SCH 50911Selective, competitive, orally active GABAB antagonist CAS# 733717-87-8 |
- MLN8237 (Alisertib)
Catalog No.:BCC2166
CAS No.:1028486-01-2
- VX-680 (MK-0457,Tozasertib)
Catalog No.:BCC2167
CAS No.:639089-54-6
- Reversine
Catalog No.:BCC1892
CAS No.:656820-32-5
- AZD1152
Catalog No.:BCC1393
CAS No.:722543-31-9
- XL228
Catalog No.:BCC2058
CAS No.:898280-07-4
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 733717-87-8 | SDF | Download SDF |
PubChem ID | 5311429 | Appearance | Powder |
Formula | C8H15NO3 | M.Wt | 173.21 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 100 mM in water and to 100 mM in phosphate buffered saline | ||
Chemical Name | 2-[(2S)-5,5-dimethylmorpholin-2-yl]acetic acid | ||
SMILES | CC1(COC(CN1)CC(=O)O)C | ||
Standard InChIKey | SEYCKMQSPUVYEF-LURJTMIESA-N | ||
Standard InChI | InChI=1S/C8H15NO3/c1-8(2)5-12-6(4-9-8)3-7(10)11/h6,9H,3-5H2,1-2H3,(H,10,11)/t6-/m0/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. |
||
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. |
||
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 | A selective, competitive and orally active GABAB antagonist. Displays an IC50 of 1.1 μM at GABAB, approximately 60 times that of CGP 35348 and no binding affinity for GABAA at concentrations up to 100 μM. |
SCH 50911 Dilution Calculator
SCH 50911 Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 5.7733 mL | 28.8667 mL | 57.7334 mL | 115.4668 mL | 144.3335 mL |
5 mM | 1.1547 mL | 5.7733 mL | 11.5467 mL | 23.0934 mL | 28.8667 mL |
10 mM | 0.5773 mL | 2.8867 mL | 5.7733 mL | 11.5467 mL | 14.4333 mL |
50 mM | 0.1155 mL | 0.5773 mL | 1.1547 mL | 2.3093 mL | 2.8867 mL |
100 mM | 0.0577 mL | 0.2887 mL | 0.5773 mL | 1.1547 mL | 1.4433 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. |
Calcutta University
University of Minnesota
University of Maryland School of Medicine
University of Illinois at Chicago
The Ohio State University
University of Zurich
Harvard University
Colorado State University
Auburn University
Yale University
Worcester Polytechnic Institute
Washington State University
Stanford University
University of Leipzig
Universidade da Beira Interior
The Institute of Cancer Research
Heidelberg University
University of Amsterdam
University of Auckland
TsingHua University
The University of Michigan
Miami University
DRURY University
Jilin University
Fudan University
Wuhan University
Sun Yat-sen University
Universite de Paris
Deemed University
Auckland University
The University of Tokyo
Korea University
- Niclosamide monohydrate
Catalog No.:BCC5212
CAS No.:73360-56-2
- 9-O-Acetyl-4,4'-di-O-methyllariciresinol
Catalog No.:BCN1367
CAS No.:73354-15-1
- Albanin A
Catalog No.:BCN3290
CAS No.:73343-42-7
- Macbecin I
Catalog No.:BCC7551
CAS No.:73341-72-7
- 3-Hydroxy-9,10-Dimethoxypterocarpan
Catalog No.:BCC8101
CAS No.:73340-41-7
- Methylnissolin
Catalog No.:BCN1368
CAS No.:733-40-4
- BAY 61-3606
Catalog No.:BCC1406
CAS No.:732983-37-8
- Deoxynojirimycin hydrochloride
Catalog No.:BCN2626
CAS No.:73285-50-4
- 1,4-Dihydro-1,2-dimethyl-4-oxo-3-quinolinecarboxylic acid
Catalog No.:BCN1369
CAS No.:73281-83-1
- 5-O-Caffeoylshikimic acid
Catalog No.:BCN7929
CAS No.:73263-62-4
- Moringin
Catalog No.:BCN7722
CAS No.:73255-40-0
- Methylnaltrexone Bromide
Catalog No.:BCC1740
CAS No.:73232-52-7
- SB 706375
Catalog No.:BCC6256
CAS No.:733734-61-7
- AR 231453
Catalog No.:BCC5143
CAS No.:733750-99-7
- Norandrostenedione
Catalog No.:BCC9103
CAS No.:734-32-7
- Dehydrobruceine A
Catalog No.:BCN7620
CAS No.:73435-47-9
- 1-Deoxymannojirimycin hydrochloride
Catalog No.:BCC6995
CAS No.:73465-43-7
- Tetrachyrin
Catalog No.:BCN4776
CAS No.:73483-88-2
- 7-Acetyllycopsamine
Catalog No.:BCN2000
CAS No.:73544-48-6
- cis-ACBD
Catalog No.:BCC6587
CAS No.:73550-55-7
- Mevastatin
Catalog No.:BCN2568
CAS No.:73573-88-3
- 27-p-Coumaroyloxyursolic acid
Catalog No.:BCN4288
CAS No.:73584-67-5
- Omeprazole
Catalog No.:BCC1254
CAS No.:73590-58-6
- (-)-Bicuculline methobromide
Catalog No.:BCC6555
CAS No.:73604-30-5
Proconvulsive effect of the GABA(B) receptor antagonist, SCH 50911, in rats undergoing ethanol withdrawal syndrome.[Pubmed:12079684]
Eur J Pharmacol. 2002 Jun 12;445(3):195-9.
The present study investigated the effect of the GABA(B) receptor antagonist, SCH 50911 [(2S)(+)-5,5-dimethyl-2-morpholineacetic acid], on the occurrence of seizures in ethanol-dependent rats undergoing ethanol withdrawal syndrome. The acute administration of nonconvulsive doses of SCH 50911 (0, 100, 170 and 300 mg/kg, i.p.) resulted in a dramatic facilitation of spontaneous seizure occurrence. This finding, together with the reported ability of the GABA(B) receptor agonist, baclofen, to suppress seizures associated to ethanol withdrawal syndrome, suggests that the GABA(B) receptor may be part of the neural substrate underlying the hyperexcitability of ethanol withdrawal syndrome.
Activation of nigral dopamine neurons by the selective GABA(B)-receptor antagonist SCH 50911.[Pubmed:10443545]
J Neural Transm (Vienna). 1999;106(5-6):383-94.
Previous studies have shown that systemic as well as local administration of the GABA(B)-receptor agonist baclofen is associated with a decrease in firing rate, a regularisation of firing rhythm and a decrease in burst firing activity of dopamine (DA) containing midbrain neurons. In the present electrophysiological study we have utilised the novel, selective and potent GABA(B)-receptor antagonist SCH 50911 in order to further analyse the importance of GABA(B)-receptors for the overall activity of rat nigral DA neurons. SCH 50911 given intravenously (1-64 mg/kg) or locally, by microiontophoretic techniques, was found to increase firing rate and to increase the burst firing activity of DA neurons. The present data suggest that the GABA(B)-receptor antagonist blocks somatodendritic receptors on nigral DA neurons. This GABA-receptor input appears to be of a tonic nature. It is proposed that the activation of nigral DA neurons may underlie the beneficial effects of GABA(B)-receptor antagonists in the modulation of cognition and that GABA(B)-receptor antagonists may be of therapeutic value in the treatment of Parkinson's disease.
Protection by the GABAB receptor antagonist, SCH 50911, of gamma-hydroxybutyric acid-induced mortality in mice.[Pubmed:15496299]
Eur J Pharmacol. 2004 Oct 25;503(1-3):77-80.
Different effects of moderate to high doses of gamma-hydroxybutyric acid, including sedation/hypnosis, have been found to be blocked by gamma-aminobutyric acidB (GABAB) receptor antagonists. The present study investigated whether the protective effect of GABAB receptor antagonists extends also to gamma-hydroxybutyric acid-induced mortality. To this aim, the present study investigated the effect of the GABAB receptor antagonist, (2S)(+)-5,5-dimethyl-2-morpholineacetic acid (SCH 50911; 100 mg/kg, ip), on mortality induced by gamma-hydroxybutyric acid (1-6 g/kg, ip) in DBA mice. Pretreatment with SCH 50911 resulted in a significant shift to the right of the dose-response curve of gamma-hydroxybutyric acid-induced mortality. Accordingly, the LD50 in SCH 50911-pretreated mice was significantly higher than that obtained in water-pretreated mice. The results of the present study support the hypothesis that (a) the GABAB receptor is a relevant site of action of gamma-hydroxybutyric acid, and (b) GABAB receptor antagonists may constitute potentially effective therapeutic interventions for gamma-hydroxybutyric acid intoxication.
Regional Fos-expression induced by gamma-hydroxybutyrate (GHB): comparison with gamma-butyrolactone (GBL) and effects of co-administration of the GABAB antagonist SCH 50911 and putative GHB antagonist NCS-382.[Pubmed:25088910]
Neuroscience. 2014 Sep 26;277:700-15.
gamma-Hydroxybutyrate (GHB) has a complex array of neural actions that include effects on its own high-affinity GHB receptor, the release of neuroactive steroids, and agonist actions at GABAA and GABAB receptors. We previously reported partial overlap in the c-Fos expression patterns produced by GHB and the GABAB agonist, baclofen in rats. The present study extends these earlier findings by examining the extent to which GHB Fos expression and behavioral sedation are prevented by (2S)-(+)-5,5-dimethyl-2-morpholineacetic acid (SCH 50911), a GABAB antagonist, and NCS-382, a putative antagonist at the high-affinity GHB receptor. We also compare Fos expression caused by GHB and its precursor gamma-butyrolactone (GBL), which is a pro-drug for GHB but lacks the high sodium content of the parent GHB molecule. Both GHB (1,000 mg/kg) and GBL (600 mg/kg) induced rapid sedation in rats that lasted over 90 min and caused similar Fos expression patterns, albeit with GBL causing greater activation of the nucleus accumbens (core and shell) and dentate gyrus (granular layer). Pretreatment with SCH 50911 (100mg/kg) partly reversed the sedative effects of GHB and significantly reduced GHB-induced Fos expression in only four regions: the tenia tecta, lateral habenula, dorsal raphe and laterodorsal tegmental nucleus. NCS-382 (50mg/kg) had no effect on GHB-induced sedation or Fos expression. When given alone, both NCS-382 and SCH 50911 increased Fos expression in the bed nucleus of the stria terminalis, central amygdala, parasubthalamic nucleus and nucleus of the solitary tract. SCH 50911 alone affected the Islands of Calleja and the medial, central and paraventricular thalamic nuclei. Overall, this study shows a surprising lack of reversal of GHB-induced Fos expression by two relevant antagonists, both of which have marked intrinsic actions. This may reflect the limited doses tested but also suggests that GHB Fos expression reflects mechanisms independent of GHB and GABAB receptors.
The morpholino-acetic acid analogue Sch 50911 is a selective GABA(B) receptor antagonist in rat neocortical slices.[Pubmed:9865527]
Eur J Pharmacol. 1998 Nov 27;362(1):35-41.
The pharmacological properties of (+)-(S)-5,5-dimethylmorpholinyl-2-acetic acid (SCH 50911) were evaluated on GABA(B) receptors in rat neocortical slices. The GABA(B) receptor agonist, baclofen, produced a concentration-dependent depression of the frequency of spontaneous discharges in slices maintained in Mg2+-free Krebs medium with an EC50 of 6 microM, reversibly antagonised by SCH 50911 (5, 10 and 25 microM) with an apparent pA2 of 6.0 +/- 0.1. The (-) enantiomer Sch 50910 (500 microM) and the racemic des-methyl analogue Sch 48588 (500 microM) were inactive. In slices preloaded with [3H]GABA, SCH 50911 antagonised GABA(B) autoreceptors, increasing the electrically-stimulated 3H overflow in a concentration-dependent manner, with an IC50 of 3 microM. The maximal effect (148 +/- 10.5%) was found at 10 microM, but at 50 microM the response was reduced to 67 +/- 19%. In contrast, evoked release was unaffected by Sch 50910 (100 microM) whilst Sch 48588 at 100 microM increased the overflow by 51.3 +/- 11.6%. In summary, SCH 50911 is a relatively potent antagonist of considerable potential in studies of GABA(B) receptor function.
The pharmacology of SCH 50911: a novel, orally-active GABA-beta receptor antagonist.[Pubmed:7562513]
J Pharmacol Exp Ther. 1995 Sep;274(3):1393-8.
Experiments were conducted to characterize the pharmacology of SCH 50911 ((+)-5,5-dimethyl-2-morpholineacetic acid hydrochloride), a structurally novel GABA-B receptor antagonist. Although more potent GABA-B antagonists have been reported, in this study SCH 50911 was compared with CGP 35348, a moderately potent and selective GABA-B antagonist with acceptable in vivo activity. SCH 50911 was more potent to inhibit the binding of GABA to the GABA-B receptor in rat brain (IC50 = 1.1 microM) than CGP 35348 (IC50 = 62 microM). SCH 50911 had no binding affinity for GABA-A, histamine H1, histamine H3, dopamine D1, dopamine D2, serotonin 5-HT2, or muscarinic m1, m2, or m4 receptors. However, SCH 50911 (IC50 = 2.2 microM) was active in a nonspecific muscarinic receptor binding assay, but was devoid of muscarinic agonist or antagonist activity in the isolated guinea pig ileum. SCH 50911 blocked inhibitory responses to baclofen of the guinea pig trachea in a competitive manner (pA2 = 5.8 +/- 0.004). CGP 35348 was 19-fold less potent in this assay (pA2 = 4.6 +/- 0.15). In vivo, SCH 50911 (ED50 = 2.9 mg kg-1, s.c.) and CGP 35348 (ED50 = 5.8 mg kg-1, s.c.) blocked the antitussive effects of baclofen in the guinea pig. In the cat, both SCH 50911 (10 mg kg-1, i.v.) and CGP 35348 (10 mg kg-1, i.v.) shifted the antitussive dose response relationship for baclofen to the right.(ABSTRACT TRUNCATED AT 250 WORDS)
Characterization of the antiabsence effects of SCH 50911, a GABA-B receptor antagonist, in the lethargic mouse, gamma-hydroxybutyrate, and pentylenetetrazole models.[Pubmed:7562514]
J Pharmacol Exp Ther. 1995 Sep;274(3):1399-403.
Recent studies have shown that gamma-aminobutyric acidB (GABAB) receptor antagonists suppress absence seizures in animal models. (+)-5,5-Dimethyl-2-morpholineacetic acid, hydrochloride (SCH 50911) is a new GABAB antagonist that is structurally dissimilar to previously studied GABAB antagonists such as 3-aminopropyl-diethoxymethyl-phosphinic acid (CGP 35348), 3-aminopropyl-n-butyl-phosphinic acid (CGP 36742) or 3-aminopropyl-cyclohexylmethyl-phosphinic acid (CGP 46381). In this study we measured the antiabsence effects of SCH 50911 in three animal models: the lethargic (lh/lh) mutant mouse, which has spontaneous absence seizures; and two rat models in which absence seizures were induced by administration of either gamma-hydroxybutyrate or pentylenetetrazole. SCH 50911 abolished seizures in all three models in a dose-dependent fashion (ID100 = 8-170 mumol/kg). In each model SCH 50911 was more potent (ID50 = 2-22 mumol/kg) than the following antiabsence compounds: the GABAB antagonist CGP 35348 (ID50 = 210-890 mumol/kg); ethosuximide (ID50 < or = 142-1240 mumol/kg); trimethadione (ID50 = 520-1100 mumol/kg); and valproic acid (ID50 = 900-2360 mumol/kg). SCH 50911 was equipotent with the GABAB antagonist CGP 46381 (ID50 = 20 mumol/kg) in the lh/lh mouse model. These findings suggest that antiabsence activity may be a defining feature of GABAB receptor antagonists and provide a rationale for pursuing clinical trials of GABAB receptor antagonists in human patients with absence seizures.