| Identification | Back Directory | [Name]
BBS 4 | [CAS]
402934-09-2 | [Synonyms]
BBS 4
2-PyrrolidinecarboxaMide, N-[2-(1,3-benzodioxol-5-yl)ethyl]-1-[2-(1H-iMidazol-1-yl)-6-Methyl-4-pyriMidinyl]-, (2R)- | [Molecular Formula]
C22H24N6O3 | [MDL Number]
MFCD20526517 | [MOL File]
402934-09-2.mol | [Molecular Weight]
420.46 |
| Hazard Information | Back Directory | [Description]
BBS4 is a potent, orally active and selective inducible nitric oxide synthase dimerization inhibitor. BBS4 inhibits the dimerization of iNOS monomers, thus preventing the formation of the dimeric, active form of the enzyme. BBS4 significantly ameliorated adjuvant-induced arthritis in a rat model. BBS4 blocks the formation of the protein-protein interaction present in the dimeric form of iNOS. BBS4 prevents systemic, cardiac, and pulmonary hemodynamic dysfunction in endotoxemic mice. | [Uses]
BBS-4 is a potent and selective inducible nitric oxide synthase (NOS2) dimerization inhibitor, with an IC50 of 0.49 nM. BBS-4 can protect mice from the cardiovascular dysfunction of sepsis[1]. | [in vivo]
BBS-4 (10 mg/kg; i.p.; 1 h after endotoxin administration) prevents endotoxin-induced hypotension in mice[1].
BBS-4 (30 mg/kg; i.p.; 1 h after endotoxin administration) prevents endotoxin-induced myocardial dysfunction in mice[1].
BBS-4 (10 mg/kg; i.p.; 1 and 8 h after endotoxin administration) prevents endotoxin-induced impairment of murine hypoxic pulmonary vasoconstriction (HPV)[1].
BBS-4 (10 mg/kg; i.p.; 1 and 8 h after endotoxin administration) does not affect the endotoxin-induced increase in pulmonary NOS2 gene expression, but it (30 mg/kg) prevents cardiac and pulmonary NOS2 protein dimerization and increases plasma nitrate and nitrite (NOx) concentration in mice[1].
BBS-2 (30 mg/kg; s.c. twice daily for 10 d) does not affect agonist-stimulated NOS3-dependent aortic relaxation ex vivo[1].
BBS-4 (10-30 mg/kg; i.p.) does not improve mortality rate in endotoxemic mice[1].
| [IC 50]
iNOS | [References]
[1] Ichinose F, et, al. A selective inducible NOS dimerization inhibitor prevents systemic, cardiac, and pulmonary hemodynamic dysfunction in endotoxemic mice. Am J Physiol Heart Circ Physiol. 2003 Dec; 285(6): H2524-30. DOI:10.1152/ajpheart.00530.2003
[2] https://pubmed.ncbi.nlm.nih.gov/12907425/ DOI:10.1152/ajpheart.00530.2003 |
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