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  • ||||||||||  J147 / Abrexa
    Preclinical, Journal:  J147 Reduces tPA-Induced Brain Hemorrhage in Acute Experimental Stroke in Rats. (Pubmed Central) -  Mar 23, 2022   
    Our results demonstrate that J147 treatment alone exerts cerebral cytoprotective effects in a suture model of acute ischemic stroke, while in an embolic stroke model co-administration of J147 with tPA reduces delayed tPA-induced intracerebral hemorrhage and confers cerebroprotection. These findings suggest that J147-tPA combination therapy could be a promising approach to improving the treatment of ischemic stroke.
  • ||||||||||  J147 / Abrexa
    Journal:  Activation of monoaminergic system contributes to the antidepressant- and anxiolytic-like effects of J147. (Pubmed Central) -  Feb 10, 2022   
    Moreover, J147-induced significant inhibition of monoamine oxidase A activity. These findings suggest that the antidepressant- and anxiolytic-like effects of J147 might be related to the monoaminergic system by the evidence that high dose of J147 inhibits monoamine oxidase (MAO)-A activity and increases synaptic monoamines in the mouse brain.
  • ||||||||||  J147 / Abrexa
    Journal:  Geroprotective effects of Alzheimer's disease drug candidates. (Pubmed Central) -  Jul 21, 2021   
    However, these two organs had distinct, tissue-specific protein level alterations that occurred with age, but in both cases, drug treatments restored a more youthful level. These data show that geroprotective AD drug candidates J147 and CMS121 prevent age-associated disease in both brain and kidney, and that their apparent mode of action in each tissue is distinct.
  • ||||||||||  J147 / Abrexa
    Journal:  Targeting of intracellular Ca stores as a therapeutic strategy against age-related neurotoxicities. (Pubmed Central) -  Feb 13, 2021   
    The molecular basis of these changes was then investigated in cell culture neurotoxicity assays that were the primary screen in the development of J147. Here we show that J147 and its molecular target, ATP synthase, regulate the maintenance of store-operated calcium entry (SOCE) and cell death during acute neurotoxicity.
  • ||||||||||  J147 / Abrexa
    Journal:  Targeting of intracellular Ca stores as a therapeutic strategy against age-related neurotoxicities. (Pubmed Central) -  Sep 5, 2020   
    The molecular basis of these changes was then investigated in cell culture neurotoxicity assays that were the primary screen in the development of J147. Here we show that J147 and its molecular target, ATP synthase, regulate the maintenance of store-operated calcium entry (SOCE) and cell death during acute neurotoxicity.
  • ||||||||||  J147 / Abrexa
    Trial completion, Trial primary completion date:  Study to Assess the Safety, Tolerability and Pharmacokinetics of Single Ascending Oral Doses of J147 (clinicaltrials.gov) -  Sep 2, 2020   
    P1,  N=64, Completed, 
    Here we show that J147 and its molecular target, ATP synthase, regulate the maintenance of store-operated calcium entry (SOCE) and cell death during acute neurotoxicity. Recruiting --> Completed | Trial primary completion date: Oct 2019 --> Feb 2020
  • ||||||||||  J147 / Abrexa
    Journal:  Elevating acetyl-CoA levels reduces aspects of brain aging. (Pubmed Central) -  May 15, 2020   
    CMS121 and J147 increased the levels of acetyl-CoA in cell culture and mice via the inhibition of acetyl-CoA carboxylase 1 (ACC1), resulting in neuroprotection and increased acetylation of histone H3K9 in SAMP8 mice, a site linked to memory enhancement. These data show that targeting specific metabolic aspects of the aging brain could result in treatments for dementia.
  • ||||||||||  J147 / Abrexa
    Journal:  The mitochondrial ATP synthase is a shared drug target for aging and dementia. (Pubmed Central) -  Sep 1, 2019   
    ...Here, we discover a novel molecular link between aging and dementia through the identification of the molecular target for the AD drug candidate J147...Our results link aging and age-associated dementia through ATP synthase, a molecular drug target that can potentially be exploited for the suppression of both. These findings demonstrate that novel screens for new AD drug candidates identify compounds that act on established aging pathways, suggesting an unexpectedly close molecular relationship between the two.