Phensuximide
(Synonyms: 密朗丁) 目录号 : GC45547An anticonvulsant
Cas No.:86-34-0
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Phensuximide is an anticonvulsant.1 It inhibits seizures induced by maximal electroshock (MES) and pentylenetetrazole in mice (ED50s = 112 and 50 mg/kg, respectively). Phensuximide (1.25 mmol/kg, i.p.) induces proteinuria and hematuria in rats.2 Formulations containing phensuximide have been used in the treatment of petit mal seizures.
References
1. Kornet, M.J., Crider, A.M., and Magarian, E.O. Potential long-acting anticonvulsants. 1. Synthesis and activity of succinimides containing an alkylating group at the 2 position. J. Med. Chem. 20(3), 405-409 (1977).
2. Rankin, G.O., Cressey-Veneziano, K., Wang, R.T., et al. Urinary tract effects of phensuximide in the Sprague-Dawley and Fischer 344 rat. J. Appl. Toxicol. 6(5), 349-356 (1986).
| Cas No. | 86-34-0 | SDF | |
| 别名 | 密朗丁 | ||
| Canonical SMILES | O=C(N1C)C(C2=CC=CC=C2)CC1=O | ||
| 分子式 | C11H11NO2 | 分子量 | 189.2 |
| 溶解度 | DMF: 1mg/mL,DMSO: 15mg/mL,DMSO:PBS (pH 7.2) (1:5): 0.16mg/mL,Ethanol: 10mg/mL | 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 5.2854 mL | 26.4271 mL | 52.8541 mL |
| 5 mM | 1.0571 mL | 5.2854 mL | 10.5708 mL |
| 10 mM | 0.5285 mL | 2.6427 mL | 5.2854 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。
Urinary tract effects of Phensuximide in the Sprague-Dawley and Fischer 344 rat
J Appl Toxicol 1986 Oct;6(5):349-56.PMID:3772011DOI:10.1002/jat.2550060509.
Phensuximide is a succinimide antiepileptic drug useful in the treatment of petit mal epilepsy. Phensuximide has been reported to be nephrotoxic in man but not in animals. In the present study, the effects of single and subacute administration for seven days of Phensuximide on renal function and urinary tract morphology were evaluated in Sprague-Dawley and Fischer 344 rats. Single administration of Phensuximide (1.25 mmol/kg, ip) induced mild changes in renal function (trace hematuria, increased proteinuria and decreased p-aminohippurate uptake). No morphological changes were observed at 24 hr. Subacute administration of Phensuximide (0.6 mmol/kg/day, ip) produced diuresis in the Sprague-Dawley rat, but little functional evidence of nephrotoxicity. Renal morphological changes in Sprague-Dawley rats were seen primarily in distal segments of the nephrons. These changes were characterized by distensions of the basal infoldings, apical protrusions, and occlusion of some lumen. In the Fischer 344 rat, subacute Phensuximide administration (0.3 or 0.6 mmol/kg/day, ip) resulted in transient hematuria and proteinuria, but no change in the other renal function parameters studied. Renal morphological changes observed in Fischer 344 rats occurred primarily in proximal tubular cells. Damaged cells were characterized by large vacuoles at the basal infoldings, accumulations of opaque granules, migration of nuclei to the lumenal membranes, occlusion of the lumen and/or loss of the brush border. Morphological damage was more widespread in Fischer 344 rats than in Sprague-Dawley rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Plasma concentrations of Phensuximide, methsuximide, and their metabolites in relation to clinical efficacy
Neurology 1979 Nov;29(11):1509-13.PMID:116142DOI:10.1212/wnl.29.11.1509.
The clinical efficacy of Phensuximide and methsuximide was studied in relation to plasma concentrations of these compounds and their desmethyl metabolites. Single- and chronic-dose studies of each drug were carried out in five patients with intractable seizures. Patients were evaluated before and during treatment by 6-hour simultaneous video and telemetered electroencephalographic recordings to characterize the seizure type and by daily determinations of plasma antiepileptic drug concentrations. Phensuximide had a mean half-life of 7.8 hours and accumulated to an average fasting level of only 5.7 micrograms per milliliter. Desmethylphensuximide averaged only 1.7 micrograms per milliliter with a similar half-life. Methsuximide had an even shorter half-life, averaging 1.4 hours, but its desmethyl metabolite had a mean half-life of 38 hours and therefore accumulated to levels in excess of 40 micrograms per milliliter. The addition of Phensuximide to their regimens benefited none of the patients, but two had an excellent response to methsuximide. The failure of Phensuximide and its desmethyl metabolite to accumulate to reasonable levels is the likely explanation for the relatively weak antiepileptic effect of Phensuximide as compared with methsuximide.
Synthesis and anticancer activity of nitrosourea derivatives of Phensuximide
J Med Chem 1980 Mar;23(3):324-6.PMID:7365750DOI:10.1021/jm00177a024.
Nitrosourea derivatives 9--13 which utilize Phensuximide (1) as the carrier were synthesized as potential central nervous system antitumor agents. The N-(2-chloroethyl)-N-nitrosourea 13 was active in the mouse ependymoblastoma brain-tumor system, as well as the intraperitoneal L1210 leukemia system.
Role of para-hydroxylation in phensuximide-induced urotoxicity in the Fischer 344 rat
Toxicology 1992 Aug;74(1):77-88.PMID:1514190DOI:10.1016/0300-483x(92)90045-g.
Phensuximide (PSX) is an antiepileptic agent which has been shown to induce hemorrhagic cystitis and mild nephrotoxicity following repeated administration in man or rats or when acutely administered to phenobarbital-pretreated rats. The purpose of this study was to explore the role of para-hydroxylation of the phenyl group of PSX in PSX-induced urotoxicity. Two PSX derivatives, 2-(4-fluorophenyl)-N-methylsuccinimide (FMPS) and N-methyl-2-(4-methylphenyl)succinimide (MMPS), were synthesized and evaluated for urotoxic potential. Male Fischer 344 rats (four rats/group) were administered intraperitoneally (i.p.) a succinimide (0.4 or 1.0 mmol/kg) or vehicle and renal function monitored for 48 h. In a separate experiment, rats were pretreated with phenobarbital (75 mg/kg/day; 3 days, i.p.) prior to succinimide or succinimide vehicle. In non-phenobarbital pretreated rats, acute FMPS or MMPS treatment had little effect on renal function or morphology at the doses tested. Hematuria (+) was noted in the FMPS (1.0 mmol/kg) group on post-treatment day 2. However, in the phenobarbital-pretreated rats, FMPS (0.4 or 1.0 mmol/kg) induced marked hematuria (++) and increased proteinuria while having little or no effect on other renal functional parameters or renal morphology. At killing, bladders of treated rats were distended with bloody urine and exhibited hemorrhagic areas within the bladder wall. In phenobarbital-pretreated rats, MMPS administration had little effect on any renal functional parameter measured or urological morphology. These results suggest that para-hydroxylation does not contribute to the hemorrhagic cystitis induced by PSX.
Acute effects of the antiepileptic succinimides on the urinary tract and potentiation of phensuximide-induced urotoxicity by phenobarbital
J Appl Toxicol 1990 Jun;10(3):203-9.PMID:2380483DOI:10.1002/jat.2550100311.
Phensuximide (PSX), methsuximide (MSX) and ethosuximide (ESX) are succinimide antiepileptic agents used worldwide in the treatment of absence seizures. A previous study from our laboratory demonstrated that PSX (0.3 or 0.6 mmol kg-1 day-1, i.p.) induced urotoxicity following daily administration for 5-7 days in Fischer 344 rats, but PSX (1.25 mmol kg-1, i.p.) induced only minimal urotoxicity following acute administration. The purpose of this study was to determine the acute nephrotoxic potential of MSX and ESX in male Fischer 344 rats and if antiepileptic succinimide-induced urotoxicity is potentiated by phenobarbital pretreatment. In one set of experiments, rats (four rats per group) were administered a single intraperitoneal (i.p.) injection of a succinimide (0.4 or 1.0 mmol kg-1) or vehicle (sesame oil, 2.5 ml kg-1), and the renal function was monitored at 24 and 48 h. Neither ESX or MSX induced substantial changes in renal function or morphology, which suggests that neither compound is acutely nephrotoxic. Similar results were obtained with PSX, which supported our earlier findings with this antiepileptic agent. In a second set of experiments, rats (four rats per group) were pretreated for 3 days with phenobarbital (75 mg kg-1 day-1, i.p.) prior to receiving a succinimide (0.4 or 1.0 mmol kg-1, i.p.) or vehicle (sesame oil, 2.5 ml kg-1, i.p.). Renal function was monitored at 24 and 48 h after the last injection. Phenobarbital pretreatment had only minor effects on ESX- or MSX-induced renal effects, with no significant morphological changes detected between treated and pair-fed control groups.(ABSTRACT TRUNCATED AT 250 WORDS)