1. GPCR/G Protein Neuronal Signaling
  2. Dopamine Receptor Adrenergic Receptor
  3. Mivazerol

Mivazerol is a selective α2-adrenoceptor agonist. Mivazerol decreases the spontaneous release of serotonin (5-HT) and significantly inhibits the immobilization stress-induced enhancement of norepinephrine (NE), dopamine (DA) and dihydroxyphenylacetic acid (DOPAC). Mivazerol inhibits intrathecal release of glutamate evoked by halothane withdrawal in rats, and exerts neuroprotective effects in forebrain ischemia rats. Mivazerol can be used for myocardial ischemia research.

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Mivazerol

Mivazerol Chemical Structure

CAS No. : 125472-02-8

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Description

Mivazerol is a selective α2-adrenoceptor agonist. Mivazerol decreases the spontaneous release of serotonin (5-HT) and significantly inhibits the immobilization stress-induced enhancement of norepinephrine (NE), dopamine (DA) and dihydroxyphenylacetic acid (DOPAC). Mivazerol inhibits intrathecal release of glutamate evoked by halothane withdrawal in rats, and exerts neuroprotective effects in forebrain ischemia rats. Mivazerol can be used for myocardial ischemia research[1][2][3].

IC50 & Target[1]

α2-adrenergic receptor

 

In Vitro

Mivazerol has a α2a1 selectivity ratio of 119, and its specificity is between Clonidine (HY-12721) and dexmedetomidine (HY-12719)[3].

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

In Vivo

Mivazerol (15 μg/kg/h; i.v.; continuous infusion; starting 30 minutes prior to halothane withdrawal) inhibits intrathecal release of glutamate evoked
by halothane withdrawal in rats[1].
Mivazerol (2.5 μg/kg; i.t.; microinjection over 1 minute; 2 minutes prior to halothane withdrawal) inhibits intrathecal release of glutamate evoked
by halothane withdrawal in rats[1].
Mivazerol (10-40 μg/kg; s.c.; single dose; 30 min pre-ischemia) exerts neuroprotective effects in rat forebrain ischemia models[2].

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

Animal Model: Male Sprague-Dawley rats (250-400 g) anesthetized with 1.1% halothane then subjected to halothane withdrawal[1]
Dosage: 15 μg/kg/h
Administration: continuous infusion; starting 30 minutes prior to halothane withdrawal
Result: Reduced the maximal halothane withdrawal-induced HR increase and reduced the maximal intrathecal glutamate release.
Attenuated the aspartate response but had no significant effect on BP response.
Animal Model: Male Sprague-Dawley rats (250-400 g) anesthetized with 1.1% halothane then subjected to halothane withdrawal[1]
Dosage: 2.5 μg/kg
Administration: i.t.; microinjection over 1 minute; 2 minutes prior to halothane withdrawal
Result: Reduced the maximal halothane withdrawal-induced HR increase and reduced the maximal intrathecal glutamate release, with inhibition lasting at least 60 minutes post-withdrawal.
Had no significant effect on BP or aspartate responses with intrathecal administration.
Animal Model: Male Sprague-Dawley rats (300-400 g) with forebrain ischemia[2]
Dosage: 10; 20; 40 μg/kg
Administration: s.c.; single dose; 30 min pre-ischemia
Result: Reduced 7-day survival rate to 40% in the 40 μg/kg group, compared to 90% in the 10 μg/kg and 20 μg/kg groups.
Recorded median neurologic deficit scores (NDS) of 10.0 at 24 h, 27.5 at 48 h, and ~5 at 7 days for the 10 μg/kg group; 30.0 at 24 h, 27.5 at 48 h, and ~5 at 7 days for the 20 μg/kg group; 43.0 at 24 h, 100.0 at 48 h, and 100 at 7 days for the 40 μg/kg group.
Observed significantly greater number of intact neurons in the hippocampal CA1 subfield in the 20 μg/kg group than in all other groups.
Lowered neocortex damage scores significantly in the 20 μg/kg group compared to the control and 40 μg/kg groups.
Molecular Weight

217.22

Formula

C11H11N3O2

CAS No.
SMILES

O=C(C1=CC=CC(CC2=CN=CN2)=C1O)N

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Room temperature in continental US; may vary elsewhere.

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

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Mivazerol
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HY-106865
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