On 16 July 2016 NeuroTau Inc. obtained US FDA orphan drug designation for tolfenamic acid in the treatment of Progressive Supranuclear Palsy (PSP)
On 17 February 2016, NeuroTau partner was granted orphan designation (EU/3/16/1613) by the European Commission for tolfenamic acid for the treatment of progressive supranuclear palsy.
On 16 July 2016 NeuroTau Inc. obtained US FDA orphan drug designation for tolfenamic acid in the treatment of Frontotemporal Dementia (FTD)
On 17 February 2016, NeuroTau Inc partner was granted orphan designation (EU/3/16/1614) by the European Commission for tolfenamic acid for the treatment of behavioural variant frontotemporal dementia.
NeuroTau Inc announces listing of its clinical trial “Evaluation of Tolfenamic Acid in Individuals with Progressive Supranuclear Palsy (PSP)” on ClinicalTrials.gov and intention to begin study in Q1/2021
This cancer paper tested various classes of NSAIDS and showed that fenamates have a unique independent mechanism of action that alters the levels of the SP family of transcription factors.
This manuscript demonstrated the first published role for a protective effect of fenamates in AD models.
The findings of these studies provide evidence that fenamates can penetrate the brain in sufficient quantities to have an impact on targets therein.
This study provides evidence for the ability of fenamates to improve cognitive function and alter amyloid biomarker levels over a short period of treatment via a mechanism that involves Sp1.
The data presented in this published work shows that fenamates can improve memory and reduce amyloid plaque burden levels in transgenic mouse models of AD.
This paper show that several clinically approved and widely used NSAIDs of the fenamate class are effective and selective inhibitors of the NLRP3 inflammasome via inhibition of the volume-regulated anion channel in macrophages, independently of COX enzymes.
In this study, treatment with tolfenamic acid improved spatial learning deficits and memory impairments in young and aged hTau mice along with reductions in total tau as well as in site specific hyperphosphorylation of tau. Furthermore immunohistochemical analysis for phosphorylated tau protein revealed reduced staining in the frontal cortex, hippocampus, and striatum in animals treated with TA.