L 733 060

Manufactured by Bio-Techne

Sourced in United States

L-733,060 is a selective, non-peptide neurokinin-1 (NK-1) receptor antagonist produced by Bio-Techne. It functions by binding to and blocking the NK-1 receptor, which is involved in the transmission of pain signals and the regulation of various physiological processes.

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L-733,060 hydrochloride (2 citations)

12 protocols using l 733 060

Peptide Reagent Characterization Protocol

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SLIGRL-amide, BAM8-22, SLIGR-amide and CGRP8-37 were supplied by Auspep (Melbourne, Australia). Stock solutions were prepared in sterile high-purity water with subsequent dilutions made in sterile saline. The concentration, purity, and composition of the peptides were determined by high-performance liquid chromatography, mass spectrometry, and quantitative amino acid analysis. Carbachol (carbamylcholine chloride), ATP, indomethacin, atropine, propranolol, terbutaline, theophylline and L-703,606 were purchased from Sigma–Aldrich (St. Louis, MO), whilst RP-67580 ((3aR,7aR)-Octahydro-2-[1-imino-2-(2-methoxy-phenyl)ethyl]-7,7-diphenyl-4H-isoindol), substance P, CGRP and L-733,060 were obtained from Tocris Bioscience (Ellisville, MO). Sodium pentobarbitone was supplied by Virbac Australia (Peakhurst, NSW), methoxyflurane by Medical Developments International Ltd (Springvale, Australia) and Schiff reagent by Australian Biostain (Vic, Australia).

Chang A.Y., Mann T.S., McFawn P.K., Han L., Dong X, & Henry P.J. (2016). Investigating the role of MRGPRC11 and capsaicin-sensitive afferent nerves in the anti-influenza effects exerted by SLIGRL-amide in murine airways. Respiratory Research, 17, 62.

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Methamphetamine-Induced Neurochemical Changes

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Mice were treated with a single dose of MA (35 mg/kg, i.p.) or saline, and sacrificed 1 h, 3 h, 6 h, 12 h, 1 day, and 3 days after MA treatment to examine prodynorphin and substance P mRNA expressions, ROS formation, and HNE and protein carbonyl levels. High-performance liquid chromatography grade GRe with greater than 99% purity was provided by Dr. Sung Kwon Ko [35 , 36 (link)]. GRe (20 mg/kg, i.p., twice a day) was given 5 days before and 1 day after MA injection. On the day of MA injection, GRe was administered at 2 h before and 10 h after MA injection. The dose of GRe was determined based on previous study [30 (link)]. Nor-binaltorphimine (Nor-B; κ-opioid receptor antagonist; Tocris Bioscience, Ellisville, MO, USA) was dissolved in sterile saline. Nor-B (3 or 6 mg/kg, i.p.) was given 3 h and 1.5 h before MA injection. The dose of Nor-B was determined based on previous study [34 (link)]. L-733,060 (NK1 receptor antagonist; Tocris Bioscience) was dissolved in sterile saline. L-733,060 (5 or 10 mg/kg, i.p.) was given 1 h before MA injection. The dose of L-733,060 was determined based on previous study [37 (link)].

Dang D.K., Shin E.J., Kim D.J., Tran H.Q., Jeong J.H., Jang C.G., Nah S.Y., Jeong J.H., Byun J.K., Ko S.K., Bing G., Hong J.S, & Kim H.C. (2018). Ginsenoside Re protects methamphetamine-induced dopaminergic neurotoxicity in mice via upregulation of dynorphin-mediated κ-opioid receptor and downregulation of substance P-mediated neurokinin 1 receptor. Journal of Neuroinflammation, 15, 52.

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Exploring Nociceptive Modulation via NK1R

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The drugs used were (i) the NK1R agonist, Substance P (SP; 1 and 2 μg/μl; #S6883, Sigma, USA), (ii) the NK1R antagonist, L-733,060 (1 ×: 0.0176 µg/µl and × 0.176 µg/µl; #1145, Tocris Bioscience, UK) and (iii) the cholinergic receptor agonist, carbamoylcholine chloride (carbachol; 0.156 μg/μl; #C4382, Sigma, USA).
The functional effects of different doses of SP and L-733,060 were explored in this study. Notably, 1 × concentration of L-733,060 in the present study is anti-nociceptive on microinjection into the rostral ventral medulla^{48 (link)}. While we initially used the lower dose of L-733,060, arising from the results, especially in behaving animals, we also examined the effect of the higher dose of L-733,060 to explore whether the different aspects of nociception are differentially sensitive to antagonism by the antagonist. The concentration of carbachol used in the experiments is based on published work^{65 (link)}.

Ng S.Y., Ariffin M.Z, & Khanna S. (2021). Neurokinin receptor mechanisms in forebrain medial septum modulate nociception in the formalin model of inflammatory pain. Scientific Reports, 11, 24358.

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Hyperosmotic Stress-Induced Apoptosis in Corneal Epithelial Cells

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Mouse corneal epithelial cell line (TKE2) was presented from Dr. Tetsuya Kawakita of Keio University (Tokyo, Japan) and cultured in keratinocyte serum-free medium (KSFM, Invitrogen, Carlsbad, CA) [39 (link)]. To induce apoptosis caused by hyperosmotic stress, TKE2 cells were incubated overnight in bovine pituitary extract (BPE)-free KSFM and subsequently exposed to hypertonic media (450, 550 and 650 mOsm) achieved by addition of glucose for 12–48 h. To detect the inhibiting effects on hyperosmotic stress-induced apoptosis, 0.1, 1 or 10 μM SP (Calbiochem, San Diego, CA) was pre-incubated 2 h before the treatment of high glucose. In some experiments, TKE2 cells were treated with the NK-1 receptor antagonist (1 μM L-733,060, Tocris, Minneapolis, MN), the AKT inhibitor V (40 μM Triciribine, Calbiochem, San Diego, CA), or glutathione depleting agent L-Buthionine-sulfoximine (100 μM, L-BSO, Sigma-Aldrich, St. Louis, MO) in the presence or absence of substance P.

Yang L., Sui W., Li Y., Qi X., Wang Y., Zhou Q, & Gao H. (2016). Substance P Inhibits Hyperosmotic Stress-Induced Apoptosis in Corneal Epithelial Cells through the Mechanism of Akt Activation and Reactive Oxygen Species Scavenging via the Neurokinin-1 Receptor. PLoS ONE, 11(2), e0149865.

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Modulation of TGF-β1 and Neuropeptide Signaling

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TGF-β1 (R&D Systems, code: 240-B-002), reconstituted in 4mM hydrochloric acid and 0.1% bovine serum albumin (BSA, Sigma, code: A9647) was used at a concentration of 1 ng/ml based on modification from Le Roux et al’s study involving human keratocytes [11 (link)]. The TGFβRI/II kinase inhibitor LY2109761 (Santa Cruz, code: sc-396262) was used at a concentration of 2 μmol/l based on Xu et al’s study [18 (link)]. LY2109761, prepared in dimethyl sulphoxide (DMSO), was used to block the effects of TGF-β1, and was added 20 min prior to TGF-β1 incubation. In addition, SP (Calbiochem, code: 05-23-0600) at 10⁻⁷ M and NK-1 R receptor blocker (L-733.060) (Tocris, code: 1145) at 10⁻⁶ M were used in concentrations as previously used in Backman et al’s study involving tenocytes [8 (link)]. SP at 10⁻⁷ M has also been used in studies involving human colonocytes [19 (link)] and human lung epithelial cell lines [10 (link)]. The concentrations of the mAChR blocker atropine at 10⁻⁵ M (Sigma, code: A0132) and ACh at 10⁻⁶ M (Sigma, code: A661) were based on our previous study involving human tenocytes [7 (link)].

Fong G., Backman L.J., Alfredson H., Scott A, & Danielson P. (2017). The effects of substance P and acetylcholine on human tenocyte proliferation converge mechanistically via TGF-β1. PLoS ONE, 12(3), e0174101.

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Intradermal Immunization in Mice

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Mice were immunized intradermally (i.d) in the right side of the cheek (behavioral experiments), base of tail (Kaede experiments), or in footpads. As indicated, mice were immunized with 50 µg of papain, heat-inactivated papain, ovalbumin, histamine, or 40 µg of Capsaicin (all from Sigma-Aldrich); or 100 µg of Alternaria alternata (Greer). Where indicated, mice were injected with 10 µg LPS (InvivoGen), 5 µg CGRP (Sigma-Aldrich), 100 nmoles Substance P (Tocris) or 1% QX314 (Tocris). All dilutions were diluted in sterile 1x phosphate buffered saline, or PBS (Corning), except for Capsaicin which was diluted in PBS and 6.4% DMSO. Where indicated, immunizations were performed with either 500 µmol of QWF or L733060 (both from Tocris) diluted in a 5% DMSO PBS solution.

Perner C., Flayer C.H., Zhu X., Aderhold P.A., Dewan Z.N., Voisin T., Camire R.B., Chow O.A., Chiu I.M, & Sokol C.L. (2020). Substance P release by sensory neurons triggers dendritic cell migration and initiates the Type-2 immune response to allergens. Immunity, 53(5), 1063-1077.e7.

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Neuropeptide Stimulation of Macrophages

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For all experiments, RAW264.7 and BMM were stimulated with 10⁻⁸ and 10⁻¹⁰ M of recombinant SP (#S6883, Sigma-Aldrich, Schnelldorf, Germany) or mouse/rat αCGRP (#4025897, Bachem, Bubendorf, Switzerland). BMM experiments also included a neuropeptide combination with 10⁻⁷ M of a respective receptor antagonist: for SP the NK1R antagonist L733,060 (#1145, Tocris, Biotechne, Minneapolis, USA) and for αCGRP the antagonist CGRP_8–37 (#4034544, Bachem, Bubendorf, CH). For RNA extraction, RAW cells were stimulated during loading. For cell assays such as adhesion, proliferation, apoptosis and ROS activity, RAW cells were either stimulated during loading (pre), during assay procedure (post) or constantly throughout the experiment (constant). BMM experiments were only stimulated during the assay procedure.

Muschter D., Beiderbeck A.S., Späth T., Kirschneck C., Schröder A, & Grässel S. (2019). Sensory Neuropeptides and their Receptors Participate in Mechano-Regulation of Murine Macrophages. International Journal of Molecular Sciences, 20(3), 503.

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Sperm Function Pharmacology

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To investigate the role of the ACE substrate pathways bradykinin/B2R, substance p/NK1R and Ac-SDKP on sperm function, WT mice were treated i.p. for 5 days (1 dose/day) before sperm isolation, as follows: the B2R blocker HOE-140 (Sigma-Aldrich) at 100 μg/kg/day, Neurokinin 1 (NK1) receptor blocker L-733060 (Tocris) at 20 mg/kg/day, or prolyl oligopeptidase inhibitor KYP-2047 (Sigma-Aldrich) at 10 mg/kg/day.

Shibata T., Bhat S.A., Cao D., Saito S., Bernstein E.A., Nishi E., Medenilla J.D., Wang E.T., Chan J.L., Pisarska M.D., Tourtellotte W.G., Giani J.F., Bernstein K.E, & Khan Z. (2023). Testicular ACE regulates sperm metabolism and fertilization through the transcription factor PPARγ. The Journal of Biological Chemistry, 300(1), 105486.

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Antagonist-Mediated TSLP Inhibition in Allergic Skin

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BQ123, SB, Ket, cetirizine, and L733060 were from Tocris. Mouse monoclonal TSLP-neutralizing Ab (MAB555) was from R&D Systems. The antagonists and Ab dosages were based on previous studies (16 (link), 42 (link), 43 (link)). Antagonists were prepared in stock solution, diluted in PBS, and injected in 5 mL/kg volume (i.p.) 45 minutes before the test. TSLP-neutralizing Ab or isotype control IgG (rat IgG, Sigma-Aldrich) was administered at 7 sites in the inflamed skin (15 μL/site) by intradermal injection via Hamilton syringe under sevoflurane anesthesia.

Liu B., Tai Y., Liu B., Caceres A.I., Yin C, & Jordt S.E. (2019). Transcriptome profiling reveals Th2 bias and identifies endogenous itch mediators in poison ivy contact dermatitis. JCI Insight, 4(14), e124497.

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Characterization of Pharmacological Compounds

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2-Bromo-α-ergocryptine methanesulfonate salt (BRM) was purchased from Sigma-Aldrich. Aprepitant was obtained from Selleck. All the other compounds tested were purchased from Tocris Biosciences, including SCH 23390 hydrochloride, rotigotine hydrochloride, sumanirole maleate, B-HT 920, Ro 10-5824 dihydrochloride, YM 202074, cinnabarinic acid, MTP, ICI 118,551 hydrochloride, GS 6201, PSB 1115, SC 19220, CP 154526, L-733060, CP 96345, TAM, DOX, A 412997 dihydrochloride, AMN 082 dihydrochloride, SKF 97541, Rac BHFF, SEW 2871, purmorphamine, (R)-(−)-α-methylhistamine dihydrobromide, methimepip dihydrobromide, VU 0155041 sodium salt, antalarmin hydrochloride, NBI 35965 hydrochloride, BQ 788 sodium salt, BAY36-7620, 3-MATIDA, MPEP hydrochloride, MRS 1754, SC 51322, SC 19220, and JTE 013.

Chen Y., Palczewska G., Masuho I., Gao S., Jin H., Dong Z., Gieser L., Brooks M.J., Kiser P.D., Kern T.S., Martemyanov K.A., Swaroop A, & Palczewski K. (2016). Synergistically acting agonists and antagonists of G protein–coupled receptors prevent photoreceptor cell degeneration. Science signaling, 9(438), ra74.

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