Alda-1 is a potent and selective ALDH2 agonist, which activates wild-type ALDH2 and restores near wild-type activity to ALDH2*2.

Alda-1 treatment results in a significant decrease of 4-HNE-protein content in the plasma of apoE^−/− mice. Alda-1 administration leads to a slight increase in gene expression related to neurogenesis (Nog), mitochondrial biogenesis (CYTB, ND1), and apoptosis (Bax, Gsk3b) in the Hp of apoE^−/− mice. Alda-1 administration leads to 2 and 10 differentially expressed proteins in the FCx and Hp of apoE^−/− mice, respectively.
Alda-1 (1.5 mg/kg, b.w., IP) administration significantly increases the climbing time, tends to reduce the immobility time and increases the swimming time of the prenatally stressed rats in the forced swim test. Moreover, treatment of prenatally stressed rats with Alda-1 significantly increases number of entries into the open arms of the maze and the time spent therein, as assessed by elevated plus-maze test. Alda-1 (8.5 mg/kg; IP) with glucose significantly lowers 4-HNE and FJB-positive cells in the cerebral cortex of Alda-1-treated rats than in DMSO-treated rats 24 h after glucose administration.
Alda-1 (10 mg/kg per day) treatment prevents aldehydic overload, mitochondrial dysfunction and improves ventricular function in post-MI cardiomyopathy rats^[4].

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

Alda-1 treatment results in a significant decrease of 4-HNE-protein content in the plasma of apoE^−/− mice. Alda-1 administration leads to a slight increase in gene expression related to neurogenesis (Nog), mitochondrial biogenesis (CYTB, ND1), and apoptosis (Bax, Gsk3b) in the Hp of apoE^−/− mice. Alda-1 administration leads to 2 and 10 differentially expressed proteins in the FCx and Hp of apoE^−/− mice, respectively.
Alda-1 (1.5 mg/kg, b.w., IP) administration significantly increases the climbing time, tends to reduce the immobility time and increases the swimming time of the prenatally stressed rats in the forced swim test. Moreover, treatment of prenatally stressed rats with Alda-1 significantly increases number of entries into the open arms of the maze and the time spent therein, as assessed by elevated plus-maze test. Alda-1 (8.5 mg/kg; IP) with glucose significantly lowers 4-HNE and FJB-positive cells in the cerebral cortex of Alda-1-treated rats than in DMSO-treated rats 24 h after glucose administration.
Alda-1 (10 mg/kg per day) treatment prevents aldehydic overload, mitochondrial dysfunction and improves ventricular function in post-MI cardiomyopathy rats^[4].

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

• . Stachowicz A, et al. Proteomic Analysis of Mitochondria-Enriched Fraction Isolated from the Frontal Cortex and Hippocampus of Apolipoprotein E Knockout Mice Treated with Alda-1, an Activator of Mitochondrial Aldehyde Dehydrogenase (ALDH2). Int J Mol Sci.  [Content Brief]

  . Stachowicz A, et al. The impact of mitochondrial aldehyde dehydrogenase (ALDH2) activation by Alda-1 on the behavioral and biochemical disturbances in animal model of depression. Brain Behav Immun. 2016 Jan;51:144-53.  [Content Brief]

  . Ikeda T, et al. Effects of Alda-1, an Aldehyde Dehydrogenase-2 Agonist, on Hypoglycemic Neuronal Death. PLoS One. 2015 Jun 17;10(6):e0128844.  [Content Brief]

  [4]. Gomes KM, et al. Aldehydic load and aldehyde dehydrogenase 2 profile during the progression of post-myocardial infarction cardiomyopathy: benefits of Alda-1. Int J Cardiol. 2015 Jan 20;179:129-138.  [Content Brief]