2,5-Dimethoxy-4-trifluoromethylamphetamine

DOTFM
Clinical data
Other names2,5-Dimethoxy-4-trifluoromethylamphetamine; DOTFM
Legal status
Legal status
Identifiers
IUPAC name
  • (RS)-1-[2,5-Dimethoxy-4-(trifluoromethyl)phenyl]propan-2-amine
CAS Number
PubChem CID
ChemSpider
UNII
ChEMBL
CompTox Dashboard (EPA)
Chemical and physical data
FormulaC12H16F3NO2
Molar mass263.260 g·mol−1
3D model (JSmol)
SMILES
  • FC(F)(F)c1cc(OC)c(cc1OC)CC(N)C
InChI
  • InChI=1S/C12H16F3NO2/c1-7(16)4-8-5-11(18-3)9(12(13,14)15)6-10(8)17-2/h5-7H,4,16H2,1-3H3 checkY
  • Key:WPGOTSORDNBMHP-UHFFFAOYSA-N checkY
  (verify)

2,5-Dimethoxy-4-trifluoromethylamphetamine (DOTFM) is a psychedelic drug of the phenethylamine, amphetamine, and DOx. It was first synthesized in 1994 by a team at Purdue University led by David E. Nichols.[1] DOTFM is the α-methylated analogue of 2C-TFM.

It acts as an agonist at the serotonin 5-HT2A and 5-HT2C receptors.[1] In drug discrimination tests in rats, DOTFM fully substituted for LSD and was slightly more potent than DOI.[1] In addition, (R)-DOTFM robustly induces the head-twitch response, a behavioral proxy of psychedelic effects, in rodents, with equivalent potency as (R)-DOI.[2] The drug is around twice as potent as 2C-TFM in animal studies.

In contrast to (R)-DOI, which has extraordinarily potent serotonin 5-HT2A receptor-mediated anti-inflammatory effects,[3][4] DOTFM shows no anti-inflammatory effects.[5] The differences between the drugs in this regard appear to be due to differences in functional selectivity at the serotonin 5-HT2A receptor.[5][2]

See also

References

  1. 1 2 3 Nichols DE, Frescas S, Marona-Lewicka D, Huang X, Roth BL, Gudelsky GA, et al. (December 1994). "1-(2,5-Dimethoxy-4-(trifluoromethyl)phenyl)-2-aminopropane: a potent serotonin 5-HT2A/2C agonist". Journal of Medicinal Chemistry. 37 (25): 4346–4351. doi:10.1021/jm00051a011. PMID 7996545.
  2. 1 2 Flanagan TW, Foster TP, Galbato TE, Lum PY, Louie B, Song G, et al. (February 2024). "Serotonin-2 Receptor Agonists Produce Anti-inflammatory Effects through Functionally Selective Mechanisms That Involve the Suppression of Disease-Induced Arginase 1 Expression". ACS Pharmacology & Translational Science. 7 (2): 478–492. doi:10.1021/acsptsci.3c00297. PMC 10863441. PMID 38357283. The effects of (R)-DOTFM were examined in the head-twitch response (HTR) assay. (R)-DOTFM produced a strong HTR with a potent ED 50 of 0.60 μmol/kg. These values are equivalent to (R)-DOI, as previously determined.{{cite journal}}: CS1 maint: overridden setting (link)
  3. ↑ Nichols DE, Johnson MW, Nichols CD (February 2017). "Psychedelics as Medicines: An Emerging New Paradigm". Clinical Pharmacology and Therapeutics. 101 (2): 209–219. doi:10.1002/cpt.557. PMID 28019026.
  4. ↑ Yu B, Becnel J, Zerfaoui M, Rohatgi R, Boulares AH, Nichols CD (November 2008). "Serotonin 5-hydroxytryptamine(2A) receptor activation suppresses tumor necrosis factor-alpha-induced inflammation with extraordinary potency". The Journal of Pharmacology and Experimental Therapeutics. 327 (2): 316–323. doi:10.1124/jpet.108.143461. PMID 18708586.
  5. 1 2 Flanagan TW, Billac G, Nichols CD (2022). "Differential Regulation of Inflammatory Responses Following 5-HT 2 Receptor Activation in Pulmonary Tissues". The FASEB Journal. 36 (S1). doi:10.1096/fasebj.2022.36.S1.R2617. ISSN 0892-6638.
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.