Fsllry nh2

Manufactured by Bio-Techne

Sourced in United States, United Kingdom

FSLLRY-NH2 is a synthetic peptide product offered by Bio-Techne. It is a chemical compound with the molecular formula C₃₅H₄₇N₇O₆. The core function of this product is to serve as a research tool for various applications, such as cell signaling studies and receptor-ligand interactions. No further details on intended use are provided.

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Lab products found in correlation

Rwj 56110, by Bio-Techne (2 mentions) Penicillin, by Thermo Fisher Scientific (2 mentions) Streptomycin, by Thermo Fisher Scientific (2 mentions) Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (2 mentions) Oxaliplatin, by Bio-Techne (1 mentions) Hc 030031, by Merck Group (1 mentions) Ac55541, by Santa Cruz Biotechnology (1 mentions) Anti β actin antibody, by Santa Cruz Biotechnology (1 mentions) Anti erk, by BD (1 mentions) Anti par2, by Santa Cruz Biotechnology (1 mentions) Anti mcp 1, by Merck Group (1 mentions) Amphotericin, by Thermo Fisher Scientific (1 mentions) Heparin sepharose, by GE Healthcare (1 mentions) Sepharose 4b, by GE Healthcare (1 mentions) Porcine pancreatic trypsin type 9, by Merck Group (1 mentions) Cyanogen bromide activated, by GE Healthcare (1 mentions) Tfllrn nh2, by Bio-Techne (1 mentions) Fetal calf serum (fcs), by Merck Group (1 mentions) Leupeptin, by Merck Group (1 mentions) Asparaginase, by Abcam (1 mentions)

9 protocols using fsllry nh2

Rat Model of Oxaliplatin-Induced Neuropathy

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Oxaliplatin (Tocris Bioscience, R&D Systems, Minneapolis, MN, USA) was dissolved in a 5% glucose solution at a final concentration of 2 mg/ml. Acute neurotoxicity was induced in rats by a single intraperitoneal (i.p.) injection of Oxaliplatin (6 mg/kg), as described previously [7 (link), 8 (link)]. Control rats received the same volume of i.p. injection of vehicle. Mechanical allodynia and cold hypersensitivity were fully developed by OXL 3 days after injection.
PAR2 antagonist FSLLRY-NH2 (Tocris Bioscience, R&D Systems, Minneapolis, MN, USA) and TRPA1 antagonist HC030031 (Sigma-Aldrich, St. Louis, MO, USA) were injected i.p. and then mechanical and cold sensitivity were determined within 8 hrs after the drugs administration. The separated animals were used for experiments of the dosage response in each group.

Tian L., Fan T., Zhou N., Guo H, & Zhang W. (2015). Role of PAR2 in regulating oxaliplatin-induced neuropathic pain via TRPA1. Translational Neuroscience, 6(1), 111-116.

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Evaluating PAR-2 Modulation in Post-ACA Outcomes

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The potential treatment effects of PAR-2 inhibition as well as the detrimental effects of PAR-2 activation on ACA outcomes were examined. Given the lack of a prior literature evidence regarding the optimum dose for the use of selective PAR-2 inhibitor, we have administered 2 different doses of FSLLRY-NH2 (50 μg/rat or 100 μg/rat; Tocris Bioscience, Minneapolis, Minnesota, USA) intranasally at 1 hour post-resuscitation. Selective PAR-2 agonist (AC55541; 30 μg/rat; Santa Cruz Biotechnology, Dallas, Texas, USA) was intranasally administered intranasally at 2 hours post-resuscitation (unpublished data). Short-term neurologic functions were assessed by using the neurological deficit score (NDS), number of seizures and T-maze test over 7 days after ACA. The effects of FSLLRY-NH2 and AC-55541 on hippocampal neuron degeneration were evaluated by Fluoro-Jade C (FJC) staining at 7 days following ACA. Based on better outcomes observed following the administration of FSLLRY-NH2 at a dose of 50 μg, this dose was used for the mechanism study.

Ocak U., Ocak P.E., Huang L., Zuo G., Yan J., Hu X., Song Z, & Zhang J.H. (2020). Inhibition of PAR-2 attenuates neuroinflammation and improves short-term neurocognitive functions via ERK1/2 signaling following asphyxia-induced cardiac arrest in rats. Shock (Augusta, Ga.), 54(4), 539-547.

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Protease-Activated Receptor Signaling

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Unless stated otherwise, trypsin, purified LPS (obtained through phenol extraction) from Escherichia coli (serotype O26:B6), salts, buffers, and all other chemicals of reagent grade were purchased from Sigma-Aldrich (St. Louis, MO, USA). The specific PAR-1 agonist (TRAP6), PAR-2 agonist (AC 55541), PAR-4 agonist (AY-NH2) and the selective PAR-2 antagonist (FSLLRY-NH2) were purchased from Tocris Bioscience (Bristol, UK). Antibody-directed phosphorylated ERK was purchased from Novus (St. Charles, MO, USA), and anti-ERK was purchased from BD (Franklin Lakes, NJ, USA). Antiphosphorylated p38, anti-p38, and anti-c-JUN N-terminal kinase (JNK) were purchased from Calbiochem (San Diego, CA, USA). Anti-MCP-1 was purchased from Sigma-Aldrich. Monoclonal antiphosphorylated JNK, anti-PAR-2 (Additional file 1: Figure S1), and anti-β-actin antibodies were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Chao H.H., Chen P.Y., Hao W.R., Chiang W.P., Cheng T.H., Loh S.H., Leung Y.M., Liu J.C., Chen J.J, & Sung L.C. (2017). Lipopolysaccharide pretreatment increases protease-activated receptor-2 expression and monocyte chemoattractant protein-1 secretion in vascular endothelial cells. Journal of Biomedical Science, 24, 85.

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Isolation and Characterization of PAR2

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Frozen or fresh human adult lung and skin samples, ranging from 15 to 20 g, were purchased through the Collaborative Human Tissue Network; cyanogen bromide–activated Sepharose 4B from GE Healthcare; heparin-Sepharose, Na-benzoyl-dl-arginine 4-nitro-anilide, porcine pancreatic type IX trypsin (13,000–20,000 U/mg), sulphinpyrazone, calcium ionophore (A23187), porcine intestinal mucosa heparin (mean mol wt 16 kD), SBTI, cellulose phosphate (fibrous form), and leupeptin from Sigma-Aldrich; FCS, DMEM, penicillin, streptomycin, and amphotericin from Thermo Fisher Scientific; anti-PAR2 IgG and anti-EMR2 from R&D Systems; and PAR2-activating peptide (SLIGRL-NH2), PAR1-activating peptide (TFLLRN-NH2), PAR2 peptide control LRGILS-NH2, and PAR2 antagonist (FSLLRY-NH2) from Tocris Bioscience. PAR2 agonists or antagonist were diluted in a buffer comprising 20% DMSO and 80% PBS.

Le Q.T., Lyons J.J., Naranjo A.N., Olivera A., Lazarus R.A., Metcalfe D.D., Milner J.D, & Schwartz L.B. (2019). Impact of naturally forming human α/β-tryptase heterotetramers in the pathogenesis of hereditary α-tryptasemia. The Journal of Experimental Medicine, 216(10), 2348-2361.

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Fluorescent Dye Labeling Protocol

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All fluorescent dyes were purchased from ThermoFisher Scientific (Invitrogen, UK), and CPA was from Merck Millipore (Calbiochem, UK). Collagenase was obtained from Worthington (USA), asparaginase was from Abcam (UK), the PAR2 inhibitor FSLLRY-NH2 from TOCRIS (UK) and GSK-7975A from GlaxsoSmithKline (UK). All other chemicals were purchased from Sigma. C57BL/6 J mice were from Charles River UK Ltd.

Peng S., Gerasimenko J.V., Tsugorka T., Gryshchenko O., Samarasinghe S., Petersen O.H, & Gerasimenko O.V. (2016). Calcium and adenosine triphosphate control of cellular pathology: asparaginase-induced pancreatitis elicited via protease-activated receptor 2. Philosophical Transactions of the Royal Society B: Biological Sciences, 371(1700), 20150423.

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Modulating Cardiomyocyte Responses to Anti-HER2 and Doxorubicin

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Patient‐specific iPSC‐derived cardiomyocytes were treated with Tmab (anti‐HER2 humanized mAb; BioVision, Inc.) or DOX (Sigma‐Aldrich) for 7 days. Human IgG (Fujifilm Wako Chemicals) or DMSO (Sigma‐Aldrich) was used as a negative control treatment unless noted. The medium containing fresh drug was replaced every 2–3 days. The KLK5 antagonist, UA (Sigma‐Aldrich),²⁶ the PAR2 antagonist (small molecules), I‐191 (AOBIOUS),²⁷ the PAR2 antagonist (peptides), FSLLRY‐NH2 (Tocris Bioscience),²⁸, ²⁹ and Recombinant Human Kallikrein 5 (R&D Systems) were cotreated for inhibition experiments.

Sasaki R., Kurebayashi N., Eguchi H., Horimoto Y., Shiga T., Miyazaki S., Kashiyama T., Akamatsu W, & Saito M. (2022). Involvement of kallikrein‐PAR2‐proinflammatory pathway in severe trastuzumab‐induced cardiotoxicity. Cancer Science, 113(10), 3449-3462.

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Investigating PAR2 Inhibition's Effects on Neurological Outcomes after Cardiac Arrest

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The treatment effects of PAR2 inhibition on ACA outcomes were examined. Selective PAR2 inhibitor (FSLLRY-NH2; 50 μg/rat; Tocris Bioscience, Minneapolis, Minnesota, USA) was intranasally administered at 1 hour postresuscitation. Short-term neurological function was assessed through neurological deficit score (NDS) (24-hour, 48-hour, and 72hour postresuscitation), and neurocognition was evaluated using T-maze test (7 days) after ACA. The effect of FSLLRY-NH2 on hippocampal neuron degeneration was evaluated through Fluoro-Jade C (FJC) staining 7 days after ACA.

Ocak U., Eser Ocak P., Huang L, & Zhang J.H. (2020). FSLLRY-NH2 Improves Neurological Outcome After Cardiac Arrest in Rats. Turkish neurosurgery, 30(2).

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Endotoxin-Depleted House Dust Mite Extract Protocol

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House dust mite extract (# B84, Dermatophagoides pteronyssinus, Greer Laboratories, Inc., Lenoir, NC) was depleted of endotoxin using Pierce^™ High Capacity Endotoxin Removal Spin Columns (# 88274, ThermoFisher Scientific, Waltham, MA) to generate a final concentration of 0.096 endotoxin units (EU) per microgram of HDM protein. Recombinant human IFN-γ(# 570204), TNF-α(# 570104), IL-13 (# 571104), IL-17A (# 570504), and M-CSF (# 574806) were from BioLegend (San Diego, CA). Poly (I:C) (# tlrl-pic) and polymyxin B (# tlrl-pmb) were from InvivoGen (San Diego, CA). E64 (# 5208), AEBSF (# 5175), protease activated receptor-1 (PAR-1) antagonist, RWJ 56110 (# 2614), and PAR-2 antagonist, FSLLRY-NH2 (# 4751), were from Tocris (Minneapolis, MN). Recombinant human APOE3 (# 350-02) and recombinant human IL-10 (# 200-10) were from PeproTech (Rocky Hill, NJ). The Recombinant human APOE3 contained 0.021 EU/μg of protein. Dexamethasone (# D4902), LPS from Escherichia coli O111:B4 (# L4391), MitoTEMPO (# SML0737), CA-074 methyl ester (# C5857), A-438079 hydrochloride hydrate (# A9736), E-64d (# E8640), potassium chloride (KCL) (# 60142), methyl-β-cyclodextrin (# C4555), α-cyclodextrin (# C4680) and cholesterol-loaded, water soluble, methyl-β-cyclodextrin (# C4951) were from Millipore Sigma (St. Louis MO). Z-YVAD-FMK (# 218746) and MCC950 (# 5.38120.0001) were from Calbiochem (Burlington, MA).

Gordon E.M., Yao X., Xu H., Karkowsky W., Kaler M., Kalchiem-Dekel O., Barochia A.V., Gao M., Keeran K.J., Jeffries K.R, & Levine S.J. (2019). Apolipoprotein E is a Concentration-dependent Pulmonary Danger Signal that Activates the NLRP3 Inflammasome and IL-1β Secretion by Asthmatic Macrophages. The Journal of allergy and clinical immunology, 144(2), 426-441.e3.

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Retinal Arteriole Vasoreactivity Assay

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Thrombin was obtained from Roche (Mannheim, Germany). RWJ 56110, FSLLRY-NH 2 , tcY-NH 2 , and H1152 were obtained from Tocris Bioscience (Bristol, UK). Other drugs Takahashi et al.--10 were obtained from Sigma-Aldrich (St. Louis, MO). Gö-6983 was in dimethylsulfoxide (DMSO). Other drugs were dissolved in PSS. The final concentrations of DMSO were less than 0.1% in the vessel bath. 26 As a pilot study, vehicle control did not affect the diameter of the retinal arterioles.

Takahashi K., Omae T., Ono S., Kamiya T., Tanner A, & Yoshida A. (2018). Thrombin-Induced Responses via Protease-Activated Receptor 1 Blocked by the Endothelium on Isolated Porcine Retinal Arterioles. Current eye research, 43(11).

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