MethyldopaAromatic L-amino acid decarboxylase inhibitor CAS# 555-30-6 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 555-30-6 | SDF | Download SDF |
PubChem ID | 38853 | Appearance | Powder |
Formula | C10H13NO4 | M.Wt | 211.21 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 75 mM in DMSO | ||
Chemical Name | 3-(3,4-Dihydroxyphenyl)-α-methyl-L-a | ||
SMILES | C[C@](N)(Cc1ccc(O)c(O)c1)C(O)=O | ||
Standard InChIKey | CJCSPKMFHVPWAR-JTQLQIEISA-N | ||
Standard InChI | InChI=1S/C10H13NO4/c1-10(11,9(14)15)5-6-2-3-7(12)8(13)4-6/h2-4,12-13H,5,11H2,1H3,(H,14,15)/t10-/m0/s1 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | L-aromatic amino acid decarboxylase inhibitor. Antihypertensive. |
Methyldopa Dilution Calculator
Methyldopa Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 4.7346 mL | 23.6731 mL | 47.3462 mL | 94.6925 mL | 118.3656 mL |
5 mM | 0.9469 mL | 4.7346 mL | 9.4692 mL | 18.9385 mL | 23.6731 mL |
10 mM | 0.4735 mL | 2.3673 mL | 4.7346 mL | 9.4692 mL | 11.8366 mL |
50 mM | 0.0947 mL | 0.4735 mL | 0.9469 mL | 1.8938 mL | 2.3673 mL |
100 mM | 0.0473 mL | 0.2367 mL | 0.4735 mL | 0.9469 mL | 1.1837 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Methyldopa is an alpha-adrenergic agonist (selective for α2-adrenergic receptors) psychoactive drug used as a sympatholytic or antihypertensive.
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A fluorescent sensor based on methyldopa drug modified gamma-Fe2O3 nanoparticles for ultrasensitive detection of calf thymus DNA.[Pubmed:26742013]
Spectrochim Acta A Mol Biomol Spectrosc. 2016 Mar 15;157:104-109.
We reported the study of calf thymus DNA (ct-DNA) adsorption by the polymer of Methyldopa (2-amino-3-(3,4-dihydroxyphenyl)-2-methyl acid, propanoic) (PMDP), magnetofluorescent PMDP-gamma-Fe2O3 nanocrystal. The method is based on the extraordinarily high quenching efficiency of ct-DNA and the specific interaction between ct-DNA and PMDP-gamma-Fe2O3 via guanine base and metal coordination, probably. It was found that the designed magnetic nanoparticles can adsorb ct-DNA in nM levels in the presence of NaCl and KCl. In acetate and phosphate buffers DNA were adsorbed completely. Also, we found that pH plays an important role in DNA adsorption onto PMDP-gamma-Fe2O3 nanocrystal. PMDP-gamma-Fe2O3 nanocrystal is highly hydrophilic and DNA desorption wasn't observed. We believe this study will further stimulate the application of PMDP-gamma-Fe2O3 nanocrystal in bioanalytical chemistry and nanotechnology. PMDP-gamma-Fe2O3 nanocrystal possesses the ability to interact with ct-DNA via a partial intercalative binding mechanism, as demonstrated by fluorescence displacement experiments and a significant red shift (ca, 10nm) in UV-vis spectra.
3-O-Methyldopa inhibits astrocyte-mediated dopaminergic neuroprotective effects of L-DOPA.[Pubmed:27456338]
BMC Neurosci. 2016 Jul 25;17(1):52.
BACKGROUND: We evaluated the effects of 3-O-Methyldopa (3-OMD), a metabolite of L-DOPA which is formed by catechol-O-methyltransferase (COMT), on the uptake, metabolism, and neuroprotective effects of L-DOPA in striatal astrocytes. We examined changes in the numbers of dopaminergic neurons after treatment with L-DOPA and 3-OMD or entacapone, a peripheral COMT inhibitor, using primary cultured mesencephalic neurons and striatal astrocytes. RESULTS: The number of tyrosine hydroxylase-positive dopaminergic neurons was not affected by L-DOPA treatment in mesencephalic neurons alone. However, the increase in viability of dopaminergic neurons in the presence of astrocytes was further enhanced after methyl-L-DOPA treatment (25 microM) in mixed cultured mesencephalic neurons and striatal astrocytes. The neuroprotective effect of 25 microM L-DOPA was almost completely inhibited by simultaneous treatment with 3-OMD (10 or 100 microM), and was enhanced by concomitant treatment with entacapone (0.3 microM). The uptake of L-DOPA into and the release of glutathione from striatal astrocytes after L-DOPA treatment (100 microM) were inhibited by simultaneous exposure to 3-OMD (100 microM). CONCLUSIONS: These data suggest that L-DOPA exerts its neuroprotective effect on dopaminergic neurons via astrocytes and that 3-OMD competes with L-DOPA by acting on target molecule(s) (possibly including glutathione) released from astrocytes. Since some amount of entacapone can cross the blood-brain barrier, this reagent may enhance L-DOPA transportation by inhibiting COMT and increase the astrocyte-mediated neuroprotective effects of L-DOPA on dopaminergic neurons.
Antihypertensive methyldopa, labetalol, hydralazine, and clonidine reversed tumour necrosis factor-alpha inhibited endothelial nitric oxide synthase expression in endothelial-trophoblast cellular networks.[Pubmed:27998008]
Clin Exp Pharmacol Physiol. 2017 Mar;44(3):421-427.
Medications used to control hypertension in pregnancy also improve trophoblast and endothelial cellular interaction in vitro. Tumour necrosis factor-alpha (TNF-alpha) inhibits trophoblast and endothelial cellular interactions and simultaneously decreases endothelial nitric oxide synthase (eNOS) expression. This study investigated whether antihypertensive medications improved these cellular interactions by modulating eNOS and inducible nitric oxide synthase (iNOS) expression. Human uterine myometrial microvascular endothelial cells (UtMVECs) were pre-incubated with (or without) low dose TNF-alpha (0.5 ng/mL) or TNF-alpha plus soluble fms-like tyrosine kinase-1 (sFlt-1) (100 ng/mL). The endothelial cells were cultured on Matrigel. After endothelial cellular networks appeared, trophoblast derived HTR-8/SVneo cells were co-cultured in the presence of clinically relevant doses of Methyldopa, labetalol, hydralazine or clonidine for 24 hours. Cells were retrieved from the Matrigel to extract mRNA and eNOS and iNOS expression were examined by quantitative PCR. Methyldopa, labetalol, hydralazine and clonidine reversed the inhibitory effect of TNF-alpha on eNOS mRNA expression. After pre-incubating endothelial cells with TNF-alpha and sFlt-1, all the medications except Methyldopa lost their effect on eNOS mRNA expression. In the absence of TNF-alpha, antihypertensive medications did not change eNOS expression. The mRNA expression of iNOS was not affected by TNF-alpha or any medications. This study shows that selected antihypertensive medications used in the treatment of hypertension in pregnancy increase eNOS expression in vitro when induced by the inflammatory TNF-alpha. The anti-angiogenic molecule sFlt-1 may antagonise the potential benefit of these medications by interfering with the NOS pathway.
3-O-methyldopa levels in newborns: Result of newborn screening for aromatic l-amino-acid decarboxylase deficiency.[Pubmed:27216367]
Mol Genet Metab. 2016 Aug;118(4):259-63.
BACKGROUND: The diagnosis of aromatic l-amino-acid decarboxylase (AADC) deficiency is often delayed because a cerebrospinal fluid analysis is required to detect a neurotransmitter deficiency. We here demonstrated that an elevated concentration of l-dopa metabolite 3-O-Methyldopa (3-OMD) in dried blood spots could be integrated into newborn screening program to precisely predict AADC deficiency. METHODS: After obtaining parental consent, an additional spot was punched from newborn filter paper, eluted, cleaned, and analyzed by tandem mass spectrometry. Newborns with a 3-OMD concentration exceeding 500ng/mL were referred for confirmatory testing. RESULTS: From September 2013 to December 2015, 127,987 newborns were screened for AADC deficiency. The mean 3-OMD concentration in these newborns was 88.08ng/mL (SD=27.74ng/mL). Four newborns exhibited an elevated 3-OMD concentration (range, 939-3241ng/mL). All four newborns were confirmed to carry two pathologic DDC mutations, indicating an incidence of AADC deficiency of 1:32,000. During the follow-up period, three patients developed typical symptoms of AADC deficiency. Among 16 newborns with mildly elevated 3-OMD levels, six were heterozygous for the DDC IVS6+4A>T mutation. CONCLUSION: Newborn screening of AADC deficiency was achieved with a 100% positive-predictive rate. An association for gestational age could be further elucidated.
Correlation between fall in blood pressure and in vivo amine release after alpha-methylDOPA.[Pubmed:2767124]
Eur J Pharmacol. 1989 May 30;164(3):531-8.
Blood pressure (BP), hypothalamic tissue concentrations and the in vivo overflow of endogenous and alpha-methylated catecholamines were measured in urethane anaesthetised rats after alpha-Methyldopa (mDOPA) administration (200 mg/kg i.p.). Four hours after mDOPA, BP fell to its lowest value, 60% of control, and slowly returned towards control levels by 24 h. This was closely correlated with the evoked overflow of alpha-methylnoradrenaline (mNA, r = 0.9) and noradrenaline (NA, r = 0.7) but not dopamine (DA) or alpha-Methyldopamine (mDA). However, the tissue content of mNA rose much more gradually and was not maximal until after 12 h while mDA content followed the development of the hypotension. The results provide direct evidence for a false transmitter role for mNA in the brain, and suggest that the release of newly synthesised mNA is responsible for the hypotensive effect of mDOPA. Differences in the time course of overflow and storage of NA and mNA suggest the presence of separate transmitter storage and releasable pools.
The hypotensive activity and side effects of methyldopa, clonidine, and guanfacine.[Pubmed:6094346]
Hypertension. 1984 Sep-Oct;6(5 Pt 2):II28-33.
Clonidine (Catapres, Catapresan), guanfacine (Estulic), and Methyldopa (Aldomet) are the prototypes of centrally acting antihypertensive drugs. Clonidine and guanfacine are lipophilic drugs that readily penetrate into the brain, where they stimulate alpha-adrenergic receptors in the pontomedullary region. The stimulation of these central alpha-adrenergic receptors has been shown to activate an inhibiting neuron, which causes a reduction of peripheral sympathetic tone and a subsequent fall in arterial blood pressure and heart rate. Both a centrally initiated reduction of vagus reflex activity and the activation of presynaptic alpha 2-adrenergic blocking agents in the heart may contribute to the bradycardia. Studies indicate that Methyldopa also penetrates into the brain, where it is converted into alpha-methylnorepinephrine. This amine may stimulate the same central alpha-adrenergic receptors as those activated by clonidine, which will result in a hypotensive effect. Possibly, alpha-Methyldopamine might also play a role. Accordingly, the modes of action of clonidine and alpha-Methyldopa probably are very similar at a basic level. The central adrenergic receptors probably are located postsynaptically. Their receptor demand corresponds more closely to that of the alpha 2-subtype. Central alpha 1-adrenergic receptors might possibly play a part in the modulation of vagally induced baroreflex bradycardia. A discussion on the pharmacological basis of the side effects of the centrally acting antihypertensives has been limited to those adverse reactions that are somehow related to alpha-adrenergic receptors. Sedation, a common side effect, appears to be mediated by central alpha 2-adrenergic receptors, at least in animal models.(ABSTRACT TRUNCATED AT 250 WORDS)