Other agents, which are involved in different pathological pathways, are in advanced phases of testing in PD patients. Isradipine, approved for hypertension treatment, is a dihydropyridine calcium channel blocker with a relatively high affinity for Cav1.3 channels. Inhibition of Cav1 channels in PD seems to reduce cytosolic Ca2+ levels, mitochondrial oxidant stress, and sensitivity to toxins in neurons [252]. Unfortunately, the STEADY-PD III study has recently shown that patients who were taking isradipine did not have any difference in MS compared to the placebo [253]. Similar negative results have been recently obtained in the SURE-PD 3, a phase 3 clinical trial conducted in order to identify the role of inosine, a urate precursor, in slowing PD progression [245]. Deferiprone has an important role in oxidative stress because it is a powerful iron chelator [254]. Exenatide, approved for the treatment of diabetes mellitus type 2, is another agent that has been investigated for its potential neuroprotective effects [255]. It is a synthetic agonist for the glucagon-like peptide-1 (GLP-1) receptor, which seems to modulate different cellular processes, enhancing mitochondrial function, neurogenesis, and synaptic function and reducing inflammation [256]. Moreover, other therapies, such as caffeine [257], statins [258], nicotine [259], and physical therapy [260], might be available to modify disease progression. Indeed, although proven neuroprotective elements have not already been found in PD, different promising agents are currently being investigated.