http://en.wikipedia.org/wiki/File:Bexarotene.svg
Systematic (IUPAC) name
4-[1-(3,5,5,8,8-pentamethyltetralin-2-yl)ethenyl]
benzoic acid
Clinical data
AHFS/Drugs.com monograph
MedlinePlus a608006
Pregnancy cat. X
Legal status ?
Routes Oral and Topical
Pharmacokinetic data
Protein binding >99%
Metabolism Bexarotene undergoes oxidative metabolism via CYP450 3A4 and its metabolites are then glucuronidated. Four bexarotene metabolites have been identified in the plasma: 6- and 7- hydroxy-bexarotene and 6-and 7-oxo-bexarotene. All of the metabolites are active in vitro, but their clinical significance is not known.
Half-life 7 hours
Excretion Parent drug and metabolites are eliminated primarily through the hepatobiliary system. Less than 1% is excreted in the urine unchanged.
Identifiers
CAS number 153559-49-0
ATC code L01XX25
PubChem CID 82146
DrugBank APRD00114
ChemSpider 74139
UNII A61RXM4375
ChEBI CHEBI:50859
ChEMBL CHEMBL1023
Chemical data
Formula C24H28O2
Mol. mass 348.478 g/mol
SMILES eMolecules & PubChem
InChI[show]
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http://www.lclabs.com/PRODFILE/A-C/B-2422.php4
EGFR TKI resistance mechanisms and c-Met inhibitors will become a hot spot
ReplyDeleteEGFR mutations in patients with EGFR TKI gradually determine the first-line treatment of status, the EGFR TKI get drug resistance mechanism of their resistance should be taken treatment strategies will gradually become the focus of attention.
The EGFR TKI acquired resistance mechanisms are not yet completely clear. Previous studies show that approximately 50% of patients after EGFR TKI treatment after acquired drug resistance may be due to tumor cells secondary mutation. This resistance mutation No. 790 sites in the EGFR gene on the 20th exon methionine is substituted with threonine (T790M mutation), thus impeding the EGFR with erlotinib combination of erlotinib or gefitinib, erlotinib, or increase in the affinity of the EGFR and its ligands ATP.
EGFR TKI acquired drug resistance in patients with no standard treatment options. EGFR TKI combined with chemotherapy, the 3rd generation EGFR TKI, second-generation EGFR TKI United Cistercian infliximab, second-generation EGFR TKI inhibitor of c-Met, the second generation the EGFR TKI United HDAC inhibitors as well as second-generation EGFR TKI United IFGF1RC inhibitors future promising drug post-processing program.
The basis of studies have shown that a new generation of irreversible EGFR inhibitors may be acquired resistance to EGFR TKI patients. EKB-569, HKI-272, Canertinib, BIBW2992 and PF-299804 and other ongoing human clinical trials of drugs.
c-Met is leading to tumor formation and metastasis of many passage cross point, the c-Met as a target can be relatively easily achieved while interference for many passages, to find efficient c-Met inhibitor antineoplastic study hot spots. Currently, capable of blocking the signal transduction pathway of c-Met has been found that many compounds, including monoclonal antibodies (such as OA-505) and small molecule kinase inhibitor of c-Met (e.g., PF-2341066, ARQ-197, XL-184 etc.). 2010 ESMO annual meeting of the multi-center, randomized, double-blind Ⅱ clinical study (OAM4588) of the Met receptor antagonist (MetMab) combined with erlotinib efficacy of the treatment of patients with advanced NSCLC. The results showed that highly expressed in the Met patients, the erlotinib Nigeria United MetMab can improve PFS and OS, and no unexpected adverse reactions, but in patients with low expression Met erlotinib Stock MetMab of group PFS and OS was poor.
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