HCQ exerts anticancer effects by acting synergistically with common chemotherapic drugs. Although it has a well-defined and favorable toxicity profile, the necessity of increasing the dose, in some cases, limits the utilization, due to the toxicity, mainly at cardiac and ocular levels. A two-compartment model, with first-order absorption and a lag time, describes the pharmacokinetics of HCQ. The long-terminal half-life prolongs the time to reach steady-state concentrations, then delays the therapeutic effects. The next-generation formulations allow modulating the pharmacokinetics of HCQ. Avoiding systemic absorption, then liver first-pass metabolism, HCQ may be used in site-specific inflammation, without toxicity [72,73,74]. The selected studies’ primary outcomes are the extent to which HCQ may limit disease progression or exacerbations (Table 2).