PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
35614224-7	2022	We identified a small molecule, the curaxin CBL0137, which potently activates ZBP1 by triggering Z-DNA formation in cells.	CBLC137	44-51	Z-DNA binding protein 1	Homo sapiens	78-82
35605992-6	2022	CBL0137-binding proteins included glycolysis enzymes (aldolase, glyceraldehyde-3-phosphate dehydrogenase, phosphofructokinase, phosphoglycerate kinase), and DNA-binding proteins (UMSBP2, RPA1, RPA2).	CBLC137	0-7	replication protein A1	Homo sapiens	187-191
35605992-6	2022	CBL0137-binding proteins included glycolysis enzymes (aldolase, glyceraldehyde-3-phosphate dehydrogenase, phosphofructokinase, phosphoglycerate kinase), and DNA-binding proteins (UMSBP2, RPA1, RPA2).	CBLC137	0-7	replication protein A2	Homo sapiens	193-197
35605992-10	2022	RNAi against RPA1 inhibited both DNA synthesis and mitosis, whereas RPA2 knockdown inhibited mitosis, consistent with both proteins being physiologic targets of CBL0137.	CBLC137	161-168	replication protein A2	Homo sapiens	68-72
33439292-7	2021	Anti-tumor activity of CBL0137 was abrogated in CD8+ T cell depleted mice but only partially lost when natural killer or CD4+ T cells were depleted.	CBLC137	23-30	CD4 antigen	Mus musculus	121-124
35323988-2	2022	The curaxin CBL0137 has demonstrated promising antitumour activities in multiple cancers such as glioblastoma, acting through p53 activation, NF-kappaB inhibition and chromatin remodelling.	CBLC137	12-19	tumor protein p53	Homo sapiens	126-129
35323988-3	2022	In the present study, it was revealed using Annexin-V/7-AAD apoptosis assays that CBL0137 has efficacy across several human acute leukaemia cell lines with wild-type TP53, but sensitivity is reduced in TP53-mutated subtypes.	CBLC137	82-89	tumor protein p53	Homo sapiens	166-170
35323988-3	2022	In the present study, it was revealed using Annexin-V/7-AAD apoptosis assays that CBL0137 has efficacy across several human acute leukaemia cell lines with wild-type TP53, but sensitivity is reduced in TP53-mutated subtypes.	CBLC137	82-89	tumor protein p53	Homo sapiens	202-206
35323988-4	2022	A heterozygous TP53 loss-of-function mutation in the KMT2A-AFF1 human RS4;11 cell line was generated, and it was demonstrated that heterozygous TP53 loss-of-function is sufficient to cause a significant reduction in CBL0137 sensitivity.	CBLC137	216-223	lysine methyltransferase 2A	Homo sapiens	53-58
35323988-4	2022	A heterozygous TP53 loss-of-function mutation in the KMT2A-AFF1 human RS4;11 cell line was generated, and it was demonstrated that heterozygous TP53 loss-of-function is sufficient to cause a significant reduction in CBL0137 sensitivity.	CBLC137	216-223	tumor protein p53	Homo sapiens	144-148
35323988-5	2022	To the best of our knowledge, this is the first evidence to suggest a clinically significant role for functional p53 in the efficacy of CBL0137 in acute leukaemia.	CBLC137	136-143	tumor protein p53	Homo sapiens	113-116
35323988-6	2022	Future CBL0137 clinical trials should include TP53 mutation screening, to establish the clinical relevance of TP53 mutations in CBL0137 efficacy.	CBLC137	128-135	tumor protein p53	Homo sapiens	110-114
33853831-7	2021	Mechanistically, CBL0137 exerted anti-hedgehog activity by targeting transcription of GLI1 and GLI2, which are core transcription factors of the hedgehog pathway.	CBLC137	17-24	GLI family zinc finger 1	Homo sapiens	86-90
33853831-7	2021	Mechanistically, CBL0137 exerted anti-hedgehog activity by targeting transcription of GLI1 and GLI2, which are core transcription factors of the hedgehog pathway.	CBLC137	17-24	GLI family zinc finger 2	Homo sapiens	95-99
33853831-9	2021	Moreover, CBL0137 synergized with BET or CDK7 inhibitors to antagonize aberrant hedgehog pathway and growth of hedgehog-driven cancer models.	CBLC137	10-17	delta/notch like EGF repeat containing	Homo sapiens	34-37
35323988-0	2022	TP53 loss-of-function mutations reduce sensitivity of acute leukaemia to the curaxin CBL0137.	CBLC137	85-92	tumor protein p53	Homo sapiens	0-4
33907746-7	2021	Surprisingly, our results revealed that SUPT16H genetic knockdown via RNAi or pharmacological inhibition by using its inhibitor, curaxin 137 (CBL0137), results in the induction of IFNs and interferon-stimulated genes (ISGs).	CBLC137	129-140	SPT16 homolog, facilitates chromatin remodeling subunit	Homo sapiens	40-47
33907746-7	2021	Surprisingly, our results revealed that SUPT16H genetic knockdown via RNAi or pharmacological inhibition by using its inhibitor, curaxin 137 (CBL0137), results in the induction of IFNs and interferon-stimulated genes (ISGs).	CBLC137	142-149	SPT16 homolog, facilitates chromatin remodeling subunit	Homo sapiens	40-47
33852836-3	2021	We show that CBL0137 displays profound cytotoxic activity against a panel of patient-derived DIPG cultures by restoring tumor suppressor TP53 and Rb activity.	CBLC137	13-20	tumor protein p53	Homo sapiens	137-141
33852836-5	2021	The FACT subunit SPT16 is found to directly interact with H3.3K27M, and treatment with CBL0137 restores both histone H3 acetylation and trimethylation.	CBLC137	87-94	SPT16 homolog, facilitates chromatin remodeling subunit	Homo sapiens	17-22
33852836-6	2021	Combined treatment of CBL0137 with the histone deacetylase inhibitor panobinostat leads to inhibition of the Rb/E2F1 pathway and induction of apoptosis.	CBLC137	22-29	E2F transcription factor 1	Homo sapiens	112-116
33570402-4	2021	More importantly, we found that CBL0137 greatly impairs the binding of CTCF but facilitates trapping FACT on DNA.	CBLC137	32-39	CCCTC-binding factor	Homo sapiens	71-75
33570402-5	2021	We revealed that CBL0137 clamps the DNA double helix that may induce a huge barrier for DNA unzipping during replication and transcription and causes the distinct binding response of CTCF and FACT on DNA.	CBLC137	17-24	CCCTC-binding factor	Homo sapiens	183-187
33439292-9	2021	CBL0137 also elevated the number of CXCR3-expressing CTLs in the tumor and the level of interferon-gamma-inducible protein 10 (IP-10) in serum, suggesting IP-10/CXCR3 controls CBL0137-elicited recruitment of effector CTLs to tumors.	CBLC137	0-7	chemokine (C-X-C motif) receptor 3	Mus musculus	36-41
33439292-9	2021	CBL0137 also elevated the number of CXCR3-expressing CTLs in the tumor and the level of interferon-gamma-inducible protein 10 (IP-10) in serum, suggesting IP-10/CXCR3 controls CBL0137-elicited recruitment of effector CTLs to tumors.	CBLC137	0-7	chemokine (C-X-C motif) ligand 10	Mus musculus	88-125
33439292-9	2021	CBL0137 also elevated the number of CXCR3-expressing CTLs in the tumor and the level of interferon-gamma-inducible protein 10 (IP-10) in serum, suggesting IP-10/CXCR3 controls CBL0137-elicited recruitment of effector CTLs to tumors.	CBLC137	0-7	chemokine (C-X-C motif) ligand 10	Mus musculus	127-132
33439292-9	2021	CBL0137 also elevated the number of CXCR3-expressing CTLs in the tumor and the level of interferon-gamma-inducible protein 10 (IP-10) in serum, suggesting IP-10/CXCR3 controls CBL0137-elicited recruitment of effector CTLs to tumors.	CBLC137	0-7	chemokine (C-X-C motif) ligand 10	Mus musculus	155-160
33439292-9	2021	CBL0137 also elevated the number of CXCR3-expressing CTLs in the tumor and the level of interferon-gamma-inducible protein 10 (IP-10) in serum, suggesting IP-10/CXCR3 controls CBL0137-elicited recruitment of effector CTLs to tumors.	CBLC137	0-7	chemokine (C-X-C motif) receptor 3	Mus musculus	161-166
33439292-9	2021	CBL0137 also elevated the number of CXCR3-expressing CTLs in the tumor and the level of interferon-gamma-inducible protein 10 (IP-10) in serum, suggesting IP-10/CXCR3 controls CBL0137-elicited recruitment of effector CTLs to tumors.	CBLC137	176-183	chemokine (C-X-C motif) ligand 10	Mus musculus	88-125
33439292-9	2021	CBL0137 also elevated the number of CXCR3-expressing CTLs in the tumor and the level of interferon-gamma-inducible protein 10 (IP-10) in serum, suggesting IP-10/CXCR3 controls CBL0137-elicited recruitment of effector CTLs to tumors.	CBLC137	176-183	chemokine (C-X-C motif) ligand 10	Mus musculus	155-160
33439292-9	2021	CBL0137 also elevated the number of CXCR3-expressing CTLs in the tumor and the level of interferon-gamma-inducible protein 10 (IP-10) in serum, suggesting IP-10/CXCR3 controls CBL0137-elicited recruitment of effector CTLs to tumors.	CBLC137	176-183	chemokine (C-X-C motif) receptor 3	Mus musculus	161-166
29440145-0	2018	The FACT inhibitor CBL0137 Synergizes with Cisplatin in Small-Cell Lung Cancer by Increasing NOTCH1 Expression and Targeting Tumor-Initiating Cells.	CBLC137	19-26	notch 1	Mus musculus	93-99
33268769-0	2020	Effective inhibition of MYC-amplified group 3 medulloblastoma by FACT-targeted curaxin drug CBL0137.	CBLC137	92-99	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	24-27
32202904-10	2020	Results showed that the expression of p-p53, p53, Bax and PUMA was upregulated after CBL0137 administration.	CBLC137	85-92	tumor protein p53	Homo sapiens	40-43
32202904-10	2020	Results showed that the expression of p-p53, p53, Bax and PUMA was upregulated after CBL0137 administration.	CBLC137	85-92	tumor protein p53	Homo sapiens	45-48
32202904-13	2020	And the protein of apoptosis-related proteins including PARP, caspase-3, caspase-7, caspase-8, and caspase-9 were increased in CBL group compared with NC group (P < 0.05), while the NF-kappaB, p-NF-kappaB and p-AKT expression levels were significantly downregulated following CBL0137 treatment (P < 0.05).	CBLC137	276-283	Cbl proto-oncogene	Homo sapiens	127-130
30989696-3	2019	Here, we report that curaxin CBL0137, an antitumor compound, can potentiate tumor necrosis factor-alpha-mediated reactivation of latently infected HIV-1cell lines.	CBLC137	29-36	tumor necrosis factor	Homo sapiens	76-103
25402820-8	2014	In mice, CBL0137 was effective against several PDA models, including orthotopic gemcitabine resistant PANC-1 model and patient derived xenografts, in which CBL0137 anti-tumor effect correlated with overexpression of FACT.	CBLC137	9-16	pancreas protein 1	Mus musculus	102-108
27370399-3	2017	One such clinical-stage drug candidate, CBL0137, is a curaxin, small molecules which simultaneously downregulate nuclear factor-kappaB (NF-kB) and activate p53 by inactivating the chromatin remodeling complex, Facilitates Chromatin Transcription (FACT).	CBLC137	40-47	tumor protein p53	Homo sapiens	156-159
27370399-8	2017	CBL0137 induced loss of chromatin-unbound FACT, activated p53, inhibited NF-kB-dependent transcription, and was toxic to GBM cells.	CBLC137	0-7	tumor protein p53	Homo sapiens	58-61
26537256-5	2015	CBL0137 exhibited strong synergy with standard chemotherapy by blocking repair of DNA damage caused by genotoxic drugs, thus creating a synthetic lethal environment in MYCN-amplified neuroblastoma cells and suggesting a treatment strategy for MYCN-driven neuroblastoma.	CBLC137	0-7	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	168-172
26537256-5	2015	CBL0137 exhibited strong synergy with standard chemotherapy by blocking repair of DNA damage caused by genotoxic drugs, thus creating a synthetic lethal environment in MYCN-amplified neuroblastoma cells and suggesting a treatment strategy for MYCN-driven neuroblastoma.	CBLC137	0-7	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	243-247
25402820-9	2014	Moreover, we observed synergy of CBL0137 with gemcitabine which may be explained by the ability of CBL0137 to inhibit several transcriptional programs induced by gemcitabine, including NF-kappaB response and expression of ribonucleotide reductase, one of the targets of gemcitabine in cells.	CBLC137	33-40	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	185-194
22689915-3	2012	In tumor cells, Curaxin-137 inhibits NF-kappaB- and HSF1-dependent transcription (prosurvival pathways) and activates p53 (a proapoptotic pathway) without inducing DNA damage.	CBLC137	16-27	heat shock factor 1	Mus musculus	52-56
22689915-3	2012	In tumor cells, Curaxin-137 inhibits NF-kappaB- and HSF1-dependent transcription (prosurvival pathways) and activates p53 (a proapoptotic pathway) without inducing DNA damage.	CBLC137	16-27	transformation related protein 53, pseudogene	Mus musculus	118-121
22689915-6	2012	On the basis of this background, we tested whether Curaxin-137 could suppress tumorigenesis in MMTV-neu transgenic mice, which spontaneously develop mammary carcinoma due to steroid receptor-regulated expression of the Her2 proto-oncogene.	CBLC137	51-62	erb-b2 receptor tyrosine kinase 2	Mus musculus	219-223
22689915-7	2012	We found that chronic administration of Curaxin-137 in a preventive regimen to MMTV-neu mice did not cause any detectable changes in normal organs and tissues, yet inhibited tumor onset, delayed tumor progression, and prolonged survival of mice in a dose-dependent manner.	CBLC137	40-51	erb-b2 receptor tyrosine kinase 2	Mus musculus	84-87
22689915-8	2012	Curaxin-137 induced changes in FACT, altered NF-kappaB localization, and activated p53 in tumor cells as expected from its defined mechanism of action.	CBLC137	0-11	transformation related protein 53, pseudogene	Mus musculus	83-86