PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 28551160-6 2017 Treatment with copper chelators (ammonium tetrathiomolybdate, bathocuproinedisulfonic acid and D-penicillamine) increased expression of hCTR1 protein in DLD-1 and SW620 cells, and potentiated the cytotoxicity of oxaliplatin in DLD-1 but not SW620 cells. tetrathiomolybdate 33-60 solute carrier family 31 member 1 Homo sapiens 136-141 28881637-7 2017 Cu2+-induced CD147 self-association also enhances the ability of HCC cells to stimulate MMP-2 expression from neighboring fibroblasts, as well as increases the invasiveness of HCC cells which is abolished by the copper chelator tetrathiomolybdate. tetrathiomolybdate 228-246 basigin (Ok blood group) Homo sapiens 13-18 28881637-7 2017 Cu2+-induced CD147 self-association also enhances the ability of HCC cells to stimulate MMP-2 expression from neighboring fibroblasts, as well as increases the invasiveness of HCC cells which is abolished by the copper chelator tetrathiomolybdate. tetrathiomolybdate 228-246 matrix metallopeptidase 2 Homo sapiens 88-93 27806319-0 2016 Ammonium tetrathiomolybdate treatment targets the copper transporter ATP7A and enhances sensitivity of breast cancer to cisplatin. tetrathiomolybdate 0-27 ATPase copper transporting alpha Homo sapiens 69-74 27769988-13 2017 In preclinical models, tetrathiomolybdate decreased metastases to lungs (P = 0.04), LOX activity (P = 0.03), and collagen crosslinking (P = 0.012). tetrathiomolybdate 23-41 lysyl oxidase Homo sapiens 84-87 28641540-7 2017 Administration of ammonium tetrathiomolybdate, a selective intracellular copper chelator, delayed onset, slowed progression, and prolonged survival of a rodent model of the disease (G93A SOD1 mice). tetrathiomolybdate 18-45 superoxide dismutase 1, soluble Mus musculus 187-191 27806319-7 2016 Cisplatin/TM treatment of cisplatin-resistant tumors reduced ATP7A protein levels, attenuated cisplatin sequestering by ATP7A, increased nuclear availability of cisplatin, and subsequently enhanced DNA damage and apoptosis. tetrathiomolybdate 10-12 ATPase copper transporting alpha Homo sapiens 61-66 27806319-7 2016 Cisplatin/TM treatment of cisplatin-resistant tumors reduced ATP7A protein levels, attenuated cisplatin sequestering by ATP7A, increased nuclear availability of cisplatin, and subsequently enhanced DNA damage and apoptosis. tetrathiomolybdate 10-12 ATPase copper transporting alpha Homo sapiens 120-125 27582053-6 2016 Specifically, the Mo-O or Mo-S bonds can flexibly rotate to bond with the cations in the layered phase, leading to the good compatibility between the thiomolybdate adsorption layer and layered cathode. tetrathiomolybdate 150-163 MOS proto-oncogene, serine/threonine kinase Homo sapiens 26-30 24788952-2 2014 We have previously shown that ATN-224, a copper chelator drug, induces cell death in murine thymic lymphoma cells transfected with Bcl-2. tetrathiomolybdate 30-37 B cell leukemia/lymphoma 2 Mus musculus 131-136 26568478-0 2015 Tetrathiomolybdate mediates cisplatin-induced p38 signaling and EGFR degradation and enhances response to cisplatin therapy in gynecologic cancers. tetrathiomolybdate 0-18 mitogen-activated protein kinase 14 Homo sapiens 46-49 26568478-0 2015 Tetrathiomolybdate mediates cisplatin-induced p38 signaling and EGFR degradation and enhances response to cisplatin therapy in gynecologic cancers. tetrathiomolybdate 0-18 epidermal growth factor receptor Homo sapiens 64-68 26469226-0 2015 Tetrathiomolybdate inhibits mitochondrial complex IV and mediates degradation of hypoxia-inducible factor-1alpha in cancer cells. tetrathiomolybdate 0-18 hypoxia inducible factor 1 subunit alpha Homo sapiens 81-112 25349139-0 2014 The copper chelator tetrathiomolybdate regressed bleomycin-induced pulmonary fibrosis in mice, by reducing lysyl oxidase expressions. tetrathiomolybdate 20-38 lysyl oxidase Mus musculus 107-120 24292713-6 2014 We found that ATN-224-induced cell death was mediated through H(2)O(2)-dependent activation of P38 MAPK and that P38 activation led to a decrease in the antiapoptotic factor MCL1, which is often upregulated in NSCLC. tetrathiomolybdate 14-21 mitogen-activated protein kinase 14 Homo sapiens 95-98 24292713-6 2014 We found that ATN-224-induced cell death was mediated through H(2)O(2)-dependent activation of P38 MAPK and that P38 activation led to a decrease in the antiapoptotic factor MCL1, which is often upregulated in NSCLC. tetrathiomolybdate 14-21 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 174-178 24292713-7 2014 Treatment with both ATN-224 and ABT-263, an inhibitor of the apoptosis regulators BCL2/BCLXL, augmented cell death. tetrathiomolybdate 20-27 BCL2 apoptosis regulator Homo sapiens 82-86 24292713-7 2014 Treatment with both ATN-224 and ABT-263, an inhibitor of the apoptosis regulators BCL2/BCLXL, augmented cell death. tetrathiomolybdate 20-27 BCL2 like 1 Homo sapiens 87-92 24292713-9 2014 Our results indicate that antioxidant inhibition by ATN-224 has potential clinical applications as a single agent, or in combination with other drugs, for the treatment of patients with various forms of NSCLC, including KRAS-driven cancers. tetrathiomolybdate 52-59 KRAS proto-oncogene, GTPase Homo sapiens 220-224 24225134-6 2014 Furthermore, TTM dose-dependently inhibited tumor necrosis factor alpha (TNFalpha)-induced activation of NF-kappaB and AP-1, as well as mRNA and protein expression of VCAM-1, ICAM-1, and MCP-1, which was abolished by preincubating the cells with 5 microM TTM and 15 microM cupric sulfate. tetrathiomolybdate 13-16 tumor necrosis factor Homo sapiens 44-71 24225134-6 2014 Furthermore, TTM dose-dependently inhibited tumor necrosis factor alpha (TNFalpha)-induced activation of NF-kappaB and AP-1, as well as mRNA and protein expression of VCAM-1, ICAM-1, and MCP-1, which was abolished by preincubating the cells with 5 microM TTM and 15 microM cupric sulfate. tetrathiomolybdate 13-16 tumor necrosis factor Homo sapiens 73-81 24225134-6 2014 Furthermore, TTM dose-dependently inhibited tumor necrosis factor alpha (TNFalpha)-induced activation of NF-kappaB and AP-1, as well as mRNA and protein expression of VCAM-1, ICAM-1, and MCP-1, which was abolished by preincubating the cells with 5 microM TTM and 15 microM cupric sulfate. tetrathiomolybdate 13-16 nuclear factor kappa B subunit 1 Homo sapiens 105-114 24225134-6 2014 Furthermore, TTM dose-dependently inhibited tumor necrosis factor alpha (TNFalpha)-induced activation of NF-kappaB and AP-1, as well as mRNA and protein expression of VCAM-1, ICAM-1, and MCP-1, which was abolished by preincubating the cells with 5 microM TTM and 15 microM cupric sulfate. tetrathiomolybdate 13-16 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 119-123 24225134-6 2014 Furthermore, TTM dose-dependently inhibited tumor necrosis factor alpha (TNFalpha)-induced activation of NF-kappaB and AP-1, as well as mRNA and protein expression of VCAM-1, ICAM-1, and MCP-1, which was abolished by preincubating the cells with 5 microM TTM and 15 microM cupric sulfate. tetrathiomolybdate 13-16 vascular cell adhesion molecule 1 Homo sapiens 167-173 24225134-6 2014 Furthermore, TTM dose-dependently inhibited tumor necrosis factor alpha (TNFalpha)-induced activation of NF-kappaB and AP-1, as well as mRNA and protein expression of VCAM-1, ICAM-1, and MCP-1, which was abolished by preincubating the cells with 5 microM TTM and 15 microM cupric sulfate. tetrathiomolybdate 13-16 intercellular adhesion molecule 1 Homo sapiens 175-181 24225134-6 2014 Furthermore, TTM dose-dependently inhibited tumor necrosis factor alpha (TNFalpha)-induced activation of NF-kappaB and AP-1, as well as mRNA and protein expression of VCAM-1, ICAM-1, and MCP-1, which was abolished by preincubating the cells with 5 microM TTM and 15 microM cupric sulfate. tetrathiomolybdate 13-16 C-C motif chemokine ligand 2 Homo sapiens 187-192 21816640-1 2013 OBJECTIVE: ATN-224 (choline tetrathiomolybdate) is an oral Cu(2+)/Zn(2+)-superoxide dismutase 1 (SOD1) inhibitor with preclinical antitumor activity. tetrathiomolybdate 11-18 superoxide dismutase 1 Homo sapiens 59-95 21816640-1 2013 OBJECTIVE: ATN-224 (choline tetrathiomolybdate) is an oral Cu(2+)/Zn(2+)-superoxide dismutase 1 (SOD1) inhibitor with preclinical antitumor activity. tetrathiomolybdate 11-18 superoxide dismutase 1 Homo sapiens 97-101 23321002-12 2013 Ammonium tetrathiomolybdate (TTM), a copper chelating agent, prolonged survival and slowed the disease progression of SOD1(G93A) mice, even when the treatment was started after the disease onset. tetrathiomolybdate 0-27 superoxide dismutase 1, soluble Mus musculus 118-122 23321002-12 2013 Ammonium tetrathiomolybdate (TTM), a copper chelating agent, prolonged survival and slowed the disease progression of SOD1(G93A) mice, even when the treatment was started after the disease onset. tetrathiomolybdate 29-32 superoxide dismutase 1, soluble Mus musculus 118-122 21399873-3 2011 Tetrathiomolybdate (TM) has been shown to decrease cell proliferation by inhibition of superoxide dismutase-1 (SOD1). tetrathiomolybdate 20-22 superoxide dismutase 1 Homo sapiens 111-115 22847786-3 2013 TM 20 mg PO QD was started 4 weeks post-op, and continued for 2 years to maintain the ceruloplasmin level between 5 and 15 mg/dl. tetrathiomolybdate 0-2 ceruloplasmin Homo sapiens 86-99 23859038-8 2013 The cells treated with tetrathiomolybdate increase the uptake of glucose, production of lactate, activate the Akt- and AMPK-signaling pathways and downregulate COX IV. tetrathiomolybdate 23-41 AKT serine/threonine kinase 1 Homo sapiens 110-113 23859038-8 2013 The cells treated with tetrathiomolybdate increase the uptake of glucose, production of lactate, activate the Akt- and AMPK-signaling pathways and downregulate COX IV. tetrathiomolybdate 23-41 cytochrome c oxidase subunit 4I1 Homo sapiens 160-166 19697878-7 2009 Although phase III trials revealed that creatine monohydrate and IGF-1 was not beneficial for patients with ALS, favorable outcomes in SOD1 mice were reported with lithium, NADPH oxidase inhibitor, free-radical scavenger, and ammonium tetrathiomolybdate. tetrathiomolybdate 226-253 superoxide dismutase 1 Homo sapiens 135-139 21399873-3 2011 Tetrathiomolybdate (TM) has been shown to decrease cell proliferation by inhibition of superoxide dismutase-1 (SOD1). tetrathiomolybdate 0-18 superoxide dismutase 1 Homo sapiens 87-109 21399873-3 2011 Tetrathiomolybdate (TM) has been shown to decrease cell proliferation by inhibition of superoxide dismutase-1 (SOD1). tetrathiomolybdate 0-18 superoxide dismutase 1 Homo sapiens 111-115 21399873-3 2011 Tetrathiomolybdate (TM) has been shown to decrease cell proliferation by inhibition of superoxide dismutase-1 (SOD1). tetrathiomolybdate 20-22 superoxide dismutase 1 Homo sapiens 87-109 19934283-0 2009 Antiangiogenic tetrathiomolybdate protects against Her2/neu-induced breast carcinoma by hypoplastic remodeling of the mammary gland. tetrathiomolybdate 15-33 erb-b2 receptor tyrosine kinase 2 Mus musculus 51-55 19934283-0 2009 Antiangiogenic tetrathiomolybdate protects against Her2/neu-induced breast carcinoma by hypoplastic remodeling of the mammary gland. tetrathiomolybdate 15-33 erb-b2 receptor tyrosine kinase 2 Mus musculus 56-59 19934283-4 2009 RESULTS: At the 1-year follow-up, 86.7% of control and 40% of TM-treated Her2/neu mice had palpable mammary tumors with a median time to tumor development of 234 days (95% confidence interval, 202-279 days) for control and >460 days for TM-treated mice (P < 0.0005, n = 15). tetrathiomolybdate 62-64 erb-b2 receptor tyrosine kinase 2 Mus musculus 73-77 20427090-0 2010 Effect of glutathione depletion on removal of copper from LEC rat livers by tetrathiomolybdate. tetrathiomolybdate 76-94 C-C motif chemokine ligand 16 Homo sapiens 58-61 20427090-6 2010 The results suggest that GSH depletion creates an oxidative environment in the livers of LEC rats, and the oxidative environment facilitates the insolubilization of Cu and Mo in the livers of LEC rats after the TTM injection. tetrathiomolybdate 211-214 C-C motif chemokine ligand 16 Homo sapiens 192-195 20814064-7 2010 Especially, LPC-induced caspase-3 activation was inhibited by superoxide dismutase (SOD) and enhanced by ammonium tetrathiomolybdate, SOD inhibitor. tetrathiomolybdate 105-132 caspase 3 Homo sapiens 24-33 20110684-6 2010 LPC concentration- and time-dependently decreased eNOS levels, but this effect was blocked by antioxidants and SOD and potentiated by the SOD1 inhibitor, ammonium tetrathiomolybdate. tetrathiomolybdate 154-181 nitric oxide synthase 3 Homo sapiens 50-54 20110684-6 2010 LPC concentration- and time-dependently decreased eNOS levels, but this effect was blocked by antioxidants and SOD and potentiated by the SOD1 inhibitor, ammonium tetrathiomolybdate. tetrathiomolybdate 154-181 superoxide dismutase 1 Homo sapiens 138-142 19323979-2 2009 It has been reported that ATN-224, a novel copper chelator, potently inhibits the activity of the copper-dependent enzyme superoxide dismutase 1 (SOD1) in endothelial cells. tetrathiomolybdate 26-33 superoxide dismutase 1 Homo sapiens 122-144 19473947-2 2009 We report a patient with WD who developed non-convulsive status epilepticus (SE) during therapy with Tetrathiomolybdate (TTM) and review the last 20 years of the relevant literature. tetrathiomolybdate 101-119 squalene epoxidase Homo sapiens 77-79 19323979-2 2009 It has been reported that ATN-224, a novel copper chelator, potently inhibits the activity of the copper-dependent enzyme superoxide dismutase 1 (SOD1) in endothelial cells. tetrathiomolybdate 26-33 superoxide dismutase 1 Homo sapiens 146-150 19323979-5 2009 Treatment of HUVEC with ATN-224 caused increased superoxide levels, phospho-ERK signalling, nuclear NRF1 expression, HO-1 expression and induction of the anti-apoptotic proteins P21, BCL2 and BCLXL. tetrathiomolybdate 24-31 nuclear respiratory factor 1 Homo sapiens 100-104 19323979-5 2009 Treatment of HUVEC with ATN-224 caused increased superoxide levels, phospho-ERK signalling, nuclear NRF1 expression, HO-1 expression and induction of the anti-apoptotic proteins P21, BCL2 and BCLXL. tetrathiomolybdate 24-31 heme oxygenase 1 Homo sapiens 117-121 19323979-5 2009 Treatment of HUVEC with ATN-224 caused increased superoxide levels, phospho-ERK signalling, nuclear NRF1 expression, HO-1 expression and induction of the anti-apoptotic proteins P21, BCL2 and BCLXL. tetrathiomolybdate 24-31 H3 histone pseudogene 16 Homo sapiens 178-181 19323979-5 2009 Treatment of HUVEC with ATN-224 caused increased superoxide levels, phospho-ERK signalling, nuclear NRF1 expression, HO-1 expression and induction of the anti-apoptotic proteins P21, BCL2 and BCLXL. tetrathiomolybdate 24-31 BCL2 apoptosis regulator Homo sapiens 183-187 19323979-5 2009 Treatment of HUVEC with ATN-224 caused increased superoxide levels, phospho-ERK signalling, nuclear NRF1 expression, HO-1 expression and induction of the anti-apoptotic proteins P21, BCL2 and BCLXL. tetrathiomolybdate 24-31 BCL2 like 1 Homo sapiens 192-197 18253124-0 2008 Identification of biomarkers for the antiangiogenic and antitumour activity of the superoxide dismutase 1 (SOD1) inhibitor tetrathiomolybdate (ATN-224). tetrathiomolybdate 123-141 superoxide dismutase 1, soluble Mus musculus 83-105 18617166-3 2008 Ammonium tetrathiomolybdate (TTM) is a copper-chelating drug that is capable of removing a copper ion from copper-thiolate clusters, such as SOD1. tetrathiomolybdate 0-27 superoxide dismutase 1, soluble Mus musculus 141-145 18617166-3 2008 Ammonium tetrathiomolybdate (TTM) is a copper-chelating drug that is capable of removing a copper ion from copper-thiolate clusters, such as SOD1. tetrathiomolybdate 29-32 superoxide dismutase 1, soluble Mus musculus 141-145 18480265-2 2008 Tetrathiomolybdate (ATN-224) has been recently identified as an inhibitor of SOD1 that attenuates FGF-2- and VEGF-mediated phosphorylation of ERK1/2 in endothelial cells. tetrathiomolybdate 0-18 superoxide dismutase 1 Homo sapiens 77-81 18480265-2 2008 Tetrathiomolybdate (ATN-224) has been recently identified as an inhibitor of SOD1 that attenuates FGF-2- and VEGF-mediated phosphorylation of ERK1/2 in endothelial cells. tetrathiomolybdate 0-18 fibroblast growth factor 2 Homo sapiens 98-103 18480265-2 2008 Tetrathiomolybdate (ATN-224) has been recently identified as an inhibitor of SOD1 that attenuates FGF-2- and VEGF-mediated phosphorylation of ERK1/2 in endothelial cells. tetrathiomolybdate 0-18 vascular endothelial growth factor A Homo sapiens 109-113 18480265-2 2008 Tetrathiomolybdate (ATN-224) has been recently identified as an inhibitor of SOD1 that attenuates FGF-2- and VEGF-mediated phosphorylation of ERK1/2 in endothelial cells. tetrathiomolybdate 0-18 mitogen-activated protein kinase 3 Homo sapiens 142-148 18480265-2 2008 Tetrathiomolybdate (ATN-224) has been recently identified as an inhibitor of SOD1 that attenuates FGF-2- and VEGF-mediated phosphorylation of ERK1/2 in endothelial cells. tetrathiomolybdate 20-27 superoxide dismutase 1 Homo sapiens 77-81 18480265-2 2008 Tetrathiomolybdate (ATN-224) has been recently identified as an inhibitor of SOD1 that attenuates FGF-2- and VEGF-mediated phosphorylation of ERK1/2 in endothelial cells. tetrathiomolybdate 20-27 fibroblast growth factor 2 Homo sapiens 98-103 18480265-2 2008 Tetrathiomolybdate (ATN-224) has been recently identified as an inhibitor of SOD1 that attenuates FGF-2- and VEGF-mediated phosphorylation of ERK1/2 in endothelial cells. tetrathiomolybdate 20-27 vascular endothelial growth factor A Homo sapiens 109-113 18480265-2 2008 Tetrathiomolybdate (ATN-224) has been recently identified as an inhibitor of SOD1 that attenuates FGF-2- and VEGF-mediated phosphorylation of ERK1/2 in endothelial cells. tetrathiomolybdate 20-27 mitogen-activated protein kinase 3 Homo sapiens 142-148 18480265-7 2008 Pretreatment with exogenous H(2)O(2) or with the phosphatase inhibitor vanadate abrogates the inhibition of ERK1/2 phosphorylation induced by ATN-224 or SOD1 siRNA treatments. tetrathiomolybdate 142-149 mitogen-activated protein kinase 3 Homo sapiens 108-114 18253124-0 2008 Identification of biomarkers for the antiangiogenic and antitumour activity of the superoxide dismutase 1 (SOD1) inhibitor tetrathiomolybdate (ATN-224). tetrathiomolybdate 123-141 superoxide dismutase 1, soluble Mus musculus 107-111 18253124-0 2008 Identification of biomarkers for the antiangiogenic and antitumour activity of the superoxide dismutase 1 (SOD1) inhibitor tetrathiomolybdate (ATN-224). tetrathiomolybdate 143-150 superoxide dismutase 1, soluble Mus musculus 83-105 18253124-0 2008 Identification of biomarkers for the antiangiogenic and antitumour activity of the superoxide dismutase 1 (SOD1) inhibitor tetrathiomolybdate (ATN-224). tetrathiomolybdate 143-150 superoxide dismutase 1, soluble Mus musculus 107-111 18253124-6 2008 Here, we present the preclinical evaluation of two potential biomarkers for the activity of ATN-224: (i) SOD activity measurements in blood cells in mice and (ii) levels of endothelial progenitor cells (EPCs) in bonnet macaques treated with ATN-224. tetrathiomolybdate 92-99 superoxide dismutase 1, soluble Mus musculus 105-108 16827103-0 2006 Tetrathiomolybdate blocks bFGF- but not VEGF-induced incipient angiogenesis in vitro. tetrathiomolybdate 0-18 fibroblast growth factor 2 Homo sapiens 26-30 18210236-1 2007 OBJECTIVE: This study examines the target specificity of tetrathiomolybdate (ATM), an anti-angiogenic, anti-tumor agent against the viability / proliferation of arterial, venous, capillary endothelial and tumor cells. tetrathiomolybdate 57-75 ATM serine/threonine kinase Homo sapiens 77-80 16914587-0 2006 Copper binding by tetrathiomolybdate attenuates angiogenesis and tumor cell proliferation through the inhibition of superoxide dismutase 1. tetrathiomolybdate 18-36 superoxide dismutase 1 Homo sapiens 116-138 12939395-0 2003 Tetrathiomolybdate inhibits angiogenesis and metastasis through suppression of the NFkappaB signaling cascade. tetrathiomolybdate 0-18 nuclear factor kappa B subunit 1 Homo sapiens 83-91 16242529-7 2005 Our working hypothesis, based on the inhibition of interleukin-2 by tetrathiomolybdate as shown here, is that tetrathiomolybdate interrupts the inflammatory cascade at the activated-T-lymphocyte stage. tetrathiomolybdate 68-86 interleukin 2 Mus musculus 51-64 16242529-7 2005 Our working hypothesis, based on the inhibition of interleukin-2 by tetrathiomolybdate as shown here, is that tetrathiomolybdate interrupts the inflammatory cascade at the activated-T-lymphocyte stage. tetrathiomolybdate 110-128 interleukin 2 Mus musculus 51-64 15623788-1 2005 PURPOSE: To determine the effects of tetrathiomolybdate (TM), a copper-chelating agent, on retinal angiogenesis and vascular endothelial growth factor (VEGF) in a mouse model of retinal neovascularization. tetrathiomolybdate 37-55 vascular endothelial growth factor A Mus musculus 116-150 15623788-1 2005 PURPOSE: To determine the effects of tetrathiomolybdate (TM), a copper-chelating agent, on retinal angiogenesis and vascular endothelial growth factor (VEGF) in a mouse model of retinal neovascularization. tetrathiomolybdate 57-59 vascular endothelial growth factor A Mus musculus 116-150 15541506-11 2004 The inhibition of tumor necrosis factor alpha suggests that diseases of tumor necrosis factor alpha overexpression are also potential targets of tetrathiomolybdate therapy. tetrathiomolybdate 145-163 tumor necrosis factor Mus musculus 18-45 15541506-11 2004 The inhibition of tumor necrosis factor alpha suggests that diseases of tumor necrosis factor alpha overexpression are also potential targets of tetrathiomolybdate therapy. tetrathiomolybdate 145-163 tumor necrosis factor Mus musculus 72-99 15337842-3 2004 Indeed, we have good evidence, not yet published, that tetrathiomolybdate inhibits pulmonary levels of transforming growth factor-beta and tumor necrosis factor-alpha expression in these bleomycin experiments. tetrathiomolybdate 55-73 tumor necrosis factor Mus musculus 139-166 15337842-6 2004 In additional experiments, tetrathiomolybdate therapy reversed the elevated serum transaminase levels despite continued concanavalin A injections, with nearly significant serum interleukin-1beta inhibition. tetrathiomolybdate 27-45 interleukin 1 beta Mus musculus 177-194 12939395-1 2003 Tetrathiomolybdate (TM), a specific copper chelator, has been shown to be a potent antiangiogenic and antimetastatic compound possibly through suppression of the NFkappaB signaling cascade. tetrathiomolybdate 0-18 nuclear factor kappa B subunit 1 Homo sapiens 162-170 12939395-1 2003 Tetrathiomolybdate (TM), a specific copper chelator, has been shown to be a potent antiangiogenic and antimetastatic compound possibly through suppression of the NFkappaB signaling cascade. tetrathiomolybdate 20-22 nuclear factor kappa B subunit 1 Homo sapiens 162-170 10474204-4 1999 The activity of glutamic-pyruvic transaminase (GPT) in serum was shown to increase significantly on the treatment of Wistar rats with sulfide produced through hydrolytic degradation of TTM and DTM, the latter being more easily degraded. tetrathiomolybdate 185-188 glutamic--pyruvic transaminase Rattus norvegicus 16-45 11377692-3 2001 As part of a series of studies to study the interactions between Cu(II), thiomolybdates and bovine serum albumin, we have performed the syntheses and characterization of small model peptides such as His-Lys, Thr(Ac)-His-Lys and Thr-His-Lys. tetrathiomolybdate 73-87 albumin Homo sapiens 99-112 12208730-3 2002 We report that copper deficiency induced by tetrathiomolybdate (TM) significantly impairs tumor growth and angiogenesis in two animal models of breast cancer: an inflammatory breast cancer xenograft in nude mice and Her2/neu cancer-prone transgenic mice. tetrathiomolybdate 64-66 erb-b2 receptor tyrosine kinase 2 Mus musculus 216-224 11432880-6 2001 Lastly, tetrathiomolybdate, a Cu2+ chelator, significantly represses in a dose-dependent manner the heat shock-induced release of FGF1 and S100A13. tetrathiomolybdate 8-26 fibroblast growth factor 1 Homo sapiens 130-134 11432880-6 2001 Lastly, tetrathiomolybdate, a Cu2+ chelator, significantly represses in a dose-dependent manner the heat shock-induced release of FGF1 and S100A13. tetrathiomolybdate 8-26 S100 calcium binding protein A13 Homo sapiens 139-146 10474204-4 1999 The activity of glutamic-pyruvic transaminase (GPT) in serum was shown to increase significantly on the treatment of Wistar rats with sulfide produced through hydrolytic degradation of TTM and DTM, the latter being more easily degraded. tetrathiomolybdate 185-188 glutamic--pyruvic transaminase Rattus norvegicus 47-50 10474204-6 1999 Cu in Cu-containing enzymes such as Cu,Zn-superoxide dismutase (SOD) in liver and ceruloplasmin (Cp) in plasma was decreased by excessive thiomolybdates, the Cu being found in the plasma in the form of a Cu/thiomolybdate/albumin complex. tetrathiomolybdate 138-152 ceruloplasmin Rattus norvegicus 82-95 10474204-6 1999 Cu in Cu-containing enzymes such as Cu,Zn-superoxide dismutase (SOD) in liver and ceruloplasmin (Cp) in plasma was decreased by excessive thiomolybdates, the Cu being found in the plasma in the form of a Cu/thiomolybdate/albumin complex. tetrathiomolybdate 138-151 ceruloplasmin Rattus norvegicus 82-95 34744706-12 2021 Moreover, tetrathiomolybdate treatment downregulates vascular endothelial growth factor (VEGF) expression, and improved lung function in bleomycin-induced pulmonary fibrosis. tetrathiomolybdate 10-28 vascular endothelial growth factor A Ovis aries 53-87 34715139-9 2021 In lesions, TM induced: (a) a decrease in tissue weight and volume, (b) a decrease in PCNA-positive cells, (c) antiangiogenic effects by decreasing the number of blood vessels, the mRNA expression of fibroblast growth factor 2 (Fgf2) and platelet-derived growth factor subunit B (Pdgfb), and the presence of endothelial cells, (d) a decrease in antioxidant activity and an increase in lipid peroxidation. tetrathiomolybdate 12-14 proliferating cell nuclear antigen Mus musculus 86-90 34715139-9 2021 In lesions, TM induced: (a) a decrease in tissue weight and volume, (b) a decrease in PCNA-positive cells, (c) antiangiogenic effects by decreasing the number of blood vessels, the mRNA expression of fibroblast growth factor 2 (Fgf2) and platelet-derived growth factor subunit B (Pdgfb), and the presence of endothelial cells, (d) a decrease in antioxidant activity and an increase in lipid peroxidation. tetrathiomolybdate 12-14 fibroblast growth factor 2 Mus musculus 200-226 34715139-9 2021 In lesions, TM induced: (a) a decrease in tissue weight and volume, (b) a decrease in PCNA-positive cells, (c) antiangiogenic effects by decreasing the number of blood vessels, the mRNA expression of fibroblast growth factor 2 (Fgf2) and platelet-derived growth factor subunit B (Pdgfb), and the presence of endothelial cells, (d) a decrease in antioxidant activity and an increase in lipid peroxidation. tetrathiomolybdate 12-14 fibroblast growth factor 2 Mus musculus 228-232 34715139-9 2021 In lesions, TM induced: (a) a decrease in tissue weight and volume, (b) a decrease in PCNA-positive cells, (c) antiangiogenic effects by decreasing the number of blood vessels, the mRNA expression of fibroblast growth factor 2 (Fgf2) and platelet-derived growth factor subunit B (Pdgfb), and the presence of endothelial cells, (d) a decrease in antioxidant activity and an increase in lipid peroxidation. tetrathiomolybdate 12-14 platelet derived growth factor, B polypeptide Mus musculus 238-278 34715139-9 2021 In lesions, TM induced: (a) a decrease in tissue weight and volume, (b) a decrease in PCNA-positive cells, (c) antiangiogenic effects by decreasing the number of blood vessels, the mRNA expression of fibroblast growth factor 2 (Fgf2) and platelet-derived growth factor subunit B (Pdgfb), and the presence of endothelial cells, (d) a decrease in antioxidant activity and an increase in lipid peroxidation. tetrathiomolybdate 12-14 platelet derived growth factor, B polypeptide Mus musculus 280-285 34818604-0 2022 Tetrathiomolybdate Partially Alleviates Erectile Dysfunction of Type 1 Diabetic Rats Through Affecting Ceruloplasmin/eNOS and Inhibiting Corporal Fibrosis and Systemic Inflammation. tetrathiomolybdate 0-18 ceruloplasmin Rattus norvegicus 103-116 34818604-0 2022 Tetrathiomolybdate Partially Alleviates Erectile Dysfunction of Type 1 Diabetic Rats Through Affecting Ceruloplasmin/eNOS and Inhibiting Corporal Fibrosis and Systemic Inflammation. tetrathiomolybdate 0-18 nitric oxide synthase 3 Rattus norvegicus 117-121 34818604-3 2022 AIM: To investigate whether Tetrathiomolybdate (TM) supplementation could ameliorate DMED by activation of eNOS. tetrathiomolybdate 28-46 nitric oxide synthase 3 Homo sapiens 107-111 34818604-3 2022 AIM: To investigate whether Tetrathiomolybdate (TM) supplementation could ameliorate DMED by activation of eNOS. tetrathiomolybdate 48-50 nitric oxide synthase 3 Homo sapiens 107-111 34818604-12 2022 The DMED group showed upregulation of Cp and inhibition of eNOS, but the inhibition was partly reversed in the DMED+TM group. tetrathiomolybdate 116-118 nitric oxide synthase 3 Rattus norvegicus 59-63 34818604-15 2022 What"s more, gavage administration of TM profoundly decreased the serum level of IL-6 in DMED rats. tetrathiomolybdate 38-40 interleukin 6 Rattus norvegicus 81-85 34818604-17 2022 Yin Y, Peng J, Zhou J, et al., Tetrathiomolybdate Partially Alleviates Erectile Dysfunction of Type 1 Diabetic Rats Through Affecting Ceruloplasmin/eNOS and Inhibiting Corporal Fibrosis and Systemic Inflammation. tetrathiomolybdate 31-49 ceruloplasmin Rattus norvegicus 134-147 34818604-17 2022 Yin Y, Peng J, Zhou J, et al., Tetrathiomolybdate Partially Alleviates Erectile Dysfunction of Type 1 Diabetic Rats Through Affecting Ceruloplasmin/eNOS and Inhibiting Corporal Fibrosis and Systemic Inflammation. tetrathiomolybdate 31-49 nitric oxide synthase 3 Rattus norvegicus 148-152 34944703-0 2021 Evaluation of ATOX1 as a Potential Predictive Biomarker for Tetrathiomolybdate Treatment of Breast Cancer Patients with High Risk of Recurrence. tetrathiomolybdate 60-78 antioxidant 1 copper chaperone Homo sapiens 14-19 34944703-4 2021 We performed ATOX1 immunohistochemical staining of breast tumor material (before TM treatment) of 47 patients enrolled in the phase II TM clinical trial and evaluated ATOX1 expression levels in relation with patient outcome after TM treatment. tetrathiomolybdate 230-232 antioxidant 1 copper chaperone Homo sapiens 167-172 34944703-5 2021 Our results show that higher ATOX1 levels in the tumor cell cytoplasm correlate with a trend towards better event-free survival after TM treatment for triple-negative breast cancer patients and patients at stage III of disease. tetrathiomolybdate 134-136 antioxidant 1 copper chaperone Homo sapiens 29-34 34744706-12 2021 Moreover, tetrathiomolybdate treatment downregulates vascular endothelial growth factor (VEGF) expression, and improved lung function in bleomycin-induced pulmonary fibrosis. tetrathiomolybdate 10-28 vascular endothelial growth factor A Ovis aries 89-93 34426581-5 2021 Preclinical studies revealed decreased collagen deposition, lower levels of myeloid-derived suppressor cells, and higher CD4+ T-cell infiltration in TM-treated mice compared with controls. tetrathiomolybdate 149-151 CD4 antigen Mus musculus 121-124 31638244-0 2019 Ammonium tetrathiomolybdate enhances the antitumor effect of cisplatin via the suppression of ATPase copper transporting beta in head and neck squamous cell carcinoma. tetrathiomolybdate 0-27 dynein axonemal heavy chain 8 Homo sapiens 94-100 6097647-0 1984 Inhibition of ceruloplasmin and other copper oxidases by thiomolybdate. tetrathiomolybdate 57-70 ceruloplasmin Homo sapiens 14-27 32387586-2 2020 Both superoxide dismutase (SOD) inhibition by tetrathiomolybdate (ATM) and catalase inhibition by 3-amino-1, 2, 4-triazole (ATZ) increase and prolong the cytosolic Fe(II) signal after UVA irradiation. tetrathiomolybdate 46-64 superoxide dismutase 1 Homo sapiens 5-25 32387586-2 2020 Both superoxide dismutase (SOD) inhibition by tetrathiomolybdate (ATM) and catalase inhibition by 3-amino-1, 2, 4-triazole (ATZ) increase and prolong the cytosolic Fe(II) signal after UVA irradiation. tetrathiomolybdate 46-64 superoxide dismutase 1 Homo sapiens 27-30 32387586-2 2020 Both superoxide dismutase (SOD) inhibition by tetrathiomolybdate (ATM) and catalase inhibition by 3-amino-1, 2, 4-triazole (ATZ) increase and prolong the cytosolic Fe(II) signal after UVA irradiation. tetrathiomolybdate 46-64 ATM serine/threonine kinase Homo sapiens 66-69 32005716-3 2020 Repurposing the clinical Cu chelator tetrathiomolybdate (TTM) is supported by efficacy in BRAFV600E-driven melanoma models, due in part to inhibition of MEK1/2 kinase activity. tetrathiomolybdate 37-55 mitogen-activated protein kinase kinase 1 Homo sapiens 153-159 32005716-3 2020 Repurposing the clinical Cu chelator tetrathiomolybdate (TTM) is supported by efficacy in BRAFV600E-driven melanoma models, due in part to inhibition of MEK1/2 kinase activity. tetrathiomolybdate 57-60 mitogen-activated protein kinase kinase 1 Homo sapiens 153-159 32005716-7 2020 Further, in BRAFV600E-positive melanoma cells evolved to be resistant to BRAF and/or MEK1/2 inhibitors, combined treatment with TTM and the clinically evaluated BCL2 inhibitor, ABT-263, restored tumor growth suppression and induced apoptosis. tetrathiomolybdate 128-131 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 12-16 32005716-7 2020 Further, in BRAFV600E-positive melanoma cells evolved to be resistant to BRAF and/or MEK1/2 inhibitors, combined treatment with TTM and the clinically evaluated BCL2 inhibitor, ABT-263, restored tumor growth suppression and induced apoptosis. tetrathiomolybdate 128-131 mitogen-activated protein kinase kinase 1 Homo sapiens 85-91 32600223-5 2020 For these reason, the following clinically approved copper chelators are being repurposed as anti-cancer agents: a) ammonium tetrathiomolybdate (TTM) used to treat Wilson"s disease (copper overload) and Menkes disease (copper deficiency); b) Disulfiram (DSF), used against alcoholism, since it inhibits Aldehyde Dehydrogenase (ALDH1), enzyme important in ethanol detoxification, and a key target against cancer stem cells. tetrathiomolybdate 145-148 aldehyde dehydrogenase 1 family member A1 Homo sapiens 327-332 35450818-6 2022 Moreover, treatment with the mitochondrial complex IV inhibitor tetrathiomolybdate dramatically abrogated the promoting effect of STMP1 on cell proliferation and the expression of cyclin E2, CDK2 and E2F1. tetrathiomolybdate 64-82 cyclin E2 Homo sapiens 180-189 35450818-6 2022 Moreover, treatment with the mitochondrial complex IV inhibitor tetrathiomolybdate dramatically abrogated the promoting effect of STMP1 on cell proliferation and the expression of cyclin E2, CDK2 and E2F1. tetrathiomolybdate 64-82 cyclin dependent kinase 2 Homo sapiens 191-195 35450818-6 2022 Moreover, treatment with the mitochondrial complex IV inhibitor tetrathiomolybdate dramatically abrogated the promoting effect of STMP1 on cell proliferation and the expression of cyclin E2, CDK2 and E2F1. tetrathiomolybdate 64-82 E2F transcription factor 1 Homo sapiens 200-204 31083627-7 2019 Moreover, tetrathiomolybdate treatment was also effective in reducing the clonogenic potential of colon cancer BRAFV600E cells resistant to BRAF pharmacological inhibition. tetrathiomolybdate 10-28 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 111-115 29358279-4 2018 A clinically approved copper chelator, tetrathiomolybdate, inhibited the canonical NLRP3 but not the AIM2, NLRC4, and NLRP1 inflammasomes or NF-kappaB-dependent priming. tetrathiomolybdate 39-57 NLR family pyrin domain containing 3 Homo sapiens 83-88 30643139-0 2019 Tetrathiomolybdate induces dimerization of the metal-binding domain of ATPase and inhibits platination of the protein. tetrathiomolybdate 0-18 dynein axonemal heavy chain 8 Homo sapiens 71-77 30643139-1 2019 Tetrathiomolybdate (TM) is used in the clinic for the treatment of Wilson"s disease by targeting the cellular copper efflux protein ATP7B (WLN). tetrathiomolybdate 0-18 ATPase copper transporting beta Homo sapiens 132-137 30643139-1 2019 Tetrathiomolybdate (TM) is used in the clinic for the treatment of Wilson"s disease by targeting the cellular copper efflux protein ATP7B (WLN). tetrathiomolybdate 20-22 ATPase copper transporting beta Homo sapiens 132-137 30792807-0 2019 Anticancer response to disulfiram may be enhanced by co-treatment with MEK inhibitor or oxaliplatin: modulation by tetrathiomolybdate, KRAS/BRAF mutations and c-MYC/p53 status. tetrathiomolybdate 115-133 mitogen-activated protein kinase kinase 7 Homo sapiens 71-74 30792807-1 2019 Ammonium tetrathiomolybdate (TTM) and disulfiram (DSF) are copper (Cu) chelators in cancer clinical trials partly because Cu chelation: a) restricts the activity of Cu-binding MEK1/2 enzymes which drive tumourigenesis by KRAS or BRAF oncogenic mutations and b) enhances uptake of oxaliplatin (OxPt), clinically used in advanced KRAS-mutant colorectal carcinomas (CRC). tetrathiomolybdate 0-27 mitogen-activated protein kinase kinase 1 Homo sapiens 176-182 30792807-1 2019 Ammonium tetrathiomolybdate (TTM) and disulfiram (DSF) are copper (Cu) chelators in cancer clinical trials partly because Cu chelation: a) restricts the activity of Cu-binding MEK1/2 enzymes which drive tumourigenesis by KRAS or BRAF oncogenic mutations and b) enhances uptake of oxaliplatin (OxPt), clinically used in advanced KRAS-mutant colorectal carcinomas (CRC). tetrathiomolybdate 0-27 KRAS proto-oncogene, GTPase Homo sapiens 221-225 30792807-1 2019 Ammonium tetrathiomolybdate (TTM) and disulfiram (DSF) are copper (Cu) chelators in cancer clinical trials partly because Cu chelation: a) restricts the activity of Cu-binding MEK1/2 enzymes which drive tumourigenesis by KRAS or BRAF oncogenic mutations and b) enhances uptake of oxaliplatin (OxPt), clinically used in advanced KRAS-mutant colorectal carcinomas (CRC). tetrathiomolybdate 0-27 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 229-233 30792807-1 2019 Ammonium tetrathiomolybdate (TTM) and disulfiram (DSF) are copper (Cu) chelators in cancer clinical trials partly because Cu chelation: a) restricts the activity of Cu-binding MEK1/2 enzymes which drive tumourigenesis by KRAS or BRAF oncogenic mutations and b) enhances uptake of oxaliplatin (OxPt), clinically used in advanced KRAS-mutant colorectal carcinomas (CRC). tetrathiomolybdate 0-27 KRAS proto-oncogene, GTPase Homo sapiens 328-332 30792807-1 2019 Ammonium tetrathiomolybdate (TTM) and disulfiram (DSF) are copper (Cu) chelators in cancer clinical trials partly because Cu chelation: a) restricts the activity of Cu-binding MEK1/2 enzymes which drive tumourigenesis by KRAS or BRAF oncogenic mutations and b) enhances uptake of oxaliplatin (OxPt), clinically used in advanced KRAS-mutant colorectal carcinomas (CRC). tetrathiomolybdate 29-32 mitogen-activated protein kinase kinase 1 Homo sapiens 176-182 30792807-1 2019 Ammonium tetrathiomolybdate (TTM) and disulfiram (DSF) are copper (Cu) chelators in cancer clinical trials partly because Cu chelation: a) restricts the activity of Cu-binding MEK1/2 enzymes which drive tumourigenesis by KRAS or BRAF oncogenic mutations and b) enhances uptake of oxaliplatin (OxPt), clinically used in advanced KRAS-mutant colorectal carcinomas (CRC). tetrathiomolybdate 29-32 KRAS proto-oncogene, GTPase Homo sapiens 221-225 30792807-1 2019 Ammonium tetrathiomolybdate (TTM) and disulfiram (DSF) are copper (Cu) chelators in cancer clinical trials partly because Cu chelation: a) restricts the activity of Cu-binding MEK1/2 enzymes which drive tumourigenesis by KRAS or BRAF oncogenic mutations and b) enhances uptake of oxaliplatin (OxPt), clinically used in advanced KRAS-mutant colorectal carcinomas (CRC). tetrathiomolybdate 29-32 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 229-233 30792807-1 2019 Ammonium tetrathiomolybdate (TTM) and disulfiram (DSF) are copper (Cu) chelators in cancer clinical trials partly because Cu chelation: a) restricts the activity of Cu-binding MEK1/2 enzymes which drive tumourigenesis by KRAS or BRAF oncogenic mutations and b) enhances uptake of oxaliplatin (OxPt), clinically used in advanced KRAS-mutant colorectal carcinomas (CRC). tetrathiomolybdate 29-32 KRAS proto-oncogene, GTPase Homo sapiens 328-332 29710396-4 2018 First, we found that the formation of Abeta plaques in the cortex was significantly reduced, and learning deficits were significantly improved in AbetaPP/PS1 transgenic mice by copper chelator tetrathiomolybdate (TM) administration. tetrathiomolybdate 193-211 amyloid beta (A4) precursor protein Mus musculus 38-43 29710396-4 2018 First, we found that the formation of Abeta plaques in the cortex was significantly reduced, and learning deficits were significantly improved in AbetaPP/PS1 transgenic mice by copper chelator tetrathiomolybdate (TM) administration. tetrathiomolybdate 193-211 amyloid beta (A4) precursor protein Mus musculus 146-153 29710396-4 2018 First, we found that the formation of Abeta plaques in the cortex was significantly reduced, and learning deficits were significantly improved in AbetaPP/PS1 transgenic mice by copper chelator tetrathiomolybdate (TM) administration. tetrathiomolybdate 193-211 presenilin 1 Mus musculus 154-157 29710396-4 2018 First, we found that the formation of Abeta plaques in the cortex was significantly reduced, and learning deficits were significantly improved in AbetaPP/PS1 transgenic mice by copper chelator tetrathiomolybdate (TM) administration. tetrathiomolybdate 213-215 amyloid beta (A4) precursor protein Mus musculus 38-43 29710396-4 2018 First, we found that the formation of Abeta plaques in the cortex was significantly reduced, and learning deficits were significantly improved in AbetaPP/PS1 transgenic mice by copper chelator tetrathiomolybdate (TM) administration. tetrathiomolybdate 213-215 amyloid beta (A4) precursor protein Mus musculus 146-153 29710396-4 2018 First, we found that the formation of Abeta plaques in the cortex was significantly reduced, and learning deficits were significantly improved in AbetaPP/PS1 transgenic mice by copper chelator tetrathiomolybdate (TM) administration. tetrathiomolybdate 213-215 presenilin 1 Mus musculus 154-157 29460662-2 2019 WTX101 (bis-choline tetrathiomolybdate) is an investigational copper (Cu)-protein-binding agent developed for the treatment of Wilson disease (WD), a rare genetic disorder caused by mutations in the ATP7B Cu-transporter and resulting in toxic Cu accumulation. tetrathiomolybdate 8-38 ATPase copper transporting beta Rattus norvegicus 199-204 30065097-4 2018 We previously found that MEK1/2 require copper (Cu) for kinase activity and can be inhibited with the well-tolerated and economical Cu chelator tetrathiomolybdate (TM). tetrathiomolybdate 144-162 mitogen-activated protein kinase kinase 1 Mus musculus 25-31 30065097-4 2018 We previously found that MEK1/2 require copper (Cu) for kinase activity and can be inhibited with the well-tolerated and economical Cu chelator tetrathiomolybdate (TM). tetrathiomolybdate 164-166 mitogen-activated protein kinase kinase 1 Mus musculus 25-31 29721562-0 2018 Tetrathiomolybdate inhibits the reaction of cisplatin with human copper chaperone Atox1. tetrathiomolybdate 0-18 antioxidant 1 copper chaperone Homo sapiens 82-87 29505238-3 2018 Here we show a facile one-pot bottom-up synthesis of Pt-MoS x composites using electrochemical reduction in an electrolytic bath of Pt precursor and ammonium tetrathiomolybdate under ambient conditions. tetrathiomolybdate 149-176 MOS proto-oncogene, serine/threonine kinase Homo sapiens 56-59 29535623-0 2018 Tetrathiomolybdate Treatment Leads to the Suppression of Inflammatory Responses through the TRAF6/NFkappaB Pathway in LPS-Stimulated BV-2 Microglia. tetrathiomolybdate 0-18 TNF receptor-associated factor 6 Mus musculus 92-97 29535623-0 2018 Tetrathiomolybdate Treatment Leads to the Suppression of Inflammatory Responses through the TRAF6/NFkappaB Pathway in LPS-Stimulated BV-2 Microglia. tetrathiomolybdate 0-18 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 98-106