2C-T-33 shows highaffinity for theserotonin5-HT2A receptor (Ki = 1.7nM) and to a much lesser extent for the serotonin5-HT2C receptor (Ki = 75nM; 44-fold lower than for 5-HT2A).[5] In terms of serotonin 5-HT2A receptor activation, itsEC50Tooltip half-maximal effective concentration is 26nM and itsEmaxTooltip maximal efficacy is 40%.[5] Hence, 2C-T-33 acts as a low-efficacypartial agonist of the serotonin 5-HT2A receptor.[6][5][7] The drug shows higher affinity for the serotonin 5-HT2A receptor but much lowerpotency and efficacy in activating the receptor compared to2C-T or2C-B (which had values of Ki = 6.9–49nM,EC50 = 2.0–2.1nM, andEmax = 75–92%).[5] In contrast to most other 2C drugs and serotonergic psychedelics, 2C-T-33 appears to be completely inactive as an agonist of the serotonin5-HT2B receptor (EC50 > 10,000nM).[5] The drug has also been assessed at a number of othertargets.[5]
The drug did not significantly produce thehead-twitch response (HTR), a behavioral proxy of psychedelic effects, in rodents, and hence may not havehallucinogenic effects in humans.[6] Itsanalogue2C-T-27 (which lacks themethoxy group on the addedbenzyl ring) significantly and potently induces the HTR in rodents.[6] However, the HTR induced by 2C-T-27 is far weaker in magnitude than that induced by other2C-T-X drugs and other serotonergic psychedelics.[6] For example,2C-T (or 2C-T-1) induced about 7-fold more HTR events than 2C-T-33.[6] In contrast to the lack of assessment of 2C-T-33 in humans, 2C-T-27 has been evaluated and found to be active as a psychedelic in humans with a dose range of 80 to 130mg.[6][1]
The lack of HTR with 2C-T-33 may be due to its low-efficacy partial agonism of the serotonin 5-HT2A receptor and the receptor not being activated strongly enoughly.[6] The potencies of psychedelics in inducing the HTR are positively correlated with their efficacies in activating the serotonin 5-HT2A receptor.[6] The bulky 4 substitution of 2C-T-33 may be too large to accommodate the binding pocket of the serotonin 5-HT2A receptor in terms of maintaining robust receptor activation.[6] Similar findings have been observed for other phenethylamines with bulky 4-position substitutions, such asDOHx,DOBz, and4-PhPr-3,5-DMA.[6]
In addition to its potential psychoactive effects, 2C-T-33 has shownanti-inflammatory effects in animal studies similarly to other serotonin 5-HT2A receptor agonists and serotonergic psychedelics.[7] However, 2C-T-33 was the least effective assessed phenethylamine and was far less effective than other phenethylamines such as2C-I,DOIB,2C-B,(R)-DOI, and2,5-DMA, among others.[7]
^abTrachsel D (2003). "Synthese von neuen (Phenylalkyl)aminen zur Untersuchung von Struktur–Aktivitätsbeziehungen. Mitteilung 2: 4-Thio-substituierte [2-(2,5-Dimethoxyphenyl)ethyl]amine (=2,5-Dimethoxybenzolethanamine)" [Synthesis of Novel (Phenylalkyl)amines for the Investigation of Structure–Activity Relationships. Part 2). 4-Thio-Substituted [2-(2,5-Dimethoxyphenyl)ethyl]amines (=2,5-Dimethoxybenzeneethanamines)].Helvetica Chimica Acta.86 (7):2610–2619.doi:10.1002/hlca.200390210.ISSN0018-019X.
^abcMeyers-Riggs B (3 April 2011)."Shulgin's Sulfur Symphony".countyourculture. Retrieved17 February 2025.2C-T-33 (2,5-dimethoxy-4-(3-methoxybenzylthio)phenethylamine) A 3-methoxy substituted 2C-T-27. Synthesized by Daniel Trachsel but has not been bioassayed to public knowledge. [...] Trachsel, D. Synthesis of novel (phenylalkyl)amines for the investigation of structure-activity relationships. Part 2. 4-Thio-substituted [2-(2,5-dimethoxyphenyl)ethyl]amines (=2,5-dimethoxybenzeneethanamines). Helv. Chim. Acta, 5 Aug 2003, 86 (7), 2610–2619.
Notes: (1) TAAR1 activity of ligands varies significantly between species. Some agents that are TAAR1 ligands in some species are not in other species. This navbox includes all TAAR1 ligands regardless of species. (2) See the individual pages for references, as well as theList of trace amines,TAAR, andTAAR1 pages. See also:Receptor/signaling modulators
