Literature DB >> 25062731

An independent study of the preclinical efficacy of C2-8 in the R6/2 transgenic mouse model of Huntington's disease.

Nan Wang1, Xiao-Hong Lu1, Susana V Sandoval1, X William Yang1.   

Abstract

BACKGROUND: C2-8 is a small molecule inhibitor of polyglutamine aggregation and can reduce photoreceptor neurodegeneration in a Drosophila model of Huntington's disease (HD). Further preclinical studies have shown that oral administration of C2-8 in R6/2 HD transgenic mice can penetrate into the brain, reduce mHTT-exon1 aggregation, improve motor performance and diminish striatal neuron atrophy.
OBJECTIVE: In this independent preclinical study, we aimed to evaluate the pharmacokinetic properties and therapeutic efficacy of C2-8 intraperitoneal (IP) delivery in the R6/2 HD mouse.
METHODS: R6/2 mice were IP injected with low dose C2-8 (10 mg/kg), high dose C2-8 (20 mg/kg), or vehicle twice daily from 3 weeks to 3 months old. Longitudinal behavioral tests (accelerating Rotarod and wire-hang) were performed to evaluate the motor deficits, and neuropathology was measured by unbiased stereology.
RESULTS: We confirmed that the compound has good blood-brain-barrier penetration after acute or sub-chronic intraperitoneal delivery. Chronic treatment with C2-8 in R6/2 mice results in a significant reduction of nuclear mHTT aggregate volume in the brains, replicating a key finding of C2-8 as a polyglutamine aggregation inhibitor in vivo. However, by comparing HD mice with C2-8 treatment to those with vehicle treatment, we were unable to demonstrate significant amelioration of motor deficits using Rotarod and wire-hang tests. Moreover, we did not observe improvement in the striatal neurodegenerative pathology, as measured by brain weight, striatal volume, and striatal neuron volume in the C2-8 treated R6/2 mice.
CONCLUSIONS: Our study supports the practice of independent preclinical studies for novel molecules in HD therapeutic development and suggests that the use of alternative delivery strategies and full-length HD mouse models are likely needed to further assess whether the aggregate-inhibiting properties of C2-8 can be consistently translated into a preclinical benefit in HD mice.

Entities:  

Keywords:  C2-8; Huntington's disease; R6/2; aggregate; huntingtin; preclinical

Mesh:

Substances:

Year:  2013        PMID: 25062731      PMCID: PMC4124458          DOI: 10.3233/JHD-130074

Source DB:  PubMed          Journal:  J Huntingtons Dis        ISSN: 1879-6397


  13 in total

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2.  Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death.

Authors:  Montserrat Arrasate; Siddhartha Mitra; Erik S Schweitzer; Mark R Segal; Steven Finkbeiner
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3.  A potent small molecule inhibits polyglutamine aggregation in Huntington's disease neurons and suppresses neurodegeneration in vivo.

Authors:  Xiaoqian Zhang; Donna L Smith; Anatoli B Meriin; Sabine Engemann; Deborah E Russel; Margo Roark; Shetia L Washington; Michele M Maxwell; J Lawrence Marsh; Leslie Michels Thompson; Erich E Wanker; Anne B Young; David E Housman; Gillian P Bates; Michael Y Sherman; Aleksey G Kazantsev
Journal:  Proc Natl Acad Sci U S A       Date:  2005-01-10       Impact factor: 11.205

4.  A small-molecule therapeutic lead for Huntington's disease: preclinical pharmacology and efficacy of C2-8 in the R6/2 transgenic mouse.

Authors:  Vanita Chopra; Jonathan H Fox; Greg Lieberman; Kathryn Dorsey; Wayne Matson; Peter Waldmeier; David E Housman; Aleksey Kazantsev; Anne B Young; Steven Hersch
Journal:  Proc Natl Acad Sci U S A       Date:  2007-10-09       Impact factor: 11.205

5.  Ataxin-1 nuclear localization and aggregation: role in polyglutamine-induced disease in SCA1 transgenic mice.

Authors:  I A Klement; P J Skinner; M D Kaytor; H Yi; S M Hersch; H B Clark; H Y Zoghbi; H T Orr
Journal:  Cell       Date:  1998-10-02       Impact factor: 41.582

Review 6.  Huntington's disease: revisiting the aggregation hypothesis in polyglutamine neurodegenerative diseases.

Authors:  Ray Truant; Randy Singh Atwal; Carly Desmond; Lise Munsie; Thu Tran
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7.  Huntingtin acts in the nucleus to induce apoptosis but death does not correlate with the formation of intranuclear inclusions.

Authors:  F Saudou; S Finkbeiner; D Devys; M E Greenberg
Journal:  Cell       Date:  1998-10-02       Impact factor: 41.582

8.  Full-length human mutant huntingtin with a stable polyglutamine repeat can elicit progressive and selective neuropathogenesis in BACHD mice.

Authors:  Michelle Gray; Dyna I Shirasaki; Carlos Cepeda; Véronique M André; Brian Wilburn; Xiao-Hong Lu; Jifang Tao; Irene Yamazaki; Shi-Hua Li; Yi E Sun; Xiao-Jiang Li; Michael S Levine; X William Yang
Journal:  J Neurosci       Date:  2008-06-11       Impact factor: 6.167

9.  Systematic behavioral evaluation of Huntington's disease transgenic and knock-in mouse models.

Authors:  Liliana Menalled; Bassem F El-Khodor; Monica Patry; Mayte Suárez-Fariñas; Samantha J Orenstein; Benjamin Zahasky; Christina Leahy; Vanessa Wheeler; X William Yang; Marcy MacDonald; A Jennifer Morton; Gill Bates; Janet Leeds; Larry Park; David Howland; Ethan Signer; Allan Tobin; Daniela Brunner
Journal:  Neurobiol Dis       Date:  2009-05-21       Impact factor: 5.996

10.  Comprehensive behavioral and molecular characterization of a new knock-in mouse model of Huntington's disease: zQ175.

Authors:  Liliana B Menalled; Andrea E Kudwa; Sam Miller; Jon Fitzpatrick; Judy Watson-Johnson; Nicole Keating; Melinda Ruiz; Richard Mushlin; William Alosio; Kristi McConnell; David Connor; Carol Murphy; Steve Oakeshott; Mei Kwan; Jose Beltran; Afshin Ghavami; Dani Brunner; Larry C Park; Sylvie Ramboz; David Howland
Journal:  PLoS One       Date:  2012-12-20       Impact factor: 3.240

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Review 2.  Protein Aggregation Inhibitors as Disease-Modifying Therapies for Polyglutamine Diseases.

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Journal:  Front Neurosci       Date:  2021-02-12       Impact factor: 4.677

Review 3.  Yeast Models for Amyloids and Prions: Environmental Modulation and Drug Discovery.

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