Catalog No.S1034

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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NVP-AEW541 Chemical Structure

NVP-AEW541 Chemical Structure
Molecular Weight: 439.55

Validation & Quality Control

Customer Product Validation(7)

Quality Control & MSDS

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Product Information

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  • Research Area
  • Inhibition Profile

Product Description

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.
Targets Insulin Receptor [1]
(Cell-free assay)
IGF-1R [1]
(Cell-free assay)
FLT3 [1]
(Cell-free assay)
Tek [1]
(Cell-free assay)

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IC50 0.14 μM 0.15 μM 0.42 μM 0.53 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]
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]

Protocol(Only for Reference)

Kinase Assay: [1]

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 Assay: [1]

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.

Animal Study: [1]

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

Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)

SpeciesMouseRatRabbitGuinea pigHamsterDog
Weight (kg)
Body Surface Area (m2)0.0070.0250.
Km factor36128520
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Rat dose (mg/kg) = mouse dose (22.4 mg/kg) ×  mouse Km(3)  = 11.2 mg/kg
rat Km(6)


[1] García-Echeverría C, et al. Cancer Cell. 2004, 5(3), 231-239.

[2] Scotlandi K, et al. Cancer Res, 2005, 65(9), 3868-3876.

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Chemical Information

Download NVP-AEW541 SDF
Molecular Weight (MW) 439.55


CAS No. 475489-16-8
Storage 3 years -20℃powder
6 months-80℃in solvent
Synonyms AEW541
Solubility (25°C) * In vitro DMSO 88 mg/mL (200.2 mM)
Water <1 mg/mL (<1 mM)
Ethanol <1 mg/mL (<1 mM)
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 Name 7-((1s,3s)-3-(azetidin-1-ylmethyl)cyclobutyl)-5-(3-(benzyloxy)phenyl)-7H-pyrrolo[2,3-d]pyrimidin-4-amine

Customer Product Validation (7)

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Source J Clin Invest 2011 121, 4311-21. NVP-AEW541 purchased from Selleck
Method Western blots
Cell Lines SW837/LoVo/HCT-116 cells
Concentrations 1 μM
Incubation Time 6 h

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Source Clin Cancer Res 2011 17, 2237-2249. NVP-AEW541 purchased from Selleck
Method MTT-assays
Cell Lines TC1889 cells
Concentrations 0-10 µM
Incubation Time 48/72 h
Results We additionally analyzed the effects of a neutralizing IGF-1R antibody (αIR3) and of the IGF-1R inhibitors NVP-AEW541 (NVP) and BMS-536924 (BMS). Notably, all of these strategies to interfere with IGF-1R signaling reduced TC1889 cell viability and significantly induced apoptosis.

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Source Clin Cancer Res 2011 17, 2237-2249. NVP-AEW541 purchased from Selleck
Method Western blot
Cell Lines TC1889 cells
Concentrations 0.5/5 µM
Incubation Time 2 h
Results IGF-1R inhibition with PPP, a IR3, BMS-536924, as well as NVPAEW541 reduced the IGF-I-induced activation of PI3K/Akt and MAPK/Erk signaling. However, inhibitory effects, particularly on Akt phosphorylation (Fig. C), were more marked with NVPAEW541 and BMS-536924 which are both known to also inhibit the insulin receptor. Treatment with the IGF-1R/IR inhibitors NVPAEW541 and BMS-536924 both induced a marked decrease in phsophorylated Akt, which corresponded to their aforementioned strong inhibitory effect on IGF-stimulated Akt signaling. Effects on MAPK/Erk signaling with these compounds were however heterogenous, with BMS-536924 rather decreasing Erk phosphorylation, whereas NVPAEW541 activated Erk (Fig. D).

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Source Mol Cancer Ther 2011 10:697-707. NVP-AEW541 purchased from Selleck
Method Western blotting/colony formation assay
Cell Lines mouse tumor primary cell
Concentrations 0-5 µmol/L
Incubation Time
Results NVP-AEW541 inhibited tumor cell growth better in the primary cell culture with the higher baseline Igf1r level (IC50 1.5 µmol/L vs. 300 nmol/L for low and high Igf1r expressing cells, respectively; Fig. A). Anchorage-dependent colony formation assays showed that the colony forming ability of the tumor cells was drastically reduced on treatment with 1 mmol/L NVP-AEW541(Fig. B), but again sensitivity was increased for the cell culture with the higher baseline level of Igf1r expression. Similar results were obtained for anchorage-independent soft agar colony formation assays (Fig. C). Biochemical interrogation revealed that phosphorylation of Igf1r and downstream mediators Mapk, Akt, IRS-1, and P70-S6 kinase were inhibited on treatment with NVP-AEW541(Fig. D)

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Source Mol Cancer Ther 2011 10:697-707. NVP-AEW541 purchased from Selleck
Method Western blot/Quantification of drug response of ARMS cells on the quail CAM/FACS
Cell Lines rhabdomyosarcoma primary cell
Concentrations 0-5 µmol/L
Incubation Time 48 h
Results NVP-AEW541 treatment of mouse primary tumor cell cultures caused cell cycle arrest in G1 phase (Fig. A). The proportion of cells in G1 phase increased from 52.2% in untreated cells to 68.4% cells in G1 phase when cells were treated with 2 µmol/L NVP-AEW541 (P < 0.05). Western blotting showed the presence of cleaved caspase-3 in tumor cells treated with 5 µmol/L NVP-AEW541 but not at lower concentrations (Fig. B). These results indicate that NVP-AEW541 reduces tumor cell growth primarily by causing cell cycle arrest and secondarily by inducing apoptosis in rhabdomyosarcoma. CAM harboring tumor cells treated withNVP-AEW541 showed 87% less growth compared to the DMSO treated tumor cells (P =0.006), which was better than the growth inhibition seen for imatinib (P = 0.039) at the dosages tested (Fig. C and D)

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Source Mol Cancer Ther 2011 10, 697-707. NVP-AEW541 purchased from Selleck
Method Cell viability assay
Cell Lines murine rhabdo myosarcom primary cell
Concentrations 5 μmol/L
Incubation Time 72 h
Results The results of the cell viability assay showed that NVP-AEW541 alone led to an unexpected increase in cell growth at moderate doses for the NVP-AEW541 resistant cell culture. However , the cell growth inhibition could be cooperatively improved by addition of lapatinib (cooperativity index 0.1) , although lapatinib alone had no substantial effect on naive or resistant tumor cells (Fig. A and B). To examine the activity of Igf1r a nd Her2 in NVP-AEW 541 resistant primary tumor cell lines, Resistant cell cultures treated with lapatinib showed decreased p-Her2 levels; however, no difference in Her2 activity was observed in cells treated with NVP-AEW541. When the resistant cells were treated with lapatinib, a surprising increase in the levels of p-Igf1r was observed in comparison vehicle treated cells (Fig. C)

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Source Breast Cancer Res 2013 15, R55. NVP-AEW541 purchased from Selleck
Method Confocal microscopy
Cell Lines MCF-7/LTED cells
Concentrations 1 uM
Incubation Time 30 min
Results PIP3 binding to the PH domain should result in translocation of the fusion protein to the plasma membrane. AKT PH-GFP was mainly cytoplasmic in control cells, whereas treatment with exogenous IGF-I induced its translocation to the membrane. Treatment with AZD5363 induced marked translocation of AKT PH-GFP to the membrane, suggestive of increased PIP3 production and, as a result, AKT phosphorylation at the T308 PDK-1 site. Pre-treatment with the IGF-IR/InsR TKI AEW541 or BKM120 prevented AZD5363-induced membrane localization of AKT PH-GFP.

Tech Support

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
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