ArticleScientific reports2018
Copper(I)-binding properties of de-coppering drugs for the treatment of Wilson disease. α-Lipoic acid as a potential anti-copper agent.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 71 citations in OpenAlex.
- Revolutionizing breast cancer treatment: Harnessing the related mechanisms and drugs for regulated cell death (Review).International journal of oncology · 2024Pooled it
- Evaluation of the protective roles of alpha-lipoic acid supplementation on nanomaterial-induced toxicity: A meta-analysis ofFrontiers in nutrition · 2022Pooled it
- Effect of tiomolibdate choline on copper balance in patients with Wilson disease: An open-label phase 2 trial.Hepatology communications · 2026Trial
- Systemic Copper Chelation Reduces Collagen Deposition and Preserves Secretory Function in Irradiated Mouse Salivary Glands.Advances in radiation oncology · 2026Article
- Distinct Effects of Copper Ionophores on Intracellular Copper and Cell Viability in Wild-Type and CTR1-Deficient SH-SY5Y Cells.ACS omega · 2026Article
- Copper homeostasis and cuproptosis: molecular mechanisms and therapeutic opportunities.Molecular biomedicine · 2026Review
- Functional partitioning of lipoic acid decouples cellular abundance from mitochondrial utilization.bioRxiv : the preprint server for biology · 2026Article
- Copper ionophore elicits calpain-dependent paraptosis coincident with proteotoxic stress.Cell communication and signaling : CCS · 2025Article
- Rapid transcellular hepatic copper depletion by ARBM-101 rescues severe liver damage in Wilson disease rodents.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Leveraging Vulnerabilities in Copper Trafficking for Synergistic Antifungal Activity.ACS chemical biology · 2025Article
- Engineering Inorganic Nanoparticles to Induce Cuproptosis: A New Strategy for Cancer Therapy.Pharmaceutics · 2025Review
- TDMQ20 as A Drug Candidate for Wilson's Disease: Comparison with D-Penicillamine, Trientine, and Tetrathiomolybdate In Vitro and In Mice.Pharmaceutics · 2025Article
- Generative Landscapes and Dynamics to Design Functional Multidomain Artificial Transmembrane Transporters.ACS central science · 2025Article
- Modulation of copper-induced neurotoxicity by monoisoamyl 2,3-dimercaptosuccinic acid loaded nanoparticles through inhibition of mitophagy and reduction of oxidative stress in SH-SY5Y cells.Toxicology reports · 2025Article
- Comparative review of copper-associated chronic hepatitis in dogs and Wilson disease in humans.Frontiers in veterinary science · 2025Review
- Copper Dyshomeostasis and Diabetic Complications: Chelation Strategies for Management.Mini reviews in medicinal chemistry · 2025Review
- Cuproptosis-related genes and agents: implications in tumor drug resistance and future perspectives.Frontiers in pharmacology · 2025Review
- TRPM7 contributes to pyroptosis and its involvement in status epilepticus.Journal of neuroinflammation · 2024Article
- Mitochondrial copper overload promotes renal fibrosis via inhibiting pyruvate dehydrogenase activity.Cellular and molecular life sciences : CMLS · 2024Article
- α-Lipoic acid: a potential regulator of copper metabolism in Alzheimer's disease.Frontiers in molecular biosciences · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wilson disease is an autosomal recessive genetic disorder caused by loss-of-function mutations in the P-type copper ATPase, ATP7B, which leads to toxic accumulation of copper mainly in the liver and brain. Wilson disease is treatable, primarily by copper-chelation therapy, which promotes copper excretion. Although several de-coppering drugs are currently available, their Cu(I)-binding affinities have not been quantitatively characterized. Here we determined the Cu(I)-binding affinities of five major de-coppering drugs - D-penicillamine, trientine, 2,3-dimercapto-1-propanol, meso-2,3-dimercaptosuccinate and tetrathiomolybdate - by exploring their ability to extract Cu(I) ions from two Cu(I)-binding proteins, the copper chaperone for cytochrome c oxidase, Cox17, and metallothionein. We report that the Cu(I)-binding affinity of these drugs varies by four orders of magnitude and correlates positively with the number of sulfur atoms in the drug molecule and negatively with the number of atoms separating two SH groups. Based on the analysis of structure-activity relationship and determined Cu(I)-binding affinity, we hypothesize that the endogenous biologically active substance, α-lipoic acid, may be suitable for the treatment of Wilson disease. Our hypothesis is supported by cell culture experiments where α-lipoic acid protected hepatic cells from copper toxicity. These results provide a basis for elaboration of new generation drugs that may provide better therapeutic outcomes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.