E-Mail Newly published papers further elucidate the mechanisms underlying pridopidine s neuroprotective properties through activation of the Sigma-1 Receptor (S1R). Pridopidine enhances mitochondrial function and reduces mHTT-induced ER stress, which are impaired in HD, mediated by the S1R. Three new peer-reviewed publications highlight pridopidine s therapeutic potential and provide data supporting the role of the S1R in neurodegenerative diseases
Prilenia Therapeutics B.V., a clinical stage biotech company focused on developing novel treatments for neurodegenerative and neurodevelopmental disorders, today announces the publication of three peer-reviewed journal articles, highlighting key aspects of the mechanism of action of its lead asset, pridopidine, and the importance of S1R activation as a mechanism to attenuate biological features of neurodegenerative diseases.
Swiss life sciences company Amazentis has combined Mitopure (urolithin A) with high protein to increase sports performance, recovery, and overall cellular health.
Background: Pulmonary arterial hypertension (PAH) is an incurable disease that urgently needs therapeutic approaches. Based on the therapeutic effects of fasudil and dichloroacetate (DCA) on PAH, we aimed to explore the effects and potential mechanism of a new salt, fasudil dichloroacetate (FDCA), in a SU5416 plus hypoxia (SuHx)-induced rat model of PAH.
Methods: The rat model of PAH was established by a single subcutaneous injection of SU5416 (20 mg/kg) followed by hypoxia (10% O
2) exposure for 3 weeks. FDCA (15, 45, or 135 mg/kg i.g. daily) or the positive control, bosentan (100 mg/kg i.g. daily), were administered from the first day after SU5416 injection. After 3-week hypoxia, hemodynamic parameters, and histological changes of the pulmonary arterial vessels and right ventricle (RV) were assessed. Additionally, in vitro, the effects of FDCA (50 μM), compared with equimolar doses of fasudil, DCA, or fasudil+DCA, on the proliferation, migration, and contraction of human pulmona