Hoe 140

Manufactured by Merck Group

Sourced in United States

HOE-140 is a synthetic peptide compound developed by the Merck Group for use in laboratory research. It functions as a specific and high-affinity antagonist of the bradykinin B2 receptor.

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Lab products found in correlation

24 protocols using hoe 140

Cytokine Inhibition in Inflammation

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Anti-IL-1β, anti-IL-6, anti-TNFα and anti-CINC-1 antibodies were supplied by R&D Systems Inc. (USA). Indomethacin, AACOCF₃ and PACOCF₃ were purchased from Biomol Research Laboratories (USA). GM6001 was supplied by USBiological (USA); whereas L-NMMA, HOE 140, Lys-(Des-Arg9,Leu8)-bradykinin, promethazine, methysergide, BQ-123, BQ-788 and fucoidan were purchased from Sigma-Aldrich Co. (USA). Celecoxib was supplied by Searle and Co (Puerto Rico). Zileuton was purchased from Abbott Laboratories (Zyflo®, USA). Carrageenin was purchased from Marine Colloids.

Dias R.G., Sampaio S.C., Sant’Anna M.B., Cunha F.Q., Gutiérrez J.M., Lomonte B., Cury Y, & Picolo G. (2017). Articular inflammation induced by an enzymatically-inactive Lys49 phospholipase A2: activation of endogenous phospholipases contributes to the pronociceptive effect. The Journal of Venomous Animals and Toxins Including Tropical Diseases, 23, 18.

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Enzymatic Generation of Vasoinhibins

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The vasoinhibins used in in vivo experiments corresponding to the 16 kDa fragment were generated by the enzymatic cleavage of rat prolactin from mammary gland extracts as previously described (Clapp et al., 1993 (link)). Recombinant human vasoinhibins (corresponding to a 14-kDa fragment of prolactin) used in cell culture experiments were generated by site-directed mutagenesis as previously described (Galfione et al., 2003 (link)). Other compounds including BK, Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME), (Z)-1-[2-(2-aminoethyl)-N-(2-ammonio-ethyl)amino]diazen-1-ium-1,2-diolate (DETANONOate), N-acetylcysteine (NAC), Luperox (tert-butyl peroxide), the kinin B2 receptor antagonist Hoe-140, and the Evans blue dye were purchased from Sigma-Aldrich (St. Louis, MO), and the 5,59,6,69-tetrachloro-1,19,3,39 tetraethylbenzimidazolylcarbocyanine iodide JC-1 dye was from Molecular probes (Eugene, OR). The monoclonal anti-kinin B2 receptor, the polyclonal anti-kinin B1 receptor, and polyclonal anti-β-tubulin antibodies were purchased from BD Biosciences (610451), Santa Cruz Biotechnology (sc-15048), and ZYMED (22833), respectively. Secondary antibodies conjugated to alkaline phosphatase (Bio-Rad Laboratories, Hercules, CA) were used.

Arredondo Zamarripa D., Díaz-Lezama N., Meléndez García R., Chávez Balderas J., Adán N., Ledesma-Colunga M.G., Arnold E., Clapp C, & Thebault S. (2014). Vasoinhibins regulate the inner and outer blood-retinal barrier and limit retinal oxidative stress. Frontiers in Cellular Neuroscience, 8, 333.

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Macrophage Invasion Assay for Leishmania

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C57BL/6 mice received an intraperitoneal injection of 2 mL of 3% thioglycolate and macrophages were harvested from peritoneal lavage 3 days later. Macrophages were plated on 13 mm coverslips in 24-well plate and after 20 h of incubation at 37°C in complete medium (RPMI + 10% FBS, 100 U/mL penicillin, and 100 μg/mL streptomycin) the nonadherent cells were removed by washing the monolayer of cells with PBS. Invasion assays were performed by adding stationary phase promastigotes to the monolayers at a ratio of 5 : 1 (parasite/macrophage) in medium containing 1 mg/mL albumin from bovine serum (BSA, Sigma). The interaction was performed during 3 h in a humidified chamber containing 5% CO₂ at 37°C. When indicated, the culture medium was supplemented with 100 nM of B₂R antagonist (HOE-140, Sigma) or 1 μM of B₁R antagonist des-Arg⁹-[Leu⁸]-BK (DAL⁸-BK; Sigma), 5 minutes before addition of parasites. After interaction, extracellular promastigotes were removed by washing the monolayers twice with PBS, which were then fixed with Bouin overnight and stained with Giemsa (Merck). The number of intracellular amastigotes was determined by counting at least 100 cells per replicate under the light microscope. All assays were done in triplicates and results were expressed as mean values ± SD.

Svensjö E., Nogueira de Almeida L., Vellasco L., Juliano L, & Scharfstein J. (2014). Ecotin-Like ISP of L. major Promastigotes Fine-Tunes Macrophage Phagocytosis by Limiting the Pericellular Release of Bradykinin from Surface-Bound Kininogens: A Survival Strategy Based on the Silencing of Proinflammatory G-Protein Coupled Kinin B2 and B1 Receptors. Mediators of Inflammation, 2014, 143450.

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Diabetic Erectile Dysfunction in Rats

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Experiments were approved by the Institutional Animal Care and Use Committee at the Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology. 16 eight-week WTR and 24 age-matched TGR were used in this study. WTR were randomly divided into two groups: the normal Control (WTR group; n = 8) and the DMED model (WTDM group; n = 8). TGR were randomly divided into the TGR group (n = 8), the transgenic diabetic rats group (TGDM; n = 8), and the transgenic diabetic rats treated with HOE140 group (TGDMH; n = 8). Rats in the WTDM, TGDM, and TGDMH groups were intraperitoneally injected with streptozotocin (STZ, 40 mg/kg, Sigma-Aldrich) dissolved in citrate buffer solution (0.1 mol/L, pH = 4.5), while rats in the WTR and TGR groups were injected with equal amount of 0.1 mol/L citric acid-sodium citrate buffer solution instead. After 72 hours, only rats with fasting glucose concentrations higher than 16.7 mmol/L were considered to have DM. In addition, rats in the TGDMH group were also intraperitoneally injected with HOE140 (10 μg/kg/d; Sigma-Aldrich), a specific inhibitor of B₂R to suppress hKLK1 signaling, after confirmation of DM. 12 weeks later, we recorded the final metabolic parameters and conducted erectile function test.

Luan Y., Cui K., Tang Z., Ruan Y., Liu K., Wang T., Chen Z., Wang S, & Liu J. (2020). Human Tissue Kallikrein 1 Improves Erectile Dysfunction of Streptozotocin-Induced Diabetic Rats by Inhibition of Excessive Oxidative Stress and Activation of the PI3K/AKT/eNOS Pathway. Oxidative Medicine and Cellular Longevity, 2020, 6834236.

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Investigating Cell Responses to Nanoparticle-Activated Plasma

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All the cell stimulations were performed in ECM medium containing 1% BSA (Sigma-Aldrich). The exposure groups included negative controls (PBS, 1% mouse plasma and 2 μg/mL MUA@AgNPs), positive control (10 μM BK), 1% mouse plasma activated by MUA@AgNPs (0.2 μg/mL for L-p@AgNPs, 2 μg/mL for H-p@AgNPs), 10 μM aprotinin with H-p@AgNPs and 2 μM HOE 140 with H-p@AgNPs. The stimulus of L-p@AgNPs and H-p@AgNPs were freshly prepared by adding 2 μL of MUA@AgNPs (0.2, 2 mg/mL) in 18 μL of mouse plasma, respectively and incubating at 37°C for 10 min before cell stimulation. As for the stimuli of aprotinin with H-p@AgNPs, 1 mM aprotinin (Sigma-Aldrich) was pre-mixed with mouse plasma and it was subsequently processed with the protocol for H-p@AgNPs preparation. In view of 2 μM HOE 140 with H-p@AgNPs, HRECs were pre-incubated with 2 μM HOE 140 (Sigma-Aldrich) for 30 min, then treated with H-p@AgNPs. The stimulations were performed by directly adding the stimulus described above to the cell exposure medium at the ratio of 1:100 (V/V). The specific details were given in the respective assays. BK stimulation was lasted for 30 min, while the exposure duration for the other stimulus was 2 h or 6 h.

Long Y.M., Zhao X.C., Clermont A.C., Zhou Q.F., Liu Q., Feener E.P., Yan B, & Jiang G.B. (2015). Negatively Charged Silver Nanoparticles Cause Retinal Vascular Permeability by Activating Plasma Contact System and Disrupting Adherens Junction. Nanotoxicology, 10(4), 501-511.

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Comparing Angiotensin II Receptor Antagonists

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Losartan potassium was purchased from Santa Cruz Biotechnology; irbesartan, PD123319, HOE-140 and BK were from Sigma. Stock solutions of losartan (10 mM), PD123319 (10 mM), BK (10 mM), HOE-140 (0.2 mM) were prepared in distilled water. Stock solution of irbesartan (10 mM) was prepared in DMSO. Final dilutions were prepared in modified Krebs-Henseleit solution immediately before use. For each drug used, concentration was chosen according to literature data indicating optimal expected effects (see below for specific references). Since drug effects were evaluated on isolated heart, no hepatic metabolic transformation could be expected on administered compounds. Based on both pharmacokinetic and pharmacodynamic properties, losartan was administered at concentration 4.5-fold higher than irbesartan.

Sgarra L., Leo V., Addabbo F., Iacobazzi D., Carratù M.R., Montagnani M, & Potenza M.A. (2014). Intermittent Losartan Administration Triggers Cardiac Post-Conditioning in Isolated Rat Hearts: Role of BK2 Receptors. PLoS ONE, 9(2), e88542.

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Vasodilation Experiments in Rats

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For the experiments, the following were used: ketamine hydrochloride and xylazine (from Syntec, São Paulo, SP, Brazil), 4-aminopyridine (4-AP), acetylcholine chloride (ACh), atropine, CaCl₂, dextrose, ethylenediaminetetraacetic acid, glibenclamide, HOE-140, KCl, KH₂PO₄, NaCl, NaHCO₃, MgSO₄, Nω-Nitro-L-arginine methyl ester (L-NAME), indomethacin, phenylephrine (Phe), sodium deoxycholate, and tetraethylammonium (TEA) were obtained from Sigma-Aldrich (St. Louis, MO, USA) and heparin from Hipolabor (São Paulo, SP, Brazil)

de Carvalho E.S., Tirloni C.A., Palozi R.A., Schaedler M.I., Guarnier L.P., Silva A.O., Mota J.D., Cardoso C.A., de Barros M.E, & Gasparotto Junior A. (2019). Endothelium-Dependent Effects of Echinodorus grandiflorus (Cham. & Schltdl.) Micheli Mediated by M3-Muscarinic and B2-Bradykininergic Receptors on Peripheral Vascular Resistance and Its Modulatory Effects on K+ Channels in Mesenteric Vascular Beds. Evidence-based Complementary and Alternative Medicine : eCAM, 2019, 4109810.

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Preparation of Angiotensin Receptor Agonists

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Telmisartan was kindly gifted by Boehringer Ingelheim. It was dissolved in dimethyl sulfoxide (DMSO). HOE-140 (Sigma-Aldrich Japan), amastatin (Santa Cruz Biotechnology), Ang II (Sigma-Aldrich Japan), and Ang III (Sigma-Aldrich Japan) were dissolved in artificial CSF (aCSF, 133.3 mM sodium chloride, 3.4 mM potassium chloride, 1.3 mM calcium chloride, 1.2 mM magnesium chloride, 0.6 mM sodium dihydrogen orthophosphate, 32.0 mM sodium bicarbonate, and 3.4 mM glucose) [15 (link)]. Mouse recombinant APA (Sino Biological) compound contains 1.28 mmol sodium chloride per 1 mg of APA. APA was dissolved and electrolyte concentration adjusted to match aCSF. For example, APA was dissolved to 0.1 mg/ml in a vehicle (5 mM sodium chloride, 3.4 mM potassium chloride, 1.3 mM calcium chloride, 1.2 mM magnesium chloride, 0.6 mM sodium dihydrogen orthophosphate, 32.0 mM sodium bicarbonate, and 3.4 mM glucose).

Nakamura T., Yamazato M., Ishida A, & Ohya Y. (2017). Excess of Aminopeptidase A in the Brain Elevates Blood Pressure via the Angiotensin II Type 1 and Bradykinin B2 Receptors without Dipsogenic Effect. International Journal of Hypertension, 2017, 3967595.

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Preparation of Bradykinin-related Compounds

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Bradykinin was purchased from Bachem (Bubendorf, Switzerland) and dissolved in acetic acid (0.1 M) to stock solutions of 10⁻² M. Lys-[Des-Arg⁹]-Bradykinin, [Phe⁸Ψ(CH-NH)-Arg⁹]-Bradykinin, HOE-140, and R-715 were purchased from Tocris (Bristol, UK) and were dissolved in saline. Stock solutions of Lys-[Des-Arg⁹]-Bradykinin, [Phe⁸Ψ(CH-NH)-Arg⁹]-Bradykinin, and R-715 were 10⁻³ M, whereas due to its poor solubility in water, stock solutions of HOE-140 were 5 × 10⁻⁴ M. Carbachol was from Sigma-Aldrich (St. Louis, MO) and dissolved in saline to a stock solution of 2 × 10⁻¹ M. Atropine (atropinum sulfuricum) was purchased from Egis Pharmaceutical PLC (Budapest, Hungary) and was diluted in water to a stock solution of 1.44 × 10⁻⁴ M. α,β-Methyleneadenosine 5′-triphosphate, PPADS, and Y-27632 were purchased from Cayman Chemical (Ann Arbor, MI) and all substances were dissolved in saline (α,β-meATP: 10⁻² M, PPADS: 10⁻² M, and Y-27632: 10⁻³ M). Indomethacin was purchased from Sigma-Aldrich (St. Louis, MO) and dissolved in DMSO (10⁻² M stock concentration), as its aqueous solutions are quite unstable (34 (link)). NS-398 was also purchased from Sigma-Aldrich (St. Louis, MO), and DMSO was applied as solvent for preparing a 10⁻² M stock solution.

Borsodi K., Balla H., Molnár P.J., Lénárt Á., Kenessey I., Horváth A., Keszthelyi A., Romics M., Majoros A., Nyirády P., Offermanns S, & Benyó Z. (2022). Signaling Pathways Mediating Bradykinin-Induced Contraction in Murine and Human Detrusor Muscle. Frontiers in Medicine, 8, 745638.

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Modulation of B2RBK in Balb/c Mice

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B2RBK was modulated using different protocols. First, for the balb/c mice, the animals were treated with an intravenous injection of the B2RBK antagonist HOE-140 (Sigma, St Louis, MO) (30 μg per animal) (Zuccollo et al., 1996a (link); Zuccollo et al., 1996b (link)) on days 1–3 after ADM injection. The animals were killed on days 4 and 21. In the second protocol (delayed treatment), the animals received HOE-140 on days 4–6 and were killed on days 7 and 21.

Pereira R.L., Felizardo R.J., Cenedeze M.A., Hiyane M.I., Bassi Ê.J., Amano M.T., Origassa C.S., Silva R.C., Aguiar C.F., Carneiro S.M., Pesquero J.B., Araújo R.C., Keller A.D., Monteiro R.C., Moura I.C., Pacheco-Silva A, & Câmara N.O. (2014). Balance between the two kinin receptors in the progression of experimental focal and segmental glomerulosclerosis in mice. Disease Models & Mechanisms, 7(6), 701-710.

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