General
Preferred name
CP-547632
Synonyms
OSI-632 ()
CP 547632 ()
VANDETANIB ()
AZD-6474 ()
CP-547632 (hydrochloride) ()
CP 547,632 ()
Cp-547,632 ()
PAN 90806 ()
PAN-90806 ()
CP-632 ()
PAN90806 ()
CP-547632 hydrochloride ()
P&D ID
PD016641
CAS
252003-65-9
252003-71-7
Tags
available
drug candidate
Drug indication
Non-small-cell lung cancer
Age-related macular degeneration
Ovarian cancer
Solid tumour/cancer
Drug Status
investigational
Max Phase
2.0
Structure
Probe scores
P&D probe-likeness score
[[ v.score ]]%
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
DESCRIPTION CP-547632 is a potent inhibitor of VEGFR2 and basic fibroblast growth factor (FGF) receptor kinases . (GtoPdb)
DESCRIPTION CP-547632 is an orally active, ATP-competitive and potent VEGFR-2 and FGF kinases inhibitor with IC50s of 11 nM and 9 nM, respectively. CP-547632 is selective for VEGFR2 and bFGF over EGFR, PDGFR¦Â, and related tyrosine kinases (TKs). CP-547632 has antitumor efficacy[1].
PRICE 101
DESCRIPTION CP-547632 is an orally available and potent, ATP-competitive dual inhibitor of VEGFR-2 and FGF kinase F with IC50s of 11 nM and 9 nM, respectively. CP-547632 is selective, with higher selectivity for VEGFR2 and bFGF than for EGFR, PDGFR?? and related tyrosine kinases (TKs). PDGFR?? and related tyrosine kinases (TKs) CP-547632 has antitumour activity.
DESCRIPTION CP-547632 hydrochloride is an orally active, ATP-competitive and potent VEGFR-2 and FGF kinases inhibitor with IC50s of 11 nM and 9 nM, respectively. CP-547632 hydrochloride is selective for VEGFR2 and bFGF over EGFR, PDGFR¦Â, and related tyrosine kinases (TKs). CP-547632 hydrochloride has antitumor efficacy[1].
DESCRIPTION CP-547632 is as a potent inhibitor of the VEGFR-2 and basic fibroblast growth factor (FGF) kinases (IC50 11 and 9 nM, respectively). It is selective relative to epidermal growth factor receptor, platelet-derived growth factor , and other related TKs. It also inhibits VEGF-stimulated autophosphorylation of VEGFR-2 in a whole cell assay with an IC50 value of 6 nM. After oral administration of CP-547,632 to mice bearing NIH3T3/H-ras tumors, VEGFR-2 phosphorylation in tumors was inhibited in a dose-dependent fashion (EC50 590 ng/ml). CP-547,632 is a well-tolerated, orally-bioavailable inhibitor presently under clinical investigation for the treatment of human malignancies. (BOC Sciences Bioactive Compounds)
DESCRIPTION CP-547632 is an orally available and potent, ATP-competitive dual inhibitor of VEGFR-2 and FGF kinase F with IC50s of 11 nM and 9 nM, respectively. CP-547632 is selective, with higher selectivity for VEGFR2 and bFGF than for EGFR, PDGFRβ and related tyrosine kinases (TKs). PDGFRβ and related tyrosine kinases (TKs) CP-547632 has antitumour activity. (TargetMol Bioactive Compound Library)
Compound Sets
16
Axon Medchem Screening Library
BOC Sciences Bioactive Compounds
Cayman Chemical Bioactives
ChEMBL Drugs
Clinical kinase drugs
Drug Repurposing Hub
DrugBank
DrugMAP
Enamine Bioactive Compounds
Guide to Pharmacology
LSP-MoA library (Laboratory of Systems Pharmacology)
LSP-OptimalKinase library (Laboratory of Systems Pharmacology)
MedChem Express Bioactive Compound Library
Novartis Chemogenetic Library (NIBR MoA Box)
ReFrame library
TargetMol Bioactive Compound Library
External IDs
34
Properties
(calculated by RDKit )
Molecular Weight
531.08
Hydrogen Bond Acceptors
6
Hydrogen Bond Donors
3
Rotatable Bonds
10
Ring Count
3
Aromatic Ring Count
2
cLogP
3.86
TPSA
109.58
Fraction CSP3
0.45
Chiral centers
0.0
Largest ring
6.0
QED
0.4
Structural alerts
0
No structural alerts detected
Custom attributes
(extracted from source data)
Targets
KDR,FGFR1
Target
VEGFR2
bFGFR
PDGFRβ
BTK
VEGFR2 inhibitor
FGFR
VEGFR
Member status
virtual
MOA
EGFR (HER1| erbB1) Inhibitors
PDGFR Inhibitors
VEGFR-2 (FLK-1/KDR) Inhibitors
Inhibitors of Signal Transduction Pathways
Angiogenesis Inhibitors
kinase inhibitor
Pathway
Angiogenesis
Tyrosine Kinase/Adaptors
Protein Tyrosine Kinase/RTK
Therapeutic Class
Anticancer Agents
Source data