| Identification | Back Directory | [Name]
JNJ 27141491 | [CAS]
871313-59-6 | [Synonyms]
JNJ 27141491
3-[(1S)-1-(3,4-Difluorophenyl)propyl]-2,3-dihydro-5-(5-isoxazolyl)-2-thioxo-1H-imidazole-4-carboxylic acid methyl ester
1H-Imidazole-4-carboxylic acid, 3-[(1S)-1-(3,4-difluorophenyl)propyl]-2,3-dihydro-5-(5-isoxazolyl)-2-thioxo-, methyl ester | [Molecular Formula]
C17H15F2N3O3S | [MDL Number]
MFCD30182264 | [MOL File]
871313-59-6.mol | [Molecular Weight]
379.38 |
| Chemical Properties | Back Directory | [Melting point ]
127.2 °C(Solv: isopropyl ether (108-20-3)) | [Boiling point ]
501.8±60.0 °C(Predicted) | [density ]
1.44±0.1 g/cm3(Predicted) | [pka]
9.01±0.70(Predicted) |
| Hazard Information | Back Directory | [Uses]
JNJ 27141491 is a noncompetitive and orally active antagonist of human chemokine receptor CCR2. | [in vivo]
JNJ-27141491 (5-40 mg/kg; oral; once or twice daily) inhibits recruitment of monocytes and neutrophils into the alveolar air space of transgenic hCCR2 knockin mice[1].
JNJ-27141491 (20 mg/kg; oral; daily for 16 days) delays experimental autoimmune encephalomyelitis (EAE) in transgenic CCR2 mice[1]. | Animal Model: | Transgenic mCCR2 knockout/hCCR2 knockin C57BL/6 mice[1] | | Dosage: | 5, 10, 20, or 40 mg/kg | | Administration: | Oral, once or twice daily | | Result: | Once-daily oral treatment with 40, 20, 10, or 5 mg/kg inhibited the monocyte influx with 77, 57, 49, and 27%, respectively, compared with vehicle treatment, whereas this value was 74 and 22% after twice-daily oral treatment with 20 or 5 mg/kg. The neutrophil influx was also reduced; neutrophil numbers were decreased, with 56, 45, 20, and 8% after 40, 20, 10, or 5 mg/kg q.d. treatments and with 45 and 20% after 20 and 5 mg/kg b.i.d. treatments. |
| [IC 50]
hCCR2 |
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