH (p&lt;0.05 compared to vehicle).	Fingolimod Hydrochloride	10-20	interleukin 17A	Mus musculus	165-170
23287783-0	2013	Fingolimod reduces hemorrhagic transformation associated with delayed tissue plasminogen activator treatment in a mouse thromboembolic model.	Fingolimod Hydrochloride	0-10	plasminogen activator, tissue	Mus musculus	70-98
23287783-5	2013	Combination of fingolimod and tPA improves the neurological outcome of the thrombolytic therapy and reduces the risk of hemorrhagic transformation associated with delayed administration of tPA.	Fingolimod Hydrochloride	15-25	plasminogen activator, tissue	Mus musculus	189-192
23287783-6	2013	CONCLUSIONS: This study confirms the protective efficacy of fingolimod as a treatment against ischemic stroke in another rodent model of stroke (thromboembolic occlusion), and suggests that fingolimod could potentially be used in combination with tPA to reduce the risk of brain hemorrhage.	Fingolimod Hydrochloride	60-70	plasminogen activator, tissue	Mus musculus	247-250
23073075-1	2013	Fingolimod (FTY720), a novel drug approved for the treatment of relapsing-remitting multiple sclerosis, activates different sphingosine-1-phosphate receptor (S1PR) subtypes.	Fingolimod Hydrochloride	12-18	sphingosine-1-phosphate receptor 1	Mus musculus	124-147
22828274-0	2012	Fingolimod inhibits PDGF-B-induced migration of vascular smooth muscle cell by down-regulating the S1PR1/S1PR3 pathway.	Fingolimod Hydrochloride	0-10	platelet derived growth factor subunit B	Rattus norvegicus	20-26
23892961-1	2013	A 49-year-old female neuromyelitis optica spectrum disorder (NMOSD) patient with positive anti-aquaporin 4 (AQP4) antibody was treated with fingolimod (FTY720).	Fingolimod Hydrochloride	140-150	aquaporin 4	Homo sapiens	95-106
23892961-1	2013	A 49-year-old female neuromyelitis optica spectrum disorder (NMOSD) patient with positive anti-aquaporin 4 (AQP4) antibody was treated with fingolimod (FTY720).	Fingolimod Hydrochloride	140-150	aquaporin 4	Homo sapiens	108-112
23892961-1	2013	A 49-year-old female neuromyelitis optica spectrum disorder (NMOSD) patient with positive anti-aquaporin 4 (AQP4) antibody was treated with fingolimod (FTY720).	Fingolimod Hydrochloride	152-158	aquaporin 4	Homo sapiens	95-106
23892961-1	2013	A 49-year-old female neuromyelitis optica spectrum disorder (NMOSD) patient with positive anti-aquaporin 4 (AQP4) antibody was treated with fingolimod (FTY720).	Fingolimod Hydrochloride	152-158	aquaporin 4	Homo sapiens	108-112
23892961-5	2013	Thus, fingolimod may be associated with the development of a fulminant course in NMOSD patients with positive anti-AQP4 antibody.	Fingolimod Hydrochloride	6-16	aquaporin 4	Homo sapiens	115-119
22828274-0	2012	Fingolimod inhibits PDGF-B-induced migration of vascular smooth muscle cell by down-regulating the S1PR1/S1PR3 pathway.	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Rattus norvegicus	99-104
22828274-0	2012	Fingolimod inhibits PDGF-B-induced migration of vascular smooth muscle cell by down-regulating the S1PR1/S1PR3 pathway.	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 3	Rattus norvegicus	105-110
22828274-5	2012	We then compared siRNA and/or fingolimod (100 nM) treatments on PDGFR-beta, S1PR1 S1PR2 and S1PR3 expression.	Fingolimod Hydrochloride	30-40	sphingosine-1-phosphate receptor 1	Rattus norvegicus	76-81
22828274-6	2012	Fingolimod induced a 50% reduction in S1PR3 protein expression which was cumulative with that obtained with anti-S1PR3 siRNA.	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 3	Rattus norvegicus	38-43
22828274-6	2012	Fingolimod induced a 50% reduction in S1PR3 protein expression which was cumulative with that obtained with anti-S1PR3 siRNA.	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 3	Rattus norvegicus	113-118
22828274-10	2012	As an S1P analogue, fingolimod is considered a potent activator of S1PR1 and S1PR3.	Fingolimod Hydrochloride	20-30	sphingosine-1-phosphate receptor 1	Rattus norvegicus	67-72
22828274-10	2012	As an S1P analogue, fingolimod is considered a potent activator of S1PR1 and S1PR3.	Fingolimod Hydrochloride	20-30	sphingosine-1-phosphate receptor 3	Rattus norvegicus	77-82
22810490-8	2012	Incubation of astrocytes with Fingolimod prior to TNF-alpha treatment reduced ceramide production and mRNA expression of ASM to control levels in astrocytes.	Fingolimod Hydrochloride	30-40	sphingomyelin phosphodiesterase 1	Homo sapiens	121-124
22949658-8	2012	Importantly, fingolimod (FTY720), a S1P analog recently approved for treatment of multiple sclerosis, also rapidly reduced P-glycoprotein activity; similar effects were found with the active, phosphorylated metabolite (FTY720P).	Fingolimod Hydrochloride	13-23	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	123-137
22949658-8	2012	Importantly, fingolimod (FTY720), a S1P analog recently approved for treatment of multiple sclerosis, also rapidly reduced P-glycoprotein activity; similar effects were found with the active, phosphorylated metabolite (FTY720P).	Fingolimod Hydrochloride	25-31	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	123-137
22999882-2	2012	Fingolimod (FTY720, Gilenya) is a S1P(1) receptor agonist that has recently been approved for the treatment of multiple sclerosis (MS).	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Homo sapiens	34-40
22999882-2	2012	Fingolimod (FTY720, Gilenya) is a S1P(1) receptor agonist that has recently been approved for the treatment of multiple sclerosis (MS).	Fingolimod Hydrochloride	12-18	sphingosine-1-phosphate receptor 1	Homo sapiens	34-40
22891354-6	2012	Ongoing synaptic activity and MAPK signaling is required for fingolimod-induced BDNF increase, a pathway that can also be activated in vivo by systemic fingolimod administration.	Fingolimod Hydrochloride	61-71	brain derived neurotrophic factor	Mus musculus	80-84
22891354-0	2012	Fingolimod, a sphingosine-1 phosphate receptor modulator, increases BDNF levels and improves symptoms of a mouse model of Rett syndrome.	Fingolimod Hydrochloride	0-10	brain derived neurotrophic factor	Mus musculus	68-72
22891354-6	2012	Ongoing synaptic activity and MAPK signaling is required for fingolimod-induced BDNF increase, a pathway that can also be activated in vivo by systemic fingolimod administration.	Fingolimod Hydrochloride	152-162	brain derived neurotrophic factor	Mus musculus	80-84
22891354-5	2012	In cultured neurons, fingolimod increases BDNF levels and counteracts NMDA-induced neuronal death in a BDNF-dependent manner.	Fingolimod Hydrochloride	21-31	brain derived neurotrophic factor	Mus musculus	42-46
22580711-6	2012	Western blot analysis showed that FTY720 induced the downregulation of cyclin D1, cyclin E, CDK2, CDK4, Bcl-2 and E2F1 and the upregulation of Kip1/p27, Cip1/p21, Bax and Rb in GMC in a dose-dependent manner.	Fingolimod Hydrochloride	34-40	cyclin-dependent kinase 4	Rattus norvegicus	98-102
22891354-5	2012	In cultured neurons, fingolimod increases BDNF levels and counteracts NMDA-induced neuronal death in a BDNF-dependent manner.	Fingolimod Hydrochloride	21-31	brain derived neurotrophic factor	Mus musculus	103-107
22580711-6	2012	Western blot analysis showed that FTY720 induced the downregulation of cyclin D1, cyclin E, CDK2, CDK4, Bcl-2 and E2F1 and the upregulation of Kip1/p27, Cip1/p21, Bax and Rb in GMC in a dose-dependent manner.	Fingolimod Hydrochloride	34-40	cyclin D1	Rattus norvegicus	71-80
22580711-6	2012	Western blot analysis showed that FTY720 induced the downregulation of cyclin D1, cyclin E, CDK2, CDK4, Bcl-2 and E2F1 and the upregulation of Kip1/p27, Cip1/p21, Bax and Rb in GMC in a dose-dependent manner.	Fingolimod Hydrochloride	34-40	BCL2, apoptosis regulator	Rattus norvegicus	104-109
22580711-6	2012	Western blot analysis showed that FTY720 induced the downregulation of cyclin D1, cyclin E, CDK2, CDK4, Bcl-2 and E2F1 and the upregulation of Kip1/p27, Cip1/p21, Bax and Rb in GMC in a dose-dependent manner.	Fingolimod Hydrochloride	34-40	cyclin E1	Rattus norvegicus	82-90
22580711-6	2012	Western blot analysis showed that FTY720 induced the downregulation of cyclin D1, cyclin E, CDK2, CDK4, Bcl-2 and E2F1 and the upregulation of Kip1/p27, Cip1/p21, Bax and Rb in GMC in a dose-dependent manner.	Fingolimod Hydrochloride	34-40	E2F transcription factor 1	Rattus norvegicus	114-118
22580711-6	2012	Western blot analysis showed that FTY720 induced the downregulation of cyclin D1, cyclin E, CDK2, CDK4, Bcl-2 and E2F1 and the upregulation of Kip1/p27, Cip1/p21, Bax and Rb in GMC in a dose-dependent manner.	Fingolimod Hydrochloride	34-40	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	143-147
22580711-6	2012	Western blot analysis showed that FTY720 induced the downregulation of cyclin D1, cyclin E, CDK2, CDK4, Bcl-2 and E2F1 and the upregulation of Kip1/p27, Cip1/p21, Bax and Rb in GMC in a dose-dependent manner.	Fingolimod Hydrochloride	34-40	cyclin dependent kinase 2	Rattus norvegicus	92-96
22580711-6	2012	Western blot analysis showed that FTY720 induced the downregulation of cyclin D1, cyclin E, CDK2, CDK4, Bcl-2 and E2F1 and the upregulation of Kip1/p27, Cip1/p21, Bax and Rb in GMC in a dose-dependent manner.	Fingolimod Hydrochloride	34-40	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	148-151
22580711-6	2012	Western blot analysis showed that FTY720 induced the downregulation of cyclin D1, cyclin E, CDK2, CDK4, Bcl-2 and E2F1 and the upregulation of Kip1/p27, Cip1/p21, Bax and Rb in GMC in a dose-dependent manner.	Fingolimod Hydrochloride	34-40	cyclin-dependent kinase inhibitor 1A	Rattus norvegicus	153-157
22580711-6	2012	Western blot analysis showed that FTY720 induced the downregulation of cyclin D1, cyclin E, CDK2, CDK4, Bcl-2 and E2F1 and the upregulation of Kip1/p27, Cip1/p21, Bax and Rb in GMC in a dose-dependent manner.	Fingolimod Hydrochloride	34-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	158-161
22580711-6	2012	Western blot analysis showed that FTY720 induced the downregulation of cyclin D1, cyclin E, CDK2, CDK4, Bcl-2 and E2F1 and the upregulation of Kip1/p27, Cip1/p21, Bax and Rb in GMC in a dose-dependent manner.	Fingolimod Hydrochloride	34-40	BCL2 associated X, apoptosis regulator	Rattus norvegicus	163-166
22494956-11	2012	In patients who relapsed and had lesion activity despite treatment with interferon beta in the previous year, the ARR ratio for fingolimod 0 5 mg versus placebo was 0 38 (95% CI 0 21-0 68, p=0 0011), and for treatment-naive patients with rapidly evolving severe disease it was 0 33 (0 18-0 62, p=0 0006).	Fingolimod Hydrochloride	128-138	interferon beta 1	Homo sapiens	72-87
22109829-6	2012	Furthermore, FTY720-induced toxicity in AML leukemic cells was mediated by restoration of PP2A activity, via down-regulation of PP2A inhibitor SET, dephosporylation of PP2A-C(TYR307), and up-regulation of relevant PP2A subunit A and B55alpha.	Fingolimod Hydrochloride	13-19	protein phosphatase 2 phosphatase activator	Homo sapiens	90-94
22281442-4	2012	We observed that FTY720 could induce caspase-3 dependent apoptosis in a dose- and time-dependent manner in U266 cells.	Fingolimod Hydrochloride	17-23	caspase 3	Homo sapiens	37-46
22109829-6	2012	Furthermore, FTY720-induced toxicity in AML leukemic cells was mediated by restoration of PP2A activity, via down-regulation of PP2A inhibitor SET, dephosporylation of PP2A-C(TYR307), and up-regulation of relevant PP2A subunit A and B55alpha.	Fingolimod Hydrochloride	13-19	protein phosphatase 2 phosphatase activator	Homo sapiens	128-132
22109829-6	2012	Furthermore, FTY720-induced toxicity in AML leukemic cells was mediated by restoration of PP2A activity, via down-regulation of PP2A inhibitor SET, dephosporylation of PP2A-C(TYR307), and up-regulation of relevant PP2A subunit A and B55alpha.	Fingolimod Hydrochloride	13-19	protein phosphatase 2 catalytic subunit alpha	Homo sapiens	168-174
22109829-6	2012	Furthermore, FTY720-induced toxicity in AML leukemic cells was mediated by restoration of PP2A activity, via down-regulation of PP2A inhibitor SET, dephosporylation of PP2A-C(TYR307), and up-regulation of relevant PP2A subunit A and B55alpha.	Fingolimod Hydrochloride	13-19	protein phosphatase 2 phosphatase activator	Homo sapiens	128-132
22109829-6	2012	Furthermore, FTY720-induced toxicity in AML leukemic cells was mediated by restoration of PP2A activity, via down-regulation of PP2A inhibitor SET, dephosporylation of PP2A-C(TYR307), and up-regulation of relevant PP2A subunit A and B55alpha.	Fingolimod Hydrochloride	13-19	protein phosphatase 2 regulatory subunit Balpha	Homo sapiens	233-241
21632869-3	2011	An impetus for the characterization of S1P-initiated signaling effects came with the discovery that FTY720 [fingolimod; 2-amino-2-(2-[4-octylphenyl]ethyl)-1,3-propanediol] modulates the immune system by acting as an agonist at S1P(1).	Fingolimod Hydrochloride	100-106	sphingosine-1-phosphate receptor 1	Mus musculus	39-42
22149256-12	2012	Fingolimod is largely cleared through metabolism by cytochrome P450 (CYP) 4F2.	Fingolimod Hydrochloride	0-10	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	52-77
22149256-13	2012	Since few drugs are metabolized by CYP4F2, fingolimod would be expected to have a relatively low potential for drug-drug interactions.	Fingolimod Hydrochloride	43-53	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	35-41
22149256-16	2012	However, blood concentrations of fingolimod and fingolimod phosphate are increased moderately when fingolimod is coadministered with ketoconazole, an inhibitor of CYP4F2.	Fingolimod Hydrochloride	33-43	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	163-169
22149256-16	2012	However, blood concentrations of fingolimod and fingolimod phosphate are increased moderately when fingolimod is coadministered with ketoconazole, an inhibitor of CYP4F2.	Fingolimod Hydrochloride	48-58	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	163-169
23285242-7	2012	infusion of FTY720 (0.1, 0.3, 1.0 mg/kg/20 min) or BAF312 (0.5, 1.5, 5.0 mg/kg/20 min) elicited acute bradycardia in anesthetized rats demonstrating an S1P1 mediated mechanism-of-action.	Fingolimod Hydrochloride	12-18	sphingosine-1-phosphate receptor 1	Rattus norvegicus	152-156
22916176-4	2012	We hypothesized that FTY720 might exert the cardioprotective effects of S1P1 and S1P3 viaprotein kinase C-beta (PKCbeta II) signaling pathway.	Fingolimod Hydrochloride	21-27	sphingosine-1-phosphate receptor 1	Rattus norvegicus	72-85
22916176-4	2012	We hypothesized that FTY720 might exert the cardioprotective effects of S1P1 and S1P3 viaprotein kinase C-beta (PKCbeta II) signaling pathway.	Fingolimod Hydrochloride	21-27	protein kinase C, beta	Rattus norvegicus	112-119
22493799-4	2012	Fingolimod (FTY720), the novel S1PR1 agonist, has been approved for the treatment of multiple sclerosis in clinical trials.	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Homo sapiens	31-36
22493799-4	2012	Fingolimod (FTY720), the novel S1PR1 agonist, has been approved for the treatment of multiple sclerosis in clinical trials.	Fingolimod Hydrochloride	12-18	sphingosine-1-phosphate receptor 1	Homo sapiens	31-36
21519925-0	2011	Non-phosphorylated FTY720 induces apoptosis of human microglia by activating SREBP2.	Fingolimod Hydrochloride	19-25	sterol regulatory element binding transcription factor 2	Homo sapiens	77-83
21519925-1	2011	A synthetic analog of sphingosine named FTY720 (Fingolimod), phosphorylated by sphingosine kinase-2, interacts with sphingosine-1-phosphate (S1P) receptors expressed on various cells.	Fingolimod Hydrochloride	40-46	sphingosine kinase 2	Homo sapiens	79-99
21519925-1	2011	A synthetic analog of sphingosine named FTY720 (Fingolimod), phosphorylated by sphingosine kinase-2, interacts with sphingosine-1-phosphate (S1P) receptors expressed on various cells.	Fingolimod Hydrochloride	48-58	sphingosine kinase 2	Homo sapiens	79-99
21872577-3	2011	Particularly, SphK2 is necessary for the phosphorylation of the sphingosine analog fingolimod (FTY720), which is protective in rodent stroke models.	Fingolimod Hydrochloride	83-93	sphingosine kinase 2	Mus musculus	14-19
21872577-9	2011	The protective effect of FTY720 was conserved in SphK1(-/-) mice but not in SphK2(-/-) mice.	Fingolimod Hydrochloride	25-31	sphingosine kinase 1	Mus musculus	49-54
21632869-3	2011	An impetus for the characterization of S1P-initiated signaling effects came with the discovery that FTY720 [fingolimod; 2-amino-2-(2-[4-octylphenyl]ethyl)-1,3-propanediol] modulates the immune system by acting as an agonist at S1P(1).	Fingolimod Hydrochloride	100-106	sphingosine-1-phosphate receptor 1	Mus musculus	227-230
21632869-3	2011	An impetus for the characterization of S1P-initiated signaling effects came with the discovery that FTY720 [fingolimod; 2-amino-2-(2-[4-octylphenyl]ethyl)-1,3-propanediol] modulates the immune system by acting as an agonist at S1P(1).	Fingolimod Hydrochloride	108-118	sphingosine-1-phosphate receptor 1	Mus musculus	39-42
21632869-3	2011	An impetus for the characterization of S1P-initiated signaling effects came with the discovery that FTY720 [fingolimod; 2-amino-2-(2-[4-octylphenyl]ethyl)-1,3-propanediol] modulates the immune system by acting as an agonist at S1P(1).	Fingolimod Hydrochloride	108-118	sphingosine-1-phosphate receptor 1	Mus musculus	227-230
21464424-1	2011	Fingolimod is a functional antagonist of the sphingosine-1-phosphate receptor 1 and thereby inhibits sphingosine-1-phosphate-dependent lymphocyte egress from secondary lymphoid tissues, resulting in a pronounced lymphopenia in the peripheral blood.	Fingolimod Hydrochloride	0-10	sphingosine-1-phosphate receptor 1	Homo sapiens	45-79
21729281-6	2011	RESULTS: Following demyelination, fingolimod significantly augmented expression of myelin basic protein in the remyelination phase.	Fingolimod Hydrochloride	34-44	myelin basic protein	Rattus norvegicus	83-103
21729281-10	2011	In addition, nitric oxide metabolites and apoptotic effectors caspase 3 and caspase 7 were reduced during demyelination in the presence of fingolimod.	Fingolimod Hydrochloride	139-149	caspase 3	Rattus norvegicus	62-71
21729281-10	2011	In addition, nitric oxide metabolites and apoptotic effectors caspase 3 and caspase 7 were reduced during demyelination in the presence of fingolimod.	Fingolimod Hydrochloride	139-149	caspase 7	Rattus norvegicus	76-85
21751747-4	2011	In a 12-month, comparative, double-blind, randomised trial including 1292 patients daily treatment with oral fingolimod (0.5 mg or 1.25 mg) modestly prolonged the interval between exacerbations compared to weekly intramuscular injections of interferon beta-1a: about one exacerbation prevented every 6 years.	Fingolimod Hydrochloride	109-119	interferon beta 1	Homo sapiens	241-256
21464128-2	2011	We have previously demonstrated that FTY720 and (S)-FTY720 vinylphosphonate are novel inhibitors of SK1 activity.	Fingolimod Hydrochloride	37-43	sphingosine kinase 1	Homo sapiens	100-103
21912422-6	2011	With the recent discovery that clinically approved drug fingolimod has SK1-inhibiting properties, SK1 has gained significant attention from both clinicians and the pharmaceutical industry and it is hoped that trials of newly developed SK1 inhibitors might follow soon.	Fingolimod Hydrochloride	56-66	sphingosine kinase 1	Homo sapiens	71-74
21912422-6	2011	With the recent discovery that clinically approved drug fingolimod has SK1-inhibiting properties, SK1 has gained significant attention from both clinicians and the pharmaceutical industry and it is hoped that trials of newly developed SK1 inhibitors might follow soon.	Fingolimod Hydrochloride	56-66	sphingosine kinase 1	Homo sapiens	98-101
21912422-6	2011	With the recent discovery that clinically approved drug fingolimod has SK1-inhibiting properties, SK1 has gained significant attention from both clinicians and the pharmaceutical industry and it is hoped that trials of newly developed SK1 inhibitors might follow soon.	Fingolimod Hydrochloride	56-66	sphingosine kinase 1	Homo sapiens	98-101
21464424-2	2011	The effects of fingolimod treatment on the CSF of patients with MS have not been studied so far.	Fingolimod Hydrochloride	15-25	colony stimulating factor 2	Homo sapiens	43-46
21464424-7	2011	Fingolimod decreased the proportion of CSF CD4+ T cells but to a lesser extent than in the peripheral blood.	Fingolimod Hydrochloride	0-10	colony stimulating factor 2	Homo sapiens	39-42
21464424-11	2011	CONCLUSION: Fingolimod treatment has a profound impact on CSF, which to some extent differs from the peripheral effects of the drug.	Fingolimod Hydrochloride	12-22	colony stimulating factor 2	Homo sapiens	58-61
24900328-3	2011	It has been postulated that fingolimod"s efficacy is due to S1P1 agonism, while its cardiovascular side effects (transient bradycardia and hypertension) are due to S1P3 agonism.	Fingolimod Hydrochloride	28-38	sphingosine-1-phosphate receptor 1	Homo sapiens	60-64
20955831-5	2011	Therapeutic administration of FTY720 (0.03 to 1 mg/kg) significantly improved the symptoms of chronic EAE induced by myelin oligodendrocyte glycoprotein in C57BL/6 mice whereas rm-IFN-beta (10,000 IU/mouse) showed no clear effect.	Fingolimod Hydrochloride	30-36	myelin oligodendrocyte glycoprotein	Mus musculus	117-152
21233840-7	2011	In conclusion, our results show that PP2A inhibition is a common event in AML cells and that PP2A activators, such as forskolin or FTY720, could represent potential novel therapeutic targets in AML.	Fingolimod Hydrochloride	131-137	protein phosphatase 2 phosphatase activator	Homo sapiens	37-41
21233840-7	2011	In conclusion, our results show that PP2A inhibition is a common event in AML cells and that PP2A activators, such as forskolin or FTY720, could represent potential novel therapeutic targets in AML.	Fingolimod Hydrochloride	131-137	protein phosphatase 2 phosphatase activator	Homo sapiens	93-97
20955831-5	2011	Therapeutic administration of FTY720 (0.03 to 1 mg/kg) significantly improved the symptoms of chronic EAE induced by myelin oligodendrocyte glycoprotein in C57BL/6 mice whereas rm-IFN-beta (10,000 IU/mouse) showed no clear effect.	Fingolimod Hydrochloride	30-36	interferon beta 1, fibroblast	Mus musculus	180-188