| Identification | Back Directory | [Name]
Benzonitrile, 4-[(5R)-5,6,7,8-tetrahydroimidazo[1,5-a]pyridin-5-yl]- | [CAS]
102676-87-9 | [Synonyms]
(R)-Fadrozole
(R)-CGS 16949A free base
(R) Fadrozole,(R)Fadrozole
(R)-4-(5,6,7,8-tetrahydroimidazo[1,5-a]pyridin-5-yl)benzonitrile
Benzonitrile, 4-[(5R)-5,6,7,8-tetrahydroimidazo[1,5-a]pyridin-5-yl]- | [Molecular Formula]
C14H13N3 | [MOL File]
102676-87-9.mol | [Molecular Weight]
223.27 |
| Chemical Properties | Back Directory | [Boiling point ]
481.7±38.0 °C(Predicted) | [density ]
1.20±0.1 g/cm3(Predicted) | [form ]
Solid | [pka]
7.16±0.40(Predicted) | [color ]
Light yellow to yellow |
| Hazard Information | Back Directory | [Uses]
Dexfadrostat ((R)-Fadrozole) is a potent nonsteroidal inhibitor[1]. Dexfadrostat also inhibits human placental aromatase (pIC50 = 6.17) and aldosterone biosynthesis. Dexfadrostat reverses cardiac fibrosis in spontaneously hypertensive heart failure rats.[1][2]. | [in vivo]
Dexfadrostat ((R)-fadrozole; 0.24 and 1.2 mg/kg; daily; oral) and (S)-fadrozole similarly decreases plasma aldosterone levels, whereas urinary aldosterone excretion rate was reduced only by S-fadrozole[2].
Dexfadrostat (0.24 and 1.2 mg/kg; daily; oral) effectively reverses preexistent left ventricular interstitial fibrosis by 50% (vs. 42% for canrenoate), S-fadrozole was devoid of an antifibrotic effect[2]. | Animal Model: | SHHF rats[2] | | Dosage: | 0.24 and 1.2 mg/kg | | Administration: | Daily; oral | | Result: | Decreased plasma aldosterone levels and reversed preexistent left ventricular interstitial fibrosis.
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| [References]
[1] Furet P, et al. Aromatase inhibitors: synthesis, biological activity, and binding mode of azole-type compounds. J Med Chem. 1993;36(10):1393-1400. DOI:10.1021/jm00062a012
[2] Minnaard-Huiban M, et al. Fadrozole reverses cardiac fibrosis in spontaneously hypertensive heart failure rats: discordant enantioselectivity versus reduction of plasma aldosterone. Endocrinology. 2008;149(1):28-31. DOI:10.1210/en.2007-0584 |
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