Nomifensine maleate - CAS 32795-47-4
Catalog number: 32795-47-4
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
Molecular Weight:
Dopamine Receptor
Nomifensine maleate is maleate salt form of Nomifensine. Nomifensine, also called as Hoe 984 or Linamiphen, as a norepinephrine-dopamine reuptake inhibitor it is an antidepressant drug but due to increased incidence of hemolytic anemia, as well as kidney
Solid powder
(Z)-but-2-enedioic acid;2-methyl-4-phenyl-3,4-dihydro-1H-isoquinolin-8-amine Hoe 984 Hoe-984 Hoe984 Linamiphen Maleate, Nomifensine Merital Nomifensin Nomifensine Nomifensine Maleate Nomifensine Maleate (1:1)
Soluble to 5.2 mg/ml in DMSO, 1 mg/ml in H2O
Store in a cool and dry place and at 0 - 4℃ for short term (days to weeks) or -93℃ for long term (months to years).
Shelf Life:
2 years
Melting Point:
199-201 °C
1.114 g/cm3
Canonical SMILES:
1.Alteration of corticotropin-releasing factor immunoreactivity in MPTP-treated rats.
Huang CC1, Lee EH. J Neurosci Res. 1995 Jul 1;41(4):471-80.
A decrease of corticotropin-releasing factor (CRF) concentration has been reported in patients with Parkinson's disease (PD). The present study further examined the role of CRF in an animal model of parkinsonism induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Results indicated that both subchronic (2 days) and chronic (7 days) MPTP treatments decreased the number of CRF immunoreactive neurons in both the paraventricular nucleus (PVN) of the hypothalamus and the central nuelcus of the amygdala (ACN). This effect lasted for almost a month after withdrawal of chronic MPTP injections. In addition, nomifensine pretreatment protected against MPTP's toxicity on DA neurons, as assessed by tyrosine hydroxylase immunoreactivity in the substantia nigra. However, the same treatment did not prevent the toxicity of MPTP on CRF neurons. Further, no significant difference was notable in the number of CRF immunoreactive neurons between normal young adult and normal middle-aged rats in both the PVN and the ACN.
2.Evaluation of the effects and mechanisms of action of mercuric chloride on striatal dopamine release by using in vivo microdialysis in freely moving rats.
Vidal L1, Alfonso M, Faro LF, Campos F, Cervantes R, Durán R. Toxicology. 2007 Jul 1;236(1-2):42-9. Epub 2007 Mar 31.
The in vivo effects of inorganic mercury (Hg(2+)) on striatal dopamine (DA) release were studied in freely moving and conscious rats using brain microdialysis techniques. Intrastriatal administration of HgCl(2) (1mM) produced an increase in extracellular DA levels of 1717+/-375% with respect to basal levels. This effect was attenuated in a Ca(2+)-free medium (361+/-66%), after pre-treatment with reserpine (231+/-66%), and was prevented in the presence of tetrodotoxin (TTX). Thus, the HgCl(2) treatment increases striatal DA according to an external calcium and vesicular dependent mechanism, being affected by the blockade of voltage sensitive sodium channels. Moreover, HgCl(2) decreased KCl-evoked DA release. Conversely, the coinfusion of HgCl(2) with nomifensine produced increases in DA extracellular levels different to that produced by nomifensine alone, suggesting that these effects probably involve an independent DA transporter (DAT) mechanism.
3.Opioid and monoamine systems mediate the discriminative stimulus of tramadol in rats.
Filip M1, Wydra K, Inan SY, Dziedzicka-Wasylewska M, Przegaliński E. Eur J Pharmacol. 2004 Sep 13;498(1-3):143-51.
We analyzed the ability of the mu opioid peptide receptor ligands morphine and naloxone and several antidepressant drugs that are serotonin (fluoxetine), noradrenaline (reboxetine), mixed serotonin and noradrenaline (milnacipram and venlafaxine), dopamine (nomifensine) reuptake inhibitors, as well as roxindole (a nonselective drug) to substitute for, or alter, tramadol discrimination. Male Wistar rats were trained to discriminate tramadol (20 mg/kg) from saline in a two-choice water-reinforced paradigm. Out of the drugs studied, only morphine substituted for tramadol. In combination experiments, naloxone (0.1-1 mg/kg) attenuated the stimulus effects of tramadol (20 mg/kg) and the substitution evoked by morphine (2 mg/kg). Milnacipram (10 mg/kg) or reboxetine (10 mg/kg) enhanced the effects of tramadol (2.5-10 mg/kg); the other antidepressant drugs used failed to modulate tramadol discrimination. Our results indicate that tramadol can be used as a stimulus cue in rats, and that mu opioid peptide mechanisms are involved in its effects, while noradrenergic uptake inhibitors can enhance tramadol discrimination.
4.Transmitter release by non-receptor activation of the alpha-subunit of guanine nucleotide regulatory protein in rat striatal slices.
Zelles T1, Chernaeva L, Baranyi M, Déri Z, Adam-Vizi V, Vizi ES. J Neurosci Res. 1995 Oct 1;42(2):242-51.
The effects of 5 mM NaF + 10 microM AlCl3, a direct activator of guanine nucleotide-binding proteins (G proteins), on the release of [3H]dopamine ([3H]DA), [3H]gamma-aminobutyric acid ([3H]GABA), and [3H]acethylcholine ([3H]ACh) were investigated in slices of rat striatum. When the tissue was exposed to NaF + AlCl3 the release of [3H]DA, [3H]GABA, and [3H]ACh was enhanced significantly. In a calcium-free solution the release of [3H]GABA and [3H]DA was increased by NaF+AlCl3 much more than in the presence of [Ca2+]o. In slice preparations taken from reserpinized animals, in which the vesicular storage of [3H]DA was therefore prevented, NaF + AlCl3 had no effect on [3H]DA release. HPLC analysis of the radioactivity of the perfusate showed that, in the presence of NaF + AlCl3, the content of dihydroxyphenylacetic acid (DOPAC) in perfusate samples increased significantly, while in pargyline-treated animals only the DA content was increased. Inhibition of DA carriers by nomifensine or low temperature prevented the effect of NaF + AlCl3.
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CAS 32795-47-4 Nomifensine maleate

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