Aspalatone
(Synonyms: Acetylsalicylic Acid Matol ester) 目录号 : GC40848
An antithrombic compound
Cas No.:147249-33-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Aspalatone is an anti-platelet aggregator (IC50 = 180 µM, in vitro) that prolongs bleeding time significantly in a rodent model of thromboembolism. Additionally at a minimal effective dose of 24 mg/kg, aspalatone generates antioxidant and neuroprotective effects against kainic acid-induced epilepsy in rat hippocampus.
| Cas No. | 147249-33-0 | SDF | |
| 别名 | Acetylsalicylic Acid Matol ester | ||
| Canonical SMILES | O=C1C(OC(C2=C(OC(C)=O)C=CC=C2)=O)=C(C)OC=C1 | ||
| 分子式 | C15H12O6 | 分子量 | 288.3 |
| 溶解度 | DMF: 10 mg/ml,DMSO: 10 mg/ml,DMSO:PBS (pH 7.2) (1:10): 0.1 mg/ml,Ethanol: 1 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.4686 mL | 17.343 mL | 34.6861 mL |
| 5 mM | 0.6937 mL | 3.4686 mL | 6.9372 mL |
| 10 mM | 0.3469 mL | 1.7343 mL | 3.4686 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Aspalatone Prevents VEGF-Induced Lipid Peroxidation, Migration, Tube Formation, and Dysfunction of Human Aortic Endothelial Cells
Oxid Med Cell Longev 2017;2017:2769347.PMID:28243353DOI:10.1155/2017/2769347.
Although Aspalatone (acetylsalicylic acid maltol ester) is recognized as an antithrombotic agent with antioxidative and antiplatelet potential; its efficacy in preventing endothelial dysfunction is not known. In this study, we examined the antiangiogenic, antioxidative, and anti-inflammatory effect of Aspalatone in human aortic endothelial cells (HAECs). Specifically, the effect of Aspalatone on VEGF-induced HAECs growth, migration, tube formation, and levels of lipid peroxidation-derived malondialdehyde (MDA) was examined. Our results indicate that the treatment of HAECs with Aspalatone decreased VEGF-induced cell migration, tube formation, and levels of MDA. Aspalatone also inhibited VEGF-induced decrease in the expression of eNOS and increase in the expression of iNOS, ICAM-1, and VCAM-1. Aspalatone also prevented the VEGF-induced adhesion of monocytes to endothelial cells. Furthermore, Aspalatone also prevented VEGF-induced release of inflammatory markers such as Angiopoietin-2, Leptin, EGF, G-CSF, HB-EGF, and HGF in HAECs. Thus, our results suggest that Aspalatone could be used to prevent endothelial dysfunction, an important process in the pathophysiology of cardiovascular diseases.
Aspalatone, a new antiplatelet agent, attenuates the neurotoxicity induced by kainic acid in the rat
Life Sci 1997;61(24):PL 373-81.PMID:9399638DOI:10.1016/s0024-3205(97)00963-6.
The antioxidant efficacy of Aspalatone (APT; acetyl salicylic acid maltol ester), a new antiplatelet agent, has been characterized in vivo as well as in vitro, and several observations indicated that the antioxidant could prevent the neuroexcitation caused by oxidative stress. In this report, the effect of APT was evaluated on kainic acid (KA)-induced neurotoxicity, since the neurotoxicity induced by KA is, at least in part, mediated via the formation of free radicals. The results showed that pretreatments with APT or maltol (MAL) significantly attenuated seizure activity, oxidative stress (lipid peroxidation and protein oxidation) and the loss of hippocampal neurons induced by KA. On the other hand, the pretreatments with aspirin (ASP), ASP together with MAL or vitamin E failed to protect against the toxicity produced by KA suggesting that the mechanism of action for APT on the KA-induced neurotoxicity is different from that of ASP. These finding raise the possibility that salicylmaltol, a metabolite of APT, plays a role in preventing the neurotoxicity evoked by KA. Therefore, our results suggest that an APT-related antioxidant mechanism, which is linked to the MAL moiety, is involved in the neuroprotective effect against KA.
Salicylate levels in rat stomach tissues after administration of Aspalatone and acetylsalicylic acid in relation to their ulcerogenicity
Arzneimittelforschung 1997 Jul;47(7):826-8.PMID:9272238doi
To study the mechanism for the low ulcerogenicity of the antithrombotic agent Aspalatone ([3-[2-methyl-4-pyronyl)]-2-acetyloxybenzoate, CAS 147249-33-0), the metabolism and disposition of Aspalatone were compared with those of acetylsalicylic acid (ASA) in the gut wall in relation to the salicylate level in the stomach tissues following oral administration in pyrolus-ligated rats. Both Aspalatone and ASA were essentially stable in gastric juice and were absorbed in stomach unchanged. In glandular portion of the stomach, salicylate level found at 10 min post-dose in Aspalatone (80 mg/kg)-and in ASA (50 mg/kg)-treated group was 67 +/- 43 nmol/g tissue and 2000 +/- 250 nmol/g tissue, respectively. In non-glandular (rumen) tissue, salicylate was not detected in the Aspalatone group, whereas it reached a concentration of up to 1100 +/- 130 nmol/g tissue in the ASA group. As a result of the relative stability of the ester bond connecting the salicylic acid and maltol groups towards hydrolysis in the stomach and entrapment of ASA due to ion trapping, a lower salicylate level was observed in the stomach after oral Aspalatone administration, and this may, at least in part, be the underlying mechanism for the low ulcerogenicity of Aspalatone.
Synthesis and antiplatelet effects of the new antithrombotic agent Aspalatone with low ulcerogenicity
Arzneimittelforschung 1994 Oct;44(10):1122-6.PMID:7818584doi
A new compound, Aspalatone (acetylsalicylic acid maltol ester), was synthesized by esterification of acetylsalicylic acid (ASA) and maltol, an antioxidant, and studied for its bleeding time prolongation effect in rats, for its antiplatelet aggregation activity in vitro and ex vivo in rats, and for its antithrombotic activity in vivo using the mouse thromboembolism test. Aspalatone treatment (15 mg/kg p.o.) for 10 days prolonged bleeding time by 57% (p < 0.005) in Sprague-Dawley rats vs control, while ASA treatment (15 mg/kg p.o.) prolonged by 44%. At the low dose of 15 mg/kg p.o. at least 8 days of treatment were necessary for Aspalatone and ASA to prolong the bleeding time significantly. On the other hand, salicylic acid maltol ester which lacks the acetyl group did not significantly affect bleeding time at a dose of 15 mg/kg. Aspalatone produced a potent inhibition of collagen-induced platelet aggregation in vitro with IC50 of 1.8 x 10(-4) mol/l, but, similar to ASA, did not significantly inhibit ADP-induced aggregation. The ability of oral Aspalatone to inhibit platelet aggregation in rats ex vivo was compared with other reference antiplatelet drugs. Relative potency was ASA > dipyridamole approximately equal to Aspalatone > ticlopidine. A single dose of Aspalatone potently prevented death due to collagen-induced platelet aggregation in mice in vivo with ED50 value of 32 mg/kg p.o., but failed to prevent death due to ADP-induced platelet aggregation. When given for 10 days, Aspalatone prevented collagen-induced death by 90% (p < 0.001) at 20 mg/kg, and this antithrombotic effect lasted after 4 days of wash-out period.(ABSTRACT TRUNCATED AT 250 WORDS)
A new antithrombotic agent, Aspalatone, attenuated cardiotoxicity induced by doxorubicin in the mouse; possible involvement of antioxidant mechanism
Life Sci 1997;60(4-5):PL75-82.PMID:9010492DOI:10.1016/s0024-3205(96)00637-6.
A new antithrombotic agent, Aspalatone (APT; acetyl salicylic acid maltol ester), was synthesized by esterification of acetyl salicylic acid (ASP) and maltol (MAL). It was suggested that APT possessed an antioxidant effect in in vitro. To evaluate the putative antioxidant effect of APT in in vivo, we developed doxorubicin (DOX)-related cardiac damage, which might be implicated by oxidative stress. Vitamin E (Vit E) was included in the present study as an example of an antioxidant. Prolonged treatments with APT, MAL and Vit E significantly reduced the mortality in animals receiving multiple dose of DOX (3 mg/kg x 4). The potential role of APT, MAL and Vit E against DOX insult may be explained by the induction of glutathione peroxidase activity accompanied by the inhibition of lipid peroxidation. Prolonged treatments of APT, MAL and Vit E also ablated histopathological evidence of DOX cardiomyopathy. ASP challenge, however, did not affect the mortality, myocardial lesion and antioxidant deficit induced by DOX treatments. In conclusion, the protective effect of APT was equipotent to that of Vit E against DOX cardiotoxicity. The results also suggest that the antiperoxidative effect of APT plays a protective role in DOX-related cardiotoxic side effect.