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SU5402 (SU-5402; SU 5402)

Alias: SU-5402; SU 5402; 215543-92-3; 3-[(3-(2-CARBOXYETHYL)-4-METHYLPYRROL-2-YL)METHYLENE]-2-INDOLINONE; 2-[(1,2-Dihydro-2-oxo-3H-indol-3-ylidene)methyl]-4-methyl-1H-pyrrole-3-propanoic acid; 3-[4-methyl-2-[(Z)-(2-oxo-1H-indol-3-ylidene)methyl]-1H-pyrrol-3-yl]propanoic acid; 3-[3-(2-Carboxyethyl)-4-methylpyrrol-2-methylidenyl]-2-indolinone; SU5402
Cat No.:V0495 Purity: ≥98%
SU5402 (SU-5402; SU 5402) is a multi-targeted RTK (receptor tyrosine kinase) inhibitor with potential antineoplastic activity.
SU5402 (SU-5402; SU 5402)
SU5402 (SU-5402; SU 5402) Chemical Structure CAS No.: 215543-92-3
Product category: VEGFR
This product is for research use only, not for human use. We do not sell to patients.
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

SU5402 (SU-5402; SU 5402) is a multi-targeted RTK (receptor tyrosine kinase) inhibitor with potential antineoplastic activity. It has IC50s of 20 nM, 30 nM, and 510 nM for VEGFR2, FGFR1, and PDGFRβ inhibition, respectively.

Biological Activity I Assay Protocols (From Reference)
Targets
VEGFR2 (IC50 = 20 nM); FGFR1 (IC50 = 30 nM); PDGFRβ (IC50 = 510 nM)
ln Vitro

SU5402 inhibits cell proliferation that is dependent on VEGF, FGF, and PDGF, with IC50 values of 0.05 μM, 2.80 μM, and 28.4 μM, respectively.[1] With an IC50 of 0.04 μM, SU5416 dose-dependently and selectively inhibits VEGF-driven mitogenesis in HUVECs.[2] SU5402 inhibits LMP1-mediated cellular transformation, invasion, migration, and aerobic glycolysis in nasopharyngeal epithelial cells.[3] SU 5402 reduces the impact of FGF23 on cell differentiation in mouse C3H10T1/2 cells.[4]

ln Vivo
SU5416 (25 mg/kg, i.p.) prevents the growth of a panel of tumor cell lines under the skin in mice by blocking the angiogenic process that is linked to tumor growth.[2]
In contrast, systemic administration of SU5416 at nontoxic doses in mice resulted in inhibition of subcutaneous tumor growth of cells derived from various tissue origins. The antitumor effect of SU5416 was accompanied by the appearance of pale white tumors that were resected from drug-treated animals, supporting the antiangiogenic property of this agent. These findings support that pharmacological inhibition of the enzymatic activity of the vascular endothelial growth factor receptor represents a novel strategy for limiting the growth of a wide variety of tumor types.[2]
Reversal of MCT-induced PH with the FGFR1 inhibitor SU5402. [5]
To confirm that the decreases in pulmonary vascular alterations and PH associated with FGF2-siRNA treatment were related to FGF2 knockdown, indicating a key role for FGF2 overproduction in PH, we investigated to determine whether the selective FGFR1 inhibitor SU5402 prevented and/or reversed PH induced by MCT in rats. In rats treated with SU5402 on days 21 to 42 after the MCT injection, evaluations on day 42 showed marked decreases in PAP, RV/(LV + S), and distal artery muscularization compared with rats treated with the vehicle (saline) (Figure 8).
Enzyme Assay
The catalytic domain of FGF-R1 and Flk-1/KDR is expressed as GST fusion proteins after baculoviruses with altered genomes infect Spodoptera frugiperda (sf9) cells. Using glutathione sepharose chromatography, infected sf9 cell lysates are purified to homogeneity for GST-FGFR1 and GST-Flk1. In 96-well microtiter plates, 2.0 μg of a polyGlu-Tyr peptide (4:1) in 0.1 mL of PBS per well is coated overnight before the assays are carried out. The diluted purified kinases are introduced to each test well at a rate of 5 ng of GST fusion protein per 0.05 mL volume buffer using kinase assay buffer (100 mM Hepes pH 7.5, 100 mM NaCl, and 0.1 mM sodium orthovanadate). Test compounds are added to test wells (0.025 mL/well) after being diluted in 4% DMSO. To start the kinase reaction, add 0.025 mL of 40 μM ATP/40 mM MnCl2. Shake the plates for 10 minutes, and then add 0.025 mL of 0.5 M EDTA to stop the reaction. The final concentration of ATP was 10 μM, which is twice the Km value of ATP as determined experimentally. MnCl2 and no ATP are added to the negative control wells. Three rounds of washing are performed on the plates using 10 mM Tris pH 7.4, 150 mM NaCl, and 0.05% Tween-20 (TBST). For one hour, the wells are filled with a 1:10000 dilution of rabbit polyclonal anti-phosphotyrosine antiserum in TBST. After that, TBST is used to wash the plates three times. Then, for one hour, each well received a conjugate of goat anti-rabbit antiserum and horseradish peroxidase. After three TBST washes of the plates, 2,2'-azinobis(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS) is added to detect the peroxidase reaction. After allowing the assay's color readout to develop for 20 to 30 minutes, it is read using a 410 nM test filter on a Dynatech MR5000 ELISA plate reader.
Cell Assay
The tumor cell lines that are utilized for the in vitro growth are grown in medium with 5–10% CO2 at 37°C. One day after the start of the culture, SU5416 is serially diluted in media containing DMSO (<0.5%) and added to tumor cell cultures. The sulforhodamine B method is used to measure the growth of the cells after 96 hours. Using four-parameter analysis and curve fitting, IC50s are determined.
Western blotting analysis: Total cell lysates (5–50 µg of protein) were separated by 10% or 4–12% SDS-PAGE and transferred to a PVDF membrane prior to immunoblotting.
Immunofluorescence and immunohistochemical staining: Immunofluorescence staining and immunohistochemical staining were performed as previously described [3].
Cell proliferation assay: Cell proliferation assay was performed with the cell proliferation reagent CCK-8 [3].
Soft agar cloning assay: Soft agar colony formation assays were performed as previously described [3].
Migration and invasion assays: Cell migration assays and Boyden chamber invasion assays were performed using the CytoSelect 24-Well Wound Healing Assay Kit and the CytoSelect 24-Well Cell Invasion Assay Kit, respectively. For collagen gel invasion assays, a collagen mixture was prepared with type I collagen solution [3].
SMC proliferation assessed by [3H]thymidine incorporation.[5]
PA-SMCs in DMEM supplemented with 15% FCS were seeded in 24-well plates at a density of 5 × 104 cells/well and allowed to adhere. The cells were subjected to 48 hours of growth arrest in serum-free medium, then treated with 1 ml of conditioned P-EC medium. We also tested the effect of exogenous PDGF (10 ng/ml) and FGF2 (10 ng/ml) on PA-SMC proliferation with or without imatinib (10–5 M), EGF antagonist (10-5 M), and SU5402 (10-5 M). Under each condition, [3H]thymidine (1 μCi/ml) was added to each well. After incubation for 24 hours, the cells were washed twice with PBS, treated with ice-cold 10% trichloroacetic acid, and dissolved in 0.1 N NaOH (0.5 ml/well). The incorporated radioactivity was counted and reported as cpm/well.
Animal Protocol
Mice: For one week, intraperitoneal injections of DMSO or SU 5402 (dissolved in DMSO at a concentration of 6 mg/mL) at 25 mg/kg body weight are given to male ΔF508 mice (CFTRtm1Eur on a 129/FVB background) and their wild-type littermates, aged 9–12 weeks. Every day, the dosages are modified based on the mice's weight. Afterwards, isoflurane is breathed into the mice to induce anesthesia until the procedure is completed. To prevent potential cholinergic stimulation of the salivary gland, 50 μL of the cholinergic antagonist atropine (1 mM) is subcutaneously injected into the right cheek. For four minutes, the injected cheek is pressed up against a tiny strip of filter paper. The same location is then subinjected with isoprenaline (10 mM, 37.5 μL) to elicit an adrenergic secretion of saliva (time 0). For thirty minutes, replace the filter strips (pre-weighed in an Eppendorf tube) every five minutes. After the collection is complete, the weight of all six filter strips is measured, and the results are normalized to mg/g body weight.
Rats: Adult male Wistar rats (200–250 g) are given MCT (60 mg/kg s.c.) and left untreated for 21 dayIn order to evaluate the possible impact of the FGFR1 inhibitor SU 5402 on established PH, adult male Wistar rats weighing 200–250 g are administered MCT (60 mg/kg s.c.), allowed to go untreated for 21 days, and then split into two groups at random (10 animals per group): one group receives treatment with SU 5402 (25 mg/kg/day), while the other group receives no treatment from day 21 to day 42. Every treatment is administered intravenously (s.c.) once daily.
Effect of treatment with SU5402 on established MCT PH. [5]
To assess the potential effects of the FGFR1 inhibitor SU5402 on established PH, adult male Wistar rats (200–250 g) were given MCT (60 mg/kg s.c.), left untreated for 21 days, then randomly divided into 2 groups (10 animals in each group), of which one was treated with SU5402 (25 mg/kg/day) and the other given the vehicle, from day 21 to day 42. All treatments were given once a day by s.c. injection
References

[1]. Design, synthesis, and evaluations of substituted 3-[(3- or 4-carboxyethylpyrrol-2-yl)methylidenyl]indolin-2-ones as inhibitors of VEGF, FGF, and PDGF receptor tyrosine kinases. J Med Chem. 1999 Dec 16;42(25):5120-30.

[2]. SU5416 is a potent and selective inhibitor of the vascular endothelial growth factor receptor (Flk-1/KDR) that inhibits tyrosine kinase catalysis, tumor vascularization, and growth of multiple tumor types. Cancer Res. 1999 Jan 1;59(1):99-106.

[3]. Activation of the FGFR1 signalling pathway by the Epstein-Barr virus-encoded LMP1 promotes aerobic glycolysis and transformation of human nasopharyngeal epithelial cells. J Pathol. 2015 Oct;237(2):238-48.

[4]. FGF23 affects the lineage fate determination of mesenchymal stem cells. Calcif Tissue Int. 2013 Dec;93(6):556-64.

[5]. Endothelial-derived FGF2 contributes to the progression of pulmonary hypertension in humans and rodents. J Clin Invest. 2009 Mar;119(3):512-23.

Additional Infomation
SU5402 is an oxindole that is 3-methyleneoxindole in which one of the hydrogens of the methylene group is substituted by a 3-(2-carboxyethyl)-4-methyl-1H-pyrrol-2-yl group. It is an ATP-competitive inhibitor of the tyrosine kinase activity of fibroblast growth factor receptor 1. It has a role as a fibroblast growth factor receptor antagonist. It is a monocarboxylic acid, a member of pyrroles and a member of oxindoles. It is functionally related to a 3-methyleneoxindole.
Receptor tyrosine kinases (RTKs) have been implicated as therapeutic targets for the treatment of human diseases including cancers, inflammatory diseases, cardiovascular diseases including arterial restenosis, and fibrotic diseases of the lung, liver, and kidney. Three classes of 3-substituted indolin-2-ones containing propionic acid functionality attached to the pyrrole ring at the C-3 position of the core have been identified as catalytic inhibitors of the vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and platelet-derived growth factor (PDGF) RTKs. Some of the compounds were found to inhibit the tyrosine kinase activity associated with isolated vascular endothelial growth factor receptor 2 (VEGF-R2) [fetal liver tyrosine kinase 1 (Flk-1)/kinase insert domain-containing receptor (KDR)], fibroblast growth factor receptor (FGF-R), and platelet-derived growth factor receptor (PDGF-R) tyrosine kinase with IC(50) values at nanomolar level. Thus, compound 1 showed inhibition against VEGF-R2 (Flk-1/KDR) and FGF-R1 tyrosine kinase activity with IC(50) values of 20 and 30 nM, respectively, while compound 16f inhibited the PDGF-R tyrosine kinase activity with IC(50) value of 10 nM. Structural models and structure-activity relationship analysis of these compounds for the target receptors are discussed. The cellular activities of these compounds were profiled using cellular proliferation assays as measured by bromodeoxyuridine (BrdU) incorporation. Specific and potent inhibition of cell growth was observed for some of these compounds. These data provide evidence that these compounds can be used to inhibit the function of these target receptors. [1]
Non-keratinizing nasopharyngeal carcinoma (NPC) is closely associated with Epstein-Barr virus (EBV) infection. The EBV-encoded latent membrane protein 1 (LMP1) is believed to play an important role in NPC pathogenesis by virtue of its ability to activate multiple cell signalling pathways which collectively promote cell proliferation, transformation, angiogenesis, and invasiveness, as well as modulation of energy metabolism. In this study, we report that LMP1 increases cellular uptake of glucose and glutamine, enhances LDHA activity and lactate production, but reduces pyruvate kinase activity and pyruvate concentrations. LMP1 also increases the phosphorylation of PKM2, LDHA, and FGFR1, as well as the expression of PDHK1, FGFR1, c-Myc, and HIF-1α, regardless of oxygen availability. Collectively, these findings suggest that LMP1 promotes aerobic glycolysis. With respect to FGFR1 signalling, LMP1 not only increases FGFR1 expression, but also up-regulates FGF2, leading to constitutive activation of the FGFR1 signalling pathway. Furthermore, two inhibitors of FGFR1 (PD161570 and SU5402) attenuate LMP1-mediated aerobic glycolysis, cellular transformation (proliferation and anchorage-independent growth), cell migration, and invasion in nasopharyngeal epithelial cells, identifying FGFR1 signalling as a key pathway in LMP1-mediated growth transformation. Immunohistochemical staining revealed that high levels of phosphorylated FGFR1 are common in primary NPC specimens and that this correlated with the expression of LMP1. In addition, FGFR1 inhibitors suppress cell proliferation and anchorage-independent growth of NPC cells. Our current findings demonstrate that LMP1-mediated FGFR1 activation contributes to aerobic glycolysis and transformation of epithelial cells, thereby implicating FGF2/FGFR1 signalling activation in the EBV-driven pathogenesis of NPC. [2]
FGF23 is a bone-derived hormone that regulates mineral metabolism by inhibiting renal tubular phosphate reabsorption and suppressing circulating 1,25(OH)2D and PTH levels. These effects are mediated by FGF-receptor binding and activation in the presence of its coreceptor Klotho, which is expressed in the distal tubules of the kidney. Recently, expression of Klotho in skeletal tissues has been reported, indicating a direct, yet unclear, extrarenal effect of FGF23 on cells involved with bone development and remodeling. In the present study, we found that bone marrow stromal cells harvested from Klotho null mice developed fewer osteoblastic but more adipocytic colonies than cells from wild-type mice. The underlying mechanism was explored by experiments on mouse C3H10T1/2 cells. We found that Klotho was weakly expressed and that FGF23 dose-dependently affected the lineage fate determination. The effects of FGF23 on cell differentiation can be diminished by SU5402, a specific tyrosine kinase inhibitor for FGF receptors. Our results indicate that FGF23 directly affects the differentiation of bone marrow stromal cells.[4]
Pulmonary hypertension (PH) is a progressive, lethal lung disease characterized by pulmonary artery SMC (PA-SMC) hyperplasia leading to right-sided heart failure. Molecular events originating in pulmonary ECs (P-ECs) may contribute to the PA-SMC hyperplasia in PH. Thus, we exposed cultured human PA-SMC to medium conditioned by P-EC from patients with idiopathic PH (IPH) or controls and found that IPH P-EC-conditioned medium increased PA-SMC proliferation more than control P-EC medium. Levels of FGF2 were increased in the medium of IPH P-ECs over controls, while there was no detectable difference in TGF-beta1, PDGF-BB, or EGF levels. No difference in FGF2-induced proliferation or FGF receptor type 1 (FGFR1) mRNA levels was detected between IPH and control PA-SMCs. Knockdown of FGF2 in P-EC using siRNA reduced the PA-SMC growth-stimulating effects of IPH P-EC medium by 60% and control P-EC medium by 10%. In situ hybridization showed FGF2 overproduction predominantly in the remodeled vascular endothelium of lungs from patients with IPH. Repeated intravenous FGF2-siRNA administration abolished lung FGF2 production, both preventing and nearly reversing a rat model of PH. Similarly, pharmacological FGFR1 inhibition with SU5402 reversed established PH in the same model. Thus, endothelial FGF2 is overproduced in IPH and contributes to SMC hyperplasia in IPH, identifying FGF2 as a promising target for new treatments against PH.[5]
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C17H16N2O3
Molecular Weight
296.32
Exact Mass
296.116
Elemental Analysis
C, 68.91; H, 5.44; N, 9.45; O, 16.20
CAS #
215543-92-3
Related CAS #
SU 5402;215543-92-3
PubChem CID
5289418
Appearance
Orange solid powder
Density
1.4±0.1 g/cm3
Boiling Point
592.6±50.0 °C at 760 mmHg
Melting Point
>222ºC (dec.)
Flash Point
312.2±30.1 °C
Vapour Pressure
0.0±1.8 mmHg at 25°C
Index of Refraction
1.688
LogP
2.03
Hydrogen Bond Donor Count
3
Hydrogen Bond Acceptor Count
3
Rotatable Bond Count
4
Heavy Atom Count
22
Complexity
488
Defined Atom Stereocenter Count
0
SMILES
O=C(CCC1=C(NC=C1C)/C=C2C(NC3=C\2C=CC=C3)=O)O
InChi Key
JNDVEAXZWJIOKB-JYRVWZFOSA-N
InChi Code
InChI=1S/C17H16N2O3/c1-10-9-18-15(11(10)6-7-16(20)21)8-13-12-4-2-3-5-14(12)19-17(13)22/h2-5,8-9,18H,6-7H2,1H3,(H,19,22)(H,20,21)/b13-8-
Chemical Name
3-[4-methyl-2-[(Z)-(2-oxo-1H-indol-3-ylidene)methyl]-1H-pyrrol-3-yl]propanoic acid
Synonyms
SU-5402; SU 5402; 215543-92-3; 3-[(3-(2-CARBOXYETHYL)-4-METHYLPYRROL-2-YL)METHYLENE]-2-INDOLINONE; 2-[(1,2-Dihydro-2-oxo-3H-indol-3-ylidene)methyl]-4-methyl-1H-pyrrole-3-propanoic acid; 3-[4-methyl-2-[(Z)-(2-oxo-1H-indol-3-ylidene)methyl]-1H-pyrrol-3-yl]propanoic acid; 3-[3-(2-Carboxyethyl)-4-methylpyrrol-2-methylidenyl]-2-indolinone; SU5402
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: ~59 mg/mL (~199.1 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In Vivo)
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

Injection Formulations
(e.g. IP/IV/IM/SC)
Injection Formulation 1: DMSO : Tween 80: Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution 50 μL Tween 80 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO 400 μLPEG300 50 μL Tween 80 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).
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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO 100 μLPEG300 200 μL castor oil 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10: 10 : 80 (i.e. 100 μL Ethanol 100 μL Cremophor 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH 400 μLPEG300 50 μL Tween 80 450 μL Saline)


Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).
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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders


Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 3.3747 mL 16.8737 mL 33.7473 mL
5 mM 0.6749 mL 3.3747 mL 6.7495 mL
10 mM 0.3375 mL 1.6874 mL 3.3747 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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In vivo Formulation Calculator (Clear solution)
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Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution 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 stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
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Biological Data
  • SU5402

    NIH 3T3 Flk-1 cells (A) or NIH 3T3 platelet-derived growth factor β cells (B) grown to confluency were preincubated with SU5416 at concentrations ranging from 0.05 to 50 μm for 1 h at 37°C. Cancer Res. 1999 Jan 1;59(1):99-106.

  • SU5402

    A375 cells (3 × 106) were implanted subcutaneous into the hindflank region of female BALB/c nu/nu mice 8–12 weeks of age. Cancer Res. 1999 Jan 1;59(1):99-106.

  • SU5402

    Rat C6 glioma cells were surgically implanted (0.5 × 106 cells/animal) under the serosa of the colon in BALB/c nu/nu mice. Beginning 1 day after implantation, animals were treated once daily with a 50 μl i.p. bolus injection of either SU5416 at 25 mg/kg/day in DMSO or DMSO alone for 16 days. On day 16 after implantation, animals were euthanized, and their local tumors in the colon were first quantitated by measurement using venier calipers and then harvested. Cancer Res. 1999 Jan 1;59(1):99-106.

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