Stobadine
(Synonyms: 2,8-二甲基-2,3,4,4A,5,9B-六氢-1H-吡啶并[4,3-B]吲哚二盐酸盐) 目录号 : GC49500
A pyridoindole antioxidant
Cas No.:85202-17-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Stobadine is a pyridoindole antioxidant.1 It scavenges hydroxyl, peroxyl, and alkoxyl radicals and quenches singlet oxygen in cell-free assays. Ex vivo, stobadine (2 mg/kg) reduces lipid peroxidation induced by hypoxia and reoxygenation in rat forebrain.2 It improves survival in a rat model of carotid artery ligation-induced cerebral ischemia. Stobadine (1 mg/kg, i.v.) increases myocardial blood flow and decreases infarct area in a dog model of myocardial infarction induced by acute occlusion of the left coronary artery.1 Dietary administration of stobadine (0.05% w/w) delays the development of cataracts and reduces eye lens protein oxidation and plasma levels of malondialdehyde (MDA) in a rat model of diabetes induced by streptozotocin .3
1.HorÁkovÁ, L., and štolc, S.Antioxidant and pharmacodynamic effects of pyridoindole stobadineGen. Pharmacol.30(5)627-638(1998) 2.štolc, S., VlkolinskÝ, R., and PavlÁsek, J.Neuroprotection by the pyridoindole stobadine: A minireviewBrain Res. Bull.42(5)335-340(1997) 3.Kyselova, Z., Gajdosik, A., Gajdosikova, A., et al.Effect of the pyridoindole antioxidant stobadine on development of experimental diabetic cataract and on lens protein oxidation in rats: Comparison with vitamin E and BHTMol. Vis.1156-65(2005)
| Cas No. | 85202-17-1 | SDF | Download SDF |
| 别名 | 2,8-二甲基-2,3,4,4A,5,9B-六氢-1H-吡啶并[4,3-B]吲哚二盐酸盐 | ||
| Canonical SMILES | CC1=CC=C2N[C@@](CCN(C3)C)([H])[C@@]3([H])C2=C1 | ||
| 分子式 | C13H18N2 | 分子量 | 202.3 |
| 溶解度 | DMSO: >100mM | 储存条件 | -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 | 4.9432 mL | 24.7158 mL | 49.4315 mL |
| 5 mM | 0.9886 mL | 4.9432 mL | 9.8863 mL |
| 10 mM | 0.4943 mL | 2.4716 mL | 4.9432 mL |
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| 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 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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工作液浓度： mg/ml；
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2.
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Antioxidant and pharmacodynamic effects of pyridoindole Stobadine
Gen Pharmacol 1998 May;30(5):627-38.PMID:9559311DOI:10.1016/s0306-3623(97)00300-5.
1. The review summarizes the most important data known so far on chemistry, pharmacodynamics, toxicology and clinics of the investigational agent, pyridoindole Stobadine. 2. Stobadine was shown to be able to scavenge hydroxyl, peroxyl and alkoxyl radicals, to quench singlet oxygen, to repair oxidized amino acids and to preserve oxidation of SH groups by one-electron donation. These effects originated from its ability to form a stable nitrogen-centered radical on indole nitrogen. Consequently, it was able to diminish lipid peroxidation and protein impairment under oxidative stress. 3. In various in vitro and in vivo animal models, Stobadine was shown to diminish the impairment of the myocardium induced by mechanisms involving reactive oxygen species (e.g., myocardial infarction, hypoxia/ reoxygenation, catecholamine overexposure). 4. The neuroprotective effect of Stobadine was demonstrated in a series of in vivo and in vitro models (brain in situ, brain slices, spinal cord, autonomic ganglia, etc.) during ischemia/reperfusion and hypoxia/ reoxygenation or in the presence of chemical systems generating free oxygen radicals, and so forth. Stobadine improved animal survival rate and synaptic transmission recovery, maintained SH tissue level and diminished lipid peroxidation as well as impairment of Ca-sequestering intracellular systems. 5. Oxidation of low-density lipoproteins (LDLs), which plays a major role in the development of atherosclerosis, was decreased by Stobadine in vitro. Both lipid and protein (apo B) components of LDL were protected against Cu(2+)-induced oxidation by this agent. 6. Stobadine proved to be an effective protectant in models of free radical pathology in vivo, such as cyclophosphamide-, MNNG- or 60Co-induced mutagenesis and alloxan-induced hyperglycemia. 7. Besides other remarkable pharmacodynamic effects, Stobadine exerts antidysrhythmic, local anesthetic, alpha-adrenolytic, antihistaminic, myorelaxant and antiulcerogenic actions. 8. Pharmacokinetic analyses demonstrated that Stobadine was readily absorbed from the gastrointestinal tract. Thanks to its balanced lipo-hydrophilic properties, it was distributed over both water and lipid phases in biological tissues. It was shown to easily penetrate the blood-brain barrier. 9. Acute, subchronic and chronic toxicity studies in several animal species, as well as numerous analyses of embryotoxicity, teratogenicity, mutagenicity and genotoxicity, revealed only a negligible toxic potential of this agent. 10. Phase-one clinical study demonstrated safety of the compound. Only slight side effects--namely, a slight hypotension and a slight sedative effect--were observed subsequent to the highest dose used. In phase-two clinical study, the patients with angina pectoris treated for 4 weeks with Stobadine showed a significant decrease in the frequency of anginal attacks, in the number of self-administrations of sublingual nitroglycerine and in plasma lipoprotein, cholesterol and triglyceride levels. A slight decrease in systolic and diastolic blood pressure also was observed. 11. It is suggested that Stobadine may be considered a contribution to the search for new effective cardio- and neuroprotectants based on antioxidant or free radical scavenging mechanisms of action.
Neuroprotection by the pyridoindole Stobadine: a minireview
Brain Res Bull 1997;42(5):335-40.PMID:9092873DOI:10.1016/s0361-9230(96)00294-8.
The minireview summarizes data documenting that pyridoindole Stobadine (STB) may protect nervous structures against oxidative stress. This was demonstrated by the impairment of synaptic transmission in hippocampal slices and sympathetic ganglia exposed to hypoxia/reoxygenation (H/R) in vitro as well as by survival of rats and dogs exposed to brain ischemia/reperfusion (I/R) in vivo. The STB effect was linked mostly to its free radical scavenging and antioxidant properties. STB seems to act primarily on phospholipids, thus protecting the integrity and function of somatic membranes in neurons as well as those in subcellular organelles, such as mitochondria and endoplasmic reticulum. STB prevented damage to Ca2+ sequestering systems in endoplasmic reticulum and synaptosomes induced by lipid peroxidation initiators. It was found to diminish changes in NMDA and adrenergic alpha1-receptors evoked in the brain by I/R or H/R. The compound prevented total thiols, participating in tissue antioxidative protection, from decreasing in brain under these conditions. It readily penetrates into both the hydrophilic and the hydrophobic compartments of the CNS. Data were obtained indicating that in I/R, protection of structures such as brain-blood vessels, endothelium, and/or erythrocytes may participate in the STB effect, besides the direct protection of nervous tissue. STB may be characterized as a potential protectant of the CNS in diseases in which oxidative injury may play an important role, for example, stroke, neurotrauma, chronic brain ischemia, or some neurodegenerative diseases. Its molecule could provide a useful model in the further search for novel compounds with even more pertinent pharmacological and pharmacokinetic profiles.
Antimutagenic effects of Stobadine: review of results
Life Sci 1999;65(18-19):2015-7.PMID:10576458DOI:10.1016/s0024-3205(99)00468-3.
The paper summarizes the results of our previously published studies testifying the hypothesis of the antimutagenic effect of Stobadine (STB) in vivo and in vitro. The micronucleus test was used in in vivo experiments with ICR mice. Oral pretreatment with STB significantly decreased the mutagenic effect of cyclophosphamide (CP) in a concentration-dependent way. The protective effect of STB was confirmed in fetuses of CP-treated mice. STB pretreatment exerted also a radioprotective effect in Co60-irradiated mice. The ineffectiveness of STB posttreatment is indicative of its effect operative in the initiation of mutagenesis and of its radical-scavenging mechanism. The ability of STB to reduce N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)induced gene mutations and MNNG-induced calcinosis/Raynaud's phenomenon/esophageal dysmotility/sclerodactyly/telangiectasia variant of scleroderma (CREST)-positive and CREST-negative micronuclei in V79 cells was tested in in vitro experiments. We found that this drug reduced the level of both gene mutations and CREST-negative micronuclei mainly if given as pretreatment before exposure of cells to MNNG. We conclude that STB may have inhibited mutagenesis not only by scavenging reactive oxygen species, but also as a result of induction of metabolic enzymes, which reduced the level of DNA lesions.
Stobadine protects rat kidney against ischaemia/reperfusion injury
Clin Exp Pharmacol Physiol 2007 Mar;34(3):210-6.PMID:17250641DOI:10.1111/j.1440-1681.2007.04574.x.
1. Ischaemia-reperfusion (I/R) injury, one of the main causes of acute renal failure, still needs satisfactory treatment for routine clinical application. Stobadine, a novel synthetic pyridoindole anti-oxidant, has the ability to reduce tissue injury induced by mechanisms involving reactive oxygen species during I/R. The aim of the present study was to determine the effects of Stobadine on renal I/R injury. 2. Forty male Wistar rats were randomly divided into four groups as follows: sham, I/R, Stobadine treated and I/R + Stobadine treated. Stobadine (2 mg/kg, i.v.) was given intravenously to two groups of rats. The stobadine-treated group was treated with Stobadine following sham operation before the abdominal wall was closed, whereas the I/R + Stobadine group received Stobadine at the beginning of reperfusion. Renal I/R was achieved by occluding the renal arteries bilaterally for 40 min, followed by 6 h reperfusion. Immediately thereafter, blood was drawn and tissue samples were harvested to assess: (i) serum levels of blood urea nitrogen and creatinine; (ii) serum and/or tissue levels of malondialdehyde (MDA), glutathione (GSH), glucose 6-phosphate dehydrogenase (G-6PD), 6-phosphogluconate dehydrogenase (6-PGD), glutathione reductase (GR) and glutathione peroxidase (GPx); (iii) renal morphology; and (iv) immunohistochemical staining for P-selectin. 3. Stobadine was able to significantly attenuate the renal dysfunction as a result of renal I/R injury. Ischaemia-reperfusion resulted in a significant increase in serum and kidney MDA levels and a decrease in serum and kidney GSH. Stobadine treatment at the beginning of reperfusion attenuated both the increased MDA levels and decreased GSH secondary to I/R injury. In addition, the decreased G-6PD activity observed after I/R was significantly attenuated by Stobadine treatment. Stobadine did not alter 6-PGD activity after I/R. Neither GR nor GPx activity was significantly changed in the I/R alone or the I/R + Stobadine groups compared with the sham group. In addition, Stobadine decreased the morphological deterioration and high P-selectin immunoreactivity secondary to renal I/R injury. 4. A pyridoindole anti-oxidant, Stobadine exerts a renal protective effect in renal I/R injury, which is probably due to its radical-scavenging and anti-oxidant activities.
Stobadine and heart mitochondria
Life Sci 1999;65(18-19):1935-7.PMID:10576441DOI:10.1016/s0024-3205(99)00451-8.
Previous work has shown, that stobadine-hydrochloride (-)cis-2,8-dimethyl-2,3,4,4a,5,9b-hexahydro-14-pyrido(4,3b) indole administered in a single dose 2 mg/kg of body weight reduces cardiotoxic effect of isoproterenol (1 mg/kg) as shown by lowered serum enzyme activities of AST, CPK, LDH and ALT. We studied the effect of Stobadine in vivo on respiration, the level of ATP, malondialdehyde (MDA) and superoxiddismutase (SOD) in heart mitochondria. Serum enzyme activities of AST, CPK and LDH after Stobadine application were significantly decreased. In mitochondria, respiration and activity of SOD were inhibited, level of MDA was increased and level of ATP was unchanged. The cardioprotective effect of Stobadine is not linked to preservation of mitochondrial function. This effect is probably more complex and mediated on the level of the whole organism.