Aims: Recently, we introduced DAD9, a chemically-modified tetracycline (TC) conjugated to DA, creating a dopaminergic agonist with neuroprotective effects for Parkinson's Disease (PD). Our aim is to deepen the understanding of the molecular mechanisms underlying DAD9's neuroprotection.Methods: Characterization of α-Synuclein (α-Syn) oligomeric species was performed using ThT fluorescence, SDS-PAGE, DLS, and microscopy. Cell culture assays measured viability, cytotoxicity, and intracellular seeding in transgenic cell models. In vivo experiments were conducted in transgenic C. elegans.Results: The TC residue within DAD9 shielded the DA residue from oxidation, preventing the formation of dopaminochrome or neuromelanin, toxic cyclic derivatives. Furthermore, α-Syn species formed in the presence of DAD9, generated a distinct type of aggregated species, which were ThS (+), SDS-sensitive, and showed reduced toxicity in vitro and in vivo. Moreover, unlike doxycycline, DAD9 did not delay growth in C. elegans, suggesting a lack of off-target effect on eukaryotic translation, adding on to the previously reported safety profile.Conclusion: These findings suggest the DA moiety in the novel concept drug DAD9 lacked the ability to oxidize into toxic species, redirected α-Syn oligomers toward distinct off-pathway species, and the TC portion did not affect eukaryotic ribosomes. In conclusion, the chemical design in DAD9 reduced off-target effects of each of its parent compounds, positioning this novel multitarget neuroprotective dopaminergic agonist as a promising candidate for future preclinical and clinical studies.