Clomipramine

Clomipramine can inhibit reuptake of both noradrenaline and 5-HT, although Clomipramine inhibits 5-HT reuptake more strongly than it inhibits noradrenaline reuptake^[1].
The antidepressant Clomipramine inhibits both venom AChE as well as human serum BChE in a concentration-dependent manner but has no effect on AChE in the rat brain striatum^[2].Clomipramine interferes with the autophagic flux and severely compromises the viability of tumorigenic cells upon cytotoxic stress^[3].
Clomipramine reduces autophagy in neuronal primary cultures. Clomipramine (1 and 5鈥壜礛) negatively regulates neuronal autophagic pathway in primary cultured cells^[3].

Clomipramine (5-20 mg/kg; i.p) elicits significant hyperglycemia in mice. Clomipramine induces hyperglycemia in mice by blocking the 5-HT2B and/or 5-HT2C receptors, which results in facilitation of adrenaline release. In mice, Clomipramine reduces immobility in the forced swimming test, which is the behavioral model for antidepressants. Clomipramine also inhibits the OCD animal model, marble burying behavior in mice^[1].Clomipramine (20鈥塵g/kg) decreases autophagic flux in murine tissues^[3].

[1]. Yumi Sugimoto, et al. The tricyclic antidepressant Clomipramine increases plasma glucose levels of mice. J Pharmacol Sci. 2003 Sep;93(1):74-9. 

[2]. Mushtaq Ahmed, et al. Comparative study of the inhibitory effect of antidepressants on cholinesterase activity in Bungarus sindanus (krait) venom, human serum and rat striatum. J Enzyme Inhib Med Chem. 2008 Dec;23(6):912-7. 

[3]. Federica Cavaliere,The tricyclic antidepressant Clomipramine inhibits neuronal autophagic flux. Sci Rep. 2019 Mar 19;9(1):4881.