product name P7C3
Description: P7C3 is a potent proneurogenic and neuroprotective chemical that targets NAMPT enzyme. P7C3 protects newborn neurons from apoptotic cell death, and promotes neurogenesis in mice and rats in the subgranular zone of the hippocampal dentate gyrus, the site of normal neurogenesis in adult mammals. P7C3 is orally available, nontoxic, stable in mice, rats, and cell culture, and capable of penetrating the blood-brain barrier.
References: Cell. 2014 Sep 11;158(6):1324-34; Cell. 2010 Jul 9;142(1):39-51; Neurosci Lett. 2015 Mar 30;591:86-92.
474.19
Formula
C21H18Br2N2O
CAS No.
301353-96-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 95 mg/mL (200.3 mM)
Water: <1 mg/mL
Ethanol: 20 mg/mL (42.2 mM)
Solubility (In vivo)
Synonyms
other peoduct :
| In Vitro |
In vitro activity: In U2OS Cells, P7C3 protects cells from doxorubicin-mediated toxicity, and enhances the flux of nicotinamide through the NAMPT-mediated salvage pathway. Kinase Assay: Cell Assay: P7C3 (1, 10, and 100 nM) preserved mitochondrial membrane potential in parallel to proneurogenic activity. Administration of P7C3 (5 μM) to U2OS cells treated with doxorubicin, which induced NAD depletion, induced an increasing in intracellular NAD levels and concomitant protection from doxorubicin-mediated toxicity through the NAMPT-mediated salvage. |
|---|---|
| In Vivo | In mouse brain, P7C3 (40 mg/kg, p.o.) induces neurogenesis and enhances survival of newborn neurons. In npas3−/− mice, P7C3 (20 mg/kg/d, p.o.) increases the magnitude of neural precursor cell proliferation, and corrects morphological and electrophysiological deficits. In the Ts65Dn mouse model of Down Syndrome, P7C3 restores hippocampal neurogenesis though a significant increase in total Ki67+, DCX+, and surviving BrdU+ cells. |
| Animal model | Mouse |
| Formulation & Dosage | Dissolved in DMSO and diluted with 3% DMSO/10% cremophor EL/87.5% D5W (5% dextrose in water, pH 7.2); 40 mg/kg; i.p. or oral administration |
| References | Cell. 2014 Sep 11;158(6):1324-34; Cell. 2010 Jul 9;142(1):39-51; Neurosci Lett. 2015 Mar 30;591:86-92. |
