NXPZ-2 functions as an orally active inhibitor of the Keap1-Nrf2 protein–protein interaction (PPI), with a Ki value of 95 nM and EC50 values of 120 and 170 nM. It exhibits dose-dependent improvement in Aβ[1-42]-induced cognitive dysfunction and mitigates brain tissue pathological changes in Alzheimer’s disease (AD) mouse models by augmenting neuron quantity and function. Additionally, NXPZ-2 inhibits oxidative stress by upregulating Nrf2 expression levels and facilitating its translocation from the cytoplasm to the nucleus, thereby aiding research on Keap1-Nrf2 PPI inhibitors and AD-associated diseases[1].
体内研究
Administered orally to male ICR mice at doses of 52.5/105/210 mg/kg once daily for 7 days, NXPZ-2 enhances learning and memory functions in AD mice. This improvement is evidenced by increased spontaneous alternation, active avoidance times, shortened escape latency, increased time spent in the target quadrant, and a higher number of platform crossings[1].
NXPZ-2 rescues brain structural damage and reduces the number of dead neurons in AD mice without causing noticeable toxicity to mouse organs[1].
NXPZ-2, administered orally to male ICR mice at doses of 52.5/105/210 mg/kg once daily for 7 days, mitigates oxidative stress by enhancing Nrf2 expression levels and facilitating its translocation from the cytoplasm to the nucleus. This action leads to an improvement in cognitive dysfunction by elevating Nrf2 levels in both the central nervous system and peripheral blood[1].
体外研究
NXPZ-2 (0-200 μM, 7 days) shows no apparent toxicity, in primary cortical neurons[1].
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