Progabide (SL 76002)
(Synonyms: 普罗加比; SL 76002) 目录号 : GC33521
Progabide (SL 76002) 是一种 γ-氨基丁酸受体 (GABA) 激动剂。
Cas No.:62666-20-0
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: | Male Wistar rats weighing 170 to 240 g are caged in groups of three under diurnal lighting conditions with free access to food and water. The rats are accustomed to handling (housing 1 per cage for 30 min, injecting with saline, 1 mL/100 g body weight) in the period of 7 days before the beginning of the experiment. Progabide is injected as a suspension in saline containing 0.1% Tween 80. Control rats are treated IP with the corresponding vehicle (1 mL/100 g body weight). Ether stress is performed and 15 min after the beginning of the stressful procedure the animals are sacrificed[1]. |
References: [1]. Manev H, et al. Progabide, a GABA mimetic drug, stimulates the secretion of plasma corticosterone in rats. Pharmacol Biochem Behav. 1987 Dec;28(4):443-6. | |
Progabide is a gamma-aminobutyric acid receptor (GABA) agonist.
Progabide is a gamma-aminobutyric acid receptor (GABA) agonist. Doses of 50, 100 and 200 mg/kg Progabide given IP to male Wistar rats increase the plasma corticosterone levels by 244, 365 and 476% respectively (t=6.44 to12.55, p<0.01). 10 mg/kg of Progabide fails to change the concentration of corticosterone in plasma (t=0.76, N.S.). The increased plasma corticosterone level induced by administration of 200 mg/kg Progabide is evident 30 (t=2.625, p<0.05), 60 (t=13.13, p<0.001) and 120 min (t=4.07, p<0.01) after drug injection, but returns to the control value 240 min after drug injection (t=0.86, N.S.). The greatest corticosterone rise (compare with the corresponding control) is reached 60 min following the administration of Progabide[1].
[1]. Manev H, et al. Progabide, a GABA mimetic drug, stimulates the secretion of plasma corticosterone in rats. Pharmacol Biochem Behav. 1987 Dec;28(4):443-6.
| Cas No. | 62666-20-0 | SDF | |
| 别名 | 普罗加比; SL 76002 | ||
| Canonical SMILES | O=C(N)CCC/N=C(C1=CC=C(Cl)C=C1)\C2=CC(F)=CC=C2O | ||
| 分子式 | C17H16ClFN2O2 | 分子量 | 334.77 |
| 溶解度 | DMSO : 250 mg/mL (746.78 mM; Need ultrasonic) | 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 | 2.9871 mL | 14.9356 mL | 29.8713 mL |
| 5 mM | 0.5974 mL | 2.9871 mL | 5.9743 mL |
| 10 mM | 0.2987 mL | 1.4936 mL | 2.9871 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。
gamma-Aminobutyric acid (GABA) receptor stimulation. II. Specificity of Progabide (SL 76002) and SL 75102 for the GABA receptor
J Pharmacol Exp Ther 1982 Mar;220(3):672-7.PMID:6121050doi
Progabide and its immediate metabolite SL 75102 displace [3H]gamma-aminobutyric acid (GABA), [3H]muscimol and [3H]isoguvacine from their binding sites to membranes prepared from rat brain or human cerebellum and increase (SL 75102) [3H]flunitrazepam binding to rat cerebral cortex membranes. In contrast, these compounds have very weak or no effects on alpha or beta noradrenergic, histamine, muscarinic cholinergic or glycine receptors or on the [3H]imipramine or [3H]kainate binding sites. Neither progabide nor SL 75102 inhibit GABA synthesis, metabolism or uptake. Also, the uptake of norepinephrine, serotonin and dopamine into synaptosomes of cerebral regions is not affected by progabide. [3H]GABA release from substantia nigra slices is decreased by SL 75102 and progabide, in agreement with the hypothesis of a GABAergic autoreceptor controlling GABA release from its nerve terminals. These data suggest a specific agonist action of progabide and SL 75102 on GABA receptors.
gamma-Aminobutyric acid (GABA) receptor stimulation. I. Neuropharmacological profiles of Progabide (SL 76002) and SL 75102, with emphasis on their anticonvulsant spectra
J Pharmacol Exp Ther 1982 Mar;220(3):660-71.PMID:6278129doi
Progabide (4-([(4-chlorophenyl) (5-fluoro-2-hydroxyphenyl)-methylene]amino) butanamide) is a gamma-aminobutyric acid (GABA) receptor agonist which readily enters the brain. In the body, progabide is metabolized to three active metabolites: SL 75102, gabamide and GABA. Progabide and SL 75102 readily enter the brain and GABA and gabamide are also formed within this organ. Both progabide and SL 75102 exhibit a broad spectrum of anticonvulsant activities against seizures which involve GABA-mediated events (bicuculline, picrotoxinin and pentylenetetrazol) or which are apparently independent of GABAergic mechanisms (penicillin, strychnine, electroshock and audiogenic seizures). These data support the hypothesis that direct GABA receptor stimulation is an effective means of controlling convulsions of various origins. Progabide and SL 75102 have relatively minor secondary effects in comparison to commonly used antiepileptics. Myorelaxation occurs, but only at doses higher than the ED50 values in convulsant tests. Furthermore, these compounds are not sedative. Finally, these GABA agonists have a complex action in the extrapyramidal system. Anticonvulsant doses are antagonistic to dopamine receptor-mediated behaviors, whereas much lower doses seem to facilitate the effects of dopaminergic transmission.
The effects of Progabide (SL 76002) on locomotor activity and conditioned place preference induced by d-amphetamine
Eur J Pharmacol 1985 Jan 2;107(2):271-4.PMID:2984007DOI:10.1016/0014-2999(85)90069-x.
The effect of prior treatment with a GABA mimetic, SL 76002 (100 mg/kg i.p.), on amphetamine-induced locomotor activity and conditioned place preferences with amphetamine (1.5 mg/kg i.p.) was investigated. SL 76002 significantly attenuated the motor stimulant effects of amphetamine, without influencing the rewarding properties at least as determined by the place preference procedure. When injected alone, SL 76002 did not affect handling-induced locomotor activation, nor did it exhibit any aversive or reinforcing properties. The results suggest that separate neural systems may subserve the motor and rewarding properties of amphetamine.
Effect of THIP and SL 76002, two clinically experimented GABA-mimetic compounds, on anterior pituitary GABA receptors and prolactin secretion in the rat
Life Sci 1987 Mar 2;40(9):871-81.PMID:3029529DOI:10.1016/0024-3205(87)90036-1.
In the present study, the ability of three direct GABA agonists, muscimol, THIP and SL 76002 to displace 3H-GABA binding from anterior pituitary and medio-basal hypothalamus membranes was evaluated. Further, the effect of both THIP and SL 76002 on baseline prolactin levels or after stimulation of hormone release with haloperidol has been also studied. Either muscimol, THIP or SL 76002 have shown to posses 7-, 7- and 3-fold higher affinity, respectively, for the central nervous system than for the anterior pituitary 3H-GABA binding sites. Moreover, THIP and SL 76002 have demonstrated to be respectively, 25- and 1000- fold less potent than muscimol in inhibiting 3H- GABA binding at the level of the anterior pituitary and about 25- and 2700- fold less potent at the level of the medio-basal hypothalamus. Under basal conditions, either THIP or SL 76002 were ineffective to reduce prolactin release. However, after stimulation of prolactin secretion through blockade of the dopaminergic neurotransmission with haloperidol (0.1 mg/kg), both THIP (10 mg/kg) and SL 76002 (200 mg/kg) significantly counteracted the neuroleptic-induced prolactin rise with a potency which is in line with their ability to inhibit 3H-GABA binding in the anterior pituitary. The present results indicate that both compounds inhibit prolactin release under specific experimental situations probably through a GABAergic mechanism. In view of the endocrine effects of these GABA-mimetic compounds, the possibility arises for an application of these type of drugs in clinical neuroendocrinology.
Progabide: a controlled trial in partial epilepsy
Epilepsia 1983 Apr;24(2):127-34.PMID:6403342DOI:10.1111/j.1528-1157.1983.tb04873.x.
Progabide (SL 76002) was studied in a randomized double-blind crossover trial using 20 outpatients suffering from partial complex seizures. Progabide was added to the concomitant antiepileptic treatment in a fixed dosage schedule. The design included an open therapy control unit. No significant difference was established between the number of partial seizures during treatment with progabide and placebo. A trend was observed for lower seizure frequency of secondary generalized seizures during treatment with progabide. Only mild and transient side effects were observed. There was no difference between the side effects of progabide and placebo.