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Fig. 1 · Structure
Cat. No.
A10835
CAS No.
14611-52-0
Formula
C13H18ClN
Mol. Weight
223.74

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Selegiline hydrochloride

MAO-B Inhibitor

Selegiline hydrochloride is a selective and irreversible monoamine oxidase B (MAO-B) inhibitor, exhibiting an IC50 of 51 nM and demonstrating a 450-fold selectivity over MAO-A (IC50=23 μM). This compound is essential for research focused on neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease, as well as major depressive disorder. Its ability to enhance dopaminergic signaling makes it a valuable tool for studying the biochemical mechanisms underlying these conditions.

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In Vitro Studies

Selegiline at 0.5 μM showed irreversible binding to recombinant human MAO-B, assessed through enzyme activity before and after dialysis. In ex vivo brain slices from untrained naïve rats, Selegiline hydrochloride at 100 μM significantly increased burst-pause firing in CINs; the increase persisted with SCH23390 and raclopride but was abolished by ouabain. In recombinant human MAO-A, Selegiline had a reported IC50 of 23.00 ± 1.00 µM. [1,2]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Irreversible binding to recombinant human MAO-B

Biochemical assay · recombinant human MAO-B [1]

Recombinant human MAO-B was incubated with Selegiline at 0.5 μM, and enzyme activity was measured before and after dialysis. Binding was confirmed to be irreversible.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
activity of the enzyme was determined before and after the dialysisReported result deprenyl (0.5 μM), before and after the dialysis: The binding of selective MAO-B inhibitor deprenyl was confirmed to be irreversible.[1]

Literature-Reported Treatment Conditions

Treatment concentration
0.5 μM
Exposure duration
20 min incubation at 37 °C; dialyzed against potassium phosphate buffer (25 mM; pH 7.4) at 4 °C for 14–18 h (three buffer changes)
Method
incubated with each inhibitor
Vehicle
100 mM potassium phosphate buffer (pH 7.4)
Methods and source locations

Compound reported in the paper: Selegiline; Compound label in the paper: Deprenyl

The paper names Selegiline without stating the salt or form; not verified as the hydrochloride form supplied as A10835. No dose conversion or lot validation.

2. Results > 2.3. Analysis of Reversibility of Binding of Inhibitor (S23); 4. Materials and Methods > 4.5. Analysis of Reversibility of Binding of Inhibitor (S93, S94, S95, S96); Figure 4 legend (S137)

activity of the enzyme was determined before and after the dialysis: activity of the enzyme was determined before and after the dialysis; comparator: Control enzyme (without inhibitor) — 2. Results > 2.3. Analysis of Reversibility of Binding of Inhibitor (S23); 4. Materials and Methods > 4.5. Analysis of Reversibility of Binding of Inhibitor (S93, S96)

Burst-pause firing in rat brain slices

Cell-based study · CIN activity in ex vivo brain slices from untrained naïve rats [2]

Selegiline (100 μM), and not pargyline (100 μM), significantly increased burst-pause firing in CINs in ex vivo brain slices from untrained naïve rats. The selegiline-induced (100 μM) increase in burst-pause firing was abolished by ouabain (100 μM; n = 9).

Measured endpoints — not treatment concentrations
EndpointReported resultReference
burst-pause firing pattern in CINsReported result Selegiline (100 μM), and not pargyline (100 μM), significantly increased burst-pause firing in CINs. The selegiline-induced (100 μM) increase in burst-pause firing persisted in the presence of SCH23390 (SCH; 10 μM) and raclopride (Rac; 10 μM) but was abolished by ouabain (100 μM; n = 9).[2]

Literature-Reported Treatment Conditions

Treatment concentration
100 μM
Exposure duration
drug effect was typically taken around the 5- to 10-min mark during application
Method
drug application
Reported limits
Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: Selegiline hydrochloride; Compound label in the paper: Selegiline

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

RESULTS > The MAO-B inhibitor selegiline increases burst-pause activity in CINs (S98, S99, S100); MATERIALS AND METHODS > Behavioral procedures > Action potential analysis (S241); Fig. 4. legend (S311, S312)

burst-pause firing pattern in CINs: burst-pause firing pattern in CINs; comparator: baseline — RESULTS > The MAO-B inhibitor selegiline increases burst-pause activity in CINs (S99); Fig. 4. legend (S311, S312)

Selegiline inhibition of recombinant human MAO-A

Biochemical assay · recombinant human MAO-A [1]

Recombinant human MAO-A was incubated with Selegiline for 20 min at 37 °C. The MAO-A IC50 was 23.00 ± 1.00 µM.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
MAO-A IC50IC50 23.00 ± 1.00 µM[1]

Literature-Reported Treatment Conditions

Exposure duration
incubated for 20 min at 37 °C
Vehicle
DMSO
Reported limits
Not stated in the sentences used: dose, route.
Methods and source locations

Compound reported in the paper: Selegiline; Compound label in the paper: Deprenyl

The paper names Selegiline without stating the salt or form; not verified as the hydrochloride form supplied as A10835. No dose conversion or lot validation.

4. Materials and Methods > 4.2. MAOs Inhibition Assay (S72, S74, S78, S79, S81); Table 1 (T1.h1, T1.r14)

MAO-A IC50: MAO-A IC50; comparator: corresponding control (enzyme-substrate reaction) without inhibitors — Table 1 (T1.h1, T1.r14)

In Vivo Studies

In male adult mice with CFA-induced inflammatory pain, Selegiline hydrochloride administered intraperitoneally at 10 mg/kg for 7 days after CFA administration increased PWT and PWL compared with the vehicle-treated group. PMA reversed the analgesic effect of selegiline. [3]

Withdrawal responses in mice with inflammatory pain

Animal study · Male C57 adult mice (6–8 weeks old); inflammatory pain; n = 6 [3]

Selegiline hydrochloride was dissolved in saline and administered intraperitoneally at 10 mg/kg for 7 days after CFA administration. Compared to the vehicle-treated group, selegiline increased the PWT and PWL of CFA mice. However, PMA reversed the analgesic effect of selegiline.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Paw withdrawal thresholdReported result 10 mg/kg for 7 days after CFA administration: Compared to the vehicle-treated group, selegiline increased the PWT and PWL of CFA mice. However, PMA reversed the analgesic effect of selegiline.[3]

Conditions shared by the study groups

Route
intraperitoneally
Treatment course
for 7 days after CFA administration
Vehicle
saline
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Selegiline hydrochloride 10 mg/kgvehicle-treated group10 mg/kg for 7 days after CFA administration: Compared to the vehicle-treated group, selegiline increased the PWT and PWL of CFA mice. However, PMA reversed the analgesic effect of selegiline.[3]
Selegiline hydrochloride 10 mg/kg
Model: Male C57 adult mice (6–8 weeks old); inflammatory pain; n = 6
Methods and source locations

Compound reported in the paper: Selegiline hydrochloride; Compound label in the paper: Selegiline

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Methods > Animals and surgery (S2, S3); Methods > Drugs and drug administration (S36); Results > MAO-B inhibition attenuates neuroinflammation and alleviates inflammatory pain by impairing NETs formation (S119, S120); Fig. 8 legend (S244)

Paw withdrawal threshold: Paw withdrawal threshold; comparator: vehicle-treated group — Methods > Drugs and drug administration (S36); Results > MAO-B inhibition attenuates neuroinflammation and alleviates inflammatory pain by impairing NETs formation (S119, S120); Fig. 8 legend (S244)

Selegiline hydrochloride 10 mg/kg · Methods > Drugs and drug administration (S36); Results > MAO-B inhibition attenuates neuroinflammation and alleviates inflammatory pain by impairing NETs formation (S119, S120)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 14611-52-0
Applications MAO-B Inhibitor
Formula C13H18ClN
Molecular Weight 223.74
Synonyms Deprenyl hydrochloride; (-)-Selegiline hydrochloride; (-)-Deprenyl hydrochloride
SMILES
CN(CC#C)[C@H](C)CC1=CC=CC=C1.Cl

Storage & Solubility

In Vitro Solubility

Reported Solubility

No reported solubility data are available for this product.

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Chaurasiya ND, Zhao J, Pandey P, et al. Selective Inhibition of Human Monoamine Oxidase B by Acacetin 7-Methyl Ether Isolated from Turnera diffusa (Damiana). Molecules (2019). PMID: 30813423 DOI: 10.3390/molecules24040810 Source material
  2. [2] Becchi S, Chieng B, Bradfield LA, et al. Cognitive effects of thalamostriatal degeneration are ameliorated by normalizing striatal cholinergic activity. Sci Adv (2023). PMID: 37352346 DOI: 10.1126/sciadv.ade8247 Source material
  3. [3] Li T, Yue Y, Ma Y, et al. Fasting-mimicking diet alleviates inflammatory pain by inhibiting neutrophil extracellular traps formation and neuroinflammation in the spinal cord. Cell Commun Signal (2023). PMID: 37735678 DOI: 10.1186/s12964-023-01258-2 Source material

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