| Stereochemistry | ABSOLUTE |
| Molecular Formula | C22H24FN5O4 |
| Molecular Weight | 441.4555 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 2 / 2 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
C[C@H](COC1=CN2N=CN=C(OC3=C(F)C4=C(NC(C)=C4)C=C3)C2=C1C)OC(=O)[C@H](C)N
InChI
InChIKey=LTEJRLHKIYCEOX-OCCSQVGLSA-N
InChI=1S/C22H24FN5O4/c1-11-7-15-16(27-11)5-6-17(19(15)23)32-21-20-13(3)18(8-28(20)26-10-25-21)30-9-12(2)31-22(29)14(4)24/h5-8,10,12,14,27H,9,24H2,1-4H3/t12-,14+/m1/s1
Brivanib is a pyrrolotriazine-based compound and an inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2) with potential antineoplastic activity. It specifically targets and strongly binds to human VEGFR-2, a tyrosine kinase receptor and pro-angiogenic growth factor expressed almost exclusively on vascular endothelial cells. Blockade of VEGFR-2 by this agent may lead to an inhibition of VEGF-stimulated endothelial cell migration and proliferation, thereby inhibiting tumor angiogenesis. Brivanib has a moderate potency compared to VEGFR-2 against VEGFR-1 and FGFR-1 as well. Brivanib is suggested to be efficient in treatment of hepatocellular carcinoma (HCC). As first-line and as second-line therapy brivanib demonstrated promising antitumor activity and a manageable safety profile in patients with advanced, unresectable HCC in phase II clinical trials. On 3 march 2011, orphan designation was granted by the European Commission to Bristol-Myers Squibb for brivanib alaninate for the treatment of hepatocellular carcinoma.[
Originator
Approval Year
Doses
AEs
Overview
OverviewOther
| Other Inhibitor | Other Substrate | Other Inducer |
|---|---|---|
Drug as perpetrator
Drug as victim
Tox targets
PubMed
Patents
Sample Use Guides
800 mg brivanib once daily until disease progression or toxicity treatment for liver cancer in Asian patients who have failed or could not tolerate sorafenib therapy
Route of Administration:
Oral
The SK-HEP1 and HepG2 cells were used to investigate the effects of brivanib on the VEGFR-2 and FGFR-1 signaling pathways in vitro.To study the effects of brivanib treatment on VEGF- and bFGF-stimulated activation of Akt and ERK1/2 pathways, SK-HEP1 and HepG2 cells were treated with 2 uM brivanib for 24 h and then stimulated with 40 ng/mL VEGF or bFGF. In addition, brivanib SK-HEP1 cells were also stimulated with IGF-1 for 15 min. The cells were lysed and the lysates were analyzed for levels of the effector proteins, including the serine/threonine kinase Akt and ERK1/2.
ACTIVE MOIETY
SUBSTANCE RECORD
