**11. Conclusions**

L1-79 inhibits the rate limiting step in the synthesis of catecholamine, including dopamine and norepinephrine. Unlike the L-isomer of AMPT (Demser), L1-79 has a better kinetic profile for the use of L1-79 as a treatment for ASD. It's presynaptic mechanism of action likely results in a diminution of both catecholamines and related growth factors which we hypothesize will reduce symptoms of ASD in a manner not possible with receptor blockers, and which with long term use may reduce the hypertrophic architecture of catecholamine synapses in ASD back to a homeostatic morphology. An exaggerated catecholaminergic mechanism underlying ASD and its associated comorbidities can explain a variety of potential influences on the disease including the effects of bile, orphan receptors, lipids, glucose and other factors.

Preliminary results observed following the administration of L1-79 to autistic juveniles and adolescents has resulted in consistent improvement in the core symptoms of in two early studies [214, 215] not seen with previous agents.

L1-79 appears to be an effective therapy for the treatment of autism in children empirically with a novel mechanism of action that is supported by the scientific literature**.**
