557795-19-4 Usage
Description
Sunitinib is an inhibitor of multiple receptor tyrosine kinases (RTKs) involved
in tumor proliferation and angiogenesis, including platelet-derived growth factor
receptors (PDGFR), vascular endothelial growth factor receptors (VEGFR), and
stem cell factor receptor (KIT). It was launched as an oral treatment for
gastrointestinal stromal tumors (GIST) and advanced renal-cell carcinoma (RCC).
In vitro, sunitib inhibits VEGFR2, PDGFRα, PDGFRβ, KIT, and FLT3 receptors
with IC50 values in the 4–14nM range, and the ligand-dependent autophosphorylation
of VEGFR2 and PDGFRb with IC50s of approximately 10 nM.
In addition, it inhibits the growth of tumor cells expressing dysregulated target RTKs in vitro and inhibits PDGFRb- and VEGFR2-dependent tumor angiogenesis
in vivo. Sunitinib exhibits broad and potent antitumor activity, causing regression
in murine models of human epidermal (A431), colon (Colo205 and HT-29), lung
(NCI-H226 and H460), breast (MDA-MB-435), prostate (PC3-3M-luc), and renal
(786-O) cancers, and suppressing or delaying the growth of many others,
including the C6 rat and SF763 T human glioma xenografts and B16 melanoma
lung cancer.
Chemical Properties
Yellow Solid
Originator
Sugen (US)
Uses
Different sources of media describe the Uses of 557795-19-4 differently. You can refer to the following data:
1. A multi-kinase inhibitor targeting several receptor tyrosine kinases (RTK). Antineoplastic
2. Sunitinib Malate is a multi-targeted RTK inhibitor targeting VEGFR2 (Flk-1) and PDGFRβ with IC50 of 80 nM and 2 nM, and also inhibits c-Kit.
Clinical Use
Tyrosine kinase inhibitor:
Treatment of metastatic renal cell carcinoma
(MRCC), gastrointestinal stromal tumours (GIST)
and pancreatic neuroendocrine tumours (pNET)
Drug interactions
Potentially hazardous interactions with other drugs
Antipsychotics: avoid with clozapine (increased risk
of agranulocytosis).
Antivirals: avoid concomitant use with boceprevir.
Avoid concomitant use with other inhibitors or
inducers of CYP3A4. Dose alterations may be
required.
Metabolism
Metabolised mainly via the cytochrome P450 isoenzyme
CYP3A4 to its primary active metabolite, which itself is
then further metabolised via CYP3A4.
Elimination is primarily via faeces. In a human mass
balance study of [14C]sunitinib, 61% of the dose was
eliminated in faeces and 16% by the renal route.
references
[1]hui ep1, lui vw, wong cs, ma bb, lau cp, cheung cs, ho k, cheng sh, ng mh, chan at. preclinical evaluation of sunitinib as single agent or in combination with chemotherapy in nasopharyngeal carcinoma. invest new drugs. 2011 dec;29(6):1123-31.
Check Digit Verification of cas no
The CAS Registry Mumber 557795-19-4 includes 9 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 6 digits, 5,5,7,7,9 and 5 respectively; the second part has 2 digits, 1 and 9 respectively.
Calculate Digit Verification of CAS Registry Number 557795-19:
(8*5)+(7*5)+(6*7)+(5*7)+(4*9)+(3*5)+(2*1)+(1*9)=214
214 % 10 = 4
So 557795-19-4 is a valid CAS Registry Number.
InChI:InChI=1/C22H27FN4O2.C4H4O4/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;5-3(6)1-2-4(7)8/h7-8,11-12,25H,5-6,9-10H2,1-4H3,(H,24,29)(H,26,28);1-2H,(H,5,6)(H,7,8)/b17-12-;2-1-
557795-19-4Relevant articles and documents
AMP-ACTIVATED PROTEIN KINASE INHIBITORS AND METHODS OF MAKING AND USING THE SAME
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Page/Page column 64-65; 66, (2021/01/23)
The present disclosure relates to compounds of Formula (I): (I); stereoisomers thereof, prodrugs thereof, and pharmaceutically acceptable salts thereof. The present disclosure also relates to uses of the compounds, e.g., to inhibit AMP-Activated protein kinase (AMPK) and treat cancer in a subject.
A high-purity malic acid lin's preparation method
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Paragraph 0042; 0043, (2019/04/04)
The invention relates to a high-purity malic acid lin's preparation method, the method comprises the following steps: (1) the formula II compound as a starting material, the use of 1 - ethyl - (3 - dimethyl amino propyl) carbonylamino-carbodiimide hydrochloride with 1 - hydroxy benzotriazole as the condensing agent, under certain temperature and N, N diethylethylenediamine reaction to obtain compound III; (2) in the step (1) the reaction solution, between the step (1) the resulting reactant with 5 - fluoro indole - 2 - one reaction at certain temperature, to obtain compound IV; (3) in the step (2) of the reaction solution, so that the step (1) the resulting reactant with L - malic acid reaction at certain temperature, to obtain compound I; providing at least to a certain extent one of the solve the above technical problems or at least provide a useful commercial choice. The reaction route is operating time is short, simple operation, reaction system is stable, higher product yield, purity of the product is relatively high, it is suitable for industrial production.
Unique physicochemical and catalytic properties dictated by the B3NO2 ring system
Noda, Hidetoshi,Furutachi, Makoto,Asada, Yasuko,Shibasaki, Masakatsu,Kumagai, Naoya
, p. 571 - 577 (2017/06/01)
The expansion of molecular diversity beyond what nature can produce is a fundamental objective in chemical sciences. Despite the rich chemistry of boron-containing heterocycles, the 1,3-dioxa-5-aza-2,4,6-triborinane (DATB) ring system, which is characterized by a six-membered B3NO2 core, remains elusive. Here, we report the synthesis of m-terphenyl-templated DATB derivatives, displaying high stability and peculiar Lewis acidity arising from the three suitably arranged boron atoms. We identify a particular utility for DATB in the dehydrative amidation of carboxylic acids and amines, a reaction of high academic and industrial importance. The three boron sites are proposed to engage in substrate assembly, lowering the entropic cost of the transition state, in contrast with the operative mechanism of previously reported catalysts and amide coupling reagents. The distinct mechanistic pathway dictated by the DATB core will advance not only such amidations, but also other reactions driven by multisite activation.
