PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
32780889-11	2020	CUDC-907 suppressed Akt, NF-kappaB and AP-1 by downregulating phosphorylated and/or total Akt, IKKalpha/beta, RelA, JunB and JunD.	CUDC-907	0-8	AKT serine/threonine kinase 1	Homo sapiens	20-23
32780889-11	2020	CUDC-907 suppressed Akt, NF-kappaB and AP-1 by downregulating phosphorylated and/or total Akt, IKKalpha/beta, RelA, JunB and JunD.	CUDC-907	0-8	JunD proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	39-43
32780889-11	2020	CUDC-907 suppressed Akt, NF-kappaB and AP-1 by downregulating phosphorylated and/or total Akt, IKKalpha/beta, RelA, JunB and JunD.	CUDC-907	0-8	AKT serine/threonine kinase 1	Homo sapiens	90-93
32780889-11	2020	CUDC-907 suppressed Akt, NF-kappaB and AP-1 by downregulating phosphorylated and/or total Akt, IKKalpha/beta, RelA, JunB and JunD.	CUDC-907	0-8	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	95-108
32780889-11	2020	CUDC-907 suppressed Akt, NF-kappaB and AP-1 by downregulating phosphorylated and/or total Akt, IKKalpha/beta, RelA, JunB and JunD.	CUDC-907	0-8	RELA proto-oncogene, NF-kB subunit	Homo sapiens	110-114
32780889-11	2020	CUDC-907 suppressed Akt, NF-kappaB and AP-1 by downregulating phosphorylated and/or total Akt, IKKalpha/beta, RelA, JunB and JunD.	CUDC-907	0-8	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	116-120
32780889-11	2020	CUDC-907 suppressed Akt, NF-kappaB and AP-1 by downregulating phosphorylated and/or total Akt, IKKalpha/beta, RelA, JunB and JunD.	CUDC-907	0-8	JunD proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	125-129
32200503-7	2020	Knockdown of DR5 abrogated apoptosis induced by the combination of CUDC-907 and TRAIL in breast cancer cells.	CUDC-907	67-75	TNF receptor superfamily member 10b	Homo sapiens	13-16
32200503-8	2020	CUDC-907 increased the phosphorylation of JNK and p38 MAPK.	CUDC-907	0-8	mitogen-activated protein kinase 8	Homo sapiens	42-45
32200503-8	2020	CUDC-907 increased the phosphorylation of JNK and p38 MAPK.	CUDC-907	0-8	mitogen-activated protein kinase 14	Homo sapiens	50-53
32200503-0	2020	CUDC-907 enhances TRAIL-induced apoptosis through upregulation of DR5 in breast cancer cells.	CUDC-907	0-8	TNF superfamily member 10	Homo sapiens	18-23
32200503-9	2020	JNK inhibitor pretreatment attenuated CUDC-907-induced upregulation of DR5.	CUDC-907	38-46	mitogen-activated protein kinase 8	Homo sapiens	0-3
32200503-0	2020	CUDC-907 enhances TRAIL-induced apoptosis through upregulation of DR5 in breast cancer cells.	CUDC-907	0-8	TNF receptor superfamily member 10b	Homo sapiens	66-69
32200503-9	2020	JNK inhibitor pretreatment attenuated CUDC-907-induced upregulation of DR5.	CUDC-907	38-46	TNF receptor superfamily member 10b	Homo sapiens	71-74
32200503-10	2020	In summary, CUDC-907 shows potent cytotoxicity against breast cancer cells and facilitates TRAIL-mediated apoptosis through DR5 upregulation.	CUDC-907	12-20	TNF superfamily member 10	Homo sapiens	91-96
32200503-1	2020	CUDC-907 is a novel dual-acting inhibitor of phosphoinositide 3-kinase (PI3K) and histone deacetylase (HDAC).	CUDC-907	0-8	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	45-70
32200503-5	2020	The combined treatment of CUDC-907 and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resulted in a marked increase in apoptosis and cleavage of caspase-8, -9 and poly (ADP-ribose) polymerase (PARP) in breast cancer cells.	CUDC-907	26-34	TNF superfamily member 10	Homo sapiens	96-101
32200503-10	2020	In summary, CUDC-907 shows potent cytotoxicity against breast cancer cells and facilitates TRAIL-mediated apoptosis through DR5 upregulation.	CUDC-907	12-20	TNF receptor superfamily member 10b	Homo sapiens	124-127
30819918-5	2019	CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bim, and c-Myc.	CUDC-907	0-8	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	70-75
32200503-5	2020	The combined treatment of CUDC-907 and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resulted in a marked increase in apoptosis and cleavage of caspase-8, -9 and poly (ADP-ribose) polymerase (PARP) in breast cancer cells.	CUDC-907	26-34	poly(ADP-ribose) polymerase 1	Homo sapiens	162-208
32200503-5	2020	The combined treatment of CUDC-907 and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resulted in a marked increase in apoptosis and cleavage of caspase-8, -9 and poly (ADP-ribose) polymerase (PARP) in breast cancer cells.	CUDC-907	26-34	poly(ADP-ribose) polymerase 1	Homo sapiens	210-214
32200503-6	2020	CUDC-907 enhanced expressions of death receptor 5 (DR5), reduced the levels of anti-apoptotic molecules XIAP, Bcl-2 and Bcl-xL.	CUDC-907	0-8	TNF receptor superfamily member 10b	Homo sapiens	33-49
32200503-6	2020	CUDC-907 enhanced expressions of death receptor 5 (DR5), reduced the levels of anti-apoptotic molecules XIAP, Bcl-2 and Bcl-xL.	CUDC-907	0-8	TNF receptor superfamily member 10b	Homo sapiens	51-54
32200503-6	2020	CUDC-907 enhanced expressions of death receptor 5 (DR5), reduced the levels of anti-apoptotic molecules XIAP, Bcl-2 and Bcl-xL.	CUDC-907	0-8	X-linked inhibitor of apoptosis	Homo sapiens	104-108
32200503-6	2020	CUDC-907 enhanced expressions of death receptor 5 (DR5), reduced the levels of anti-apoptotic molecules XIAP, Bcl-2 and Bcl-xL.	CUDC-907	0-8	BCL2 apoptosis regulator	Homo sapiens	110-115
32200503-6	2020	CUDC-907 enhanced expressions of death receptor 5 (DR5), reduced the levels of anti-apoptotic molecules XIAP, Bcl-2 and Bcl-xL.	CUDC-907	0-8	BCL2 like 1	Homo sapiens	120-126
33069237-0	2020	The dual HDAC-PI3K inhibitor CUDC-907 displays single-agent activity and synergizes with PARP inhibitor olaparib in small cell lung cancer.	CUDC-907	29-37	poly(ADP-ribose) polymerase 1	Homo sapiens	89-93
33069237-7	2020	RESULTS: CUDC-907 treatment downregulated MYC paralogs and FoxM1, induced G1 cell-cycle arrest, and impaired DNA double-strand break (DSB) repair capacity in SCLC cells, which produced a potent antiproliferative effect.	CUDC-907	9-17	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	42-45
33069237-7	2020	RESULTS: CUDC-907 treatment downregulated MYC paralogs and FoxM1, induced G1 cell-cycle arrest, and impaired DNA double-strand break (DSB) repair capacity in SCLC cells, which produced a potent antiproliferative effect.	CUDC-907	9-17	forkhead box M1	Homo sapiens	59-64
33069237-8	2020	Furthermore, we showed that CUDC-907 treatment enhanced the therapeutic efficacy of PARP inhibitor olaparib in SCLC cellular models and a PDX model.	CUDC-907	28-36	poly(ADP-ribose) polymerase 1	Homo sapiens	84-88
33069237-9	2020	Mechanistic investigations demonstrated that CUDC-907 synergized with olaparib through the blockade of DSB repair pathways and downregulation of MYC paralogs and FoxM1.	CUDC-907	45-53	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	145-148
33069237-9	2020	Mechanistic investigations demonstrated that CUDC-907 synergized with olaparib through the blockade of DSB repair pathways and downregulation of MYC paralogs and FoxM1.	CUDC-907	45-53	forkhead box M1	Homo sapiens	162-167
33069237-10	2020	CONCLUSIONS: Our study uncovers that dual PI3K and HDAC inhibition by CUDC-907 exerts significant single-agent activity and strong synergistic effects with PARP inhibitor olaparib in SCLC, which thus provides a rational combination treatment strategy for SCLC clinical investigation.	CUDC-907	70-78	poly(ADP-ribose) polymerase 1	Homo sapiens	156-160
32943605-8	2020	CUDC-907 not only inhibited myofibroblasts markers expression, but also significantly inhibited the phosphorylation level of AKT, mTOR, Smad2/3, and promoted acetylation of histones.	CUDC-907	0-8	SMAD family member 2	Mus musculus	136-143
32943605-10	2020	Overall, these data suggest that dual inhibition of HDAC and the tyrosine kinase signaling pathways with CUDC-907 is a promising treatment strategy for TGFbeta1-induced lung and tumor fibrosis.	CUDC-907	105-113	transforming growth factor, beta 1	Mus musculus	152-160
32459381-6	2020	CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bcl-xL, Bim and c-Myc.	CUDC-907	0-8	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	54-59
32459381-6	2020	CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bcl-xL, Bim and c-Myc.	CUDC-907	0-8	BCL2 like 1	Homo sapiens	61-67
32459381-6	2020	CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bcl-xL, Bim and c-Myc.	CUDC-907	0-8	BCL2 like 11	Homo sapiens	69-72
32459381-6	2020	CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bcl-xL, Bim and c-Myc.	CUDC-907	0-8	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	77-82
32459381-7	2020	Further, down-regulation of Wee1, CHK1, RRM1 and RRM2 contributed to CUDC-907-induced DNA damage and apoptosis.	CUDC-907	69-77	WEE1 G2 checkpoint kinase	Homo sapiens	28-32
32459381-7	2020	Further, down-regulation of Wee1, CHK1, RRM1 and RRM2 contributed to CUDC-907-induced DNA damage and apoptosis.	CUDC-907	69-77	checkpoint kinase 1	Homo sapiens	34-38
32459381-7	2020	Further, down-regulation of Wee1, CHK1, RRM1 and RRM2 contributed to CUDC-907-induced DNA damage and apoptosis.	CUDC-907	69-77	ribonucleotide reductase catalytic subunit M1	Homo sapiens	40-44
32459381-7	2020	Further, down-regulation of Wee1, CHK1, RRM1 and RRM2 contributed to CUDC-907-induced DNA damage and apoptosis.	CUDC-907	69-77	ribonucleotide reductase regulatory subunit M2	Homo sapiens	49-53
31901955-3	2020	Furthermore, CUDC-907 is an oral inhibitor of class I phosphoinositide 3-kinase (PI3K) as well as class I and II histone deacetylase (HDAC) enzymes.	CUDC-907	13-21	histone deacetylase 9	Homo sapiens	113-132
31901955-3	2020	Furthermore, CUDC-907 is an oral inhibitor of class I phosphoinositide 3-kinase (PI3K) as well as class I and II histone deacetylase (HDAC) enzymes.	CUDC-907	13-21	histone deacetylase 9	Homo sapiens	134-138
31901955-4	2020	METHODS: In this study, we evaluated the effect of combination therapy of CUDC-907 and ABL TKIs, using BCR-ABL-positive cell lines and primary samples.	CUDC-907	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
31901955-10	2020	CONCLUSION: Taken together, our results indicate that administration of CUDC-907, a dual PI3K and HDAC inhibitor, may be an effective strategy against ABL TKI-resistant cells, including cells harboring the T315I mutation.	CUDC-907	72-80	histone deacetylase 9	Homo sapiens	98-102
31901955-10	2020	CONCLUSION: Taken together, our results indicate that administration of CUDC-907, a dual PI3K and HDAC inhibitor, may be an effective strategy against ABL TKI-resistant cells, including cells harboring the T315I mutation.	CUDC-907	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-154
31901955-11	2020	Moreover, CUDC-907 may enhance the cytotoxic effects of ABL TKI when a combined treatment strategy is used against Philadelphia chromosome-positive leukemia cells.	CUDC-907	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
32943605-0	2020	Dual inhibition of HDAC and tyrosine kinase signaling pathways with CUDC-907 attenuates TGFbeta1 induced lung and tumor fibrosis.	CUDC-907	68-76	transforming growth factor, beta 1	Mus musculus	88-96
32943605-5	2020	CUDC-907 is a first-in-class compound, functioning as a dual inhibitor of HDACs and PI3K/AKT pathway.	CUDC-907	0-8	thymoma viral proto-oncogene 1	Mus musculus	89-92
32943605-8	2020	CUDC-907 not only inhibited myofibroblasts markers expression, but also significantly inhibited the phosphorylation level of AKT, mTOR, Smad2/3, and promoted acetylation of histones.	CUDC-907	0-8	thymoma viral proto-oncogene 1	Mus musculus	125-128
32943605-8	2020	CUDC-907 not only inhibited myofibroblasts markers expression, but also significantly inhibited the phosphorylation level of AKT, mTOR, Smad2/3, and promoted acetylation of histones.	CUDC-907	0-8	mechanistic target of rapamycin kinase	Mus musculus	130-134
30819918-5	2019	CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bim, and c-Myc.	CUDC-907	0-8	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	54-59
30819918-5	2019	CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bim, and c-Myc.	CUDC-907	0-8	BCL2 like 11	Homo sapiens	61-64
30819918-7	2019	Downregulation of CHK1, Wee1, and RRM1, and induction of DNA damage also contributed to CUDC-907-induced apoptosis of acute myeloid leukemia cells.	CUDC-907	88-96	checkpoint kinase 1	Homo sapiens	18-22
30819918-7	2019	Downregulation of CHK1, Wee1, and RRM1, and induction of DNA damage also contributed to CUDC-907-induced apoptosis of acute myeloid leukemia cells.	CUDC-907	88-96	WEE1 G2 checkpoint kinase	Homo sapiens	24-28
30819918-7	2019	Downregulation of CHK1, Wee1, and RRM1, and induction of DNA damage also contributed to CUDC-907-induced apoptosis of acute myeloid leukemia cells.	CUDC-907	88-96	ribonucleotide reductase catalytic subunit M1	Homo sapiens	34-38
30696721-12	2019	However, a dual HDAC/PI3K inhibitor, CUDC-907, was most potent against NUT carcinoma cells, with an IC50 of 5.5-9.0 pmol/L.	CUDC-907	37-45	histone deacetylase 9	Homo sapiens	16-20
30696721-20	2019	Among MYC-targeting agents, including BET and HDAC inhibitors, CUDC-907 (a dual PI3K/HDAC inhibitor) was most effective against NC cells, followed by panobinostat (an HDAC inhibitor) and AZD5153 (a bivalent BET inhibitor).	CUDC-907	63-71	delta/notch like EGF repeat containing	Homo sapiens	38-41
31545402-0	2019	CUDC-907 reverses pathological phenotype of keloid fibroblasts in vitro and in vivo via dual inhibition of PI3K/Akt/mTOR signaling and HDAC2.	CUDC-907	0-8	AKT serine/threonine kinase 1	Homo sapiens	112-115
31545402-0	2019	CUDC-907 reverses pathological phenotype of keloid fibroblasts in vitro and in vivo via dual inhibition of PI3K/Akt/mTOR signaling and HDAC2.	CUDC-907	0-8	mechanistic target of rapamycin kinase	Homo sapiens	116-120
31545402-0	2019	CUDC-907 reverses pathological phenotype of keloid fibroblasts in vitro and in vivo via dual inhibition of PI3K/Akt/mTOR signaling and HDAC2.	CUDC-907	0-8	histone deacetylase 2	Homo sapiens	135-140
31545402-4	2019	The present study aimed to explore the possibility of reversing the KF pathological phenotype using CUDC-907, a dual inhibitor of PI3K/Akt/mTOR pathway and HDACs.	CUDC-907	100-108	AKT serine/threonine kinase 1	Homo sapiens	135-138
31545402-4	2019	The present study aimed to explore the possibility of reversing the KF pathological phenotype using CUDC-907, a dual inhibitor of PI3K/Akt/mTOR pathway and HDACs.	CUDC-907	100-108	mechanistic target of rapamycin kinase	Homo sapiens	139-143
31545402-7	2019	A mechanistic study of CUDC-907 revealed the initiation of cell cycle arrest at G2/M phase along with the enhanced expression of cyclin-dependent kinase inhibitor 1 and decreased expression of cyclin B in cells treated with CUDC-907.	CUDC-907	23-31	cyclin dependent kinase inhibitor 1A	Homo sapiens	129-164
31545402-7	2019	A mechanistic study of CUDC-907 revealed the initiation of cell cycle arrest at G2/M phase along with the enhanced expression of cyclin-dependent kinase inhibitor 1 and decreased expression of cyclin B in cells treated with CUDC-907.	CUDC-907	224-232	cyclin dependent kinase inhibitor 1A	Homo sapiens	129-164
31545402-8	2019	CUDC-907 not only inhibited AKT and mTOR phosphorylation and promoted the acetylation of histone H3, but also significantly inhibited the phosphorylation levels of Smad2/3 and Erk.	CUDC-907	0-8	AKT serine/threonine kinase 1	Homo sapiens	28-31
31545402-8	2019	CUDC-907 not only inhibited AKT and mTOR phosphorylation and promoted the acetylation of histone H3, but also significantly inhibited the phosphorylation levels of Smad2/3 and Erk.	CUDC-907	0-8	mechanistic target of rapamycin kinase	Homo sapiens	36-40
31545402-8	2019	CUDC-907 not only inhibited AKT and mTOR phosphorylation and promoted the acetylation of histone H3, but also significantly inhibited the phosphorylation levels of Smad2/3 and Erk.	CUDC-907	0-8	SMAD family member 2	Homo sapiens	164-171
31545402-8	2019	CUDC-907 not only inhibited AKT and mTOR phosphorylation and promoted the acetylation of histone H3, but also significantly inhibited the phosphorylation levels of Smad2/3 and Erk.	CUDC-907	0-8	mitogen-activated protein kinase 1	Homo sapiens	176-179
30696721-20	2019	Among MYC-targeting agents, including BET and HDAC inhibitors, CUDC-907 (a dual PI3K/HDAC inhibitor) was most effective against NC cells, followed by panobinostat (an HDAC inhibitor) and AZD5153 (a bivalent BET inhibitor).	CUDC-907	63-71	histone deacetylase 9	Homo sapiens	46-50
30696721-20	2019	Among MYC-targeting agents, including BET and HDAC inhibitors, CUDC-907 (a dual PI3K/HDAC inhibitor) was most effective against NC cells, followed by panobinostat (an HDAC inhibitor) and AZD5153 (a bivalent BET inhibitor).	CUDC-907	63-71	histone deacetylase 9	Homo sapiens	85-89
30696721-20	2019	Among MYC-targeting agents, including BET and HDAC inhibitors, CUDC-907 (a dual PI3K/HDAC inhibitor) was most effective against NC cells, followed by panobinostat (an HDAC inhibitor) and AZD5153 (a bivalent BET inhibitor).	CUDC-907	63-71	histone deacetylase 9	Homo sapiens	85-89
30696721-20	2019	Among MYC-targeting agents, including BET and HDAC inhibitors, CUDC-907 (a dual PI3K/HDAC inhibitor) was most effective against NC cells, followed by panobinostat (an HDAC inhibitor) and AZD5153 (a bivalent BET inhibitor).	CUDC-907	63-71	delta/notch like EGF repeat containing	Homo sapiens	207-210
30696721-12	2019	However, a dual HDAC/PI3K inhibitor, CUDC-907, was most potent against NUT carcinoma cells, with an IC50 of 5.5-9.0 pmol/L.	CUDC-907	37-45	NUT midline carcinoma family member 1	Homo sapiens	71-74
30224636-8	2019	Furthermore, we revealed the antitumor mechanism of CUDC-907 in Aspc-1, PANC-1, and Capan-1 pancreatic cancer cells: it suppressed the HDAC6 subunit, thus downregulating c-Myc protein levels, which was a mode of action distinct from the existing mechanisms.	CUDC-907	52-60	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	170-175
30224636-9	2019	Consistently, the extraordinary antitumor activity of CUDC-907 accompanied by downregulation of c-Myc and Ki67 expression in tumor tissue was observed in a human pancreatic cancer Aspc-1 xenograft nude mouse model in vivo.	CUDC-907	54-62	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	96-101
30224636-0	2019	CUDC-907 displays potent antitumor activity against human pancreatic adenocarcinoma in vitro and in vivo through inhibition of HDAC6 to downregulate c-Myc expression.	CUDC-907	0-8	histone deacetylase 6	Homo sapiens	127-132
30224636-0	2019	CUDC-907 displays potent antitumor activity against human pancreatic adenocarcinoma in vitro and in vivo through inhibition of HDAC6 to downregulate c-Myc expression.	CUDC-907	0-8	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	149-154
30353642-4	2019	CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1.	CUDC-907	0-8	AKT serine/threonine kinase 1	Homo sapiens	24-27
30224636-4	2019	CUDC-907 is a novel dual-acting inhibitor of phosphoinositide 3-kinase (PI3K) and histone deacetylase (HDAC).	CUDC-907	0-8	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	45-70
30224636-8	2019	Furthermore, we revealed the antitumor mechanism of CUDC-907 in Aspc-1, PANC-1, and Capan-1 pancreatic cancer cells: it suppressed the HDAC6 subunit, thus downregulating c-Myc protein levels, which was a mode of action distinct from the existing mechanisms.	CUDC-907	52-60	histone deacetylase 6	Homo sapiens	135-140
30353642-4	2019	CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1.	CUDC-907	0-8	mitogen-activated protein kinase kinase 7	Homo sapiens	84-87
30353642-4	2019	CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1.	CUDC-907	0-8	mitogen-activated protein kinase 1	Homo sapiens	88-91
30353642-4	2019	CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1.	CUDC-907	0-8	signal transducer and activator of transcription 3	Homo sapiens	96-101
30353642-4	2019	CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1.	CUDC-907	0-8	BCL2 apoptosis regulator	Homo sapiens	158-163
30353642-4	2019	CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1.	CUDC-907	0-8	BCL2 apoptosis regulator	Homo sapiens	180-185
30353642-4	2019	CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1.	CUDC-907	0-8	BCL2 like 1	Homo sapiens	187-193
30353642-4	2019	CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1.	CUDC-907	0-8	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	199-204
30353642-5	2019	Moreover, CUDC-907 downregulated cytokines BAFF and APRIL and their receptors BAFFR, TACI, and BCMA, thus blocking BAFF-induced NF-kappaB signalling.	CUDC-907	10-18	TNF superfamily member 13b	Homo sapiens	43-47
30353642-5	2019	Moreover, CUDC-907 downregulated cytokines BAFF and APRIL and their receptors BAFFR, TACI, and BCMA, thus blocking BAFF-induced NF-kappaB signalling.	CUDC-907	10-18	TNF receptor superfamily member 13C	Homo sapiens	78-83
30353642-5	2019	Moreover, CUDC-907 downregulated cytokines BAFF and APRIL and their receptors BAFFR, TACI, and BCMA, thus blocking BAFF-induced NF-kappaB signalling.	CUDC-907	10-18	TNF receptor superfamily member 13B	Homo sapiens	85-89
30353642-5	2019	Moreover, CUDC-907 downregulated cytokines BAFF and APRIL and their receptors BAFFR, TACI, and BCMA, thus blocking BAFF-induced NF-kappaB signalling.	CUDC-907	10-18	TNF receptor superfamily member 17	Homo sapiens	95-99
30353642-5	2019	Moreover, CUDC-907 downregulated cytokines BAFF and APRIL and their receptors BAFFR, TACI, and BCMA, thus blocking BAFF-induced NF-kappaB signalling.	CUDC-907	10-18	TNF superfamily member 13b	Homo sapiens	78-82
30353642-5	2019	Moreover, CUDC-907 downregulated cytokines BAFF and APRIL and their receptors BAFFR, TACI, and BCMA, thus blocking BAFF-induced NF-kappaB signalling.	CUDC-907	10-18	nuclear factor kappa B subunit 1	Homo sapiens	128-137
30353642-6	2019	T cell chemokines CCL3/4/17/22 and phosphorylation of CXCR4 were also reduced by CUDC-907.	CUDC-907	81-89	C-C motif chemokine ligand 3	Homo sapiens	18-30
30353642-6	2019	T cell chemokines CCL3/4/17/22 and phosphorylation of CXCR4 were also reduced by CUDC-907.	CUDC-907	81-89	C-X-C motif chemokine receptor 4	Homo sapiens	54-59
30353642-8	2019	Indeed, combinations of low concentrations of CUDC-907 with inhibitors of BCL2, BTK, or the NF-kappaB pathway showed a potent synergistic effect.	CUDC-907	46-54	BCL2 apoptosis regulator	Homo sapiens	74-78
30353642-8	2019	Indeed, combinations of low concentrations of CUDC-907 with inhibitors of BCL2, BTK, or the NF-kappaB pathway showed a potent synergistic effect.	CUDC-907	46-54	Bruton tyrosine kinase	Homo sapiens	80-83
30353642-8	2019	Indeed, combinations of low concentrations of CUDC-907 with inhibitors of BCL2, BTK, or the NF-kappaB pathway showed a potent synergistic effect.	CUDC-907	46-54	nuclear factor kappa B subunit 1	Homo sapiens	92-101
29760046-5	2018	The radiosensitizing effects of CUDC-907 were mediated by decreased NFkappaB/Forkhead box M1 (FOXM1) recruitment to promoters of genes involved in the DNA damage response; exogenous expression of NFkappaB/FOXM1 protected from CUDC-907-induced cytotoxicity.	CUDC-907	32-40	nuclear factor kappa B subunit 1	Homo sapiens	68-76
29760046-5	2018	The radiosensitizing effects of CUDC-907 were mediated by decreased NFkappaB/Forkhead box M1 (FOXM1) recruitment to promoters of genes involved in the DNA damage response; exogenous expression of NFkappaB/FOXM1 protected from CUDC-907-induced cytotoxicity.	CUDC-907	32-40	forkhead box M1	Homo sapiens	77-92
29760046-5	2018	The radiosensitizing effects of CUDC-907 were mediated by decreased NFkappaB/Forkhead box M1 (FOXM1) recruitment to promoters of genes involved in the DNA damage response; exogenous expression of NFkappaB/FOXM1 protected from CUDC-907-induced cytotoxicity.	CUDC-907	32-40	nuclear factor kappa B subunit 1	Homo sapiens	196-204
29760046-5	2018	The radiosensitizing effects of CUDC-907 were mediated by decreased NFkappaB/Forkhead box M1 (FOXM1) recruitment to promoters of genes involved in the DNA damage response; exogenous expression of NFkappaB/FOXM1 protected from CUDC-907-induced cytotoxicity.	CUDC-907	32-40	forkhead box M1	Homo sapiens	94-99
28819699-0	2018	CUDC-907, a dual HDAC and PI3K inhibitor, reverses platinum drug resistance.	CUDC-907	0-8	histone deacetylase 9	Homo sapiens	17-21
29760046-5	2018	The radiosensitizing effects of CUDC-907 were mediated by decreased NFkappaB/Forkhead box M1 (FOXM1) recruitment to promoters of genes involved in the DNA damage response; exogenous expression of NFkappaB/FOXM1 protected from CUDC-907-induced cytotoxicity.	CUDC-907	32-40	forkhead box M1	Homo sapiens	205-210
29760046-5	2018	The radiosensitizing effects of CUDC-907 were mediated by decreased NFkappaB/Forkhead box M1 (FOXM1) recruitment to promoters of genes involved in the DNA damage response; exogenous expression of NFkappaB/FOXM1 protected from CUDC-907-induced cytotoxicity.	CUDC-907	226-234	nuclear factor kappa B subunit 1	Homo sapiens	196-204
28819699-3	2018	CUDC-907 is a potent molecular targeted anticancer agent, rationally designed to simultaneously inhibit histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K).	CUDC-907	0-8	histone deacetylase 9	Homo sapiens	104-123
28819699-3	2018	CUDC-907 is a potent molecular targeted anticancer agent, rationally designed to simultaneously inhibit histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K).	CUDC-907	0-8	histone deacetylase 9	Homo sapiens	125-129
28819699-3	2018	CUDC-907 is a potent molecular targeted anticancer agent, rationally designed to simultaneously inhibit histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K).	CUDC-907	0-8	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	135-164
28819699-13	2018	In Pt-resistant cancer cells, CUDC-907 apparently circumvented the resistance through inhibition of ABCC2 and DNA repair but induction of cell cycle arrest.	CUDC-907	30-38	ATP binding cassette subfamily C member 2	Homo sapiens	100-105
28819699-14	2018	In the presence of CUDC-907, cellular accumulation of Pt drugs and formation of DNA-Pt adducts were found to be increased whereas expression levels of ABCC2 and ERCC1 was inhibited in Pt-resistant cells.	CUDC-907	19-27	ATP binding cassette subfamily C member 2	Homo sapiens	151-156
28819699-14	2018	In the presence of CUDC-907, cellular accumulation of Pt drugs and formation of DNA-Pt adducts were found to be increased whereas expression levels of ABCC2 and ERCC1 was inhibited in Pt-resistant cells.	CUDC-907	19-27	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	161-166
28600475-4	2017	Our aim was to determine the therapeutic efficacy of simultaneously targeting these pathways in thyroid cancer with a single agent and to evaluate biomarkers of treatment response.Experimental Design: CUDC-907 is a first-in-class compound, functioning as a dual inhibitor of HDACs and the PI3K/AKT pathway.	CUDC-907	201-209	thymoma viral proto-oncogene 1	Mus musculus	294-297
28600475-5	2017	We investigated its antiproliferative effect in vitro and in vivoResults: CUDC-907 significantly inhibited cellular proliferation in thyroid cancer cell lines, induced G2-M arrest with decreased levels of the checkpoint regulators cyclin B1, AURKA, AURKB, PLK1, and increased p21 and p27.	CUDC-907	74-82	cyclin B1	Mus musculus	231-240
28600475-5	2017	We investigated its antiproliferative effect in vitro and in vivoResults: CUDC-907 significantly inhibited cellular proliferation in thyroid cancer cell lines, induced G2-M arrest with decreased levels of the checkpoint regulators cyclin B1, AURKA, AURKB, PLK1, and increased p21 and p27.	CUDC-907	74-82	aurora kinase A	Mus musculus	242-247
28600475-5	2017	We investigated its antiproliferative effect in vitro and in vivoResults: CUDC-907 significantly inhibited cellular proliferation in thyroid cancer cell lines, induced G2-M arrest with decreased levels of the checkpoint regulators cyclin B1, AURKA, AURKB, PLK1, and increased p21 and p27.	CUDC-907	74-82	aurora kinase B	Mus musculus	249-254
28600475-5	2017	We investigated its antiproliferative effect in vitro and in vivoResults: CUDC-907 significantly inhibited cellular proliferation in thyroid cancer cell lines, induced G2-M arrest with decreased levels of the checkpoint regulators cyclin B1, AURKA, AURKB, PLK1, and increased p21 and p27.	CUDC-907	74-82	polo like kinase 1	Mus musculus	256-260
28600475-5	2017	We investigated its antiproliferative effect in vitro and in vivoResults: CUDC-907 significantly inhibited cellular proliferation in thyroid cancer cell lines, induced G2-M arrest with decreased levels of the checkpoint regulators cyclin B1, AURKA, AURKB, PLK1, and increased p21 and p27.	CUDC-907	74-82	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	276-279
28600475-5	2017	We investigated its antiproliferative effect in vitro and in vivoResults: CUDC-907 significantly inhibited cellular proliferation in thyroid cancer cell lines, induced G2-M arrest with decreased levels of the checkpoint regulators cyclin B1, AURKA, AURKB, PLK1, and increased p21 and p27.	CUDC-907	74-82	cyclin-dependent kinase inhibitor 1B	Mus musculus	284-287
28600475-7	2017	CUDC-907 treatment caused H3 hyperacetylation and decreased HDAC2 expression.	CUDC-907	0-8	histone deacetylase 2	Mus musculus	60-65
28600475-9	2017	CUDC-907 treatment reduced both p-AKT and p-ERK1/2 levels.	CUDC-907	0-8	thymoma viral proto-oncogene 1	Mus musculus	34-37
27829312-0	2017	CUDC-907 Promotes Bone Marrow Adipocytic Differentiation Through Inhibition of Histone Deacetylase and Regulation of Cell Cycle.	CUDC-907	0-8	histone deacetylase 9	Homo sapiens	79-98
27829312-6	2017	Chromatin immune precipitation combined with quantitative polymerase chain reaction showed significant increase in H3K9ac epigenetic marker in the promoter regions of AdipoQ, FABP4, PPARgamma, KLF15, and CEBPA in CUDC-907-treated hBMSCs.	CUDC-907	213-221	fatty acid binding protein 4	Homo sapiens	175-180
27829312-6	2017	Chromatin immune precipitation combined with quantitative polymerase chain reaction showed significant increase in H3K9ac epigenetic marker in the promoter regions of AdipoQ, FABP4, PPARgamma, KLF15, and CEBPA in CUDC-907-treated hBMSCs.	CUDC-907	213-221	peroxisome proliferator activated receptor gamma	Homo sapiens	182-191
27829312-6	2017	Chromatin immune precipitation combined with quantitative polymerase chain reaction showed significant increase in H3K9ac epigenetic marker in the promoter regions of AdipoQ, FABP4, PPARgamma, KLF15, and CEBPA in CUDC-907-treated hBMSCs.	CUDC-907	213-221	Kruppel like factor 15	Homo sapiens	193-198
27829312-6	2017	Chromatin immune precipitation combined with quantitative polymerase chain reaction showed significant increase in H3K9ac epigenetic marker in the promoter regions of AdipoQ, FABP4, PPARgamma, KLF15, and CEBPA in CUDC-907-treated hBMSCs.	CUDC-907	213-221	CCAAT enhancer binding protein alpha	Homo sapiens	204-209
27980108-6	2017	Consistently, the antitumor activity of CUDC-907 against multiple MYC-driven cancer types was also demonstrated in animal models, including DLBCL and NMC xenograft models, Myc transgenic tumor syngeneic models, and MYC-amplified solid tumor patient-derived xenograft (PDX) models.	CUDC-907	40-48	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	66-69
28147336-5	2017	CUDC-907 treatment down-regulated the phosphorylation of PI3K downstream targets, including AKT, PRAS40, S6, and 4EBP1, increased histone 3 acetylation, and decreased Myc protein levels.	CUDC-907	0-8	AKT serine/threonine kinase 1	Homo sapiens	92-95
28147336-5	2017	CUDC-907 treatment down-regulated the phosphorylation of PI3K downstream targets, including AKT, PRAS40, S6, and 4EBP1, increased histone 3 acetylation, and decreased Myc protein levels.	CUDC-907	0-8	AKT1 substrate 1	Homo sapiens	97-103
28147336-5	2017	CUDC-907 treatment down-regulated the phosphorylation of PI3K downstream targets, including AKT, PRAS40, S6, and 4EBP1, increased histone 3 acetylation, and decreased Myc protein levels.	CUDC-907	0-8	ribosomal protein S6	Homo sapiens	105-118
28147336-5	2017	CUDC-907 treatment down-regulated the phosphorylation of PI3K downstream targets, including AKT, PRAS40, S6, and 4EBP1, increased histone 3 acetylation, and decreased Myc protein levels.	CUDC-907	0-8	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	167-170
28147336-9	2017	Collectively, these data provide a mechanistic rationale for evaluating CUDC-907 for the treatment of patients with Myc and PI3K-dependent lymphomas.	CUDC-907	72-80	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	116-119
27980108-6	2017	Consistently, the antitumor activity of CUDC-907 against multiple MYC-driven cancer types was also demonstrated in animal models, including DLBCL and NMC xenograft models, Myc transgenic tumor syngeneic models, and MYC-amplified solid tumor patient-derived xenograft (PDX) models.	CUDC-907	40-48	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	215-218
27980108-7	2017	Our findings suggest that dual function HDAC and PI3K inhibitor CUDC-907 is an effective agent targeting MYC and thus may be developed as potential therapy for MYC-dependent cancers.	CUDC-907	64-72	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	105-108
27980108-7	2017	Our findings suggest that dual function HDAC and PI3K inhibitor CUDC-907 is an effective agent targeting MYC and thus may be developed as potential therapy for MYC-dependent cancers.	CUDC-907	64-72	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	160-163
26796063-0	2016	Human ATP-Binding Cassette Transporter ABCG2 Confers Resistance to CUDC-907, a Dual Inhibitor of Histone Deacetylase and Phosphatidylinositol 3-Kinase.	CUDC-907	67-75	histone deacetylase 9	Homo sapiens	97-116
27980108-0	2017	Dual HDAC and PI3K Inhibitor CUDC-907 Downregulates MYC and Suppresses Growth of MYC-dependent Cancers.	CUDC-907	29-37	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	52-55
27980108-5	2017	Furthermore, CUDC-907, a small-molecule dual-acting inhibitor of both class I and II HDACs and class I PI3Ks, effectively suppresses the growth and survival of MYC-altered or MYC-dependent cancer cells, such as DH DLBCL and BRD-NUT fusion-positive NUT midline carcinoma (NMC) cells, and MYC protein downregulation is an early event induced by CUDC-907 treatment.	CUDC-907	13-21	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	160-163
27980108-5	2017	Furthermore, CUDC-907, a small-molecule dual-acting inhibitor of both class I and II HDACs and class I PI3Ks, effectively suppresses the growth and survival of MYC-altered or MYC-dependent cancer cells, such as DH DLBCL and BRD-NUT fusion-positive NUT midline carcinoma (NMC) cells, and MYC protein downregulation is an early event induced by CUDC-907 treatment.	CUDC-907	13-21	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	175-178
27980108-5	2017	Furthermore, CUDC-907, a small-molecule dual-acting inhibitor of both class I and II HDACs and class I PI3Ks, effectively suppresses the growth and survival of MYC-altered or MYC-dependent cancer cells, such as DH DLBCL and BRD-NUT fusion-positive NUT midline carcinoma (NMC) cells, and MYC protein downregulation is an early event induced by CUDC-907 treatment.	CUDC-907	13-21	NUT midline carcinoma family member 1	Homo sapiens	228-231
27980108-5	2017	Furthermore, CUDC-907, a small-molecule dual-acting inhibitor of both class I and II HDACs and class I PI3Ks, effectively suppresses the growth and survival of MYC-altered or MYC-dependent cancer cells, such as DH DLBCL and BRD-NUT fusion-positive NUT midline carcinoma (NMC) cells, and MYC protein downregulation is an early event induced by CUDC-907 treatment.	CUDC-907	13-21	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	175-178
28139498-10	2017	Furthermore, CRC cells treated with CUDC-907 exhibited a higher degree of histone H3 lysine 9 acetylation (H3K9ac) and reduced AKT phosphorylation (Ser473).	CUDC-907	36-44	AKT serine/threonine kinase 1	Homo sapiens	127-130
26796063-0	2016	Human ATP-Binding Cassette Transporter ABCG2 Confers Resistance to CUDC-907, a Dual Inhibitor of Histone Deacetylase and Phosphatidylinositol 3-Kinase.	CUDC-907	67-75	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	121-150
26796063-1	2016	CUDC-907 is a novel, dual-acting small molecule compound designed to simultaneously inhibit the activity of histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K).	CUDC-907	0-8	histone deacetylase 9	Homo sapiens	108-127
26796063-1	2016	CUDC-907 is a novel, dual-acting small molecule compound designed to simultaneously inhibit the activity of histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K).	CUDC-907	0-8	histone deacetylase 9	Homo sapiens	129-133
26796063-1	2016	CUDC-907 is a novel, dual-acting small molecule compound designed to simultaneously inhibit the activity of histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K).	CUDC-907	0-8	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	139-168
26796063-2	2016	Treatment with CUDC-907 led to sustained inhibition of HDAC and PI3K activity, inhibition of RAF-MEK-MAPK signaling pathway, and inhibition of cancer cell growth.	CUDC-907	15-23	histone deacetylase 9	Homo sapiens	55-59
26796063-2	2016	Treatment with CUDC-907 led to sustained inhibition of HDAC and PI3K activity, inhibition of RAF-MEK-MAPK signaling pathway, and inhibition of cancer cell growth.	CUDC-907	15-23	zinc fingers and homeoboxes 2	Homo sapiens	93-96
26796063-2	2016	Treatment with CUDC-907 led to sustained inhibition of HDAC and PI3K activity, inhibition of RAF-MEK-MAPK signaling pathway, and inhibition of cancer cell growth.	CUDC-907	15-23	mitogen-activated protein kinase kinase 7	Homo sapiens	97-100
26796063-6	2016	In this study, we reveal that ABCG2 reduces the intracellular accumulation of CUDC-907 and confers significant resistance to CUDC-907, which leads to reduced activity of CUDC-907 to inhibit HDAC and PI3K in human cancer cells.	CUDC-907	78-86	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	30-35
26796063-6	2016	In this study, we reveal that ABCG2 reduces the intracellular accumulation of CUDC-907 and confers significant resistance to CUDC-907, which leads to reduced activity of CUDC-907 to inhibit HDAC and PI3K in human cancer cells.	CUDC-907	78-86	histone deacetylase 9	Homo sapiens	190-194
26796063-6	2016	In this study, we reveal that ABCG2 reduces the intracellular accumulation of CUDC-907 and confers significant resistance to CUDC-907, which leads to reduced activity of CUDC-907 to inhibit HDAC and PI3K in human cancer cells.	CUDC-907	125-133	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	30-35
26796063-6	2016	In this study, we reveal that ABCG2 reduces the intracellular accumulation of CUDC-907 and confers significant resistance to CUDC-907, which leads to reduced activity of CUDC-907 to inhibit HDAC and PI3K in human cancer cells.	CUDC-907	125-133	histone deacetylase 9	Homo sapiens	190-194
26796063-6	2016	In this study, we reveal that ABCG2 reduces the intracellular accumulation of CUDC-907 and confers significant resistance to CUDC-907, which leads to reduced activity of CUDC-907 to inhibit HDAC and PI3K in human cancer cells.	CUDC-907	125-133	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	30-35
26796063-6	2016	In this study, we reveal that ABCG2 reduces the intracellular accumulation of CUDC-907 and confers significant resistance to CUDC-907, which leads to reduced activity of CUDC-907 to inhibit HDAC and PI3K in human cancer cells.	CUDC-907	125-133	histone deacetylase 9	Homo sapiens	190-194
26796063-7	2016	Moreover, although CUDC-907 affects the transport function of ABCG2, it was not potent enough to reverse drug resistance mediated by ABCG2 or affect the expression level of ABCG2 in human cancer cells.	CUDC-907	19-27	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	62-67
26796063-8	2016	Taken together, our findings indicate that ABCG2-mediated CUDC-907 resistance can have serious clinical implications and should be further investigated.	CUDC-907	58-66	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	43-48
26796063-9	2016	More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials.	CUDC-907	54-62	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	66-71
26796063-9	2016	More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials.	CUDC-907	54-62	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	146-151
26796063-9	2016	More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials.	CUDC-907	54-62	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	146-151
26796063-9	2016	More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials.	CUDC-907	207-215	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	66-71
26796063-9	2016	More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials.	CUDC-907	207-215	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	146-151
26796063-9	2016	More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials.	CUDC-907	207-215	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	146-151
26796063-9	2016	More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials.	CUDC-907	207-215	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	66-71
26796063-9	2016	More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials.	CUDC-907	207-215	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	146-151
26796063-9	2016	More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials.	CUDC-907	207-215	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	146-151
35291899-9	2022	Additionally, CIITA expression levels were significantly increased with pFF alpha-synuclein administration and intensified with the co-treatment of CUDC-907 and TMP-195.	CUDC-907	148-156	class II transactivator	Mus musculus	14-19
26796063-0	2016	Human ATP-Binding Cassette Transporter ABCG2 Confers Resistance to CUDC-907, a Dual Inhibitor of Histone Deacetylase and Phosphatidylinositol 3-Kinase.	CUDC-907	67-75	ATP binding cassette subfamily A member 4	Homo sapiens	6-38
26796063-0	2016	Human ATP-Binding Cassette Transporter ABCG2 Confers Resistance to CUDC-907, a Dual Inhibitor of Histone Deacetylase and Phosphatidylinositol 3-Kinase.	CUDC-907	67-75	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	39-44
34776939-9	2021	The study data show that CUDC-907 (fimepinostat), a novel dual acting inhibitor of phosphoinositide 3-kinase (PI3K) and histone deacetylase (HDAC), has potent inhibitory effects on HCC cell lines and primary HCC cells in vitro, Animal studies have shown that CUDC-907 can also suppress HCC cells in vivo.	CUDC-907	25-33	phosphoinositide-3-kinase regulatory subunit 1	Mus musculus	83-108
34776939-9	2021	The study data show that CUDC-907 (fimepinostat), a novel dual acting inhibitor of phosphoinositide 3-kinase (PI3K) and histone deacetylase (HDAC), has potent inhibitory effects on HCC cell lines and primary HCC cells in vitro, Animal studies have shown that CUDC-907 can also suppress HCC cells in vivo.	CUDC-907	259-267	phosphoinositide-3-kinase regulatory subunit 1	Mus musculus	83-108
34776939-10	2021	Furthermore, we found that CUDC-907 inhibits the PI3K/AKT/mTOR pathway and downregulates the expression of c-Myc, leading to the suppression of HCC cells.	CUDC-907	27-35	thymoma viral proto-oncogene 1	Mus musculus	54-57
34776939-10	2021	Furthermore, we found that CUDC-907 inhibits the PI3K/AKT/mTOR pathway and downregulates the expression of c-Myc, leading to the suppression of HCC cells.	CUDC-907	27-35	mechanistic target of rapamycin kinase	Mus musculus	58-62
34099621-5	2021	Upregulation of FLT3 and activation of ERK are mechanisms of resistance to gilteritinib, while activation of JAK2/STAT5 is a mechanism of resistance to CUDC-907.	CUDC-907	152-160	Janus kinase 2	Homo sapiens	109-113
34099621-5	2021	Upregulation of FLT3 and activation of ERK are mechanisms of resistance to gilteritinib, while activation of JAK2/STAT5 is a mechanism of resistance to CUDC-907.	CUDC-907	152-160	signal transducer and activator of transcription 5A	Homo sapiens	114-119
22693356-4	2012	RESULTS: CUDC-907 potently inhibits class I PI3Ks as well as classes I and II HDAC enzymes.	CUDC-907	9-17	histone deacetylase 9	Homo sapiens	78-82
22693356-5	2012	Through its integrated HDAC inhibitory activity, CUDC-907 durably inhibits the PI3K-AKT-mTOR pathway and compensatory signaling molecules such as RAF, MEK, MAPK, and STAT-3, as well as upstream receptor tyrosine kinases.	CUDC-907	49-57	histone deacetylase 9	Homo sapiens	23-27
22693356-5	2012	Through its integrated HDAC inhibitory activity, CUDC-907 durably inhibits the PI3K-AKT-mTOR pathway and compensatory signaling molecules such as RAF, MEK, MAPK, and STAT-3, as well as upstream receptor tyrosine kinases.	CUDC-907	49-57	zinc fingers and homeoboxes 2	Homo sapiens	146-149
22693356-5	2012	Through its integrated HDAC inhibitory activity, CUDC-907 durably inhibits the PI3K-AKT-mTOR pathway and compensatory signaling molecules such as RAF, MEK, MAPK, and STAT-3, as well as upstream receptor tyrosine kinases.	CUDC-907	49-57	mitogen-activated protein kinase kinase 7	Homo sapiens	151-154
22693356-5	2012	Through its integrated HDAC inhibitory activity, CUDC-907 durably inhibits the PI3K-AKT-mTOR pathway and compensatory signaling molecules such as RAF, MEK, MAPK, and STAT-3, as well as upstream receptor tyrosine kinases.	CUDC-907	49-57	signal transducer and activator of transcription 3	Homo sapiens	166-172
35291899-10	2022	Furthermore, pFF alpha-synuclein caused a time-dependent increase in the IFN-gamma(IFN-gamma) and interleukin-16(IL-16) levels, and that increase was potentiated with CUDC-907 and TMP-195.	CUDC-907	167-175	synuclein, alpha	Mus musculus	17-32
35291899-10	2022	Furthermore, pFF alpha-synuclein caused a time-dependent increase in the IFN-gamma(IFN-gamma) and interleukin-16(IL-16) levels, and that increase was potentiated with CUDC-907 and TMP-195.	CUDC-907	167-175	interferon gamma	Mus musculus	73-82
35291899-10	2022	Furthermore, pFF alpha-synuclein caused a time-dependent increase in the IFN-gamma(IFN-gamma) and interleukin-16(IL-16) levels, and that increase was potentiated with CUDC-907 and TMP-195.	CUDC-907	167-175	interferon gamma	Mus musculus	83-92
35291899-10	2022	Furthermore, pFF alpha-synuclein caused a time-dependent increase in the IFN-gamma(IFN-gamma) and interleukin-16(IL-16) levels, and that increase was potentiated with CUDC-907 and TMP-195.	CUDC-907	167-175	interleukin 16	Mus musculus	98-112
35291899-10	2022	Furthermore, pFF alpha-synuclein caused a time-dependent increase in the IFN-gamma(IFN-gamma) and interleukin-16(IL-16) levels, and that increase was potentiated with CUDC-907 and TMP-195.	CUDC-907	167-175	interleukin 16	Mus musculus	113-118
35205815-7	2022	Our results show that CUDC-907 significantly inhibits NB proliferation and colony growth, induces apoptosis, blocks cell cycle progression, inhibits MYCN, and enhances H3K9Ac levels by inhibiting the PI3K/AKT signaling pathway and HDAC function.	CUDC-907	22-30	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	149-153
35205815-7	2022	Our results show that CUDC-907 significantly inhibits NB proliferation and colony growth, induces apoptosis, blocks cell cycle progression, inhibits MYCN, and enhances H3K9Ac levels by inhibiting the PI3K/AKT signaling pathway and HDAC function.	CUDC-907	22-30	AKT serine/threonine kinase 1	Homo sapiens	205-208
35205815-9	2022	Overall, our findings highlight that the dual inhibition of PI3K and HDAC by CUDC-907 is an effective therapeutic strategy for NB and other MYC-dependent cancers.	CUDC-907	77-85	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	140-143
33663586-8	2021	Akt activity and expression of BCL-XL, MCL-1, and NF-kappaB p65 were reduced by CUDC-907 in a dose-dependent manner.	CUDC-907	80-88	AKT serine/threonine kinase 1	Homo sapiens	0-3
33663586-8	2021	Akt activity and expression of BCL-XL, MCL-1, and NF-kappaB p65 were reduced by CUDC-907 in a dose-dependent manner.	CUDC-907	80-88	BCL2 like 1	Homo sapiens	31-37
33663586-8	2021	Akt activity and expression of BCL-XL, MCL-1, and NF-kappaB p65 were reduced by CUDC-907 in a dose-dependent manner.	CUDC-907	80-88	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	39-44
33663586-8	2021	Akt activity and expression of BCL-XL, MCL-1, and NF-kappaB p65 were reduced by CUDC-907 in a dose-dependent manner.	CUDC-907	80-88	RELA proto-oncogene, NF-kB subunit	Homo sapiens	60-63
33077264-8	2021	Notably, and during this short period, there are four HDAC inhibitor hybrids have entered different phases of clinical trials for treatment of different types of blood and solid tumors, namely; CUDC-101, CUDC-907, Tinostamustine, and Domatinostat.	CUDC-907	204-212	histone deacetylase 9	Homo sapiens	54-58
33000123-10	2021	RESULTS: From a kinase inhibitor library, we identified the dual PI3K/HDAC inhibitor CUDC-907 as a potent inhibitor of murine and human corticotroph tumor ACTH secretion (EC50 1-5nM), and cell proliferation (IC50 5nM).	CUDC-907	85-93	proopiomelanocortin	Homo sapiens	155-159
33000123-12	2021	We also demonstrated that CUDC-907 acts through HDAC1/2 inhibition at the POMC transcriptional level combined with its PI3K-mediated inhibition of corticotroph cell viability to reduce ACTH secretion.	CUDC-907	26-34	histone deacetylase 1	Homo sapiens	48-55
33000123-12	2021	We also demonstrated that CUDC-907 acts through HDAC1/2 inhibition at the POMC transcriptional level combined with its PI3K-mediated inhibition of corticotroph cell viability to reduce ACTH secretion.	CUDC-907	26-34	proopiomelanocortin	Homo sapiens	74-78
33000123-12	2021	We also demonstrated that CUDC-907 acts through HDAC1/2 inhibition at the POMC transcriptional level combined with its PI3K-mediated inhibition of corticotroph cell viability to reduce ACTH secretion.	CUDC-907	26-34	pro-opiomelanocortin-alpha	Mus musculus	185-189
32165486-3	2021	In this study, we combine venetoclax with the dual PI3K and histone deacetylase inhibitor CUDC-907, which can downregulate Mcl-1, upregulate Bim, and induce DNA damage, as well as downregulate c-Myc.	CUDC-907	90-98	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	123-128
32165486-3	2021	In this study, we combine venetoclax with the dual PI3K and histone deacetylase inhibitor CUDC-907, which can downregulate Mcl-1, upregulate Bim, and induce DNA damage, as well as downregulate c-Myc.	CUDC-907	90-98	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	193-198
32165486-5	2021	CUDC-907 downregulates CHK1, Wee1, RRM1, and c-Myc, which were found to play a role in venetoclax-induced apoptosis.	CUDC-907	0-8	checkpoint kinase 1	Homo sapiens	23-27
32165486-5	2021	CUDC-907 downregulates CHK1, Wee1, RRM1, and c-Myc, which were found to play a role in venetoclax-induced apoptosis.	CUDC-907	0-8	WEE1 G2 checkpoint kinase	Homo sapiens	29-33
32165486-5	2021	CUDC-907 downregulates CHK1, Wee1, RRM1, and c-Myc, which were found to play a role in venetoclax-induced apoptosis.	CUDC-907	0-8	ribonucleotide reductase catalytic subunit M1	Homo sapiens	35-39
32165486-5	2021	CUDC-907 downregulates CHK1, Wee1, RRM1, and c-Myc, which were found to play a role in venetoclax-induced apoptosis.	CUDC-907	0-8	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	45-50
33757580-15	2021	The dual HDAC and PI3K inhibitor, CUDC-907, exhibited cytotoxic and immunotherapy-enhancing effects in MM cells, including multi-drug-resistant lines and primary cells from lenalidomide-resistant patients.	CUDC-907	34-42	histone deacetylase 9	Homo sapiens	9-13
33392641-12	2021	Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines.	CUDC-907	38-46	AKT serine/threonine kinase 1	Homo sapiens	74-77
33392641-12	2021	Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines.	CUDC-907	38-46	ribosomal protein S6	Homo sapiens	83-103
33392641-12	2021	Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines.	CUDC-907	38-46	mitogen-activated protein kinase 1	Homo sapiens	110-113
33392641-12	2021	Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines.	CUDC-907	38-46	mitogen-activated protein kinase 1	Homo sapiens	115-153
33392641-12	2021	Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines.	CUDC-907	38-46	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	180-209
33392641-12	2021	Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines.	CUDC-907	38-46	mechanistic target of rapamycin kinase	Homo sapiens	212-216
33392641-12	2021	Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines.	CUDC-907	38-46	mechanistic target of rapamycin kinase	Homo sapiens	218-247
33392641-12	2021	Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines.	CUDC-907	38-46	mitogen-activated protein kinase 1	Homo sapiens	253-256
33280267-4	2021	Here we performed high-throughput compound screening (HTS) using this PSC-derived NNS model to find potential therapeutic candidates and identified CUDC-907 as an effective inhibitor of the release of MCP-1 and IP-10.	CUDC-907	148-156	C-C motif chemokine ligand 2	Homo sapiens	201-206
33280267-4	2021	Here we performed high-throughput compound screening (HTS) using this PSC-derived NNS model to find potential therapeutic candidates and identified CUDC-907 as an effective inhibitor of the release of MCP-1 and IP-10.	CUDC-907	148-156	C-X-C motif chemokine ligand 10	Homo sapiens	211-216
33402194-0	2021	Correction to: The dual HDAC-PI3K inhibitor CUDC-907 displays single-agent activity and synergizes with PARP inhibitor olaparib in small cell lung cancer.	CUDC-907	44-52	poly(ADP-ribose) polymerase 1	Homo sapiens	104-108