Benznidazol (Ro 07-1051)
(Synonyms: 苄硝唑; Ro 07-1051; Ro 71051) 目录号 : GC32326
An antiprotozoal agent
Cas No.:22994-85-0
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
Benznidazole is an orally bioavailable antiprotozoal agent.1 It is a 2-nitroimidazole prodrug that becomes active when the nitro group is reduced within the parasite.2 It inhibits the growth of the parasites T. cruzi, T. vaginalis, G. lamblia, and E. histolytica (IC50s = 8.1, 18.62, 22.58, and 4.27 μM, respectively).3,4 It also inhibits clonogenic growth of human C33A cervical and KNS42 glioblastoma cancer cells under hypoxic, but not normoxic, conditions when used at a concentration of 100 μM.5 Benznidazole (100 mg/kg per day) decreases T. cruzi blood parasitemia to below detectable levels in a mouse model of chronic stable Chagas disease.1 Formulations containing benznidazole have been used in the treatment of Chagas disease caused by T. cruzi.
1.Khare, S., Liu, W., Stinson, M., et al.Antitrypanosomal teatment with benznidazole is superior to posaconazole regimens in mouse models of Chagas diseaseAntimicrob. Agents Chemother.59(10)6385-6394(2015) 2.Trochine, A., Creek, D.J., Faral-Tello, P., et al.Benznidazole biotransformation and multiple targets in Trypanosoma cruzi revealed by metabolomicsPLoS Negl. Trop. Dis.8(5)e2844(2014) 3.Cogo, J., de Oliveira Caleare, A., Ueda-Nakamura, T., et al.Trypanocidal activity of guaianolide obtained from Tanacetum parthenium (L.) Schultz-Bip. and its combinational effect with benznidazolePhytomedicine20(1)59-66(2012) 4.Hernández-Nú?ez, E., Tlahuext, H., Moo-Puc, R., et al.Design, synthesis and biological evaluation of 2-(2-amino-5(6)-nitro-1H-benzimidazol-1-yl)-N-arylacetamides as antiprotozoal agentsMolecules22(4)E579(2017) 5.Li, Q., Lin, Q., and Yun, Z.Hypoxia-activated cytotoxicity of benznidazole against clonogenic tumor cellsCancer Biol. Ther.17(12)1266-1273(2016)
| Cas No. | 22994-85-0 | SDF | |
| 别名 | 苄硝唑; Ro 07-1051; Ro 71051 | ||
| Canonical SMILES | O=C(NCC1=CC=CC=C1)CN2C=CN=C2[N+]([O-])=O | ||
| 分子式 | C12H12N4O3 | 分子量 | 260.25 |
| 溶解度 | DMSO : 160 mg/mL (614.79 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 | 3.8425 mL | 19.2123 mL | 38.4246 mL |
| 5 mM | 0.7685 mL | 3.8425 mL | 7.6849 mL |
| 10 mM | 0.3842 mL | 1.9212 mL | 3.8425 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。
The pharmacokinetics in mice and dogs of nitroimidazole radiosensitizers and chemosensitizers more lipophilic than misonidazole
Int J Radiat Oncol Biol Phys 1982 Mar-Apr;8(3-4):473-6.PMID:7107369DOI:10.1016/0360-3016(82)90664-2.
We have examined the pharmacokinetic properties of nitroimidazole radiosensitizers and chemosensitizers more lipophilic than misonidazole (MISO). In dogs, 2 analogues showed comparable peak plasma concentrations with considerably shorter half-lives (t1/2) and reduced areas under curves (AUC). Benznidazole (Ro 07-1051) had a much longer t1/2, a higher AUC, and somewhat higher peak concentrations. In mice tumor/plasma, brain/plasma, and tumor/brain ratios were generally similar to MISO, as was penetration of brain and peripheral nerve by benznidazole in dogs. Selection of lipophilic analogues with appropriate pharmacokinetic properties may facilitate accommodation of the potentially different requirements for improved radiosensitization or chemosensitization.
Chemosensitization by lipophilic nitroimidazoles
Br J Cancer 1983 Jul;48(1):17-26.PMID:6871076DOI:10.1038/bjc.1983.152.
We have carried out experiments to determine the response of tumours and normal tissues in the C3H mouse to the combination of lipophilic nitroimidazoles and CCNU, cyclophosphamide or melphalan. The nitroimidazoles studied were Ro 07-1902 (1902) and benznidazole (Ro 07-1051, BENZO). Maximum enhancement of CCNU response in the KHT sarcoma by 2.5 mmol kg-1 1902 or 0.3 mmol kg-1 BENZO occurred at low doses of CCNU where dose modifying factors (DMF) of 2.5-3.0 and 1.5-2.0 respectively were found. The DMFs for depression of white cell count at day 3 were 1.6 and 1.2 respectively whilst the DMFs for LD50/30 were 1.5 and 1.3. There appears, therefore, to be a therapeutic gain at low doses of CCNU of about the same magnitude as produced by 2.5 mmol kg-1 misonidazole. The production of this gain at relatively low doses of BENZO is of possible clinical significance. Some sensitization of the KHT tumour to CCNU by 0.3 mmol kg-1 BENZO was maintained even with an interval of 25 h between BENZO and CCNU injection. A multiple injection regime of BENZO administration designed to maintain plasma concentrations for prolonged periods was, however, no more effective than a single dose. The response of the RIF-1 sarcoma to cyclophosphamide was not enhanced by the lipophilic sensitizers at the doses previously stated. Considerable enhancement of tumour response to melphalan (DMF 2.0) was produced by both lipophilic sensitizers. Enhancement of acute LD50 was similar in magnitude but no large enhancement by BENZO of melphalan induced white blood cell depression was observed. The evidence regarding the therapeutic potential of this combination is, therefore, equivocal.
Structure/activity relationships for the enhancement by electron-affinic drugs of the anti-tumour effect of CCNU
Br J Cancer 1982 Aug;46(2):249-59.PMID:7150475DOI:10.1038/bjc.1982.190.
Using a regrowth-delay assay, we investigated structure/activity relationships for the enhancement by electron-affinic agents of the anti-tumour effect of the nitrosourea CCNU against the KHT sarcoma in C3H mice. A series of neutral 2-nitroimidazoles similar in electron affinity but varying in octanol/water partition coefficient (PC) over 4 orders of magnitude (0.016- greater than 200, Misonidazole = 0.43) were examined at a fixed dose of 2.5 mmol/kg. A parabolic (quadratic) dependence of activity on log PC was observed. Analogues more hydrophilic than misonidazole (MISO) were inactive as were those with very high PCs (greater than 20). Those with PC 0.43--20 were usually more active than MISO, some considerably so. The fairly lipophilic 5-nitroimidazoles nimorazole and metronidazole (METRO) had similar activity to MISO, despite their reduced electron affinity. Two basic 2-nitroimidazoles more efficient as radiosensitizers in vitro likewise showed activity comparable to MISO. We also investigated several agents more electron-affinic than MISO, including some non-nitro compounds. Most were inactive at maximum tolerated doses, but nitrofurazone showed reasonable activity. Sensitizer dose-response curves were obtained for MISO, METRO and two of the most effective agents, benznidazole (Ro 07-1051) and Ro 07-1902. The two latter agents were both considerably more active than MISO at low doses (0.1--0.9 mmol/kg). These studies indicate that the structural features of electron-affinic agents responsible for the enhancement of KHT tumour response to CCNU, are quite different from those affecting radiosensitization, lipophilicity being particularly important. The microsomal enzyme-inhibitor SKF 525A increased the anti-tumour effect of CCNU, suggesting inhibition of CCNU metabolism as one possible mechanism contributing to chemosensitization by lipophilic electron-affinic agents in mice.