Most cited papers from AGADA Biosciences

AGADA Biosciences

What are the most cited papers from AGADA Biosciences?

The most cited paper from AGADA Biosciences is "Safety, Tolerability, and Efficacy of Viltolarsen in Boys With Duchenne Muscular Dystrophy Amenable to Exon 53 Skipping" (Paula R. Clemens, Vamshi K. Rao, Anne M. Connolly et al., 2020), with 275 citations. Next come "Genetic tool development in marine protists: emerging model organisms for experimental cell biology" (174) and "Vamorolone targets dual nuclear receptors to treat inflammation and dystrophic cardiomyopathy" (90).

Published TypeFieldAccessAuthors

Showing 24 of 24 papers. Every paper is listed.

Most cited papers, sortable by citations and release date
#	Paper
1	Safety, Tolerability, and Efficacy of Viltolarsen in Boys With Duchenne Muscular Dystrophy Amenable to Exon 53 Skipping Paula R. Clemens, Vamshi K. Rao, Anne M. Connolly et al. · JAMA Neurology Open access	26 May 2020	275
2	Genetic tool development in marine protists: emerging model organisms for experimental cell biology Drahomíra Faktorová et al. · Nature Methods Open access113 authors	6 Apr 2020	174
3	Vamorolone targets dual nuclear receptors to treat inflammation and dystrophic cardiomyopathy Christopher R. Heier, Qing Yuan Yu, Alyson A. Fiorillo et al. · Life Science Alliance Open access	Feb 2019	90
4	Ryanodine channel complex stabilizer compound S48168/ARM210 as a disease modifier in dystrophin‐deficient mdx mice: proof‐of‐concept study and independent validation of efficacy Roberta Francesca Capogrosso, Paola Mantuano, Kitipong Uaesoontrachoon et al. · The FASEB Journal Open access	2 Nov 2017	61
5	Human JAK1 gain of function causes dysregulated myelopoeisis and severe allergic inflammation Catherine M. Biggs et al. · JCI Insight Open access	21 Dec 2022	31
6	Mechanism of action and therapeutic route for a muscular dystrophy caused by a genetic defect in lipid metabolism Mahtab Tavasoli et al. · Nature Communications Open access	23 Mar 2022	30
7	Tyrosine kinase-mediated axial motility of basal cells revealed by intravital imaging Jeremy W. Roy, Bong-Ki Kim, Eric Hill et al. · Nature Communications Open access	12 Feb 2016	29
8	Osteopontin is linked with AKT, FoxO1, and myostatin in skeletal muscle cells Peter P. Nghiem, Joe N. Kornegay, Kitipong Uaesoontrachoon et al. · Muscle & Nerve Open access	26 Jul 2017	18
9	Biomarker-focused multi-drug combination therapy and repurposing trial in mdx mice Michael Ziemba, Molly Barkhouse, Kitipong Uaesoontrachoon et al. · PLoS ONE Open access	22 Feb 2021	14
10	Orthogonal Analysis of Dystrophin Protein and Mrna As A Surrogate Outcome for Drug Development Kitipong Uaesoontrachoon et al. · Biomarkers in Medicine Open access	5 Aug 2019	13
11	A mouse model of inherited choline kinase β-deficiency presents with specific cardiac abnormalities and a predisposition to arrhythmia Mahtab Tavasoli, Tiam Feridooni, Hirad A. Feridooni et al. · Journal of Biological Chemistry Open access	10 Feb 2022	11
12	Loss of calpain3b in Zebrafish, a Model of Limb-Girdle Muscular Dystrophy, Increases Susceptibility to Muscle Defects Due to Elevated Muscle Activity Sergey V. Prykhozhij, Lucía Cáceres, Kevin Ban et al. · Genes Open access	15 Feb 2023	9
13	The effect of IL-1β inhibitor canakinumab (Ilaris®) on IL-6 production in human skeletal muscle cells Anna Cordeiro, Fiorella Morales, Maria del Carmen Parquet et al. · PLoS ONE Open access	6 Mar 2025	8
14	Genome Editing in Zebrafish Using High-Fidelity Cas9 Nucleases: Choosing the Right Nuclease for the Task Sergey V. Prykhozhij, Anna Cordeiro, Lucía Cáceres et al. · Methods in molecular biology Book chapter	2020	7
15	Enhancing AAV-microdystrophin gene therapy after repeat dosing by blocking phagocytosis Rita Spathis, Deeva Robles Kuriplach, Sabrina Narvesen et al. · Frontiers in Immunology Open access	3 Mar 2025	6
16	Loss of Dnajc21 leads to cytopenia and altered nucleotide metabolism in zebrafish Sarada Ketharnathan, Sujata Pokharel, Sergey V. Prykhozhij et al. · Leukemia Open access	13 Aug 2024	6
17	Mechanistic analysis of MLKL-driven cell survival Peijia Jiang, Xiaoyang Liu, Mauricio J. Reginato et al. · Cell Death Discovery Open access	10 Jun 2026	0
18	Neurodevelopmental disease-causing variants in choline kinase CHKA gene couple phosphatidylcholine synthesis to oxidative stress damage and disease etiology Mahtab Tavasoli, Mariam Alkandari, Gabriel G. Dorighello et al. · Journal of Biological Chemistry Open access	26 Nov 2025	0
19	High mobility group box 1 (HMGB1) is a potential disease biomarker in cell and mouse models of Duchenne muscular dystrophy Rebecca A. Slick, Jessica R. P. Sutton, Margaret Haberman et al. · Biology Open Open access	19 Aug 2024	0
20	REGISTRIES AND CARE OF NEUROMUSCULAR DISORDERS A. Mullen, Kitipong Uaesoontrachoon, Sadish Srinivassane et al. · Neuromuscular Disorders	5 Sep 2018	0
21	DMD CLINICAL THERAPIES II P R Clemens, Vamshi K. Rao, Anne M. Connolly et al. · Neuromuscular Disorders	5 Sep 2018	0
22	Progression of a Muscular Dystrophy Due to a Genetic Defect in Membrane Synthesis is Driven by Large Changes in Neutral Lipid Metabolism Mahtab Tavasoli, Sarah Lahire, Stanislav Sokolenko et al. · Research Square PreprintOpen access	19 May 2021	0
23	DMD – ANIMAL MODELS & PRECLINICAL TREATMENT Heather Gordish‐Dressman, Kitipong Uaesoontrachoon, Alexandra MacKinnon et al. · Neuromuscular Disorders	28 Sep 2020	0
24	Success of preclinical drug trials using reliable and reproducible endpoints in mouse models of neuromuscular diseases Kanneboyina Nagaraju, A. Mullen, Alexandra MacKinnon et al. · Neuromuscular Disorders	12 Sep 2017	0

Citations are OpenAlex's own counts, from its 2026-09-23 snapshot, so the ranking can differ from Google Scholar or Web of Science. A paper is listed for an institution when any of its authors gave it as an affiliation; retracted papers and papers whose citation count cannot be traced to citing works are left out, and a preprint and the article it became are shown once. Release dates are OpenAlex's: where a source gave only a month or a year, that is what is shown. How the lists are chosen.