Stereochemistry | ACHIRAL |
Molecular Formula | C26H25N3O4 |
Molecular Weight | 443.4944 |
Optical Activity | NONE |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
CNC(=O)C1=C2C=CC(OC3=CC=NC4=CC(OCC5(N)CC5)=C(OC)C=C34)=CC2=CC=C1
InChI
InChIKey=CUDVHEFYRIWYQD-UHFFFAOYSA-N
InChI=1S/C26H25N3O4/c1-28-25(30)19-5-3-4-16-12-17(6-7-18(16)19)33-22-8-11-29-21-14-24(23(31-2)13-20(21)22)32-15-26(27)9-10-26/h3-8,11-14H,9-10,15,27H2,1-2H3,(H,28,30)
Molecular Formula | C26H25N3O4 |
Molecular Weight | 443.4944 |
Charge | 0 |
Count |
MOL RATIO
1 MOL RATIO (average) |
Stereochemistry | ACHIRAL |
Additional Stereochemistry | No |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Optical Activity | NONE |
Lucitanib (E-3810) is a novel multi-kinase inhibitor currently in clinical trials for its anti-angiogenic and anti-tumor activity. A Phase I/IIa clinical trial of lucitanib was initiated in 2010 and has demonstrated multiple objective responses in FGFR1 gene-amplified breast cancer patients, and objective responses were also observed in patients with tumors often sensitive to VEGFR inhibitors, such as renal cell and thyroid cancer. Lucitanib is an oral, potent inhibitor of the tyrosine kinase activity of fibroblast growth factor receptors 1 through 3 (FGFR1-3), vascular endothelial growth factor receptors 1 through 3 (VEGFR1-3) and platelet-derived growth factor receptors alpha and beta (PDGFR alpha-beta). The most common adverse events were hypertension, asthenia, and proteinuria.
Originator
Approval Year
Overview
CYP3A4 | CYP2C9 | CYP2D6 | hERG |
---|---|---|---|
OverviewOther
Other Inhibitor | Other Substrate | Other Inducer |
---|---|---|
Drug as perpetrator
Sourcing
PubMed
Sample Use Guides
Once daily (q.d.), on a continuous schedule over 28-day cycles, in fasting conditions (at least 2 hours prior to and 2 hours after any meal), until progressive disease or unacceptable toxicity.
Starting dose is 10 mg/day and can be reduced in 2.5 mg decrements to 5 mg/day based on individual tolerability.
Route of Administration:
Oral
the recovery of VEGFR2 phosphorylation after AL3810 washout was examined in HUVEC cells. Treatment with 1 uM/L of AL3810 for 4 hrs caused a dramatic decrease in the level of phospho-VEGFR2. Upon the removal of the inhibitor, VEGFR2 phosphorylation was recovered substantially at 6 hrs, followed by a total restoration at 24 hrs after inhibitor washout, indicating that AL3810 is a reversible inhibitor.