ArticleFrontiers in pharmacology2025
A new Jun amino-terminal kinase inhibitor, KRev-202, inhibits rat ischemic acute injury and the progression to renal fibrosis.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Ischemia is an important cause of acute kidney injury (AKI). Ischemia-induced hypoxia rapidly induces activation of the Jun amino-terminal kinase (JNK) in tubular epithelial cells of the kidney, and blockade of this enzyme is protective in short-term animal models of renal ischemia. However, the clinical translation of this finding requires a water-soluble JNK inhibitor. This study investigated whether KRev-202, a soluble prodrug of the potent and selective JNK inhibitor CC930, can prevent ischemia-induced AKI and whether short-term inhibition of JNK can prevent AKI from transitioning to renal fibrosis. Methods: In a rat model of bilateral renal ischemia/reperfusion injury (IRI), the animals received prophylactic treatment with KRev-202, the parent compound (CC-930), or a vehicle by oral gavage, starting 1 h prior to surgery. Results and Discussion: In study 1, the animals were killed on day 1 after IRI to assess the AKI peak. Vehicle-treated animals exhibited a 4.5-fold increase in plasma creatinine levels, substantial tubular necrosis, increased tubular damage markers, and inflammation on day 1. Both KRev-202 and CC-930 treatment inhibited JNK activation, caused a 50% reduction in plasma creatinine levels, and substantially reduced tubular necrosis, tubular damage, and inflammation. In studies 2 and 3, treatments were administered from -1 h until day 4, and then the animals were killed on days 7 and 21, respectively. Compared to the vehicle group, a 4-day treatment with KRev-202 or CC-930 improved the recovery of tubular structure on day 7 and substantially reduced the development of renal fibrosis on day 21. Furthermore, KRev-202 treatment administered only during the first 24 h of IRI provided the same benefits as the 4-day treatment regimen, demonstrating the importance of early blockade of this pathway. In conclusion, KRev-202 is a new water-soluble JNK inhibitor with therapeutic potential for preventing ischemia-induced AKI.
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