PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
2674359-3	1989	The drug Lonidamine [1-(2,4-dichlorobenzyl)-1H-indazol-3 carboxylic acid)] (LND) is able to selectively block hexokinase (HK) activity and, consequently, lactate production only in highly glycolytic (highly malignant) gliomas, stimulating, on the contrary, that of low grade gliomas; this basically depends on the different HK patterns between low and high grade gliomas.	lonidamine	9-19	hexokinase 1	Homo sapiens	110-120
2715079-0	1989	Potentiation of radiation effects on multicellular tumor spheroids (MTS) of HeLa cells by lonidamine.	lonidamine	90-100	MLRL	Homo sapiens	68-71
2715079-4	1989	When the MTS were treated with lonidamine in combination with fractionated irradiation, remarkable enhancement of growth inhibition was observed at the drug concentration of 10 micrograms/ml.	lonidamine	31-41	MLRL	Homo sapiens	9-12
2674359-3	1989	The drug Lonidamine [1-(2,4-dichlorobenzyl)-1H-indazol-3 carboxylic acid)] (LND) is able to selectively block hexokinase (HK) activity and, consequently, lactate production only in highly glycolytic (highly malignant) gliomas, stimulating, on the contrary, that of low grade gliomas; this basically depends on the different HK patterns between low and high grade gliomas.	lonidamine	9-19	hexokinase 1	Homo sapiens	122-124
2674359-3	1989	The drug Lonidamine [1-(2,4-dichlorobenzyl)-1H-indazol-3 carboxylic acid)] (LND) is able to selectively block hexokinase (HK) activity and, consequently, lactate production only in highly glycolytic (highly malignant) gliomas, stimulating, on the contrary, that of low grade gliomas; this basically depends on the different HK patterns between low and high grade gliomas.	lonidamine	9-19	hexokinase 1	Homo sapiens	324-326
2674359-3	1989	The drug Lonidamine [1-(2,4-dichlorobenzyl)-1H-indazol-3 carboxylic acid)] (LND) is able to selectively block hexokinase (HK) activity and, consequently, lactate production only in highly glycolytic (highly malignant) gliomas, stimulating, on the contrary, that of low grade gliomas; this basically depends on the different HK patterns between low and high grade gliomas.	lonidamine	76-79	hexokinase 1	Homo sapiens	110-120
2674359-3	1989	The drug Lonidamine [1-(2,4-dichlorobenzyl)-1H-indazol-3 carboxylic acid)] (LND) is able to selectively block hexokinase (HK) activity and, consequently, lactate production only in highly glycolytic (highly malignant) gliomas, stimulating, on the contrary, that of low grade gliomas; this basically depends on the different HK patterns between low and high grade gliomas.	lonidamine	76-79	hexokinase 1	Homo sapiens	122-124
2674359-3	1989	The drug Lonidamine [1-(2,4-dichlorobenzyl)-1H-indazol-3 carboxylic acid)] (LND) is able to selectively block hexokinase (HK) activity and, consequently, lactate production only in highly glycolytic (highly malignant) gliomas, stimulating, on the contrary, that of low grade gliomas; this basically depends on the different HK patterns between low and high grade gliomas.	lonidamine	76-79	hexokinase 1	Homo sapiens	324-326
3922932-11	1985	When another indazole carboxylic acid derivative, lonidamine, was administered (250 mg/kg), similar changes were evident in epididymal and serum rABP at 32 hours, but the rapid decrease in testicular rABP suggested a different mechanism of action.	lonidamine	50-60	sex hormone binding globulin	Rattus norvegicus	145-149
3245672-0	1988	The role of mitochondrial hexokinase in neoplastic phenotype and its sensitivity to lonidamine.	lonidamine	84-94	hexokinase 1	Homo sapiens	26-36
3631888-1	1987	An experiment was conducted using lonidamine and gossypol against Ehrlich tumour in the foot pad of CD-1 mice.	lonidamine	34-44	CD1 antigen complex	Mus musculus	100-104
3922932-11	1985	When another indazole carboxylic acid derivative, lonidamine, was administered (250 mg/kg), similar changes were evident in epididymal and serum rABP at 32 hours, but the rapid decrease in testicular rABP suggested a different mechanism of action.	lonidamine	50-60	sex hormone binding globulin	Rattus norvegicus	200-204
28668829-0	2017	Effect of Lonidamine on Systemic Therapy of DB-1 Human Melanoma Xenografts with Temozolomide.	lonidamine	10-20	vascular endothelial zinc finger 1	Homo sapiens	44-48
3156759-7	1985	This interpretation is supported by the finding that lonidamine, which specifically inhibits mitochondria-bound hexokinase only when mitochondria are in a condensed state, decreases lactate production to a value similar to that found in unstimulated cells.	lonidamine	53-63	hexokinase 1	Homo sapiens	112-122
31848318-4	2019	Knockdown of HK2 or pharmacological inhibition of HK2 activity with Lonidamine decreased TGF-beta-stimulated fibrogenic processes, including profibrotic gene expression, cell migration, colony formation, and activation of the transcription factors YAP and TAZ, with no apparent effect on cellular viability.	lonidamine	68-78	hexokinase 2	Homo sapiens	50-53
31848318-4	2019	Knockdown of HK2 or pharmacological inhibition of HK2 activity with Lonidamine decreased TGF-beta-stimulated fibrogenic processes, including profibrotic gene expression, cell migration, colony formation, and activation of the transcription factors YAP and TAZ, with no apparent effect on cellular viability.	lonidamine	68-78	transforming growth factor beta 1	Homo sapiens	89-97
31848318-4	2019	Knockdown of HK2 or pharmacological inhibition of HK2 activity with Lonidamine decreased TGF-beta-stimulated fibrogenic processes, including profibrotic gene expression, cell migration, colony formation, and activation of the transcription factors YAP and TAZ, with no apparent effect on cellular viability.	lonidamine	68-78	Yes1 associated transcriptional regulator	Homo sapiens	248-251
31848318-6	2019	In a mouse model of bleomycin-induced lung fibrosis, Lonidamine reduced the expression of genes encoding profibrotic markers (collagenIotaalpha1, EDA-fibronectin, alpha smooth muscle actin, and connective tissue growth factor) and stabilized or improved lung function as assessed by measurement of peripheral blood oxygenation.	lonidamine	53-63	cellular communication network factor 2	Mus musculus	194-225
33292203-0	2020	Lonidamine potentiates the oncolytic efficiency of M1 virus independent of hexokinase 2 but via inhibition of antiviral immunity.	lonidamine	0-10	hexokinase 2	Mus musculus	75-87
33292203-15	2020	In contrast, lonidamine, a reported hexokinase 2 (HK2) inhibitor, enhanced the infection and oncolytic effect of M1 virus independent of HK2.	lonidamine	13-23	hexokinase 2	Mus musculus	36-48
33292203-15	2020	In contrast, lonidamine, a reported hexokinase 2 (HK2) inhibitor, enhanced the infection and oncolytic effect of M1 virus independent of HK2.	lonidamine	13-23	hexokinase 2	Mus musculus	50-53
32838518-3	2020	One complex (PFL) that consists of cisplatin, tegafur, and lonidamine exhibits strong cytotoxicity against triple negative breast cancer (TNBC) cells.	lonidamine	59-69	profilin 2	Homo sapiens	13-16
30279592-1	2018	Lonidamine (LND), a metabolic modulator, sensitizes DB-1 human melanoma to doxorubicin (DOX) chemotherapy by acidifying and de-energizing the tumor.	lonidamine	0-10	vascular endothelial zinc finger 1	Homo sapiens	52-56
30279592-1	2018	Lonidamine (LND), a metabolic modulator, sensitizes DB-1 human melanoma to doxorubicin (DOX) chemotherapy by acidifying and de-energizing the tumor.	lonidamine	12-15	vascular endothelial zinc finger 1	Homo sapiens	52-56
28935467-6	2017	While inhibition of HK2 either by Lonidamine or siRNA further elevated PMA induced Chibby, mitochondrial ROS, TIGAR and LC3II levels; siRNA mediated knock-down of SIRT6 exhibited contradictory effects as compared to HK2.	lonidamine	34-44	hexokinase 2	Homo sapiens	20-23
26597758-4	2016	siRNA mediated knockdown of HIF-1alpha as well as enzymatic inhibition of HK II by Lonidamine, delocalized mitochondrially bound HKII.	lonidamine	83-93	hexokinase 2	Homo sapiens	74-79
27234586-5	2016	It has been known for a long time that lonidamine interferes with energy production in tumour cells by inhibiting hexokinase II (HKII), a glycolytic enzyme.	lonidamine	39-49	hexokinase 2	Homo sapiens	114-127
27234586-5	2016	It has been known for a long time that lonidamine interferes with energy production in tumour cells by inhibiting hexokinase II (HKII), a glycolytic enzyme.	lonidamine	39-49	hexokinase 2	Homo sapiens	129-133
27234586-5	2016	It has been known for a long time that lonidamine interferes with energy production in tumour cells by inhibiting hexokinase II (HKII), a glycolytic enzyme.	lonidamine	39-49	hexokinase 1	Homo sapiens	138-155
27610044-14	2016	(iv) 2-DG and lonidamine stimulated defensive Akt and ERK phosphorylation/activation, while glucose starvation was ineffective.	lonidamine	14-24	AKT serine/threonine kinase 1	Homo sapiens	46-49
27610044-14	2016	(iv) 2-DG and lonidamine stimulated defensive Akt and ERK phosphorylation/activation, while glucose starvation was ineffective.	lonidamine	14-24	mitogen-activated protein kinase 1	Homo sapiens	54-57
26597758-4	2016	siRNA mediated knockdown of HIF-1alpha as well as enzymatic inhibition of HK II by Lonidamine, delocalized mitochondrially bound HKII.	lonidamine	83-93	hexokinase 2	Homo sapiens	129-133
26597758-5	2016	This altered subcellular HKII localization affected TNFalpha-induced cofilin activation and actin turnover, as pharmacological inhibition of HKII by Lonidamine decreased Actin-related protein 2 (ARP2)/cofilin interaction.	lonidamine	149-159	hexokinase 2	Homo sapiens	25-29
26597758-5	2016	This altered subcellular HKII localization affected TNFalpha-induced cofilin activation and actin turnover, as pharmacological inhibition of HKII by Lonidamine decreased Actin-related protein 2 (ARP2)/cofilin interaction.	lonidamine	149-159	tumor necrosis factor	Homo sapiens	52-60
26597758-5	2016	This altered subcellular HKII localization affected TNFalpha-induced cofilin activation and actin turnover, as pharmacological inhibition of HKII by Lonidamine decreased Actin-related protein 2 (ARP2)/cofilin interaction.	lonidamine	149-159	cofilin 1	Homo sapiens	69-76
26597758-5	2016	This altered subcellular HKII localization affected TNFalpha-induced cofilin activation and actin turnover, as pharmacological inhibition of HKII by Lonidamine decreased Actin-related protein 2 (ARP2)/cofilin interaction.	lonidamine	149-159	hexokinase 2	Homo sapiens	141-145
26597758-5	2016	This altered subcellular HKII localization affected TNFalpha-induced cofilin activation and actin turnover, as pharmacological inhibition of HKII by Lonidamine decreased Actin-related protein 2 (ARP2)/cofilin interaction.	lonidamine	149-159	actin related protein 2	Homo sapiens	170-193
26597758-5	2016	This altered subcellular HKII localization affected TNFalpha-induced cofilin activation and actin turnover, as pharmacological inhibition of HKII by Lonidamine decreased Actin-related protein 2 (ARP2)/cofilin interaction.	lonidamine	149-159	actin related protein 2	Homo sapiens	195-199
26597758-5	2016	This altered subcellular HKII localization affected TNFalpha-induced cofilin activation and actin turnover, as pharmacological inhibition of HKII by Lonidamine decreased Actin-related protein 2 (ARP2)/cofilin interaction.	lonidamine	149-159	cofilin 1	Homo sapiens	201-208
26597758-6	2016	Photobleaching studies revealed destabilization of TNFalpha- induced stable MHC-I membrane clusters in the presence of Lonidamine and ARP2 inhibitor CK666.	lonidamine	119-129	tumor necrosis factor	Homo sapiens	51-59
21932172-8	2011	Extension of lifespan requires activation of pmk-1, an orthologue of p38 MAP kinase, and is abolished by co-application of an antioxidant, indicating that increased ROS formation is required for the extension of lifespan by lonidamine.	lonidamine	224-234	Mitogen-activated protein kinase pmk-1	Caenorhabditis elegans	45-50
26111690-9	2015	Western blotting showed that lonidamine up-regulated the expression of GRP78, down-regulated the expression of cIAP1 and promoted caspase-8 activation as the treatment time extended.	lonidamine	29-39	baculoviral IAP repeat containing 2	Homo sapiens	111-116
26111690-9	2015	Western blotting showed that lonidamine up-regulated the expression of GRP78, down-regulated the expression of cIAP1 and promoted caspase-8 activation as the treatment time extended.	lonidamine	29-39	caspase 8	Homo sapiens	130-139
26111690-10	2015	CONCLUSION: Lonidamine can inhibit the proliferation and induce apoptosis in MCF-7 cells, and these effects are probably mediated by reducing ATP level, inducing endoplasmic reticulum stress response, down-regulating cIAP1, and promoting caspase-8 activation in the cells.	lonidamine	12-22	baculoviral IAP repeat containing 2	Homo sapiens	217-222
26111690-10	2015	CONCLUSION: Lonidamine can inhibit the proliferation and induce apoptosis in MCF-7 cells, and these effects are probably mediated by reducing ATP level, inducing endoplasmic reticulum stress response, down-regulating cIAP1, and promoting caspase-8 activation in the cells.	lonidamine	12-22	caspase 8	Homo sapiens	238-247
25501281-4	2015	Hexokinase and CPT-1 activities were examined in the presence of different concentrations of their inhibitors, lonidamine and etomoxir, to find the concentration of maximum inhibition ([I max]).	lonidamine	111-121	hexokinase 1	Homo sapiens	0-10
25501281-4	2015	Hexokinase and CPT-1 activities were examined in the presence of different concentrations of their inhibitors, lonidamine and etomoxir, to find the concentration of maximum inhibition ([I max]).	lonidamine	111-121	carnitine palmitoyltransferase 1A	Homo sapiens	15-20
22745015-0	2013	(31) P and (1) H MRS of DB-1 melanoma xenografts: lonidamine selectively decreases tumor intracellular pH and energy status and sensitizes tumors to melphalan.	lonidamine	50-60	vascular endothelial zinc finger 1	Homo sapiens	24-28
26387611-0	2015	The energy blockers bromopyruvate and lonidamine lead GL15 glioblastoma cells to death by different p53-dependent routes.	lonidamine	38-48	tumor protein p53	Homo sapiens	100-103
26111690-9	2015	Western blotting showed that lonidamine up-regulated the expression of GRP78, down-regulated the expression of cIAP1 and promoted caspase-8 activation as the treatment time extended.	lonidamine	29-39	heat shock protein family A (Hsp70) member 5	Homo sapiens	71-76
25501281-9	2015	Hexokinase and CPT-1 activities were significantly inhibited by lonidamine [600 muM] and etomoxir [100 muM] in both cell lines.	lonidamine	64-74	hexokinase 1	Homo sapiens	0-10
25501281-9	2015	Hexokinase and CPT-1 activities were significantly inhibited by lonidamine [600 muM] and etomoxir [100 muM] in both cell lines.	lonidamine	64-74	carnitine palmitoyltransferase 1A	Homo sapiens	15-20
25501281-9	2015	Hexokinase and CPT-1 activities were significantly inhibited by lonidamine [600 muM] and etomoxir [100 muM] in both cell lines.	lonidamine	64-74	latexin	Homo sapiens	80-83
25501281-10	2015	Treatment of the cells with lonidamine [600 muM] resulted in a significant ATP reduction, cell viability and apoptosis, caspase-3 activity elevation, MMP reduction, and appearance of apoptosis-related morphological changes in the cells.	lonidamine	28-38	latexin	Homo sapiens	44-47
25501281-10	2015	Treatment of the cells with lonidamine [600 muM] resulted in a significant ATP reduction, cell viability and apoptosis, caspase-3 activity elevation, MMP reduction, and appearance of apoptosis-related morphological changes in the cells.	lonidamine	28-38	caspase 3	Homo sapiens	120-129
23967175-8	2013	In addition, we found that combination treatment with the TSPO ligands (PK 11195 or Ro5-4864) and lonidamine, a clinical phase II drug targeting mitochondria, decreased viability of ER-negative breast cancer cell lines.	lonidamine	98-108	estrogen receptor 1	Homo sapiens	182-184
21889928-6	2011	Lonidamine/ATO stimulates JNK phosphorylation/activation, and apoptosis is attenuated by the JNK inhibitor SP600125.	lonidamine	0-10	mitogen-activated protein kinase 8	Homo sapiens	26-29
21889928-6	2011	Lonidamine/ATO stimulates JNK phosphorylation/activation, and apoptosis is attenuated by the JNK inhibitor SP600125.	lonidamine	0-10	mitogen-activated protein kinase 8	Homo sapiens	93-96
21889928-7	2011	In addition, lonidamine elicits ERK and Akt/mTOR pathway activation, as indicated by increased ERK, Akt, p70S6K and rpS6 phosphorylation, and these effects are reduced by co-treatment with ATO.	lonidamine	13-23	mitogen-activated protein kinase 1	Homo sapiens	32-35
21889928-7	2011	In addition, lonidamine elicits ERK and Akt/mTOR pathway activation, as indicated by increased ERK, Akt, p70S6K and rpS6 phosphorylation, and these effects are reduced by co-treatment with ATO.	lonidamine	13-23	AKT serine/threonine kinase 1	Homo sapiens	40-43
21889928-7	2011	In addition, lonidamine elicits ERK and Akt/mTOR pathway activation, as indicated by increased ERK, Akt, p70S6K and rpS6 phosphorylation, and these effects are reduced by co-treatment with ATO.	lonidamine	13-23	mechanistic target of rapamycin kinase	Homo sapiens	44-48
21889928-7	2011	In addition, lonidamine elicits ERK and Akt/mTOR pathway activation, as indicated by increased ERK, Akt, p70S6K and rpS6 phosphorylation, and these effects are reduced by co-treatment with ATO.	lonidamine	13-23	mitogen-activated protein kinase 1	Homo sapiens	95-98
21889928-7	2011	In addition, lonidamine elicits ERK and Akt/mTOR pathway activation, as indicated by increased ERK, Akt, p70S6K and rpS6 phosphorylation, and these effects are reduced by co-treatment with ATO.	lonidamine	13-23	AKT serine/threonine kinase 1	Homo sapiens	100-103
21889928-7	2011	In addition, lonidamine elicits ERK and Akt/mTOR pathway activation, as indicated by increased ERK, Akt, p70S6K and rpS6 phosphorylation, and these effects are reduced by co-treatment with ATO.	lonidamine	13-23	ribosomal protein S6 kinase B1	Homo sapiens	105-111
21889928-7	2011	In addition, lonidamine elicits ERK and Akt/mTOR pathway activation, as indicated by increased ERK, Akt, p70S6K and rpS6 phosphorylation, and these effects are reduced by co-treatment with ATO.	lonidamine	13-23	ribosomal protein S6	Homo sapiens	116-120
21889928-8	2011	Importantly, co-treatment with MEK/ERK inhibitor (U0126) and PI3K/Akt (LY294002) or mTOR (rapamycin) inhibitors, instead of ATO, also potentiates lonidamine-provoked apoptosis.	lonidamine	146-156	mitogen-activated protein kinase kinase 7	Homo sapiens	31-34
21889928-8	2011	Importantly, co-treatment with MEK/ERK inhibitor (U0126) and PI3K/Akt (LY294002) or mTOR (rapamycin) inhibitors, instead of ATO, also potentiates lonidamine-provoked apoptosis.	lonidamine	146-156	mitogen-activated protein kinase 1	Homo sapiens	35-38
21889928-8	2011	Importantly, co-treatment with MEK/ERK inhibitor (U0126) and PI3K/Akt (LY294002) or mTOR (rapamycin) inhibitors, instead of ATO, also potentiates lonidamine-provoked apoptosis.	lonidamine	146-156	AKT serine/threonine kinase 1	Homo sapiens	66-69
21889928-8	2011	Importantly, co-treatment with MEK/ERK inhibitor (U0126) and PI3K/Akt (LY294002) or mTOR (rapamycin) inhibitors, instead of ATO, also potentiates lonidamine-provoked apoptosis.	lonidamine	146-156	mechanistic target of rapamycin kinase	Homo sapiens	84-88
21889928-9	2011	These results indicate that: (i) lonidamine efficacy is restrained by drug-provoked activation of MEK/ERK and Akt/mTOR defensive pathways, which therefore represent potential therapeutic targets.	lonidamine	33-43	mitogen-activated protein kinase kinase 7	Homo sapiens	98-101
21889928-9	2011	These results indicate that: (i) lonidamine efficacy is restrained by drug-provoked activation of MEK/ERK and Akt/mTOR defensive pathways, which therefore represent potential therapeutic targets.	lonidamine	33-43	mitogen-activated protein kinase 1	Homo sapiens	102-105
21889928-9	2011	These results indicate that: (i) lonidamine efficacy is restrained by drug-provoked activation of MEK/ERK and Akt/mTOR defensive pathways, which therefore represent potential therapeutic targets.	lonidamine	33-43	AKT serine/threonine kinase 1	Homo sapiens	110-113
21889928-9	2011	These results indicate that: (i) lonidamine efficacy is restrained by drug-provoked activation of MEK/ERK and Akt/mTOR defensive pathways, which therefore represent potential therapeutic targets.	lonidamine	33-43	mechanistic target of rapamycin kinase	Homo sapiens	114-118
21932172-9	2011	Consistent with the concept of mitohormesis, lonidamine is capable of promoting longevity in a pmk-1 sensitive manner by increasing formation of ROS.	lonidamine	45-55	Mitogen-activated protein kinase pmk-1	Caenorhabditis elegans	95-100
21220050-0	2011	Pharmacokinetics and biodistribution of lonidamine/paclitaxel loaded, EGFR-targeted nanoparticles in an orthotopic animal model of multi-drug resistant breast cancer.	lonidamine	40-50	epidermal growth factor receptor	Mus musculus	70-74
21220050-1	2011	UNLABELLED: The aim of this study was to assess the biodistribution and pharmacokinetics of epidermal growth factor receptor (EGFR)-targeted polymer-blend nanoparticles loaded with the anticancer drugs lonidamine and paclitaxel.	lonidamine	202-212	epidermal growth factor receptor	Mus musculus	92-124
21220050-1	2011	UNLABELLED: The aim of this study was to assess the biodistribution and pharmacokinetics of epidermal growth factor receptor (EGFR)-targeted polymer-blend nanoparticles loaded with the anticancer drugs lonidamine and paclitaxel.	lonidamine	202-212	epidermal growth factor receptor	Mus musculus	126-130
21220050-7	2011	Lonidamine-paclitaxel combination therapy administered via EGFR-targeted polymer-blend nanocarriers may become a viable platform for the future treatment of multidrug-resistant cancer.	lonidamine	0-10	epidermal growth factor receptor	Mus musculus	59-63
21220050-8	2011	FROM THE CLINICAL EDITOR: In this study the biodistribution and pharmacokinetics of epidermal growth factor receptor (EGFR)-targeted polymer-blend nanoparticles loaded with lonidamine and paclitaxel were assessed.	lonidamine	173-183	epidermal growth factor receptor	Mus musculus	84-116
21220050-8	2011	FROM THE CLINICAL EDITOR: In this study the biodistribution and pharmacokinetics of epidermal growth factor receptor (EGFR)-targeted polymer-blend nanoparticles loaded with lonidamine and paclitaxel were assessed.	lonidamine	173-183	epidermal growth factor receptor	Mus musculus	118-122
20942457-7	2011	Treatment with a nanoparticle dose of 1 muM paclitaxel/10 muM lonidamine resulted in less than 10% cell viability for all hypoxic/MDR cell lines and less than 5% cell viability for all normoxic cell lines.	lonidamine	62-72	latexin	Homo sapiens	40-43
21537843-6	2011	An MCT inhibitor, lonidamine, regulated the acidification of extracellular pH, also inhibiting both increased cancer cell migration and infiltration and MMP2/9 activity.	lonidamine	18-28	solute carrier family 16 member 1	Homo sapiens	3-6
21537843-6	2011	An MCT inhibitor, lonidamine, regulated the acidification of extracellular pH, also inhibiting both increased cancer cell migration and infiltration and MMP2/9 activity.	lonidamine	18-28	matrix metallopeptidase 2	Homo sapiens	153-159
20942457-0	2011	Development of EGFR-targeted polymer blend nanocarriers for combination paclitaxel/lonidamine delivery to treat multi-drug resistance in human breast and ovarian tumor cells.	lonidamine	83-93	epidermal growth factor receptor	Homo sapiens	15-19
20942457-7	2011	Treatment with a nanoparticle dose of 1 muM paclitaxel/10 muM lonidamine resulted in less than 10% cell viability for all hypoxic/MDR cell lines and less than 5% cell viability for all normoxic cell lines.	lonidamine	62-72	latexin	Homo sapiens	58-61
20942457-10	2011	This system treats MDR by inhibiting the Warburg effect and promoting mitochondrial binding of pro-apoptotic Bcl-2 proteins (lonidamine), while hyperstabilizing microtubules (paclitaxel).	lonidamine	125-135	BCL2 apoptosis regulator	Homo sapiens	109-114
20942457-11	2011	This nanocarrier system actively targets a MDR associated phenotype (EGFR receptor overexpression), further enhancing the therapeutic index of both drugs and potentiating the use of lonidamine/paclitaxel combination therapy in the treatment of MDR cancer.	lonidamine	182-192	epidermal growth factor receptor	Homo sapiens	69-73
20605902-4	2010	Curcumin plus ATO or lonidamine stimulates typical events of the mitochondrial executioner pathway (Bax and Bid activation, cytochrome c release, X-linked inhibitor of apoptosis down-regulation, and caspase-9/-3 activation) and causes mitochondrial transmembrane potential dissipation, which nevertheless represents a late event in the apoptotic response.	lonidamine	21-31	BCL2 associated X, apoptosis regulator	Homo sapiens	100-103
21931642-0	2011	Therapeutic efficacy and safety of paclitaxel/lonidamine loaded EGFR-targeted nanoparticles for the treatment of multi-drug resistant cancer.	lonidamine	46-56	epidermal growth factor receptor	Homo sapiens	64-68
21931642-3	2011	We exploit this expression through the development of EGFR-targeted, polymer blend nanocarriers for the treatment of MDR cancer using paclitaxel (a common chemotherapeutic agent) and lonidamine (an experimental drug; mitochondrial hexokinase 2 inhibitor).	lonidamine	183-193	epidermal growth factor receptor	Homo sapiens	54-58
21931642-3	2011	We exploit this expression through the development of EGFR-targeted, polymer blend nanocarriers for the treatment of MDR cancer using paclitaxel (a common chemotherapeutic agent) and lonidamine (an experimental drug; mitochondrial hexokinase 2 inhibitor).	lonidamine	183-193	hexokinase 2	Homo sapiens	231-243
21931642-9	2011	In addition, treatment with the EGFR-targeted lonidamine/paclitaxel nanoparticles decreased tumor density and altered the MDR phenotype of the tumor xenografts.	lonidamine	46-56	epidermal growth factor receptor	Homo sapiens	32-36
20605902-4	2010	Curcumin plus ATO or lonidamine stimulates typical events of the mitochondrial executioner pathway (Bax and Bid activation, cytochrome c release, X-linked inhibitor of apoptosis down-regulation, and caspase-9/-3 activation) and causes mitochondrial transmembrane potential dissipation, which nevertheless represents a late event in the apoptotic response.	lonidamine	21-31	BH3 interacting domain death agonist	Homo sapiens	108-111
20605902-4	2010	Curcumin plus ATO or lonidamine stimulates typical events of the mitochondrial executioner pathway (Bax and Bid activation, cytochrome c release, X-linked inhibitor of apoptosis down-regulation, and caspase-9/-3 activation) and causes mitochondrial transmembrane potential dissipation, which nevertheless represents a late event in the apoptotic response.	lonidamine	21-31	cytochrome c, somatic	Homo sapiens	124-136
20605902-4	2010	Curcumin plus ATO or lonidamine stimulates typical events of the mitochondrial executioner pathway (Bax and Bid activation, cytochrome c release, X-linked inhibitor of apoptosis down-regulation, and caspase-9/-3 activation) and causes mitochondrial transmembrane potential dissipation, which nevertheless represents a late event in the apoptotic response.	lonidamine	21-31	X-linked inhibitor of apoptosis	Homo sapiens	146-177
20605902-4	2010	Curcumin plus ATO or lonidamine stimulates typical events of the mitochondrial executioner pathway (Bax and Bid activation, cytochrome c release, X-linked inhibitor of apoptosis down-regulation, and caspase-9/-3 activation) and causes mitochondrial transmembrane potential dissipation, which nevertheless represents a late event in the apoptotic response.	lonidamine	21-31	caspase 9	Homo sapiens	199-208
18978206-4	2009	Treatment of prednisolone-resistant Jurkat and Molt4 cells with 2-deoxy-D-glucose (2-DG), lonidamine (LND), or 3-bromopyruvate (3-BrPA) increased the in vitro sensitivity to glucocorticoids, while treatment of the prednisolone-sensitive cell lines Tom-1 and RS4; 11 did not influence drug cytotoxicity.	lonidamine	90-100	target of myb1 membrane trafficking protein	Homo sapiens	248-253
20060930-6	2010	As expected, ANT3 enhanced mitochondria-mediated apoptosis in response to lonidamine, a mitochondriotoxic chemotherapeutic drug, and staurosporine, a protein kinase inhibitor.	lonidamine	74-84	solute carrier family 25 member 6	Homo sapiens	13-17
20060930-10	2010	Finally, stable ANT4 overexpression protected cancer cells from lonidamine and staurosporine apoptosis in a manner independent of Bcl-2 expression.	lonidamine	64-74	solute carrier family 25 member 31	Homo sapiens	16-20
16982757-8	2006	Most importantly, ANT2, but not ANT1, silencing facilitated MMP induction by lonidamine, a mitochondrion-targeted antitumor compound already used in clinical studies for breast, ovarian, glioma, and lung cancer as well as prostate adenoma.	lonidamine	77-87	solute carrier family 25 member 6	Homo sapiens	18-22
16986057-2	2005	Lonidamine, an orally administered small molecule that inhibits glycolysis by the inactivation of hexokinase, may represent a unique and novel approach to the treatment of benign prostatic hyperplasia (BPH).	lonidamine	0-10	hexokinase 1	Homo sapiens	98-108
16181969-0	2005	Lonidamine transiently affects spermatogenesis in pubertal CD1 mice.	lonidamine	0-10	CD1 antigen complex	Mus musculus	59-62
14766935-7	2004	Ru360 (10 microm), a mitochondrial Ca(2+) uptake blocker, and lonidamine (100 microm), a permeability transition pore (PTP) opener, inhibited transient K(Ca) currents similarly to mitochondrial depolarization.	lonidamine	62-72	protein tyrosine phosphatase, non-receptor type 13	Rattus norvegicus	119-122
12606488-6	2003	This potentiation was markedly reduced by phloretin and lonidamine (inhibitors of AQP-9 and CFTR, respectively).	lonidamine	56-66	aquaporin 9	Rattus norvegicus	82-87
12606488-6	2003	This potentiation was markedly reduced by phloretin and lonidamine (inhibitors of AQP-9 and CFTR, respectively).	lonidamine	56-66	CF transmembrane conductance regulator	Rattus norvegicus	92-96
12444067-5	2002	Spectral analysis of this variance suggested a block at a rate of 3.68 micro mol(-1)/sec(-1) and an off rate of 69.01 sec(-1) for lonidamine, and an on rate of 3.27 micro mol(-1)/sec(-1) and an off rate of 108 sec(-1) for AF2785.	lonidamine	130-140	secretory blood group 1	Rattus norvegicus	118-124
12444067-5	2002	Spectral analysis of this variance suggested a block at a rate of 3.68 micro mol(-1)/sec(-1) and an off rate of 69.01 sec(-1) for lonidamine, and an on rate of 3.27 micro mol(-1)/sec(-1) and an off rate of 108 sec(-1) for AF2785.	lonidamine	130-140	secretory blood group 1	Rattus norvegicus	118-124
12444067-5	2002	Spectral analysis of this variance suggested a block at a rate of 3.68 micro mol(-1)/sec(-1) and an off rate of 69.01 sec(-1) for lonidamine, and an on rate of 3.27 micro mol(-1)/sec(-1) and an off rate of 108 sec(-1) for AF2785.	lonidamine	130-140	secretory blood group 1	Rattus norvegicus	118-124
12444067-6	2002	Single CFTR-Cl(-) channel activity using excised inside-out membrane patches from rat epididymal epithelial cells revealed that addition of lonidamine to the intracellular solution caused a flickery block (a reduction in channel-open time) at lower concentration (10 micro M) without any effect on open channel probability or single-channel current amplitude.	lonidamine	140-150	CF transmembrane conductance regulator	Rattus norvegicus	7-11
12444067-9	2002	These results suggest that lonidamine and AF2785, which are open-channel blockers of CFTR at low concentrations, also affect CFTR gating at high concentrations.	lonidamine	27-37	CF transmembrane conductance regulator	Rattus norvegicus	85-89
12444067-9	2002	These results suggest that lonidamine and AF2785, which are open-channel blockers of CFTR at low concentrations, also affect CFTR gating at high concentrations.	lonidamine	27-37	CF transmembrane conductance regulator	Rattus norvegicus	125-129
12411425-0	2002	Mechanism of lonidamine inhibition of the CFTR chloride channel.	lonidamine	13-23	CF transmembrane conductance regulator	Homo sapiens	42-46
12411425-3	2002	Here we investigate the effects of the indazole compound lonidamine on CFTR channels expressed in mammalian cell lines using patch clamp recording.	lonidamine	57-67	CF transmembrane conductance regulator	Homo sapiens	71-75
12411425-5	2002	Application of lonidamine to the intracellular face of excised membrane patches caused a voltage-dependent block of CFTR currents, with an apparent K(d) of 58 micro M at -100 mV.	lonidamine	15-25	CF transmembrane conductance regulator	Homo sapiens	116-120
12411425-13	2002	Several point mutations within the sixth transmembrane region of CFTR (R334C, F337S, T338A and S341A) significantly weakened block of macroscopic CFTR current, suggesting that lonidamine enters deeply into the channel pore from its intracellular end.	lonidamine	176-186	CF transmembrane conductance regulator	Homo sapiens	65-69
12411425-13	2002	Several point mutations within the sixth transmembrane region of CFTR (R334C, F337S, T338A and S341A) significantly weakened block of macroscopic CFTR current, suggesting that lonidamine enters deeply into the channel pore from its intracellular end.	lonidamine	176-186	CF transmembrane conductance regulator	Homo sapiens	146-150
12411425-15	2002	These results identify and characterize lonidamine as a novel CFTR open channel blocker and provide important information concerning its molecular mechanism of action.	lonidamine	40-50	CF transmembrane conductance regulator	Homo sapiens	62-66
11090432-0	2000	Testin induction: the role of cyclic 3",5"-adenosine monophosphate/protein kinase A signaling in the regulation of basal and lonidamine-induced testin expression by rat sertoli cells.	lonidamine	125-135	testin gene	Rattus norvegicus	0-6
11753636-4	2001	In a cell-free system, lonidamine, arsenite, and CD437 induced the permeabilization of ANT proteoliposomes, yet had no effect on protein-free liposomes.	lonidamine	23-33	solute carrier family 25 member 6	Homo sapiens	87-90
11753636-6	2001	Lonidamine, arsenite, and CD437, added to synthetic planar lipid bilayers containing ANT, elicited ANT channel activities with clearly distinct conductance levels of 20+/-7, 100+/-30, and 47+/-7 pS, respectively.	lonidamine	0-10	solute carrier family 25 member 6	Homo sapiens	85-88
11753636-6	2001	Lonidamine, arsenite, and CD437, added to synthetic planar lipid bilayers containing ANT, elicited ANT channel activities with clearly distinct conductance levels of 20+/-7, 100+/-30, and 47+/-7 pS, respectively.	lonidamine	0-10	solute carrier family 25 member 6	Homo sapiens	99-102
11753636-8	2001	Inhibition of F(0)F(1)ATPase without glycolysis inhibition sensitized to lonidamine-induced cell death.	lonidamine	73-83	ATP synthase F1 subunit epsilon	Homo sapiens	14-28
11753636-11	2001	These results indicate that ANT is a target of lonidamine, arsenite, and CD437 and unravel an unexpected heterogeneity in the mode of action of these three compounds.	lonidamine	47-57	solute carrier family 25 member 6	Homo sapiens	28-31
11090432-3	2000	In contrast, lonidamine, an antispermatogenic drug that rearranges the Sertoli cell membrane microfilament structure causing a disruption of Sertoli-germ cell adhesion junctions, induced a drastic increase in testicular testin expression when administered orally.	lonidamine	13-23	testin gene	Rattus norvegicus	220-226
11090432-0	2000	Testin induction: the role of cyclic 3",5"-adenosine monophosphate/protein kinase A signaling in the regulation of basal and lonidamine-induced testin expression by rat sertoli cells.	lonidamine	125-135	testin gene	Rattus norvegicus	144-150
11090432-4	2000	Lonidamine-induced Sertoli cell testin expression involved both ongoing RNA and de novo protein synthesis.	lonidamine	0-10	testin gene	Rattus norvegicus	32-38
11140278-1	2000	It has been shown previously that the antifertility agents Lonidamine and its analogue AF2785, [1-(2,4-dichlorobenzyl)-indazole-3-acrylic acid] are potent inhibitors of the cAMP-activated chloride channel (CFTR) in rat epididymal cells.	lonidamine	59-69	CF transmembrane conductance regulator	Rattus norvegicus	206-210
11090432-7	2000	However, lonidamine can abolish the inhibitory effect of cAMP analogues on Sertoli cell testin expression.	lonidamine	9-19	testin gene	Rattus norvegicus	88-94
10952928-5	2000	We report for the first time two indazole compounds: lonidamine and 1-(2, 4-dichlorobenzyl)-indazole-3-acrylic acid (AF2785) are potent blockers of CFTR in the epididymis.	lonidamine	53-63	CF transmembrane conductance regulator	Rattus norvegicus	148-152
9747871-3	1998	We sought to inhibit glioblastoma metabolism by simultaneously inhibiting hexokinase with lonidamine and binding benzodiazepine receptors with diazepam.	lonidamine	90-100	hexokinase 1	Homo sapiens	74-84
10360831-0	1999	bcl-2 inhibits mitochondrial metabolism and lonidamine-induced apoptosis in adriamycin-resistant MCF7 cells.	lonidamine	44-54	BCL2 apoptosis regulator	Homo sapiens	0-5
10360831-1	1999	Lonidamine (LND), a selective inhibitor of the energy metabolism of tumor cells, induces apoptosis, independently of the p53 gene, in the adriamycin(ADR)-resistant MCF7 breast-cancer cell line (MCF7 ADR).	lonidamine	0-10	tumor protein p53	Homo sapiens	121-124
10353597-0	1999	Lonidamine triggers apoptosis via a direct, Bcl-2-inhibited effect on the mitochondrial permeability transition pore.	lonidamine	0-10	BCL2 apoptosis regulator	Homo sapiens	44-49
9752269-8	1998	Disturbance of HK binding to mitochondria by lonidamine led to inhibition of cells and xenografted-glioma growth.	lonidamine	45-55	hexokinase 1	Homo sapiens	15-17
8823807-9	1996	The extent of inhibition in sensitive and resistant cells overlapped that found for mitochondrially bound hexokinase, thus indicating that the greater sensitivity of resistant cells to lonidamine was due to their higher amount of bound hexokinase.	lonidamine	185-195	hexokinase 1	Homo sapiens	106-116
9472640-7	1998	In the breast carcinoma MX-1, hypersensitive to cisplatin and to the lonidamine+cisplatin combination, the efficacy of drug treatment was associated with phosphorylation of bcl-2 followed by down-regulation of the protein.	lonidamine	69-79	MX dynamin like GTPase 1	Homo sapiens	24-28
9472640-7	1998	In the breast carcinoma MX-1, hypersensitive to cisplatin and to the lonidamine+cisplatin combination, the efficacy of drug treatment was associated with phosphorylation of bcl-2 followed by down-regulation of the protein.	lonidamine	69-79	BCL2 apoptosis regulator	Homo sapiens	173-178
9472640-8	1998	Lonidamine itself caused a delayed phosphorylation of bcl-2.	lonidamine	0-10	BCL2 apoptosis regulator	Homo sapiens	54-59
8787680-5	1996	The evaluation of bcl-2 protein expression suggests that this different effect of lonidamine treatment in drug-resistant and -sensitive cell lines might not simply be due to dissimilar expression levels of bcl-2 protein.	lonidamine	82-92	BCL2 apoptosis regulator	Homo sapiens	18-23
8787680-6	1996	To determine whether the lonidamine-induced apoptosis is mediated by p53 protein, we used cells lacking endogenous p53 and overexpressing either wild-type p53 or dominant-negative p53 mutant.	lonidamine	25-35	tumor protein p53	Homo sapiens	69-72
8616901-0	1996	Efficacy of lonidamine combined with different DNA-damaging agents in the treatment of the MX-1 tumor xenograft.	lonidamine	12-22	MX dynamin like GTPase 1	Homo sapiens	91-95
8823807-9	1996	The extent of inhibition in sensitive and resistant cells overlapped that found for mitochondrially bound hexokinase, thus indicating that the greater sensitivity of resistant cells to lonidamine was due to their higher amount of bound hexokinase.	lonidamine	185-195	hexokinase 1	Homo sapiens	236-246
21556629-1	1995	The antiproliferative activity of lonidamine, alone or in combination with the antiestrogen tamoxifen, was studied on estrogen receptor-positive and estrogen receptor-negative human breast cancer cell lines.	lonidamine	34-44	estrogen receptor 1	Homo sapiens	118-135
8634352-4	1995	The within-day (n = 5) and between-day (n = 5) relative standard deviations for lonidamine determination in serum samples spiked at the 2.5 micrograms ml-1 level were 2.7% and 4.5%, respectively.	lonidamine	80-90	interleukin 17F	Homo sapiens	151-155
7796408-6	1995	Combined administration of LND and the metabolic inhibitor 2-deoxyglucose yielded additive but not synergistic cytotoxicity and enabled assessment of hexokinase activity.	lonidamine	27-30	hexokinase 1	Homo sapiens	150-160
21556629-2	1995	Lonidamine by itself induced an appreciable cytotoxic effect on all five cell lines, with 50% inhibitory concentrations (IC50) ranging from 19.5 to 54 mu M. The combination of lonidamine and tamoxifen, simultaneously administered or in sequence, provided additive effects on the estrogen receptor-negative MCF/DX cell line and a sub-additive interaction in the estrogen receptor-positive MCF7 cells.	lonidamine	0-10	estrogen receptor 1	Homo sapiens	279-296
21556629-2	1995	Lonidamine by itself induced an appreciable cytotoxic effect on all five cell lines, with 50% inhibitory concentrations (IC50) ranging from 19.5 to 54 mu M. The combination of lonidamine and tamoxifen, simultaneously administered or in sequence, provided additive effects on the estrogen receptor-negative MCF/DX cell line and a sub-additive interaction in the estrogen receptor-positive MCF7 cells.	lonidamine	0-10	estrogen receptor 1	Homo sapiens	361-378
21556629-3	1995	The negative interference between the two drugs could be ascribed to the marked reduction induced by lonidamine in the expression of estrogen receptor in the MCF7 cells.	lonidamine	101-111	estrogen receptor 1	Homo sapiens	133-150
2031191-9	1991	One component, a compound that eluted from the HPLC more rapidly than lonidamine, was found in some patients to be sensitive to hydrolysis with beta-glucuronidase.	lonidamine	70-80	glucuronidase beta	Homo sapiens	144-162
1650226-1	1991	Pharmacokinetic studies of lonidamine (1-[2,4-dichlorobenzyl]- 1H- indazole- 3-carboxylic acid, Doridamina: CAS 50264-69-2) in humans showed a wide variation of the plasma concentration-time profiles following a single peroral dose of 300 mg (Cmax between 6.5 and 40.9 micrograms/ml, tmax between 0.75 and 5.5 h).	lonidamine	27-37	BCAR1 scaffold protein, Cas family member	Homo sapiens	108-111
8272575-0	1993	Morphological changes in the hearts of CD1 mice following chronic treatment with doxorubicin and lonidamine.	lonidamine	97-107	CD1 antigen complex	Mus musculus	39-42
1718588-0	1991	Combination therapy: lonidamine, hyperthermia, and chemotherapy against the RIF-1 tumor in vivo.	lonidamine	21-31	replication timing regulatory factor 1	Homo sapiens	76-81
2031197-2	1991	In human malignant gliomas and cell lines from a glioblastoma multiform, lonidamine has been shown to interfere with aerobic glycolysis with a decrease of lactate production by the inhibition of a mitochondrially-bound hexokinase; this selective reduction of the energetic capabilities of glioma cells would be a limiting factor for processes requiring energy, such as cell growth and recovery from potentially lethal damage after radiotherapy or chemotherapy.	lonidamine	73-83	hexokinase 1	Homo sapiens	219-229
2098504-2	1990	Lonidamine (LND) is a drug that interferes with energy metabolism of cancer cells, principally inhibiting aerobic glycolytic activity, by its effect on mitochondrially-bound hexokinase (HK).	lonidamine	0-10	hexokinase 1	Homo sapiens	174-184
2382989-1	1990	Lonidamine combined with cisplatin treatment was tested in human glioma (U87MG) human squamous cell carcinoma (UMSCCl) and Chinese hamster (HA1) cells.	lonidamine	0-10	Rho GTPase activating protein 45	Homo sapiens	140-143
2382989-3	1990	Lonidamine caused little sensitization in U87MG cells, moderate sensitization in HA1 cells and large sensitization in UMSCCl cells.	lonidamine	0-10	Rho GTPase activating protein 45	Homo sapiens	81-84
2253227-0	1990	Cytotoxicity of lonidamine alone and in combination with other drugs against murine RIF-1 and human HT1080 cells in vitro.	lonidamine	16-26	replication timing regulatory factor 1	Mus musculus	84-89
2098504-2	1990	Lonidamine (LND) is a drug that interferes with energy metabolism of cancer cells, principally inhibiting aerobic glycolytic activity, by its effect on mitochondrially-bound hexokinase (HK).	lonidamine	0-10	hexokinase 1	Homo sapiens	186-188
2098504-2	1990	Lonidamine (LND) is a drug that interferes with energy metabolism of cancer cells, principally inhibiting aerobic glycolytic activity, by its effect on mitochondrially-bound hexokinase (HK).	lonidamine	12-15	hexokinase 1	Homo sapiens	174-184
2098504-2	1990	Lonidamine (LND) is a drug that interferes with energy metabolism of cancer cells, principally inhibiting aerobic glycolytic activity, by its effect on mitochondrially-bound hexokinase (HK).	lonidamine	12-15	hexokinase 1	Homo sapiens	186-188
33237147-0	2020	Potentiation of the Effect of Lonidamine by Quercetin in MCF-7 human breast cancer cells through downregulation of MMP-2/9 mRNA Expression.	lonidamine	30-40	matrix metallopeptidase 2	Homo sapiens	115-122
33237147-7	2020	In this study, the combination of quercetin and lonidamine has been evaluated for the first time and the combination treatment decreased MMP-2/-9 mRNA expression more potently than the effects of the compounds alone.	lonidamine	48-58	matrix metallopeptidase 2	Homo sapiens	137-145
35286638-3	2022	The Pt(IV)-lonidamine complex interacts with albumin relatively slowly but possesses high stability and lipophilicity (log P 1.62), which makes it possible the cellular uptake in a free (of proteins) form.	lonidamine	11-21	albumin	Homo sapiens	45-52
34912792-2	2021	To overcome this phenomenon, herein, a mitochondrial-directed pH-sensitive polyvinyl alcohol (PVA) nanogel incorporating the hexokinase inhibitor lonidamine (LND) and the chemotherapeutic drug paclitaxel (PTX) was developed to restore the activity of PTX and synergistically treat drug-resistant tumors.	lonidamine	146-156	hexokinase 1	Homo sapiens	125-135