Purpose: To evaluate the efficacy and safety of latanoprostene bunod 0.024% (LBN) in Korean patients with glaucoma or ocular hypertension in a real-world clinical setting. Methods: This retrospective study included patients who initiated LBN treatment between March 1, 2022, and December 31, 2024. Patients were categorized into monotherapy, switched therapy, and concomitant therapy groups. Changes in intraocular pressure (IOP) were assessed at baseline, month 1, and month 6 according to treatment group and diagnosis. The type and frequency of adverse events were also analyzed. Results: Among the 138 patients initially identified, 129 were included in the analysis. The mean IOP for all patients was 17.4 ± 4.9 mmHg at baseline, 16.0 ± 4.6 mmHg at month 1, and 14.6 ± 3.7 mmHg at month 6. The mean IOP reduction was -1.4 ± 2.8 mmHg at month 1 (p < 0.001) and -2.2 ± 3.3 mmHg at month 6 (p < 0.001). Subgroup analyses by treatment type (monotherapy, switched, and concomitant) and diagnosis revealed significant IOP reductions at both time points across all groups. Adverse events occurred in 22 patients (17.1%), with eye pain being the most frequent. No serious adverse events were observed, including systemic side effects, severe visual impairment, or significant ocular complications. Conclusions LBN significantly reduced IOP in Korean patients with glaucoma and ocular hypertension, irrespective of prior IOP-lowering medication use and was well tolerated with a favorable safety profile. These findings support the use of LBN as an effective treatment option for Korean patients with glaucoma or ocular hypertension in diverse clinical settings.

Oolonghomobisflavan B (OHBFB) is a prominent and specific polyphenolic constituent of oolong tea. We previously identified a cell membrane receptor for OHBFB and showed that it induces cancer-selective cell death in vitro and in vivo, although its standalone anticancer efficacy is limited. 5,7-Dimethoxyflavone (5,7-DMF), a principal bioactive component of black ginger (Kaempferia parviflora), also exhibits anticancer activity.Here, we demonstrate that 5,7-DMF synergistically enhances the anticancer effect of OHBFB in multiple myeloma cells by boosting OHBFB-induced intracellular cyclic guanosine monophosphate (cGMP) production. Moreover, co-treatment with OHBFB and 5,7-DMF triggers apoptotic cell death in multiple myeloma cells, accompanied by activation of the cGMP/acid sphingomyelinase (ASM) pathway. In summary, 5,7-DMF amplifies the anticancer activity of OHBFB by upregulating cGMP in multiple myeloma cells.

Cognitive impairment, including memory deficits, is a major concern in neurological disorders.Natural polyphenolic compounds have emerged as promising neuroprotective agents due to their antioxidant and anti-inflammatory properties. Previously, we identified a receptor for oolonghomobisflavan B (OHBFB).OHBFB, a polyphenol derived from oolong tea, has shown strong radical-scavenging activity, but its effects on cognitive function and underlying mechanisms remain largely unknown. In this study, mice were orally administered OHBFB (10, 30, 50 mg/kg) for 15 days, followed by scopolamine-induced memory impairment.Behavioral assessments were performed using the novel object recognition (NOR) test and the closed-arm Tmaze test. Molecular analyses of brain tissues included Western blotting for brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP response element-binding protein (p-CREB). Safety assessments (body weight and organ weights) and antioxidant capacity (DPPH assay, IC50 = 4.40 μM and ABTS assay, IC50 = 4.08 μM) were also conducted. NOR: novel-object exploration rose from 49.7% (control) to 51.5%, 54.2%, and 59.9% with OHBFB 10, 30, 50 mg/kg. T-maze: performance shifted from 50.5% (control) to 49.6%, 55.1%, and 61.5% at the same doses. Expression of BDNF and p-CREB in brain tissue was restored to near-normal levels in OHBFB -treated groups. OHBFB also exhibited potent antioxidant activity, consistent with its neuroprotective effects, while showing no adverse effects on body weight or organ indices. These findings suggest that, within a scopolamine-induced amnesia mouse model, OHBFB improves cognitive performance while engaging the BDNF-CREB pathway. Given its safety profile, OHBFB may serve as a promising candidate for the treatment of cognitive impairments, including those associated with neurodegenerative disorders.

As the elderly population is increasing, Alzheimer's disease (AD) has become a global issue and many clinical trials have been conducted to evaluate treatments for AD. As these clinical trials have been conducted and have failed, the development of new theraphies for AD with fewer adverse effects remains a challenge. In this study, we examined the effects of Theracurmin on cognitive decline using 5XFAD mice, an AD mouse model. Theracurmin is more bioavailable form of curcumin, generated with submicron colloidal dispersion. Mice were treated with Theracurmin (100, 300 and 1,000 mg/kg) for 12 weeks and were subjected to the novel object recognition test and the Barnes maze test. Theracurmin-treated mice showed significant amelioration in recognition and spatial memories compared those of the vehicle-treated controls. In addition, the antioxidant activities of Theracurmin were investigated by measuring the superoxide dismutase (SOD) activity, malondialdehyde (MDA) and glutathione (GSH) levels. The increased MDA level and decreased SOD and GSH levels in the vehicle-treated 5XFAD mice were significantly reversed by the administration of Theracurmin. Moreover, we observed that Theracurmin administration elevated the expression levels of synaptic components, including synaptophysin and post synaptic density protein 95, and decreased the expression levels of ionized calcium-binding adapter molecule 1 (Iba-1), a marker of activated microglia. These results suggest that Theracurmin ameliorates cognitive function by increasing the expression of synaptic components and by preventing neuronal cell damage from oxidative stress or from the activation of microglia. Thus, Theracurmin would be useful for treating the cognitive dysfunctions observed in AD.
Aged ; Alzheimer Disease ; Animals ; Cognition ; Colloids ; Curcumin ; Glutathione ; Humans ; Malondialdehyde ; Mice ; Microglia ; Neurons ; Oxidative Stress ; Post-Synaptic Density ; Spatial Memory ; Superoxide Dismutase ; Synaptophysin