Semaxanib (SU5416)

Catalog No.S2845 Synonyms: semaxinib

For research use only.

Semaxanib (SU5416, semaxinib) 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.

Semaxanib (SU5416) Chemical Structure

CAS No. 194413-58-6, 204005-46-9

Selleck's Semaxanib (SU5416) has been cited by 16 publications

Purity & Quality Control

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Biological Activity

Description Semaxanib (SU5416, semaxinib) 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 MkHTR5l1d3SxeHnjbZR6KGG|c3H5 M3PzZlQ5KGh? M{WwfmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1ETjdiY3XscJMh[W[2ZYKgOFghcHK|IHL5JGNEUzhiYYPzZZktKEmFNUC9N{4yKG6P MmfaNlM4Pzd6OUi=
mouse B16F10 cells MoXwR5l1d3SxeHnjbZR6KGG|c3H5 NXflOFBmPDhiaB?= M{[zPWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KG2xdYPlJGIyPkZzMDDj[YxteyCjZoTldkA1QCCqcoOgZpkhS0ONODDhd5NigSxiSVO1NF0{NjZibl2= NVX5RpJjOjN5N{e4PVg>
human U251 cells NWX1PZJNTnWwY4Tpc44h[XO|YYm= NXr0eGJSUW6qaXLpeIlwdiCxZjDWSWdHWjJiaX6gbJVu[W5iVUK1NUBk\WyuczDifUBxcG:|cHjveJlzd3OrbnWgSWxKW0FuIFnDOVA:OTJwOTDuUS=> M17lflI1QTByOE[1
human A431 cells MkjWSpVv[3Srb36gZZN{[Xl? NUfISZd5SW62aXHu[4lw\2WwaXOgZYN1cX[rdImgZYdicW6|dDDoeY1idiCDNEOxJINmdGy|LDDJR|UxRTBwMEi1JO69VQ>? MVeyNFQxOzZ7Mx?=
CHO cells MlHQSpVv[3Srb36gZZN{[Xl? NELudVVKdmirYnn0bY9vKG:oIG\FS2ZTKGmwZIXj[YQh[XW2b4Doc5NxcG:{eXzheIlwdiCxZjDoeY1idiCYYYPjeYxieiCnbnTveIhmdGmjbDDndo94fGhiZnHjeI9zKHKnY3XweI9zKDJiKG\FS2ZTOilidILhcpNn\WO2ZXSgbY4hS0iRIHPlcIx{NCCLQ{WwQVAvQDh2IN88US=> NF7WRmgyOjR5N{O1Ni=>
human MCF7 cells MWHQdo9tcW[ncnH0bY9vKGG|c3H5 MV60JIRigXN? M3TnXWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTVPGO{Bk\WyuczDh[pRmeiB2IHThfZMh[nliY3;1cJRmeiClb4XueIVzKG2ndHjv[EwhUUN3ME2xMlkh|ryP M1fpTVI{OTJ2MkGz
human SF539 cells NF2xZ2xHfW6ldHnvckBie3OjeR?= NEDRU2pKdmirYnn0bY9vKG:oIGDES2ZT[mW2YTDpckBpfW2jbjDTSlU{QSClZXzsd{BjgSCyaH;zdIhwfHm{b4PpcoUhTUyLU1GsJGlEPTB;Mj60JO69VQ>? MVyxPVc1QDd6NR?=
A431 cells NHzZNItHfW6ldHnvckBie3OjeR?= NW\GZnRXUW6qaXLpeIlwdiCxZjDWSWdHWjJiZYjwdoV{e2WmIHnuJIh2dWGwIFG0N|Eh[2WubIOsJGlEPTB;MUKuPUDPxE1? MoLVNlA2PThyN{K=
HUVEC cells MXfQdo9tcW[ncnH0bY9vKGG|c3H5 Mn7MO|IhcA>? NYPMTZVRSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDIWXZGSyClZXzsd{Bie3Onc4Pl[EBieyC{ZXT1Z5Rqd25iaX6gZ4VtdCC4aXHibYxqfHliYX\0[ZIhPzJiaILzJIJ6KHS{eYDhckBjdHWnIHHzd4F6NCCJSUWwQVE{NjZizszN NF;uNJMzPjNzOEC1Oi=>
human HMEC1 cells M4PTdXBzd2yrZnXyZZRqd25iYYPzZZk> NV[0Vo9CPyCmYYnz NX;xUmd2SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDIUWVEOSClZXzsd{Bi\nSncjC3JIRigXNiYomgZ492dHSncjDjc5VvfGW{IH3leIhw\CxiSVO1NF0yPSEQvF2= MnnUNlMyOjR{MUO=
human HeLa cells M2\sZ3Bzd2yrZnXyZZRqd25iYYPzZZk> Mlf1OEBl[Xm| NFfNcHZCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjlUIEh[2WubIOgZYZ1\XJiNDDkZZl{KGK7IHPveYx1\XJiY3;1cpRmeiCvZYToc4QtKEmFNUC9NlAh|ryP M1zHVFI{OTJ2MkGz
Assay
Methods Test Index PMID
Western blot p-VEGFR2 / VEGFR2 / p-PLCγ1 / PLCγ1 / p-ERK / ERK 21699503
Immunofluorescence CD31 / OCT-4 / SOX-2 25665868
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 (from reference)

Kinase Assay:[1]
  • 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]
  • 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.
Animal Research:[1]
  • Animal Models: Human melanoma xenografts A375
  • Dosages: 25 mg/kg
  • Administration: i.p. daily

Solubility (25°C)

In vitro

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

Chemical Information

Molecular Weight 238.28
Formula

C15H14N2O

CAS No. 194413-58-6, 204005-46-9
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles CC1=CC(=C(N1)C=C2C3=CC=CC=C3NC2=O)C

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)

mg/kg g μL

Step 2: Enter the in vivo formulation (This is only the calculator, not formulation. Please contact us first if there is no in vivo formulation at the solubility Section.)

% DMSO % % Tween 80 % ddH2O
%DMSO %

Calculation results:

Working concentration: mg/ml;

Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such
as vortex, ultrasound or hot water bath can be used to aid dissolving.

Molarity Calculator

Mass Concentration Volume Molecular Weight

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

(data from https://clinicaltrials.gov, updated on 2022-08-01)

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

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