Lerisetron
(Synonyms: F 0930, F 0930RS) 目录号 : GC25569Lerisetron (F 0930, F 0930RS) is a 5-HT3 receptor antagonist with IC50 of 0.81μM.
Cas No.:143257-98-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
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- SDS (Safety Data Sheet)
- Datasheet
Lerisetron (F 0930, F 0930RS) is a 5-HT3 receptor antagonist with IC50 of 0.81μM.
[1] Cooper M, et al. Arzneimittelforschung. 2002;52(9):689-94.
| Cas No. | 143257-98-1 | SDF | Download SDF |
| 别名 | F 0930, F 0930RS | ||
| 分子式 | C18H20N4 | 分子量 | 292.38 |
| 溶解度 | DMSO: 58 mg/mL (198.37 mM);Water: Insoluble;Ethanol: 58 mg/mL (198.37 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 | 3.4202 mL | 17.101 mL | 34.2021 mL |
| 5 mM | 0.684 mL | 3.4202 mL | 6.8404 mL |
| 10 mM | 0.342 mL | 1.7101 mL | 3.4202 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。
Lerisetron. FAES
Curr Opin Investig Drugs 2003 Jul;4(7):874-7.PMID:14619411doi
Lerisetron is a 5-hydroxytryptamine3 receptor antagonist under development by FAES Farma for the potential treatment of emesis resulting from chemotherapy. Phase I trials of Lerisetron were underway in Spain by 1994, and as of June 2000, the compound was in phase II trials in the UK. By the end of 2001, phase II trials had been completed and phase III trials had commenced.
Lerisetron Analogues with Antimalarial Properties: Synthesis, Structure-Activity Relationship Studies, and Biological Assessment
ACS Omega 2020 Mar 17;5(12):6967-6982.PMID:32258933DOI:10.1021/acsomega.0c00327.
A phenotypic whole cell high-throughput screen against the asexual blood and liver stages of the malaria parasite identified a benzimidazole chemical series. Among the hits were the antiemetic benzimidazole drug Lerisetron 1 (IC50 NF54 = 0.81 μM) and its methyl-substituted analogue 2 (IC50 NF54 = 0.098 μM). A medicinal chemistry hit to lead effort led to the identification of chloro-substituted analogue 3 with high potency against the drug-sensitive NF54 (IC50 NF54 = 0.062 μM) and multidrug-resistant K1 (IC50 K1 = 0.054 μM) strains of the human malaria parasite Plasmodium falciparum. Compounds 2 and 3 gratifyingly showed in vivo efficacy in both Plasmodium berghei and P. falciparum mouse models of malaria. Cardiotoxicity risk as expressed in strong inhibition of the human ether-a-go-go-related gene (hERG) potassium channel was identified as a major liability to address. This led to the synthesis and biological assessment of around 60 analogues from which several compounds with improved antiplasmodial potency, relative to the lead compound 3, were identified.
Antiemetic effects of Lerisetron in radiation-induced emesis in the dog
Acta Oncol 1998;37(7-8):759-63.PMID:10050999DOI:10.1080/028418698430160.
The 5-HT3 receptor antagonists are the most potent antiemetics known at present. Lerisetron is a new 5-HT3 receptor antagonist chemically unrelated to other antagonists like Ondansetron. An emesis model in the dog induced by irradiation with 60Co was used, and 8 Gy were administered over the total body surface. An irradiated control group was established and received no medication, and two irradiated groups received treatment with either Ondansetron or Lerisetron. The 'up-down' technique was employed to determine the effective dose (ED50). A logarithmic-scale was used to increase or decrease the doses in each case. The initial doses were 300 microg/kg for Ondansetron and 100 microg/kg for Lerisetron. All animals in the control group vomited. The ED50 of Ondansetron was 178+/-151 microg/kg body wt and that of Lerisetron was 63+/-18 microg/kg. Lerisetron is more potent and presented less individual variability than Ondansetron, but its antiemetic effects were equally effective.
Effects of Lerisetron, a new 5-HT3 receptor antagonist, on ipecacuanha-induced emesis in healthy volunteers
Arzneimittelforschung 2002;52(9):689-94.PMID:12404884DOI:10.1055/s-0031-1299952.
The purpose of these studies was to evaluate the effect of Lerisetron (1-phenyl-methyl-2-piperazinyl-1H-benzimidazole hydrochloride, CAS 143257-98-1, F-0930-RS2), a new 5-HT3 receptor antagonist, on ipecacuanha-induced nausea and vomiting. The ipecacuanha model of emesis has been used to test the anti-emetic activity of several different 5-HT3 antagonists and the anti-emetic doses that were effective in the ipecacuanha model have been found to correlate well with the clinically effective doses. Study 1 investigated oral doses of Lerisetron from 4 mg to 40 mg. Study 2 evaluated the duration of effect of a single dose of 20 mg oral Lerisetron. Study 3 evaluated intravenous doses of 18 mg and 12 mg Lerisetron. In Study 1, the 40 mg dose of oral Lerisetron inhibited emesis in all test subjects. The percentage of subjects who experienced an emetic episode increased as the dose of Lerisetron decreased. At the lowest dose level tested five of six subjects had an emetic episode compared with four out of five in the placebo group. In Study 2, 20 mg oral Lerisetron was effective up to 12 h after administration. When ipecacuanha was administered at 18 h post-dose three of seven subjects had an emetic episode and at 24 h post-dose the incidence of emesis was similar to the placebo treatment groups in the previous study. Study 3 demonstrated the effectiveness of intravenous doses of Lerisetron. The 18 mg intravenous dose reduced the number of patients experiencing emetic episodes by 75% compared with placebo, doses below 12 mg i.v. were not evaluated because of the reduced efficacy of the compound at this dose level. In conclusion, Lerisetron has been shown to be effective in the treatment of ipecacuanha-induced nausea and vomiting at intravenous doses of 18 mg and at oral doses of 20 mg for up to 12 hours.
Serum protein binding of Lerisetron, a novel specific 5HT3 antagonist, in patients with cancer
Cancer Chemother Pharmacol 1998;42(5):418-22.PMID:9771958DOI:10.1007/s002800050839.
The aim of this study was, (1) to characterize the serum protein binding of Lerisetron, a new 5-hydroxytryptamine (5-HT3) receptor antagonist under investigation as an antiemetic agent, and (2) to measure the percentage of unbound Lerisetron in cancer patients. The binding parameters were determined in human serum albumin (HSA), alpha1-acid glycoprotein (AAG) and in pooled serum from six healthy volunteers. Concentrations of Lerisetron ranging from 50 ng/ml to 2 microg/ml were used. The serum protein binding of 14C-lerisetron (2 microg/ml) was determined by ultrafiltration in three groups of individuals. Group I comprised healthy subjects (n = 11), group II comprised cancer patients undergoing radiotherapy (n = 9), and group III comprised cancer patients receiving chemotherapy (n = 18). The unbound concentration of Lerisetron was measured in all samples by liquid scintillation counting. Concentrations of both AAG and HSA were also measured in all serum samples. The drug was extensively bound in pooled serum, involving a nonsaturated process. In HSA, Lerisetron was also highly bound (4.04+/-0.8% unbound) and the protein binding was essentially unchanged within the studied concentration range of Lerisetron. The extent of binding to AAG was high but significantly lower than in serum and in HSA and was also independent of Lerisetron concentration. The unbound Lerisetron was significantly decreased in group II cancer patients when compared with group I subjects (2.38+/-0.64% vs 3.70+/-0.70%; P < 0.001). No significant changes in Lerisetron binding were observed in group III patients. HSA was diminished in both groups of patients and AAG was only significantly increased in group II. Unbound Lerisetron was correlated with AAG in group II and with HSA in group III.