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NVP-BEZ235, Free Base, >99% N-4288

NVP-BEZ235, Free Base, >99%
N-4288-50mg
N-4288-100mg
N-4288-200mg
N-4288-500mg

M.W. 469.54 C
30H23N5O [915019-65-7]
Storage
: Store at or below -20 ºC. Solubility: Soluble in
anhydrous dimethylformamide at 10 mg/mL after warming

to 75 °C and cooling; soluble in DMSO at 1.33 mg/mL
with warming; soluble in 1-methyl-2-pyrrolidinone at
about 2 mg/mL after warming to 75 °C and cooling; very
poorly soluble in ethanol; very poorly soluble in water;

maximum solubility in plain water is estimated to be about
10-20 µM; buffers, serum, or other additives may increase
or decrease the aqueous solubility.
• NVP-BEZ235 is an imidazo[4,5-c]quinoline derivative that
inhibits PI3K and mTOR kinase activity by binding to the ATPbinding cleft of these enzymes. NVP-BEZ235 is able to effectively
and specifically block the dysfunctional activation of the PI3K
pathway and induce G(1) arrest. It also inhibits the growth of
human cancer in animal models. Maira, S.M. et al., “Identification
and characterization of NVP-BEZ235, a new orally available dual
phosphatidylinositol 3-kinase/mammalian target of rapamycin
inhibitor with potent in vivo antitumor activity.”
Mol. Cancer Ther.
7
: 1851-1863 (2008).
• NVP-BEZ235 strongly inhibits VEGF-induced cell proliferation
and survival in vitro and VEGF-induced angiogenesis in vivo
.
Schnell, C.R. et al., “Effects of the Dual Phosphatidylinositol
3-Kinase/Mammalian Target of Rapamycin Inhibitor NVPBEZ235 on the Tumor Vasculature: Implications for Clinical
Imaging.” Cancer Res. 68
: 6598-6607 (2008).
• NVP-BEZ235 abrogated phosphatidylinositol 3-kinase
(PI3K)-induced lapatinib resistance. Eichhorn, P.J. et al.,
“Phosphatidylinositol 3-Kinase Hyperactivation Results
in Lapatinib Resistance that Is Reversed by the mTOR/
Phosphatidylinositol 3-Kinase Inhibitor NVP-BEZ235.”
Cancer Res. 68
: 9221-9230 (2008).
• NVP-BEZ235 induced melanoma cells to arrest in the G1 phase
of cell cycle, reduced cyclin D1 expression, and increased
p27(KIP1), but had negligible apoptotic activity. In a syngeneic
B16 mouse melanoma tumor model, NVP-BEZ235 significantly
attenuated tumor growth at primary and lymph node metastatic
sites without obvious toxicity. In addition, NVP-BEZ235 blocked
neovascularization and increased tumoral necrosis. Marone, R.,
et al., “Targeting melanoma with dual phosphoinositide 3-kinase/
mammalian target of rapamycin inhibitors.”
Mol. Cancer Res.
7
: 601-613 (2009).
• NVP-BEZ235 inhibits the PI3K/mTOR pathway and results in
inhibition of proliferation of cancer cells with both wild-type and
mutated p110α
. Serra, V. et al., “NVP-BEZ235, a dual PI3K/
mTOR inhibitor, prevents PI3K signaling and inhibits the growth
of cancer cells with activating PI3K mutations.”
Cancer Res.
68
: 8022-8030 (2008).
Sold for laboratory or manufacturing purposes only; not for
human, medical, veterinary, food, or household use.

• This product is offered for R&D use in accordance with (i) 35
USC 271(e)+A13(1) in the U.S.; (ii) Section 69.1 of Japanese
Patent Law in Japan; (iii) Section 11, No. 2 of the German Patent

Act of 1981 in Germany; (iv) Section 60, Paragraph 5b of the U.K.
Patents Act of 1977 in the U.K.; (v) Sections 55.2(1) and 55.2(6)
and other common law exemptions of Canadian patent law; (vi)
Section 68B of the Patents Act of 1953 in New Zealand together
with the amendment of same by the Statutes Amendment Bill of
2002; (vii) such related legislation and/or case law as may be or
become applicable in the aforementioned countries; and (viii) such
similar laws and rules as may apply in various other countries.

• Not available in some countries; not available to some institutions;
not available for some uses.