| Stereochemistry | ABSOLUTE |
| Molecular Formula | C10H17N3O2S |
| Molecular Weight | 243.326 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 3 / 3 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
[H][C@]12CS[C@@H](CCCCC(O)=O)[C@@]1([H])NC(=N)N2
InChI
InChIKey=WWVANQJRLPIHNS-ZKWXMUAHSA-N
InChI=1S/C10H17N3O2S/c11-10-12-6-5-16-7(9(6)13-10)3-1-2-4-8(14)15/h6-7,9H,1-5H2,(H,14,15)(H3,11,12,13)/t6-,7-,9-/m0/s1
| Molecular Formula | C10H17N3O2S |
| Molecular Weight | 243.326 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ABSOLUTE |
| Additional Stereochemistry | No |
| Defined Stereocenters | 3 / 3 |
| E/Z Centers | 0 |
| Optical Activity | UNSPECIFIED |
2-Iminobiotin (2-IB) is a cyclic guanidino analog of biotin (Vitamin B7) and combined neuronal and inducible (but not endothelial) nitric oxide synthase inhibitor that has been demonstrated to improve neuroprotection in animal models of hypoxic-ischemic Brain Injury. While the exact mechanism of action has yet to be defined, 2-Iminobiotin potentially protects against hypoxic-ischemic brain damage by preventing nitric oxide or peroxynitrite-induced mitochondrial damage. In preclinical models, 2-Iminobiotin provides gender-specific neuroprotection against hypoxia-ischemia in neonatal rats by a NO-independent mechanism.
Originator
Approval Year
Cmax
AUC
Doses
AEs
Sourcing
PubMed
Patents
Sample Use Guides
2-Iminobiotin is formulated as a 0.75 mg/ml isotonic, iso-osmotic, saline solution with a pH of 4. It is administered as a solution for I.V.infusion through a central catheter. Six pulse doses will be given in 20 hours. Dosage will starts with 0.2 mg/kg/dose, but may be adapted during the study.
Route of Administration:
Intravenous
Neuronal IMR-32 cells were exposed to hypoxia employing an enzymatic hypoxia system and were thereafter incubated with various concentrations of 2-IB (10 to 300ng/ml). Cell damage, metabolic activity and generation of reactive oxygen species were quantified using colorimetric/fluorometric lactate dehydrogenase (LDH), tetrazolium-based (MTS) and reactive oxygen species assays. Proteome profiling arrays were performed to evaluate the regulation of cell stress protein expression by hypoxia and 2-IB. Seven hours of hypoxia led to morphological changes in IMR-32 cultures, increased neuronal cell damage, reduction of metabolic activity and enhanced reactive oxygen species production. Post-hypoxic application of 2-IB (30ng/ml) attenuated hypoxia-induced LDH release and increased metabolic activity of IMR-32 cells, while reactive oxygen species production was only by trend decreased.