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Key Documents
M8877
α-Methyl-DL-m-tyrosine
Synonim(y):
α-MMT, DL-2-Methyl-3-(3-hydroxyphenyl)alanine, AMMT
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About This Item
Wzór empiryczny (zapis Hilla):
C10H13NO3
Numer CAS:
Masa cząsteczkowa:
195.22
Numer MDL:
Kod UNSPSC:
12352200
Polecane produkty
temp. przechowywania
−20°C
ciąg SMILES
CC(N)(Cc1cccc(O)c1)C(O)=O
Certyfikaty analizy (CoA)
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Dokumenty związane z niedawno zakupionymi produktami zostały zamieszczone w Bibliotece dokumentów.
K Ishikawa et al.
European journal of pharmacology, 120(1), 63-68 (1986-01-14)
A comparative study of the ability to block the amine pump was carried out on tricyclic antidepressants including dothiepin and northiaden in vivo. Dothiepin was found to prevent the 6-OHDA-induced depletion of cardiac noradrenaline but not the PCA-induced depletion of
J Arita et al.
Neuroendocrinology, 38(1), 62-67 (1984-01-01)
To address the issue of whether, after morphine treatment, the reduced release of dopamine (DA) into portal blood is entirely responsible for the increased prolactin (PRL) release, the following study was conducted. The concentration of DA in plasma from a
T Abrahamsson et al.
Journal of cardiovascular pharmacology, 7 Suppl 5, S81-S85 (1985-01-01)
In the adrenergic neurons the amino acid alpha-methyl-meta-tyrosine (alpha-MmT) is converted to metaraminol via the noradrenaline (NA) synthetic pathway. Metaraminol thereby displaces NA from its neuronal stores, and as a consequence NA levels can be drastically reduced, although normal sympathetic
Smriti Iyengar et al.
The Journal of pharmacology and experimental therapeutics, 311(2), 576-584 (2004-07-16)
5-Hydroxytryptamine (serotonin) (5-HT) and norepinephrine (NE) are implicated in modulating descending inhibitory pain pathways in the central nervous system. Duloxetine is a selective and potent dual 5-HT and NE reuptake inhibitor (SNRI). The ability of duloxetine to antagonize 5-HT depletion
M Oide
Pharmacology, 28(3), 130-138 (1984-01-01)
alpha-Methyldopa (alpha-MD) was administered intraperitoneally into adult male mice and its effect on alpha 1- and alpha 2-noradrenergic receptor binding sites in the brain was investigated, using [3H]WB-4101 and [3H]clonidine, respectively. A single injection of 50-200 mg/kg alpha-MD abolished the
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