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Piribedil dihydrochloride

Dopamine agonist CAS# 1451048-94-4

Piribedil dihydrochloride

Catalog No. BCC6898----Order now to get a substantial discount!

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Chemical structure

Piribedil dihydrochloride

3D structure

Chemical Properties of Piribedil dihydrochloride

Cas No. 1451048-94-4 SDF Download SDF
PubChem ID 56972173 Appearance Powder
Formula C16H20Cl2N4O2 M.Wt 371.27
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 25 mM in water
Chemical Name 2-[4-(1,3-benzodioxol-5-ylmethyl)piperazin-1-yl]pyrimidine;dihydrochloride
SMILES C1CN(CCN1CC2=CC3=C(C=C2)OCO3)C4=NC=CC=N4.Cl.Cl
Standard InChIKey LTXWEVPOJXPWAD-UHFFFAOYSA-N
Standard InChI InChI=1S/C16H18N4O2.2ClH/c1-4-17-16(18-5-1)20-8-6-19(7-9-20)11-13-2-3-14-15(10-13)22-12-21-14;;/h1-5,10H,6-9,11-12H2;2*1H
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Piribedil dihydrochloride

DescriptionA direct dopamine agonist, in clinical use for treatment of dopaminergic system dysfunction. Recent work suggests that it is selective for the D3 subtype, for which it has 20 times higher affinity than for D2, and possesses no significant affinity for D1 receptors.

Piribedil dihydrochloride Dilution Calculator

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Preparing Stock Solutions of Piribedil dihydrochloride

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.6935 mL 13.4673 mL 26.9346 mL 53.8692 mL 67.3364 mL
5 mM 0.5387 mL 2.6935 mL 5.3869 mL 10.7738 mL 13.4673 mL
10 mM 0.2693 mL 1.3467 mL 2.6935 mL 5.3869 mL 6.7336 mL
50 mM 0.0539 mL 0.2693 mL 0.5387 mL 1.0774 mL 1.3467 mL
100 mM 0.0269 mL 0.1347 mL 0.2693 mL 0.5387 mL 0.6734 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Piribedil dihydrochloride

In vitro affinity of piribedil for dopamine D3 receptor subtypes, an autoradiographic study.[Pubmed:8905329]

Eur J Pharmacol. 1996 Oct 10;313(1-2):63-7.

Receptor binding autoradiography, using the selective ligand [3H]7-OH-(R)DPAT (R(+)-2-dipropylamino-7-hydroxy 1,2,3,4-tetrahydronaphthalene), showed that piribedil is a potent inhibitor at dopamine D3 receptors in limbic regions (island of Calleja), with affinity (IC50) between 30 and 60 nM. The in vitro IC50 of piribedil for inhibition of [3H]spiperone binding to receptors of the dopamine D2-like family (D2, D3 and D4), ranged between 10(-7) and 10(-6) M in different brain regions (medial and lateral caudate putamen, olfactory tubercles, and nucleus accumbens). At the highest concentration tested (10(-5 M) piribedil inhibited dopamine D1 receptor binding by < 50%. It is concluded that piribedil has 20 times higher affinity for dopamine D3 than for dopamine D2-like receptors, and very low affinity for the dopamine D1 receptor subtype in rat brain. How this pattern of receptor affinity is related to the pharmacological profile of piribedil deserves further investigation.

Parkinson's disease: pathological mechanisms and actions of piribedil.[Pubmed:1634907]

J Neurol. 1992;239 Suppl 1:S2-8.

The cause of the degeneration of dopamine-containing cells in the zona compacta of the substantia nigra in Parkinson's disease remains unknown. The ability of the selective nigral toxin 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) (via its metabolite MPP+) to destroy nigral dopamine cells selectively by inhibiting complex I of the mitochondrial energy chain may provide a clue. Indeed, recent studies of post-mortem brain tissue have suggested the presence of an on-going toxic process in the substantia nigra in Parkinson's disease leading to excess lipid peroxidation. This appears also to involve a disruption of mitochondrial function since mitochondrial superoxide dismutase activity is increased and there is impairment of complex I. These changes may in turn relate to a selective increase in the total iron content of substantia nigra coupled to a generalised decrease in brain ferritin content. Piribedil is used in the symptomatic treatment of Parkinson's disease and is particularly effective against tremor. Piribedil (and its metabolites) acts as a dopamine D-2 receptor agonist. However, in our studies in contrast to other dopamine agonists, in vivo piribedil interacts with dopamine receptors in the substantia nigra and nucleus accumbens but not those in the striatum. In patients with Parkinson's disease the beneficial effects of piribedil may be limited by nausea and drowsiness. Indeed, in MPTP-treated primates piribedil reverses motor deficits but marked side-effects occur. However, pre-treatment with the peripheral dopamine receptor antagonist domperidone prevents the unwanted effects and piribedil produces a profound and longer-lasting reversal of all components of the motor syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

A comparative study of the locomotor activity effects of apomorphine and the "atypical dopamine agonists" (piribedil and S3608).[Pubmed:3081774]

Life Sci. 1986 Mar 10;38(10):895-903.

Apomorphine and the "atypical dopamine agonists" (piribedil and S3608) dose dependently increase locomotor activity (LA) in rats. The LA effects of all 3 drugs are readily attenuated by pretreatment with pimozide or sulpiride. Reserpine pretreatment or bilateral 6-hydroxydopamine lesions of the nucleus accumbens (NAS) potentiates apomorphine-induced LA but attenuates piribedil- and S3608-induced LA. The latter suggests an indirect mode of action for piribedil and for S3608. However, piribedil and S3608 at concentrations up to 10(-4)M do not cause release or inhibition of 3H-dopamine uptake in synaptosomes prepared from the rat NAS. Sulpiride antagonism of apomorphine-induced LA is surmountable by increasing the dose of apomorphine. Antagonism of piribedil- or S3608-induced LA by sulpiride is not surmountable by increasing the dose of either of the "atypical dopamine agonists". Furthermore, pretreatment with either piribedil or S3608 substantially increases the peak LA inducible by apomorphine. The effects of simultaneous injections of piribedil and S3608 are, however, not additive. These findings suggest that the LA stimulant effects of piribedil and S3608 are mediated via receptors or systems which differ from the receptors involved in the mediation of apomorphine-induced LA.

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