Desciclovir
(Synonyms: DCV, 6-Deoxyacyclovir, BW A515U) 目录号 : GC25341Desciclovir (DCV, 6-Deoxyacyclovir, BW A515U) is a prodrug of the antiherpetic agent acyclovir (ACV) that converted into ACV by xanthine oxidase in humans.
Cas No.:84408-37-7
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
Desciclovir (DCV, 6-Deoxyacyclovir, BW A515U) is a prodrug of the antiherpetic agent acyclovir (ACV) that converted into ACV by xanthine oxidase in humans.
[1] H C Krasny, B G Petty. J Clin Pharmacol. 1987 Jan;27(1):74-7.
| Cas No. | 84408-37-7 | SDF | Download SDF |
| 别名 | DCV, 6-Deoxyacyclovir, BW A515U | ||
| 分子式 | C8H11N5O2 | 分子量 | 209.21 |
| 溶解度 | DMSO: 42 mg/mL (200.76 mM);Water: 25 mg/mL (119.50 mM);Ethanol: 3 mg/mL (14.34 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 | 4.7799 mL | 23.8994 mL | 47.7989 mL |
| 5 mM | 0.956 mL | 4.7799 mL | 9.5598 mL |
| 10 mM | 0.478 mL | 2.3899 mL | 4.7799 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。
Metabolism of Desciclovir, a prodrug of acyclovir, in humans after multiple oral dosing
J Clin Pharmacol 1987 Jan;27(1):74-7.PMID:3680558DOI:10.1177/009127008702700112.
Desciclovir (DCV), a prodrug of the antiherpetic agent acyclovir (ACV), is converted in humans to ACV, presumably by xanthine oxidase. Further metabolism of these two compounds was investigated in six human volunteers given 250 mg DCV orally every eight hours for ten days plus one dose on day 11. The mean percent dose recovered in urine (24 hr) on days 2, 5, and 10 as carboxy-DCV (2%) and as carboxy-ACV (14%) along with recoveries of DCV (6%) and ACV (62%) gave a mean total of 84% cleared over a 24-hour period at steady state. Carboxyl metabolites were not found in the plasma of these same subjects at peak DCV concentration on dose day 11. The ratios of DCV and ACV to their corresponding carboxyl metabolites in urine were 4:1 and 3:1, respectively, suggesting that there is little or no difference in the efficiency of these two substrates for oxidation to their carboxylic acid metabolites.
Pharmacokinetics and tolerance of Desciclovir, a prodrug of acyclovir, in healthy human volunteers
Antimicrob Agents Chemother 1987 Sep;31(9):1317-22.PMID:3674844DOI:10.1128/AAC.31.9.1317.
Because of the incomplete absorption of acyclovir (ACV) when given orally in humans, efforts have been made to develop a prodrug of ACV that would be better absorbed from the gastrointestinal tract and then converted in vivo to ACV. One such compound, Desciclovir (DCV), is converted to acyclovir in vivo by xanthine oxidase. We gave each of 13 healthy volunteers 250 mg (about 3.25 mg/kg of body weight) of DCV orally thrice daily for 10 days, collected serial plasma and urine specimens, and measured DCV and ACV concentrations. The absorption of DCV was at least 75%, and almost two-thirds of the administered oral dose was recovered in the urine as ACV. Peak ACV levels in plasma were about 5 micrograms/ml and were reached in less than 1 h. The levels of ACV achieved in plasma were of the same magnitude as those reported for subjects given intravenous ACV at a dose of 2.5 mg/kg and approximately 10-fold higher than levels attained after administration of 200 mg of oral ACV every 4 h as measured in previous studies. The half-life of DCV was 0.85 +/- 0.16 h, compared with 2.6 +/- 0.5 h for ACV, indicating rapid conversion of DCV to ACV. There was no substantial increase in ACV levels in plasma on day 11 compared with day 2. No serious or consistent adverse effects were noted. In particular, the creatinine level in serum did not significantly rise in any subject and remained within the normal range in all.
Efficacy of Desciclovir in the treatment of Epstein-Barr virus infection in oral hairy leukoplakia
J Acquir Immune Defic Syndr (1988) 1990;3(6):571-8.PMID:2159990doi
The efficacy of Desciclovir, an analog of acyclovir, in eliminating lesions of oral hairy leukoplakia (HL) and suppressing Epstein-Barr virus (EBV) infection was evaluated in a double-blind, placebo-controlled study of 14 patients. Patients were randomized to receive either the active drug, 250 mg three times a day for 14 days, or placebo. In all eight patients receiving Desciclovir, lesions of HL were either completely resolved or significantly reduced during the treatment period, whereas lesions in patients receiving placebo showed no change. The histological features of HL were significantly diminished in patients on Desciclovir, and cytochemical, in situ hybridization, and ultrastructural studies showed that EBV infection was eliminated or dramatically reduced in the Desciclovir group only. Four patients on Desciclovir reported side effects, but none required withdrawal from the study. The reappearance of HL in all eight subjects on Desciclovir within 1-4 months after therapy was discontinued suggests the need for additional study.
Open study of 2-amino-9-(hydroxyethoxymethyl)-9H-purine (Desciclovir) in the treatment of herpes zoster
J Antimicrob Chemother 1987 Nov;20(5):743-51.PMID:3429375DOI:10.1093/jac/20.5.743.
An oral pro-drug of acyclovir, 2-amino-9-(2-hydroxyethoxymethyl)-9H-purine (Desciclovir) was evaluated in an open study comprising of 20 patients with herpes zoster. The clinical effects were comparable to those obtained with oral and intravenous acyclovir, even with a dosage of only 125 mg thrice daily. There was adequate absorption though considerable individual variation occurred. No effects of concomitant food intake were demonstrated. The finding of possible impaired conversion of Desciclovir to acyclovir in one patient was unexplained and deserves attention in future studies. Likewise, more studies are needed to understand the occurrence of transient high peak plasma concentrations of acyclovir. Side-effects other than those already known with the use of acyclovir, namely reversible tubular damage, were not observed.
Desciclovir permeation of the human erythrocyte membrane by nonfacilitated diffusion
Biochem Pharmacol 1991 Jun 21;42(1):147-52.PMID:2069588DOI:10.1016/0006-2952(91)90693-y.
The mechanism of transport of Desciclovir (DCV)--a structural analogue and prodrug of acyclovir (ACV) which provides an improved oral bioavailability of ACV--was investigated in human erythrocytes with a "papaverine-stop" assay. DCV influx was nonconcentrative, linearly dependent on DCV concentration (0.9 microM to 15 mM), insensitive (less than or equal to 20% inhibition) to nucleobases, nucleosides, or potent inhibitors of nucleoside transport, and occurred without permeant metabolism. However, DCV was a weak competitive inhibitor of the influx of adenine (Ki = 1.3 mM) and of 5-iodo-2'-deoxyuridine (Ki = 2.9 mM). permeants of the erythrocyte nucleobase and nucleoside carriers, respectively. This indicates that DCV has an affinity for both of these transporters, even though it appears not to be an effective permeant. We conclude that, in contrast to ACV which enters human erythrocytes primarily via the nucleobase carrier, DCV permeates these cells chiefly (greater than or equal to 80%) by nonfacilitated diffusion. This mechanistic difference in transport between ACV and DCV is attributed to differences in their desolvation energies and suggests an explanation for the differences in the oral bioavailability of ACV which is observed after the administration of these two "acyclic nucleosides."