NicergolineCAS# 27848-84-6 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 27848-84-6 | SDF | Download SDF |
PubChem ID | 11869400 | Appearance | Powder |
Formula | C24H26BrN3O3 | M.Wt | 484.39 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | DMSO : 100 mg/mL (206.45 mM; Need ultrasonic) | ||
Chemical Name | [(6aR,9R,10aS)-10a-methoxy-4,7-dimethyl-6,6a,7,8,9,10-hexahydroindolo[4,3-fg]quinoline-7-ium-9-yl]methyl 5-bromopyridine-3-carboxylate | ||
SMILES | C[NH+]1CC(CC2(C1CC3=CN(C4=CC=CC2=C34)C)OC)COC(=O)C5=CC(=CN=C5)Br | ||
Standard InChIKey | YSEXMKHXIOCEJA-FVFQAYNVSA-O | ||
Standard InChI | InChI=1S/C24H26BrN3O3/c1-27-13-17-8-21-24(30-3,19-5-4-6-20(27)22(17)19)9-15(12-28(21)2)14-31-23(29)16-7-18(25)11-26-10-16/h4-7,10-11,13,15,21H,8-9,12,14H2,1-3H3/p+1/t15-,21-,24+/m1/s1 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | α-adrenergic, vasodilator. Cognitive enhancer. |
Nicergoline Dilution Calculator
Nicergoline Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.0645 mL | 10.3223 mL | 20.6445 mL | 41.289 mL | 51.6113 mL |
5 mM | 0.4129 mL | 2.0645 mL | 4.1289 mL | 8.2578 mL | 10.3223 mL |
10 mM | 0.2064 mL | 1.0322 mL | 2.0645 mL | 4.1289 mL | 5.1611 mL |
50 mM | 0.0413 mL | 0.2064 mL | 0.4129 mL | 0.8258 mL | 1.0322 mL |
100 mM | 0.0206 mL | 0.1032 mL | 0.2064 mL | 0.4129 mL | 0.5161 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Nicergoline inhibits human platelet Ca(2+) signalling through triggering a microtubule-dependent reorganization of the platelet ultrastructure.[Pubmed:26450366]
Br J Pharmacol. 2016 Jan;173(1):234-47.
BACKGROUND AND PURPOSE: Recently, we demonstrated that a pericellular Ca(2+) recycling system potentiates agonist-evoked Ca(2+) signalling and granule secretion in human platelets and hypothesized a role for the membrane complex (MC) in orchestrating the accumulation of Ca(2+) in the pericellular region. Previous work has demonstrated that treatment with high concentrations of Nicergoline may disrupt the MC through an ability to trigger a re-organization of the dense tubular system. Experiments were therefore performed to assess whether Nicergoline-induced changes in platelet ultrastructure affects thrombin-evoked Ca(2+) fluxes and dense granule secretion. EXPERIMENTAL APPROACH: Thrombin-evoked Ca(2+) fluxes were monitored in Fura-2- or Fluo-5N-loaded human platelets, or using platelet suspensions containing Fluo-4 or Rhod-5N K(+) salts. Fluorescence microscopy was utilized to monitor microtubule structure and intracellular Ca(2+) store distribution in TubulinTracker- and Fluo-5N-loaded platelets respectively. Dense granule secretion was monitored using luciferin-luciferase. KEY RESULTS: Nicergoline treatment inhibited thrombin-evoked Ca(2+) signalling and induced alterations in the microtubule structure and the distribution of intracellular Ca(2+) stores in platelets. Nicergoline altered the generation and spreading of thrombin-induced pericellular Ca(2+) signals and almost completely prevented dense granule secretion. Stabilization of microtubules using taxol reversed most effects of Nicergoline on platelet Ca(2+) signalling and partially reversed its effects on dense granule secretion. CONCLUSIONS AND IMPLICATIONS: Nicergoline-induced alterations to platelet ultrastructure disrupt platelet Ca(2+) signalling in a manner that would be predicted if the MC had been disrupted. These data suggest that Nicergoline may be a useful prototype for the discovery of novel MC-disrupting anti-thrombotics.
Ergotamine and nicergoline - facts and myths.[Pubmed:25712664]
Pharmacol Rep. 2015 Apr;67(2):360-3.
Ergotamine, being a representative of naturally occurring ergoline alkaloids, derived from d-lysergic acid, and Nicergoline, a d-lumilysergic acid derivative belonging to semi-synthetic ergot-derived alkaloids, display diversified affinity for adrenergic, serotoninergic, and dopamine receptors. Although introduction of triptans marginalized use of ergotamine, Nicergoline is used in cerebral metabolic-vascular disorders, and dementia. Additionally, Nicergoline exhibits a safety profile comparable to that of placebo, and none of the reviewed studies reported any incidence of fibrosis or ergotism with Nicergoline treatment. In line with the recent data, activation of 5-HT2B receptor by ergot derivatives i.e. ergotamine, methysergide, pergolide, and carbegoline is involved in pathogenesis of drug-induced valvulopathy. In contrary structurally related drugs - lisuride and terguride do not increase the risk of valvular heart disease. It seems, that more detailed mechanistic studies on Nicergoline and ergotamine might be beneficial for determining structural requirements related to activation of G-protein as well as alternative signal transduction pathways e.g. beta-arrestins or different kinases, and responsible for drug liabilities.
[Identification of related substances in nicergoline by HPLC-MS].[Pubmed:26669004]
Yao Xue Xue Bao. 2015 Aug;50(8):1026-31.
To study the related substances in Nicergoline, electrospray positive ionization high resolution TOF/MS was used for the determination of the accurate mass and elemental composition of the related substances. Triple quadrupoles tandem MS/MS was employed for the determination of the fragmentations of the parent ions. 16 related substances were detected and identified to be eight synthetic by-products and eight degradation products, by using impurity references matching, product mass spectra fragmentations elucidation, and verified further according to synthetic processes and stress testing results. The results obtained are valuable for Nicergoline manufacturing process control and quality assurance.
Treatment of neurotrophic keratopathy with nicergoline.[Pubmed:25625360]
Cornea. 2015 Mar;34(3):303-7.
PURPOSE: The aim of this study was to determine the effect of Nicergoline in patients with neurotrophic keratopathy. METHODS: This is a prospective, noncomparative interventional study. The study included 27 eyes of 24 patients with neurotrophic keratopathy who were unresponsive to conventional therapy. Patients were treated with 10 mg of oral Nicergoline twice daily for at least 2 weeks. Slit-lamp examination, photography, corneal fluorescein dye testing, Cochet-Bonnet corneal sensitivity, and best-corrected visual acuity tests were performed before and after treatment. Tear nerve growth factor levels were measured before and after treatment. RESULTS: In 23 eyes (85%), epithelial defects healed completely between 7 and 30 days of treatment with Nicergoline (mean, 15.6 +/- 8.0 days). Epithelial defects persisted in 4 eyes (15%). The mean corneal sensitivity before and after treatment with Nicergoline was 20.5 +/- 8.5 and 30.2 +/- 10.8 mm, respectively (P < 0.001). The best-corrected visual acuity (measured in units according to the logarithm of the minimum angle of resolution) was significantly improved from 1.1 +/- 0.6 to 0.8 +/- 0.6 (P < 0.001). The tear nerve growth factor levels were significantly higher ranging from 3.2 +/- 0.3 to 6.2 +/- 0.3 pg/mL (P < 0.001). CONCLUSIONS: Treatment with Nicergoline helps patients with neurotrophic keratopathy in whom conventional treatment has failed.
Modulation of phosphoinositide turnover by chronic nicergoline in rat brain.[Pubmed:8736642]
Neurosci Lett. 1996 May 17;209(3):189-92.
Basal and agonist-stimulated phosphoinositide (PI) turnover and inositol 1,4,5 -trisphospate (InsP3) content in rat brain were investigated after chronic Nicergoline (SERMION) treatment. Oral administration of Nicergoline (5 mg/kg b.i.d. for 7 weeks) enhanced the basal turnover of PI in the cerebral cortex compared to controls. This effect was paralleled by a significant rise of cortical InsP3 levels. No significant changes of noradrenaline- or carbachol-induced accumulation of [3H]-inositol-I-phophate ([3H]-InsP1) were found in cortices from Nicergoline-treated rats. On the contrary, in the striatum Nicergoline significantly potentiated the responsiveness of noradrenaline- and carbachol-stimulated PI turnover, leaving unchanged the basal production of [3H]-InsP1 and InsP3 levels. The results suggest that the interaction of Nicergoline with PI transducing pathway might have relevance to the mechanisms of action of Nicergoline.
Modulation of hippocampal ACh release by chronic nicergoline treatment in freely moving young and aged rats.[Pubmed:8552297]
Neurosci Lett. 1995 Sep 15;197(3):195-8.
The effects of Nicergoline on basal and K(+)-stimulated release of ACh in the hippocampus of 3- and 19-month old rats has been studied by microdialysis. A significant decrease of basal ACh release (59%) was found in aged vehicle treated rats in comparison to young rats. High-K+ (100 mM) in the perfusate strongly increased the release of ACh by up to 6-fold over the baseline of both young and aged rats. Chronic oral administration of Nicergoline to aged rats (5 mg/kg b.i.d. for 6 weeks) significantly reversed (93%) the age-related decrease of basal release of ACh, leaving the increase due to K+ depolarization unchanged. In young animals, Nicergoline did not affect the basal output of ACh, but enhanced the K(+)-evoked release of ACh by 39%. Results from this study demonstrate that Nicergoline treatment increases the ability of hippocampal cholinergic terminals to release ACh, and suggest that this drug can reset the cholinergic impairement associated with aging.
Effects of four non-cholinergic cognitive enhancers in comparison with tacrine and galanthamine on scopolamine-induced amnesia in rats.[Pubmed:1738791]
Psychopharmacology (Berl). 1992;106(1):26-30.
Amnesia can be induced in rats in the passive avoidance paradigm by administration of scopolamine, a central muscarinic receptor antagonist. Tacrine or galanthamine, inhibitors of acetylcholinesterase, given in conjunction with scopolamine partially reversed the scopolamine-induced deficit in passive avoidance performance. Four so-called cognitive enhancers, all widely used for the treatment of the symptoms associated with mental aging, cerebral insufficiency and senile memory disorder, were investigated in this paradigm. Piracetam, an extract of Ginkgo biloba, dihydroergocristine and a combination of raubasine with dihydroergocristine, all attenuated the amnesia induced by scopolamine. In contrast, Nicergoline had no significant effect. Raubasine alone also failed to significantly attenuate scopolamine-induced amnesia, although some doses of raubasine had a non-significant tendency (P less than 0.10) to reduce the amnesia.