In a forensic case involving 5-MeO-MiPT, blood concentrations of 160 ng/mL and urine concentrations of 3,380 ng/mL were documented.supported
Blood concentration 160 ng/mL, urine 3380 ng/mL. dta.2245
In a calcium mobilization assay using cells expressing the human 5-HT₂A receptor, MiPT produced an EC₅₀ of 44.9 ± 1.7 nM with an Emax of 74 ± 5% relative to serotoninsupported
MiPT: 5-HT2A EC50 = 44.9 ± 1.7 nM, Emax = 74 ± 5% s00213-014-3557-7
MiPT does not recruit β-arrestin at 5-HT₂A, consistent with a G protein-biased signaling profile.supported
no β-arrestin recruitment s00213-014-3557-7
MiPT is inactive at the 5-HT₁A receptor at concentrations up to 10 µMsupported
inactive at 5-HT1A (>10 µM) s00213-014-3557-7
Kozell et al. confirmed that non-ring-substituted tryptamines — the structural class to which MiPT belongs — generally exhibit variable and low 5-HT₁A affinity, in contrast to 5-substituted compounds (e.g., 5-MeO-MiPT) which consistently show high 5-HT₁A activity.supported
5-substituted: high 5-HT1A affinity, low 5-HT2C. Non-ring-substituted (e.g. MiPT) most consistently bind SERT. jpet.122.001454
At monoamine transporters, MiPT is inactive as a reuptake inhibitor (Ki >10,000 nM at SERT, DAT, and NET)supported
inactive at SERT, DAT, NET (>10,000 nM each) s00213-014-3557-7
However, it functions as a substrate at the serotonin transporter (SERT uptake inhibition Ki = 8.88 ± 4.7 µM) and at vesicular monoamine transporter 2 (VMAT2 inhibition Ki = 20 ± 4.3 µM)supported
MiPT KI at SERT = 8.88 ± 4.7 µM; KI at VMAT2 = 20 ± 4.3 µM. High binding-to-uptake ratios support substrate (not blocker) hypothesis. s00702-009-0308-8
This substrate behavior may permit intraneuronal accumulation to concentrations sufficient for activation of intracellular sigma-1 receptors, though no direct sigma-1 binding data for MiPT have been published.supported
Tryptamines may accumulate in neurons for sigma-1 receptor activation. s00702-009-0308-8
Among 21 tryptamines studied by Kozell et al., non-ring-substituted tryptamines most consistently exhibited SERT binding, corroborating the substrate classification.supported
21 substituted tryptamines... Non-ring-substituted (e.g. MiPT) most consistently bind SERT. jpet.122.001454
Repke et al. confirmed that MiPT shows substantial increases in both potency and oral activity compared to DMT, which is rapidly degraded by intestinal and hepatic MAO-A and requires co-administration with an MAOI for oral activity.supported
MiPT (Ar H) and 5-MeO-MiPT (Ar 5-OCH3) showed substantial increase in potency and oral activity vs N,N-dimethyl homologues. pmid:4009612
Claim in pharmacology — inconclusiveinconclusiveworking →
Caspar et al. identified CYP1A2, CYP2C19, CYP2D6, and CYP3A4 as responsible for hydroxylation, with CYP2C19, CYP2D6, and CYP3A4 mediating N-dealkylation, and glucuronidation and sulfation as phase II pathwayssupported
CYP1A2, CYP2C19, CYP2D6, CYP3A4 in hydroxylation; CYP2C19, CYP2D6, CYP3A4 in N-dealkylation. Glucuronidation and sulfation of phase I metabolites. dta.2197