LC-PDA-01 is a selective peroxiredoxin 1 (PRDX1) activator with an EC 50 of 111.8 nM and a human K D of 123.2 nM. LC-PDA-01 inhibits the expression of pro-inflammatory cytokines IL-1β, IL-6 and TNF-α. LC-PDA-01 can be used in antioxidant/anti-inflammatory research [1].
In Vitro, LC-PDA-01 (100 μM; 3 h) significantly stabilizes endogenous PRDX1 protein in HEK-293T human embryonic kidney cells, as measured by cellular thermal shift assay[1]. LC-PDA-01 (20 μM) significantly suppresses LPS -induced expression of IL-1β, IL-6, and TNF-α mRNA in RAW 264.7 mouse macrophages[1]. LC-PDA-01 (Incubated to measure half-life of 381.6 min) shows excellent metabolic stability in mouse liver microsomes, with a half-life of 381.6 min and a hepatic extraction ratio of 13.7%[1]. LC-PDA-01 has low apparent permeability (Papp A→B = 0.06 × 10-6 cm/s) across Caco-2 monolayers, with a high efflux ratio of 5.23, suggesting potential P-gp-mediated active efflux[1].
References:
[1]. Zhu YY, et al. Design and evaluation of peroxiredoxin 1 agonist based on scaffold hopping of salvianolic acids and combinatorial click chemistry. Acta Pharmacol Sin. 2026 Mar 9.
In Vitro, LC-PDA-01 (100 μM; 3 h) significantly stabilizes endogenous PRDX1 protein in HEK-293T human embryonic kidney cells, as measured by cellular thermal shift assay[1]. LC-PDA-01 (20 μM) significantly suppresses LPS -induced expression of IL-1β, IL-6, and TNF-α mRNA in RAW 264.7 mouse macrophages[1]. LC-PDA-01 (Incubated to measure half-life of 381.6 min) shows excellent metabolic stability in mouse liver microsomes, with a half-life of 381.6 min and a hepatic extraction ratio of 13.7%[1]. LC-PDA-01 has low apparent permeability (Papp A→B = 0.06 × 10-6 cm/s) across Caco-2 monolayers, with a high efflux ratio of 5.23, suggesting potential P-gp-mediated active efflux[1].
References:
[1]. Zhu YY, et al. Design and evaluation of peroxiredoxin 1 agonist based on scaffold hopping of salvianolic acids and combinatorial click chemistry. Acta Pharmacol Sin. 2026 Mar 9.