Semaxanib (SU5416)

Catalog No.S2845

Semaxanib (SU5416) Chemical Structure

Molecular Weight(MW): 238.28

Semaxanib (SU5416) is a potent and selective VEGFR(Flk-1/KDR) inhibitor with IC50 of 1.23 μM, 20-fold more selective for VEGFR than PDGFRβ, lack of activity against EGFR, InsR and FGFR. Phase 3.

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Cited by 6 Publications

3 Customer Reviews

  • Injected tumor cells move to the tail via blood vessels. Tg (flil1:egfp) embryos at 20 hpf were treated with 2 μM SU5416 for 1 hr (+SU5416) to inhibit vasculogenesis24; the control fish were treated with 0.02% DMSO for 1 hr (-SU5416). After 1 hr, SU5416 or DMSO was washed out by changing fish media. At 48 hpf, tfRFP-B16 cells were injected into the pericardium cavity of fish. Representative images show that tumor cells moved to the tail in a drug-free larva, while no tumor cells moved to the tail in a drug-treated larva after new vessels were inhibited by SU5416. Insets are enlarged images from each corresponding tip of the tail indicated by white arrows. Dashed white lines mark extravasated tumor cells at 12 hpi. Vessels are green and tumor cells are red. –SU5416, 6 other larvae exhibit similar behaviors; +SU5416, 3 other larvae exhibit similar behaviors. Scale bars, 500 μm. Insets, 100 μm.

    Sci Rep, 2016, 6:19304. . Semaxanib (SU5416) purchased from Selleck.

    HUVEC spheroids embedded in fibrin gel were incubated with a pool of PDR vitreous fluid samples (1:4 dilution) in the absence or in the presence of different extracellular pathway. Formation of radially growing sprouts was evaluated after 24 h of incubation. Data are the mean ± S.E.M. of 30 spheroids per experimental point. *p《0.05, **p《0.01 versus PDR vitreous

    Angiogenesis, 2017, 20(4):629-640. Semaxanib (SU5416) purchased from Selleck.

  • VEGFR inhibition mitigates JNA fibroblast-induced tubule formation in HUVECS. (A) HUVEC tubule formation was assessed in the presence of JNA CM or SFM with or without SU5416 or vehicle control (DMSO). The photograph represents characteristic HUVEC tubules in each treatment group. (B) HUVECs were plated on a layer of Matrigel in the presence of SFM or JNA CM and subsequently treated with vehicle control (DMSO) or SU5416 at an IC50 concentration of 1.23µM. After a 6-hour incubation at 37°C, the HUVECs were examined under magnification ×100 and tubule formation and length were assessed using Pipeline software. The experiment was repeated 3 times. CM = conditioned media; DMSO = dimethylsulfoxide; HUVEC = human umbilical vein endothelial cell; IC50 = the dose that is cytotoxic to 50% of the cells treated in vitro; JNA = juvenile nasopharyngeal angiofibroma; SFM = serum-free media.

    Int Forum Allergy Rhinol, 2017, 7(10):973-979. Semaxanib (SU5416) purchased from Selleck.

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Biological Activity

Description Semaxanib (SU5416) is a potent and selective VEGFR(Flk-1/KDR) inhibitor with IC50 of 1.23 μM, 20-fold more selective for VEGFR than PDGFRβ, lack of activity against EGFR, InsR and FGFR. Phase 3.
Targets
VEGFR2/Flk1 [1]
(Cell-free assay)
1.23 μM
In vitro

Semaxanib inhibits VEGF-dependent phosphorylation of the Flk-1 receptor in Flk-1-overexpressing NIH 3T3 cells with IC50 of 1.04 μM. Semaxanib inhibits PDGF-dependent autophosphorylation in NIH 3T3 cells with IC50 of 20.3 μM. Semaxanib inhibits VEGF- and FGF-driven mitogenesis in a dose-dependent manner with IC50 of 0.04 and 50 μM, respectively. Semaxanib treatment has no effect on the in vitro growth of C6 glioma, Calu 6 lung carcinoma, A375 melanoma, A431 epidermoid carcinoma, and SF767T glioma cells (all IC50s > 20 μM). [1]
Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
MCF7 cells Mln1R5l1d3SxeHnjbZR6KGG|c3H5 NXLwTmZVPDhiaB?= NFPQV3FEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOS0Z5IHPlcIx{KGGodHXyJFQ5KGi{czDifUBES0t6IHHzd4F6NCCLQ{WwQVMvOSCwTR?= MnXiNlM4Pzd6OUi=
mouse B16F10 cells NUHZfFBuS3m2b4TvfIlkcXS7IHHzd4F6 MVO0PEBp NXK1T|BtS3m2b4TvfIlkcXS7IHHnZYlve3RibX;1d4UhSjF4RkGwJINmdGy|IHHmeIVzKDR6IHjyd{BjgSCFQ1u4JIF{e2G7LDDJR|UxRTNwNjDuUS=> MlfmNlM4Pzd6OUi=
human U251 cells M3nrdmZ2dmO2aX;uJIF{e2G7 MWXJcohq[mm2aX;uJI9nKF[HR1\SNkBqdiCqdX3hckBWOjVzIHPlcIx{KGK7IIDoc5NxcG:2eYLvd4lv\SCHTFnTRUwhUUN3ME2xNk46KG6P MW[yOFkxODh4NR?=
human A431 cells NWL1UHV2TnWwY4Tpc44h[XO|YYm= MY\BcpRq[W6paX;n[Y5q[yCjY4Tpeol1gSCjZ3HpcpN1KGi3bXHuJGE1OzFiY3XscJMtKEmFNUC9NE4xQDVizszN MVOyNFQxOzZ7Mx?=
CHO cells M3PtbWZ2dmO2aX;uJIF{e2G7 MofTTY5pcWKrdHnvckBw\iCYRVfGVkBqdmS3Y3XkJIF2fG:yaH;zdIhwenmuYYTpc44hd2ZiaIXtZY4hXmG|Y4XsZZIh\W6mb4To[Yxq[WxiZ4Lve5RpKG[jY4TvdkBz\WOncITvdkAzKCiYRVfGVlIqKHS{YX7z[oVkfGWmIHnuJGNJVyClZXzsd{whUUN3ME2wMlg5PCEQvF2= MWGxNlQ4PzN3Mh?=
human MCF7 cells M1zVOHBzd2yrZnXyZZRqd25iYYPzZZk> MXG0JIRigXN? MW\BcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE2FRkegZ4VtdHNiYX\0[ZIhPCCmYYnzJIJ6KGOxdXz0[ZIh[2:3boTldkBu\XSqb3SsJGlEPTB;MT65JO69VQ>? M2Wx[VI{OTJ2MkGz
human SF539 cells MoPWSpVv[3Srb36gZZN{[Xl? MmfiTY5pcWKrdHnvckBw\iCSRFfGVoJmfGFiaX6gbJVu[W5iU1[1N|kh[2WubIOgZpkheGixc4Doc5R6em:|aX7lJGVNUVODLDDJR|UxRTJwNDFOwG0> MWGxPVc1QDd6NR?=
A431 cells Mn30SpVv[3Srb36gZZN{[Xl? NF3COIVKdmirYnn0bY9vKG:oIG\FS2ZTOiCneIDy[ZN{\WRiaX6gbJVu[W5iQUSzNUBk\WyuczygTWM2OD1zMj65JO69VQ>? NULJ[mJZOjB3NUiwO|I>
HUVEC cells Mn34VJJwdGmoZYLheIlwdiCjc4PhfS=> MkC1O|IhcA>? Mn;pRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCKVW\FR{Bk\WyuczDhd5Nme3OnZDDhd{Bz\WS3Y4Tpc44hcW5iY3XscEB3cWGkaXzpeJkh[W[2ZYKgO|IhcHK|IHL5JJRzgXCjbjDicJVmKGG|c3H5MEBIUTVyPUGzMlYh|ryP MWSyOlMyQDB3Nh?=
human HMEC1 cells MYjQdo9tcW[ncnH0bY9vKGG|c3H5 NYLiXJQyPyCmYYnz MVHBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEiPRVOxJINmdGy|IHHmeIVzKDdiZHH5d{BjgSClb4XseIVzKGOxdX70[ZIhdWW2aH;kMEBKSzVyPUG1JO69VQ>? MmrFNlMyOjR{MUO=
human HeLa cells M3m3[3Bzd2yrZnXyZZRqd25iYYPzZZk> NEOxb4s1KGSjeYO= NHH3N2hCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjlUIEh[2WubIOgZYZ1\XJiNDDkZZl{KGK7IHPveYx1\XJiY3;1cpRmeiCvZYToc4QtKEmFNUC9NlAh|ryP M3rwWVI{OTJ2MkGz

... Click to View More Cell Line Experimental Data
Assay
Methods Test Index PMID
Western blot
p-VEGFR2 / VEGFR2 / p-PLCγ1 / PLCγ1 / p-ERK / ERK ; 

PubMed: 21699503     


SU5416 dose-dependently inhibited VEGF-A and bFGF-regulated intracellular signalling in primary endothelial cells. Cells were treated for 7.5 min with VEGF-A or bFGF (25 ng/mL) and processed for immunoblotting using anti-phospho-PLCγ1 (Y783), anti-PLCγ1, anti-phospho-ERK1/2 (T202/Y204), anti-ERK1/2 and anti-α-tubulin antibodies. Data shown are representative of four independent experiments.

21699503
Immunofluorescence
CD31 / OCT-4 / SOX-2 ; 

PubMed: 25665868     


Immunofluorescent detection of Oct-4, Sox-2, or CD31 in vehicle control (top row) and SU5416 treated cells (bottom row). Representative images are from one of three experiments. Scale bar = 70 μm.

25665868
Growth inhibition assay
Cell viability; 

PubMed: 25794107     


MTT assay showed that SU5416 treatment significantly suppressed Daoy cell growth.

25794107
In vivo Semaxanib dose-related inhibits growth of A375 tumor in vivo. A >85% inhibition of subcutaneous tumor growth is observed with daily i.p. administration of SU5416 in DMSO at Semaxanib, without measurable toxicity. Semaxanib shows broad spectrum antitumor activity. SU5416 significantly inhibits the subcutaneous growth of 8 of 10 tumor lines tested (A431, Calu-6, C6, LNCAP, EPH4-VEGF, 3T3HER2, 488G2M2 and SF763T cells) with an average mortality rate of 2.5%. [1] Semaxanib (25 mg/kg/day) displays potent antiangiogenic activity, resulting in a significant reduction of both the total and functional vascular density of the tumor microvasculature. [2]

Protocol

Kinase Assay:[1]
+ Expand

Biochemical kinase assays:

Solubilized membranes from 3T3 Flk-1 cells are added to polystyrene ELISA plates that had been precoated with a monoclonal antibody that recognizes Flk-1. After an overnight incubation with lysate at 4 ℃, serial dilutions of SU5416 are added to the immunolocalized receptor. To induce autophosphorylation of the receptor, various concentrations of ATP are added to the ELISA plate wells containing serially diluted solutions of SU5416. The autophosphorylation is allowed to proceed for 60 min at room temperature and then stopped with EDTA. The amount of phosphotyrosine present on the Flk-1 receptors in the individual wells is determined by incubating the immunolocalized receptor with a biotinylated monoclonal antibody directed against phosphotyrosine. After removal of the unbound anti-phosphotyrosine antibody, avidin-conjugated horseradish pero-idase H is added to the wells. A stabilized form of 3,3 9,5,5 9-tetramethyl benzidine dihydrochloride and H2O2 is added to the wells. The color readout of the assay is allowed to develop for 30 min, and the reaction is stopped with H2SO4.
Cell Research:[1]
+ Expand
  • Cell lines: HUVECs
  • Concentrations: ~100 μM
  • Incubation Time: 2 days
  • Method: HUVECs are plated in 96-well, flat-bottomed plates (1×104 cells/100 μL/well) in F-12K media containing 0.5% heat-inactivated FBS and cultured at 37 ℃ for 24 h to quiesce the cells. Serial dilutions of compounds prepared in medium containing 1% DMSO are then added for 2 h, followed by the addition of mitogenic concentrations of either VEGF at 5 ng/mL or 20 ng/mL or acidic fibroblast growth factor at 0.25–5 ng/mL in media. The final concentration of DMSO in the assay is 0.25%. After 24 h, either [3H]thymidine (1 μCi/well) or BrdUrd is added, and the cell monolayers are incubated for another 24 h. The uptake of either [3H]thymidine or BrdUrd into cells is quantitated using a liquid scintillation counter or a BrdUrd ELISA, respectively.
    (Only for Reference)
Animal Research:[1]
+ Expand
  • Animal Models: Human melanoma xenografts A375
  • Formulation: DMSO
  • Dosages: 25 mg/kg
  • Administration: i.p. daily
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 22 mg/mL (92.32 mM)
Ethanol 2 mg/mL (8.39 mM)
Water Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5% DMSO+40%PEG 300+ 5% Tween80 + ddH2O
For best results, use promptly after mixing. 		0.5mg/mlmg/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 238.28
Formula

C15H14N2O
CAS No. 194413-58-6
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT00006247 Terminated Drug: semaxanib Brain and Central Nervous System Tumors Pediatric Brain Tumor Consortium|National Cancer Institute (NCI) August 2000 Phase 1
NCT00005642 Completed Drug: semaxanib Unspecified Adult Solid Tumor Protocol Specific Case Comprehensive Cancer Center|National Cancer Institute (NCI) May 2000 Phase 1
NCT00005647 Completed Drug: paclitaxel|Drug: semaxanib Head and Neck Cancer Case Comprehensive Cancer Center|National Cancer Institute (NCI) May 2000 Phase 1

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID