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Su1498

Manufactured by Merck Group
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SU1498 is a lab equipment product manufactured by Merck Group. It is a chemical compound used for research and scientific applications. The core function of SU1498 is to inhibit the activity of the epidermal growth factor receptor (EGFR) tyrosine kinase.

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Lab products found in correlation

Ve cadherin, by Santa Cruz Biotechnology (2 mentions) P enoss1177, by Cell Signaling Technology (2 mentions) Pvegfr2 y1175, by Cell Signaling Technology (2 mentions) Tvegfr2, by Cell Signaling Technology (2 mentions) Piezo1, by Abcam (2 mentions) T enos, by BD (2 mentions) P vinculiny822, by Abcam (2 mentions) T vinculin, by Merck Group (2 mentions) Integrin αvβ3 clone lm609, by Merck Group (2 mentions) Plxnd1, by Thermo Fisher Scientific (2 mentions) Gq 11, by Santa Cruz Biotechnology (2 mentions) Nrp1 blocking antibody, by R&D Systems (2 mentions) Semaphorin 3e, by R&D Systems (2 mentions) T akt, by Cell Signaling Technology (2 mentions) Pakt s473, by Cell Signaling Technology (2 mentions) Igg2a, by BioLegend (1 mentions) Pitstop 2, by Merck Group (1 mentions) Hydroxy dynasore, by Merck Group (1 mentions) Amine coupling kit, by GE Healthcare (1 mentions) Recombinant human vegf 165 293 ve 010 cf, by R&D Systems (1 mentions)

8 protocols using su1498

1

Retinal Explant VEGF Modulation

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Retinal explants were incubated for 24 h with different concentrations of recombinant mouse VEGF (ThermoFisher Scientific), with 100 µM H2O2 (Sigma-Aldrich), or with 25 µM of the VEGFR2 inhibitor SU1498 (Sigma-Aldrich).
Rossino M.G., Lulli M., Amato R., Cammalleri M., Dal Monte M, & Casini G. (2020). Oxidative Stress Induces a VEGF Autocrine Loop in the Retina: Relevance for Diabetic Retinopathy. Cells, 9(6), 1452.
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2

Inhibiting VEGFR-2 and Neutralizing VEGF-A in C. difficile Infection

Cited 1 time
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To inhibit VEGFR-2, mice were treated with daily intraperitoneal injections of 100μl SU1498 (30 mg/kg in dimethyl sulfoxide, Sigma Aldrich, Inc.) or dimethyl sulfoxide alone starting on the day of C. difficile gavage and continuing daily for 3 days49 (link). To neutralize VEGF-A, mice were treated with intraperitoneal injection of 250 μg rat anti-mouse VEGF-A antibody (2G11–2A05) or the isotype control IgG2a (each at 12.5 mg/kg, Biolegend, Inc.)50 (link) at 12 and 36 hours after C. difficile challenge. To stabilize HIF-1α prolyl hydroxylase, mice were treated with intraperitoneal injections of 100μl DMOG (400mg/kg in saline, Cayman Chemical) starting on the day of C. difficile gavage for 2 days.
Huang J., Kelly C.P., Bakirtzi K., Gálvez J.A., Lyras D., Mileto S.J., Larcombe S., Xu H., Yang X., Shields K.S., Zhu W., Zhang Y., Goldsmith J.D., Patel I.J., Hansen J., Huang M., Yla-Herttuala S., Moss A.C., Paredes-Sabja D., Pothoulakis C., Shah Y.M., Wang J, & Chen X. (2018). Clostridium difficile toxins induce VEGF-A and vascular permeability to promote disease pathogenesis. Nature microbiology, 4(2), 269-279.
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3

Shear Stress Effects on HUVEC Adhesion Molecules

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HUVECs were pretreated with SU‐1498 (SML1193, Sigma Aldrich) at 20 μM for 4 h or Hydroxy‐Dynasore (SML0340, Sigma Aldrich) at 100 μM or Pitstop‐2 (SML1169, Sigma Aldrich) at 30 μM for 1 h. The resulting cells were exposed to 15 dyn/cm2 of shear stress for 5, 10 and 30 min. The cells were fixed and analyzed by immunofluorescence staining for VE‐PTP and VE‐cadherin.
Shirakura K., Baluk P., Nottebaum A.F., Ipe U., Peters K.G., McDonald D.M, & Vestweber D. (2023). Shear stress control of vascular leaks and atheromas through Tie2 activation by VE‐PTP sequestration. EMBO Molecular Medicine, 15(4), e16128.
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4

VEGFR2 and Semaphorin 3E Signaling

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The antibodies used for western blotting included phospho(p)-ERK1/2T-202;Y-204, total(t)-ERK1/2, pAktS473, tAkt, p-eNOSS1177, pVEGFR2Y1175, tVEGFR2 (all antibodies from Cell Signaling Technology), t-eNOS (BD Biosciences), p-VinculinY822 (AbCam), t-Vinculin (Sigma Aldrich), PI3K/P85 (Upstate), integrin αvβ3 (clone LM609, Merck), Shc (Abcam),VE-cadherin (Santa Cruz), PlxnD1 (Thermo Fisher Scientific and Abcam), Piezo1 (Abcam), Gq/11 (Santa Cruz Biotechnology), Src (Upstate)
The inhibitors used in the study included VEGFR2 tyrosine kinase inhibitor SU1498 (Sigma Aldrich). Recombinant Semaphorin 3E was purchased from R&D Systems (Bio-techne, Minneapolis, MN, USA) and used at 10 μM. NRP1 blocking antibody was purchased from R&D Systems and Sema3E blocking antibody was from Thermo Fisher Scientific USA.
Mehta V., Pang K.L., Rozbesky D., Nather K., Keen A., Lachowski D., Kong Y., Karia D., Ameismeier M., Huang J., Fang Y., del Rio Hernandez A., Reader J.S., Yvonne Jones E, & Tzima E. (2020). The Guidance Receptor Plexin D1 Moonlights as an Endothelial Mechanosensor. Nature, 578(7794), 290-295.
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5

VEGFR2 and Semaphorin 3E Signaling

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The antibodies used for western blotting included phospho(p)-ERK1/2T-202;Y-204, total(t)-ERK1/2, pAktS473, tAkt, p-eNOSS1177, pVEGFR2Y1175, tVEGFR2 (all antibodies from Cell Signaling Technology), t-eNOS (BD Biosciences), p-VinculinY822 (AbCam), t-Vinculin (Sigma Aldrich), PI3K/P85 (Upstate), integrin αvβ3 (clone LM609, Merck), Shc (Abcam),VE-cadherin (Santa Cruz), PlxnD1 (Thermo Fisher Scientific and Abcam), Piezo1 (Abcam), Gq/11 (Santa Cruz Biotechnology), Src (Upstate)
The inhibitors used in the study included VEGFR2 tyrosine kinase inhibitor SU1498 (Sigma Aldrich). Recombinant Semaphorin 3E was purchased from R&D Systems (Bio-techne, Minneapolis, MN, USA) and used at 10 μM. NRP1 blocking antibody was purchased from R&D Systems and Sema3E blocking antibody was from Thermo Fisher Scientific USA.
Mehta V., Pang K.L., Rozbesky D., Nather K., Keen A., Lachowski D., Kong Y., Karia D., Ameismeier M., Huang J., Fang Y., del Rio Hernandez A., Reader J.S., Yvonne Jones E, & Tzima E. (2020). The Guidance Receptor Plexin D1 Moonlights as an Endothelial Mechanosensor. Nature, 578(7794), 290-295.
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6

Hyaluronan Modification and VEGFR-2 Inhibition

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Hyaluronan (HA) (from Streptococcus, MW = 1.1 × 106 g mol−1) was obtained from Aqua Biochem (Dessau, Germany). Sulfur trioxide/dimethylformamide complex (SO3–DMF, purum, 97%, active SO3 48%) as well as sulfur trioxide/pyridine complex (SO3–pyridine, pract.; 45% SO3) were acquired from Fluka Chemie, (Buchs, Switzerland). Hep extracted from porcine intestinal mucosa and the specific VEGFR-2 inhibitor SU1498 were available from Sigma-Aldrich (Schnelldorf, Germany). Hep hexasaccharide (dp 6) was obtained from Iduron (Manchester, UK). Recombinant human VEGF165 (293-VE-010/CF) and neutralizing VEGFR-2 antibody (MAB3572-100) were obtained from R&D Systems (Wiesbaden-Nordenstadt, Germany). For SPR measurements, the Series S Sensor Chips C1, CM5 and CM3, the Amine Coupling Kit and HBS-EP (10x) from GE Healthcare Europe GmbH (Freiburg, Germany) were used. The VEGF165 HBD was purified as previously described26 (link).
Koehler L., Ruiz-Gómez G., Balamurugan K., Rother S., Freyse J., Möller S., Schnabelrauch M., Köhling S., Djordjevic S., Scharnweber D., Rademann J., Pisabarro M.T, & Hintze V. (2019). Dual Action of Sulfated Hyaluronan on Angiogenic Processes in Relation to Vascular Endothelial Growth Factor-A. Scientific Reports, 9, 18143.
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7

Intracerebroventricular Delivery of VEGF Inhibitors in Ischemic Stroke Model

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VEGF and the VEGFRs inhibitors were administered by intracerebroventricular (i.c.v.) injections in the corresponding animal groups 30 min after intraluminal filament removal, which marked the beginning of reperfusion, with the following stereotaxic coordinates: AP -0.8 and L -1.5 from Bregma and V -4 from dura matter. Injections were performed with graduated glass microcapillary pipettes that were pulled to produce a tip < 50 μm in diameter (McCluskey et al., 2008 (link)) at a flux rate of 0.8 μL/min. Because of the non-polar nature of the inhibitors used in this study, we injected a corresponding volume of DMSO in all experimental groups to control for DMSO possible effects. Control sham- and MCAO-operated animals were injected with vehicle solutions consisting of 2 μL DMSO followed by 2 μL 0.1% BSA (4 μL final volume). Recombinant rat VEGF-A164 (Sigma) was prepared in a 0.1% BSA at a final concentration of 25 ng/μL, 2 μL VEGF were injected followed by 2 μL DMSO. SU1498 and Axitinib (both from Sigma) were prepared in DMSO at a concentration of 6.4 mM. Two μL of each inhibitor were administered in the corresponding groups followed by 2 μL 0.1% BSA or 25 ng/μL VEGF depending on the experimental condition.
Cárdenas-Rivera A., Campero-Romero A.N., Heras-Romero Y., Penagos-Puig A., Rincón-Heredia R, & Tovar-y-Romo L.B. (2019). Early Post-stroke Activation of Vascular Endothelial Growth Factor Receptor 2 Hinders the Receptor 1-Dependent Neuroprotection Afforded by the Endogenous Ligand. Frontiers in Cellular Neuroscience, 13, 270.
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8

Signaling Pathway Modulation Protocol

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All cell culture serum and media were purchased from Gibico,while cell culture supplements were purchased from Sigma. Theantibody against Flag (ab190059) wasfrom Abcam. The antibodies against XBP1 (M-186,sc-7160), IRE1α (sc-20790),eNOS(sc-376542), Akt1/2/3 (sc-81434) and GAPDH (sc-25778) were fromSanta CruZ Biotech. All secondary antibodies werefrom Dakocytomation. All microRNA reagents were purchased from Thermo Fisher Scientific. SU1498, L-NAME, LY294002, KT-5823, DMSO, DAPI, crystal violet and Nitrite/Nitrate Assay Kit (23479)were purchased from Sigma.
Yang J., Xu J., Danniel M., Wang X., Wang W., Zeng L, & Shen L. (2018). The interaction between XBP1 and eNOS contributes to endothelial cell migration. Experimental cell research, 363(2).
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