TAE226 (NVP-TAE226)

For research use only.

Catalog No.S2820

18 publications

TAE226 (NVP-TAE226) Chemical Structure

CAS No. 761437-28-9

TAE226 (NVP-TAE226) is a potent FAK inhibitor with IC50 of 5.5 nM and modestly potent to Pyk2, ~10- to 100-fold less potent against InsR, IGF-1R, ALK, and c-Met. TAE226 (NVP-TAE226) induces apoptosis.

Selleck's TAE226 (NVP-TAE226) has been cited by 18 publications

3 Customer Reviews

  • Targeting the actin cytoskeleton overcomes resistance to HDACi in primary MM. Graphs representing the proportion of cell death induced in MM patients (n=6) treated LBH589 (5 nM), TAE226 (0.5 uM) and combination.

    Cell Death Dis 2014 5, e1134. TAE226 (NVP-TAE226) purchased from Selleck.

  • Role of Tyr397-FAK phosphorylation on HCT-116 cell adhesion and migration. A) Real time adhesion assay and B) Real time migration assay in the presence of P(Tyr397)-FAK inhibitor. HCT-116 cells were treated with the P(Tyr397)-FAK inhibitor NPV-TAE226 at 0.1, 1 and 10 μM for 24 h at 37 °C, 5% CO2, and then seeded on a xCELLigence Roche 16-well plate after it had been functionalized with fibronectin. Cell adhesion and cell migration were monitored for 4 h and 24 h respectively. Each condition was analysed in quadruplicate and the experiment repeated two times.

    J Inorg Biochem, 2016, 160:225-35. TAE226 (NVP-TAE226) purchased from Selleck.

  • The numbers of BrdU-positive cells were significantly increased by pre-treatment of NGF in SVZ and SGZ. Compared with the IgG group (a1 and a2), the numbers of BrdU-positive cells were significantly higher in the NGF group (b1 and b2). Compared with the NGF group, the numbers of BrdU-positive cells were significantly lower than in the TAE226 groups (c1 and c2) (n=3/group; *P < 0.01; **P < 0.05; 200×).

    Neurosci Lett, 2018, 672:96-102. TAE226 (NVP-TAE226) purchased from Selleck.

Purity & Quality Control

Choose Selective FAK Inhibitors

Biological Activity

Description TAE226 (NVP-TAE226) is a potent FAK inhibitor with IC50 of 5.5 nM and modestly potent to Pyk2, ~10- to 100-fold less potent against InsR, IGF-1R, ALK, and c-Met. TAE226 (NVP-TAE226) induces apoptosis.
PYK2 [1]
(cell-free assay)
FAK [1]
(cell-free assay)
Insulin Receptor [1]
(cell-free assay)
IGF-1R [1]
(cell-free assay)
c-Met [1]
(cell-free assay)
3.5 nM 5.5 nM 43.5 nM 140 nM 160 nM
In vitro

NVP-TAE226 (< 1 μM) inhibits extracellular matrix-induced autophosphorylation of FAK (Tyr397) in serum-starved U87 cells. NVP-TAE226 (< 1 μM) also inhibits IGF-I-induced phosphorylation of IGF-1R and activity of its downstream target genes such as MAPK and Akt in both U87 and U251 cells. NVP-TAE226 (<10 μM) retards tumor cell growth and attenuats G(2)-M cell cycle progression associated with a decrease in cyclin B1 and phosphorylated cdc2 (Tyr15) protein expression in both U87 and U251 cells. NVP-TAE226 (1 μM) inhibits tumor cell invasion by at least 50% compared with the control in an in vitro Matrigel invasion assay in glioma cell lines. NVP-TAE226 (1 μM) treatment of glioma cell lines containing wild-type p53 mainly exhibits G(2)-M arrest, whereas glioma cell lines bearing mutant p53 undergoes apoptosis, as evidence by detection of caspase-3/7 activation and poly(ADP-ribose) polymerase cleavage and by an Annexin V apoptosis assay. [1] NVP-TAE226 (5 μM) inhibits phosphorylation of FAK in the human neuroblastoma cell line SK-N-AS. NVP-TAE226 (<10 μM) treatment of the human neuroblastoma cell line SK-N-AS leads to decrease in cellular viability, cell cycle arrest, and an increase in apoptosis. [2] NVP-TAE226 (0.1 μM-10 μM) inhibits tube formation of HMEC1 cells. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HCT116 cells M3nkdHBzd2yrZnXyZZRqd25iYYPzZZk> Ml;SOFghcA>? NYP1WYxISW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDIR3QyOTZiY3XscJMh[W[2ZYKgOFghcHK|IHL5JHdUXC1zIHHzd4F6NCCLQ{WwQVAvPCEQvF2= MnvhNlUyQDB4NUS=
HUVEC Mn3lSpVv[3Srb36gZZN{[Xl? Mnf3O|IhcA>? NYfpcpJkSW62aXHu[4lw\2WwaXOgZYN1cX[rdImgbY4hUFWYRVOgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDWSWdHNXO2aX31cIF1\WRicILvcIln\XKjdHnvckBi\nSncjC3NkBpenNiYomgW3NVNTFiYYPzZZktKEmFNUC9NUDPxE1? M4qyOlI{QDR3MkG3
U87MG cells MWHQdo9tcW[ncnH0bY9vKGG|c3H5 NGHqVlQ1QCCq MYjBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKFV6N13HJINmdGy|IHHmeIVzKDR6IHjyd{BjgSCZU2StNUBie3OjeTygTWM2OD1zLkKg{txO M{TueFI2OThyNkW0
PC3 cells NVnHd5lUWHKxbHnm[ZJifGmxbjDhd5NigQ>? MYC0PEBp MUDBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKFCFMzDj[YxteyCjZoTldkA1QCCqcoOgZpkhX1OWLUGgZZN{[XluIFnDOVA:OS54IN88US=> Mmf4NlUyQDB4NUS=
MDA-MB-231 cells MnfLVJJwdGmoZYLheIlwdiCjc4PhfS=> M2\pZVQ5KGh? NH;nSmhCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF3ERU1OSi1{M{GgZ4VtdHNiYX\0[ZIhPDhiaILzJIJ6KFeVVD2xJIF{e2G7LDDJR|UxRTJwODFOwG0> MXeyOVE5ODZ3NB?=
BT474 cells NUn6dVkxTnWwY4Tpc44h[XO|YYm= M2XzZVEh|ryP M1i5NVI1KGh? M2fJc2lv\HWldHnvckBw\iCjcH;weI9{cXNiaX6gbJVu[W5iQmS0O|Qh[2WubIOgZZN{\XO|ZXSgZZMh[2ynYY\h[4Uhd2ZiOEmgb2RiKFCDUmCgZZQhOSC3TTDh[pRmeiB{NDDodpMh[nliV3XzeIVzdiCkbH;0eIlv\w>? M3THRVE5QTh7OUWw

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot
FAK / p-FAK(Y397) / p-AKT(S473) / AKT / pERK / ERK ; 

PubMed: 31215459     

Effects of TAE226 on phosphorylation of FAK at Y397, Akt at S473 and ERK1/2 in MIA PaCa-2 cells treated for 1 h.

Growth inhibition assay
Cell viability; 

PubMed: 21196322     

FAK inhibition is achieved with TAE226, a specific FAK kinase inhibitor. Neuroblastoma cells, SK-N-BE(2) (amplified MYCN) and SK-N-AS (non-amplified MYCN) are treated with TAE226 for 24 hours and viability is measured using Alamar Blue Assay. After 24 hours, cellular viability is significantly decreased in the MYCN amplified neuroblastoma cell line, SK-N-BE(2), compared to that in the non-amplified, SK-N-AS, cell line, demonstrating the biologic importance of FAK in MYCN amplified neuroblastoma cells.

In vivo NVP-TAE226 (75 mg/kg) significantly increases the survival rate of mice bearing intracranial glioma xenografts. [1] NVP-TAE226 (100 mg/kg, oral) exerts significant decrease in microvessel density in a human colon cancer model in SCID mice. [3] NVP-TAE226 (100 mg/kg, oral) efficiently inhibits MIA PaCa-2 human pancreatic tumor growth without body weight loss in vivo model. [4] NVP-TAE226 inhibits 4T1 murine breast tumor growth and metastasis to the lung in a dose-dependent manner in vivo model, associated with inhibition of FAK autophosphorylation at Y397 and Akt phosphorylation at Serine473. [5]


Cell Research:[1]
- Collapse
  • Cell lines: U87 and U251 cell lines
  • Concentrations: 10 μM
  • Incubation Time: 5 days
  • Method: Cell cultures are harvested with 0.05% trypsin and seeded in triplicate at 2 × 104 in 24-well culture plates for 24 h before drug treatment. Culture medium is used for mock treatment. Cells are harvested at the indicated day after treatment, and viable cells are counted using the Vi-cell viability analyze
    (Only for Reference)
Animal Research:[1]
- Collapse
  • Animal Models: Male nude mice bearing intracranial glioma xenografts
  • Dosages: 75 mg/kg
  • Administration: Administered via oral gavage
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 94 mg/mL (200.45 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
0.5% methylcellulose
For best results, use promptly after mixing.
30 mg/mL

* 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 468.94


CAS No. 761437-28-9
Storage powder
in solvent
Synonyms N/A

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FAK Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID