Pramiracetamnootropic drug CAS# 68497-62-1 |
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Quality Control & MSDS
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| Cas No. | 68497-62-1 | SDF | Download SDF |
| PubChem ID | 51711 | Appearance | Powder |
| Formula | C14H27N3O2 | M.Wt | 269.38 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | DMSO : ≥ 100 mg/mL (371.22 mM) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | N-[2-[di(propan-2-yl)amino]ethyl]-2-(2-oxopyrrolidin-1-yl)acetamide;sulfuric acid | ||
| SMILES | CC(C)N(CCNC(=O)CN1CCCC1=O)C(C)C.OS(=O)(=O)O | ||
| Standard InChIKey | ACSROKXFXFNERX-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C14H27N3O2.H2O4S/c1-11(2)17(12(3)4)9-7-15-13(18)10-16-8-5-6-14(16)19;1-5(2,3)4/h11-12H,5-10H2,1-4H3,(H,15,18);(H2,1,2,3,4) | ||
| 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 | Pramiracetam is a nootropic drug derived from piracetam, and is more potent. Pramiracetam reportedly improved cognitive deficits associated with traumatic brain injuries.
IC50 Value:
Target:
in vitro: Pramiracetam sulfate did not exhibit any affinity in vitro for dopaminergic , GABAergic, serotoninergic, adrenergic, muscarinic, adenosine (IC50 > 10 uM), and benzodiazepine receptors (IC50 > 1 uM) binding sites [1].
in vivo: In a double-blind, randomized design, two groups of six subjects each received alternating placebo and single 400, 800, 1,200, and 1,600 mg oral doses of pramiracetam after an overnight fast. Mean (+/- SD) peak plasma concentrations of the four dose groups (2.71 +/- 0.54, 5.40 +/- 1.34, 6.13 +/- 0.71, 8.98 +/- 0.71 micrograms/mL) were attained between two to three hours following drug administration [2]. Two doses of pramiracetam (7.5 mg/kg and 15 mg/kg) were administered daily prior to testing for 7 weeks in a 16-arm radial maze in which nine arms were baited with food [3]. References: | |||||
Pramiracetam Dilution Calculator
Pramiracetam Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.7122 mL | 18.5611 mL | 37.1223 mL | 74.2446 mL | 92.8057 mL |
| 5 mM | 0.7424 mL | 3.7122 mL | 7.4245 mL | 14.8489 mL | 18.5611 mL |
| 10 mM | 0.3712 mL | 1.8561 mL | 3.7122 mL | 7.4245 mL | 9.2806 mL |
| 50 mM | 0.0742 mL | 0.3712 mL | 0.7424 mL | 1.4849 mL | 1.8561 mL |
| 100 mM | 0.0371 mL | 0.1856 mL | 0.3712 mL | 0.7424 mL | 0.9281 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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Pramiracetam is a nootropic drug [1].
Pramiracetam is investigated for its cognition-enhancing properties. A lower dosage of pramiracetam (100 mg/kg i.p.) was inadequate on NOS mRNA expression and chemical action. Interestingly, organization of pramiracetam (300 mg/kg i.p.) in rats pretreated (24 h before) with lithium chloride (LiCl) (3 mEq/kg i.p.) yielded a 40% expansion in cortical NOS action. Be that as it may, in LiCl-pretreated rats this nootropic neglected to influence cortical NOS mRNA expression; LiCl (3 mEq/kg i.p.) given alone delivered no impact. In summary, the present information show that pramiracetam given alone or in blend with LiCl builds NOS movement in mind cortical homogenates of rats and this might add to the components fundamental learning and memory change created by this nootropic. [1]
Antidementia viability of pramiracetam in 10 patients with likely Alzheimer's sickness was assessed utilizing a 2-phase, placebo-controlled, enhancement-type trial design. Eight patients prove a best dosage in the measurement finding stage, however in the ensuing replication stage just two again enhanced to a comparable degree. PETs with fluorodeoxyglucose got in two people demonstrated no distinct change. Dosages up to 4,000 mg pramiracetam are unrealistic to give symptomatic advantage to Alzheimer's infection patients. [2]
References:
Systemic administration of pramiracetam increases nitric oxide synthase activity in the cerebral cortex of the rat. Funct Neurol. 1995 May-Jun;10(3):151-5.
Nootropic drugs in Alzheimer's disease: symptomatic treatment with pramiracetam. Neurology. 1991 Apr;41(4):570-4.
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[Pharmacokinetics of pramiracetam in animals].[Pubmed:11387954]
Hua Xi Yi Ke Da Xue Xue Bao. 1999 Dec;30(4):411-3.
Pharmacokinetic rules of Pramiracetam were studied here. After giving Pramiracetam orally to dogs, we drew their blood at various times. The drug concentrations in blood plasma were detected by HPLC. 3p87 program was used to calculate the pharmacokinetic parameters. The time-concentration curve corresponded to one apartment model. T1/2 was about 2.3-3.9 hours in various doses. After Pramiracetam was given to rats per os, high concentrations of Pramiracetam were detected in the rats' tissues. The kidney had the highest concentration of Pramiracetam; the liver had the next highest concentration, and then the intestine, lung, muscle, heart, gonad, spleen and sebum had the high concentration in order. The drug was also detected in the brain. 0.7% of the given dose was excreted in unchanged form in bile in 24 hours. 28.26% and 6.35% were excreted in urine and feces respectively in 72 hours. The plasma protein combining rate detected by the method of balance dialysis was 20.1-22.2%.
The action of pramiracetam on consequences of hypobaric hypoxia is only moderate.[Pubmed:9200217]
Physiol Res. 1996;45(3):245-8.
The possible protective action of Pramiracetam, a pyrrolidinone nootropic drug, against hypobaric hypoxia was studied in two age groups of immature rats with implanted electrodes. Epileptic afterdischarges induced by hippocampal stimulation were used as a measure of hypoxic damage. Pramiracetam did not substantially change these afterdischarges in 12- and 18-day-old rat pups which were not exposed to hypoxia. Hypobaric hypoxia (simulated altitude of 7000 m for one hour) led to prolongation of the first afterdischarge in both age groups. Pramiracetam did not influence this prolongation in 12-day-old rats. The first afterdischarge was shortened significantly in 18-day-old animals but not to the level of rats not exposed to hypoxia. The afterdischarges elicited by repeated stimulations (four times at 10 min intervals) did not differ in Pramiracetam-treated and control rats.
Systemic administration of pramiracetam increases nitric oxide synthase activity in the cerebral cortex of the rat.[Pubmed:8557218]
Funct Neurol. 1995 May-Jun;10(3):151-5.
The effect of systemic administration of Pramiracetam on neuronal type nitric oxide synthase (NOS) activity and NOS mRNA expression were studied in the hippocampus and cerebral cortex in rats. A dose of 300 mg/kg (i.p.) of this nootropic produced an approximately 20% increase in NOS activity in rat brain cortical homogenates but not in hippocampal homogenates; no significant changes were observed in NOS mRNA expression in the cortex and hippocampus. A lower dose of Pramiracetam (100 mg/kg i.p.) was ineffective on NOS mRNA expression and enzyme activity. Interestingly, administration of Pramiracetam (300 mg/kg i.p.) in rats pretreated (24 h before) with lithium chloride (LiCl) (3 mEq/kg i.p.) yielded a 40% increase in cortical NOS activity. However, in LiCl-pretreated rats this nootropic failed to affect cortical NOS mRNA expression; LiCl (3 mEq/kg i.p.) given alone produced no effect. In conclusion, the present data demonstrate that Pramiracetam given alone or in combination with LiCl increases NOS activity in brain cortical homogenates of rats and this may contribute to the mechanisms underlying learning and memory improvement produced by this nootropic.
Pramiracetam effects on scopolamine-induced amnesia in healthy volunteers.[Pubmed:15374306]
Arch Gerontol Geriatr. 1994 Mar-Apr;18(2):133-9.
Pramiracetam has been evaluated for its potential antiamnesic properties in scopolamine-induced amnesia in healthy volunteers. Two groups of twelve males, 18-42 and 55-65 years old, respectively, were randomly assigned to oral treatment with Pramiracetam (600 mg twice a day) or with placebo for 10 consecutive days. On day 11 each subject was injected intramuscularly with scopolamine hydrobromide (0.5 mg). Before scopolamine injection and then 1, 3 and 6 h after it, subjects were administered the following psychometric tests: simple and choice visual reaction times, digit symbol substitution test, Rey's 15 words test for short and long term verbal memory. Scopolamine significantly impaired episodic memory and selective attention tests in both scopolamine and placebo groups. Instead visuo-motor and incidental learning measures were unaffected. Pramiracetam, when compared to placebo, was able to partially reduce the amnesic effects induced by scopolamine both in young and old subjects.
