Deprenyl inhibits apoptosis and displays neuroprotective effects in a variety of in vitro and in vivo systems. In vivo it rescues nigral dopaminergic neurons after systemic MPTP treatment. In vitro it rescues PC12 cells from apoptotic cell death induced by trophic withdrawal. The putative target responsible for the anti-apoptotic effects is glyceraldehyde-3-phosphate dehydrogenase. Deprenyl also inhibits monoamine oxidase-B, which is not involved in its anti-apoptotic mechanism. Parkinson’s disease therapeutic.
Product Details
| Alternative Name: | Selegiline hydrochloride |
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| Formula: | C13H17N . HCl |
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| MW: | 223.7 |
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| CAS: | 14611-52-0 |
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| Purity: | ≥98% (HPLC) |
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| Appearance: | White solid. |
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| Solubility: | Soluble in water. |
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| Shipping: | Ambient |
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| Long Term Storage: | Ambient |
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| Regulatory Status: | RUO - Research Use Only |
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Product Literature References
Glyceraldehyde-3-phosphate dehydrogenase, the putative target of the antiapoptotic compounds CGP 3466 and R-(-)-deprenyl: E. Kragten, et al.; J. Biol. Chem.
273, 5821 (1998),
Abstract;
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(-)-Deprenyl reduces PC12 cell apoptosis by inducing new protein synthesis: W. G. Tatton, et al.; J. Neurochem.
63, 1572 (1994),
Abstract;
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Rescue of dying neurons: a new action for deprenyl in MPTP parkinsonism: W. G. Tatton & C. E. Greenwood; J. Neurosci. Res.
30, 666 (1991),
Abstract;
The effect of deprenyl (selegiline) on the natural history of Parkinson's disease: J. W. Tetrud & J. W. Langston; Science
245, 519 (1989),
Abstract;
