Search

The internal quantum efficiency of organic light-emitting diodes (OLEDs) has reached nearly 100%, and thus further improvement in the external quantum efficiency can be achieved only through outcoupling enhancement. However, light propagation in OLEDs for achieving high outcoupling has mainly been controlled not by the internal organic semiconductor layers but by external optical elements, which inevitably increase process cost. Here, a method is proposed for outcoupling enhancement that actively controls the refractive index of a hole transport layer (HTL) in OLEDs using a stably evaporable perfluororesin, which has a low refractive index and high amorphousness. The co-deposition of the perfluororesin with a hole transport material lowers the refractive index of the HTL to 1.56 at 550 nm without deteriorating the electrical properties. Owing to the nano-sized pillar-like phase separation between the perfluororesin and the hole transport material, the path of charge transport is retained. Using the low-index co-deposited HTL, a 1.22-fold enhancement of the outcoupling efficiency of a phosphorescent OLED is demonstrated. The proposed method can be generally applied to OLEDs to significantly enhance their outcoupling efficiency without increasing process cost. The results show the potential of active refractive index control as a major strategy for achieving further high-efficiency OLEDs.

Ridaifen-G (RID-G), a tamoxifen analog that we previously synthesized, has potent growth inhibitory activity against various cancer cell lines. Tamoxifen is an anticancer drug known to act on an estrogen receptor (ER) and other proteins. However, our previous studies interestingly suggested that the mechanism of action of RID-G was different from that of tamoxifen. In order to investigate the molecular mode of action of RID-G, we developed a novel chemical genetic approach that combined a phage display screen with a statistical analysis of drug potency and gene expression profiles in thirty-nine cancer cell lines. Application of this method to RID-G revealed that three proteins, calmodulin (CaM), heterogeneous nuclear ribonucleoproteins A2/B1 (hnRNP A2/B1), and zinc finger protein 638 (ZNF638) were the candidates of direct targets of RID-G. Moreover, cell lines susceptible to RID-G show similar expression profiles of RID-G target genes. These results suggest that RID-G involves CaM, hnRNP A2/B1, and ZNF638 in its growth inhibitory activity.