Diethylcarbamazine citrate
(Synonyms: 枸橼酸乙胺嗪) 目录号 : GC32241
Diethylcarbamazine citrate is an inhibitor of arachidonic acid metabolism in filarial microfilaria and is highly specific for several parasites and does not contain any toxic metallic elements.
Cas No.:1642-54-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Diethylcarbamazine citrate is an inhibitor of arachidonic acid metabolism in filarial microfilaria and is highly specific for several parasites and does not contain any toxic metallic elements.
| Cas No. | 1642-54-2 | SDF | |
| 别名 | 枸橼酸乙胺嗪 | ||
| Canonical SMILES | O=C(N1CCN(C)CC1)N(CC)CC.O=C(CC(C(O)=O)(O)CC(O)=O)O | ||
| 分子式 | C16H29N3O8 | 分子量 | 391.42 |
| 溶解度 | DMSO : ≥ 39 mg/mL (99.64 mM) | 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 | 2.5548 mL | 12.774 mL | 25.548 mL |
| 5 mM | 0.511 mL | 2.5548 mL | 5.1096 mL |
| 10 mM | 0.2555 mL | 1.2774 mL | 2.5548 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。
Diethylcarbamazine citrate-fortified salt for lymphatic filariasis elimination in India
Indian J Med Res 2022 Mar;155(3&4):347-355.PMID:36124509DOI:10.4103/ijmr.ijmr_171_22.
Lymphatic filariasis (LF) is a vector-borne neglected tropical disease, causing permanent disability. The disease is debilitating and widespread, leading to tremendous productivity and economic loss. The Government of India (GOI) prioritized the elimination of LF through the annual mass drug administration (MDA) programme in 2004 and continued with a single dose of Diethylcarbamazine citrate (DEC), 6 mg/kg of body weight, plus albendazole annually over a period of 5-6 years. The GOI had set the target to achieve LF elimination by 2015 and now by 2030. The progress so far has been suboptimal. Much remains to be done as about 84 per cent of the total 328 endemic districts are still under MDA. The major challenge in implementing MDA is poor compliance. It is necessary to have a feasible alternative strategy addressing the above challenge to achieve the desired goal of LF elimination. At this juncture, a well-researched approach, i.e. the use of DEC-fortified salt, also advocated by the World Health Organization, as a unique form of MDA, is proposed. As per this strategy, a low dose of DEC (0.2% w/w) is added to the cooking salt at the manufacturing facility of iodized salt and consumed by the LF-endemic communities for about two years. Many examples of successful use of this strategy for LF elimination in small- and large-scale trials have been documented in India and several other endemic countries in the world. Implementing DEC-iodine-fortified salt is a safe, less expensive, more efficient and prompt approach for achieving the elimination of LF in India. Adverse effects are none or minor and self-limiting. The DEC-fortified salt strategy can easily piggyback on the existing countrywide deployment of iodized salt under the National Iodine Deficiency Disorders Control Programme (NIDDCP), which has achieved a great success in reducing iodine-deficiency disorders such as hypothyroidism. This existing robust programme can be leveraged to launch DEC-fortified salt for the community. If implemented appropriately, this strategy will ensure the complete cessation of LF transmission within two years from its introduction. If the said strategy is implemented in 2022, it is expected that India will be able to achieve the LF elimination by 2024, much before the global target of 2030.
Diethylcarbamazine citrate, an antifilarial drug, stimulates human granulocyte adherence
Antimicrob Agents Chemother 1983 Sep;24(3):453-6.PMID:6639005DOI:10.1128/AAC.24.3.453.
Incubation with Diethylcarbamazine citrate caused significant augmentation of human neutrophil and eosinophil adherence to tissue culture plastic. This effect was dose dependent and cell dependent, with eosinophils showing greater sensitivity and a greater adhesive response to the drug than did neutrophils. Eosinophils preincubated with Diethylcarbamazine citrate demonstrated decreased adhesive responses to other adherence-augmenting stimuli. Use of Fc-treated plastic augmented diethylcarbamazine citrate-stimulated neutrophil (but not eosinophil) adherence. Direct stimulation of host effector cell adherence may explain, in part, the therapeutic action of Diethylcarbamazine citrate in vivo.
Diethylcarbamazine citrate ameliorates insulin resistance in high-fat diet-induced obese mice via modulation of adipose tissue inflammation
Int Immunopharmacol 2015 Dec;29(2):607-612.PMID:26432178DOI:10.1016/j.intimp.2015.09.021.
Diethylcarbamazine citrate (DEC) had been known as anti-inflammatory drug but its effect on obesity-induced insulin resistance as a result of released inflammatory mediators from adipose tissue (AT) was not known. White male albino mice were fed with high fat diet (HFD) for 18weeks to induce obesity. DEC at different three doses (12, 50 and 200mg/kg) was orally administered twice a week starting at week 6. Body, liver and adipose tissue weights were taken, while glucose tolerance, insulin resistance, blood triglycerides and levels of adipokines (leptin, TNF-伪, IL-6 and MCP-1) were tested. The activity of cyclooxygenase (COX) in the liver tissue homogenate was also tested. In addition, NF-魏Bp65 localization in liver cell cytoplasmic and nuclear fractions was detected using Western blotting. The only effective anti-inflammatory dose was 50mg/kg to reduce (p<0.05) the high levels of glucose, insulin and triglycerides in serum. DEC was not anti-obesity drug because the weights of body, liver and adipose tissues were not changed. Hyperleptinemia was decreased (p<0.001) and associated with a reduction in serum levels of TNF-伪, IL-6 and MCP-1 (p<0.001). In addition, the activity of COX in DEC treatment decreased significantly (p<0.01), while NF-魏Bp65 localization in nuclear extracts was obviously inhibited in 50mg/kg treated group. It could be concluded that DEC was the only effective dose against mouse insulin resistance but not lipid accumulation.
Immunomodulatory effect of Diethylcarbamazine citrate plus filarial excretory-secretory product on rat hepatocarcinogenesis
Int Immunopharmacol 2015 Feb;24(2):173-181.PMID:25499729DOI:10.1016/j.intimp.2014.12.004.
Diethylcarbamazine citrate (DEC) had a significance in anti-filarial chemotherapy, while excretory-secretory product (ES) is released from adult filarial females. The target of the current study was to examine the immunomodulatory effect of DEC, Setaria equina ES or a combination of them on rat hepatocellular carcinoma (HCC) induced by diethylnitrosamine (DEN). In vitro effect of combined DEC and ES or ES alone on lipopolysaccharide (LPS)-stimulated rat peripheral blood mononuclear cells (PBMCs) was tested through IFN-纬 assay in culture supernatants. In addition, single or repeated doses of DEC, ES or DEC+ES have been applied in white albino rats to test the effect on HCC. Levels of IFN-纬 and anti-ES IgG antibodies in rat serum were assayed using ELISA. Hemolytic complement activity (CH50) was determined in serum while the concentration of nitric oxide (NO) was assayed in liver tissue. The infiltration of NK cells as well as the expression of MHC Iproliferating cell nuclear antigen (PCNA), inducible NO synthase (iNOS), Bcl2 and p53 were determined using immunohistochemistry. There was a dose-dependent increase in IFN-纬 after in vitro exposure to DEC+ES. Repeated ES doses increased NO concentration (p<0.05) and expression of iNOS but reduced CH50 (p<0.001), while repeated DEC+ES doses could increase anti-ES IgG (p<0.01), IFN-纬 level (p<0.05) and NK cell infiltration. The same treatments could also reduce the expression of MHC I expression, PCNA, Bcl2 and p53. This study has shown immunomodulatory and protective effects of DEC+ES repeated doses on rat HCC.
Cardiovascular effects of Diethylcarbamazine citrate
Br J Pharmacol 1976 Feb;56(2):219-27.PMID:1252670DOI:10.1111/j.1476-5381.1976.tb07445.x.
1 The cardiovascular effects of the anthelmintic drug Diethylcarbamazine citrate (DECC) were examined in cats anaesthetized with pentobarbitone. There were two quite distinct haemodynamic responses, an initial transient hypotension (occurring within 10 s of an intravenous injection) and a pronounced secondary hypertension which reached a peak 30-60 s after the injection. 2 Within 10 s of an intravenous injection of DECC (2.5 to 10 mg/kg) there was hypotension, bradycardia and there were reductions in left ventricular and carotid artery dP/dt max. These effects were most pronounced following injections into the pulmonary artery; they were not observed after bilateral vagotomy or after injections into the lumen of the left ventricle. It is suggested that DECC, like nicotine, stimulates vagal receptors in the pulmonary vascular bed. 3 The secondary phase was characterized by marked systemic and pulmonary hypertension, by contractions of the nictitating membrane and by increases in left ventricular dP/dt (at fixed isovolumic pressures), in cardiac output and in myocardial blood flow. All these effects were prevented, or markedly reduced, following the administration of hexamethonium or bethanidine and the pressor response was prevented by phentolamine. It is concluded that, in doses similar to those used in therapeutics, DECC stimulates sympathetic ganglia and releases noradrenaline. The relevance of this finding to the reported side effects of the drug are discussed. 4 DECC (5 or 10 mg/kg) significantly inhibited prostaglandin F2alpha-induced increases in peak inspiratory intra-tracheal pressure without modifying its pulmonary hypertensive effect. The possible relevance of this finding to the use of DECC in asthma is discussed.