Sb225002

Manufactured by Bio-Techne

Sourced in United Kingdom

SB225002 is a lab equipment product from Bio-Techne. It is a small molecule inhibitor used in scientific research.

Automatically generated - may contain errors

Lab products found in correlation

Cxcl1 neutralizing antibody, by Boster Bio (2 mentions) Carrageenan, by Merck Group (2 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (2 mentions) Tnf α, by Thermo Fisher Scientific (1 mentions) Timolol, by Bio-Techne (1 mentions) Tamsulosin, by Bio-Techne (1 mentions) Pd98059, by Merck Group (1 mentions) Normal goat serum (ngs), by Southern Biotech (1 mentions) Mouse igg1 anti ctbp2, by BD (1 mentions) Alexa fluortm 488 goat anti mouse igg2a, by Thermo Fisher Scientific (1 mentions) Alexa fluortm 647 donkey anti goat igg, by Thermo Fisher Scientific (1 mentions) Aqua ad iniectabilia, by B. Braun (1 mentions) Alzet, by Durect (1 mentions) Bay11 7082, by Merck Group (1 mentions) Par4 ap aypgkf nh2, by Peptide Institute (1 mentions) Yapgkf nh2, by Peptide Institute (1 mentions) H e staining reagents, by Thermo Fisher Scientific (1 mentions) Amd3100, by Bio-Techne (1 mentions) Vevo 1100 high resolution imaging system, by Fujifilm (1 mentions) 30 mhz high frequency scan head, by Fujifilm (1 mentions)

30 protocols using sb225002

Genetically-Engineered Lung Tumor Mouse Model

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Mice carrying the Stat3^floxed allele20 (link) were crossed with the Kras^LSLG12D/+ knock-in mice19 (link) to generate Stat3^flox/flox:Kras^G12D/+ mice maintained on a C57BL6/N background. In all experiments described, littermates were used as controls. All mice were bred and maintained according to an ethical animal licence protocol complying with the current Austrian law. Induction of lung tumours via intranasal AdCre inhalation was performed with 2.5 × 10⁷ plaque-forming unit as described64 (link). Stat3^ΔLep/ΔLep:Kras^G12D/+ and Stat3^+/+:Kras^G12D/+ mice were treated with SB225002 (Tocris#2725) as following: 1 week or 6 weeks post Adenoviral Cre infection, mice were injected either with vehicle or SB225002 (dissolved in PBS+0.25% Tween-20) with doses of 0.5 mg kg⁻¹ bodyweight intraperitoneally 5 days per week for 5 or 7 weeks, respectively. Treatment was performed according to an animal licence protocol approved by the Bundesministerium für Wissenschaft und Forschung (BMWF-66.009/0252-II/3b/2013).

Grabner B., Schramek D., Mueller K.M., Moll H.P., Svinka J., Hoffmann T., Bauer E., Blaas L., Hruschka N., Zboray K., Stiedl P., Nivarthi H., Bogner E., Gruber W., Mohr T., Zwick R.H., Kenner L., Poli V., Aberger F., Stoiber D., Egger G., Esterbauer H., Zuber J., Moriggl R., Eferl R., Győrffy B., Penninger J.M., Popper H, & Casanova E. (2015). Disruption of STAT3 signalling promotes KRAS-induced lung tumorigenesis. Nature Communications, 6, 6285.

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Microscale Bioparticle Cluster Arrays for Neutrophil Assays

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Microscale arrays of bioparticle clusters were manufactured as described (12 (link)). For pattern design, heat-killed S. aureus (SA) Texas Red particle conjugates (Sigma-Aldrich) were used. The slides had an eight-well table format consisting of 10 patterns per row arranged in eight columns with single pattern diameters of 130 µm. Before neutrophils were added, wells were coated with 10% SA-opsonization reagent (Thermo Fisher Scientific) and fibronectin (10 μg/ml) in FBS for 1 hour followed by three washes with 1× PBS. Control and GRK2-depleted neutrophils were differentially labeled with CellTracker Green and 5-TAMRA SE, mixed 1:1 and preactivated with TNF-α (50 ng/ml; PeproTech) for 10 min. Neutrophils were then suspended in bovine collagen I (Nutacon) at a final gel concentration of 1 mg/ml and a density of 2 × 10⁶ cells/ml, before 180 µl of the neutrophil-gel suspension was added to each well. To inhibit leukotriene biosynthesis, neutrophils were pre-incubated with 10 µM MK-886 (5-lipoxygenase-activating protein inhibitor, Calbiochem) for 30 min. To inhibit CXCL2 signaling, neutrophils were pre-incubated with 50 µM SB225002 (CXCR2 antagonist, Tocris) for 30 min. Loaded slides were incubated for 2 to 3 hours at 37°C before image acquisition. Images of whole slides were acquired at 10× magnification using the confocal spinning-disk microscope system as described above.

Kienle K., Glaser K.M., Eickhoff S., Mihlan M., Knöpper K., Reátegui E., Epple M.W., Gunzer M., Baumeister R., Tarrant T.K., Germain R.N., Irimia D., Kastenmüller W, & Lämmermann T. (2021). Neutrophils self-limit swarming to contain bacterial growth in vivo. Science (New York, N.Y.), 372(6548), eabe7729.

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Pharmacological Modulation of Corneal Wound Healing

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Immediately post wounding, the mice were topically administered the selective β2-AR agonist isoepinephrine (5 µL, 0.05 molL⁻¹; Tocris Bioscience, UK), the selective β2-AR antagonist timolol (5 µL, 0.01 molL⁻¹; Tocris Bioscience, UK), the α1-AR antagonist tamsulosin (5 µL, 20 molL⁻¹; Tocris Bioscience, UK). The aforementioned drugs were dissolved in a balanced salt solution (BSS), and the BSS was administered as the vehicle for the control mice. In some experiments, the mice received i.p. injections of the chemokine receptor CXCR2 antagonist SB 225002 (Tocris, 1 molL⁻¹, using dimethyl sulfoxide as vehicle) to inhibit neutrophil trafficking 5 min before ATSE^{39 (link)}. The effect of isoepinephrine, timolol, tamsulosin, and SB 225002 on corneal wound healing without ATSE was documented in Supplementary Figure 8 as the control data.

Xiao C., Wu M., Liu J., Gu J., Jiao X., Lu D., He J., Lin C., Xue Y., Fu T., Wang H., Wang G., Yang X, & Li Z. (2019). Acute tobacco smoke exposure exacerbates the inflammatory response to corneal wounds in mice via the sympathetic nervous system. Communications Biology, 2, 33.

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Intrathecal Delivery of CXCR2 Antagonist

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SB225002, a potent and selective antagonist of CXCR2, was purchased from Tocris (Bristol, UK). MEK inhibitor PD98059 was purchased from Merck KGaA (Darmstadt, Germany). The CXCL1 neutralizing antibody was purchased from Boster (Wuhan, China). For intrathecal injection, spinal cord puncture was made with a 30 G needle between the L5 and L6 level to deliver the reagents to the cerebral spinal fluid (Hylden and Wilcox, 1980 (link)).

Cao D.L., Zhang Z.J., Xie R.G., Jiang B.C., Ji R.R, & Gao Y.J. (2014). Chemokine CXCL1 enhances inflammatory pain and increases NMDA receptor activity and COX-2 expression in spinal cord neurons via activation of CXCR2. Experimental neurology, 0, 328-336.

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Antagonizing CXCR2 in Endotoxemia

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CXCR2 was blocked using its potent and selective antagonist SB225002 (Tocris, Bristol, UK). Mice were injected i.p. with the compound at 10 mg/kg b.w. 30 min before endotoxemia induction (1 mg/kg b.w. LPS, i.p.). The mice were imaged at 24 h of systemic inflammation.

Cichon I., Ortmann W., Santocki M., Opydo-Chanek M, & Kolaczkowska E. (2021). Scrutinizing Mechanisms of the ‘Obesity Paradox in Sepsis’: Obesity Is Accompanied by Diminished Formation of Neutrophil Extracellular Traps (NETs) Due to Restricted Neutrophil–Platelet Interactions. Cells, 10(2), 384.

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Combination Therapy for Autoimmune Disease

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IFNβ (3×10⁴ unit/mouse) were i.p. injected every other day from day 0 to 8 as previously performed^{24 (link)}. rLT (rLTα2β1)(1008-LY-010/CF, R&D; 10 μg/kg mouse) was i.p. administered every day from day 0 to 9. CXCR2 inhibitor (SB225002, Tocris: 0.1 mg/kg mouse) was i.p. injected every day from day 0 to day 20. LTβR-Fc (PRO154527, Genentech)(150 ng/mouse) was i.p. injected every other day from day 0.

Inoue M., Chen P.H., Siecinski S., Li Q.J., Liu C., Steinman L., Gregory S.G., Benner E, & Shinohara M.L. (2016). Mechanism to develop inflammasome-independent and interferon-β-resistant EAE with neuronal damages. Nature neuroscience, 19(12), 1599-1609.

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Comprehensive Antibody Sourcing Protocol

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SB225002 was purchased from TOCRIS bioscience (#2725/10). Antibodies used in this study were purchased from different companies: anti-CtBP2 mouse IgG1 was purchased from BD Biosciences (#612044), Rabbit polyclonal Myosin-VIIa was obtained from Proteus Biosciences (#25-6790), Rabbit polyclonal IgG CXCL1 (ab269939), Rabbit monoclonal IBA1 (ab178846) and Mouse monoclonal IgG1 CD68 (ab31630) were purchased from Abcam, Mouse monoclonal IgG2a CD45 (05-1410) and anti-glutamate receptor 2 (GluR2) IgG2a were purchased from Millipore (#MAB397). Rhodamine (TRITC) AffiniPure Donkey Anti-Rabbit IgG secondary antibody was purchased from Jackson ImmunoResearch Laboratories (711-025-152). Secondary antibodies used were as follows: Alexa FluorTM 568 goat anti-mouse IgG1 (A-21124), Alexa FluorTM 488 goat anti-mouse IgG2a (A-21131) and Alexa FluorTM 647 donkey anti-goat IgG (A-21447) were purchased from Life Technologies. All primers were purchase from integrated DNA technologies (IDT DNA) (Iowa. USA). Normal Goat serum was purchased from SouthernBiotech (0060-01) (Alabama. USA).

Al Aameri R.F., Alanisi E.M., Oluwatosin A., Al Sallami D., Sheth S., Alberts I., Patel S., Rybak L.P, & Ramkumar V. (2023). Targeting CXCL1 chemokine signaling for treating cisplatin ototoxicity. Frontiers in Immunology, 14, 1125948.

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Intrathecal CXCR2 Antagonist for Glioblastoma

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SB was administered intrathecally as recently described [40 (link)]. In short, a mini-osmotic pump (model 2002/2001; ALZET, DURECT Corporation, Cupertino, CA, USA) was prepared and filled with the small molecule CXCR2 Antagonist SB225002 (Tocris, Bristol, UK) according to the manufacturer’s protocol prior to implantation on day 14. The intraventricular catheter was placed 0.8 mm laterally of the bregma into the lateral ventricle contralateral to the tumor site and a subcutaneous pocket was prepared for mini-osmotic pump reservoir placement. Treatments started immediately with implantation of a mini-osmotic pump on day 14. SB was administered continuously with a rate of 1 µL per hour at a dosage of 30 µg per day.
The intraperitoneal administration of TMZ (TEMODAL^®, MSD, Kenilworth, NJ, USA) was conducted daily with a weight-adapted dosage of 60 µg/g/d. The control group received Aqua ad iniectabilia (B.Braun, Mesungen, Germany) intraperitoneally.

Urbantat R.M., Jelgersma C., Brandenburg S., Nieminen-Kelhä M., Kremenetskaia I., Zollfrank J., Mueller S., Rubarth K., Koch A., Vajkoczy P, & Acker G. (2021). Tumor-Associated Microglia/Macrophages as a Predictor for Survival in Glioblastoma and Temozolomide-Induced Changes in CXCR2 Signaling with New Resistance Overcoming Strategy by Combination Therapy. International Journal of Molecular Sciences, 22(20), 11180.

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CXCR2 Antagonist Intrathecal Injection

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The CXCL1 neutralizing antibody was purchased from Boster (Wuhan, China). SB225002, a potent and selective antagonist of CXCR2, was purchased from Tocris (Bristol, UK). BAY11-7082, a NFκB inhibitor, was purchased from Merck (Merck KGaA, Darmstadt, Germany). Intrathecal injection was made with a 30 G needle between the L5 and L6 intervertebral space to deliver the reagents to the cerebral spinal fluid [21 (link)].

Xu J., Zhu M.D., Zhang X., Tian H., Zhang J.H., Wu X.B, & Gao Y.J. (2014). NFκB-mediated CXCL1 production in spinal cord astrocytes contributes to the maintenance of bone cancer pain in mice. Journal of Neuroinflammation, 11, 38.

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Evaluating anti-MIF and anti-CD74 Modulators

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PAR4-AP (AYPGKF-NH2)] and corresponding scrambled peptide (YAPGKF-NH2) as control were from Peptides International, Inc. (Louisville, KY). Anti-MIF monoclonal antibody, isotope control (mIgG1) and anti-CD74 monoclonal antibodies were provided by Dr. Richard Bucala from Yale University. Rat IgG2b monoclonal antibodies (isotype controls for anti-CD74) were from BD Biosciences (San Jose, CA). AMD3100 and SB225002 were purchased from Tocris (Minneapolis, MN). HE staining reagents were from Fisher Scientific. The rest of the materials used were from Sigma-Aldrich or as described in the methods.

Ye S., Ma F., Mahmood D.F., Meyer-Siegler K.L., Menard R.E., Hunt D.E., Leng L., Bucala R, & Vera P.L. (2021). Intravesical CD74 and CXCR4, macrophage migration inhibitory factor (MIF) receptors, mediate bladder pain. PLoS ONE, 16(8), e0255975.

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