Core Viewpoint - Enhua Pharmaceutical has entered into exclusive commercial cooperation agreements with Green Leaf Pharmaceutical and its subsidiary, allowing Enhua to promote and sell three long-acting injectable antipsychotic products in mainland China, marking a significant strategic partnership in the CNS field [1][2]. Group 1: Agreement Details - Enhua's subsidiary, Jiangsu Enhua Hexin Pharmaceutical Marketing Co., Ltd., will receive exclusive rights to promote and sell three products: Risperidone microspheres (Riketu®), Paliperidone palmitate injection (Ruibailai®), and Paliperidone palmitate injection (Meibiru®) [1]. - Enhua will pay a one-time non-refundable licensing fee of $20 million to Green Leaf Pharmaceutical and Green Leaf Jiaao [1]. - The agreement stipulates that Enhua must achieve a minimum sales target of 2.7 billion RMB (approximately $400 million) for the licensed products between 2026 and 2035 [1]. Group 2: Strategic Importance - The exclusive authorization for these three long-acting injectables creates a differentiated product portfolio that addresses the treatment needs of schizophrenia patients at all stages of the disease [2]. - This strategic collaboration between two leading companies in the CNS field is expected to enhance the market presence of these products in primary healthcare centers, facilitating standardized treatment for more patients and reducing the burden of the disease [2].

香港交易及結算所有限公司及香港聯合交易所有限公司對本公告的內容概不 負 責，對 其 準 確 性 或 完 整 性 亦 不 發 表 任 何 聲 明，並 明 確 表 示，概 不 就 因 本 公 告 的全部或任何部份內容而產生或因倚賴該等內容而引致的任何損失承擔任何 責 任。 LUYE PHARMA GROUP LTD. 綠葉製藥集團有限公司 （於 百 慕 達 註 冊 成 立 之 有 限 公 司） （股 份 代 號：02186） 自願性公告 授予恩華三款抗精神病藥長效針劑產品 於中國大陸的獨家商業化權利 綠葉製藥集團 有限公司（「本公司」，連 同 其 附 屬 公 司 統 稱「本集團」），董 事 會（「董 事 會」）宣 佈，本 集 團 的 若 干 附 屬 公 司 與 江 蘇 恩 華 藥 業 股 份 有 限 公 司 的 附 屬 公 司 江蘇恩華和信醫藥營銷有限公司（「恩 華」）簽 署 合 作 協 議，授 予 恩 華 三 款 抗 精 神 病 藥 長 效 針 劑 產 品 在 中 國 大 陸 地 區 的 獨 家 商 業 化 權 利。該 三 款 產 品 分 別 為 瑞 可 妥（注 射 用 利 培 酮 微 球（Ⅱ））、瑞 百 萊（ ...

Core Insights - The article discusses the critical role of thyroid hormone transport to the brain for normal neural development, mediated by the transport proteins MCT8 and OATP1C1 [2][3]. Group 1: Research Findings - A recent study published in the journal Cell by researchers from Baylor College of Medicine and the National Institutes of Health provides structural insights into the transport mechanisms of thyroid hormones via MCT8 and OATP1C1 [4][5]. - The study utilized cryo-electron microscopy to analyze the structures of MCT8 and OATP1C1 in complex with active thyroid hormones T3 and its precursor T4, achieving resolutions of 2.9 Å and 2.3 Å respectively [7]. - Key findings include the high transport specificity of MCT8 for thyroid hormones, the selective transport mechanism of OATP1C1 for thyroxine, and the discovery of a conserved extracellular regulatory site in OATP1C1 that can be allosterically inhibited by E1G [9][11].

Core Viewpoint - The research published by Yale University confirms the presence of T cells in the healthy brains of mice and humans, specifically in the subfornical organ (SFO), indicating that T cells can reside in the brain under normal conditions, contrary to previous beliefs about the blood-brain barrier and immune cell isolation [3][11]. Group 1: Research Findings - The study reveals that T cells in the SFO are enriched and play a crucial role in monitoring gut and fat tissue information, which is essential for regulating feeding and behavior [3][11]. - T cells in the SFO are distinct from those in the meninges, as they express proteins like CXCR6 that allow them to remain in brain tissue and secrete immune signaling proteins such as IFNγ [8][11]. - The research indicates a relationship between dietary habits and the quantity of T cells in the brain, with high-fat diets leading to an increase in T cells in both fat tissue and the brain [8][9]. Group 2: Mechanisms of Interaction - The study demonstrates that fasting increases T cell numbers in the brain while decreasing them in fat tissue, suggesting that dietary intake can dynamically regulate T cell migration to the central nervous system [9][11]. - Antibiotic intervention to deplete gut microbiota resulted in a significant reduction of T cells in the brain, indicating that gut microbiota may influence immune cell homeostasis in the central nervous system [9][11]. - The presence of T cells in the brain is linked to feeding behavior, as T cell-deficient mice took longer to find food when hungry compared to normal mice, highlighting their role in foraging and eating behaviors [9][11].

Core Viewpoint - Metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), are increasingly serious public health burdens with limited treatment options. Recent studies indicate that fibroblast growth factor-21 (FGF21) analogs can significantly improve MASH, although the mechanisms remain unclear [2]. Group 1 - A study published by researchers from the University of Iowa in Cell Metabolism demonstrates that FGF21 reverses MASH through coordinated actions on the central nervous system (CNS) and liver [3]. - The research team established that FGF21 exerts beneficial metabolic effects to reverse MASH by independently reducing liver triglyceride and cholesterol levels through different mechanisms [5]. - FGF21 signaling directly acts on glutamatergic neurons in the CNS, stimulating the reduction of liver triglycerides and reversing fibrosis, while also directly signaling liver cells to lower cholesterol levels [6][8]. Group 2 - Mechanistically, FGF21 increases sympathetic nervous activity in the liver, thereby inhibiting de novo lipogenesis [7]. - The core findings of the study include that FGF21 can reverse diet-induced MASH, directly signals the CNS to lower liver triglyceride levels and fibrosis, signals liver cells to reduce cholesterol during MASH, and enhances liver sympathetic nervous activity while decreasing de novo lipogenesis [8]. - Overall, these findings provide a promising drug target and new insights for the treatment of MASH [10].