Fiacitabine
(Synonyms: 非西他滨; NSC 382097; FIAC; FOAC) 目录号 : GC36039
Fiacitabine(NSC 382097; FIAC; FOAC)是选择性HSV DNA复制抑制剂，对HSV1和HSV2的IC50分别为2.5 nM和12.6 nM。
Cas No.:69123-90-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Fiacitabine(NSC 382097; FIAC; FOAC) is a selective inhibitior of DNA replication of herpes simplex virus(HSV) with IC50 values of 2.5 nM and 12.6 nM for HSV1 and HSV2, respectively. IC50 value: 2.5/12.6 nM (HSV1/2) [2]Target: HSVFIAC suppressed by 90% the replication of various strains of herpes simplex virus types 1 and 2 at concentrations of 0.0025 to 0.0126 microM. Cytotoxicity was minimal, as determined by trypan blue dye exclusion with norman Vero, WI-38, and NC-37 cell proliferation; the 50% inhibitory dose was 4 to 10 microM in a 4-day assay. FIAC was active at much lower concentrations than arabinosylcytosine, iododeoxyuridine, and arabinosyladenine. It was slightly more active against herpes simplex virus type 1 than acycloquanosine and slightly more toxic to normal cells. FIAC was about 8,000 times more active against the replication of wild-type herpes simplex virus type 1 than against a mutant strain lacking the expression of virus-specified thymidine kinase [2].
[1]. Allaudeen HS, et al. Selective inhibition of DNA replication in herpes simplex virus infected cells by 1-(2'-deoxy-2'-fluoro-beta-D-arabinofuranosyl)-5-iodocytosine. J Biol Chem. 1982 Oct 25;257(20):11879-82. [2]. Lopez C, et al. 2'-fluoro-5-iodo-aracytosine, a potent and selective anti-herpesvirus agent. Antimicrob Agents Chemother. 1980 May;17(5):803-6.
| Cas No. | 69123-90-6 | SDF | |
| 别名 | 非西他滨; NSC 382097; FIAC; FOAC | ||
| Canonical SMILES | O=C(N=C1N)N([C@@H]([C@H]([C@@H]2O)F)O[C@@H]2CO)C=C1I | ||
| 分子式 | C9H11FIN3O4 | 分子量 | 371.1 |
| 溶解度 | DMSO: ≥ 37 mg/mL (99.70 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 | 2.6947 mL | 13.4735 mL | 26.9469 mL |
| 5 mM | 0.5389 mL | 2.6947 mL | 5.3894 mL |
| 10 mM | 0.2695 mL | 1.3473 mL | 2.6947 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。
Recognition and treatment of shingles
Drugs 1994 Oct;48(4):528-48.PMID:7528128DOI:10.2165/00003495-199448040-00004.
Varicella zoster virus (VZV) is responsible for a primary infection (varicella) followed by a latency, eventually resulting in herpes zoster (shingles). The replication cycle of VZV is normally interrupted after varicella. Consequently, VZV remains dormant in the organism. Reactivation occurs after viraemia, and the development of tissue alterations (skin and viscera) depends on the immunological status of the patient. Diagnosis of herpes zoster relies on clinical recognition and cytological and histological evaluations combined with immunohistochemistry and molecular biology techniques. Treatment of herpes zoster primarily relies upon antiviral drugs and incidentally on immunomodulating agents, specific immunoglobulins, antimicrobial agents, antiviral enzymes and corticosteroids. Drugs with a clinically relevant activity against varicella zoster virus infections include aciclovir, adenosine monophosphate, bromodeoxyuridine, desciclovir, Fiacitabine, idoxuridine, interferon-alpha and vidarabine. Among them, aciclovir appears to be a first-line agent. Its efficacy has been well established by many clinical studies. Promising drugs for the future include famciclovir, penciclovir, valaciclovir and other molecules currently under investigation. Recent and promising improvements in antiviral drug development may increase patient compliance, cost-benefit ratios and therapeutic efficacy.
Current pharmacological approaches to the therapy of varicella zoster virus infections: a guide to treatment
Drugs 1999 Feb;57(2):187-206.PMID:10188760DOI:10.2165/00003495-199957020-00005.
Varicella zoster virus (VZV), a member of the herpesvirus family, is responsible for both primary (varicella, chickenpox) as well as reactivation (zoster, shingles) infections. In immunocompetent patients, the course of varicella is generally benign. For varicella zoster, post-herpetic neuralgia is the most common complication. In immunocompromised patients (particularly those with AIDS), transplant recipients and cancer patients, VZV infections can be life-threatening. For these patients and also for immunocompetent patients at risk such as pregnant women or premature infants, the current treatment of choice is based on either intravenous or oral aciclovir (acyclovir). The low oral bioavailability of aciclovir, as well as the emergence of drug-resistant virus strains, have stimulated efforts towards the development of new compounds for the treatment of individuals with VZV infections. Among these new compounds, penciclovir, its oral prodrug form famciclovir and the oral pro-drug form of aciclovir (valaciclovir), rank among the most promising. As with aciclovir itself, all of these drugs are dependent on the virus-encoded thymidine kinase (TK) for their intracellular activation (phosphorylation), and, upon conversion to their triphosphate form, they act as inhibitors/alternative substrate of the viral DNA polymerase. Therefore, cross-resistance to these drugs may be expected for those virus mutants that are TK-deficient and thus resistant to aciclovir. Other classes of nucleoside analogues dependent for their phosphorylation on the viral TK that have been pursued for the treatment of VZV infections include sorivudine, brivudine, fialuridine, Fiacitabine and netivudine. Among oxetanocins, which are partially dependent on viral TK, lobucavir is now under clinical evaluation. Foscarnet, which does not require any previous metabolism to interact with the viral DNA polymerase, is used in the clinic when TK-deficient VZV mutants emerge during aciclovir treatment. TK-deficient mutants are also sensitive to the acyclic nucleoside phosphonates (i.e. [s]-1-[3-hydroxy-2-phosphonylmethoxypropyl]cytosine; HPMPC); these agents do not depend on the virus-encoded TK for their phosphorylation but depend on cellular enzymes for conversion to their diphosphoryl derivatives which then inhibit viral DNA synthesis. Vaccination for VZV has now come of age. It is recommended for healthy children, patients with leukaemia, and patients receiving immunosuppressive therapy or those with chronic diseases. The protection induced by the vaccine seems, to some extent, to include zoster and associated neuralgia. Passive immuniatin based on specific immunoglobulins does not effectively prevent VZV infection and is therefore restricted to high risk individuals (i.e. immunocompromised children and pregnant women).