Fig. 1 · Structure

Cat. No.: A11547
CAS No.: 168273-06-1
Formula: C₂₂H₂₁Cl₃N₄O
Mol. Weight: 463.79

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Other Forms

Form	MW
Rimonabant (SR141716) This page	463.79
Rimonabant hydrochloride	500.25

Rimonabant (SR141716)

Name: Rimonabant (SR141716)
Brand: Adooq Bioscience
SKU: A11547
Availability: InStock
Rating: 5 (1 reviews)

Cat. No. A11547 CAS 168273-06-1

Rimonabant is a selective antagonist of CB1 with IC50 of 13.6 nM and EC50 of 17.3 nM in hCB1 transfected HEK 293 membrane.

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Biological Activity

Bioactivity / Mechanism

SR141716A showed functional inverse-agonist activity in CB1-expressing superior cervical ganglion neurons: acute 1 μM application reversed tonic inhibition of calcium current. The response depended on the expressed receptor construct, supporting a model-specific interpretation of CB1 constitutive activity. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target	Activity	Value
hCB1		13.6 nM
hCB2		1.64 μM
ACAT		1.5 μM-2.9 μM

In Vitro Studies

In isolated rat neurons expressing wild-type CB1, SR141716A (1 μM) increased calcium current by 60.2 ± 13.7% (mean ± SEM; n = 10 neurons). The D164N construct showed a smaller increase, 11.6 ± 6.9% (n = 5), while retaining responsiveness to the agonist WIN 55,212-2. These are electrophysiological responses in a receptor-expression model. [1]

Reversal of tonic calcium-current inhibition in CB1-expressing neurons

Cell-based study · Isolated superior cervical ganglion neurons from adult male Wistar rats expressing wild-type CB1 or CB1-D164N; 100 ng/μl receptor cDNA injection for the Fig. 4 comparison. Methods identify human wild-type CB1 cDNA; Results identify D164N as rat CB1. [1]

At 1 μM, SR 141716A enhanced calcium current in wild-type CB1-expressing neurons, consistent with reversal of tonic receptor activity. Enhancement was smaller with D164N, although that construct retained agonist responsiveness. This is a cellular functional endpoint, not a binding affinity or IC50.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Calcium-current increase with SR 141716A in wild-type CB1-expressing neurons	Calcium-current change 60.2 ± 13.7%; n = 10 neurons; mean ± SEM	[1]
Calcium-current increase with SR 141716A in CB1-D164N-expressing neurons	Calcium-current change 11.6 ± 6.9%; n = 5 neurons; mean ± SEM; p < 0.05 versus wild-type CB1	[1]
Calcium-current inhibition with WIN 55,212-2 in wild-type CB1 versus CB1-D164N neurons	Calcium-current change 43.7 ± 6.5% (n = 7) versus 34.2 ± 4.8% (n = 6); mean ± SEM	[1]

Literature-Reported Treatment Conditions

Treatment concentration: 1 μM SR 141716A
Method: Acute perfusion during whole-cell patch-clamp recording at 22–26 °C, 16–20 h after receptor-cDNA injection.
Vehicle: DMSO stock diluted into external recording solution; the matched DMSO concentration had no effect on calcium current.
Co-treatment: WIN 55,212-2 (1 μM) was an agonist comparator/control, not a combination efficacy treatment.
Reported limits: No single fixed SR exposure duration is stated. Neuron counts are not numbers of donor animals; donor-animal replication is not specified for these comparisons.

Methods and source locations

Compound reported in the paper: SR 141716A (rimonabant); Compound label in the paper: SR

Functional inverse-agonist interpretation is restricted to the expressed-CB1 neuronal system and calcium-current endpoint.

Results: D164N constitutive-activity comparison; Fig. 4A–B; Fig. 1A,C and captions; Materials and Methods: receptor constructs, electrophysiology, Solutions

Calcium-current increase with SR 141716A in wild-type CB1-expressing neurons: Whole-cell patch clamp; agonist comparator was 1 μM WIN 55,212-2. — Fig. 4A–B and corresponding Results; Materials and Methods: electrophysiology, Solutions and statistics

Calcium-current increase with SR 141716A in CB1-D164N-expressing neurons: Whole-cell patch clamp; agonist comparator was 1 μM WIN 55,212-2. — Fig. 4A–B and corresponding Results; Materials and Methods: electrophysiology, Solutions and statistics

Calcium-current inhibition with WIN 55,212-2 in wild-type CB1 versus CB1-D164N neurons: Whole-cell patch clamp; agonist comparator was 1 μM WIN 55,212-2. — Fig. 4A–B and corresponding Results; Materials and Methods: electrophysiology, Solutions and statistics

In Vivo Studies

In male mice with diet-induced obesity, rimonabant at 10 mg/kg/day by oral gavage for four weeks produced sustained lower body weight despite recovery of food intake. Total fat mass was lower than in body-weight-matched controls. Plasma MCP-1 was lower than in obese vehicle and intake-matched controls, but was not significantly lower than in weight-matched controls, limiting inference of a direct anti-inflammatory effect. [2]

Chronic rimonabant in diet-induced obesity with intake- and weight-matched controls

Animal study · Male C57BL/6J mice rendered obese by 6 months of high-fat feeding; lean normal-diet mice supplied a reference group. [2]

One four-week controlled design assessed weight, adiposity and plasma inflammation. Food-intake suppression was transient; lower body weight persisted. Fat mass was lower than in weight-matched controls, but plasma MCP-1 was not significantly different from those controls.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Body weight and food intake	Reported group comparison Food intake fell initially, then recovered; body weight remained lower than obese vehicle controls.	[2]
Total fat mass as percentage of total body mass	Reported group comparison Lower in HFD-R than body-weight-matched HFD-BW controls (P < 0.05); n = 12–19 mice/group in Fig. 1 caption.	[2]
Plasma MCP-1 measured by ELISA	Reported group comparison Lower than HFD-V and HFD-DI (P < 0.01); difference versus HFD-BW was not statistically significant; n = 9–19 mice/group.	[2]

Conditions shared by the study groups

Route: Oral gavage
Frequency: Daily
Treatment course: 4 weeks
Vehicle: 0.1% Tween 80

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
HFD-R: rimonabant 10 mg/kg/day	HFD-V: obese vehicle, ad libitum; HFD-BW: vehicle, intake adjusted to match treated body weight; HFD-DI: vehicle, intake matched to HFD-R one day behind; ND-V: lean vehicle reference.	Persistent lower weight and reduced fat mass; lower plasma MCP-1 versus HFD-V and HFD-DI, but no significant plasma MCP-1 advantage over HFD-BW.	[2]

HFD-R: rimonabant: Model: Obese male C57BL/6J mice maintained on high-fat diet ad libitum.; Reported limits: Exact endpoint-specific group sizes are given as ranges in captions; no allocation/randomization details extracted.

Methods and source locations

Compound reported in the paper: Rimonabant; Compound label in the paper: HFD-R

Findings apply to this male mouse diet-induced-obesity design; direct weight-independent anti-inflammatory action is not established by plasma MCP-1.

Methods and Procedures: Animals and rimonabant treatment, Statistical analysis; Results: diet intake/body weight and plasma MCP-1; Fig. 1a–b and Fig. 5 with captions

Body weight and food intake: Daily weight/intake recording; densitometry 2 days before treatment end; terminal plasma ELISA, as applicable. Group values summarized as mean ± SEM; one-way ANOVA/Bonferroni for multiple groups. — Fig. 1a–b; Results: Effect of rimonabant on diet intake and body weight

Total fat mass as percentage of total body mass: Daily weight/intake recording; densitometry 2 days before treatment end; terminal plasma ELISA, as applicable. Group values summarized as mean ± SEM; one-way ANOVA/Bonferroni for multiple groups. — Fig. 1b (total fat mass); caption and corresponding Results

Plasma MCP-1 measured by ELISA: Daily weight/intake recording; densitometry 2 days before treatment end; terminal plasma ELISA, as applicable. Group values summarized as mean ± SEM; one-way ANOVA/Bonferroni for multiple groups. — Fig. 5 and caption; Results: Effect of rimonabant on plasma levels of MCP-1

HFD-R: rimonabant · Methods and Procedures: Animals and rimonabant treatment, Statistical analysis; Results: diet intake/body weight and plasma MCP-1; Fig. 1a–b and Fig. 5 with captions

Specifications

Manufacturer	Adooq Bioscience
Actions	Antagonist
CAS Number	168273-06-1
Formula	C₂₂H₂₁Cl₃N₄O
Molecular Weight	463.79
Synonyms	SR141716
SMILES	CC1=C(N(N=C1C(=O)NN2CCCCC2)C3=C(C=C(C=C3)Cl)Cl)C4=CC=C(C=C4)Cl

Storage & Solubility

In Vitro Solubility

Reported Solubility

Solvent	Reported Solubility
DMSO	22 mg/mL (47.43 mM)
Water	Insoluble
Ethanol	2 mg/mL

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration: 28 mg/mL
Vehicle: 30% PEG400+0.5% Tween80+5% propylene glycol

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

[1] Nie J, Lewis DL. Structural domains of the CB1 cannabinoid receptor that contribute to constitutive activity and G-protein sequestration. The Journal of neuroscience : the official journal of the Society for Neuroscience (2001). PMID: 11698587 DOI: 10.1523/jneurosci.21-22-08758.2001 Source material
[2] Wang Q, Perrard XD, Perrard JL, et al. Effect of the cannabinoid receptor-1 antagonist rimonabant on inflammation in mice with diet-induced obesity. Obesity (Silver Spring, Md.) (2011). PMID: 20885384 DOI: 10.1038/oby.2010.213 Source material

Publications

1 publication citing this product

Marie-Eve Di Raddo, .et al. , Curr Res Neurobiol, 2023, Sep 4:5:100107 PMID: 38020805