AD-9308
Based on 1 Customer Validation
AD-9308 is an orally active, highly selective aldehyde dehydrogenase 2 (ALDH2) activator. AD-9308 alleviates oxidative stress, improves mitochondrial function, restores cell viability, reduces renal tubular injury, fibrosis and inflammatory responses, reverses ventricular remodeling, restores the activities of Dicer and superoxide dismutase, inhibits the IL-6 signaling pathway, reduces the accumulation of 4-HNE-protein adducts, and improves glucose homeostasis. AD-9308 can be used in studies related to acrolein-induced kidney injury, diabetes, cardiomyopathy, heart failure, diet-induced obesity, fatty liver, insulin resistance and glucose intolerance.
For research use only. We do not sell to patients.
- CAS No.: 1804942-56-0
- Formula: C30H36FN3O5
- Molecular Weight:537.62
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Storage:
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
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ALDH2 |
IL-6 |
In Vitro
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J Aldh22/2 (Glu504Lys knock-in) (male, 6 weeks old, chronic oral acrolein-induced renal injury)[1]
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Dosage:20 mg/kg
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Administration:p.o.; daily; 12 consecutive weeks
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Result:Markedly reduced acrolein-induced increases in urine albumin-to-creatinine ratio (UACR) and blood urea nitrogen (BUN) levels.
Ameliorated acrolein-induced tubular damage including vacuolar degeneration, epithelial swelling, tubular dilation, and interstitial fibrosis.
Reversed acrolein-induced kidney GSH depletion, reduced acrolein-increased renal ferrous iron (Fe2+) accumulation, and lowered elevated renal malondialdehyde (MDA) levels.
Substantially attenuated acrolein-induced increases in renal acrolein-protein conjugates (Acr-PC), neutrophil gelatinase-associated lipocalin (NGAL), fibronectin, and alpha-smooth muscle actin (α-SMA) protein expression.
Reduced acrolein-induced upregulation of mRNA expression for tubular injury markers (NGAL, KIM-1) and pro-inflammatory cytokines (IL-6, TGF-β).
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Animal Model:C57BL6/J mice (8-week-old at study initiation; streptozotocin-induced hyperglycemia)[2]
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Dosage:60 mg/kg/day; 180 mg/kg/day
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Administration:p.o.; daily; ~4 months
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Result:Improved left ventricular diastolic function with significant linear trends for E/A ratio (p-for-trend = 0.0180), e’ wave velocity (p-for-trend = 0.0002), E/e’ ratio (p-for-trend = 0.0202), e’/a’ ratio (p-for-trend = 0.0019), and isovolumic relaxation time (p-for-trend = 0.0107).
Improved systolic function with significant linear trends for fractional shortening (p-for-trend = 0.0055), ejection fraction (p-for-trend = 0.0042), stroke volume (p-for-trend = 0.0006), cardiac output (p-for-trend = 0.0004), and s wave velocity (p-for-trend = 0.0167).
Mitigated reductions in interventricular septum thickness at end diastole (p-for-trend = 0.0022) and left ventricular mass (p-for-trend = 0.0015).
Reduced serum 4-hydroxy-2-nonenal (4-HNE) levels, cardiac tissue 4-HNE protein adducts, and cardiac heme oxygenase 1 (Ho-1) expression.
Enhanced cardiac ALDH2 enzymatic activity.
Reduced cardiac mRNA expression of fibrosis markers Tgf-β1 (p-for-trend < 0.0001), Ctgf (p-for-trend < 0.0001), Fsp1 (p-for-trend = 0.0026), Postn (p-for-trend = 0.0046), Fn-1 (p-for-trend = 0.0001), and Tgf-β2 (p-for-trend = 0.0004), as well as α-Sma (p-for-trend = 0.0367) and Col IV (p-for-trend = 0.0113) mRNA and protein deposition.
Reduced cardiac mRNA expression of inflammatory markers Il-1β (p-for-trend = 0.0010), Il-6 (p-for-trend = 0.0002), Infγ (p-for-trend = 0.0054), Mcp-1 (p-for-trend = 0.0047), Sap (p-for-trend = 0.0005), and Tnf-α (p-for-trend < 0.0001).
Increased cardiac Bcl-2 expression, reduced iNOS, Bax, and cleaved caspase 3 expression, stabilized IκBα protein, and reduced NF-κB p65 nuclear translocation and activity.
Improved cardiac mitochondrial electron transfer chain complex II and III activities, reversed diabetic shifts in mitochondrial dynamic regulators (reduced Drp1, normalized Opa1 processing), and lowered cardiac autophagy markers Beclin 1 and LC3A/B II expression.
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Animal Model:Wistar normotensive male rats (12 weeks of age at study initiation; myocardial infarction-induced heart failure model)[3]
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Dosage:40 mg/kg/day
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Administration:oral gavage; twice daily; six weeks
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Result:Restored cardiac Dicer activity to levels comparable to vehicle-treated sham rats.
Reduced left ventricular end-diastolic diameter, cardiomyocyte cross-sectional area, left ventricular fibrosis, and inflammatory cell infiltration compared to vehicle-treated heart failure controls.
Improved left ventricular ejection fraction, re-established cardiac ALDH2 catalytic activity, and reduced cardiac 4-HNE protein adduct levels in heart failure rats.
Showed no significant effects on cardiac morphology, function, aldehyde clearance, or Dicer function in sham-treated rats.
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Animal Model:heterozygous ALDH2*1/*2 knock-in (male, 10-week-old, chronic 10% O2 hypoxia for 4 weeks induced pulmonary hypertension)[4]
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Dosage:60 mg/kg
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Administration:p.o.; daily; 4 weeks
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Result:Significantly reduced hypoxia-induced increases in right ventricular systolic pressure.
Reduced the Fulton index (right ventricular hypertrophy marker).
Restored lung superoxide dismutase activity.
Decreased the percentage of pulmonary arterial wall thickness.
Lowered the signal intensity of 4-HNE-protein adducts in pulmonary arteries.
Attenuated hypoxia-induced increases in proximity ligation assay signal (indicating reduced interleukin-6 association with pulmonary arterial endothelial cells).
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Animal Model:C57BL/6J Aldh2 wild-type (male; fed high-fat high-sucrose diet from 10 weeks of age)[5]
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Dosage:20 mg/kg/day; 60 mg/kg/day
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Administration:p.o.; daily; 20 weeks
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Result:Reduced diet-induced weight gain dose-dependently.
Decreased weights of perigonadal fat, inguinal fat, and omental fat.
Reduced adipocyte hypertrophy.
Decreased hepatic steatosis severity and hepatic triglyceride levels.
Lowered fasting glucose levels.
Improved insulin sensitivity and glucose tolerance.
Reduced serum 4-hydroxynonenal (4-HNE) levels.
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Animal Model:C57BL/6J Aldh2 homozygous knock-in (male; mimicking human Glu504Lys mutation; fed high-fat high-sucrose diet from 10 weeks of age)[5]
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Dosage:20 mg/kg/day; 60 mg/kg/day
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Administration:p.o.; daily; 20 weeks
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Result:Reduced diet-induced weight gain dose-dependently.
Decreased weights of perigonadal fat, inguinal fat, and omental fat.
Reduced adipocyte hypertrophy.
Decreased hepatic steatosis severity and hepatic triglyceride levels.
Lowered fasting glucose levels.
Improved insulin sensitivity and glucose tolerance.
Reduced serum 4-hydroxynonenal (4-HNE) levels.
Reduced the number of 4-HNE-adducted mitochondrial proteins involved in fatty acid oxidation and electron transport chain in brown adipose tissue.
- Collagen: Sirius Red Staining
- Mitochondrial membrane-potential fluorescent assay
- Nephrotoxicity Study
- Mammalian live/dead viability and cytotoxicity staining
- ROS/oxidative-stress fluorescent staining
- Connective Tissue: Masson's Trichrome/Collagen Trichrome Staining
- CCK-8/WST-8 Cell Proliferation Assay
- Research Protocol for Cardiovascular Diseases
- Research Protocol for Metabolic Diseases
- Cell Viability Determination by MTT Colorimetric Assay
- Fibrosis/Collagen Morphometry
- Cell Cytotoxicity Assay
- Research Protocol for Endocrine Diseases
- Mitochondrial membrane-potential and mitochondrial mass staining
- MTT Cell Proliferation Assay
Chemical Information
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CAS No. 1804942-56-0
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Appearance Oil
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Molecular Weight 537.62
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Formula C30H36FN3O5
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SMILES
CC(C)[C@H](N)C(OCC1=C(C2=CC(C(NCC3=CC(F)=C(C=C3)OC)=O)=C(C=C2)OCC(C)C)N=CC=C1)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Solvent & Solubility
In Vitro:
DMSO : ≥ 100 mg/mL (186.00 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
* "≥" means soluble, but saturation unknown.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Purity & Documentation
References
[1]. Kuo YM, et al. Aldehyde dehydrogenase 2 mitigates acrolein-driven ferroptosis to preserve kidney function. Environmental pollution (Barking, Essex : 1987). 2026 Feb 01;390:127555. [Content Brief]
[2]. Lee HL, et al. A Novel ALDH2 Activator AD-9308 Improves Diastolic and Systolic Myocardial Functions in Streptozotocin-Induced Diabetic Mice. Antioxidants (Basel, Switzerland). 2021 Mar 13;10(3):450. [Content Brief]
[3]. Kiyuna LA, et al. 4-Hydroxynonenal impairs miRNA maturation in heart failure via Dicer post-translational modification. European heart journal. 2023 Nov 21;44(44):4696-4712. [Content Brief]
[4]. Chou YH, et al. Deciphering endothelial aldehyde dehydrogenase 2, oxidative stress, and interleukin-6 interactions in pulmonary hypertension: Implications for precision medicine. Biochemical pharmacology. 2026 Jan;243(Pt 1):117510. [Content Brief]
[5]. Chang YC, et al. A common East-Asian ALDH2 mutation causes metabolic disorders and the therapeutic effect of ALDH2 activators. Nature communications. 2023 Sep 25;14(1):5971. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
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| DMSO | 1 mM | 1.8600 mL | 9.3002 mL | 18.6005 mL | 46.5012 mL |
| 5 mM | 0.3720 mL | 1.8600 mL | 3.7201 mL | 9.3002 mL | |
| 10 mM | 0.1860 mL | 0.9300 mL | 1.8600 mL | 4.6501 mL | |
| 15 mM | 0.1240 mL | 0.6200 mL | 1.2400 mL | 3.1001 mL | |
| 20 mM | 0.0930 mL | 0.4650 mL | 0.9300 mL | 2.3251 mL | |
| 25 mM | 0.0744 mL | 0.3720 mL | 0.7440 mL | 1.8600 mL | |
| 30 mM | 0.0620 mL | 0.3100 mL | 0.6200 mL | 1.5500 mL | |
| 40 mM | 0.0465 mL | 0.2325 mL | 0.4650 mL | 1.1625 mL | |
| 50 mM | 0.0372 mL | 0.1860 mL | 0.3720 mL | 0.9300 mL | |
| 60 mM | 0.0310 mL | 0.1550 mL | 0.3100 mL | 0.7750 mL | |
| 80 mM | 0.0233 mL | 0.1163 mL | 0.2325 mL | 0.5813 mL | |
| 100 mM | 0.0186 mL | 0.0930 mL | 0.1860 mL | 0.4650 mL |
AD-9308 Related Classifications
HY-160475 Related Classifications
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Keywords
- AD-9308
- 1804942-56-0
- AD9308
- AD 9308
- Aldehyde Dehydrogenase (ALDH)
- Interleukin Related
- acrolein
- C57BL/6J Aldh2 wild-type mice
- aldehyde dehydrogenase 2
- myocardial infarction-induced heart failure
- H9c2 cardiomyoblasts
- 4-hydroxy-2-nonenal
- human pulmonary arterial endothelial cells
- streptozotocin-induced diabetic mice
- Inhibitor
- inhibitor
- inhibit