xjb-5-131 and Weight-Loss

xjb-5-131 has been researched along with Weight-Loss* in 2 studies

Other Studies

2 other study(ies) available for xjb-5-131 and Weight-Loss

Article	Year
Mitochondrial targeting of XJB-5-131 attenuates or improves pathophysiology in HdhQ150 animals with well-developed disease phenotypes. Human molecular genetics, 2016, 05-01, Volume: 25, Issue:9 Oxidative damage to mitochondria (MT) is a major mechanism for aging and neurodegeneration. We have developed a novel synthetic antioxidant, XJB-5-131, which directly targets MT, the primary site and primary target of oxidative damage. XJB-5-131 prevents the onset of motor decline in an HdhQ(150/150) mouse model for Huntington's disease (HD) if treatment starts early. Here, we report that XJB-5-131 attenuates or reverses disease progression if treatment occurs after disease onset. In animals with well-developed pathology, XJB-5-131 promotes weight gain, prevents neuronal death, reduces oxidative damage in neurons, suppresses the decline of motor performance or improves it, and reduces a graying phenotype in treated HdhQ(150/150) animals relative to matched littermate controls. XJB-5-131 holds promise as a clinical candidate for the treatment of HD. Topics: Animals; Behavior, Animal; Cells, Cultured; Cyclic N-Oxides; Disease Models, Animal; Huntington Disease; Mice; Mice, Inbred C57BL; Mitochondria; Motor Activity; Neurons; Oxidative Stress; Weight Loss	2016
Targeting of XJB-5-131 to mitochondria suppresses oxidative DNA damage and motor decline in a mouse model of Huntington's disease. Cell reports, 2012, Nov-29, Volume: 2, Issue:5 Oxidative damage and mitochondrial dysfunction are implicated in aging and age-related neurodegenerative diseases, including Huntington's disease (HD). Many naturally occurring antioxidants have been tested for their ability to correct for deleterious effects of reactive oxygen species, but often they lack specificity, are tissue variable, and have marginal efficacy in human clinical trials. To increase specificity and efficacy, we have designed a synthetic antioxidant, XJB-5-131, to target mitochondria. We demonstrate in a mouse model of HD that XJB-5-131 has remarkably beneficial effects. XJB-5-131 reduces oxidative damage to mitochondrial DNA, maintains mitochondrial DNA copy number, suppresses motor decline and weight loss, enhances neuronal survival, and improves mitochondrial function. The findings poise XJB-5-131 as a promising therapeutic compound. Topics: Animals; Antioxidants; Cell Survival; Cells, Cultured; Cyclic N-Oxides; Disease Models, Animal; DNA Damage; DNA, Mitochondrial; Gene Dosage; Huntington Disease; Mice; Mice, Inbred C57BL; Mitochondria; Motor Activity; Neurons; Oxidative Stress; Weight Loss	2012

Article

Year

Mitochondrial targeting of XJB-5-131 attenuates or improves pathophysiology in HdhQ150 animals with well-developed disease phenotypes.

Human molecular genetics, 2016, 05-01, Volume: 25, Issue:9

Oxidative damage to mitochondria (MT) is a major mechanism for aging and neurodegeneration. We have developed a novel synthetic antioxidant, XJB-5-131, which directly targets MT, the primary site and primary target of oxidative damage. XJB-5-131 prevents the onset of motor decline in an HdhQ(150/150) mouse model for Huntington's disease (HD) if treatment starts early. Here, we report that XJB-5-131 attenuates or reverses disease progression if treatment occurs after disease onset. In animals with well-developed pathology, XJB-5-131 promotes weight gain, prevents neuronal death, reduces oxidative damage in neurons, suppresses the decline of motor performance or improves it, and reduces a graying phenotype in treated HdhQ(150/150) animals relative to matched littermate controls. XJB-5-131 holds promise as a clinical candidate for the treatment of HD.

Topics: Animals; Behavior, Animal; Cells, Cultured; Cyclic N-Oxides; Disease Models, Animal; Huntington Disease; Mice; Mice, Inbred C57BL; Mitochondria; Motor Activity; Neurons; Oxidative Stress; Weight Loss

2016

Targeting of XJB-5-131 to mitochondria suppresses oxidative DNA damage and motor decline in a mouse model of Huntington's disease.

Cell reports, 2012, Nov-29, Volume: 2, Issue:5

Oxidative damage and mitochondrial dysfunction are implicated in aging and age-related neurodegenerative diseases, including Huntington's disease (HD). Many naturally occurring antioxidants have been tested for their ability to correct for deleterious effects of reactive oxygen species, but often they lack specificity, are tissue variable, and have marginal efficacy in human clinical trials. To increase specificity and efficacy, we have designed a synthetic antioxidant, XJB-5-131, to target mitochondria. We demonstrate in a mouse model of HD that XJB-5-131 has remarkably beneficial effects. XJB-5-131 reduces oxidative damage to mitochondrial DNA, maintains mitochondrial DNA copy number, suppresses motor decline and weight loss, enhances neuronal survival, and improves mitochondrial function. The findings poise XJB-5-131 as a promising therapeutic compound.

Topics: Animals; Antioxidants; Cell Survival; Cells, Cultured; Cyclic N-Oxides; Disease Models, Animal; DNA Damage; DNA, Mitochondrial; Gene Dosage; Huntington Disease; Mice; Mice, Inbred C57BL; Mitochondria; Motor Activity; Neurons; Oxidative Stress; Weight Loss

2012