Pivagabine
(Synonyms: 匹伐加宾,CXB-722) 目录号 : GC38939
Pivagabine (CXB 722)，一种精神药物，是具有神经调节活性的疏水性4-氨基丁酸衍生物。Pivagabine 能穿透大鼠的血脑屏障。Pivagabine 拮抗足部休克对大鼠脑内 GABAA 受体功能和促肾上腺皮质激素释放因子 (CRF) 浓度的影响。
Cas No.:69542-93-4
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
Pivagabine (CXB 722), a psychoactive drug, is a hydrophobic 4-aminobutyric acid derivative with neuromodulatory activity. Pivagabine penetrates the blood-brain barrier in rats. Pivagabine antagonizes the effects of foot shock on both GABAA receptor function and corticotropin-releasing factor (CRF) concentrations in rat brain[1][2].
Pivagabine (CXB 722) (200 mg/kg; i.p.; twice a day for 4 days and 1 hour before killing on the 5th day) prevents the effects of foot-shock stress on CRF concentration in both brain regions[2]. Animal Model: Adult male Sprague-Dawley CD rats (200-250 g)[2]
[1]. Esposito G, et al. Pivagabine: a novel psychoactive drug. Arzneimittelforschung. 1997 Nov;47(11A):1306-9. [2]. Serra M, et al. Antagonism by pivagabine of stress-induced changes in GABAA receptor function and corticotropin-releasing factor concentrations in rat brain. Psychoneuroendocrinology. 1999 Apr;24(3):269-84.
| Cas No. | 69542-93-4 | SDF | |
| 别名 | 匹伐加宾,CXB-722 | ||
| Canonical SMILES | O=C(O)CCCNC(C(C)(C)C)=O | ||
| 分子式 | C9H17NO3 | 分子量 | 187.24 |
| 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 | 5.3407 mL | 26.7037 mL | 53.4074 mL |
| 5 mM | 1.0681 mL | 5.3407 mL | 10.6815 mL |
| 10 mM | 0.5341 mL | 2.6704 mL | 5.3407 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。
Therapeutic Interventions for Adjustment Disorder: A Systematic Review
Am J Ther 2020 Jul/Aug;27(4):e375-e386.PMID:32520732DOI:10.1097/MJT.0000000000001170.
Background: Adjustment disorder requires therapeutic intervention because of its complications, which include a significant risk of suicide, but evidence-based therapeutic guidelines are not available. Areas of uncertainty: The main problem is related to answer to the following question: What is the optimal therapeutic approach to adjustment disorder? In this respect we review all randomized controlled trials that aimed to investigate therapeutic interventions for adjustment disorder in adult populations. Data sources: Comprehensive search of the electronic database PubMed (January 1980-June 2019). The review included clinical trials that aimed to investigate a psychological or pharmacological treatment for adjustment disorder in adult population and reported outcome data for therapeutic interventions. Results: The search identified 23 studies that fulfilled the inclusion criteria for this review. Pharmacotherapy interventions were the focus of 11 studies that used various medications and dosages including viloxazine, lormetazepam, S-adenosylmethionine, Pivagabine, trazodone, clorazepate, etifoxine, lorazepam, diazepam, afobazole, and plant extracts (Kava-kava, Euphytose, and Ginkgo biloba) on a total number of 1020 patients. Psychotherapy interventions were identified in 12 studies that used mirror therapy, short-term dynamic psychotherapy, yoga meditation, body-mind-spirit technique, mindfulness, bibliotherapy (self-help manual), humor training, and cognitive behavioral therapy. Conclusions: Psychotherapy seems indicated for mildly symptomatic adjustment disorder. Given the fact that adjustment disorder with severe symptoms is associated with a high risk of suicidal ideation and suicide attempts, clinicians must consider the potential benefit of using psychotropic agents such as benzodiazepines, antidepressants, or etifoxine.
Pivagabine: a novel psychoactive drug
Arzneimittelforschung 1997 Nov;47(11A):1306-9.PMID:9450153doi
Pivagabine (4-[(2,2-dimethyl-1-oxopropyl)amino]butanoic acid, CAS 69542-93-4, Tonerg) is a metabolically stable compound with a modulatory effect on some biochemical parameters involved in stress conditions (corticotropin releasing factor, neurosteroids). The compound, tested in several animal models, prevents stress-correlated behavioural deficits. Moreover, Pivagabine has a highly significant therapeutic potential in clinical conditions characterized by manifestations of psychological distress due to an inadequate management of stressful events.
Pivagabine decreases stress-related hormone secretion in women with hypothalamic amenorrhea
J Endocrinol Invest 2000 Sep;23(8):526-32.PMID:11021769DOI:10.1007/BF03343769.
Stress-induced neuroendocrine activities influence the regulation of endocrine glands and axes. Weight loss-related hypothalamic amenorrhea is a typical stress-induced physiopathological condition. It is characterized by increased adrenal cortex activation and by reduced GH, LH, FSH and gonadal steroid hormone levels. The aim of the present study was to investigate the effects of Pivagabine, a neurotropic drug (1800 mg/day for 7 days) or placebo administration on ACTH, cortisol, GH, LH, FSH and PRL plasma levels in patients with hypothalamic amenorrhea related to weight loss. Hormonal parameters and the pulsatile release of cortisol (6-hour pulsatility, sampling every 10 minutes) were evaluated before and after 7 days of treatment. Pivagabine administration significantly reduced mean plasma ACTH (from 21.7+/-1.7 to 15.4+/-1.2 pg/ml, p<0.05) and cortisol levels (from 12.2+/-0.7 to 9.7+/-0.7 ng/ml, p<0.05) and increased GH levels (from 1.4+/-0.5 to 3.0+/-0.9 ng/ml, p<0.05). A significant reduction of cortisol pulse amplitude was observed (p<0.01) while no change in pulse frequency occurred. No changes were observed in placebo-treated subjects. LH, FSH and PRL levels were not modified by placebo or Pivagabine administration. In conclusion, in patients with hypothalamic amenorrhea related to weight loss Pivagabine induced a significant decrease of cortisol secretion and an increase of GH release by Pivagabine administration, suggesting that this drug exerts a specific neuroendocrine modulatory role.
Pivagabine effects on neuroendocrine responses to experimentally-induced psychological stress in humans
Behav Brain Res 2001 Jul;122(1):93-101.PMID:11287080DOI:10.1016/s0166-4328(01)00177-2.
Neuroendocrinology of chronic stress seems to be characterized by HPA axis hyperactivity and early childhood stressors have been hypothesized to predispose individuals to adult onset depression by means of dysregulation of the HPA axis. Pivagabine (PVG), a hydrophobic 4-aminobutyric acid derivative, has been used experimentally recently in the treatment of different disorders related to stress-maladaptation, because of its possible inhibitory action on corticotrophin releasing factor secretion and HPA axis function. In the present study, 20 healthy male subjects were each exposed twice to the same psychosocial stressor (stroop color-word interference task, public speaking and mental arithmetic in front of an audience) during a first session (day 1) and a second session (day 8). Plasma concentrations of norepinephrine (NE), epinephrine (EPI), adrenocorticotropic hormone (ACTH) and cortisol (CORT), heart rate (HR) and systolic blood pressure (SBP) were measured immediately before the beginning of the tests and at their end, 30 min later, on both experimental days. Utilizing a double blind schedule, the subjects received Pivagabine (900 mg, twice a day)(PVG group: nine subjects) or placebo (PBO group: 11 subjects) during the 7 days between the two stress sessions. NE, EPI, ACTH, and CORT levels were significantly elevated after stress exposure on day 1 and day 8 in PBO group subjects. After PVG treatment, on day 8, ACTH, CORT, NE and EPI responses to stress were significantly blunted, together with HR and SBP, in PVG group subjects. These results add to the evidence concerning PVG capacity to inhibit the HPA axis in humans, in response to stressful stimuli, and suggest that the action of PVG may be mediated not only by GABAergic receptors, but also by the suppression of catecholamines response. PVG treatment could modulate HPA hyper-responsiveness to stress in subjects with negative affectivity and depressive traits.
Effects of Pivagabine on psychophysical performance and behavioural response in experimental models of stress
Arzneimittelforschung 1997 Nov;47(11A):1310-4.PMID:9450154doi
The effect of Pivagabine (4-[(2,2-dimethyl-1-oxopropyl)amino]butanoic acid, CAS 69542-93-4, Tonerg), a synthetic molecule with neuromodulatory activity, was evaluated on a series of behavioural parameters in rats exposed to various stimuli, with the aim of evaluating the response to stress (open field exploration, water maze, psychic conflict), conditioning (active and passive avoidance and avoidance retention, aggressiveness, extinction of conditioned responses), learning and performing of specific psychophysical tests (rota-rod, ballasted swimming, taut thread). Pivagabine induced significant improvement of stress-related tests by reducing the anxiety-producing reactions related to the various experimental settings. In conditioning tests an improvement in learning of conditioned responses was observed at lower dosages (10 and 50 mg/kg); an opposite effect was obtained with higher dosages (100 and 200 mg/kg). Pivagabine did not influence the retention nor the extinction of conditioned responses. Pivagabine induced a marked improvement of all motor performance tests in young and in aged animals. By contrast with benzodiazepines, Pivagabine did not alter the ability of learning tasks, the motor performance and the aggressive behaviours. It is likely that the observed effects of Pivagabine are mediated by inhibition of release of corticotropin-releasing factor, a neurohormone involved in stress-generating mechanisms.