Minaprine

Cat. No.: HY-B0884: Data Sheet Handling Instructions
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Minaprine is a brain-penetrant monoamine oxidase inhibitor. Minaprine also weakly inhibits acetylcholinesterase (AChE) activity. Minaprine reduces intraneuronal dopamine metabolism, lowers striatal homovanillic acid and dihydroxyphenylacetic acid levels, and raises striatal 3-methoxytyramine and 5-hydroxytryptamine levels. Minaprine exhibits convulsant, antidepressant properties.

At equivalent molar concentrations, both the salt and free forms of a compound exhibit comparable biological activity. Nevertheless, the salt form (Minaprine dihydrochloride) usually boasts enhanced water solubility and stability.

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Minaprine Chemical Structure

CAS No. : 25905-77-5

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Other In-stock Forms of Minaprine:

Minaprine dihydrochloride

Other Forms of Minaprine:

Minaprine dihydrochloride In-stock

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•Related Small Molecules:

•Related Proteins:

View All Monoamine Oxidase Isoform Specific Products:

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MAO-A MAO-B

View All Cholinesterase (ChE) Isoform Specific Products:

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AChE BChE

Biological Activity
Purity & Documentation
References
Customer Review

Description

IC₅₀ & Target^[1]

AChE

In Vitro

Minaprine (5×10^-4 M) does not interact with dopaminergic receptors in rat striatal membranes, as it fails to displace [³H]spiperone binding^[1].
Minaprine (40-160 μM) does not alter choline acetyltransferase activity in rat striatal or hippocampal tissue preparations in vitro^[2].
Minaprine (40-160 μM) inhibits acetylcholinesterase activity in rat striatal and hippocampal tissue preparations in vitro^[2].
Minaprine weakly displaces (³H) dexetimide from specific muscarinic receptors in rat striatal homogenates in vitro, with an IC₅₀ of 2×10^-4 M^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Minaprine (2.5-30 mg/kg; i.p.; single dose) induces dose-dependent and time-dependent reductions in striatal HVA and DOPAC, alongside increases in striatal 3-MT, with maximal effects observed 30 minutes after administration, and appears to act via partial, reversible inhibition of monoamine oxidase activity^[1].
Minaprine (7.5-30 mg/kg; i.p.; single dose or once daily for 10 consecutive days) dose-dependently increases acetylcholine levels in multiple rat brain regions^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	CD-COBS (male, 225-250 g)^[1]
Dosage:	2.5, 5, 10, 15, 30 mg/kg
Administration:	i.p.; single dose
Result:	Reduced striatal DOPAC to 403 ± 32 ng/g wet tissue (P < 0.01 vs control) and increased 3-MT to 19.1 ± 1.2 ng/g wet tissue at 2.5 mg/kg, 30 minutes post-administration. Reduced striatal DOPAC to 364 ± 11 ng/g wet tissue (P < 0.01 vs control) and increased 3-MT to 24.5 ± 3.5 ng/g wet tissue (P < 0.05 vs control) at 5 mg/kg, 30 minutes post-administration. Reduced striatal HVA to 355 ± 37 ng/g wet tissue (P < 0.05 vs control) and DOPAC to 294 ± 12 ng/g wet tissue (P < 0.01 vs control), and increased 3-MT to 35 ± 2.5 ng/g wet tissue (P < 0.01 vs control) at 10 mg/kg, 30 minutes post-administration. Reduced striatal HVA to 321 ± 34 ng/g wet tissue (P < 0.01 vs control) and DOPAC to 239 ± 25 ng/g wet tissue (P < 0.01 vs control), and increased 3-MT to 43.6 ± 2.8 ng/g wet tissue (P < 0.01 vs control) at 15 mg/kg, 30 minutes post-administration. Reduced striatal HVA to 312 ± 16 ng/g wet tissue (P < 0.01 vs control) and DOPAC to 241 ± 12 ng/g wet tissue (P < 0.01 vs control), and increased 3-MT to 56.6 ± 2.3 ng/g wet tissue (P < 0.01 vs control) at 30 mg/kg, 30 minutes post-administration. Reduced striatal HVA to 283 ± 13 ng/g wet tissue (P < 0.05 vs control) and DOPAC to 471 ± 13 ng/g wet tissue (P < 0.01 vs control), and increased 3-MT to 66 ± 5 ng/g wet tissue (P < 0.01 vs control) at 15 mg/kg, 15 minutes post-administration. Reduced striatal HVA to 190 ± 26 ng/g wet tissue (P < 0.01 vs control) and DOPAC to 288 ± 14 ng/g wet tissue (P < 0.01 vs control), and increased 3-MT to 86 ± 8 ng/g wet tissue (P < 0.01 vs control) at 15 mg/kg, 30 minutes post-administration. Reduced striatal HVA to 222 ± 28 ng/g wet tissue (P < 0.01 vs control) and DOPAC to 339 ± 57 ng/g wet tissue (P < 0.01 vs control), and increased 3-MT to 73 ± 14 ng/g wet tissue (P < 0.01 vs control) at 15 mg/kg, 60 minutes post-administration. Reduced striatal HVA to 231 ± 24 ng/g wet tissue (P < 0.01 vs control) and DOPAC to 488 ± 21 ng/g wet tissue (P < 0.01 vs control), and increased 3-MT to 41 ± 3 ng/g wet tissue (P < 0.01 vs control) at 15 mg/kg, 90 minutes post-administration. Reduced striatal HVA to 247 ± 27 ng/g wet tissue (P < 0.01 vs control) and DOPAC to 442 ± 31 ng/g wet tissue (P < 0.01 vs control) at 15 mg/kg, 120 minutes post-administration; 3-MT was not significantly different from control. Did not alter pargyline-induced changes in striatal HVA, DOPAC, or 3-MT levels when administered 5 minutes after Pargyline (HY-A0091A) (100 mg/kg i.p.) at 15 mg/kg. Did not significantly alter striatal DA concentrations at any dose or time point tested.

Animal Model:	CD-COBS (female, 200-300 g)^[2]
Dosage:	7.5 mg/kg; 15 mg/kg; 30 mg/kg; 15 mg/kg (daily for 10 days) followed by 30 mg/kg (challenge dose)
Administration:	i.p.; single dose or once daily for 10 consecutive days
Result:	Showed no significant change in striatal acetylcholine or choline levels at 7.5 mg/kg. Produced a 17% increase in striatal acetylcholine levels; showed no change in choline levels at 15 mg/kg. Produced a 59% increase in striatal acetylcholine levels, which persisted for at least 2 h; decreased striatal choline levels by 20% (significant only at 30 min post-administration) at 30 mg/kg. Increased acetylcholine levels by 35% in the hippocampus, 14% in the midbrain-hindbrain, and 37% in the forebrain (excluding striatum and hippocampus), without altering choline levels in these regions at 30 mg/kg. Caused an 18% inhibition of striatal acetylcholinesterase activity at 5 min post-administration (corresponding to peak brain drug levels), which resolved by 30 min at 30 mg/kg. Showed no change in choline acetyltransferase activity after in vivo administration of 30 mg/kg. Produced an increase in striatal acetylcholine comparable to that seen in drug-naive rats (no tolerance) after 10 days of daily 15 mg/kg treatment followed by a 30 mg/kg challenge dose.

Molecular Weight

298.38

Formula

C₁₇H₂₂N₄O

CAS No.

25905-77-5

SMILES

CC1=CC(C2=CC=CC=C2)=NN=C1NCCN3CCOCC3

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Solvent & Solubility

In Vitro:

DMSO : ≥ 35 mg/mL (117.30 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

*"≥" means soluble, but saturation unknown.

Preparing
Stock Solutions

Concentration Solvent Mass	1 mg	5 mg	10 mg

1 mM	3.3514 mL	16.7572 mL	33.5143 mL
5 mM	0.6703 mL	3.3514 mL	6.7029 mL
10 mM	0.3351 mL	1.6757 mL	3.3514 mL

View the Complete Stock Solution Preparation Table

Molarity Calculator
Dilution Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

This equation is commonly abbreviated as: C₁V₁ = C₂V₂

Concentration _(start)

Volume _(start)

Concentration _(final)

Volume _(final)

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

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mg/kg

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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Calculation results:

Working solution concentration: mg/mL

Purity & Documentation

Handling Instructions (2659 KB)

References

[1]. Ferretti P, et al. Biochemical effects of minaprine on striatal dopaminergic neurons in rats. J Pharm Pharmacol. 1984;36(1):48-50. [Content Brief]

[2]. Garattini S, et al. Neurochemical effects of minaprine, a novel psychotropic drug, on the central cholinergic system of the rat. Psychopharmacology (Berl). 1984;82(3):210-214. [Content Brief]

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg

DMSO	1 mM	3.3514 mL	16.7572 mL	33.5143 mL	83.7858 mL
	5 mM	0.6703 mL	3.3514 mL	6.7029 mL	16.7572 mL
	10 mM	0.3351 mL	1.6757 mL	3.3514 mL	8.3786 mL
	15 mM	0.2234 mL	1.1171 mL	2.2343 mL	5.5857 mL
	20 mM	0.1676 mL	0.8379 mL	1.6757 mL	4.1893 mL
	25 mM	0.1341 mL	0.6703 mL	1.3406 mL	3.3514 mL
	30 mM	0.1117 mL	0.5586 mL	1.1171 mL	2.7929 mL
	40 mM	0.0838 mL	0.4189 mL	0.8379 mL	2.0946 mL
	50 mM	0.0670 mL	0.3351 mL	0.6703 mL	1.6757 mL
	60 mM	0.0559 mL	0.2793 mL	0.5586 mL	1.3964 mL
	80 mM	0.0419 mL	0.2095 mL	0.4189 mL	1.0473 mL
	100 mM	0.0335 mL	0.1676 mL	0.3351 mL	0.8379 mL

Minaprine Related Classifications

Neurological Disease

Help & FAQs

Do most proteins show cross-species activity?
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Minaprine25905-77-5Monoamine OxidaseCholinesterase (ChE)MAOdopaminemuscarinic receptors5-hydroxytryptaminemonoamine oxidase inhibitoracetylcholinesteraseglycine receptorsblood-brain barrierglycine receptor blockermonoamine oxidaserat striatumInhibitorinhibitorinhibit

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