ChemicalBook CAS DataBase List 402934-09-2

402934-09-2

Name	BBS 4
CAS	402934-09-2
Molecular Formula	C22H24N6O3
MDL Number	MFCD20526517
Molecular Weight	420.46
MOL File	402934-09-2.mol

Chemical Properties

density	1.43±0.1 g/cm3(Predicted)
form	Solid
pka	14.54±0.20(Predicted)
color	White to off-white

Hazard Information

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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