Catalog No.S1034 Synonyms: AEW541

NVP-AEW541 Chemical Structure

Molecular Weight(MW): 439.55

NVP-AEW541 is a potent inhibitor of IGF-1R/InsR with IC50 of 150 nM/140 nM in cell-free assays, greater potency and selectivity for IGF-1R in a cell-based assay.

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In DMSO USD 414 In stock
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7 Customer Reviews

  • (A) KRAS mutant (SW837 and LoVo) or KRAS/PIK3CA mutant (HCT-116) colorectal cancers were treated with the indicated compounds for 6 hours (gef, gefitinib 1 μM; NVP, NVP-AEW541 1 μM; PHA, PHA-665752 1 μM), and the resulting protein lysates were immunoprecipitated with an anti-p85 antibody. The precipitated proteins were analyzed by Western blots with the indicated antibodies. Whole cell extracts were probed with the indicated antibodies. Asterisks indicate the IRS proteins for SW837 and HCT-116 cells, and ERBB3 for LoVo cells. (B) SW837 cells were grown in either normal serum (5% FBS) or low serum (0.5% FBS) and treated with vehicle, R1507 anti–IGF-IR antibody (25 μg/ml), or NVP-AEW541 (1 μM) for 6 hours. The cells were lysed and probed with the indicated antibodies.

    J Clin Invest 2011 121, 4311-21. NVP-AEW541 purchased from Selleck.

    A, cell viability reduction. TC1889 cells were treated with pharmacological inhibitors against IGF-1R (NVP and BMS), as well as a neutralizing IGF-1R antibody (aIR3) and cell viability was assessed using MTT-assays. Mouse IgG1 antibody was employed as a reference control for the effects of aIR3 at respective concentrations. Assays were performed in sextuple. Data are expressed as the mean SD (n 3). B, induction of cell death. TC1889 cells were treated with pharmacological inhibitors against IGF-1R as well as a neutralizing IGF-1R antibody and cell death was evaluated by FACS-analyses following PI-staining. Data are expressed as the mean SD (n ?3).

    Clin Cancer Res 2011 17, 2237-2249. NVP-AEW541 purchased from Selleck.

  • C, TC1889 cells were serum-starved for 16 hours, treated with vehicle or the IGF-1R inhibitor PPP, NVP, BMS, or the neutralizing IGF1R antibody aIR3 for 2 hours, and then stimulated with IGF-I (100 ng/mL) for 15 min. The activity of PI3K/Akt- and MAPK/Erk-signaling was investigated by an analysis of the expression of phosphorylated Akt, GSK3b, MEK1/2, and Erk using Western immunoblotting. Representative results are shown (n ?3). Actin served as a loading control. D, TC1889 cells were treated with vehicle or PPP, NVP, BMS, or aIR3. The activity of PI3K/Akt- and MAPK/Erk-signaling was investigated as mentioned earlier. Representative results are shown (n ?3). Actin served as a loading control.

    Clin Cancer Res 2011 17, 2237-2249. NVP-AEW541 purchased from Selleck.

    A, cell viability assay for mouse rhabdomyosarcoma cultures treated with various doses of NVP-AEW541 and immunoblot showing expression levels of Igf1r in mouse rhabdomyosarcoma primary cell cultures (U20325 and U21089) compared with the mouse myoblast cell line C2C12. B, anchorage-dependent colony formation assay showing increased inhibition of colony formation by mouse rhabdomyosarcoma cultures compared to mouse myoblast cell line C2C12 on treatment with increasing doses of NVPAEW541. C, anchorageindependent colony formation by mouse rhabdomyosarcoma cultures (U20325) is inhibited on treatment with NVP-AEW541, indicated by a decrease in colony size. The scale bar represents 50mm. The number of colonies formed in soft agar also is reduced on treatment with NVP-AEW541. D, Western blot showing decrease in the phosphorylation of Igf1r, P70 S6 kinase, IRS1, Akt, Mapk, and Shc on treatment of the mouse rhabdomyosarcoma primary cell cultures (U20325) with increasing amounts of NVPAEW541.

    Mol Cancer Ther 2011 10:697-707. NVP-AEW541 purchased from Selleck.

  • A, treating the mouse rhabdomyosarcoma primary cell cultures (U20325) with increasing amount of NVP-AEW541 induces cell cycle arrest in the G1 phase. B, at moderately high concentrations of NVP-AEW541, the mouse rhabdomyosarcoma cells (U20325) show increased apoptosis as evident by the presence of cleaved caspase-3 at 5 mmol/L (but not at 2 mmol/L, unpublished data). C, representative (median) images of luminescence emitted by rhabdomyosarcoma primary cell cultures grown on quail CAM and being treated with DMSO, imatinib, and NVP-AEW541. The images are displayed with a minimum–maximum scale of 2 106 to 2 107 photons/s/cm2/steradian. D, graphical representation of the intensity of bioluminescence signal emitted by rhabdomyosarcoma primary cell cultures grown on quail CAM that were being treated with DMSO, imatinib (100 mmol/L), or NVPAEW541(10 mmol/L).

    Mol Cancer Ther 2011 10:697-707. NVP-AEW541 purchased from Selleck.

    Combination of NVP-AEW541 and lapatinib cooperatively inhibits the growth of NVP-AEW541 resistant murine rhabdomyosarcoma primary cell cultures with Igf1r/Her2 complexes. Cell viability assay for Naïve, untreated (U20325; A) and NVP-AEW541 innately resistant mouse rhabdomyosarcoma primary culture (U44676; B) treated with varying concentrations of NVP-AEW541, lapatinib, or a combination of both. Naïve cells (U20325) were sensitive to NVP-AEW541, but lapatinib had no cooperativity. In contrast, NVP-AEW541 at moderate doses increased cell growth in resistant cell cultures (U44676). However, this paradoxical effect was reduced by the addition of lapatinib, although lapatinib treatment alone had very little effect. C, the NVP-AEW541 resistant primary tumor cell line (U44676) was treated with DMSO, 5mmol/L lapatinib, 5 mmol/L NVP-AEW541, and a combination of 5 mmol/L NVP-AEW541 t lapatinib for 25 minutes and Western blot analysis was done on lysates for p-Igf1r and p-Her2.

    Mol Cancer Ther 2011 10, 697-707. NVP-AEW541 purchased from Selleck.

  • Inhibition of IGF-IR/InsR or PI3K abrogates AKT membrane localization and phosphorylation. MCF-7/LTED cells were transfected with an AKT PH-GFP plasmid. On day four, cells were treated with 100 ng/ml IGF-I in serum-free medium for 15 minutes, or pre-incubated with 10% DCC-FBS ?1 uM AEW541 or 1 uM BKM120 for 30 minutes followed by treatment with 2 uM AZD5363 for four hours. Cells were viewed in a LSM 510Meta confocal microscope at 40x magnification.

    Breast Cancer Res 2013 15, R55. NVP-AEW541 purchased from Selleck.

Purity & Quality Control

Choose Selective IGF-1R Inhibitors

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2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.

Biological Activity

Description NVP-AEW541 is a potent inhibitor of IGF-1R/InsR with IC50 of 150 nM/140 nM in cell-free assays, greater potency and selectivity for IGF-1R in a cell-based assay.
Insulin Receptor [1]
(Cell-free assay)
IGF-1R [1]
(Cell-free assay)
FLT3 [1]
(Cell-free assay)
Tek [1]
(Cell-free assay)
FLT1 [1]
(Cell-free assay)
0.14 μM 0.15 μM 0.42 μM 0.53 μM 0.6 μM
In vitro

NVP-AEW541 also inhibits InsR, Tek, Flt1 and Flt3 with IC50 of 140 nM, 530 nM, 600 nM and 420 nM in purified kinases/recombinant kinase domains assay. NVP-AEW541 is more selective and shows 27-fold more potent than InsR at the cellular level. NVP-AEW541 suppresses the IGF-I-mediated survival, soft agar and proliferation of MCF-7 cells with IC50 of 0.162 μM, 0.105 μM and 1.64 μM, respectively. NVP-AEW541 also reduces the level of phospho-IGF-1R and phospho-PKB in NWT-21 cells. [1] NVP-AEW541 shows growth inhibitory effect on TC-71 musculoskeletal sarcoma cells in low-serum medium as well as in 10% FBS–containing medium. NVP-AEW541 inhibits cell cycle progression and induces specific G1 arrest in sarcoma cell lines (TC-71, SK-N-MC, SaoS-2, RD/18 and RH4). [2] NVP-AEW541 could inhibit the growth of human neuroblastoma cells with IC50 of 0.4-6.8 μM. An increase in the hypodiploid fraction and the depletion of the S and G2-M compartments could be detected in these cell lines. NVP-AEW541-driven inhibition of IGF-1R causes a reduction of phosphorylation of Akt, but not of Erk1 and Erk2 in neuroblastoma cells. [3] NVP-AEW541 inhibits glioma cell growth and disrupts the autocrine loop initiated by HIF1α stabilization. [4] A recent study shows that NVP-AEW541 suppresses the proliferation and viability of PC3, DU145, and 22Rv1 prostate cancer cells, without necessarity of associated cell death. NVP-AEW541 decreases phospho-Akt levels in 22Rv1 and DU415 cells but not PC3 cells, without affecting total Akt levels, which shows that PTEN status could determine the effectiveness of NVP-AEW541 with essential Akt. NVP-AEW541-induced radiosensization is dependent on Akt activation status. NVP-AEW541 could increase the H2AX phosphorylation (a measure of DSBs) in PC3, DU145, and 22Rv1 cells. [5]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
A431  NFSwTWhMcW6jc3WgZZN{[Xl? MkP4glEx6oDMzszN NVvsR2VZTE2VTx?= NHv1fZJqdmirYnn0d{BJTVJzIIfpeIghUUN3MDDv[kA,OTBizszN NYHFWW1WOTVyNUC5NVU>
A31  M3n2dmtqdmG|ZTDhd5NigQ>? NF74cpJ,OTEkgJtOwG0> MVnEUXNQ NYnINYJycW6qaXLpeJMhWESJRmKge4l1cCCLQ{WwJI9nKD5zMDFOwG0> M{mwUVE2ODVyOUG1
GIST882 M3\mRWtqdmG|ZTDhd5NigQ>? M{PY[54yOOLCit88US=> MX;EUXNQ NGO5VVlqdmirYnn0d{BkNUurdDD3bZRpKEmFNUCgc4YhRjVizszN MVGxOVA2ODlzNR?=
32D-Bcr-Abl M4q4O2tqdmG|ZTDhd5NigQ>? MYT+NVDjiIsQvF2= M33zOmROW09? NX3YPWFIcW6qaXLpeJMhSmO{LVHicEBxOjFyIIfpeIghUUN3MDDv[kA,OTBizszN NGX6fWUyPTB3MEmxOS=>
NWT-21 M1zWc2dzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NH3obm1FVVOR NHLyeYRKSzVyPUCuNVY{KM7:TR?= NYfXcVVPOTVyNUC5NVU>
TC-71 MkLqS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? NFi4c3N,OSEQvF2= MmWwSG1UVw>? MYDpcohq[mm2czDpcpN2dGmwLXzpb4Uh\3Kxd4ToJIZi[3Sxcj3J5qCUdWWmaXH0[YQh\3Kxd4To Mn\0NVU5Pjd|OE[=
TC-71 MojVS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? MoXrglfjiIsQvF2= MUjEUXNQ MX3JR|UxRDBwNTFOwG0> M{T3SFE2QDZ5M{i2
Saos-2 M1XD[Gdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NGPPS2d,P+LCit88US=> M{XpTGROW09? M1rXXGlEPTB:MzFOwG0> MnrENVU5Pjd|OE[=
U-2OS M4rqe2dzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MnfoglfjiIsQvF2= Mm\ISG1UVw>? NFvkOYpKSzVyPECuOUDPxE1? MWOxOVg3PzN6Nh?=
SK-N-MC NWmwcll1T3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= M1THUJ446oDMzszN M3noc2ROW09? Mn2wTWM2ODxyLkWg{txO NHXvN3UyPTh4N{O4Oi=>
RD-ES Mnu2S5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? NEXiTop,P+LCit88US=> NYThcIhDTE2VTx?= MWjJR|UxRDBwNTFOwG0> MWexOVg3PzN6Nh?=
SJ-Rh 30 MkjFS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? MVL+O-KBks7:TR?= Ml31SG1UVw>? NXe5cIhKUUN3MEywMlUh|ryP NUTwO|JyOTV6NkezPFY>
SJ-Rh 4 NH3Ec5dIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= MkXyglfjiIsQvF2= NG\jcnpFVVOR NYf6eJFvUUN3MEywMlUh|ryP MUCxOVg3PzN6Nh?=
6647 NECxWIJIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NHq3S2p,P+LCit88US=> MVHEUXNQ M2DTd2lEPTB:MD61JO69VQ>? NFS5W5gyPTh4N{O4Oi=>
SARG MnzOS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? NEO4Rpp,P+LCit88US=> MnjPSG1UVw>? NXj0U2FrUUN3MEyzJO69VQ>? M1nJb|E2QDZ5M{i2
MOS MmHkS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? MmjFglfjiIsQvF2= NHrhV2JFVVOR NY[0[JVSUUN3MEy0JO69VQ>? MlfqNVU5Pjd|OE[=
IOR/OS7 M{PvZWdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NV30cIQ4hjgkgJtOwG0> NVHzdIQyTE2VTx?= MoLITWM2ODxzIN88US=> MVSxOVg3PzN6Nh?=
IOR/OS9 M3zIcmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NWntOXlYhjgkgJtOwG0> NXrsXYY6TE2VTx?= NYDq[WtYUUN3MEy2JO69VQ>? NWTnSVV3OTV6NkezPFY>
IOR/OS10 MV7Hdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? M{WwOJ446oDMzszN MXvEUXNQ NFfWU21KSzVyPEWg{txO MWWxOVg3PzN6Nh?=
IOR/OS14 NGTldIJIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= M17xR5446oDMzszN MVLEUXNQ NYLuSoZkUUN3MEy0JO69VQ>? M4jaUFE2QDZ5M{i2
LAP35 MVLHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? MWX+O-KBks7:TR?= NXHLO4VxTE2VTx?= M3LUd2lEPTB:MD61JO69VQ>? NYHreJc{OTV6NkezPFY>
IOR/BRZ MlTSS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? NGTrWG9,P+LCit88US=> MYjEUXNQ NWnNSWpbUUN3MEywMlUh|ryP MUixOVg3PzN6Nh?=
IOR/CAR MVzHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? MnXJglfjiIsQvF2= MYLEUXNQ NHTVO3RKSzVyPEGg{txO MY[xOVg3PzN6Nh?=
IOR/RCH MmL4S5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? NH\leY5,P+LCit88US=> Mmi1SG1UVw>? NUjWcIdnUUN3MEywMlUh|ryP NWG2PYt7OTV6NkezPFY>
RMZ-RC2 MofQS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? MlHIglfjiIsQvF2= NUHDdYJyTE2VTx?= NGjhNWhKSzVyPECuOUDPxE1? NVvp[3Z4OTV6NkezPFY>
CCA MVjHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? MnnIglfjiIsQvF2= M1nCV2ROW09? NE\DSYJKSzVyPEKg{txO M3nTTlE2QDZ5M{i2
RD/18 M{iwbmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MYn+O-KBks7:TR?= M37kSWROW09? NVHxeGU3UUN3MEy0JO69VQ>? Mli1NVU5Pjd|OE[=
OVCAR-3 M{LZ[2dzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MoS1glE26oDMzszN MYfEUXNQ Mn[zbY5pcWKrdIOgZ4VtdCCycn;sbYZmemG2aX;u MlfxNVY{ODB6MkC=
OVCAR-4 NYPvdZVDT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NVPrcmRXhjF34pEK{txO MV\EUXNQ MmrTbY5pcWKrdIOgZ4VtdCCycn;sbYZmemG2aX;u MXqxOlMxODh{MB?=
OVCAR-3 NHWzSHlCeG:ydH;zbZMh[XO|YYm= Ml3ZglE26oDMzszN MnK3SG1UVw>? Mm\ibY5lfWOnczDhdI9xfG:|aYO= NYPNXFN1OTZ|MEC4NlA>
OVCAR-4 M175Z2Fxd3C2b4Ppd{Bie3OjeR?= MkO5glE26oDMzszN M1y3e2ROW09? MWXpcoR2[2W|IHHwc5B1d3Orcx?= M3vlXlE3OzByOEKw
OVCAR-3 MXnGeY5kfGmxbjDhd5NigQ>? MYL+NVXjiIsQvF2= Mmq5SG1UVw>? M2fGbmRm[3KnYYPld{BxcG:|cHjvdplt[XSrb36gc4YhSUuW NUXEN40zOTZ|MEC4NlA>
Huh-7 M{X0cmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MWL+NVDjiIsQvF2= NIKxSYpFVVOR MXPJR|UxRTFwNDFOwG0> NXLoXXdlOTZ3M{C3N|Q>
Hep-G2 NFfjSZNIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= Ml7EglEx6oDMzszN MoXmSG1UVw>? NYHBboVYUUN3ME2xMlgh|ryP MYexOlU{ODd|NB?=
Hep-3B NFuxZo9Iem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NX;zZ5U6hjFy4pEK{txO NXzPdFFYTE2VTx?= NHfhS4lKSzVyPUGuPUDPxE1? MYexOlU{ODd|NB?=
SK-Hep-1 NX76dnZ2T3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= M{DLW54yOOLCit88US=> MmPNSG1UVw>? MXrJR|UxRTZwOTFOwG0> MX2xOlU{ODd|NB?=
Huh-7 MYfGeY5kfGmxbjDhd5NigQ>? MWj+NVDjiIsQvF2= NWHUbmUzTE2VTx?= MXjJcoR2[2W|IHPlcIwh[3mlbHWgZZJz\XO2 M3LpcVE3PTNyN{O0
Hep-G2 MYrGeY5kfGmxbjDhd5NigQ>? NGPpU45,OTEkgJtOwG0> MmPkSG1UVw>? M2fNbGlv\HWlZYOgZ4VtdCCleXPs[UBienKnc4S= NHrzfpgyPjV|MEezOC=>
SK-Hep-1 MlnJSpVv[3Srb36gZZN{[Xl? M2DzU54yOOLCit88US=> NWfPcYNGTE2VTx?= NE\vc4VKdmS3Y3XzJINmdGxiY4njcIUh[XK{ZYP0 MmTvNVY2OzB5M{S=
BON NFT3Z5VMcW6jc3WgZZN{[Xl? M1HY[Z43KM7:TR?= MVfEUXNQ MoPmbY5lfWOnczDk[ZBpd3OyaH;yfYxifGmxbjDv[kBKT0ZvMWK= MXKxOlYxOTJ6NB?=
CM Mn71S5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? MkXRglXjiIsQvF2= NH3ZWWdFVVOR MnjVTWM2OD1|LkOg{txO MlSwNVY3ODF{OES=
BON M1HzSWZ2dmO2aX;uJIF{e2G7 NUTVOYoyhjdwNfMAju69VQ>? M37lW2ROW09? MkSzbY5lfWOnczDj[YxtKGO7Y3zlJIFzemW|dB?= NUmwTo5XOTZ4MEGyPFQ>
CM NEfsU|FHfW6ldHnvckBie3OjeR?= NFG0RW1,PeLCit88US=> NEfqXVNFVVOR MWrpcoR2[2W|IHPlcIwh[3mlbHWgZZJz\XO2 MU[xOlYxOTJ6NB?=
BON NF3QcXRCeG:ydH;zbZMh[XO|YYm= NGH0WXl,Py534pEK{txO NGnKZYFFVVOR NGfDcmRqdmS3Y3XzJGFxd3C2b4Ppdy=> NHuxXFkyPjZyMUK4OC=>
HT-29 NUjV[2dpT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= MljOglEx6oDMzszN NIHJcYxFVVOR NWL4bYdXUUN3ME2xMlch|ryP NEDPOZkyPzByN{CxOS=>
HCT-116 MWrHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? M4\jR54yOOLCit88US=> NV\sT5VITE2VTx?= M4f0dmlEPTB;Mj61JO69VQ>? NVXXUYEyOTdyMEewNVU>
primary colorectal cancer cells M4jmT2Z2dmO2aX;uJIF{e2G7 NGnLeXB,PeLCit88US=> NEfvbGVFVVOR MVHhcJRmenNidHjlJI1wenCqb3zv[5khd2ZidHjlJJJmdWGrbnnu[{Bk\Wyucx?= MVKxO|AxPzBzNR?=
HTLA-230 Mlf5SpVv[3Srb36gZZN{[Xl? M{\DSJ45KM7:TR?= NXjJbZVLTE2VTx?= M1fFZ4lvcGmkaYTzJGlITi2LST3t[YRq[XSnZDDzeIlufWyjdHnvckBw\iCLR1[tTXIh[W6mIFHreC=> MmfCNVcyOjF6OUi=
KCNR M3n6bWZ2dmO2aX;uJIF{e2G7 M3HlWJ45KM7:TR?= M{XMOWROW09? MX;pcohq[mm2czDJS2YuUUlvbXXkbYF1\WRic4TpcZVt[XSrb36gc4YhUUeILVnSJIFv\CCDa4S= M3TY[|E4OTJzOEm4
SK-N-BE2c NWn3U4I6TnWwY4Tpc44h[XO|YYm= NHPuWol,QCEQvF2= NGL0eIVFVVOR MUTpcohq[mm2czDJS2YuUUlvbXXkbYF1\WRic4TpcZVt[XSrb36gc4YhUUeILVnSJIFv\CCDa4S= M1y0NVE4OTJzOEm4
SK-N-BE NVjMRZVsTnWwY4Tpc44h[XO|YYm= NX;qR|FQhjhizszN NH;CNFBFVVOR NG[1R3pqdmirYnn0d{BKT0ZvSVmtcYVlcWG2ZXSgd5RqdXWuYYTpc44hd2ZiSVfGMWlTKGGwZDDBb5Q> NYTrN5psOTdzMkG4PVg>
LAN-5 MVHGeY5kfGmxbjDhd5NigQ>? NVuzPGR5hjhizszN NFuycGhFVVOR NYXwbWJWcW6qaXLpeJMhUUeILVnJMY1m\GmjdHXkJJN1cW23bHH0bY9vKG:oIFnHSk1KWiCjbnSgRYt1 NYPUXpQ2OTdzMkG4PVg>
GI-CA-N M2HCOGZ2dmO2aX;uJIF{e2G7 NFG3VpJ,QCEQvF2= NWOxN2txTE2VTx?= MVvpcohq[mm2czDJS2YuUUlvbXXkbYF1\WRic4TpcZVt[XSrb36gc4YhUUeILVnSJIFv\CCDa4S= MX[xO|EzOTh7OB?=
SH-EP MmfISpVv[3Srb36gZZN{[Xl? M4rNbp45KM7:TR?= MUjEUXNQ Ml\GbY5pcWKrdIOgTWdHNUmLLX3l[IlifGWmIIP0bY12dGG2aX;uJI9nKEmJRj3JVkBidmRiQXv0 M2m1cFE4OTJzOEm4
RN-GA NInRNYlHfW6ldHnvckBie3OjeR?= MlTTglgh|ryP NIPRWJlFVVOR M{PaZolvcGmkaYTzJGlITi2LST3t[YRq[XSnZDDzeIlufWyjdHnvckBw\iCLR1[tTXIh[W6mIFHreC=> M2\qcFE4OTJzOEm4
SY-5Y(N) MoTISpVv[3Srb36gZZN{[Xl? NI\vb|F,QCEQvF2= M4rXbmROW09? MljsbY5pcWKrdIOgTWdHNUmLLX3l[IlifGWmIIP0bY12dGG2aX;uJI9nKEmJRj3JVkBidmRiQXv0 NH;KdngyPzF{MUi5PC=>
GI-CA-N M2jw[mdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 M1yzNJ45KM7:TR?= MkfPSG1UVw>? M3ztXWlEPTB;IE[uPEDPxE1? NGfU[mkyPzF{MUi5PC=>
SH-EP MWHHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? M3vEXJ45KM7:TR?= MnvhSG1UVw>? M3vYNWlEPTB;IEOg{txO M{D4OFE4OTJzOEm4
HTLA-230 NVLpWmw5T3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= M2TyfJ45KM7:TR?= MoDYSG1UVw>? NYfJNFNRUUN3ME2gNE42KM7:TR?= MlKwNVcyOjF6OUi=
SK-N-BE2c NVXPcZczT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NH:yVo5,QCEQvF2= MlO5SG1UVw>? M{CxSmlEPTB;IEGuNUDPxE1? NELj[lUyPzF{MUi5PC=>
SK-N-BE2 MV7Hdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? NILSeI1,QCEQvF2= NY\HWGNHTE2VTx?= MlvOTWM2OD1iMzFOwG0> NHraflIyPzF{MUi5PC=>
SY-5Y (N) M4HRdGdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MmTmglgh|ryP NY[1d4I{TE2VTx?= M2\yb2lEPTB;IEKuOEDPxE1? MnXPNVcyOjF6OUi=
LAN-5 MoiwS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? NF7ScFB,QCEQvF2= M2m2SGROW09? NWO1bVFbUUN3ME2gNE41KM7:TR?= MWexO|EzOTh7OB?=
KCNR Ml3BS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? M2jXdp45KM7:TR?= NYjFZ2JVTE2VTx?= MXrJR|UxRSByLkSg{txO NEjSTo8yPzF{MUi5PC=>
RN-GA MXnHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? MlHhglgh|ryP MlPvSG1UVw>? M1;yRWlEPTB;IEGuN{DPxE1? MV[xO|EzOTh7OB?=
SK-N-AS NFjvemVIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= M4[5dp45KM7:TR?= MVvEUXNQ MYHpcoR2[2W|IHHwc5B1d3Orcx?= MU[xO|EzOTh7OB?=
KCNR Mn\FRZBweHSxc3nzJIF{e2G7 MlPOglgh|ryP MVzEUXNQ MUfpcoR2[2W|IHHwc5B1d3Orcx?= MWexO|EzOTh7OB?=
GI-CA-N NEKze5BCeG:ydH;zbZMh[XO|YYm= NUWwfVhXhjhizszN NIH2RnZFVVOR M1vmZ4lv\HWlZYOgZZBweHSxc3nz M1uzcVE4OTJzOEm4
SK-N-BE2c MkiyRZBweHSxc3nzJIF{e2G7 NWTURpo4hjhizszN NF;WeGhFVVOR MXfpcoR2[2W|IHHwc5B1d3Orcx?= MYmxO|EzOTh7OB?=
SY-5Y (N) NUDlPYQ3SXCxcITvd4l{KGG|c3H5 Mn3lglgh|ryP NVf1fXpITE2VTx?= Ml7WbY5lfWOnczDhdI9xfG:|aYO= M3rsXlE4OTJzOEm4
HL60AR NWPyV45TTnWwY4Tpc44h[XO|YYm= NGTrRnIyPjBibl2= NEjNNo9mdmijbnPld{B1cGVibHX2[Yx{KG:oIICyO2tqeDF? Mk\TNVc{PjF{MkW=
HL60AR MXrBdI9xfG:|aYOgZZN{[Xl? MkK0glIxOCCwTR?= NH3xeI1qdmS3Y3XzJIFxd3C2b4Ppdy=> MoqwNVc{PjF{MkW=
HPAF-II NGKweYFMcW6jc3WgZZN{[Xl? NVn2UopYhjFizszN NFXKS2NFVVOR MWXpcohq[mm2czDJS2YuUS2vZXTpZZRm\CC|aXfuZYxtcW6p NWrzRm5{OTh2NEW1NlA>
HPAF-II M4O3OWdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 M4PIXp4zKM7:TR?= NGHpe3pFVVOR NHm4OJBqdmirYnn0d{Bk\WyuIIDyc4xq\mW{YYTpc44> MknjNVg1PDV3MkC=
HPAF-II NEDkdJhHfW6ldHnvckBie3OjeR?= M{XYN54zKM7:TR?= M3;SfmROW09? MkXzbY5pcWKrdIOgZoF{[WxiYX7kJGlITi2LLX3l[IlifGWmIIDhcoNz\WG2aXOgZ4Fv[2W{IHPlcIwhdWmpcnH0bY9v NIXGeFQyQDR2NUWyNC=>
TFK-1 NV7FWmJnT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= Ml3VglI2OCCwTR?= Mn7LSG1UVw>? NFXiUYNKSzVyPUCuNlYh|ryP NYPEWJB2OjByNk[3N|Q>
CC-LP-1 NXLBdWZZT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NHfHe|N,OjVyIH7N NUPod5pmTE2VTx?= MVLJR|UxRTBwMUWg{txO NVXhZ3NnOjByNk[3N|Q>
CC-SW-1 MV;Hdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? Ml;DglI2OCCwTR?= MVzEUXNQ M4iwdmlEPTB;MD61OEDPxE1? MV6yNFA3Pjd|NB?=
Sk-ChA-1 Mlj6S5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? MlnLglI2OCCwTR?= NILC[|hFVVOR NFPHbJlKSzVyPUCuNkDPxE1? NIXuW|IzODB4NkezOC=>
Mz-ChA-1 M1i0[mdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MUj+NlUxKG6P Ml[2SG1UVw>? M2HjcWlEPTB;MT6zPUDPxE1? M2ThflIxODZ4N{O0
Mz-ChA-2 M1\0dmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MmjuglI2OCCwTR?= MXvEUXNQ NH6yVGxKSzVyPUCuO|Mh|ryP MnnsNlAxPjZ5M{S=
Ishikawa NVT0RZZxU2mwYYPlJIF{e2G7 Mo\iglExKM7:TR?= M4\3cGROW09? MlXWbY5pcWKrdIOgTWdHNUmUIHHjeIl3[XSrb36gZpkhQTNn NWTO[JBjOjF{OUWzN|U>
USPC-1 M1\JN2tqdmG|ZTDhd5NigQ>? Ml3DglExKM7:TR?= NXu0PFZ[TE2VTx?= MlK4bY5pcWKrdIOgTWdHNUmUIHHjeIl3[XSrb36gZpkhOTByJR?= MUWyNVI6PTN|NR?=
ECC-1 NXLURWZ[T3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NV7mNZRNhjFyIN88US=> NYjPe25sTE2VTx?= NILMWFFl\WO{ZXHz[ZMh[2WubDDwdo9tcW[ncnH0bY9v NX;hXlh3OjF{OUWzN|U>
Ishikawa NHracYlIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= M1TyXZ4yOCEQvF2= MYHEUXNQ NGrMcnRl\WO{ZXHz[ZMh[2WubDDwdo9tcW[ncnH0bY9v NUDIVJdEOjF{OUWzN|U>
USPC-1 NF\NZ49Iem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NVWzeWV3hjFyIN88US=> MX3EUXNQ MlXj[IVkemWjc3XzJINmdGxicILvcIln\XKjdHnvci=> MWeyNVI6PTN|NR?=
USPC-2 NGn1[XhIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NGXyd3V,OTBizszN NFPxWJVFVVOR MVXk[YNz\WG|ZYOgZ4VtdCCycn;sbYZmemG2aX;u Mmf2NlEzQTV|M{W=

... Click to View More Cell Line Experimental Data

In vivo NVP-AEW541 (50 mg/kg, p.o.) results in abrogation of basal and IGF-I-induced receptor, and PKB and MAPK phosphorylation, with T/C value of 14% in the NWT-21 tumor xenograft. [1] NVP-AEW541 (50 mg/kg) causes tumor shrinkage in both HTLA-230 and SK-N-BE2c xenografts, without signs of systemic toxicity. NVP-AEW541 could inhibit tumor invasion both in Matrigel-coated chambers and in HTLA-230 xenografts. [3]


Kinase Assay:[1]
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In vitro kinase assays:

NVP-AEW541 is dissolved in DMSO (10 mM) and stored at -20 °C. Dilutions are freshly made in DMSO/water 1:1. The final concentration of DMSO in the enzyme assays is <0.5 %. The protein kinase assays are carried out in 96-well plates at RT and terminated by the addition of 20 μL of 125 mM EDTA. Subsequently, 30 μL (c-Abl, c-Src, IGF-1R) of the reaction mixture are transferred onto Immobilon-PVDF presoaked for 5 min with methanol, rinsed with water, then soaked for 5 min with 0.5 % H3PO4 and mounted on vacuum manifold. After spotting all samples, vacuum is connected and each well rinsed with 200 μL 0.5 % H3PO4. Membranes are removed and washed 4× on a shaker with 1.0 % H3PO4, once with ethanol. After drying, mounting in Packard TopCount 96-well frame, and adding of 10 μL/well of Microscint, membranes are counted. IC50 values are calculated by linear regression analysis of the percentage inhibition of NVP-AEW541 in duplicate, at four concentrations (usually 0.01, 0.1, 1, and 10 μM). One unit of protein kinase activity is defined as 1 nmol of 33P transferred from [γ33P]ATP to the substrate protein per minute per mg of protein at 37 °C.
Cell Research:[1]
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  • Cell lines: MCF-7 cells
  • Concentrations: ~ 10 μM
  • Incubation Time: 72 hours
  • Method: Between 3 × 103 and 6 × 103 cells/well are seeded in 96-well plates with a total media volume of 100 μL/well. Increasing concentrations of NVP-AEW541 is added 24 hours thereafter in quadruplicate. 72 hours later, cells are fixed by addition of 25 μL/well Glutaraldehyde (20%) and incubation for 10 min at RT. Cells are then washed 2× with 200 μL/well H2O and 100 μL Methylene Blue (0.05%) is added. After incubation for 10 min at RT, cells are washed 3× with 200 μL/well H2O. 200 μL/well HCl (3%) is added, and following incubation for 30 min at RT on a plate shaker, absorbance is measured at 650 nm.
    (Only for Reference)
Animal Research:[1]
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  • Animal Models: Female Harlan athymic nude mice weighing 18-25 g with NWT-21 cells
  • Formulation: Dissolved in 25 mM L(+)-tartaric acid
  • Dosages: 20, 30, or 50 mg/kg
  • Administration: Administered via p.o. twice daily
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 88 mg/mL (200.2 mM)
Water <1 mg/mL
Ethanol <1 mg/mL
In vivo 30% PEG400+0.5% Tween80+5% propylene glycol 20 mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 439.55


CAS No. 475489-16-8
Storage powder
in solvent
Synonyms AEW541

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Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID