IL-6 levels are elevated in the plasma of patients suffering from TIA or ischemic stroke, and are predictive of stroke severity and outcome (Hoshi et al. 2005; Lambertsen et al. 2012; Shaafi et al. 2014).

Tocilizumab (TB) is a FDA approved recombinant, humanized anti–IL-6 receptor monoclonal antibody that is safe in humans and approved for the treatment of inflammatory disorders, including rheumatoid arthritis and systemic Juvenile Idiopathic Arthritis, Giant Cell Arteritis, or Cytokine Release Syndrome (https://www.gene.com/download/pdf/actemra_prescribing.pdf). TB blocks the action of IL-6 without increasing the IL-6 half-life (as was seen with other anti-IL-6 strategies), and humanization led to an increase in the half-life of the antibody. Most importantly, the action of the soluble IL-6 receptor is also blocked, which mediates many of the detrimental effects of IL-6 (Kishimoto 2006). More recently, the efficacy of TB has been investigated in patients with acute coronary syndromes.  TB attenuated inflammation and reduced the peri-procedural rise in troponin in patients with non‐ST‐elevation MI, again with a favorable safety profile(Kleveland et al. 2016). A recent community‐based study in RA patients showed that TB had beneficial effects on endothelial function (Bacchiega et al. 2017), further strengthening the biological plausibility that TB will be neuroprotective in patients.

In our translational studies, we have demonstrated that TB effectively reduced injury produced by focal cerebral ischemia in different occlusion models and in aged animals of both sexes, with a therapeutic window of at least 6 hours and with a sustained beneficial effect on functional outcomes lasting for at least 28 days.