Description
(+)-Dihydrexidine hydrochloride ((+)-DAR-0100 hydrochloride) is a dopamine D1 receptor agonist with an EC50 of 72± 21 nM.
Product information
CAS Number: 158704-02-0
Molecular Weight: 303.78
Formula: C17H18ClNO2
Chemical Name: (6aR,12bS)-5H,6H,6aH,7H,8H,12bH-benzo[a]phenanthridine-10,11-diol hydrochloride
Smiles: Cl.OC1=CC2CC[C@H]3NCC4=CC=CC=C4[C@@H]3C=2C=C1O
InChiKey: IJYUPBNUPIRQEP-SATBOSKTSA-N
InChi: InChI=1S/C17H17NO2.ClH/c19-15-7-10-5-6-14-17(13(10)8-16(15)20)12-4-2-1-3-11(12)9-18-14;/h1-4,7-8,14,17-20H,5-6,9H2;1H/t14-,17-;/m1./s1
Technical Data
Appearance: Solid Power
Purity: ≥98% (or refer to the Certificate of Analysis)
Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis
Storage Condition: Dry, dark and -20 oC for 1 year or refer to the Certificate of Analysis.
Shelf Life: ≥12 months if stored properly.
Stock Solution Storage: 0 - 4 oC for 1 month or refer to the Certificate of Analysis.
Drug Formulation: To be determined
HS Tariff Code: 382200
How to use
In Vitro:
(+)-Dihydrexidine hydrochloride (DHX) is a high-potency, bioavailable D1 dopamine receptor agonist. (+)-Dihydrexidine is screened for activity against 40 other binding sites, and is inactive (IC50 greater than 10 microM) against all except D2 dopamine receptors (IC50=130 nM) and alpha 2 adrenoreceptors (IC50=230 nM). Dihydrexidine competes stereoselectively and potently for D1 binding sites in rat striatal membranes labeled with [3H]SCH23390 with an IC50 of about 10 nM compared to about 30 nM for the prototypical D1 agonist SKF38393.
In Vivo:
To examine the functional state of striatal neurons in response to D1 receptor activation, AC5+/+ and AC5-/- mice are injected with the D1 agonist (+)-Dihydrexidine (30 mg/kg, i.p.) and obtained the dorso-lateral striatum and NAc, separately, 45 min later for RT-PCR analysis. These experiments reveal that (+)-Dihydrexidine -triggered induction of the immediate early genes, c-fos, egr-1, and junB, in the NAc is markedly enhanced in AC5-/- mice compared with that in AC5+/+ mice, while the induction in the dorso-lateral striatum is suppressed in AC5-/- mice.
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