Alda 1 - CAS 349438-38-6
Catalog number: 349438-38-6
Category: Inhibitor
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Molecular Formula:
C15H11Cl2NO3
Molecular Weight:
324.16
COA:
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Targets:
Aldehyde dehydrogenase (ALDH)
Description:
ALDH2 is the activator of both the wild-type ALDH2*1 and the asian E487K mutant ALDH2*2 forms of mitochondrial aldehyde dehydrogenase 2 (mtALDH2).
Purity:
≥98%
Appearance:
White Solid
Synonyms:
N-(1,3-Benzodioxol-5-ylmethyl)-2,6-dichlorobenzamide;
Solubility:
Soluble in DMSO
Storage:
Store at 2-8 °C
MSDS:
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Application:
Activator of aldehyde dehydrogenase 2 (ALDH2).
Quality Standard:
Enterprise Standard
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Quantity:
Milligrams-Grams
InChIKey:
FQUAFMNPXPXOJE-UHFFFAOYSA-N
InChI:
1S/C16H19NO3S/c1-11-9-12(2)16(13(3)10-11)17-21(18,19)15-7-5-14(20-4)6-8-15/h5-10,17H,1-4H3
Canonical SMILES:
COC1=CC=C(S(NC2=C(C)C=C(C)C=C2C)(=O)=O)C=C1
1.ALDH2 protects against alcoholic cardiomyopathy through a mechanism involving the p38 MAPK/CREB pathway and local renin-angiotensin system inhibition in cardiomyocytes.
Liu B;Zhang R;Wei S;Yuan Q;Xue M;Hao P;Xu F;Wang J;Chen Y Int J Cardiol. 2018 Apr 15;257:150-159. doi: 10.1016/j.ijcard.2017.11.094.
BACKGROUND: ;Angiotensin II (Ang II) in the local cardiac renin-angiotensin system (RAS) is closely associated with alcoholic cardiomyopathy (ACM). Inhibition of local cardiac RAS has great significance in the treatment of ACM. Although aldehyde dehydrogenase 2 (ALDH2) has been demonstrated to protect against ACM through detoxification of aldehydes, the precise mechanisms are largely unknown. In the present study, we determined whether ALDH2 improved cardiac damage by inhibiting the local RAS in ACM and investigated the related regulatory mechanisms.;METHODS AND RESULTS: ;Adult male mice were fed with 5% ethanol or a control diet for 2months, with or without the ALDH2 activator Alda-1. Heavy ethanol consumption induced cardiac damage, increased angiotensinogen (AGT) and Ang II and decreased myocardial ALDH2 activity in hearts. ALDH2 activation improved ethanol-induced cardiac damage and decreased AGT and Ang II in hearts. In vitro, ALDH2 activation or overexpression decreased AGT and Ang II in cultured cardiomyocytes treated with 400mmol/L ethanol for 24h. Furthermore, p38 MAP kinase (p38 MAPK)/cyclic adenosine monophosphate response element-binding protein (CREB) pathway activation by ethanol increased AGT and Ang II in cardiomyocytes.
2.Mitochondrial aldehyde dehydrogenase obliterates insulin resistance-induced cardiac dysfunction through deacetylation of PGC-1α.
Hu N;Ren J;Zhang Y Oncotarget. 2016 Nov 22;7(47):76398-76414. doi: 10.18632/oncotarget.11977.
Insulin resistance contributes to the high prevalence of type 2 diabetes mellitus, leading to cardiac anomalies. Emerging evidence depicts a pivotal role for mitochondrial injury in oxidative metabolism and insulin resistance. Mitochondrial aldehyde dehydrogenase (ALDH2) is one of metabolic enzymes detoxifying aldehydes although its role in insulin resistance remains elusive. This study was designed to evaluate the impact of ALDH2 overexpression on insulin resistance-induced myocardial damage and mechanisms involved with a focus on autophagy. Wild-type (WT) and transgenic mice overexpressing ALDH2 were fed sucrose or starch diet for 8 weeks and cardiac function and intracellular Ca2+ handling were assessed using echocardiographic and IonOptix systems. Western blot analysis was used to evaluate Akt, heme oxygenase-1 (HO-1), PGC-1α and Sirt-3. Our data revealed that sucrose intake provoked insulin resistance and compromised fractional shortening, cardiomyocyte function and intracellular Ca2+ handling (p < 0.05) along with unaltered cardiomyocyte size (p > 0.05), mitochondrial injury (elevated ROS generation, suppressed NAD+ and aconitase activity, p < 0.05 for all), the effect of which was ablated by ALDH2.
3.Alda‑1, an aldehyde dehydrogenase‑2 agonist, improves long‑term survival in rats with chronic heart failure following myocardial infarction.
Hua Y;Chen H;Zhao X;Liu M;Jin W;Yan W;Wu Y;Tan Z;Fan H;Wu Y;Xie L;Zhang W;Liu B;Zhou Y Mol Med Rep. 2018 Sep;18(3):3159-3166. doi: 10.3892/mmr.2018.9309. Epub 2018 Jul 24.
Alda‑1, an aldehyde dehydrogenase 2 (ALDH2) agonist, has been demonstrated to reduce injury caused by acute myocardial infarction (MI) and ischemia/reperfusion. The present study aimed to investigate whether oral administration of Alda‑1 improved long‑term survival of rats with chronic heart failure (CHF) post‑MI. MI model rats treated daily with Alda‑1 exhibited an increase in 20‑week survival rate compared with untreated MI rats. Alda‑1 treatment decreased the heart weight/body weight ratio, collagen volume, left ventricular (LV) internal diameter at the end of diastole and LV internal diameter at the end of systole, while increasing LV ejection fraction with evident LV fractional shortening. Myocardial cell apoptosis index, the activity of caspase‑3 and the expression of cleaved‑caspase‑3 were also reduced by Alda‑1 treatment. The protective effects of Alda‑1 were associated with reduced 4‑hydroxynonenal accumulation. The results of the present study revealed that the long‑term treatment with Alda‑1 prevented the progression of ventricular remodeling and improved the long‑term survival of rats with CHF post‑MI.
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CAS 349438-38-6 Alda 1

Alda 1
(CAS: 349438-38-6)

ALDH2 is the activator of both the wild-type ALDH2*1 and the asian E487K mutant ALDH2*2 forms of mitochondrial aldehyde dehydrogenase 2 (mtALDH2).

Chemical Structure

CAS 349438-38-6 Alda 1

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