204005-46-9 Usage
Description
SU 5416 is a vascular endothelial growth factor receptor blocker, which plays a crucial role in inhibiting angiogenesis, a process that involves the formation of new blood vessels. It is a potent compound that has been extensively studied for its potential applications in various fields, particularly in the context of cancer treatment and vascular remodeling.
Uses
Used in Pharmaceutical Industry:
SU 5416 is used as an angiogenesis inhibitor for deep penetration into tumor tissues. By blocking the vascular endothelial growth factor receptor, it helps in limiting the growth of new blood vessels that supply nutrients and oxygen to the tumor, thereby inhibiting tumor growth and progression.
Used in Cancer Treatment:
SU 5416 is used as a therapeutic agent in the treatment of various types of cancer. Its ability to inhibit angiogenesis makes it a promising candidate for targeting solid malignancies, as it can help in starving the tumor of essential nutrients and oxygen, leading to reduced tumor growth and metastasis.
Used in Pulmonary Hypertension Research:
SU 5416 is used as a research tool to study the mechanism of development of cerebral vasculature in zebrafish hindbrain and to investigate the pulmonary vascular remodeling in response to hypoxia in mouse models of pulmonary arterial hypertension. These studies contribute to a better understanding of the underlying pathophysiology of pulmonary hypertension and may lead to the development of novel therapeutic strategies.
Used in Preclinical Studies:
SU 5416 is used in preclinical studies to evaluate its potential as a therapeutic agent in various disease models, including cancer and pulmonary hypertension. These studies help in assessing the safety, efficacy, and pharmacokinetics of the compound, providing valuable insights into its potential clinical applications.
Biological Activity
Inhibitor of vascular endothelial growth factor receptor (VEGFR) that also inhibits other tyrosine kinases KIT, MET, FLT3 and RET. Displays no activity against EGFR, HER2, IGF1R and PDGFR. Inhibits tumor vascularization and growth of multiple tumor types.
Biochem/physiol Actions
SU 516 inhibits the activity of neuronal nitric oxide synthase and protects the neuronal cells from nitric oxide-mediated neurotoxicity.1 It also acts an agonist of aryl hydrocarbon receptor and is an effective clinical agent for treating autoimmune diseases and transplant rejection.2
Check Digit Verification of cas no
The CAS Registry Mumber 204005-46-9 includes 9 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 6 digits, 2,0,4,0,0 and 5 respectively; the second part has 2 digits, 4 and 6 respectively.
Calculate Digit Verification of CAS Registry Number 204005-46:
(8*2)+(7*0)+(6*4)+(5*0)+(4*0)+(3*5)+(2*4)+(1*6)=69
69 % 10 = 9
So 204005-46-9 is a valid CAS Registry Number.
InChI:InChI=1/C15H14N2O/c1-9-7-10(2)16-14(9)8-12-11-5-3-4-6-13(11)17-15(12)18/h3-8,16H,1-2H3,(H,17,18)/b12-8-
204005-46-9Relevant articles and documents
Virtual screening and further development of novel ALK inhibitors
Okamoto, Masako,Kojima, Hirotatsu,Saito, Nae,Okabe, Takayoshi,Masuda, Yoshiaki,Furuya, Toshio,Nagano, Tetsuo
experimental part, p. 3086 - 3095 (2011/06/26)
Anaplastic lymphoma kinase (ALK) has been in the spotlight in recent years as a promising new target for therapy of non-small-cell lung cancer (NSCLC). Since the identification of the echinoderm microtubule-associated protein-like 4 (EML4)-ALK fusion gene in some NSCLC patients was reported in 2007, various research groups have been seeking ALK inhibitors. Above all, crizotinib (PF-02341066) has been under clinical trial, and its therapeutic efficacy of inhibiting ALK in NSCLC has been reported. Among anticancer drugs, drug resistance appears frequently necessitating various kinds of inhibitors. We identified novel ALK inhibitors by virtual screening from the public chemical library collected by the Chemical Biology Research Initiative (CBRI) at the University of Tokyo, and inhibitors that are more potent were developed.