Vandetanib (ZD6474)

Catalog No.S1046

Vandetanib (ZD6474) Chemical Structure

Molecular Weight(MW): 475.35

Vandetanib (ZD6474) is a potent inhibitor of VEGFR2 with IC50 of 40 nM in a cell-free assay. It also inhibits VEGFR3 and EGFR with IC50 of 110 nM and 500 nM, respectively. Not sensitive to PDGFRβ, Flt1, Tie-2 and FGFR1 with IC50 of 1.1-3.6 μM. No activity against MEK, CDK2, c-Kit, erbB2, FAK, PDK1, Akt and IGF-1R with IC50 above 10 μM.

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7 Customer Reviews

  • (A) Representative in vivo bioluminescence of mice at and during time of treatment. Derived cell lines with either BCR-ABL1 WT or V299L was tail-vein injected into immunocompetent recipient mice. Initial imaging was performed at day 10 post-transplantation. Mice were subsequently treated once daily with vehicle, 10 mg/kg dasatinib, 50 mg/kg imatinib, 50 mg/kg vandetanib, or 50 mg/kg foretinib.
    (B) Fold change in total whole-mouse bioluminescence signal between post- and pre-treatment. Mice bearing BCR-ABL1 V299L ALLs showed significant tumor burden reduction upon treatment with foretinib or vandetanib. Statistical significance determined by Mann-Whitney test. *p < 0.05, **p < 0.01.

    Cell, 2016, 165(1):234-46.. Vandetanib (ZD6474) purchased from Selleck.

    Vandetanib reduced extracellular nitrite levels in endothelial cells. MS1 endothelial cells (ECs) were incubated with 1 mol/L of vandetanib or matched vehicle (dimethyl sulfoxide [DMSO]), 50 ng/mL of vascular endothelial growth factor (VEGF) or matched vehicle (PBS; 0.5 hours), and L-arginine and soluble N-ethylmaleamide sensitive factor attachment protein (SNAP) added (1.5 hours). Vandetanib lowered nitrite levels in MS1 Ecs (*P0.0003). VEGF was used a positive control and increased nitrite levels (**P0.02). These findings indicate that vandetanib lowered endothelial cell NO levels.

    hypertension 2011 58, 85-92. Vandetanib (ZD6474) purchased from Selleck.

  • Vandetanib reduced phosphorylation of Akt in endothelial cells (ECs). MS1 ECs were incubated with 1 μmol/L of vandetanib or matched vehicle (dimethyl sulfoxide [DMSO]; 1 hour). Western blotting analysis showed that vandetanib decreased phosphorylation of Akt (S473) in MS1 ECs (*P<0.01; n=6 per group, studies done in triplicate). These findings show that vandetanib reduced Akt activity.

    hypertension 2011 58, 85-92. Vandetanib (ZD6474) purchased from Selleck.

    Vandetanib increases membrane localization of endothelial NO synthase (eNOS). MS1 endothelial cells (ECs) were incubated with 1 μmol/L of vandetanib or matched vehicle (dimethyl sulfoxide [DMSO]). Western blotting analysis showed that vandetanib increases membrane localization of eNOS compared with control (*P<0.04; n=4 per group, studies done in triplicate). These findings show that vandetanib increased the membrane localization of eNOS compared with control.

    hypertension 2011 58, 85-92. Vandetanib (ZD6474) purchased from Selleck.

  • (H) Anti-pSTAT3Y705, total STAT3, pSRCy416 of RWPE-1 transfectants treated for 6 hours with vandetanib at the indicated concentrations. Actin was used as loading control.

    J Cancer, 2017, 8(1):140-145. Vandetanib (ZD6474) purchased from Selleck.

    LS-007 inhibits CDK1/CDK7/CDK9 activity in AL cells. HL-60 (A), CCRF-CEM (B) cells were treated with increasing concentrations of LS-007 or flavopiridol for 2 h, and cell lysates were collected and examined by immunoblotting with the indicated antibodies.

    Acta Pharmacol Sin, 2016, 37(11):1481-1489. Vandetanib (ZD6474) purchased from Selleck.

  • Breast cancer cells were pretreated with 100ng/ml EGF for 15 min and then treated with the indicated concentrations of Vandetanib for 24 hours.

     

     

    Dr. Zhang of Tianjin Medical University. Vandetanib (ZD6474) purchased from Selleck.

Purity & Quality Control

Choose Selective VEGFR Inhibitors

Biological Activity

Description Vandetanib (ZD6474) is a potent inhibitor of VEGFR2 with IC50 of 40 nM in a cell-free assay. It also inhibits VEGFR3 and EGFR with IC50 of 110 nM and 500 nM, respectively. Not sensitive to PDGFRβ, Flt1, Tie-2 and FGFR1 with IC50 of 1.1-3.6 μM. No activity against MEK, CDK2, c-Kit, erbB2, FAK, PDK1, Akt and IGF-1R with IC50 above 10 μM.
Targets
VEGFR2 [1]
(Cell-free assay)
VEGFR3 [1]
(Cell-free assay)
EGFR [1]
(Cell-free assay)
40 nM 110 nM 500 nM
In vitro

Vandetanib also inhibits VEGFR3 and EGFR with IC50 of 110 nM and 500 nM, respectively. Vandetanib is not sensitive to PDGFRβ, Flt1, Tie-2 and FGFR1 with IC50 of 1.1-3.6 μM, while almost has no activity against MEK, CDK2, c-Kit, erbB2, FAK, PDK1, Akt and IGF-1R with IC50 above 10 μM. Vandetanib inhibits VEGF-, EGF- and bFGF-stimulated HUVEC proliferation with IC50 of 60 nM, 170 nM and 800 nM, with no effect on basal endothelial cell growth. Vandetanib inhibits tumor cell growth with IC50 of 2.7 μM (A549) to 13.5 μM (Calu-6). [1] Vandetanib displays an inhibitory effect on the basal ABCG2-ATPase. Parental and ABCG2-expressing A431 cells showed similar sensitivities toward Vandetanib. Exposure to EGFR inhibitors decreases pEGFR levels in A431 cells, with Vandetanib displaying only a moderate effect. Vandetanib displays a slight but measurable effect, whereas gefitinib, pelitinib and neratinib completely inhibit ABCG2-mediated efflux of mitoxantrone from A431/ABCG2 cells, similarly to the specific ABCG2 inhibitor Ko143. [2] Vandetanib inhibits both PC3wt and PC3R cell lines with similar IC50 of 13.3 μM and 11.5 μM, respectively. [3] Vandetanib suppresses phosphorylation of VEGFR2 in HUVEC and EGFR in hepatoma cells and inhibits cell proliferation. [4] Vandetanib causes an accumulation of cells in the G0-G1 phases in GEO and OVCAR-3 cells and increases apoptosis in OVCAR-3, ZR-75-1, MCF-10A ras, and GEO cells. Vandetanib causes a dose-dependent inhibition of EGFR phosphorylation in mouse NIH-EGFR fibroblasts and human MCF-10A ras breast cancer cells, two cell lines that overexpress the human EGFR. Vandetanib treatment results in a dose-dependent inhibition of soft agar growth in seven human cell lines (breast, colon, gastric, and ovarian) with functional EGFR but lacking VEGFR2. [5]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
SN179  MYnGeY5kfGmxbjDBd5NigQ>? NUKzWGhjPTBy4pEJcm3DqA>? NGGzd4UyPiCq NVHGTXhncW6lcnXhd4V{KEO[Q2K0JIV5eHKnc4Ppc44he2mpbnnmbYNidnSueR?= M4nQSFI2Pjd4Nkmx
SN186 Ml24SpVv[3Srb36gRZN{[Xl? MXm1NFDjiImwTdMg MXyxOkBp MWPpcoNz\WG|ZYOgR3hEWjRiZYjwdoV{e2mxbjDzbYdvcW[rY3HueIx6 M3vGOlI2Pjd4Nkmx
SN179  NEnaXWJHfW6ldHnvckBCe3OjeR?= NG\aenU2ODEkgJnuUeKh NF3SUGIyPiCq MUXlcohidmOnczD0bIUhS1iFTEGyJIRqemWldHXkJI1q\3KjdHnvci=> NYH5OJU{OjV4N{[2PVE>
SN179  NXS0fHpLTnWwY4Tpc44hSXO|YYm= M1POO|UxOOLCiX7NxsA> NV:2coFLOTZiaB?= MofLbY5kemWjc3XzJIJie2GuIH3p[5JifGmxbtMg MmP6NlU3PzZ4OUG=
Jurkat MonBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkLSO|LDqGkEoB?= NYfkTYxoT0l3ME2xMlUhyrFiMD6yJO69VQ>? MVqyOFY5OTJyNR?=
K-562 M1rLd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGq2Ulc4OsLiaNMg MYLHTVUxRTFwODFCtUAxNjFizszN NGX2WZQzPDZ6MUKwOS=>
NCTC-2544 NHTleodIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3XVbFczyqCqwrC= MoDtS2k2OD12Lk[gxtEhOC5|IN88US=> M4DHVVI1PjhzMkC1
A-431 M3ixVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2PF[|czyqCqwrC= M3zldGdKPTB;Mj60JOKyKDBwMzFOwG0> Mn7wNlQ3QDF{MEW=
SK-N-SH M4LsUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4DiTlAvPjJ3LUKwJO69VQ>? M2Pn[FQ5KGh? NG\EOFJFVVOR M1nIV4lvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz MY[yOFM6QTB5NB?=
SH-SY5Y NVvnSmJrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnnlNE43OjVvMkCg{txO NWrQepNtPDhiaB?= M1uyeWROW09? MY\pcohq[mm2czDj[YxtKGe{b4f0bEBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> M2jVelI1Ozl7MEe0
SK-N-SH MmLHRZBweHSxc3nzbUBCe3OjeR?= M16wPVUwOTBxMkCg{txO NH7jb2c1QCCq NGe5XItFVVOR MWnpcoR2[2W|IHHwc5B1d3OrczDkc5NmKGSncHXu[IVvfGy7 NV3KUG1UOjR|OUmwO|Q>
SH-SY5Y NGXqcmZCeG:ydH;zbZNqKEG|c3H5 MVu1M|ExNzJyIN88US=> M{PCcVQ5KGh? M4HTemROW09? NUjDXWVWcW6mdXPld{BieG:ydH;zbZMh\G:|ZTDk[ZBmdmSnboTsfS=> MXWyOFM6QTB5NB?=
SK-N-SH NGDOfHlHfW6ldHnvckBCe3OjeR?= MYK1M|ExNzJyIN88US=> NEPjPIQ1QCCq MXHEUXNQ M2PH[4lv\HWlZYOgS|EheGijc3WgZ4VtdCCleXPs[UBienKnc4S= M3rE[|I1Ozl7MEe0
SH-SY5Y MVrGeY5kfGmxbjDBd5NigQ>? MVO1M|ExNzJyIN88US=> NFK1ZVY1QCCq Ml7DSG1UVw>? NIe1OVNqdmS3Y3XzJGcyKHCqYYPlJINmdGxiY4njcIUh[XK{ZYP0 NHHiXY4zPDN7OUC3OC=>
SK-N-SH MlvVSpVv[3Srb36gRZN{[Xl? MWmxM|UwOTBizszN MYW0PEBp NYfVb5RWTE2VTx?= MmWzbY5pcWKrdIOgVmVVKHCqb4PwbI9zgWyjdHnvci=> MkDPNlQ{QTlyN{S=
SH-SY5Y MWrGeY5kfGmxbjDBd5NigQ>? NYrBc4NHOS93L{GwJO69VQ>? MUi0PEBp NYnIWYNJTE2VTx?= NX\OR|JmcW6qaXLpeJMhWkWWIIDoc5NxcG:{eXzheIlwdg>? MknaNlQ{QTlyN{S=
SK-N-SH MlzYSpVv[3Srb36gRZN{[Xl? NYDEbW8xPS9zMDFOwG0> MnXlOFghcA>? M2D3d2ROW09? MnTBbY5pcWKrdIOgbJVu[W5iTlKgZ4VtdCCvaXfyZZRqd25? NWOxWmwzOjR|OUmwO|Q>
SH-SY5Y MX\GeY5kfGmxbjDBd5NigQ>? NIrRR5U2NzFyIN88US=> M1;SWVQ5KGh? NEfSOZBFVVOR M13JZolvcGmkaYTzJIh2dWGwIF7CJINmdGxibXnndoF1cW:w NH3KWXgzPDN7OUC3OC=>
SK-N-SH MWXGeY5kfGmxbjDBd5NigQ>? NGrZNGY2NzFyIN88US=> NYju[I9jPDhiaB?= MUHEUXNQ MULpcohq[mm2czDoeY1idiCQQjDj[YxtKGmwdnHzbY9v M2Hi[FI1Ozl7MEe0
SH-SY5Y NUDDSG9qTnWwY4Tpc44hSXO|YYm= MkPSOU8yOCEQvF2= MoLYOFghcA>? M4jV[mROW09? MVjpcohq[mm2czDoeY1idiCQQjDj[YxtKGmwdnHzbY9v MorONlQ{QTlyN{S=
SK-N-SH NIfteVdHfW6ldHnvckBCe3OjeR?= NFTDZ|U2KM7:TR?= NGjSSXAzPC92OD:3NkBp NUDqOJRyTE2VTx?= NHXuN4t{fXCycnXzd4V{KHSqZTDlfJBz\XO|aX;uJI9nKEO[Q2K0JIFv\CCPTWCxOEBuWk6D MknoNlQ{QTlyN{S=
SH-SY5Y NUDudHNZTnWwY4Tpc44hSXO|YYm= NV7vZo1qPSEQvF2= NXXac2VqOjRxNEivO|IhcA>? MlG5SG1UVw>? NF7hTlJ{fXCycnXzd4V{KHSqZTDlfJBz\XO|aX;uJI9nKEO[Q2K0JIFv\CCPTWCxOEBuWk6D MXiyOFM6QTB5NB?=
SK-N-SH MknuSpVv[3Srb36gRZN{[Xl? MkHaOUDPxE1? MmHiOFgwPzJiaB?= MX3EUXNQ M1jreJN2eHC{ZYPz[ZMh\XiycnXzd4lwdiCxZjD0bIUhS1iFUkSgZY5lKE2PUEG0JJBzd3SnaX6= MVyyOFM6QTB5NB?=
SH-SY5Y M3PQNGZ2dmO2aX;uJGF{e2G7 NVPvUWlvPSEQvF2= Mo\4OFgwPzJiaB?= MY\EUXNQ M4\OfJN2eHC{ZYPz[ZMh\XiycnXzd4lwdiCxZjD0bIUhS1iFUkSgZY5lKE2PUEG0JJBzd3SnaX6= NEeyPWYzPDN7OUC3OC=>
HMEpC NYPHSXhGT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF\TdGMyKG6PLUGwNEDPxE1? MkS2OFjDqGkEoB?= NH[zOG1FVVOR NYm5R5NbcW6qaXLpeJMh[2WubDDndo94fGhiaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MlPBNlQyOzh6NEO=
MCF-7 M2Gxemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGTsUo0yKG6PLUGwNEDPxE1? MVi0POKhcMLi MnzOSG1UVw>? MWHpcohq[mm2czDj[YxtKGe{b4f0bEBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> NED6[JIzPDF|OEi0Ny=>
ZR-75-1 NYXEeJpqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3y5ZlEhdk1vMUCwJO69VQ>? MmH6OFjDqGkEoB?= NGHLVHpFVVOR M3XERYlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz NUXacYR1OjRzM{i4OFM>
MDA-MB-231 M{HnfGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXfWcm5qOSCwTT2xNFAh|ryP NH3Femc1QMLiaNMg MnPpSG1UVw>? NHjTZYdqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? M1nnWlI1OTN6OESz
MDA-MB-468 NW\VNJkzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVP2WnhuOSCwTT2xNFAh|ryP NFPFVmQ1QMLiaNMg M3zuUmROW09? M{n0TIlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz MojDNlQyOzh6NEO=
T-47-D MkPNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUexJI5ONTFyMDFOwG0> M4j0cVQ5yqCqwrC= NFnPR29FVVOR NWLNT3E{cW6qaXLpeJMh[2WubDDndo94fGhiaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MoH2NlQyOzh6NEO=
U251  NUjyNYNxTnWwY4Tpc44hSXO|YYm= M2D2fVIwPC964pEJ{tzjjLQEoB?= M3;PN|YwOTJxMkSgbC=> MmjxSG1UVw>? NGXl[ppqdmO{ZXHz[ZMhfGinIFzDN{1KUSCuZY\lcEBqdiCjIITpcYUu\GWyZX7k[Y51KGGwZDDkc5NmNWSncHXu[IVvfCCvYX7u[ZI> Mmr3NlM4QTl6NUK=
U87MG NV:1XIpVTnWwY4Tpc44hSXO|YYm= NGXKNHQzNzRxOPMAje696oT|wrC= MmX6Ok8yOi9{NDDo NEm4VnVFVVOR MnjZbY5kemWjc3XzJJRp\SCOQ{OtTWkhdGW4ZXygbY4h[SC2aX3lMYRmeGWwZHXueEBidmRiZH;z[U1l\XCnbnTlcpQhdWGwbnXy MVGyN|c6QTh3Mh?=
U251  MX3GeY5kfGmxbjDBd5NigQ>? NFLKdJE16oDLzs|iiNPDqA>? Ml3FNk83NzF{IHi= MVfEUXNQ M2jMV5N2eHC{ZYPz[ZMh[mG|YXygcIV3\Wy|IH;mJJBpd3OyaH;yfYxifGmxbjDv[kBUPiBqU{KzOU8zOzZrLDC0SU1DWDFiKGSzO{81PiluIHHu[EBCc3RiKGO0O|MqKGmwIHGgeIlu\S2mZYDlcoRmdnRibXHucoVzyqB? NYmzRXo2OjN5OUm4OVI>
U87MG NXHLNGU1TnWwY4Tpc44hSXO|YYm= MWm05qCK|r{khMRCpC=> NEnoS3czNzZxMUKgbC=> Mn7ZSG1UVw>? MXLzeZBxemW|c3XzJIJie2GuIHzleoVteyCxZjDwbI9{eGixconsZZRqd25ib3[gV|YhMFN{M{WvNlM3MSxiNFWtRnAyKCiWM{evOFYqNCCjbnSgRYt1KCiVNEezLUBqdiCjIITpcYUu\GWyZX7k[Y51KG2jbn7lduKh MVGyN|c6QTh3Mh?=
H1650  M2jjXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVzJR|UxRTNwNdMxNU4zKM7:TR?= NFrwTlMzOzJ5NEe1PC=>
HUVECs  NX3HWHQ4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYTZPXVMPzJiaB?= NGXm[oZKSzVywrC9JFcvOSEQvH3vcE9N MViyNlYyOTB{Nx?=
KYN-2  NYTifJMyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVjJdo9vPzJiaB?= MV;JR|UxyqB;IEiuNUDPxG2xbD;M NWXld2tVOjJ4MUGwNlc>
HuH-7  M3XtR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmfWO|IhcA>? NWrsW|ZwUUN3MNMgQUA6NjRizsztc4wwVA>? M3XJe|IzPjFzMEK3
HUVECs  Mlj5SpVv[3Srb36gRZN{[Xl? NWT4fVF[OS93L{GwJO69VQ>? MVexJIg> M4\2[5Nq\26rZnnjZY51dHliaX7obYJqfHNiVlXHSnIuOiCyaH;zdIhwenmuYYTpc44> MUWyNlYyOTB{Nx?=
HAK1-B NEjOSGZHfW6ldHnvckBCe3OjeR?= Mn3vNU82NzFyIN88US=> MoLtNUBp MlK4d5VxeHKnc4Pld{BGT0[UIIDoc5NxcG:{eXzheIlwdg>? NHG3eGwzOjZzMUCyOy=>
UM-22A MoLES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWm2VmZ4OC14IN88US=> MXi3NkBp NXX4U2lFTE2VTx?= NGHTPFBqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NWnUcFJ{OjJ|MEe3N|U>
UM-22B NXP5XWc5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWPuV4dZOC14IN88US=> MVi3NkBp NE\0UWxFVVOR M3G3TolvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz MoLSNlI{ODd5M{W=
PCI-37A MlzKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX7iWXF5OC14IN88US=> NXToWFlsPzJiaB?= NGHqd3ZFVVOR NHLqbZRqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? MnvKNlI{ODd5M{W=
PCI-37B NUXSTZlCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYewMVYh|ryP NWS0eWlyPzJiaB?= M1;1SmROW09? NGfZfJhqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? MlTGNlI{ODd5M{W=
PCI-15B NXj2bZFnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml3XNE03KM7:TR?= NEXQe3M4OiCq M4LsVGROW09? NYL5Vm5HcW6qaXLpeJMh[2WubDDndo94fGhiaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? M4DXNFIzOzB5N{O1
SCC-25 M{XCemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXfid3NYOC14IN88US=> NVex[Hh2PzJiaB?= NYDsNGY3TE2VTx?= M3PNfYlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz M2X1R|IzOzB5N{O1
UM-22A MX7GeY5kfGmxbjDBd5NigQ>? NETacZgxNTFyIN88US=> NF35cJAzPCCq MkS4SG1UVw>? M4TKXolvcGmkaYTzJJRp\SCjY4TpeoF1cW:wIH;mJJRp\SCHR1\SJJR6em:|aX7lJItqdmG|ZTDhcoQh[Wy|bzDk[YNz\WG|ZYOgeIhmKGW6cILld5Nqd25ib3[gdIhwe3Cqb4L5cIF1\WRiZn;ycZMhd2ZidHjlJIRwf26|dILlZY0he2mpbnHsbY5oKGWuZX3lcpR{NCCVVFHUN{BidmRiTVHQTy=> MnXENlI{ODd5M{W=
UM-22B M17nZ2Z2dmO2aX;uJGF{e2G7 NFPCPJoxNTFyIN88US=> M{jXW|I1KGh? M2D4TmROW09? NULsR4NncW6qaXLpeJMhfGinIHHjeIl3[XSrb36gc4YhfGinIFXHSnIhfHm{b4PpcoUhc2mwYYPlJIFv\CCjbIPvJIRm[3KnYYPld{B1cGViZYjwdoV{e2mxbjDv[kBxcG:|cHjvdplt[XSnZDDmc5JueyCxZjD0bIUh\G:5boP0doVidSC|aXfuZYxqdmdiZXzlcYVvfHNuIGPURXQ{KGGwZDDNRXBM NUnsOZp2OjJ|MEe3N|U>
PCI-15B MlHoSpVv[3Srb36gRZN{[Xl? NW\mW|lTOC1zMDFOwG0> Mo[wNlQhcA>? NYnLNYt3TE2VTx?= NHX1PYpqdmirYnn0d{B1cGViYXP0bZZifGmxbjDv[kB1cGViRVfGVkB1gXKxc3nu[UBscW6jc3WgZY5lKGGuc3:g[IVkemWjc3XzJJRp\SCneIDy[ZN{cW:wIH;mJJBpd3OyaH;yfYxifGWmIH\vdo1{KG:oIITo[UBld3ewc4Ty[YFuKHOrZ37hcIlv\yCnbHXt[Y51eyxiU2TBWFMh[W6mIF3BVGs> M3jFNFIzOzB5N{O1
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ACCM NUXjXVBnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1vvWlAuOTBizszN MkOyO|IhcA>? Mnu0bY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> M3roTlE5Pjl6MEK1
ACC3 M3WzcGFxd3C2b4Ppd4khSXO|YYm= M4mxNVAuOTBizszN NWqzclZYPzJiaB?= NUj1bYdncW6mdXPld{BieG:ydH;zbZMh\G:|ZTDk[ZBmdmSnboTsfS=> M17SdVE5Pjl6MEK1
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H2452 M13jOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkPOO|IhcA>? MkiwSG1UVw>? M2P2XWlEPTB;NT61JO69VQ>? NFXYdIwyQDN4NEK0PC=>
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CNE-1 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVjqSlRiOC5zLUK1MlYh|ryP MoPKO|IhcA>? M4fqdGlEPTB;Mj6zJO69VQ>? MVyxO|Y{OTZ2Nh?=
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C666-1 M{[3Tmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGi4WW8xNjFvMkWuOkDPxE1? MV63NkBp NWDM[pVwUUN3ME20Mlg3KM7:TR?= MoruNVc3OzF4NE[=
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CNE-2 NInWXZRHfW6ldHnvckBCe3OjeR?= NEi5d|U3KM7:TR?= Mmn4NlQhcA>? NWLmVFJ[\GWuYYnzJGcxN0dzIHPlcIwh[3mlbHWgdJJw\3Knc4Ppc44> M1rhXFE4PjNzNkS2
C666-1 MY\GeY5kfGmxbjDBd5NigQ>? MoftOkDPxE1? M3XZXFI1KGh? MlS0[IVt[Xm|IFewM2cyKGOnbHygZ5lkdGVicILv[5Jme3Orb36= MlzjNVc3OzF4NE[=

... Click to View More Cell Line Experimental Data

In vivo Vandetanib (2.5 mg/kg, i.v.), reverses a VEGF-induced hypotension by 63% but does not significantly affect a bFGF-induced hypotension. Vandetanib (100 mg/kg) inhibits the tumor-induced blood vessel formation by 79%. Vandetanib (12.5-100 mg/kg, orally) shows great tumor growth inhibition in human tumor xenografts including Calu-6, PC-3, MDA-MA-231, SKOV-3, SW620, A549, A431, B16-F10(AP3) and Lewis Lung, with little effects on body weight. [1] In PC3wt xenografts, administration of Vandetanib alone exerts paradoxical tumor growth stimulating effects. In PC3R xenografts, the low dose of Vandetanib (25 mg/kg) has no significant effect relative to control, whereas the high dose (50 mg/kg) significantly inhibits tumor growth compared with control. In contrast, the high-dose combination reveals a significant negative interaction between Vandetanib 50 mg/kg and docetaxel 30 mg/kg in PC3R cells. [3] In tumor-bearing mice, Vandetanib suppresses phosphorylation of VEGFR2 and EGFR in tumor tissues, significantly decreases tumor vessel density, enhances tumor cell apoptosis, suppresses tumor growth, improves survival, reduces number of intrahepatic metastases, and up-regulates VEGF, TGF-alpha and EGF in tumor tissues. Treatment with Vandetanib is not associated with serious adverse events, including ALT abnormality, bone marrow suppression or body weight loss. [4] Vandetanib treatment of nude mice bearing palpable GEO colon cancer xenografts (which are sensitive to inhibition of EGFR signaling) induces dose-dependent tumor growth inhibition. [5]

Protocol

Kinase Assay:

[1]

+ Expand

Kinase inhibition:

Vandetanib is incubated with enzyme, 10 mM MnCl2, and 2 μM ATP in 96-well plates coated with a poly(Glu, Ala, Tyr) 6:3:1 random copolymer substrate. Phosphorylated tyrosine is then detected by sequential incubation with a mouse IgG anti-phosphotyrosine 4G10 antibody, a horseradish peroxidase-linked sheep antimouse immunoglobulin antibody, and 2,2′-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid). This methodology is adapted to examine selectivity versus tyrosine kinases associated with EGFR, PDGFRβ, Tie-2, FGFR1, c-kit, erbB2, IGF-1R, and FAK. All enzyme assays (tyrosine or serine-threonine) used appropriate ATP concentrations at or just below the respective Km (0.2–14 μM). Selectivity versus serine-threonine kinases (CDK2, AKT, and PDK1) is examined using a relevant scintillation proximity-assay (SPA) in 96-well plates. CDK2 assays contained 10 mM MnCl2, 4.5 μM ATP, 0.15 μCi of [γ-33 P]ATP/reaction, 50 mM HEPES (pH 7.5), 1 mM DTT, 0.1 mM sodium orthovanadate, 0.1 mM sodium fluoride, 10 mM sodium glycerophosphate, 1 mg/mL BSA fraction V, and a retinoblastoma substrate (part of the retinoblastoma gene, 792–928, expressed in a glutathione S-transferase expression system; 0.22 μM final concentration). Reactions are allowed to proceed at room temperature for 60 minutes before quenching for 2 hours with 150 μL of a solution containing EDTA (62 mM final concentration), 3 μg of a rabbit immunoglobulin anti-glutathione S-transferase antibody and protein A SPA-polyvinyltoluene beads (0.8 mg/reaction). Plates are then sealed, centrifuged (1200× g for 5 minutes), and counted on a Microplate scintillation counter for 30 seconds.
Cell Research:

[1]

+ Expand
  • Cell lines: Calu-6, PC-3, MDA-MA-231, SKOV-3, SW620, A549, A431, B16-F10(AP3) and Lewis Lung cells
  • Concentrations: 0.1–100 μM
  • Incubation Time: 72 hours
  • Method:

    Tumor cells are plated in their respective media at predetermined densities that are known to enable logarithmic cell growth during the period of assay (PC-3, 500 cells/well; all others, 1000 cells/well). Plates are incubated for 24 hours (37 °C with CO2) before the addition of Vandetanib (0.1–100 μM) or vehicle (0.1% DMSO in medium). Plates are reincubated for an additional 72 hours before assessing cell proliferation by [3 H]thymidine incorporation by a beta counter.


    (Only for Reference)
Animal Research:

[5]

+ Expand
  • Animal Models: Female athymic (nu/nu genotype) Swiss mice with PC-3, Calu-6, SKOV-3, and MDA-MB-231 tumors
  • Formulation: 1% (v/v) solution of polyoxyethylene
  • Dosages: 12.5 mg/kg/day, 25 mg/kg/day, 50 mg/kg/day, or 100 mg/kg/day
  • Administration: Oral administration
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 4 mg/mL (8.41 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order:
1% CMC Na
For best results, use promptly after mixing.
30mg/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 475.35
Formula

C22H24BrFN4O2

CAS No. 443913-73-3
Storage powder
Synonyms N/A

Bio Calculators

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Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT00514046 Active, not recruiting Medullary Thyroid Carcinoma|Multiple Endocrine Neoplasia Type 2A|Multiple Endocrine Neoplasia Type 2B National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) July 9, 2007 Phase 1|Phase 2
NCT02495103 Recruiting Renal Cell Carcinoma|Hereditary Leiomyomatosis and Renal Cell Cancer|Papillary Renal Cell Carcinoma, Sporadic National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) June 30, 2015 Phase 1|Phase 2
NCT00272350 Completed Recurrent High-Grade Gliomas|Progressive Low-Grade Gliomas|Malignant Gliomas National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) December 29, 2005 Phase 1
NCT02638428 Recruiting Relapsed Pediatric Solid Tumor|Refractory Pediatric Solid Tumor|Relapsed Pediatric AML|Refractory Pediatric AML Samsung Medical Center|Ministry of health & welfare, Republic of Korea December 2015 Phase 2
NCT02530411 Recruiting Neoplasms Velindre NHS Trust|Cancer Research UK|AstraZeneca April 2015 Phase 2
NCT02239952 Recruiting Cancer|High-grade Glioma VU University Medical Center November 2014 --

Tech Support

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.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID