Mirificin

Mirificin (Puerarin apioside) is a blood-brain barrier-permeable tyrosinase inhibitor, with an IC₅₀ value of 12.66 μM against mushroom tyrosinase. Mirificin reduces the expression of ALOX12 in cardiomyocytes and alleviates hypoxia/reoxygenation-induced apoptosis. The neuroprotective effect of Mirificin depends on the activation of VEGFR2 and HSP1A1, which reduces cerebral infarct size and improves neurological function. Mirificin can be used in the research of hyperpigmentation, acute myocardial infarction and ischemic stroke^[1][2][3]. IC50 & Target:IC50: 12.66 μM (TYR)^[1] In Vitro:Mirificin (20.0 μM) shows no toxicity to H9c2 rat cardiomyocytes, even at the highest concentration tested^[2].
Mirificin (5-50 μM; 24 h) dose-dependently increases the viability and reduces the cytotoxicity of differentiated PC12 cells with oxygen-glucose deprivation/reperfusion (OGD/R) injury^[3].
Mirificin (0.1-10.0 μM) significantly reduces the mRNA expression level of Alox12 in H9c2 rat cardiomyocytes^[2].
Mirificin (0.1 μM; 3 h) protects H9c2 rat cardiomyocytes against hypoxia/reoxygenation (H/R)-induced injury by inhibiting ALOX12 protein expression, restoring the BCL-2/BAX ratio, and reducing apoptosis^[2]. In Vivo:Mirificin is the absorbable component of DLP in mice, and exhibits strong binding affinity to ALOX12, a key target in the pathogenesis of AMI^[2].
Mirificin (12.5-25 mg/kg; i.p.; two administrations) reduces the cerebral infarction volume and improves neurological function in mice with ischemic stroke induced by middle cerebral artery occlusion (MCAO)^[3].