Loxoprofen sodium
(Synonyms: 洛索洛芬钠) 目录号 : GC60228
An NSAID and a prodrug form of loxoprofen-SRS
Cas No.:80382-23-6
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
Loxoprofen is a non-steroidal anti-inflammatory drug (NSAID) and prodrug form of loxoprofen-SRS.1 It inhibits COX-1 and COX-2 in isolated human whole blood (IC50s = 6.5 and 13.5 ?M, respectively). Loxoprofen reduces acetic acid-induced writhing in mice and carrageenan-induced paw edema and LPS-induced fever in rats (ED30s = 20.1, 0.7, and 2.79 mg/kg, respectively).2 Formulations containing loxoprofen have been used in the treatment of pain associated with osteoarthritis, myalgia, and post-traumatic swelling.
1.Riendeau, D., Salem, M., Styhler, A., et al.Evaluation of loxoprofen and its alcohol metabolites for potency and selectivity of inhibition of cyclooxygenase-2Bioorg. Med. Chem. Lett.14(5)1201-1203(2004) 2.Futaki, N., Yoshikawa, K., Hamasaka, Y., et al.NS-398, a novel non-steroidal anti-inflammatory drug with potent analgesic and antipyretic effects, which causes minimal stomach lesionsGen. Pharmacol.24105-110(1993)
| Cas No. | 80382-23-6 | SDF | |
| 别名 | 洛索洛芬钠 | ||
| Canonical SMILES | O=C1C(CCC1)CC2=CC=C(C(C)C(O[Na])=O)C=C2 | ||
| 分子式 | C15H17NaO3 | 分子量 | 268.28 |
| 溶解度 | Water : 53mg/mL | 储存条件 | 4°C, stored under nitrogen |
| 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 | 3.7274 mL | 18.6372 mL | 37.2745 mL |
| 5 mM | 0.7455 mL | 3.7274 mL | 7.4549 mL |
| 10 mM | 0.3727 mL | 1.8637 mL | 3.7274 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。
Loxoprofen sodium Alleviates Oxidative Stress and Apoptosis Induced by Angiotensin II in Human Umbilical Vein Endothelial Cells (HUVECs)
Drug Des Devel Ther 2020 Nov 18;14:5087-5096.PMID:33239867DOI:10.2147/DDDT.S266175.
Background and purpose: Endothelium exerts an important role in releasing vasoactive substances, maintaining the blood flow, regulating the growth of vessels, moderating the process of coagulation, and the balance of fibrinolytic system, the dysfunction of which is reported to result in arterial stiffness. The present study aimed to investigate the effects of Loxoprofen sodium against HUVECs injury induced by angiotensin II. Methods: The injury model on HUVECs was established through incubation with angiotensin II. The expression levels of AT2R, NOX-4, Bax, Bcl-2, and caspase-3 were evaluated using qRT-PCR and Western Blot. DCFH-DA assay was used to detect the production of ROS and ELISA assay was used to evaluate the level of reduced glutathione. Mitochondrial membrane potential (MMP) was measured using dihydrorhodamine 123 assay. MTT and LDH assays were utilized to determine the proliferation ability of HUVECs. The apoptosis rate of HUVECs was evaluated using flow cytometry. Results: Loxoprofen sodium suppressed endothelial AT2R elevation by angiotensin II. Loxoprofen ameliorated Angiotensin II-induced production of ROS, reduced GSH, and NOX-2 and NOX-4 expression. Furthermore, Loxoprofen mitigated Angiotensin II, reduced mitochondrial membrane potential and improved cell viability, and suppressed LDH release by angiotensin II. Importantly, loxoprofen showed a beneficial role in protecting endothelial apoptosis by mitigating apoptotic machinery including the balanced expression of Bax, Bcl-2, and caspase-3 cleavage. Conclusion: Loxoprofen sodium might alleviate the high ROS levels and apoptosis induced by angiotensin II in HUVECs.
Loxoprofen sodium induces the production of complement C5a in human serum
Int Immunopharmacol 2016 Apr;33:55-62.PMID:26854577DOI:10.1016/j.intimp.2016.01.025.
Basophil activation test (BAT) is an in vitro allergy test that is useful to identify allergens that cause IgE-dependent allergies. The test has been used to detect not only food allergies and allergies caused by environmental factors but also to detect drug hypersensitivity, which has been known to include IgE-independent reactions. In our preliminary studies in which BAT was applied to detect hypersensitivity of loxoprofen, a non-steroidal anti-inflammatory drug (NSAID), conventional BAT with incubation for 30min did not show basophil activation by means of increased CD203c expression. In this study, we extended the incubation time to 24h on the basis of the hypothesis that loxoprofen indirectly activates basophils. Basophils from healthy control donors as well as allergic patients showed up-regulation of CD203c after incubation with loxoprofen for 24h. Activation was induced using loxoprofen-treated serum. Proteomic and pharmacologic analyses revealed that serum incubation with loxoprofen generated an active complement component C5a, which induced CD203c expression via binding to the C5a receptor on basophils. Because C3a production was also detected after incubation for 24h, loxoprofen is likely to stimulate the complement classical pathway. Our findings suggest that the complement activation is involved in drug hypersensitivity and the suppression of this activation may contribute to the elimination of false positive of BAT for drug allergies.
Enzymologic and pharmacologic profile of Loxoprofen sodium and its metabolites
Biol Pharm Bull 2005 Nov;28(11):2075-9.PMID:16272692DOI:10.1248/bpb.28.2075.
We investigated the mechanism of inhibition of Loxoprofen sodium, a non-steroidal anti-inflammatory drug (NSAID), and its active metabolite (loxoprofen-SRS) on cyclooxygenase (COX). In in vitro assays, Loxoprofen sodium appeared inactive against recombinant human COX-1 and COX-2, whereas loxoprofen-SRS inhibited both. In the investigation of kinetic behavior, loxoprofen-SRS showed time-dependent inhibition for both isozymes. Human whole blood assay also showed that loxoprofen-SRS possesses the profile of a non-selective inhibitor for COX. In a rat air pouch model, oral administration of Loxoprofen sodium lowered prostaglandin (PG) E2 in both fluid exudates of the inflammatory pouch and stomach tissue with ED50 values of 2.0 and 2.1 mg/kg, respectively. Additionally, platelet thromboxane B2 production was also inhibited by Loxoprofen sodium (ED50 of 0.34 mg/kg). In a rat carrageenan-induced paw edema model, Loxoprofen sodium dose-dependently reduced the paw edema, accompanied by a decrease in PGE2 content in inflamed paw exudates. These findings suggest that the COX inhibitory activity of Loxoprofen sodium is attributable to its active metabolite, loxoprofen-SRS, and that loxoprofen-SRS shows non-selective inhibition for COX.
Loxoprofen sodium, a Non-Selective NSAID, Reduces Atherosclerosis in Mice by Reducing Inflammation
J Clin Biochem Nutr 2010 Sep;47(2):138-47.PMID:20838569DOI:10.3164/jcbn.10-33.
Recently, it is suggested that the use of nonsteroidal anti-inflammatory drugs (NSAID) may contribute to the occurrence of cardiovascular events, while the formation of atherosclerotic lesions is related to inflammation. Loxoprofen sodium, a non-selective NSAID, becomes active after metabolism in the body and inhibits the activation of cyclooxygenase. We fed apoE(-/-) mice a western diet from 8 to 16 weeks of age and administered Loxoprofen sodium. We measured atherosclerotic lesions at the aortic root. We examined serum levels of cholesterol and triglycerides with HPLC, platelet aggregation, and urinary prostaglandin metabolites with enzyme immune assay. Atherosclerotic lesion formation was reduced to 63.5% and 41.5% as compared to the control in male and female apoE(-/-) mice treated with Loxoprofen sodium respectively. Urinary metabolites of prostaglandin E(2), F(1α), and thromboxane B(2), and platelet aggregation were decreased in mice treated with Loxoprofen sodium. Serum levels of cholesterol and triglycerides were not changed. We conclude that Loxoprofen sodium reduced the formation of early to intermediate atherosclerotic lesions at the proximal aorta in mice mediated by an anti-inflammatory effect.
Loxoprofen sodium Versus Diclofenac Potassium for Post-Dental Extraction Pain Relief: A Randomized, Triple-Blind, Clinical Trial
Dent J (Basel) 2019 Dec 25;8(1):2.PMID:31881670DOI:10.3390/dj8010002.
One of the most common post-operative complications of tooth extraction is pain. Oral analgesics, namely Loxoprofen sodium and diclofenac potassium, are often prescribed; however, the efficacy of these drugs irrespective of gender and type of extraction has not been tested. Therefore, this study aimed to compare the efficacy of these two drugs in post-dental extraction pain relief among male and female patients in cases of simple and surgical tooth extraction. A single-center, triple-blind, randomized clinical trial was conducted among 100 male and female patients who underwent tooth extraction at Taibah University Dental College and Hospital in Al-Madinah, Saudi Arabia. The patients reported their pain post-operatively after 6 hours and every 12 h for 3 days using the Verbal Descriptor Scale (e.g., "no pain", "mild pain"). Descriptive statistics and chi-square tests were run to analyze the data. An equal number of patients received either the drug Loxoprofen sodium or diclofenac potassium and completed the study follow-up. Patients allocated to the diclofenac potassium drug group after 36 h were statistically significantly in their reporting of "no pain" and "mild pain" compared to patients allocated to the Loxoprofen sodium group (86% vs. 66%, respectively; p = 0.019), irrespective of gender or type of tooth extraction. However, both groups demonstrated comparable (p > 0.05) post-operative pain relief over the other aforementioned allocated time intervals. In conclusion, the diclofenac potassium group had slightly better control over post-operative pain than the group receiving Loxoprofen sodium.