Rimonabant

The meta-analysis was conducted and reported according to recommendations of the Meta-analysis of Observational Studies in Epidemiology (MOOSE) group [36] (link). A review protocol was construed following the MOOSE guidelines. This was not published but only for internal use of this study.
A PubMed and Embase search was conducted for articles on metabolic side effect profiles of antipsychotic medication. The search term used was: ((“weight gain” OR “BMI” OR “7% weight”) AND (chlorpromazine OR haloperidol OR bromperidol OR fluphenazine OR zuclopenthixol OR pentixol OR flupentixol OR levopromazine OR perphenazine OR pimozide OR penfluridol OR sulpiride OR amisulpride OR amoxapine OR asenapine OR aripiprazole OR blonanserine OR clozapine OR iloperidone OR melperone OR olanzapine OR risperidone OR paliperidone OR quetiapine OR sertindole OR lurasidone OR ziprasidone)) NOT (addition OR additive OR adjunctive OR augmentation OR lithium OR valproate OR carbamazepine OR metformin OR topiramate OR ramelteon OR rimonabant OR modafinil OR sibutramine OR genetics OR pharmacokinetics OR vomiting OR nausea OR review OR “cognitive behavioural therapy” OR “cognitive behavioral therapy” OR delirium OR steroids OR ropinirole OR sleep OR “brain volume”)
Limits Activated: Humans, Clinical Trial, Randomized Controlled Trial, Clinical Trial, Phase IV, Controlled Clinical Trial, English, German, All Adult: 18+ years, Publication Date from 1999/01/01 to 2011/12/31.

The Animal Study Protocol (IACUC; 536/2018) was approved by the Italian Ministry of Health and Ethics Committee for the use of experimental animals being conformed to guidelines for the safe use and care of experimental animals following the Italian D.L. no. 116 of 27 January 1992 and associated guidelines in the European Communities Council (86/609/ECC and 2010/63/UE). In this study, 5‐week‐old control (C57BL/10ScSnJ) and dystrophic (C57BL/10ScSn‐DMDmdx/J) mice weighing approximately 20–25 g were purchased from Charles River Laboratories (Milan IT). All mice were housed in an individually ventilated cage system with a 12‐h light–dark cycle and received standard mouse chow (Harlan Teklad) and water ab libitum. Animals belonging to each cage were randomly assigned to the different experimental groups. Each experimental group included at least five mice. The experimenter(s) performing the treatments and locomotor testing was blind to the genotype and treatment. Control or mdx mice were treated orally for 3 weeks with (i) vehicle (dimethyl sulfoxide – DMSO Cat# 276855 Sigma‐Aldrich), (ii) deflazacort (DFZ) 1.2 mg/kg/day (Cat# SML0123 Sigma‐Aldrich), (iii) sodium butyrate (NaB) 100 mg/kg/day (Cat# 303410, Sigma‐Aldrich); (iii) ACEA 2.5 mg/Kg (Cat# A9719 Sigma‐Aldrich), or (iv) rimonabant 0.5 mg/Kg (Cat# 9000484, Cayman) were intraperitoneally (IP) injected three times a week for 2 weeks (Iannotti et al, 2018 (link)).

Gemcitabine, cisplatin, Δ⁹-tetrahydrocannabinol, and cannabidiol were obtained from Millipore-Sigma. Cannabichromene, cannabivarin, rimonabant, SR 144,528, and A-967079 were obtained from Cayman Chemical.

Morphine (20 mg/kg, SIGMA^®) was freshly diluted in 0.9% NaCl (Saline) solution. Saline was used as the control solution. Rimonabant (1 or 10 mg/kg, SR141716; Sanofi-Aventis^®, Paris, France) was dissolved in 1% Tween 80 and then diluted in distilled water. Solution of 1% Tween 80 in distilled water was used as the Rimonabant control (Vehicle). The solutions were administered intraperitoneally (i.p.) at a volume of 10 mL/kg body weight.