Semaxanib (SU5416)

Name: Semaxanib (SU5416)
Brand: Selleck Chemicals
SKU: S2845
Rating: 5 (9 reviews)

For research use only. Not for use in humans.

Catalog No.S2845

9 publications

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.

Selleck's Semaxanib (SU5416) has been cited by 9 publications

ACS Appl Mater Interfaces, 2019, 101021/acsami9b20178

PubMed: 31816241 ( click the link to review the publication )

Angiogenesis, 2017, 20(4):629-640

PubMed: 28905243 ( click the link to review the publication )

Epilepsy Behav, 2017, 68:159-167

PubMed: 28193596 ( click the link to review the publication )

Int Forum Allergy Rhinol, 2017, 7(10):973-979

PubMed: 28707818 ( click the link to review the publication )

PLoS One, 2016, 11(11):e0167218

PubMed: 27880824 ( click the link to review the publication )

Sci Rep, 2016, 6:19304

PubMed: 26787224 ( click the link to review the publication )

Oncoimmunology, 2015, 10.1080/2162402X.2014.998107

PubMed: ( click the link to review the publication )

Oncoimmunology, 2015, 4(4):e998107

PubMed: 26137411 ( click the link to review the publication )

Clin Cancer Res, 2013, 19(9):2381-92

PubMed: 23532890 ( click the link to review the publication )

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.

Purity & Quality Control

Choose Selective VEGFR Inhibitors

Biological Activity

Description

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	Incubation Time	Activity Description	PMID
MCF7 cells	M{ntRWN6fG:2b4jpZ4l1gSCjc4PhfS=>	MlThOFghcA>?	NWDWSoxlS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVUOINzDj[YxteyCjZoTldkA1QCCqcoOgZpkhS0ONODDhd5NigSxiSVO1NF0{NjFibl2=	NVzMTZVuOjN5N{e4PVg>
mouse B16F10 cells	MnLoR5l1d3SxeHnjbZR6KGG\|c3H5	Mn3sOFghcA>?	NEH1UmdEgXSxdH;4bYNqfHliYXfhbY5{fCCvb4Xz[UBDOT[IMUCgZ4VtdHNiYX\0[ZIhPDhiaILzJIJ6KEOFS{igZZN{[XluIFnDOVA:Oy54IH7N	NGTMUGYzOzd5N{i5PC=>
human U251 cells	M4nJVmZ2dmO2aX;uJIF{e2G7		MofZTY5pcWKrdHnvckBw\iCYRVfGVlIhcW5iaIXtZY4hXTJ3MTDj[YxteyCkeTDwbI9{eGixdInyc5NqdmViRVzJV2EtKEmFNUC9NVIvQSCwTR?=	NIrMOWYzPDlyMEi2OS=>
human A431 cells	MmHxSpVv[3Srb36gZZN{[Xl?		M1\JUWFvfGmjbnfpc4dmdmmlIHHjeIl3cXS7IHHnZYlve3RiaIXtZY4hSTR\|MTDj[YxteyxiSVO1NF0xNjB6NTFOwG0>	M2nkflIxPDB\|Nkmz
CHO cells	NInMXGpHfW6ldHnvckBie3OjeR?=		NFPKcWdKdmirYnn0bY9vKG:oIG\FS2ZTKGmwZIXj[YQh[XW2b4Doc5NxcG:{eXzheIlwdiCxZjDoeY1idiCYYYPjeYxieiCnbnTveIhmdGmjbDDndo94fGhiZnHjeI9zKHKnY3XweI9zKDJiKG\FS2ZTOilidILhcpNn\WO2ZXSgbY4hS0iRIHPlcIx{NCCLQ{WwQVAvQDh2IN88US=>	MmXPNVI1Pzd\|NUK=
human MCF7 cells	M4ewcnBzd2yrZnXyZZRqd25iYYPzZZk>	MkXjOEBl[Xm\|	MoLBRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6\|dDDoeY1idiCPQ1[3JINmdGy\|IHHmeIVzKDRiZHH5d{BjgSClb4XseIVzKGOxdX70[ZIhdWW2aH;kMEBKSzVyPUGuPUDPxE1?	MX6yN\|EzPDJzMx?=
human SF539 cells	MX7GeY5kfGmxbjDhd5NigQ>?		MYfJcohq[mm2aX;uJI9nKFCGR1\SZoV1[SCrbjDoeY1idiCVRkWzPUBk\WyuczDifUBxcG:\|cHjveJlzd3OrbnWgSWxKW0FuIFnDOVA:Oi52IN88US=>	NFnjbpAyQTd2OEe4OS=>
A431 cells	NEnsO2xHfW6ldHnvckBie3OjeR?=		MWLJcohq[mm2aX;uJI9nKF[HR1\SNkBmgHC{ZYPz[YQhcW5iaIXtZY4hSTR\|MTDj[YxteyxiSVO1NF0yOi57IN88US=>	MlrDNlA2PThyN{K=
HUVEC cells	NHG1eXpRem:uaX\ldoF1cW:wIHHzd4F6	NIDsbok4OiCq	MnrqRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6\|dDDoeY1idiCKVW\FR{Bk\WyuczDhd5Nme3OnZDDhd{Bz\WS3Y4Tpc44hcW5iY3XscEB3cWGkaXzpeJkh[W[2ZYKgO\|IhcHK\|IHL5JJRzgXCjbjDicJVmKGG\|c3H5MEBIUTVyPUGzMlYh\|ryP	M1f6TFI3OzF6MEW2
human HMEC1 cells	MX7Qdo9tcW[ncnH0bY9vKGG\|c3H5	M{PpV\|ch\GG7cx?=	NXLaeJh3SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDIUWVEOSClZXzsd{Bi\nSncjC3JIRigXNiYomgZ492dHSncjDjc5VvfGW{IH3leIhw\CxiSVO1NF0yPSEQvF2=	Ml\3NlMyOjR{MUO=
human HeLa cells	M4i4O3Bzd2yrZnXyZZRqd25iYYPzZZk>	NUDVPGlRPCCmYYnz	M2DocGFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iSHXMZUBk\WyuczDh[pRmeiB2IHThfZMh[nliY3;1cJRmeiClb4XueIVzKG2ndHjv[EwhUUN3ME2yNEDPxE1?	NF3LR5EzOzF{NEKxNy=>

... 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 Br J Pharmacol 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 Microvasc Res 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 PLoS One 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]	- Collapse 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]	- Collapse 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]	- Collapse Animal Models: Human melanoma xenografts A375 Formulation: DMSO Dosages: 25 mg/kg Administration: i.p. daily (Only for Reference)

References

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 Download Semaxanib (SU5416) SDF

Molecular Weight	238.28
Formula	C₁₅H₁₄N₂O
CAS No.	194413-58-6
Storage	3 years -20°C powder
Storage	2 years -80°C in solvent
Synonyms	N/A
Smiles	CC1=CC(=C([NH]1)/C=C/2C(=O)NC3=CC=CC=C23)C

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Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2019-10-14)

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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Semaxanib (SU5416)