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MedKoo product information:
Sunitinib
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MedKoo Code#: 100790
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Name:
Sunitinib
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CAS#: 341031-54-7
Synonym: Synonym:
sunitinib. US brand name: Sutent. Abbreviation: SU11248;
Code names: SU011248; SU11248. Chemical structure name:
5-[5-fluoro-2-oxo-1,2-dihydroindol-(3Z)-ylidenemethyl]-2,4-dimethyl-1H-pyrrole-3-carboxylic
acid (2-diethylaminoethyl)amide)
IUPAC/Chemical name:
(Z)-N-(2-(diethylamino)ethyl)-5-((5-fluoro-2-oxoindolin-3-ylidene)methyl)-2,4-dimethyl-1H-pyrrole-3-carboxamide
malate
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Chemical structure:
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Theoretical analysis
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Sunitinib (free base form)
Chemical Formula: C22H27FN4O2
Exact Mass: 398.21180
Molecular Weight: 398.47
m/z: 398.21180 (100.0%), 399.21516 (23.8%),
400.21851 (2.7%), 399.20884 (1.5%)
Elemental Analysis: C, 66.31; H, 6.83; F,
4.77; N, 14.06; O, 8.03
Sunitinib malate
Chemical Formula: C26H33FN4O7
Molecular Weight: 532.56
Elemental Analysis: C, 58.64; H, 6.25; F,
3.57; N, 10.52; O, 21.03
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Availability and price:
Sunitinib (99%) is in stock.
For quotation, question, and order, please send email to
sales@medkoo.com to describe your needs. A representative
will respond your email shortly. We offer significant discount
for larger quantity order.
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Quality control
data:
Product will be shipped with
supporting analytical data.
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Information about this agent
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Sunitinib malate is the orally bioavailable malate salt of an
indolinone-based tyrosine kinase inhibitor with potential
antineoplastic activity. Sunitinib blocks the tyrosine kinase
activities of vascular endothelial growth factor receptor 2
(VEGFR2), platelet-derived growth factor receptor b (PDGFRb), and
c-kit, thereby inhibiting angiogenesis and cell proliferation. This
agent also inhibits the phosphorylation of Fms-related tyrosine
kinase 3 (FLT3), another receptor tyrosine kinase expressed by some
leukemic cells.
Sunitinib malate is a yellow to orange powder with a pKa of 8.95. The
solubility of sunitinib malate in aqueous media over the range pH 1.2 to
pH 6.8 is in excess of 25 mg/mL. The log of the distribution coefficient
(octanol/water) at pH 7 is 5.2. SUTENT (sunitinib malate) capsules are
supplied as printed hard shell capsules containing sunitinib malate
equivalent to 12.5 mg, 25 mg or 50 mg of sunitinib together with
mannitol, croscarmellose sodium, povidone (K-25) and magnesium stearate
as inactive ngredients. The orange gelatin capsule shells contain
titanium dioxide, and red iron oxide. The caramel gelatin capsule shells
also contain yellow iron oxide and black iron oxide. The printing ink
contains shellac, propylene glycol, sodium hydroxide, povidone and
titanium dioxide.
Sunitinib (marketed as Sutent by Pfizer, and
previously known as SU11248) 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 was
the first cancer drug simultaneously approved for two different
indications. Sunitinib has become a standard of care for both of these
cancers, and is currently being studied for the treatment of many
others.
According to
http://en.wikipedia.org/wiki/Sunitinib, Sunitinib is a standard of
care in the first-line treatment of metastatic RCC, other therapeutic
options in this setting are sorafenib (Nexavar), temsirolimus (Torisel)
and interleukin-2 (Proleukin). RCC is generally resistant to
chemotherapy or radiation. Prior to RTKs, metastatic disease could only
be treated with the cytokines interferon alpha (IFNα) or Interleukin 2
(IL-2). However, these agents demonstrated low rates of efficacy
(5%-20%). In two separate Phase II studies, sunitinib demonstrated
consistent response rates of approximately 40% in patients who had
already failed cytokine therapy. Although these were Phase II studies,
these results were impressive enough for the FDA to approve sunitinib
for first-line use even before Phase III data were available. The
results of the Phase III study, published in the New England Journal of
Medicine in 2007, proved that sunitinib offers superior efficacy
compared with IFNα. Progression-free survival (primary endpoint) was
more than doubled: 11 months for sunitinib compared with 5 months for
IFNα (P<.000001). The benefit for sunitinib was significant across all
major patient subgroups, including those with a poor prognosis at
baseline. Secondary endpoints also favored sunitinib. 28% of sunitinib
patients had significant tumor shrinkage (objective response) compared
with only 5% of patients who received IFNα (P<.001). Although overall
survival data are not yet mature, there is a clear trend toward improved
survival with sunitinib. Patients receiving sunitinib also reported a
significantly better quality of life than those treated with IFNα
(P<.001).
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13: Girardi F, Franceschi E, Brandes AA. Cardiovascular Safety of
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15: Kutach AK, Villaseñor AG, Lam D, Belunis C, Janson C, Lok S, Hong
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19: Bäuerle T, Merz M, Komljenovic D, Zwick S, Semmler W. Drug-induced
vessel remodeling in bone metastases as assessed by dynamic contrast
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21: Coriat R, Ropert S, Mir O, Billemont B, Chaussade S, Massault PP,
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23: von Bubnoff N, Rummelt C, Menzel H, Sigl M, Peschel C, Duyster J.
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24: Hanzer M, Nebl A, Spendel S, Pilhatsch A, Urban C, Benesch M.
Necrosis of a skin autograft after short-term treatment with sunitinib
in a 14-year-old girl with metastatic alveolar soft part sarcoma of the
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25: Sjölund K, Andersson A, Nilsson E, Nilsson O, Ahlman H, Nilsson B.
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26: van Erp NP, Baker SD, Zandvliet AS, Ploeger BA, den Hollander M,
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Marginal increase of sunitinib exposure by grapefruit juice. Cancer
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31: Schmidinger M, Arnold D, Szczylik C, Wagstaff J, Ravaud A.
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33: Hammers HJ, Verheul HM, Salumbides B, Sharma R, Rudek M, Jaspers J,
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42: Levashova Z, Backer M, Hamby CV, Pizzonia J, Backer JM, Blankenberg
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67: Norum J, Nieder C, Kondo M. Sunitinib, sorafenib, temsirolimus or
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68: Goemans BF, Zwaan CM, Cloos J, de Lange D, Loonen AH, Reinhardt D,
Hählen K, Gibson BE, Creutzig U, Kaspers GJ. FLT3 and KIT mutated
pediatric acute myeloid leukemia (AML) samples are sensitive in vitro to
the tyrosine kinase inhibitor SU11657. Leuk Res. 2010 Apr 30. [Epub
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69: Antoniu SA, Kolb MR. Intedanib, a triple kinase inhibitor of VEGFR,
FGFR and PDGFR for the treatment of cancer and idiopathic pulmonary
fibrosis. IDrugs. 2010 May;13(5):332-45. PubMed PMID: 20432191.
70: Scagliotti G, Govindan R. Targeting angiogenesis with multitargeted
tyrosine kinase inhibitors in the treatment of non-small cell lung
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73: Fléchon A, Boyle H, Négrier S. [Management of side effects
associated with antiangiogenic treatment in renal cell carcinoma]. Bull
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combined treatments]. Bull Cancer. 2010;97:65-71. French. PubMed PMID:
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75: Barrascout E, Medioni J, Scotte F, Ayllon J, Mejean A, Cuenod CA,
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activity of sorafenib, sunitinib and bevacizumab]. Bull Cancer.
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