SunifiramCAS# 314728-85-3 |
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CAS No.:103628-48-4
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Chemical structure
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Cas No. | 314728-85-3 | SDF | Download SDF |
PubChem ID | 4223812 | Appearance | Powder |
Formula | C14H18N2O2 | M.Wt | 246.3 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | DM-235 | ||
Solubility | H2O : 50 mg/mL (203.00 mM; Need ultrasonic) DMSO : ≥ 2.6 mg/mL (10.56 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | 1-(4-benzoylpiperazin-1-yl)propan-1-one | ||
SMILES | CCC(=O)N1CCN(CC1)C(=O)C2=CC=CC=C2 | ||
Standard InChIKey | DGOWDUFJCINDGI-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C14H18N2O2/c1-2-13(17)15-8-10-16(11-9-15)14(18)12-6-4-3-5-7-12/h3-7H,2,8-11H2,1H3 | ||
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 | Sunifiram (DM-235) is a piperazine derived ampakine-like drug which has nootropic effects in animal studies with significantly higher potency than piracetam.
IC50 value:
Target:
in vitro: DM 232 and DM 235 are novel antiamnesic compounds structurally related to ampakines. The involvement of AMPA receptors in the mechanism of action of DM 232 and DM 235 was, therefore, investigated in vivo and in vitro. Both compounds (0.1 mg/kg i.p.) were able to reverse the amnesia induced by the AMPA receptor antagonist NBQX (30 mg/kg i.p.) in the mouse passive avoidance test. At the effective doses, the investigated compounds did not impair motor coordination, as revealed by the rota rod test, nor modify spontaneous motility and inspection activity, as revealed by the hole board test [1]. In mouse hippocampal slices, sunifiram at 10-100 nM significantly enhanced LTP in a bell-shaped dose-response relationship which peaked at 10 nM. The enhancement of LTP by sunifiram treatment was inhibited by 7-chloro-kynurenic acid (7-ClKN), an antagonist for glycine-binding site of NMDAR, but not by ifenprodil, an inhibitor for polyamine site of NMDAR [2].
in vivo: OBX mice were administered once a day for 7-12 days with sunifiram (0.01-1.0 mg/kg p.o.) from 10 days after operation with or without gavestinel (10 mg/kg i.p.), which is glycine-binding site inhibitor of N-methyl-d-aspartate receptor (NMDAR) [3]. References: |
Sunifiram Dilution Calculator
Sunifiram Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 4.0601 mL | 20.3004 mL | 40.6009 mL | 81.2018 mL | 101.5022 mL |
5 mM | 0.812 mL | 4.0601 mL | 8.1202 mL | 16.2404 mL | 20.3004 mL |
10 mM | 0.406 mL | 2.03 mL | 4.0601 mL | 8.1202 mL | 10.1502 mL |
50 mM | 0.0812 mL | 0.406 mL | 0.812 mL | 1.624 mL | 2.03 mL |
100 mM | 0.0406 mL | 0.203 mL | 0.406 mL | 0.812 mL | 1.015 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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Sunifiram (DM-235) is a piperazine derived ampakine-like drug which has nootropic effects in animal studies with significantly higher potency than piracetam.
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Design, synthesis and preliminary pharmacological evaluation of new analogues of DM232 (unifiram) and DM235 (sunifiram) as cognition modulators.[Pubmed:18954993]
Bioorg Med Chem. 2008 Dec 1;16(23):10034-42.
A series of amides, structurally related to DM232 (unifiram) and DM235 (Sunifiram), characterized by a 1,2,3,4-tetrahydropyrazino[2,1-a]isoindol-6(2H)-one, 1,4-diamino-cyclohexane or 1,4-diaminobenzene ring, have been synthesized and tested for cognition-enhancing activity in the mouse passive-avoidance test. Some of the compounds display good antiamnesic and procognitive activity, with higher potency than piracetam, while some cyclohexane derivatives are endowed with amnesia inducing properties.
Novel nootropic drug sunifiram improves cognitive deficits via CaM kinase II and protein kinase C activation in olfactory bulbectomized mice.[Pubmed:23295391]
Behav Brain Res. 2013 Apr 1;242:150-7.
Alzheimer's disease (AD) shows degeneration of the cholinergic system in the medial septum, thereby eliciting down-regulation of the olfactory function in patients. We have previously reported that olfactory bulbectomized (OBX) mice show hippocampus-dependent memory impairment as assessed by memory-related behavioral tasks and hippocampal long-term potentiation (LTP). In the present study, we focused whether novel pyrrolidone nootropic drug Sunifiram improves both memory impairment and depression observed in OBX mice. OBX mice were administered once a day for 7-12 days with Sunifiram (0.01-1.0mg/kg p.o.) from 10 days after operation with or without gavestinel (10mg/kg i.p.), which is glycine-binding site inhibitor of N-methyl-d-aspartate receptor (NMDAR). The spatial reference memory assessed by Y-maze and short-term memory assessed by novel object recognition task were significantly improved by Sunifiram treatment in OBX mice. Sunifiram also restored hippocampal LTP injured in OBX mice without treatment with gavestinel. By contrast, Sunifiram treatment did not ameliorate the depressive behaviors assessed by tail suspension task in OBX mice. Notably, Sunifiram treatment restored CaMKIIalpha (Thr-286) autophosphorylation and GluR1 (Ser-831) phosphorylation in the hippocampal CA1 region from OBX mice to the levels of control mice. Likewise, Sunifiram treatment improved PKCalpha (Ser-657) autophosphorylation and NR1 (Ser-896) phosphorylation to the control levels. Stimulation of CaMKII and PKC autophosphorylation by Sunifiram was significantly inhibited by pre-treatment with gavestinel. However, Sunifiram treatment did not affect the phosphorylation of CaMKIV (Thr-196) and ERK. Taken together, Sunifiram ameliorates OBX-induced deficits of memory-related behaviors and impaired LTP in the hippocampal CA1 region via stimulation of glycine-binding site of NMDAR.
Design, synthesis and nootropic activity of new analogues of sunifiram and sapunifiram, two potent cognition-enhancers.[Pubmed:19786353]
Bioorg Med Chem. 2009 Nov 1;17(21):7606-14.
A series of amides and sulfonamides, structurally related to DM235 (Sunifiram) and MN19 (sapunifiram), derived by ring expansion or contraction, or by inversion of the exocyclic amide function, have been synthesized and tested for cognition-enhancing activity in the mouse passive-avoidance test. Some of the compounds display good antiamnesic and procognitive activity, with higher potency than piracetam, and with a potency similar to the parent compounds.
Novel nootropic drug sunifiram enhances hippocampal synaptic efficacy via glycine-binding site of N-methyl-D-aspartate receptor.[Pubmed:23733502]
Hippocampus. 2013 Oct;23(10):942-51.
Sunifiram is a novel pyrrolidone nootropic drug structurally related to piracetam, which was developed for neurodegenerative disorder like Alzheimer's disease. Sunifiram is known to enhance cognitive function in some behavioral experiments such as Morris water maze task. To address question whether Sunifiram affects N-methyl-D-aspartate receptor (NMDAR)-dependent synaptic function in the hippocampal CA1 region, we assessed the effects of Sunifiram on NMDAR-dependent long-term potentiation (LTP) by electrophysiology and on phosphorylation of synaptic proteins by immunoblotting analysis. In mouse hippocampal slices, Sunifiram at 10-100 nM significantly enhanced LTP in a bell-shaped dose-response relationship which peaked at 10 nM. The enhancement of LTP by Sunifiram treatment was inhibited by 7-chloro-kynurenic acid (7-ClKN), an antagonist for glycine-binding site of NMDAR, but not by ifenprodil, an inhibitor for polyamine site of NMDAR. The enhancement of LTP by sunifilam was associated with an increase in phosphorylation of alpha-amino-3-hydroxy-5-methylisozazole-4-propionate receptor (AMPAR) through activation of calcium/calmodulin-dependent protein kinase II (CaMKII) and an increase in phosphorylation of NMDAR through activation of protein kinase Calpha (PKCalpha). Sunifiram treatments at 1-1000 nM increased the slope of field excitatory postsynaptic potentials (fEPSPs) in a dose-dependent manner. The enhancement was associated with an increase in phosphorylation of AMPAR receptor through activation of CaMKII. Interestingly, under the basal condition, Sunifiram treatments increased PKCalpha (Ser-657) and Src family (Tyr-416) activities with the same bell-shaped dose-response curve as that of LTP peaking at 10 nM. The increase in phosphorylation of PKCalpha (Ser-657) and Src (Tyr-416) induced by Sunifiram was inhibited by 7-ClKN treatment. The LTP enhancement by Sunifiram was significantly inhibited by PP2, a Src family inhibitor. Finally, when pretreated with a high concentration of glycine (300 muM), Sunifiram treatments failed to potentiate LTP in the CA1 region. Taken together, Sunifiram stimulates the glycine-binding site of NMDAR with concomitant PKCalpha activation through Src kinase. Enhancement of PKCalpha activity triggers to potentiate hippocampal LTP through CaMKII activation.