Recent years have seen an impressive amount of research devoted to understanding the etiopathology of Autism Spectrum Disorder (ASD) and developing therapies to treat this complex syndrome. This work has been largely based on the employment of rodent models, based on a multitude of genetic and environmental manipulations. Unfortunately, the task of identifying suitable candidates playing a relevant etiopathological role in ASD is highly challenging, due to a number of problems specifically affecting the research in this field. These include (i) the heterogeneity of ASD itself, including several disorders, (ii) the complexity of ASD etiology, involving a plethora of genetic and environmental factors, (iii) the presence of a huge variety of rodent models, without a universal consensus on their validity. Here we highlight how the endocannabinoid system (ECS) emerges within this complex context as a valid therapeutic target and etiopathological factor in ASD. The multiple roles of the ECS in modulating neuronal functions are described, to underline the overall relevance of this system. We summarize then the most recent results showing alterations of the ECS in rodent models of ASD (with an emphasis on mouse studies), and demonstrating ASD-like behaviours in mice with altered ECS, induced either by genetic or pharmacological manipulations.We also give a critical overview of the most relevant advances in designing treatments and novel mouse models for ASD targeting the ECS, highlighting the approaches that seem more promising to simplify the complex field of research on treatments for ASD.

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Multi‐stage drugs have been prioritized in antimalarial drug discovery, as targeting more than one process in the Plasmodium life cycle is likely to increase efficiency, while decreasing the chances of emergence of resistance by the parasite. Herein, we disclose two novel acridine‐based families of compounds that combine the structural features of primaquine and chloroquine. Compounds prepared and studied thus far retained the in vitro activity displayed by the parent drugs against the erythrocytic stages of chloroquine‐sensitive and ‐resistant Plasmodium falciparum strains, and against the hepatic stages of Plasmodium berghei, hence acting as dual‐stage antiplasmodial hits.