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| Type | HazMat fee for 500 gram (Estimated) |
| Excepted Quantity | USD 0.00 |
| Limited Quantity | USD 15-60 |
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| Inaccessible (Haz class 6.1), International | USD 150+ |
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| 描述 | Mitochondrial aldehyde dehydrogenase (ALDH2) plays roles in either toxic environmental aldehydes or organic ethanol metabolism as well as in disease therapy like cardiovascular disease. Alda-1 is an agonist that activates both wild-type ALDH2 and ALDH2*2 by bounding to the apo-form of them at the exit of the substrate tunnel and extends in toward the active site. At pH 7.5, the length and nature of 100 μM aldehydes that were acetaldehyde, propionaldehyde and butyraldehyde were activated in dependent ways with the concentrations of Alda-1 of 0, 3, 6, 20, 30 μM respectively. Alda-1 also antagonized daidzin inhibition of both ALDH2 and ALDH2*2 in a dependent way with concentrations of 10 μM. Furthermore, the combined activatory could significantly increase the effects of both Alda-1 and NAD+ on ester hydrolysis for the two enzymes, which inversely became antagonistic for ALDH2 if the concentration is very high[1]. In male sprague-dawley rats study model with lung ischemia/reperfusion (I/R) injuries, 10 mg/kg Alda-1 treatment could significantly alleviate the I/R injury. The hepatic I/R could increase ROC which was reduced by Alda-1 treatment and damage ALDH2 activity without changing ALDH2 expression and the ALDH2 activity could also be increased by Alda-1. The accumulation of MDA and 4-HNE due to I/R could also be inhibited, indicating that Alda-1 could activate ALDH2 activity and thus diminish the accumulation of toxic products. Furthermore, Alda-1 was proved to reduce the inflammatory response, ROS level, cell viability and mitochondrial membrane potential[2]. In sum, Alda-1 could enhance the catalytic ALDH2 activity by 2-times with EC50 of 20 μM and inhibit 4-HNE-induced inactivation of ALDH2. 8 mg/kg Injection of Alda-1 could decrease creatine kinase release into the blood by 50%[3]. |
| Concentration | Treated Time | Description | References | |
| Recombinant ALDH2 | 20 µM | 1 hour | Alda-1 prevented nitroglycerin-induced ALDH2 inactivation | Sci Transl Med. 2011 Nov 2;3(107):107ra111. |
| H9c2 cells | 20 µM | 12 hours | Alda-1 treatment significantly increased ALDH2 activation in H9c2 cells and promoted mitochondrial respiration. | Bioact Mater. 2021 Jan 8;6(7):2058-2069. |
| Cardiomyocytes | 20 µM | 12 hours | Alda-1 treatment significantly increased ALDH2 activation in cardiomyocytes and promoted mitochondrial respiration. | Bioact Mater. 2021 Jan 8;6(7):2058-2069. |
| T84 human colon cells | 20 µM | 12 hours | Alda-1 restored the levels of ALDH2 protein and activity, and significantly blocked ethanol-induced increase in cell permeability and reduction in TJ/AJ protein levels. | Redox Biol. 2023 Feb;59:102577. |
| A549 cells | 0 nM, 100 nM, 350 nM, 1 µM | 2 days | Alda-1 treatment significantly reduced the side population of A549 cells, indicating that Alda-1 inhibits the stem cell-like properties of lung cancer cells. | Neoplasia. 2019 Jun;21(6):602-614. |
| H1299 cells | 0 nM, 100 nM, 1 µM | 2 days | Alda-1 treatment significantly reduced the CD44+/CD24− population of H1299 cells, indicating that Alda-1 inhibits the stem cell-like properties of lung cancer cells. | Neoplasia. 2019 Jun;21(6):602-614. |
| H9C2 cells | 20 µM | 2 hours | To evaluate the protective effect of Alda-1 on LPS-induced apoptosis and inflammation in H9C2 cells, the results showed that Alda-1 pretreatment significantly reduced LPS-induced mitochondrial membrane permeability, ROS levels, and apoptosis rate, and decreased the expression of inflammatory factors. | Mol Med. 2023 Dec 20;29(1):171. |
| H9C2 myoblasts | 20 µM | 24 hours | To evaluate the protective effect of Alda-1 on Aβ-induced lipid peroxidation, results showed that Alda-1 significantly alleviated Aβ-induced lipid peroxidation. | Acta Pharmacol Sin. 2022 Jan;43(1):39-49. |
| Human renal proximal tubular epithelial cells (HK-2) | 20 µM | 24 hours | To evaluate the effect of Alda-1 on MA-induced mitochondrial dysfunction and apoptosis in HK-2 cells. Results showed that Alda-1 treatment significantly improved mitochondrial function and reduced apoptosis. | Cell Death Dis. 2023 Jan 20;14(1):45. |
| 3T3 cells | 20 µM | 48 hours | Evaluate the activation effect of Alda-1 on ALDH2 variants. The results showed that Alda-1 increased the activity of the ALDH2*2 variant by approximately 14-fold, but had limited activation effects on other variants. | EBioMedicine. 2020 May;55:102753. |
| Human-derived fibroblasts | 20 µM | 48 hours | Evaluate the activation effect of Alda-1 on ALDH2 variants. The results showed that Alda-1 had poor activation effects on ALDH2*3 and ALDH2*6 variants, and did not significantly improve their activity. | EBioMedicine. 2020 May;55:102753. |
| Cardiac fibroblasts | 20 µM | 96 hours | Alda-1 treatment reduced fibroblast proliferation under aldehydic load stress | Cardiovasc Res. 2014 Sep 1;103(4):498-508. |
| ALDH2*1 | 0.03–0.06 µM | To study the activation effect of Alda-1 on ALDH2*1 dehydrogenase activity | Nat Struct Mol Biol. 2010 Feb;17(2):159-64. | |
| ALDH2*2 | 0.3–0.5 µM | To study the activation effect of Alda-1 on ALDH2*2 dehydrogenase activity | Nat Struct Mol Biol. 2010 Feb;17(2):159-64. | |
| HepG2 cells | 40 µM | Alda-1 prevented HNE-induced HepG2 cell death by activating ALDH2 to degrade HNE | Cell Mol Gastroenterol Hepatol. 2022;14(4):925-944. | |
| Huh-7 cells | 40 µM | Alda-1 prevented HNE-induced Huh-7 cell death by activating ALDH2 to degrade HNE | Cell Mol Gastroenterol Hepatol. 2022;14(4):925-944. | |
| Administration | Dosage | Frequency | Description | References | ||
| C57BL/6 mice | LPS-induced myocardial injury model | Intraperitoneal injection | 10 mg/kg | Single injection, lasting 12 hours | To evaluate the protective effect of Alda-1 on LPS-induced cardiac dysfunction, inflammation, and apoptosis, the results showed that Alda-1 pretreatment significantly improved cardiac function, reduced the expression of cardiac injury markers CKMB and LDH, and decreased the levels of inflammatory cytokines and apoptosis rate. | Mol Med. 2023 Dec 20;29(1):171. |
| C57BL/6 mice | Intestinal ischemia-reperfusion injury model | Intraperitoneal injection | 10 mg/kg | Single dose, 1 hour before ischemia | Alda-1 pretreatment significantly alleviated intestinal ischemia-reperfusion injury, accompanied by up-regulated ALDH2 activity and reduced accumulation of 4-HNE and MDA. | Clin Sci (Lond). 2017 Jun 1;131(11):1123-1136 |
| Rats | Myocardial infarction-induced heart failure model | Subcutaneous injection | 10 mg/kg/day | Continuous for 6 weeks | Alda-1 treatment improved cardiac function, reduced left ventricular dilation, and decreased myocardial hypertrophy and cardiac fibrosis | Cardiovasc Res. 2014 Sep 1;103(4):498-508. |
| Wistar rats | Myocardial infarction model | Continuous infusion via Alzet pump | 16 mg/kg/day | 16 hours | Alda-1 prevented nitroglycerin-induced increase in myocardial infarction injury | Sci Transl Med. 2011 Nov 2;3(107):107ra111. |
| Mice and rats | ALDH2*1/*2 knock-in mice and Wistar rats | Subcutaneous injection | 2 mg/kg | 15 minutes before, and again at 30 and 150 minutes after | Alda-1 reduced the response to nociceptive stimulus in ALDH2*1/*2 mice and reversed the carrageenan-induced pain behavior, restoring thresholds to baseline values for both wild type and ALDH2*1/*2 mice. | Sci Transl Med. 2014 Aug 27;6(251):251ra118 |
| Mice | Choline-deficient, amino acid-defined (CDAA) mouse model | Intraperitoneal injection | 20 mg/kg | 3 times a week for 8 weeks | Alda-1 reduced liver inflammation and fibrosis by degrading HNE | Cell Mol Gastroenterol Hepatol. 2022;14(4):925-944. |
| C57BL/6 mice | Cisplatin or maleic acid-induced acute kidney injury model | Intraperitoneal injection | 20 mg/kg | Once daily for 3 days | To evaluate the protective effect of Alda-1 on cisplatin or maleic acid-induced acute kidney injury. Results showed that Alda-1 pretreatment significantly improved renal function and reduced tubular injury and apoptosis. | Cell Death Dis. 2023 Jan 20;14(1):45. |
| C57BL/6 mice | Bile duct ligation model | Subcutaneous injection | 20 mg/kg | Once daily for 14 days | Alda-1 accelerates aldehyde degradation by activating ALDH2, reducing BDL-induced liver necrosis, inflammation, and fibrosis, indicating that aldehydes play an important role in the pathogenesis of cholestatic liver injury and fibrosis. | Free Radic Biol Med. 2019 Dec;145:136-145 |
| Mice | GSNO-R−/− mice | Perfusion | 20 μmol/L | 10 minutes prior to the onset of ischemia and for 10 minutes at the start of reperfusion | Alda-1 significantly reduced infarct size in female GSNO-R?/? hearts, suggesting that excess mitochondrial formaldehyde may exacerbate I/R injury in female hearts with the disruption of GSNO-R. | Circ Res. 2018 Nov 9;123(11):1232-1243 |
| C57BL/6J mice | Alcoholic liver disease model | Intraperitoneal injection | 5 mg/kg | Every other day for 10 days | To test the therapeutic potential of Alda-1 for alcoholic liver disease, results showed that Alda-1 treatment alleviated liver damage, reduced hepatic steatosis, and apoptosis. | J Hepatol. 2015 Jun;62(6):1375-81. |
| C57BL/6J mice | GFP-LC3 transgenic mice | Intraperitoneal injection | 50 mg/kg | Single dose | Alda-1 pretreatment reduced ethanol-induced mitochondrial depolarization and GFP-LC3 puncta formation. | Autophagy. 2022 Nov;18(11):2671-2685 |
| Dose | Rat: 12.5 mg/kg - 50 mg/kg[4] (i.p.), 1.5 mg/kg[5] (i.p.) |
| Administration | i.p. |
| 计算器 | ||||
| 存储液制备 | ![]() |
1mg | 5mg | 10mg |
|
1 mM 5 mM 10 mM |
3.08mL 0.62mL 0.31mL |
15.42mL 3.08mL 1.54mL |
30.85mL 6.17mL 3.08mL |
|
| CAS号 | 349438-38-6 |
| 分子式 | C15H11Cl2NO3 |
| 分子量 | 324.16 |
| SMILES Code | O=C(NCC1=CC=C(OCO2)C2=C1)C3=C(Cl)C=CC=C3Cl |
| MDL No. | MFCD02055160 |
| 别名 | |
| 运输 | 蓝冰 |
| InChI Key | NMKJFZCBCIUYHI-UHFFFAOYSA-N |
| Pubchem ID | 831629 |
| 存储条件 |
In solvent -20°C: 3-6个月 -80°C: 12个月 Pure form Sealed in dry,2-8°C |
| 溶解方案 |
DMSO: 50 mg/mL(154.25 mM),注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO 以下溶解方案都请先按照体外实验的方式配制澄清的储备液,再依次添加助溶剂: ——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议现用现配,当天使用; 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶
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