2-DPMP
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Collated from TripSit, Pharmacology. Where sources differ (e.g. dosing), Compare shows them side by side.
Also known as desoxypipradrol, 2dpmp, 2-desoxypiperadol, desoxypipradolTS
A very potent stimulant that is a NDRI. Developed by Novartis in the 1950s, to treat narcolepsy and ADHD, however dropped when Methylphenidate was produced a few years later, which was seen as superior due to its shorter T½. 2-DPMP Half life 16-20 hours. Warning: subjective reports suggest this drug is caustic to the nasal mucosa and may cause damage to the nasal cavity.TS
Insufflated
Route dataTripSit
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| 1 mg | 2–3 mg | 3–4 mg | 4–6 mg | —+ |
| Onset | 60–120 minutes |
|---|---|
| Total | 16–72 hours |
| After-effects | 1–72 hours |
Oral
Route dataTripSit
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| 1 mg | 2–4 mg | 4–6 mg | 6–8 mg | —+ |
| Onset | 60–120 minutes |
|---|---|
| Total | 16–72 hours |
| After-effects | 1–72 hours |
🧬 Receptor activityPH
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.
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