Pirlindole hydrochloride
(Synonyms: Pyrazidole hydrochloride; Pirazidole hydrochloride)
Pirlindole (Pyrazidole; Pirazidole) hydrochloride is an orally active, selective, reversible, blood-brain barrier-permeable MAO-A inhibitor with weak inhibitory effects on norepinephrine transporters and serotonin transporters. Pirlindole hydrochloride secondarily inhibits the reuptake of norepinephrine and serotonin to elevate central neurotransmitter levels, thereby producing antidepressant effects, and also exhibits multiple activities including anticonvulsant, analgesic, local anesthetic, blood pressure-regulating, and platelet aggregation-inhibiting properties. Pirlindole hydrochloride is widely applicable to research on major depressive disorder and related depressive conditions.
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- No. CAS: 16154-78-2
- Fòrmula: C15H19ClN2
- Peso molecular:262.78
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Almacenamiento:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Actividad biológica
Descripciòn
Pirlindole (Pyrazidole; Pirazidole) hydrochloride is an orally active, selective, reversible, blood-brain barrier-permeable MAO-A inhibitor with weak inhibitory effects on norepinephrine transporters and serotonin transporters. Pirlindole hydrochloride secondarily inhibits the reuptake of norepinephrine and serotonin to elevate central neurotransmitter levels, thereby producing antidepressant effects, and also exhibits multiple activities including anticonvulsant, analgesic, local anesthetic, blood pressure-regulating, and platelet aggregation-inhibiting properties. Pirlindole hydrochloride is widely applicable to research on major depressive disorder and related depressive conditions[1][2].
IC50 & Target[1]
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MAO-A |
In Vitro
In Vivo
Pirlindole (5-25 mg/kg; i.p.; acute; 10 mg/kg; i.p.; twice daily; 14 days) produces a significant antidepressant-like effect in the Porsolt forced swimming test in rats and mice, with potency equivalent to standard antidepressants[2].
Pirlindole (10 mg/kg; i.p.; daily; 5 days) reverses hypoactive self-stimulation behavior in rats with internal capsule lesions, indicating antidepressant-like activity[2].
Pirlindole (10 mg/kg; i.p.; daily; 7-14 days) improves escape/avoidance learning deficits in mice exposed to in vivo inescapable electric shock, demonstrating antidepressant-like activity[2].
Pirlindole (1-50 mg/kg; i.p., p.o.) antagonizes Reserpine (HY-N0480)- and Tetrabenazine (HY-B0590)-induced behavioral deficits in mice and rats, with ED50 values of 13.66 mg/kg i.p. and 13.39 mg/kg i.p. for respective effects in rats[2].
Pirlindole (up to 25 mg/kg; i.p., s.c., p.o.) does not antagonize Apomorphine (HY-12723)-induced hypothermia in mice[2].
Pirlindole (11.4-20 mg/kg; i.p.) potentiates 5-hydroxytryptophan-induced head twitches in mice with an ED50 of 11.4-20 mg/kg i.p[2].
Pirlindole potentiates tryptamine-induced clonic seizures in rats with an ED50 of 11.07 mg/kg i.p. or 25 mg/kg p.o[2].
Pirlindole (up to 50 mg/kg; p.o., s.c., i.p.) does not antagonize Oxotremorine (HY-170032)-induced hypothermia or tremors in mice at tested doses[2].
Pirlindole (0.01-1.00 mg/kg; i.v.) does not reinforce intravenous self-administration in Rhesus monkeys, indicating low addiction risk[2].
Pirlindole (1 mg/kg/min; i.v.; 10 minutes) does not alter the firing rate of central noradrenergic or serotonergic neurons in rats[2].
Pirlindole (5 mg/kg; p.o.) induces EEG activation in squirrel monkeys, and at 10 mg/kg i.v. modulates clonidine-induced EEG effects in rabbits[2].
Pirlindole (10-150 mg/kg; i.p.) produces selective, reversible inhibition of MAO-A in rats, with an ED50 of 21 mg/kg i.p., and minimal MAO-B inhibition[2].
Pirlindole (15-30 mg/kg; i.p.) protects mice against Picrotoxin (HY-101391)-induced tonic spasms, has analgesic effects in mice and rats at 10-30 mg/kg i.p., and acts as a local anesthetic in guinea pigs at a 0.3% solution, while high doses (up to 324 mg/kg i.p.) cause nervous system disturbances in mice[2].
Pirlindole (10 mg/kg; i.p.; daily; 5 days) reverses hypoactive self-stimulation behavior in rats with internal capsule lesions, indicating antidepressant-like activity[2].
Pirlindole (10 mg/kg; i.p.; daily; 7-14 days) improves escape/avoidance learning deficits in mice exposed to in vivo inescapable electric shock, demonstrating antidepressant-like activity[2].
Pirlindole (1-50 mg/kg; i.p., p.o.) antagonizes Reserpine (HY-N0480)- and Tetrabenazine (HY-B0590)-induced behavioral deficits in mice and rats, with ED50 values of 13.66 mg/kg i.p. and 13.39 mg/kg i.p. for respective effects in rats[2].
Pirlindole (up to 25 mg/kg; i.p., s.c., p.o.) does not antagonize Apomorphine (HY-12723)-induced hypothermia in mice[2].
Pirlindole (11.4-20 mg/kg; i.p.) potentiates 5-hydroxytryptophan-induced head twitches in mice with an ED50 of 11.4-20 mg/kg i.p[2].
Pirlindole potentiates tryptamine-induced clonic seizures in rats with an ED50 of 11.07 mg/kg i.p. or 25 mg/kg p.o[2].
Pirlindole (up to 50 mg/kg; p.o., s.c., i.p.) does not antagonize Oxotremorine (HY-170032)-induced hypothermia or tremors in mice at tested doses[2].
Pirlindole (0.01-1.00 mg/kg; i.v.) does not reinforce intravenous self-administration in Rhesus monkeys, indicating low addiction risk[2].
Pirlindole (1 mg/kg/min; i.v.; 10 minutes) does not alter the firing rate of central noradrenergic or serotonergic neurons in rats[2].
Pirlindole (5 mg/kg; p.o.) induces EEG activation in squirrel monkeys, and at 10 mg/kg i.v. modulates clonidine-induced EEG effects in rabbits[2].
Pirlindole (10-150 mg/kg; i.p.) produces selective, reversible inhibition of MAO-A in rats, with an ED50 of 21 mg/kg i.p., and minimal MAO-B inhibition[2].
Pirlindole (15-30 mg/kg; i.p.) protects mice against Picrotoxin (HY-101391)-induced tonic spasms, has analgesic effects in mice and rats at 10-30 mg/kg i.p., and acts as a local anesthetic in guinea pigs at a 0.3% solution, while high doses (up to 324 mg/kg i.p.) cause nervous system disturbances in mice[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:strain not specified (rat); strain not specified (mouse)[2]
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Dosage:10 mg/kg (rat, acute); 20 mg/kg (rat, acute); 5 mg/kg (mouse, acute); 25 mg/kg (mouse, acute); 10 mg/kg (mouse, chronic)
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Administration:i.p.; acute (rat); i.p.; acute (mouse); i.p.; twice daily; 14 days (mouse)
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Result:Significantly decreased immobility time in the forced swimming test.
Showed potency equivalent to classical tricyclic antidepressants and classical monoamine oxidase inhibitors.
Demonstrated a clear dose-effect relationship between 5 and 25 mg/kg i.p. in mice.
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Animal Model:strain not specified[2]
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Dosage:10 mg/kg
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Administration:i.p.; daily; 5 days
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Result:Increased self-stimulation behavior, an effect also observed with other antidepressants like imipramine and tranylcypromine.
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Animal Model:strain not specified[2]
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Dosage:10 mg/kg
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Administration:i.p.; daily; 7-14 days
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Result:Improved the escape/avoidance learning deficit induced by inescapable electric shock.
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Animal Model:strain not specified (mouse); strain not specified (rat)[2]
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Dosage:1 mg/kg (mouse); 50 mg/kg (mouse); 2.5 mg/kg (mouse); 50 mg/kg (mouse); 25 mg/kg (mouse, tetrabenazine-induced blepharoptosis); 13.66 mg/kg (rat, reserpine-induced effects ED50); 13.39 mg/kg (rat, tetrabenazine-induced catalepsy ED50)
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Administration:i.p. (mouse); p.o. (mouse); i.p. (rat)
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Result:Antagonized reserpine-induced blepharoptosis and hypothermia in mice, and tetrabenazine-induced blepharoptosis in mice.
Achieved an ED50 of 13.66 mg/kg i.p. for antagonizing reserpine-induced effects in rats, and an ED50 of 13.39 mg/kg i.p. for antagonizing tetrabenazine-induced catalepsy in rats.
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Animal Model:strain not specified[2]
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Dosage:10 mg/kg (p.o.); 25 mg/kg (p.o.); 5 mg/kg (i.p.); 20 mg/kg (i.p.)
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Administration:p.o.; i.p.
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Result:Exerted a dose-dependent potentiation of amphetamine stereotypy in rats, but was largely less active than imipramine, nialamide, and clorgyline.
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Animal Model:strain not specified (mouse); strain not specified (rat)[2]
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Dosage:25 mg/kg (mouse, s.c.); 1 mg/kg (mouse, i.p.); 25 mg/kg (mouse, i.p.); 25 mg/kg (mouse, p.o.); >65 mg/kg (rat, i.p.)
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Administration:s.c. (mouse); i.p. (mouse, rat); p.o. (mouse)
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Result:Was unable to antagonize apomorphine-induced hypothermia in mice.
Had an ED50 >65 mg/kg i.p. for antagonizing fluphenazine-induced catalepsy in rats, showing no meaningful activity compared to imipramine and tranylcypromine.
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Animal Model:strain not specified[2]
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Dosage:20 mg/kg; 11.4 mg/kg
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Administration:i.p.
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Result:Potentiated 5-hydroxytryptophan-induced head twitches in mice with ED50 values of 20 mg/kg i.p. and 11.4 mg/kg i.p.
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Animal Model:strain not specified[2]
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Dosage:25 mg/kg (p.o.); 11.07 mg/kg (i.p.)
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Administration:p.o.; i.p.
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Result:Potentiated tryptamine-induced clonic seizures in rats with ED50 values of 25 mg/kg p.o. and 11.07 mg/kg i.p.
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Animal Model:strain not specified[2]
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Dosage:25 mg/kg (s.c.); 50 mg/kg (p.o.); 30 mg/kg (i.p.)
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Administration:s.c.; p.o.; i.p.
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Result:Was unable to antagonize oxotremorine-induced hypothermia or tremors in mice, similar to tranylcypromine but unlike tricyclic antidepressants.
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Animal Model:strain not specified (mouse); strain not specified (rat)[2]
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Dosage:10 mg/kg (p.o.); 25 mg/kg (p.o.); 25 mg/kg (i.p.)
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Administration:p.o.; i.p.
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Result:Antagonized diazepam-induced sedation in mice and rats, and prevented nitrazepam-induced loss of the righting reflex in mice.
Had no effect on diazepam's anxiolytic activity.
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Animal Model:strain not specified[2]
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Dosage:0.01 mg/kg; 1.00 mg/kg
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Administration:i.v.
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Result:Did not reinforce intravenous self-administration behavior in Rhesus monkeys.
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Animal Model:strain not specified[2]
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Dosage:1 mg/kg/min
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Administration:i.v.; 10 minutes
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Result:Did not significantly modify the firing rate of noradrenergic (locus coeruleus) or serotonergic (dorsal raphe nucleus) neurons in rats.
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Animal Model:strain not specified (squirrel monkey); strain not specified (rabbit)[2]
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Dosage:5 mg/kg (squirrel monkey); 10 mg/kg (rabbit)
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Administration:p.o. (squirrel monkey); i.v. (rabbit)
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Result:Produced EEG activation (increased beta and gamma waves) without overt motor stimulation in squirrel monkeys.
Antagonized clonidine-induced EEG synchronization and amplified clonidine-induced EEG desynchronization in rabbits.
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Animal Model:strain not specified[2]
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Dosage:10 mg/kg; 150 mg/kg; 21 mg/kg (MAO-A inhibition ED50); 163 mg/kg (MAO-B inhibition extrapolated ED50)
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Administration:i.p.
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Result:Produced selective, reversible inhibition of MAO-A; the ED50 for selective MAO-A inhibition was 21 mg/kg i.p.
Reduced brain MAO activity to half its initial value 1 hour after 10 mg/kg i.p.
Inhibited MAO-B by approximately 30% at 50 mg/kg i.p., with an extrapolated ED50 of 163 mg/kg i.p. for MAO-B inhibition.
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Animal Model:strain not specified[2]
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Dosage:10 mg/kg (s.c.); 40 mg/kg (s.c.); 50 mg/kg (i.p.); 25 mg/kg (i.p., three times within 24 hours)
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Administration:s.c.; i.p.; three times within 24 hours
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Result:Increased noradrenaline levels in all rat brain structures (particularly the hypothalamus), and increased serotonin levels in the hypothalamus, cortex, and raphe nucleus.
Did not significantly modify dopamine or homovanillic acid (HVA) levels.
Increased serotonin levels by 37% and decreased 5-hydroxyindoleacetic acid (5-HIAA) levels after administration of 25 mg/kg i.p. three times in 24 hours.
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Animal Model:strain not specified (mouse); strain not specified (rat); strain not specified (guinea pig)[2]
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Dosage:324 mg/kg (mouse, Irwin test); 15 mg/kg (mouse, anticonvulsive); 30 mg/kg (mouse, anticonvulsive); 10 mg/kg (mouse/rat, analgesic); 30 mg/kg (mouse/rat, analgesic); 0.3% solution (guinea pig, local anesthetic)
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Administration:i.p. (mouse, rat); topical (guinea pig)
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Result:Caused ataxia, motor disturbances, tremor, and clonic spasms in mice at up to 324 mg/kg i.p.
Protected mice against picrotoxin-induced tonic spasms at 15-30 mg/kg i.p.
Had analgesic properties in mice and rats at 10-30 mg/kg i.p., and exhibited local anesthetic activity in guinea pigs at a 0.3% solution.
Chemical Information
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No. CAS 16154-78-2
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Appearance Solid
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Peso molecular 262.78
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Fòrmula C15H19ClN2
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SMILES
CC1=CC(C2=C3N4CCNC3CCC2)=C4C=C1.Cl
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Synonyms
Pyrazidole hydrochloride; Pirazidole hydrochloride
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Pureza y Documentación
Referencias
[1]. Macedo A, et al. Pirlindole in the treatment of depression: a meta-analysis. Clinical drug investigation. 2011;31(1):61-71. [Content Brief]
[2]. Bruhwyler J, et al. Pirlindole: a selective reversible inhibitor of monoamine oxidase A. A review of its preclinical properties. Pharmacological research. 1997 Jul;36(1):23-33. [Content Brief]
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