Selegiline hydrochloride Property

Melting point:

141-142°C

alpha 

D25 -10.8° (c = 6.48 in water)

storage temp. 

2-8°C

solubility 

H₂O: >10 mg/mL

form 

solid

color 

white

optical activity

[α]25/D 10.8°, c = 6.48 in H2O(lit.)

Water Solubility 

Soluble in water at 100mM

Stability:

Stable for 2 years from date of purchase as supplied. Solutions in DMSO may be stored at -20°C for up to 3 months.

CAS DataBase Reference

14611-52-0(CAS DataBase Reference)

Safety

Safety Statements 

22-36

RIDADR 

3249

WGK Germany 

3

RTECS 

DA0292500

HazardClass 

6.1(b)

PackingGroup 

III

HS Code 

2921490002

Hazardous Substances Data

14611-52-0(Hazardous Substances Data)

Toxicity

LD50 in rats (mg/kg): 81 i.v., 280 s.c. (Magyar)

Hazard and Precautionary Statements (GHS)

Symbol(GHS)

Signal word

Warning

Hazard statements

H302Harmful if swallowed

H336May cause drowsiness or dizziness

Selegiline hydrochloride Chemical Properties,Usage,Production

Description

Deprenyl (14611-52-0) is a potent inhibitor of monoamine oxidase B (MAO- B) which has been used for the treatment of Parkinson’s disease.1,2 Displays neuroprotective effects rescuing nigral dopaminergic neurons after systemic MPTP treatment.3 Rescues PC12 cells from trophic withdrawal-induced apoptosis.4 Glyceraldehyde-3-phosphate dehydrogenase has been found to be the putative target responsible for its neuroprotective effects.5

Chemical Properties

Crystalline Solid

Uses

antibacterial

Uses

Antidepressant, Antiparkinsonian

Uses

Selegiline hydrochloride is used to alleviate the symptonms of Parkinsons disease

brand name

Eldepryl (Somerset); Zelapar (Valeant).

Biological Activity

Selective inhibitor of monoamine oxidase B (MAO-B).

Clinical Use

Monoamine-oxidase-B inhibitor:
Treatment of Parkinson’s disease

Veterinary Drugs and Treatments

Selegiline is approved for use in dogs for the treatment of Cushing’s disease and for Canine Cognitive Dysfunction (so-called “old dog dementia”). Its use for Cushing’s disease is somewhat controversial as clinical studies evaluating its efficacy have shown disappointing results. In humans, selegiline’s primary indication is for the adjunctive treatment of Parkinson’s disease.

Drug interactions

Potentially hazardous interactions with other drugs
Analgesics: hyperpyrexia and CNS toxicity reported with pethidine - avoid; avoid with opioid analgesics.
Antidepressants: avoid with citalopram and escitalopram; increased risk of hypertension and CNS excitation with fluvoxamine, sertraline or venlafaxine, do not start selegiline until 1 week after stopping them, avoid for 2 weeks after stopping selegiline; increased risk of hypertension and CNS excitation with paroxetine, do not start selegiline until 2 weeks after stopping paroxetine, avoid for 2 weeks after stopping selegiline avoid concomitant use with other MAOIs and moclobemide (can lead to hypertensive crisis) - allow at least 14 days before starting a MAOI; avoid concomitant use with fluoxetine, allow 5 weeks between stopping fluoxetine and starting selegiline; allow 14 days between stopping selegiline and starting fluoxetine; increased CNS toxicity with tricyclics and vortioxetine.
Oestrogens and progestogens: concentration of selegiline increased - avoid.
Sympathomimetics: concomitant use is not recommended; risk of hypertensive crisis with dopamine.

Metabolism

Extensive first-pass metabolism in the liver to produce at least 5 metabolites, including desmethylselegiline (norselegiline), N-methylamfetamine, and amfetamine. Plasma concentrations of selegiline metabolites are greatly reduced after doses of the oral lyophilisate preparation, the majority of which undergoes absorption through the buccal mucosa.
Selegiline is excreted as metabolites mainly in the urine and about 15% appears in the faeces.

References

Gerlach et al. (1992), The molecular pharmacology of L-deprenyl; Eur. J. Pharmacol., 226 97 Tetrud and Langston (1989), The effect of deprenyl (selegiline) on the natural history of Parkinson’s disease; Science, 245 519 Tatton and Greenwood (1991), Rescue of dying neurons: a new action of deprenyl in MPTP parkinsonism; J. Neurosci Res., 30 666 Tatton et al. (1994), (-)-Deprenyl reduces PC12 cell apoptosis by inducing new protein synthesis; J. Neurochem, 63 1572 Kargten et al. (1998), Glyceraldehyde-3-phosphate dehydrogenase, the putative target of the antiapoptotic compounds CGP 3466 and R-(-)-deprenyl; J. Biol. Chem., 273 5821