Like LSD, the drug is known to be a highly potentserotonin5-HT2A and5-HT2C receptoragonistin vitro.[1] Itsaffinities (IC50Tooltip half-maximal inhibitory concentration) are in the ranges of 10–100nM for the serotonin 5-HT2A receptor and 100–1,000nM for the serotonin 5-HT2C receptor, while itsactivationalpotencies (EC50Tooltip half-maximal effective concentration) are less than 10nM for the serotonin 5-HT2A receptor and in the range of 10–100nM for the serotonin 5-HT2C receptor.[1] DEIMDHPCA was the most potent serotonin 5-HT2A receptor agonist of 27evaluated ergoline-like compounds.[1] In line with its serotonin 5-HT2A receptor agonism, and similarly to LSD and other psychedelics,[3][4] DEIMDHPCA has been found to producepsychoplastogenic effects onneurite growthin vitro.[1]
Many serotonin 5-HT2A receptor agonists, for instance LSD, producepsychedelic effects in humans.[1][5][6][7] The publication that reported DEIMDHPCA specifically pertained to psychoplastogenic ergoline-like compounds with no or reducedhallucinogenic activity for potential therapeutic use.[1] However, the hallucinogenic-related properties of DEIMDHPCA and the other reported compounds, for instance their effects in thehead-twitch response (HTR)assay, were not individually described.[1] As such, it remains unclear whether or not DEIMDHPCA could have psychedelic effects in humans.[1]
Other related compounds in which one or more other carbons have been removed from theLSD's ergoline ring system to produce simplified and less-rigid phenethylamines andtryptamines includeN-DEAOP-NMT[8][9] andNDTDI.[10][11][12]N-DEAOP-NMT is the analogue of LSD in which the carbon atoms at positions 9 and 10 of the ergoline ring system have been removed to make a fully non-rigid tryptamine,[8][9] while NDTDI is the analogue of LSD in which only the carbon at position 9 has been removed to make a rigidtricyclic tryptamine.[10][11][12]N-DEAOP-NMT has been found to produce LSD-like effects in rodents,[8][9] while NDTDI has been encountered as a novelrecreational anddesigner drug andmade illegal in parts ofEurope.[10][11]
The analogue of DEIMDHPCA without theethyl groups on theamide has been described.[8][13] In addition, DEIMDHPCA's analogue without the amide ethyl groups and with aphenyl ring instead of theindole ring has been described.[8][13] Their activities were not reported.[8][13]
WXVL_BT0793LQ2118, an analogue of DEIMDHPCA lacking theN,N-diethyl-carboxamidemoiety and with afluorine at the 6-position, has been reported.[14][15] It was identified viain silico screening of 1.6billion molecules for serotonin 5-HT2A receptor agonism withAlphaFold2.[14] Following identification, the drug was assessed and found to be apotentserotonin5-HT2A,5-HT2B, and5-HT2C receptoragonist.[14]
^abcNorris PE, Blicke FF (December 1952). "Potential ergot substitutes: esters and amides of beta-amino acids".Journal of the American Pharmaceutical Association (Scientific Ed.).41 (12):637–639.doi:10.1002/jps.3030411204.PMID13022416.Six esters and amides of derivatives of β-alanine which are related to lysergic acid have been prepared and tested for oxytocic activity. None of these products possess a significant oxytocic activity. [...] The purpose of this investigation was to synthesize amides and also esters of compounds (II–V) which represent fragments of the lysergic acid molecule in the hope that some of these products might possess oxytocic activity. Various modified fragments of the lysergic acid molecule have been synthesized previously; it was claimed that some of the compounds are active oxytocics (1—7). [...] Pharmacologic data indicated that none of the esters or amides of compounds II—V which were prepared possess a significant oxytocic action when compared to the clinically used oxytocics. However, the diethylamide of N-methyl-N-[β′-(3-indolyl)-ethyl]-β-alanine (IIIc) appeared to have an oxytocic activity approximately ten times stronger than that of the diethylamide of N-methyl-N-(β′-phenethyl)-β-alanine (IIc).
