Organic long‐persistent luminescence (OLPL) is one of the most promising methods for long‐lived‐emission applications. However, present room‐temperature OLPL emitters are mainly based on a bimolecular exciplex system which usually needs an expensive small molecule such as 2,8‐bis(diphenyl‐phosphoryl)dibenzo[b,d]thiophene (PPT) as the acceptor. In this study, a new thermally activated delayed fluorescence (TADF) compound, 3‐(4‐(9H‐carbazol‐9‐yl)phenyl)acenaphtho[1,2‐b]pyrazine‐8,9‐dicarbonitrile (CzPhAP), is designed, which also shows OLPL in many well‐known hosts such as PPT, 2,2′,2″‐(1,3,5‐benzinetriyl)‐tris(1‐phenyl‐1‐H‐benzimidazole) (TPBi), and poly(methyl methacrylate) (PMMA), without any exciplex formation, and its OLPL duration reaches more than 1 h at room temperature. Combining the low cost of PMMA manufacture and flexible designs of TADF molecules, pure organic, large‐scale, color tunable, and low‐cost room‐temperature OLPL applications become possible. Moreover, it is found that the onset of the 77 K afterglow spectra from a TADF‐emitter‐doped film is not necessarily reliable for determining the lowest triplet state energy level. This is because in some TADF‐emitter‐doped films, optical excitation can generate charges (electron and holes) that can later recombine to form singlet excitons during the phosphorescence spectrum measurement. The spectrum taken in the phosphorescence time window at low temperature may consequently consist of both singlet and triplet emission.

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Osteoporosis is a devastating disease that features reduced bone quantity and microstructure, which causes fragility fracture and increases mortality, especially in the aged population. Due to the long-term side-effects of current drugs for osteoporosis, it is of importance to find other safe and effective medications. Ellagic acid (EA) is a phenolic compound found in nut galls, plant extracts, and fruits, and exhibits antioxidant and antineoplastic effects. Here, we showed that EA attenuated the formation and function of osteoclast dose-dependently. The underlying mechanism was further discovered by western blot, immunofluorescence assay, and luciferase assay, which elucidated that EA suppressed osteoclastogenesis and bone resorption mainly through attenuating receptor activator of nuclear factor-κB (NF-κB) ligand-induced NF-κB activation and extracellular signal-regulated kinase signaling pathways, accompanied by decreased protein expression of nuclear factor of activated T-cells calcineurin-dependent 1 and c-Fos. Moreover, EA inhibits osteoclast marker genes expression including Dc-stamp, Ctsk, Atp6v0d2, and Acp5. Intriguingly, we also found that EA treatment could significantly protect ovariectomy-induced bone loss in vivo. Conclusively, this study suggested that EA might have the therapeutic potentiality for preventing or treating osteoporosis. K E Y W O R D S ellagic acid, ERK, NF-κB, osteoclast, osteoporosis, RANKL Xixi Lin and Guixin Yuan contributed equally to this work.