Alda-1

Research use only, not for human use.

A small-molecule activator of ALDH2.

A small-molecule activator of ALDH2, particularly effective activator of ALDH2*2 (EC50= 20 uM; increases the activity of the mutant, ALDH2*2 (11-fold); causes slight inhibition of GTN denitration and did not increase GTN-induced sGC activation in the presence of either variant; no effect on ADH1.

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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.

Alda-1 | Alda1 | Alda 1

Metabolic Enzyme/Protease

ALDH

ALDH2

Other Indications

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349438-38-6

324.1588

C15H11Cl2NO3

>98% (HPLC)

DMSO: ≥ 51 mg/mL

O=C(NCC1=CC=C(OCO2)C2=C1)C3=C(Cl)C=CC=C3Cl

Benzamide, N-(1,3-benzodioxol-5-ylmethyl)-2,6-dichloro-

(-20℃)

With Ice Pack

≥ 2 years