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557795-19-4 分子结构
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N-[2-(diethylamino)ethyl]-5-{[(3Z)-5-fluoro-2-oxo-2,3-dihydro-1H-indol-3-ylidene]methyl}-2,4-dimethyl-1H-pyrrole-3-carboxamide

ChemBase编号:1135
分子式:C22H27FN4O2
平均质量:398.4737832
单一同位素质量:398.21180434
SMILES和InChIs

SMILES:
Fc1cc2/C(=C/c3[nH]c(c(c3C)C(=O)NCCN(CC)CC)C)/C(=O)Nc2cc1
Canonical SMILES:
CCN(CCNC(=O)c1c(C)[nH]c(c1C)/C=C/1\C(=O)Nc2c1cc(F)cc2)CC
InChI:
InChI=1S/C22H27FN4O2/c1-5-27(6-2)10-9-24-22(29)20-13(3)19(25-14(20)4)12-17-16-11-15(23)7-8-18(16)26-21(17)28/h7-8,11-12,25H,5-6,9-10H2,1-4H3,(H,24,29)(H,26,28)/b17-12-
InChIKey:
WINHZLLDWRZWRT-ATVHPVEESA-N

引用这个纪录

CBID:1135 http://www.chembase.cn/molecule-1135.html

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名称和登记号

名称和登记号

名称 登记号
IUPAC标准名
N-[2-(diethylamino)ethyl]-5-{[(3Z)-5-fluoro-2-oxo-2,3-dihydro-1H-indol-3-ylidene]methyl}-2,4-dimethyl-1H-pyrrole-3-carboxamide
IUPAC传统名
sunitinib
商标名
Sutent
sunitinib
SU-11248
别名
SU11248
Sunitinib malate
Sutent
Sunitinib
N-[2-(diethylamino)ethyl]-5-[(Z)-(5-fluoro-2-oxo-1,2-dihydro-3H-indol-3-ylidene)methyl]-2,4-dimethyl-1H-pyrrole-3-carboxamide
CAS号
557795-19-4
MDL号
MFCD09260778
PubChem SID
160964598
46507140
PubChem CID
5329102

数据来源

数据来源

所有数据来源 商品来源 非商品来源

理论计算性质

理论计算性质

JChem ALOGPS 2.1
Acid pKa 11.462899  质子受体
质子供体 LogD (pH = 5.5) -0.2940415 
LogD (pH = 7.4) 1.2792807  Log P 2.9273767 
摩尔折射率 116.2663 cm3 极化性 42.123272 Å3
极化表面积 77.23 Å2 可自由旋转的化学键
里宾斯基五规则 true 
Log P 3.24  LOG S -4.11 
溶解度 3.08e-02 g/l 

分子性质

分子性质

理化性质 产品相关信息 生物活性(PubChem)
疏水性(logP)
2.5 expand 查看数据来源
纯度
95+% expand 查看数据来源
98% expand 查看数据来源

详细说明

详细说明

DrugBank DrugBank
DrugBank -  DB01268 external link
Item Information
Drug Groups approved; investigational
Description Sunitinib is an oral, small-molecule, multi-targeted receptor tyrosine kinase (RTK) inhibitor that was approved by the FDA for the treatment of renal cell carcinoma (RCC) and imatinib-resistant gastrointestinal stromal tumor (GIST) on January 26, 2006. Sunitinib inhibits cellular signaling by targeting multiple RTKs. These include all platelet-derived growth factor receptors (PDGF-R) and vascular endothelial growth factor receptors (VEGF-R). Sunitinib also inhibits KIT (CD117), the RTK that drives the majority of GISTs. In addition, sunitinib inhibits other RTKs including RET, CSF-1R, and flt3.
Indication For the treatment of advanced renal cell carcinoma as well as the treatment of gastrointestinal stromal tumor after disease progression on or intolerance to imatinib mesylate.
Pharmacology Sunitinib is an oral, small-molecule, multi-targeted receptor tyrosine kinase (RTK) inhibitor that was approved by the FDA on January 26, 2006.
Affected Organisms
Humans and other mammals
Biotransformation Sunitinib is metabolized primarily by the cytochrome P450 enzyme, CYP3A4, to produce its primary active metabolite, which is further metabolized by CYP3A4.
Absorption Maximum plasma concentrations (Cmax) of sunitinib are generally observed between 6 and 12 hours (Tmax) following oral administration. Food has no effect on the bioavailability of sunitinib. Sunitinib may be taken with or without food.
Half Life Following administration of a single oral dose in healthy volunteers, the terminal half-lives of sunitinib and its primary active metabolite are approximately 40 to 60 hours and 80 to 110 hours, respectively.
Protein Binding Binding of sunitinib and its primary metabolite to human plasma protein in vitro was 95% and 90%, respectively.
Elimination Sunitinib is metabolized primarily by the cytochrome P450 enzyme, CYP3A4, to produce its primary active metabolite, which is further metabolized by CYP3A4. Elimination is primarily via feces. In a human mass balance study of [14C]sunitinib, 61% of the dose was eliminated in feces, with renal elimination accounting for 16% of the administered dose.
Distribution * 2230 L
Clearance * Oral cl=34 - 62 L/h
References
Motzer RJ, Hutson TE, Tomczak P, Michaelson MD, Bukowski RM, Rixe O, Oudard S, Negrier S, Szczylik C, Kim ST, Chen I, Bycott PW, Baum CM, Figlin RA: Sunitinib versus interferon alfa in metastatic renal-cell carcinoma. N Engl J Med. 2007 Jan 11;356(2):115-24. [Pubmed]
Demetri GD, van Oosterom AT, Garrett CR, Blackstein ME, Shah MH, Verweij J, McArthur G, Judson IR, Heinrich MC, Morgan JA, Desai J, Fletcher CD, George S, Bello CL, Huang X, Baum CM, Casali PG: Efficacy and safety of sunitinib in patients with advanced gastrointestinal stromal tumour after failure of imatinib: a randomised controlled trial. Lancet. 2006 Oct 14;368(9544):1329-38. [Pubmed]
External Links
Wikipedia
RxList
Drugs.com
DrugBank -  DB07417 external link
Drug information: experimental

参考文献

参考文献

供应商提供 Google Scholar IconGoogle Scholar PubMed iconPubMed Google Books IconGoogle Books
  • Motzer RJ, Hutson TE, Tomczak P, Michaelson MD, Bukowski RM, Rixe O, Oudard S, Negrier S, Szczylik C, Kim ST, Chen I, Bycott PW, Baum CM, Figlin RA: Sunitinib versus interferon alfa in metastatic renal-cell carcinoma. N Engl J Med. 2007 Jan 11;356(2):115-24. Pubmed
  • Demetri GD, van Oosterom AT, Garrett CR, Blackstein ME, Shah MH, Verweij J, McArthur G, Judson IR, Heinrich MC, Morgan JA, Desai J, Fletcher CD, George S, Bello CL, Huang X, Baum CM, Casali PG: Efficacy and safety of sunitinib in patients with advanced gastrointestinal stromal tumour after failure of imatinib: a randomised controlled trial. Lancet. 2006 Oct 14;368(9544):1329-38. Pubmed
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专利

专利

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