(±)-MDMA hydrochlorideInhibitor of 5-HT and dopamine uptake; hallucinogenic CAS# 92279-84-0 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 92279-84-0 | SDF | Download SDF |
PubChem ID | 71285 | Appearance | Powder |
Formula | C11H16ClNO2 | M.Wt | 229.7 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | Methylenedioxymethamphetamine hydrochloride | ||
Solubility | Soluble to 100 mM in water | ||
Chemical Name | 1-(1,3-benzodioxol-5-yl)-N-methylpropan-2-amine;hydrochloride | ||
SMILES | CC(CC1=CC2=C(C=C1)OCO2)NC.Cl | ||
Standard InChIKey | LUWHVONVCYWRMZ-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C11H15NO2.ClH/c1-8(12-2)5-9-3-4-10-11(6-9)14-7-13-10;/h3-4,6,8,12H,5,7H2,1-2H3;1H | ||
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 | Hallucinogenic compound that inhibits 5-HT and dopamine uptake. |
(±)-MDMA hydrochloride Dilution Calculator
(±)-MDMA hydrochloride Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 4.3535 mL | 21.7675 mL | 43.535 mL | 87.0701 mL | 108.8376 mL |
5 mM | 0.8707 mL | 4.3535 mL | 8.707 mL | 17.414 mL | 21.7675 mL |
10 mM | 0.4354 mL | 2.1768 mL | 4.3535 mL | 8.707 mL | 10.8838 mL |
50 mM | 0.0871 mL | 0.4354 mL | 0.8707 mL | 1.7414 mL | 2.1768 mL |
100 mM | 0.0435 mL | 0.2177 mL | 0.4354 mL | 0.8707 mL | 1.0884 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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Development of a Library Search-Based Screening System for 3,4-Methylenedioxymethamphetamine in Ecstasy Tablets Using a Portable Near-Infrared Spectrometer.[Pubmed:27362667]
J Forensic Sci. 2016 Sep;61(5):1208-14.
This is the first report on development of a library search-based screening system for 3,4-methylenedioxymethamphetamine (MDMA) in ecstasy tablets using a portable near-infrared (NIR) spectrometer. The spectrum library consisted of spectra originating from standard substances as well as mixtures of (±)-MDMA hydrochloride (MDMA-HCl) and diluents. The raw NIR spectra were mathematically pretreated, and then, a library search was performed using correlation coefficient. To enhance the discrimination ability, the wavelength used for the library search was limited. Mixtures of MDMA-HCl and diluents were used to decide criteria to judge MDMA-positive or MDMA-negative. Confiscated MDMA tablets and medicinal tablets were used for performance check of the criteria. Twenty-two of 27 MDMA tablets were truly judged as MDMA-positive. Five false-negative results may be caused by compounds not included in the library. No false-positive results were obtained for medicinal tablets. This system will be a useful tool for on-site screening of MDMA tablets.
MDMA ("Ecstasy") suppresses the innate IFN-gamma response in vivo: a critical role for the anti-inflammatory cytokine IL-10.[Pubmed:17689526]
Eur J Pharmacol. 2007 Oct 31;572(2-3):228-38.
Here we demonstrate that the widely abused drug methylenedioxymethamphetamine (MDMA; "Ecstasy") suppresses innate interferon (IFN)-gamma production in mice following an in vivo lipopolysaccharide (LPS) challenge. IFN-gamma signalling was also impaired by MDMA, as indicated by reduced phosphorylation of signal transducer and activator of transcription-1 (STAT1) and reduced expression of interferon-gamma inducible protein 10 (IP-10/CXCL10); a chemokine induced by IFN-gamma. MDMA also suppressed production of interleukin (IL)-12 and IL-15; two cytokines that induce IFN-gamma production. Our results demonstrate that in vitro exposure to MDMA does not mimic the suppression of innate IFN-gamma observed in vivo, indicating that observed suppression is most likely due to the release of endogenous immunomodulatory substances following drug administration. In this regard, we previously demonstrated that MDMA increases production of the anti-inflammatory cytokine IL-10 in vivo, an event that is mediated by beta-adrenoceptor activation on immune cells. Considering that increased IL-10 production precedes suppression of IFN-gamma induced by MDMA, and also considering that IL-10 can inhibit IL-12 and IFN-gamma production, we examined the possibility that IL-10 was an essential mediator of the suppressive effect of MDMA on the IFN-gamma response. By pre-treating mice with an anti-IL-10 receptor antibody we demonstrate that IL-10 is a critical mediator of MDMA-induced suppression of IFN- gamma production and signalling. Consistent with a role for beta-adrenoceptor activation in the immunosuppressive actions of MDMA, pre-treatment with the beta-adrenoceptor antagonist nadolol blocked the MDMA-induced increase in IL-10, and also inhibited the suppressive action of MDMA on the innate IFN-gamma response. The potential clinical significance of these findings for MDMA users is discussed.
New insights into the mechanism of action of amphetamines.[Pubmed:17209801]
Annu Rev Pharmacol Toxicol. 2007;47:681-98.
Amphetamine is a psychostimulant commonly used to treat several disorders, including attention deficit, narcolepsy, and obesity. Plasmalemmal and vesicular monoamine transporters, such as the neuronal dopamine transporter and the vesicular monoamine transporter-2, are two of its principal targets. This review focuses on new insights, obtained from both in vivo and in vitro studies, into the molecular mechanisms whereby amphetamine, and the closely related compounds methamphetamine and methylenedioxymethamphetamine, cause monoamine, and particularly dopamine, release. These mechanisms include amphetamine-induced exchange diffusion, reverse transport, and channel-like transport phenomena as well as the weak base properties of amphetamine. Additionally, amphetamine analogs may affect monoamine transporters through phosphorylation, transporter trafficking, and the production of reactive oxygen and nitrogen species. All of these mechanisms have potential implications for both amphetamine- and methamphetamine-induced neurotoxicity, as well as dopaminergic neurodegenerative diseases.
Direct effects of 3,4-methylenedioxymethamphetamine (MDMA) on serotonin or dopamine release and uptake in the caudate putamen, nucleus accumbens, substantia nigra pars reticulata, and the dorsal raphe nucleus slices.[Pubmed:10819905]
Synapse. 2000 Jun 15;36(4):275-85.
We examined the effects of pressure ejected 3, 4-methylenedioxymethamphetamine (MDMA) from a micropipette on direct chemically stimulated release, and on electrically stimulated serotonin (5-HT) or dopamine (DA) release in the caudate putamen (CPu), nucleus accumbens (NAc), substantia nigra pars reticulata (SNr), and the dorsal raphe nucleus (DRN) brain slices of rat, using fast cyclic voltammetry (FCV). MDMA is electroactive, oxidising at +1100 mV. When the anodic input waveform was reduced from +1.4 to +1.0 volt, MDMA was not electroactive. Using this waveform, pressure ejection of MDMA did not release 5-HT or DA in brain slices prepared from any of the nuclei studied. MDMA significantly potentiated electrically stimulated 5-HT release in the SNr and DA release in CPu. In the DRN or in the NAc, MDMA was without effect on peak electrically stimulated 5-HT or DA release. The rates of neurotransmitter uptake, expressed as t(1/2), were in all cases significantly decreased after MDMA. The results indicate that MDMA, unlike (+)amphetamine, is not as a releaser of DA or 5-HT, it is a potent inhibitor of both DA and 5-HT uptake.