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Desoxypipradrol

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Collated from PsychonautWiki, Pharmacology. Where sources differ (e.g. dosing), Compare shows them side by side.

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Also known as Desoxypipradol, 2-DPMP, Ivory WavePW

Desoxypipradrol may lead to states of psychosis, mania and addiction at a significantly higher rate than other stimulants. Due to its unusually long half-life and extreme potency, it is strongly discouraged to abuse this substance in high doses, multiple days in a row, or in combination with other substances known to increase the risk of psychosis. Please see this section for more details.PW

Addiction potentialPW
moderately addictive with a high potential for abuse
TolerancePW
full tolerance develops with prolonged and repeated use; half after 3 - 7 days; baseline after 1 - 2 weeks
Cross-tolerancePW
dopamine, stimulant

Insufflated

Route dataPsychonautWiki

ThresholdLightCommonStrongHeavy
0.25 mg0.5–1.5 mg1.5–3.5 mg3.5–5 mg5 mg+
06.25 mg
LightCommonStrongHeavy
Onset15–240 minutes
Come-up2–6 hours
Peak6–30 hours
Offset6–40 hours
Total10–72 hours
OnsetCome-upPeakOffset

Oral

Route dataPsychonautWiki

ThresholdLightCommonStrongHeavy
0.25 mg1–2 mg2–6 mg6–8 mg8 mg+
010 mg
LightCommonStrongHeavy
Onset1–4 hours
Peak9–30 hours
Offset6–40 hours
Total16–72 hours
OnsetCome-upPeakOffset

Dangerous interactionsPW

Unsafe interactionsPW

Caution / uncertainPW

Mechanism of actionPH

The ATP-Mg++-dependent uptake of (3)H dopamine and l-(3)H norepinephrine into purified synaptic vesicles of whole rat brain, rat striatum and rat hypothalamus was inhibited 10-fold more effectively by S-(+)-amphetamine as compared to its corresponding (R-(-)-enantiomer. In contrast, S-(+)-deoxypipradrol and its R-(-)-enantiomer were approximately equipotent inhibitors of 3H-amine uptake into these synaptic vesicular preparations. The 1R:2R-methylphenidate was twice as potent as its 1R:2S-enantiomer as an inhibitor of (3)H-catecholamine uptake. These data suggest that the receptor sites on the amine pumps present in the membranes of all three vesicular preparations are similar in so far as they are all sensitive to the stereochemical configuration around the alpha-carbon of amphetamine but are not sensitive to the stereochemical configuration around the analogous carbon of deoxypipradrol and methylphenidate. These observations are the reverse of those previously observed for the phenethylamine pumps present in peripheral and central neuronal membranes.
... Rat brain slices from the nucleus accumbens core, which were exposed to either cocaine (1, 3 or 10 uM) or desoxypipradrol (1, 3 or 10 uM) for 60 min. Dopamine efflux was electrically evoked and recorded using fast cyclic voltammetry. Both drugs increased the peak dopamine efflux and also slowed dopamine re-uptake. Desoxypipradrol was more potent than cocaine causing a sevenfold increase in peak dopamine levels (versus a threefold increase for cocaine) and increasing dopamine re-uptake half-life 15-fold (versus fivefold for cocaine). These data suggest that desoxypipradrol is more potent than cocaine at dopamine terminals, and this could account for its psychotogenic effects.

Plan when to take Desoxypipradrol — see where onset, peak and comedown land on the clock

Fact-sheets from PsychonautWiki. Harm-reduction reference only — not medical advice.