| Stereochemistry | ACHIRAL |
| Molecular Formula | C6H10N2O2 |
| Molecular Weight | 142.1558 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
NC(=O)CN1CCCC1=O
InChI
InChIKey=GMZVRMREEHBGGF-UHFFFAOYSA-N
InChI=1S/C6H10N2O2/c7-5(9)4-8-3-1-2-6(8)10/h1-4H2,(H2,7,9)
| Molecular Formula | C6H10N2O2 |
| Molecular Weight | 142.1558 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
Piracetam (sold under many brand names) is a nootropic drug in the racetams group, with chemical name 2-oxo-1-pyrrolidine acetamide. It shares the same 2-oxo-pyrrolidone base structure with pyroglutamic acid. Piracetam is a cyclic derivative of the neurotransmitter gamma-aminobutyric acid (GABA), originally marketed in 1971 by UCB Pharma. Presently piracetam is used in many European countries, Asia and South America. In the United States, it is not approved by the US Food and Drug Administration for any medical use and it is not permitted to be sold as a dietary supplement. In the UK, piracetam is prescribed mainly for myoclonus but is used off-label for other conditions. Evidence to support its use for many conditions is unclear. Piracetam's mechanism of action, as with racetams in general, is not fully understood. The drug influences neuronal and vascular functions and influences cognitive function without acting as a sedative or stimulant. It is hypothesized to act on ion channels or ion carriers, thus leading to increased neuron excitability. GABA brain metabolism and GABA receptors are not affected by piracetam. It has been found to increase blood flow and oxygen consumption in parts of the brain, but this may be a side effect of increased brain activity rather than a primary effector mechanism of action for the drug.
CNS Activity
Approval Year
Cmax
AUC
T1/2
Doses
AEs
PubMed
Patents
Sample Use Guides
The dosing of piracetam varies according to indication. For cognitive disorders and vertigo it is 2.4–4.8 g daily p.o., for dyslexia it is 3.2 g daily p.o., for cortical myoclonus it is 7.2–24.0 g daily p.o., for prophylaxis of vaso-occlusive crises in sickle cell anemia it is 160 mg/kg/day p.o., and for remission of vaso-occlusive crises it is 300 mg/kg/day i.v. in four divided doses.
Route of Administration:
Oral
Primary cultures of mice cortical neurons were washed twice in glucose-free Earle’s solution (143 mM NaCl, 5.4 mM KCl, 1.8 mM CaCl2, 1.0 mM MgSO4, 1.0 mM NaH2PO4, 2.4 mM HEPES, and pH 7.4) at 37 OC and placed in an incubator containing 95 % N2 and 5 % CO2 for 4 h. The neurons were then fed with high glucose DMEM (Earle’s solution), and returned to the normal incubator for a 4 h recovery. Those neurons for control underwent the same procedure except the oxygen/glucose deprivation treatment. For the drug treatment groups, piracetam (PIR, 500 or 1,000 mkM/l) or nimodipine (NIMO, 10 mkM/l) was given 12 h before OGD or during OGD and for the following 4 h. The OGD control group was treated with vehicle (PBS).
