ArticleMolecular genetics and metabolism
A rapid, noninvasive immunoassay for frataxin: utility in assessment of Friedreich ataxia.
Article in Molecular genetics and metabolism. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 5 registered trials, which are not on this map. Cited by 63 papers.
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.
A Study to Determine the Range of Tissue Frataxin Concentrations and Other Potential Biomarkers for Friedreich's Ataxia in Normal Healthy Volunteers
A Phase 2, Randomized, Double-Blind, Placebo-Controlled, Dose Exploration Study to Assess the Safety, Pharmacokinetics, and Pharmacodynamics of Subcutaneous CTI-1601 in Adult Subjects With Friedreich's Ataxia
An Open-Label Extension Study to Assess the Long-Term Safety, Efficacy, Pharmacodynamics, Pharmacokinetics, and Tolerability of Subcutaneous CTI-1601 in Subjects With Friedreich's Ataxia
A Phase 1 Study to Assess the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of Subcutaneous Nomlabofusp in Adolescents and Children With Friedreich's Ataxia
A Phase 3 Randomized, Double-Blind, Placebo-Controlled, Multicenter Study to Evaluate the Efficacy and Safety of Subcutaneous Nomlabofusp in Subjects With Friedreich's Ataxia
Who cites it
63 citing papers in PubMed, 103 citations in OpenAlex.
- Safety, pharmacokinetics, and pharmacodynamics of nomlabofusp (CTI-1601) in Friedreich's ataxia.Annals of clinical and translational neurology · 2024Trial
- Randomized, double-blind, placebo-controlled study of interferon-Annals of clinical and translational neurology · 2019Trial
- Advances in Gene and Cellular Therapy in Friedreich Ataxia.Molecular diagnosis & therapy · 2026Review
- Transcription and cohesin direct domain boundary spatial positioning and are linked to Friedreich's ataxia.Molecular cell · 2026Article
- Nomlabofusp Treatment Produces Frataxin Levels That Correlate Across Peripheral Tissues: Preclinical and Clinical Support for Surrogate Tissue Sampling.Clinical and translational science · 2026Article
- Peripheral frataxin levels govern long-term clinical progression in Friedreich ataxia.BMJ neurology open · 2026Article
- Nomlabofusp, a Fusion Protein of Human Frataxin and a Cell Penetrant Peptide, Delivers Mature and Functional Frataxin into Mitochondria.The AAPS journal · 2025Article
- Anatomical and functional analysis of the corticospinal tract in an FRDA mouse model.bioRxiv : the preprint server for biology · 2024Article
- Phenotypic variation of FXN compound heterozygotes in a Friedreich ataxia cohort.Annals of clinical and translational neurology · 2024Article
- Frataxin analysis using triple quadrupole mass spectrometry: application to a large heterogeneous clinical cohort.Journal of neurology · 2024Article
- METTL17 is an Fe-S cluster checkpoint for mitochondrial translation.Molecular cell · 2024Article
- Insights into the effects of Friedreich ataxia on the left ventricle using T1 mapping and late gadolinium enhancement.PloS one · 2024Article
- Long non-coding RNABrain communications · 2024Article
- A peptide derived from TID1S rescues frataxin deficiency and mitochondrial defects in FRDA cellular models.Frontiers in pharmacology · 2024Article
- Novel intragenic deletion within the FXN gene in a patient with typical phenotype of Friedreich ataxia: may be more prevalent than we think?BMC medical genomics · 2023Article
- Patient-derived iPSC models of Friedreich ataxia: a new frontier for understanding disease mechanisms and therapeutic application.Translational neurodegeneration · 2023Review
- Neurobehavioral deficits of mice expressing a low level of G127V mutant frataxin.Neurobiology of disease · 2023Article
- Clinical Evidence for Variegated Silencing in Patients With Friedreich Ataxia.Neurology. Genetics · 2022Article
- Simultaneous Quantification of Mitochondrial Mature Frataxin and Extra-Mitochondrial Frataxin Isoform E in Friedreich's Ataxia Blood.Frontiers in neuroscience · 2022Article
- Friedreich's Ataxia Frequency in a Large Cohort of Genetically Undetermined Ataxia Patients.Frontiers in neurology · 2021Article
3 more citing papers are in PubMed but not listed here.
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 3 institutions in 1 country.
Funding
Abstract
Friedreich ataxia (FRDA) is an autosomal recessive neurodegenerative disorder caused by reduced amounts of the mitochondrial protein frataxin. Frataxin levels in research studies are typically measured via Western blot analysis from patient fibroblasts, lymphocytes, or muscle biopsies; none of these is ideal for rapid detection in large scale clinical studies. Recently, a rapid, noninvasive lateral flow immunoassay was developed to accurately measure picogram levels of frataxin protein and shown to distinguish lymphoblastoid cells from FRDA carriers, patients and controls. We expanded the immunoassay to measure frataxin directly in buccal cells and whole blood from a large cohort of controls, known carriers and patients typical of a clinical trial population. The assay in buccal cells shared a similar degree of variability with previous studies conducted in lymphoblastoid cells (~10% coefficient of variation in controls). Significant differences in frataxin protein quantity were seen between the mean group values of controls, carriers, and patient buccal cells (100, 50.2, and 20.9% of control, respectively) and in protein extracted from whole blood (100, 75.3, and 32.2%, respectively), although there was some overlap between the groups. In addition, frataxin levels were inversely related to GAA repeat length and correlated directly with age of onset. Subjects with one expanded GAA repeat and an identified frataxin point mutation also carried frataxin levels in the disease range. Some patients displaying an FRDA phenotype but carrying only a single identifiable mutation had frataxin levels in the FRDA patient range. One patient from this group has a novel deletion that included exons 2 and 3 of the FXN gene based on multiplex ligation-dependent probe amplification (MLPA) analysis of the FXN gene. The lateral flow immunoassay may be a useful means to noninvasively assess frataxin levels repetitively with minimal discomfort in FRDA patients in specific situations such as clinical trials, and as a complementary diagnostic tool to aid in identification and characterization of atypical patients.
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.