deferoxamine has been researched along with Nerve Degeneration in 21 studies
Deferoxamine: Natural product isolated from Streptomyces pilosus. It forms iron complexes and is used as a chelating agent, particularly in the mesylate form.
desferrioxamine B : An acyclic desferrioxamine that is butanedioic acid in which one of the carboxy groups undergoes formal condensation with the primary amino group of N-(5-aminopentyl)-N-hydroxyacetamide and the second carboxy group undergoes formal condensation with the hydroxyamino group of N(1)-(5-aminopentyl)-N(1)-hydroxy-N(4)-[5-(hydroxyamino)pentyl]butanediamide. It is a siderophore native to Streptomyces pilosus biosynthesised by the DesABCD enzyme cluster as a high affinity Fe(III) chelator.
Nerve Degeneration: Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
Excerpt | Relevance | Reference |
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" Considering that creatine kinase (CK) is important for brain energy homeostasis and is inhibited by free radicals, and that oxidative stress is probably involved in the pathogenesis of uremic encephalopathy, we measured CK activity (hippocampus, striatum, cerebellum, cerebral cortex and prefrontal cortex) in brain if rats submitted to renal ischemia and the effect of administration of antioxidants (N-acetylcysteine, NAC and deferoxamine, DFX) on this enzyme." | 7.74 | Inhibition of brain creatine kinase activity after renal ischemia is attenuated by N-acetylcysteine and deferoxamine administration. ( Burigo, M; Constantino, L; Dal-Pizzol, F; Di-Pietro, PB; Dias, ML; Machado, RA; Scaini, G; Streck, EL, 2008) |
" Considering that creatine kinase (CK) is important for brain energy homeostasis and is inhibited by free radicals, and that oxidative stress is probably involved in the pathogenesis of uremic encephalopathy, we measured CK activity (hippocampus, striatum, cerebellum, cerebral cortex and prefrontal cortex) in brain if rats submitted to renal ischemia and the effect of administration of antioxidants (N-acetylcysteine, NAC and deferoxamine, DFX) on this enzyme." | 3.74 | Inhibition of brain creatine kinase activity after renal ischemia is attenuated by N-acetylcysteine and deferoxamine administration. ( Burigo, M; Constantino, L; Dal-Pizzol, F; Di-Pietro, PB; Dias, ML; Machado, RA; Scaini, G; Streck, EL, 2008) |
" An understanding of a possible enhanced bioavailability of Al in this type of exposure, versus other exposures such as antacid intake or industrial exposure, needs to be considered and explored." | 2.39 | Can the controversy of the role of aluminum in Alzheimer's disease be resolved? What are the suggested approaches to this controversy and methodological issues to be considered? ( Exley, C; Forbes, WF; Huang, Y; Joshi, JG; Kruck, T; McLachlan, DR; Savory, J; Wakayama, I, 1996) |
"Rat model of cerebral ischemia was established by middle cerebral artery occlusion with or without DFO administration." | 1.35 | Desferoxamine preconditioning protects against cerebral ischemia in rats by inducing expressions of hypoxia inducible factor 1 alpha and erythropoietin. ( Ding, SJ; Guo, W; Li, YX; Xiao, L; Zhan, Q, 2008) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 0 (0.00) | 18.7374 |
1990's | 7 (33.33) | 18.2507 |
2000's | 10 (47.62) | 29.6817 |
2010's | 4 (19.05) | 24.3611 |
2020's | 0 (0.00) | 2.80 |
Authors | Studies |
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Gotsbacher, MP | 1 |
Telfer, TJ | 1 |
Witting, PK | 1 |
Double, KL | 1 |
Finkelstein, DI | 1 |
Codd, R | 1 |
Guo, X | 1 |
Qi, X | 1 |
Li, H | 1 |
Duan, Z | 1 |
Wei, Y | 1 |
Zhang, F | 1 |
Tian, M | 1 |
Ma, L | 1 |
You, C | 1 |
Selim, M | 1 |
van der Kooij, MA | 1 |
Groenendaal, F | 1 |
Kavelaars, A | 1 |
Heijnen, CJ | 1 |
van Bel, F | 1 |
Yu, J | 1 |
Guo, Y | 1 |
Sun, M | 1 |
Li, B | 1 |
Zhang, Y | 1 |
Li, C | 1 |
Zhang, Z | 1 |
Zhang, K | 1 |
Du, X | 1 |
Li, Y | 1 |
Chaudhary, N | 1 |
Gemmete, JJ | 1 |
Thompson, BG | 1 |
Xi, G | 1 |
Pandey, AS | 1 |
Pelit, A | 1 |
Haciyakupoglu, G | 1 |
Zorludemir, S | 1 |
Mete, U | 1 |
Daglioglu, K | 1 |
Kaya, M | 1 |
Karelson, E | 1 |
Fernaeus, S | 1 |
Reis, K | 1 |
Bogdanovic, N | 1 |
Land, T | 1 |
Zhang, X | 1 |
Xie, W | 1 |
Qu, S | 1 |
Pan, T | 1 |
Wang, X | 1 |
Le, W | 1 |
Di-Pietro, PB | 1 |
Dias, ML | 1 |
Scaini, G | 1 |
Burigo, M | 1 |
Constantino, L | 1 |
Machado, RA | 1 |
Dal-Pizzol, F | 1 |
Streck, EL | 1 |
Li, YX | 1 |
Ding, SJ | 1 |
Xiao, L | 1 |
Guo, W | 1 |
Zhan, Q | 1 |
Huang, Y | 2 |
Savory, J | 3 |
Herman, MM | 2 |
Nicholson, JR | 1 |
Reyes, MR | 1 |
Boyd, JC | 2 |
Wills, MR | 2 |
Erasmus, RT | 1 |
Kondo, T | 1 |
Exley, C | 1 |
Forbes, WF | 1 |
Joshi, JG | 1 |
Kruck, T | 1 |
McLachlan, DR | 1 |
Wakayama, I | 1 |
Lan, J | 1 |
Jiang, DH | 1 |
Rauhala, P | 1 |
Khaldi, A | 1 |
Mohanakumar, KP | 1 |
Chiueh, CC | 1 |
de la Monte, SM | 1 |
Neely, TR | 1 |
Cannon, J | 1 |
Wands, JR | 1 |
Yoshida, H | 1 |
Imaizumi, T | 1 |
Tanji, K | 1 |
Matsumiya, T | 1 |
Sakaki, H | 1 |
Kimura, D | 1 |
Cui, XF | 1 |
Kumagai, M | 1 |
Tamo, W | 1 |
Shibata, T | 1 |
Hatakeyama, M | 1 |
Sato, Y | 1 |
Satoh, K | 1 |
Ben-Shachar, D | 1 |
Eshel, G | 1 |
Finberg, JP | 1 |
Youdim, MB | 1 |
Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
Safety and Effectiveness Study of Deferoxamine and Xingnaojing Injection in Intracerebral Hemorrhage[NCT02367248] | Phase 1/Phase 2 | 180 participants (Anticipated) | Interventional | 2015-03-31 | Recruiting | ||
Futility Study of Deferoxamine in Intracerebral Hemorrhage[NCT01662895] | Phase 2 | 42 participants (Actual) | Interventional | 2013-03-18 | Terminated (stopped due to By DSMB on October 18, 2013 due to increased incidence of ARDS. See modified protocol [NCT02175225) | ||
Study of Deferoxamine Mesylate in Intracerebral Hemorrhage[NCT02175225] | Phase 2 | 294 participants (Actual) | Interventional | 2014-10-31 | Completed | ||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
Mortality at any time from randomization through day-90 (NCT01662895)
Timeframe: 90 days
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine | 3 |
Normal Saline | 0 |
(NCT01662895)
Timeframe: within 7 days or discharge
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine | 1 |
Normal Saline | 1 |
(NCT01662895)
Timeframe: within 7 days or discharge
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine | 0 |
Normal Saline | 1 |
(NCT01662895)
Timeframe: 90 days
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine | 9 |
Normal Saline | 6 |
(NCT01662895)
Timeframe: 90 days
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine | 6 |
Normal Saline | 0 |
(NCT01662895)
Timeframe: within 7 days or discharge
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine | 0 |
Normal Saline | 0 |
"The primary outcome measure of efficacy is the modified Rankin Scale (mRS) score, dichotomized to define good functional outcome as mRS 0-2 at 90 days.~The minimum mRS score is 0 (i.e. no disability). The maximum score is 6 (i.e. dead)." (NCT01662895)
Timeframe: 90 days
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine | 6 |
Normal Saline | 10 |
The proportion of DFO- and placebo-treated subjects with mRS 0-3 vs. 4-6 at 90 days (NCT01662895)
Timeframe: 90 days
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine | 12 |
Normal Saline | 14 |
Adverse event of special interest: anaphylaxis at any time during the study infusion (NCT02175225)
Timeframe: during the study infusion
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine Mesylate | 3 |
Normal Saline | 0 |
Hypotension requiring medical intervention at any time during the study infusion that could not be explained by other causes (NCT02175225)
Timeframe: during the study infusion
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine Mesylate | 1 |
Normal Saline | 2 |
Adverse event of special interest: development of new and unexplained visual or auditory changes after initiation of the study infusion (NCT02175225)
Timeframe: after initiation of study infusion
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine Mesylate | 3 |
Normal Saline | 4 |
Edema accompanied by an unexplained increase of more than four points on the US National Institutes of Health Stroke Scale or a decrease of more than two points in Glasgow Coma Scale score during the first week after the intracerebral haemorrhage. (NCT02175225)
Timeframe: 7 days
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine Mesylate | 9 |
Normal Saline | 5 |
Number of subjects experiencing Serious adverse events at any time from randomization through day 90 (NCT02175225)
Timeframe: 90 days
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine Mesylate | 39 |
Normal Saline | 49 |
Number of Subjects Experiencing Serious Adverse Events within 7 days of randomization (NCT02175225)
Timeframe: 7 days
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine Mesylate | 24 |
Normal Saline | 26 |
Another measure of efficacy is the modified Rankin Scale (mRS) score, dichotomized to define good functional outcome as mRS 0-2 at 180 days. The mRS ranges from 0 to 6, with higher scores indicating worse outcome. (NCT02175225)
Timeframe: 180 days
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine Mesylate | 61 |
Normal Saline | 48 |
The primary outcome measure of efficacy is the modified Rankin Scale (mRS) score, dichotomized to define good functional outcome as mRS 0-2 at 90 days. The mRS ranges from 0 to 6, with higher scores indicating worse outcome. (NCT02175225)
Timeframe: 90 days
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine Mesylate | 48 |
Normal Saline | 47 |
Another measure of efficacy is the modified Rankin Scale (mRS) score, dichotomized to define good functional outcome as mRS 0-3 at 180 days. The mRS ranges from 0 to 6, with higher scores indicating worse outcome. (NCT02175225)
Timeframe: 180 days
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine Mesylate | 97 |
Normal Saline | 92 |
"Another measure of efficacy is the modified Rankin Scale (mRS) score, dichotomized to define good functional outcome as mRS 0-3 at 90 days. The mRS ranges from 0 to 6, with higher scores indicating worse outcome.~Although mRS 0-3 is less favorable than the primary outcome of mRS 0-2, it would still be a desirable effect in patients with ICH given that no treatments exist to reduce disability." (NCT02175225)
Timeframe: 90 days
Intervention | Participants (Count of Participants) |
---|---|
Deferoxamine Mesylate | 91 |
Normal Saline | 82 |
Adverse event of special interest: Respiratory compromise of any cause, including acute respiratory distress syndrome, in hospital until day 7 or discharge [whichever was earlier] (NCT02175225)
Timeframe: 7 days
Intervention | Participants (Count of Participants) | |
---|---|---|
All cause | Cause by acute respiratory distress syndrome | |
Deferoxamine Mesylate | 20 | 2 |
Normal Saline | 23 | 1 |
Analyses will be expanded to include an interaction between treatment and OTT window and the magnitude of the treatment effect, and corresponding confidence interval, will be estimated for each time window (<12 hours vs. >/= 12 hours) in order to explore the presence of a differential treatment effect in the OTT windows. (NCT02175225)
Timeframe: 90 days
Intervention | Participants (Count of Participants) | |
---|---|---|
Onset to treatment time <=12 hours | Onset to treatment time >12 hours | |
Deferoxamine Mesylate | 15 | 33 |
Normal Saline | 19 | 28 |
4 reviews available for deferoxamine and Nerve Degeneration
Article | Year |
---|---|
Deferoxamine mesylate: a new hope for intracerebral hemorrhage: from bench to clinical trials.
Topics: Animals; Cerebral Hemorrhage; Chemotherapy, Adjuvant; Deferoxamine; Disease Models, Animal; Hemoglob | 2009 |
Deferoxamine mesylate: a new hope for intracerebral hemorrhage: from bench to clinical trials.
Topics: Animals; Cerebral Hemorrhage; Chemotherapy, Adjuvant; Deferoxamine; Disease Models, Animal; Hemoglob | 2009 |
Deferoxamine mesylate: a new hope for intracerebral hemorrhage: from bench to clinical trials.
Topics: Animals; Cerebral Hemorrhage; Chemotherapy, Adjuvant; Deferoxamine; Disease Models, Animal; Hemoglob | 2009 |
Deferoxamine mesylate: a new hope for intracerebral hemorrhage: from bench to clinical trials.
Topics: Animals; Cerebral Hemorrhage; Chemotherapy, Adjuvant; Deferoxamine; Disease Models, Animal; Hemoglob | 2009 |
Deferoxamine mesylate: a new hope for intracerebral hemorrhage: from bench to clinical trials.
Topics: Animals; Cerebral Hemorrhage; Chemotherapy, Adjuvant; Deferoxamine; Disease Models, Animal; Hemoglob | 2009 |
Deferoxamine mesylate: a new hope for intracerebral hemorrhage: from bench to clinical trials.
Topics: Animals; Cerebral Hemorrhage; Chemotherapy, Adjuvant; Deferoxamine; Disease Models, Animal; Hemoglob | 2009 |
Deferoxamine mesylate: a new hope for intracerebral hemorrhage: from bench to clinical trials.
Topics: Animals; Cerebral Hemorrhage; Chemotherapy, Adjuvant; Deferoxamine; Disease Models, Animal; Hemoglob | 2009 |
Deferoxamine mesylate: a new hope for intracerebral hemorrhage: from bench to clinical trials.
Topics: Animals; Cerebral Hemorrhage; Chemotherapy, Adjuvant; Deferoxamine; Disease Models, Animal; Hemoglob | 2009 |
Deferoxamine mesylate: a new hope for intracerebral hemorrhage: from bench to clinical trials.
Topics: Animals; Cerebral Hemorrhage; Chemotherapy, Adjuvant; Deferoxamine; Disease Models, Animal; Hemoglob | 2009 |
Parkinson's disease and free radicals. Mechanism of neurodegeneration and neuroprotection.
Topics: Corpus Striatum; Deferoxamine; Free Radicals; Humans; Hydroxyl Radical; Nerve Degeneration; Neurons; | 1996 |
Can the controversy of the role of aluminum in Alzheimer's disease be resolved? What are the suggested approaches to this controversy and methodological issues to be considered?
Topics: Aluminum; Alzheimer Disease; Amyloid beta-Protein Precursor; Animals; Deferoxamine; Environmental Ex | 1996 |
Desferrioxamine and vitamin E protect against iron and MPTP-induced neurodegeneration in mice.
Topics: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; 3,4-Dihydroxyphenylacetic Acid; Animals; Brain Disease | 1997 |
17 other studies available for deferoxamine and Nerve Degeneration
Article | Year |
---|---|
Analogues of desferrioxamine B designed to attenuate iron-mediated neurodegeneration: synthesis, characterisation and activity in the MPTP-mouse model of Parkinson's disease.
Topics: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Animals; Antioxidants; Ascorbic Acid; Benzothiazoles; | 2017 |
Deferoxamine Alleviates Iron Overload and Brain Injury in a Rat Model of Brainstem Hemorrhage.
Topics: Animals; Brain Stem Hemorrhage, Traumatic; Chelating Agents; Collagenases; Deferoxamine; Heme Oxygen | 2019 |
Combination of deferoxamine and erythropoietin: therapy for hypoxia-ischemia-induced brain injury in the neonatal rat?
Topics: Animals; Animals, Newborn; Anti-Inflammatory Agents; Antioxidants; Brain Infarction; Caspase 3; Cere | 2009 |
Iron is a potential key mediator of glutamate excitotoxicity in spinal cord motor neurons.
Topics: Analysis of Variance; Animals; Aspartic Acid; Cation Transport Proteins; Deferoxamine; Ferritins; Gl | 2009 |
Neuroprotection of desferrioxamine in lipopolysaccharide-induced nigrostriatal dopamine neuron degeneration.
Topics: Animals; Behavior, Animal; Deferoxamine; Dopaminergic Neurons; Iron; Lipopolysaccharides; Male; Mice | 2012 |
Iron--potential therapeutic target in hemorrhagic stroke.
Topics: Cerebral Hemorrhage; Deferoxamine; Humans; Iron; Iron Chelating Agents; Nerve Degeneration; Stroke | 2013 |
Preventative effect of deferoxamine on degenerative changes in the optic nerve in experimental retrobulbar haematoma.
Topics: Animals; Deferoxamine; Disease Models, Animal; Hematoma; Iron Chelating Agents; Nerve Degeneration; | 2003 |
Stimulation of G-proteins in human control and Alzheimer's disease brain by FAD mutants of APP(714-723): implication of oxidative mechanisms.
Topics: Aged; Alzheimer Disease; Amyloid beta-Protein Precursor; Antioxidants; Cell Membrane; Cerebral Corte | 2005 |
Neuroprotection by iron chelator against proteasome inhibitor-induced nigral degeneration.
Topics: Acetylcysteine; Animals; Deferoxamine; Iron Chelating Agents; Male; Mice; Mice, Inbred C57BL; Nerve | 2005 |
Inhibition of brain creatine kinase activity after renal ischemia is attenuated by N-acetylcysteine and deferoxamine administration.
Topics: Acetylcysteine; Animals; Antioxidants; Brain; Brain Diseases, Metabolic; Creatine Kinase; Deferoxami | 2008 |
Desferoxamine preconditioning protects against cerebral ischemia in rats by inducing expressions of hypoxia inducible factor 1 alpha and erythropoietin.
Topics: Animals; Brain Ischemia; Cells, Cultured; Cerebral Infarction; Deferoxamine; Disease Models, Animal; | 2008 |
Quantitative evaluation of Al maltolate-induced neurodegeneration with subsequent Al removal by desferrioxamine treatment.
Topics: Aluminum; Animals; Chelating Agents; Deferoxamine; Male; Nerve Degeneration; Organometallic Compound | 1995 |
Partial reversal of aluminium-induced neurofibrillary degeneration by desferrioxamine in adult male rabbits.
Topics: Aluminum Compounds; Animals; Brain Diseases; Deferoxamine; Histocytochemistry; Injections, Intravent | 1994 |
Apparent role of hydroxyl radicals in oxidative brain injury induced by sodium nitroprusside.
Topics: Animals; Ascorbic Acid; Brain Injuries; Deferoxamine; Hydrogen Peroxide; Hydroxyl Radical; In Vitro | 1998 |
Oxidative stress and hypoxia-like injury cause Alzheimer-type molecular abnormalities in central nervous system neurons.
Topics: Alzheimer Disease; Animals; Apoptosis; Cell Division; Cell Hypoxia; Cell Survival; Cells, Cultured; | 2000 |
Platelet-activating factor enhances the expression of vascular endothelial growth factor in normal human astrocytes.
Topics: Anti-Inflammatory Agents; Astrocytes; Brain; Cells, Cultured; Cycloheximide; Deferoxamine; Dexametha | 2002 |
The iron chelator desferrioxamine (Desferal) retards 6-hydroxydopamine-induced degeneration of nigrostriatal dopamine neurons.
Topics: 3,4-Dihydroxyphenylacetic Acid; Animals; Deferoxamine; Dopamine; Homovanillic Acid; Hydroxydopamines | 1991 |