Unmet Need:
It is estimated that 13.3 million people worldwide are affected by acute kidney injury (AKI) (see Bjornstad et. al). AKI is an especially prevalent condition in kidney transplant recipients, with one study showing that 35% of recipients had at least one episode of AKI (see Palmisiano et. al). These injury events lead to worsening kidney function, which can only be managed through hospitalization and often leads to poor long-term outcomes in native and transplanted kidneys (see UptoDate). There is a broad list of inciting causes of injury and currently there no approved pharmacological agents that can prevent AKI events (see Gameiro et. al). There is a strong need for therapies to be developed that can prevent the incidence and severity of acute kidney injury in patients at risk of having an AKI event.
Technology Overview:
Researchers at Johns Hopkins have developed a drug, JHU083, which attenuates worsening kidney function in a mouse model of Acute Kidney Injury (AKI). Previous studies done by the investigators have shown that changes in T-cell metabolism and proliferation occur after AKI and can exacerbate the injury and repair. Data suggests that pre-treating mice before AKI with JHU083, a drug that targets T-cell metabolism, improves renal injury outcomes and prevents pathogenic T-cell metabolic reprograming, activation, and proliferation in-vivo. In summary, researchers have discovered and tested a promising drug that can help patients who are at risk of having an acute kidney injury.
Stage of Development:
Drug has been developed and tested in-vivo in a preclinical mouse model.
Publication:
Lee, K., Thompson, E.A., Gharaie, S., Patel, C.H., Kurzhagen, J.T., Pierorazio, P.M., Arend, L.J., Thomas, A.G., Noel, S., Slusher, B.S. and Rabb, H., 2023. T cell metabolic reprogramming in acute kidney injury and protection by glutamine blockade. JCI insight, 8(12).
