Sr141716a

Manufactured by Merck Group

Sourced in Spain, Germany, United States

SR141716A is a synthetic compound that acts as a cannabinoid receptor type 1 (CB1) antagonist. It is commonly used in scientific research and laboratory settings.

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Lab products found in correlation

6 protocols using sr141716a

Cannabinoid Receptor-Mediated Effects of CBD

Cited 2 times

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CBD was obtained from Jazz Pharmaceuticals (Dublin, Ireland) and dissolved in ethanol: cremophor: saline (1:1:18) to obtain the required doses of 10, 20 and 30 mg/kg for wild-type (WT) animals, and the dose of 20 mg/kg for knockout mice (CB1KO, CB2KO and GPR55KO). The drug was prepared immediately before its intraperitoneal (i.p.) administration at a volume of 10 mL/kg of weight (0.3 mL for each mouse). According to its pharmacokinetic properties, CBD was administered 1h and a half before the behavioral evaluation [54 (link),93 (link)].
The CB1r-antagonist SR141716A was purchased from Sigma-Aldrich (Madrid, Spain) and dissolved in ethanol, cremophor and saline (1:1:18) to obtain the required dose of 2 mg/kg for its i.p. administration 30 min before CBD administration and 2 h before the behavioral evaluation. The dose of SR141716A was selected based on previous studies demonstrating that this dose does not produce any effects by itself [94 (link),95 (link)].

Austrich-Olivares A., García-Gutiérrez M.S., Illescas L., Gasparyan A, & Manzanares J. (2022). Cannabinoid CB1 Receptor Involvement in the Actions of CBD on Anxiety and Coping Behaviors in Mice. Pharmaceuticals, 15(4), 473.

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Preparation and Storage of Cannabinoid Ligands

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Forskolin (FSK, F), CP55940, 2‐arachidonoyl glycerol (2‐AG), NESS‐0327, and SR141716A were purchased from Cayman Chemical Company; AM4113 was purchased both from Cayman Chemical Company and Sigma Aldrich.
FSK, and EG‐018 and all analogues were constituted at 31.6 mM in dimethyl sulfoxide (DMSO, Sigma Aldrich); NESS‐0327, AM4113 and SR141716A were constituted at 10 mM in DMSO. FSK was stored in large aliquots at room temperature and reused for multiple experiments, while all other drugs were aliquoted for single use in 0.2 ml tubes and stored at −80°C until use. Vehicle (DMSO and ethanol) content was controlled within each experiment, at 0.1% for each agonist in either DMSO or ethanol, with an additional 0.015% DMSO (for FSK) and an additional 0.1% ethanol for coelenterazine H in cAMP assays (see below).

Finlay D.B., Nguyen T., Gamage T.F., Chen S., Barrus D.G., Patel P.R., Thomas B.F., Wiley J.L., Zhang Y, & Glass M. (2022). Exploring determinants of agonist efficacy at the CB1 cannabinoid receptor: Analogues of the synthetic cannabinoid receptor agonist EG‐018. Pharmacology Research & Perspectives, 10(1), e00901.

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Cannabinoid Receptor Targeting in Brain Tumors

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All solvents and reagents were used as obtained from Sigma Aldrich (St. Louis, MO) and Thermo Fisher Scientific (Pittsburgh, PA), unless otherwise stated. 3-Bormo-5-aminopyrazole from Ark Pharm, Inc. (Libertyville, IL). 0.1% Triton X-100 in PBS, SR-141716A, indocyanine green (ICG), and DAPI from Sigma-Aldrich (St. Louis, MO). 4% paraformaldehyde in PBS from Affymetrix (Santa Clara, CA). Doxorubucin from A Chemtek Inc. (Worcester, MA). CellTiter-Glo® Luminescent Cell Viability Assay kit from Promega (Madison, WI). RNAzol Reagent, and Platinum Taq DNA polymerase from Invitrogen (Carlsbad, CA). Primers for CB₂R, CB₁R and GAPDH (housekeeping gene) from Integrated DNA Technologies (Coralville, IA). ProLong® Gold antifade reagent from Life Technologies (Carlsbad, CA). DRAQ-5 from Cell Signaling Technology (Beverly, MA). Transfected mouse delayed brain tumor (DBT) cell line that expresses CB₂R (DBT-CB₂) or CB₁R (DBT-CB₁). 6 - 8 week old female nu/nu mice were obtained from The Jackson Laboratory (Bar Harbor, ME).

Ling X., Zhang S., Shao P., Li W., Yang L., Ding Y., Xu C., Stella N, & Bai M. (2015). A novel near-infrared fluorescence imaging probe that preferentially binds to cannabinoid receptors CB2R over CB1R. Biomaterials, 57, 169-178.

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Cannabinoid Receptor Ligands in Hypoxic-Ischemic Injury

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URB447 was synthesized as previously
described.^{17 (link)} SR141716A and WIN-55,212-2
were purchased from Sigma-Aldrich. Drugs were dissolved in 1:9 PBS:DMSO
(vehicle) and injected intraperitoneally to a final concentration
of 1 mg/kg. This dose was chosen based on what was previously reported
in the literature for the CB₁ antagonist SR141716A^{21 (link)} and WIN-55,212-2,^{19 (link)} and on preliminary experiments performed with URB447 and SR141716A
administered before the HI induction.

Carloni S., Crinelli R., Palma L., Álvarez F.J., Piomelli D., Duranti A., Balduini W, & Alonso-Alconada D. (2020). The Synthetic Cannabinoid URB447 Reduces Brain Injury and the Associated White Matter Demyelination after Hypoxia-Ischemia in Neonatal Rats. ACS Chemical Neuroscience, 11(9), 1291-1299.

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Cannabinoid-Induced CPP and Dependence

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All drugs were administered by i.p. route. For conditioned place preference (CPP)
procedure the dose of non-selective cannabinoid receptor agonist R(+)-WIN55,212-2 mesylate salt (Sigma Chemical Co., Madrid Spain) was administered at 0.5 mg/kg (Manzanedo et al., 2010) (link), whereas for physical dependence induction it was administered at 1mg/kg in a volume of 0.1ml/10g of body weight, following Hutcheson et al., (1998) (link).
The selective CB1 cannabinoid receptor antagonist SR141716A (Rimonabant; Sigma-Aldrich, Darmstadt, Germany) was administered at 10mg/kg in a volume of 0.2ml/10g of body weight, as previously described (Hutcheson et al., 1998; (link)Valverde et al., 2000) . Both drugs were respectively dissolved in the vehicle solution consisting of ethanol/cremophor EL (Kelliphor; Sigma-Aldrich, Darmstadt, Germany)/distilled water (1:1:18).

Martín-Sánchez A., García-Baos A., Castro-Zavala A., Alegre-Zurano L, & Valverde O. (2021). Early-life stress exacerbates the effects of WIN55,212-2 and modulates the cannabinoid receptor type 1 expression. Neuropharmacology, 184.

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Pharmacological Modulation of Rodent Behavior

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URB597 (0.3 or 1 mg/kg; Sigma-Aldrich, St. Louis, MO, USA) and SR141716A (3 mg/kg; Sigma-Aldrich) were dissolved in 15% dimethyl sulfoxide, 4.25% polyethylene glycol, 4.25% Tween 80, and 76.5% saline. Diazepam (DZP, 1 mg/kg; Ratiopharm, Ulm, Germany) was dissolved in physiological saline. The drugs were injected intraperitoneally (i.p. at 10 mL/kg) 1 h prior to the behavioral paradigm. To activate DREADDs, clozapine N-oxide (CNO; Tocris, Bristol, Great Britain) dissolved in physiological saline was injected i.p. at 10 mg/kg and 10 mL/kg 45 min before exposure to the behavioral test.
Muscimol (MUSC; Sigma-Aldrich) and fluorescently-labeled MUSC (fMUSCL; BODIPY™ TMR-X conj., Thermo Fisher Scientific, Waltham, MA, USA) were dissolved in freshly-prepared artificial cerebrospinal fluid (aCSF) and injected locally via guide cannulas 45 min prior to behavioral testing at 0.1 ng/nL. Vocalization experiments were conducted using fMUSC in a crossover design whereby half of the animals received fMUSC and the other half vehicle (aCSF). On the next day, the treatment was switched. For the elevated plus maze (EPM) experiment mice received MUSC or vehicle.

Ruat J., Genewsky A.J., Heinz D.E., Kaltwasser S.F., Canteras N.S., Czisch M., Chen A, & Wotjak C.T. (2022). Why do mice squeak? Toward a better understanding of defensive vocalization. iScience, 25(7), 104657.

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