Denopamine ((R)-(-)-Denopamine) is an orally active, selective β1-adrenergic agonist. Denopamine prolongs survival in a murine model of congestive heart failure induced by viral myocarditis: suppression of tumor necrosis factor-α production in the heart. Cardiovascular effects[1].
Denopamine (0.1-100 μM) suppresses LPS-induced TNF-α production in a concentration-dependent manner[1].
Cell Viability Assay[1]
| Cell Line: | Murine spleen cells |
| Concentration: | 0, 0.1, 1, 10, 100 μM |
| Incubation Time: | 5 hours |
| Result: | Decreased TNF-α levels by 96.9±6.7%, 62.7±6.5%, 53.2±8.8%, and 40.3±1.5% at 0.1, 1, 10 and 100 μmol/L, respectively. |
Denopamine (14 μmol/kg per day; oral administration; for 14 days) significantly improves the survival of the animals, attenuates myocardial lesions, and suppresses TNF-α production in vivo[1].
The plasma concentration of Denopamine is 13.1±1.9 nmol/L at 1 h, 4.3±0.9 nmol/L at 2 h, 1.8±0.5 nmol/L at 3 h, and <0.6 nmol/L at 5 h after its administration. A single 14 μmol/kg dose of denopamine in mice produces a peak level at 1 h[1].
| Animal Model: | Four-week-old inbred male DBA/2 mice[1] |
| Dosage: | 14 μmol/kg per day |
| Administration: | Oral administration; 14 days |
| Result: | Treatment significantly improved the survival of the animals (14 of 25 (56%) treated, vs 5 of 25 (20%) control mice). At day 14, the survival rate of 57.1% (16 of 28 mice) in the treated group was significantly higher than the 33.3% (10 of 30 mice) survival rate in the control group. The survival rate from day 6 to day 14 was also significantly improved in the treated group (69.6%; 16 of 23 mice) versus the control group (45.5%; 10 of 22 mice, p < 0.05). |