132874-73-8

Basic information

• Product Name: 5-(dipropylamino)-5,6-dihydro-4H-imidazo-(5,1ij)quinolin-2(1H)-one
• Synonyms: 5-(dipropylamino)-5,6-dihydro-4H-imidazo-(5,1ij)quinolin-2(1H)-one
• CAS NO: 132874-73-8
• Molecular Formula: C₁₆H₂₃N₃O
• Molecular Weight: 273.37332
• Mol File: 132874-73-8.mol

Chemical Properties

• Boiling Point: °Cat760mmHg
• Flash Point: °C
• Appearance: /
• Density: 1.16g/cm³
• Refractive Index: 1.604
• CAS DataBase Reference: 5-(dipropylamino)-5,6-dihydro-4H-imidazo-(5,1ij)quinolin-2(1H)-one(CAS DataBase Reference)
• NIST Chemistry Reference: 5-(dipropylamino)-5,6-dihydro-4H-imidazo-(5,1ij)quinolin-2(1H)-one(132874-73-8)
• EPA Substance Registry System: 5-(dipropylamino)-5,6-dihydro-4H-imidazo-(5,1ij)quinolin-2(1H)-one(132874-73-8)

Safety Data

• Hazardous Substances Data: 132874-73-8(Hazardous Substances Data)

Usage

InChI:InChI=1/C16H23N3O/c1-3-8-18(9-4-2)13-10-12-6-5-7-14-15(12)19(11-13)16(20)17-14/h5-7,13H,3-4,8-11H2,1-2H3,(H,17,20)/t13-/m1/s1

Upstream product

• 2448-45-5 Cbz-D-Phe 

Relevant articles and documents

Novel Analogues of (R)-5-(Methylamino)-5,6-dihydro-4H-imidazo[4,5,1-ij]quinolin-2(1H)-one (Sumanirole) Provide Clues to Dopamine D2/D3 Receptor Agonist Selectivity

Novel 1-, 5-, and 8-substituted analogues of sumanirole (1), a dopamine D2/D3 receptor (D2R/D3R) agonist, were synthesized. Binding affinities at both D2R and D3R were higher when determined in competition with the agonist radioligand [3H]7-hydroxy-N,N-dipropyl-2-aminotetralin (7-OH-DPAT) than with the antagonist radioligand [3H]N-methylspiperone. Although 1 was confirmed as a D2R-preferential agonist, its selectivity in binding and functional studies was lower than previously reported. All analogues were determined to be D2R/D3R agonists in both GoBRET and mitogenesis functional assays. Loss of efficacy was detected for the N-1-substituted analogues at D3R. In contrast, the N-5-alkyl-substituted analogues, and notably the n-butyl-arylamides (22b and 22c), all showed improved affinity at D2R over 1 with neither a loss of efficacy nor an increase in selectivity. Computational modeling provided a structural basis for the D2R selectivity of 1, illustrating how subtle differences in the highly homologous orthosteric binding site (OBS) differentially affect D2R/D3R affinity and functional efficacy.