2025年末将至，距离港股通最新一轮调整考察期结束仅有最后20天时间，这意味着目前已是不少标的"入通"的最后冲刺阶段。 恒生指数和港股通下一轮定期调整时间在明年3月，检讨结果公布时间在2月25日，检讨周期则为2025年1月1日至2025年12月31日。据智通财经APP测算，目 前预计新纳入港股通的标的数量共有31只。除去3只标的将以"A+H"形式获纳入外，剩下28只则有望因满足"入通门槛"获纳入，劲方医药-B(02595)便是其中 之一。 上市以来稳健走势成"入通"关键 目前数据显示，劲方医药在本次检讨周期内的日平均市值为102.96亿港元，较最新的92.42亿港元市值门槛高出超10亿港元。考虑到现已时至12月11日，距离 港股通最新一轮调整考察期结束仅有20天时间，因此劲方医药在保证市值稳定前提下，在新一期港股通调整中顺利入通的概率较大。 从劲方医药上市以来的表现来看，经历上市前期震荡下跌后实现止跌回稳的股价走势无疑是其"冲通"的关键因素。 据智通财经APP观察，9月18日，劲方医药辉立暗盘以40.00港元高开，经过短暂震荡便快速拉升至45.58港元高点，并后续保持中高位震荡以41.22港元报 收，最终收涨 ...

Core Insights - The research conducted by Fudan University reveals a novel role of Acetyl-CoA as a "metabolic messenger" that directly regulates mitochondrial autophagy, providing a new therapeutic target for overcoming resistance to KRAS inhibitors in pancreatic cancer [1][7]. Group 1: Research Findings - The study highlights that during nutrient scarcity, Acetyl-CoA bypasses the well-known AMPK and mTOR pathways, directly signaling to mitochondria through the protein NLRX1 [1][2]. - The research team utilized CRISPR/Cas9 technology to identify NLRX1 as a key protein involved in this newly discovered signaling pathway [3][4]. - The interaction between Acetyl-CoA and NLRX1 was confirmed through a "molecular fishing" experiment, demonstrating a direct binding relationship [4][5]. Group 2: Implications for Cancer Treatment - The findings indicate that in nutrient-rich conditions, high levels of Acetyl-CoA inhibit mitochondrial autophagy by locking NLRX1 in a dormant state, while nutrient deprivation releases this inhibition, promoting autophagy [6][7]. - The study also uncovers a mechanism by which cancer cells develop resistance to KRAS inhibitors by activating mitochondrial autophagy in response to decreased Acetyl-CoA levels, suggesting a potential new treatment strategy [7][8]. - Targeting the Acetyl-CoA-NLRX1 axis could enhance the effectiveness of KRAS inhibitors, offering new hope for cancer patients facing treatment resistance [7][8].

Core Insights - The research published by Fudan University reveals a novel signaling function of Acetyl-Coenzyme A (AcCoA) in regulating mitophagy through the receptor NLRX1, independent of classical pathways like AMPK and mTOR [3][14][16] - This discovery provides new potential targets and strategies for overcoming resistance to KRAS inhibitors in cancer treatment [3][14][16] Group 1: Mechanism of AcCoA in Mitophagy - AcCoA levels decrease during nutrient deprivation, such as short-term fasting, leading to the activation of mitophagy [5][6] - NLRX1 is identified as a key mediator that directly binds to AcCoA, regulating its signaling role in mitophagy [8][11] Group 2: Experimental Validation - In animal models, fasting resulted in a significant decrease in AcCoA levels in tissues, correlating with increased mitophagy [11] - Supplementing with acetate or knocking out NLRX1 gene can block the fasting-induced mitophagy, indicating the critical role of AcCoA and NLRX1 in this process [11][12] Group 3: Implications for Cancer Treatment - The study indicates that KRAS inhibitors downregulate ACLY expression, reducing AcCoA levels and triggering NLRX1-dependent mitophagy, which may contribute to cancer cell resistance [14] - Short-term fasting may have dual effects in cancer treatment, potentially enhancing immune response while also promoting resistance through mitophagy [14][16] Group 4: Future Directions - Targeting the AcCoA-NLRX1 signaling axis may enhance cancer treatment efficacy and could have implications in various metabolic and neurodegenerative diseases [16]