Vibunazole (BAY-N-7133)
(Synonyms: 维布纳唑) 目录号 : GC32321
Vibunazole是一种新型的抗真菌唑。
Cas No.:80456-55-9
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
Animal experiment: | Under pentobarbital anesthesia 26 to 30 g female Swiss-Webster albino mice are injected intratracheally with either 0.05 mL sterile 0.9 % NaCI solution or 150 arthroconidia of Coccidioides imrnitis (strain Silveira) suspended in 0.05 mL of 0.9 % NaCI solution. Treatment of cohorts of ten infected and ten uninfected mice is begun 72 h after inoculation. Daily i.v. injections (tail vein) of 0.1 mL of 5 % glucose solution delivering either 0, 2.5, 5 or 10 mg/kg/dose of Vibunazole are given for 30 days[1]. |
References: [1]. Hoeprich PD, et al. Activity of BAY n 7133 and BAY 1 9139 in vitro and in experimental murine coccidioidomycosis. Eur J Clin Microbiol. 1985 Aug;4(4):400-3. | |
Vibunazole is a new antifungal azole.
Vibunazole is an antifungal azole. Low concentrations of all three drugs inhibit Coccidioides immitis, strain Silveira, in vitro with a descending order of activity ketoconazole>Vibunazole>BAY 1 9139[1].
The untreated, infected mice lost weight initially and progressively, whereas treated mice gain weight after an initial loss with Vibunazole (all doses), BAY 1 9139 and ketoconazole at 2.5 mg/kg/day. With both Vibunazole and BAY 1 9139, the 5 and 10 mg/kg doses yield serum concentrations exceeding the MICs for the Coccidioides immitis test strain (0.8 and 1.5 μg/mL respectively) for periods in excess of 30 min after injection[1].
[1]. Hoeprich PD, et al. Activity of BAY n 7133 and BAY 1 9139 in vitro and in experimental murine coccidioidomycosis. Eur J Clin Microbiol. 1985 Aug;4(4):400-3.
| Cas No. | 80456-55-9 | SDF | |
| 别名 | 维布纳唑 | ||
| Canonical SMILES | OC(C(C)(C)C)(COC1=CC=C(Cl)C=C1)CN2N=CN=C2 | ||
| 分子式 | C15H20ClN3O2 | 分子量 | 309.79 |
| 溶解度 | Soluble in DMSO | 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 | 3.228 mL | 16.14 mL | 32.2799 mL |
| 5 mM | 0.6456 mL | 3.228 mL | 6.456 mL |
| 10 mM | 0.3228 mL | 1.614 mL | 3.228 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。
Pharmacokinetics of Vibunazole (BAY n 7133) administered orally to healthy subjects
J Antimicrob Chemother 1985 Jul;16(1):75-9.PMID:4044466DOI:10.1093/jac/16.1.75.
The role of gastric acidity in the absorption of the new antifungal drug Vibunazole was studied in six healthy volunteers. Vibunazole was administered orally as 400 mg tablets to fasting subjects under three conditions: after 400 mg cimetidine orally, after 30 ml diluted hydrochloric acid orally, and alone. Plasma concentrations of Vibunazole were determined with HPLC. The plasma concentration profile of Vibunazole could be described adequately by a one-compartmental open model with first-order absorption. Kinetic parameters after oral administration did not differ between the three modes of administration. The mean peak time was 1 h 29 min (after lag-time). The mean peak concentration was 2.76 mg/l. The mean elimination half-life of Vibunazole was 2 h 22 min. The mean absorption lag-time was 30 min, with considerable variation.
A direct comparison of oral treatments with BAY-N-7133, BAY-1-9139 and ketoconazole in experimental murine coccidioidomycosis
Sabouraudia 1984;22(1):37-46.PMID:6322362DOI:10.1080/00362178485380071.
Two new experimental antifungal azole drugs were compared with ketoconazole for the management of experimental murine coccidioidomycosis. The first, BAY-N-7133, a triazole, was superior to the second, BAY-1-9139, an imidazole derivative. Neither BAY drug was as effective as ketoconazole in early fulminant coccidioidomycosis of mice, in later disseminated disease and in deep-seated chronic disease. A possible limitation of BAY-N-7133 in the mouse model was its reported capacity to induce enzyme changes that accelerated its clearance from serum. Induction of such an enzyme response in human beings has been reported not to occur.
Antifungal relative inhibition factors: BAY l-9139, bifonazole, butoconazole, isoconazole, itraconazole (R 51211), oxiconazole, Ro 14-4767/002, sulconazole, terconazole and Vibunazole (BAY n-7133) compared in vitro with nine established antifungal agents
J Antimicrob Chemother 1984 Aug;14(2):105-14.PMID:6094418DOI:10.1093/jac/14.2.105.
Nine new antifungal agents were tested for their activity in vitro in terms of relative inhibition factors (RIFs) against 26 isolates of Candida species, eight isolates of Aspergillus species and six isolates of dermatophyte fungi. Eight of the new compounds were azole antifungals, the ninth was a phenylmorpholine derivative. Against Candida species, all the novel compounds gave RIFs that were of a similar order to RIFs for established imidazole compounds. Two topical antifungals, butoconazole and terconazole, and two systemic antifungals, itraconazole and Vibunazole, gave mean RIFs less than 60% in tests with Candida species, and therefore matched clotrimazole, ketoconazole and tioconazole in terms of RIF. However, none of the new compounds gave RIFs as low as amphotericin B against the Candida isolates. Against Aspergillus isolates, itraconazole, with a mean RIF of 25%, was even more active in vitro than amphotericin B. Vibunazole was as active as ketoconazole against Aspergillus isolates. All the new antifungals except Bay l-9139 gave very low RIFs against dermatophyte isolates, and thus matched established imidazole antifungals for inhibitory effects in vitro. In terms of RIF data, all the nine new compounds tested appear to offer reasonable potential for antifungal chemotherapy in vivo. A similar conclusion would not have been drawn from minimal inhibitory concentration data, which tended to show most of the new antifungals in a very poor light. Tests with amphotericin B, 5-fluorocytosine and ketoconazole showed that RIF can vary substantially with the pH of the test medium. For amphotericin B and ketoconazole the best activity was seen at neutral pH values; for 5-fluorocytosine the greatest inhibitory activity was found at lower pH values.
New azole compounds: Vibunazole (Bay n7133) and Bay L9139, compared with ketoconazole in the therapy of systemic candidosis and in pharmacokinetic studies, in mice
J Antimicrob Chemother 1985 Jan;15(1):69-75.PMID:3972759DOI:10.1093/jac/15.1.69.
Ketoconazole, a new imidazole: Bay L9139, and a new triazole: Vibunazole (Bay n7133) were compared in therapy of systemic candidosis. CD-1 male mice were challenged with Candida albicans intravenously (greater than LD80), and treated twice a day, orally, for one month. The isolate of Can. albicans used, and isolates obtained after treatment with the antifungals, were susceptible to all three drugs (MICs less than or equal to 0.5 mg/l). No drug was lethal to uninfected mice in doses of 200 mg/kg/day for one month. With therapy started on the day after infection, all three drugs at 50 or 100 mg/kg/day prolonged survival, compared with controls (P less than 0.05), with ketoconazole slightly superior to the other two drugs, but none did so at 25 mg/kg/day. At 200 mg/kg/day ketoconazole and Vibunazole were protective, but L9139 was not, and this suggested synergistic toxicity of L9139 with Can. albicans infection, at this dose. With treatment begun on day 4, ketoconazole prolonged survival (P less than 0.005) at 200 or 100 mg/kg/day compared with controls, but ketoconazole at 10-50 mg/kg/day, and Vibunazole and L9139 at 10-200 mg/kg/day were ineffective. Survivors had renal lesions and culture-proven residual infection. Pharmacokinetic studies indicated lower peak Vibunazole and 9139 serum concentrations, and reduced area-under-curve (AUC), after 26 days of treatment, as against single dose administration. The relative inefficacy of Vibunazole and L9139 appears to be related to unfavourable pharmacokinetic properties with continued administration.
Managing fungal and viral infection in the immunocompromised host
Recent Results Cancer Res 1988;108:61-70.PMID:3051213DOI:10.1007/978-3-642-82932-1_9.
The increasing number of opportunistic fungal infections in neutropenic cancer patients has become of major concern. Postmortem examinations have shown that more than half of the deaths attributed to infection were due to disseminated fungal infections. Candida species are the major pathogens. Unfortunately, the early diagnosis of serious fungal invasion is exceedingly difficult in these patients, since the manifestations of infection are ill-defined and the organisms can only rarely be isolated from blood cultures. Therefore, empirical antifungal therapy in febrile patients early in the course of disease appears necessary to prevent fungal superinfections and to control clinically undetected fungal invasion. Even if a fungal infection is diagnosed, treatment options are limited to a small number of drugs, and the chance of successful treatment is slim. Amphotericin B remains the most effective drug for systemic fungal infection; however, it is also the most toxic antimicrobical in use. Reduction of its toxicity and, simultaneously, improvement of its effectiveness can be achieved by incorporation into liposomes, although liposomal amphotericin B is not yet available commercially. The newer azoles, such as ketoconazole, Vibunazole, and itraconazole are orally active and less toxic. Azoles have been successfully used in the treatment of superficial candidal infections; they are not very active in systemic candidiasis. Inhibitors of the cell wall biosynthesis of candida species include inhibitors of chitin and glucan biosynthesis. Echinocandins and papulacandins interfer with the glucan synthesis and show good anticandidal activity. Their therapeutic potential is currently being explored in clinical trials. Neutropenic patients and particularly bone marrow transplant (BMT) recipients are, in addition to fungal infections, at very high risk for herpesvirus infections: herpes simplex virus (HSV) 0-20 days after BMT, cytomegalovirus (CMV) 40-80 days after BMT, varicella zoster virus (VZV) 100-160 days after BMT, and Epstein-Barr virus (EBV) 14-21 days after BMT. Acyclovir and vidarabine are, at present, the only antiviral drugs available for HSV and VZV infections, acyclovir apparently being the more effective. It is also the drug of choice for prevention of HSV infections in severely immunocompromised, i.e., BMT, patients. Bromovinyldeoxyuridine seems to be suitable for systemic treatment of HSV-1 and VZV infections in these patients. Its potency in inhibiting HSV-1 and VZV replication is superior to that of ACV, and in therapeutic doses it is nontoxic to hematopoietic progenitor cells.(ABSTRACT TRUNCATED AT 400 WORDS)