8-OH-DPAT (8-Hydroxy-DPAT)

Catalog No.S8447

For research use only.

8-OH-DPAT (8-Hydroxy-DPAT) is a kind of classic 5-HT1A agonist with the pIC50 of 8.19. It has a selectivity of almost-1000 fold for a subtype of the 5-HT1 binding site; Its biological half-life is 1.5 hous.

8-OH-DPAT (8-Hydroxy-DPAT) Chemical Structure

CAS No. 78950-78-4

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Biological Activity

Description 8-OH-DPAT (8-Hydroxy-DPAT) is a kind of classic 5-HT1A agonist with the pIC50 of 8.19. It has a selectivity of almost-1000 fold for a subtype of the 5-HT1 binding site; Its biological half-life is 1.5 hous.
5-HT1A [1]
In vitro

The drug is only weakly effective at 5-HT1B subtype, the pIC50 being 5.42 ± 0.08 (n = 5). Since 8-OH-DPAT has no effect on 5-HT1B binding at concentrations lower than 100 nM[1]. 8-OH-DPAT is able to reduce the accumulation of both autophagic-derived and photoreceptor outer segment-derived lipofuscin, increase antioxidant protection and reduce oxidative damage in cultured human RPE cells[4].

In vivo Intravenous administration of the selective 5-HT1A-receptor agonist 8-OH-DPAT rapidly reverses the hypotensive and bradycardic responses established during severe hemorrhage with relatively little variability. 8-OH-DPAT is relatively lipophilic and readily crosses the blood-brain barrier[3].

Protocol (from reference)

Cell Research:


  • Cell lines: Retinal pigment epithelial (RPE) cells
  • Concentrations: 10 μM
  • Incubation Time: 24 h
  • Method:

    Cells are exposed to H2O2 (200 µM) for 1 hour and either pre-or post treated with 8-OH DPAT (10 µM) for 24 hours. In the case of pretreatment all measurements are made 24 hr after H2O2 and for post treatment 8-OH DPAT is added immediately following H2O2 exposure. 5HT1A agonist treatment: To assess the ability of the 5-HT1A receptor agonist, 8-OH DPAT, to reduce lipofuscin formation in cultured RPE cells, this compound is added to the culture medium every 48 hours at concentrations ranging from 0.1 to 20 µM. All experiments are undertaken in basal medium, and cells receiving vehicle alone (PBS) acted as negative controls. To determine if the effect of 8-OH DPAT is sustained following discontinuation of 5-HT1A receptor agonist treatment, 8-OH DPAT treatment is discontinued after 28 days and the cells maintained in basal medium or fed POS for a further 28 days. To assess the ability of 8-OH DPAT to remove existing lipofuscin, autophagy-derived lipofuscin and phagocytic-derived lipofuscin are allowed to accumulate as described above and then 8-OH DPAT is added every second day for up to 28 days. To confirm that 8-OH DPAT is acting via the 5-HT1A receptor agonist we include the 5-HT1A receptor antagonist S(-)-UH-301 at 5 µM in some experiments. To determine the effect of timing of 8-OH DPAT treatment on oxidative stress markers, RPE cultures are either pre-treated with 8-OH DPAT (at 1 or 10 µM) for 3 or 24 hours prior to exposure to 200 µM H2O2 for 1 hour or treated with the 5HT1A agonist for 3 or 24 hours post-exposure to H2O2. Cells not exposed to oxidative stressor serve as a negative control, and cells exposed to oxidative stressor but not 8-OH DPAT serve as a positive control. Cells exposed to 8-OH DPAT only act as an additional control.

Animal Research:


  • Animal Models: Male Lister hooded rats
  • Dosages: 0, 3.0, 10, 100 and 300 μg/kg
  • Administration: i.p.

Solubility (25°C)

In vitro

DMSO 49 mg/mL
(198.07 mM)
Ethanol 49 mg/mL
(198.07 mM)
Water Insoluble

Chemical Information

Molecular Weight 247.38


CAS No. 78950-78-4
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles CCCN(CCC)C1CCC2=C(C1)C(=CC=C2)O

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