2C-T-7
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Mechanism of action
Studies involving a bromine-substituted analogue, 2C-B (4-bromo-2,5- dimethoxyphenethylamine), have shown it to be a partial agonist for 5-HT2 (5-HT2A and 5-HT2C) serotonergic receptors and 1-adrenergic receptors. At 10-6 M, 2C-B also acted as a competitive 5-HT antagonist, but, at higher concentrations (2.8 x 10-5M), it acted as a non-competitive 5-HT antagonist. ... As 2C-T-7 is phenethylamine based, it is possible that it may have serotonergic receptor affinity similar to 2C-B (i.e. binding to 5-HT2 and, to some degree, 5-HT1 receptors).
The subjective effects of 2C-T-7, like those of 2C-B and DOM, appear to be mediated through central serotonin receptors. 2C-T-7 selectively binds to the 5-HT receptor system.
Pharmacokinetics
Absorption
... the primary route of administration is oral. However, insufflation (snorting) is also commonly mentioned in user reports. Some less common routes of administration include smoking, rectal administration and intravenous or intramuscular administration.
Metabolism
... it is likely that its metabolism may proceed via similar pathways as 2C-B, possibly with additional metabolic reactions.
The phenethylamine-derived designer drug 4-ethyl-2,5-dimethoxy-beta-phenethylamine (2C-E) was found to be mainly metabolized in rats by O-demethylation, N-acetylation, hydroxylation of the ethyl side chain at C2' or at C1' followed by oxidation at C1' to the corresponding ketone, by deamination followed by reduction to the corresponding alcohols or by oxidation to the corresponding acids, and finally combinations of these steps. Most of the metabolites were excreted in conjugated form. The authors' systematic toxicological analysis (STA) procedure using full-scan GC-MS allowed the detection of an intake of a dose of 2C-E in rat urine that corresponds to a common drug users' dose. Assuming similar metabolism, the described STA procedure should be suitable for proof of an intake of 2C-E in human urine. /4-Ethyl-2,5-dimethoxy-beta-phenethylamine (2C-E)/
The in vivo metabolism of 2,5-dimethoxy-4-propylthiophenethylamine (2C-T-7), a ring-substituted psychoactive phenethylamine, was studied in rat. Male Wistar rats were administered 10 mg/kg 2C-T-7 hydrochloride orally, and 24-hr urine fractions were collected. After enzymatic hydrolysis of the urine sample, the metabolites were extracted by liquid-liquid extraction and analyzed by liquid chromatography/mass spectrometry. 2C-T-7-sulfoxide, N-acetyl-2C-T-7-sulfoxide, N-acetyl-2,5-dimethoxy-4-methylthiophenethylamine-sulfoxide, N-acetyl-2,5-dimethoxy-4-(2-hydroxypropylthio)phenethylamine-sulfoxide, and N-acetyl-2,5-dimethoxy-4-(2-hydroxypropylthio)phenethylamine-sulfone were detected as the primary metabolites of 2C-T-7. These findings suggest that sulfoxidation, sulfone formation, hydroxylation of the propyl side chain at the beta-position, and S-depropylation followed by methylation of thiol were the major metabolic pathways of 2C-T-7 in rat.
Studies are described on the metabolism and the toxicological analysis of the phenethylamine-derived designer drug 2,5-dimethoxy-4-ethylthio-beta-phenethylamine (2C-T-2) in rat urine using gas chromatography/mass spectrometry (GC/MS) after enzymatic cleavage of conjugates, liquid-liquid extraction and derivatization. The structures of 14 metabolites were assigned tentatively by detailed interpretation of their mass spectra. Identification of these metabolites indicated that 2C-T-2 was metabolized by sulfoxidation followed by N-acetylation and either hydroxylation of the S-ethyl side chain or demethylation of one methoxy group, O-demethylation of the parent compound followed by N-acetylation and sulfoxidation, deamination followed by reduction to the corresponding alcohol followed by partial glucuronidation and/or sulfation or by oxidation to the corresponding acid followed either by partial glucuronidation or by degradation to the corresponding benzoic acid derivative followed by partial glucuronidation. Furthermore, 2C-T-2 was metabolized by N-acetylation of the parent compound followed either by O-demethylation and sulfoxidation or by S-dealkylation, S-methylation and sulfoxidation. The authors' systematic toxicological analysis (STA) procedure using full-scan GC/MS after acid hydrolysis, liquid-liquid extraction microwave-assisted acetylation allowed the detection of an intake of a dose of 2C-T-2 in rat urine, which corresponds to a common drug users' dose. Assuming similar metabolism, the described STA procedure should be suitable for proof of an intake of 2C-T-2 in human urine. /2,5-Dimethoxy-4-ethylthio-beta-phenethylamine (2C-T-2)/
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