更新于：2024-05-01

ANXA1

annexin A1

更新于：2024-05-01

基本信息

别名

annexin A1、Annexin Ac2-26、Annexin I

+ [10]

简介

Plays important roles in the innate immune response as effector of glucocorticoid-mediated responses and regulator of the inflammatory process. Has anti-inflammatory activity (PubMed:8425544). Plays a role in glucocorticoid-mediated down-regulation of the early phase of the inflammatory response (By similarity). Contributes to the adaptive immune response by enhancing signaling cascades that are triggered by T-cell activation, regulates differentiation and proliferation of activated T-cells (PubMed:17008549). Promotes the differentiation of T-cells into Th1 cells and negatively regulates differentiation into Th2 cells (PubMed:17008549). Has no effect on unstimulated T cells (PubMed:17008549). Negatively regulates hormone exocytosis via activation of the formyl peptide receptors and reorganization of the actin cytoskeleton (PubMed:19625660). Has high affinity for Ca(2+) and can bind up to eight Ca(2+) ions (By similarity). Displays Ca(2+)-dependent binding to phospholipid membranes (PubMed:2532504, PubMed:8557678). Plays a role in the formation of phagocytic cups and phagosomes. Plays a role in phagocytosis by mediating the Ca(2+)-dependent interaction between phagosomes and the actin cytoskeleton (By similarity). Functions at least in part by activating the formyl peptide receptors and downstream signaling cascades (PubMed:22879591, PubMed:15187149, PubMed:25664854). Promotes chemotaxis of granulocytes and monocytes via activation of the formyl peptide receptors (PubMed:15187149). Promotes rearrangement of the actin cytoskeleton, cell polarization and cell migration (PubMed:15187149). Promotes resolution of inflammation and wound healing (PubMed:25664854). Acts via neutrophil N-formyl peptide receptors to enhance the release of CXCL2 (PubMed:22879591).

关联

项与 ANXA1 相关的药物

Annexuzlimab

靶点

ANXA1

作用机制

ANXA1拮抗剂

在研机构

MedAnnex Ltd.

原研机构

MedAnnex Ltd.

在研适应症

实体瘤 [+2]

非在研适应症-

最高研发阶段临床1期

首次获批国家/地区-

首次获批日期1800-01-20

125I-AnnA1 IgG

靶点

ANXA1

作用机制

ANXA1 modulators

在研机构-

原研机构

Kimmel Cancer Center

在研适应症-

非在研适应症

肿瘤

最高研发阶段无进展

首次获批国家/地区-

首次获批日期1800-01-20

项与 ANXA1 相关的临床试验

ISRCTN78740398 / Recruiting临床1期

A modular, multi-arm, first-in-human trial to evaluate the safety and tolerability of MDX-124 alone and in combination with anti-cancer treatments, in participants with locally advanced, unresectable or metastatic solid malignancies

开始日期2022-12-01

申办/合作机构

MedAnnex Ltd.

100 项与 ANXA1 相关的临床结果

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100 项与 ANXA1 相关的转化医学

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0 项与 ANXA1 相关的专利（医药）

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2,316

项与 ANXA1 相关的文献（医药）

2024-02-20·Biomaterials science

Extracellular vesicles produced by 3D cultured MSCs promote wound healing by regulating macrophage activation through ANXA1.

Article

作者: Hao Deng ; Yuheng Jiang ; Junhao Deng ; Feifan Chang ; Junyu Chen ; Xinyu Sun ; Dongliang Cheng ; Zhongqi Wang ; Ran Li ; Jiang Liu ; Yi Li ; Licheng Zhang ; Pengbin Yin

The conundrum of wound healing has transformed into an imminent medical challenge. Presently, cell-free therapy centered around extracellular vesicles (EVs) has become a pivotal and promising research avenue. EVs generated from three-dimensional (3D) cell cultures have been previously established to possess enhanced tissue regeneration potential, although the underlying mechanisms remain elusive. In this study, we observed higher expression of annexin ANXA1 in 3D-cultured EVs. Remarkably, 3D-EVs with elevated ANXA1 expression demonstrated a more potent capacity to promote macrophage polarization from the M1 phenotype to the M2 phenotype. Concurrently, they exhibited superior abilities to enhance cell migration and tube formation, facilitating expedited wound healing in animal experiments. Conversely, the application of an ANXA1 inhibitor counteracted the positive effects of 3D-EVs. Taken together, our data validate that extracellular vesicles derived from 3D-cultured MSCs regulate macrophage polarization via ANXA1, thereby fostering wound healing.

2024-02-15·Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Loss of Endothelial Annexin A1 Aggravates Inflammation-Induched Vascular Aging.

Article

作者: Qinyi You ; Yilang Ke ; Xiaofeng Chen ; Wanhong Yan ; Dang Li ; Lu Chen ; Run Wang ; Jie Yu ; Huashan Hong

Chronic inflammation is increasingly considered as the most important component of vascular aging, contributing to the progression of age-related cardiovascular diseases. To delay the process of vascular aging, anti-inflammation may be an effective measure. The anti-inflammatory factor annexin A1 (ANXA1) is shown to participate in several age-related diseases; however, its function during vascular aging remains unclear. Here, an ANXA1 knockout (ANXA1^-/- ) and an endothelial cell-specific ANXA1 deletion mouse (ANXA1^△EC ) model are used to investigate the role of ANXA1 in vascular aging. ANXA1 depletion exacerbates vascular remodeling and dysfunction while upregulates age- and inflammation-related protein expression. Conversely, Ac2-26 (a mimetic peptide of ANXA1) supplementation reverses this phenomenon. Furthermore, long-term tumor necrosis factor-alpha (TNF-α) induction of human umbilical vein endothelial cells (HUVECs) increases cell senescence. Finally, the senescence-associated secretory phenotype and senescence-related protein expression, rates of senescence-β-galactosidase positivity, cell cycle arrest, cell migration, and tube formation ability are observed in both ANXA1-knockdown HUVECs and overexpressed ANXA1-TNF-α induced senescent HUVECs. They also explore the impact of formyl peptide receptor 2 (a receptor of ANXA1) in an ANXA1 overexpression inflammatory model. These data provide compelling evidence that age-related inflammation in arteries contributes to senescent endothelial cells that promote vascular aging.

2024-02-15·FASEB journal : official publication of the Federation of American Societies for Experimental Biology

The pro-resolving mediator, annexin A1 regulates blood pressure, and age-associated changes in cardiovascular function and remodeling.

Article

作者: Jaideep Singh ; Kristy L Jackson ; Feng Shii Tang ; Ting Fu ; Cameron Nowell ; Ekaterina Salimova ; Helen Kiriazis ; Rebecca H Ritchie ; Geoffrey A Head ; Owen L Woodman ; Cheng Xue Qin

Aging is associated with chronic, low-level inflammation which may contribute to cardiovascular pathologies such as hypertension and atherosclerosis. This chronic inflammation may be opposed by endogenous mechanisms to limit inflammation, for example, by the actions of annexin A1 (ANXA1), an endogenous glucocorticoid-regulated protein that has anti-inflammatory and pro-resolving activity. We hypothesized the pro-resolving mediator ANXA1 protects against age-induced changes in blood pressure (BP), cardiovascular structure and function, and cardiac senescence. BP was measured monthly in conscious mature (4-month) and middle-aged (12-month) ANXA1-deficient (ANXA1^-/- ) and wild-type C57BL/6 mice. Body composition was measured using EchoMRI, and both cardiac and vascular function using ultrasound imaging. Cardiac hypertrophy, fibrosis and senescence, vascular fibrosis, elastin, and calcification were assessed histologically. Gene expression relevant to structural remodeling, inflammation, and cardiomyocyte senescence were also quantified. In C57BL/6 mice, progression from 4 to 12 months of age did not affect the majority of cardiovascular parameters measured, with the exception of mild cardiac hypertrophy, vascular calcium, and collagen deposition. Interestingly, ANXA1^-/- mice exhibited higher BP, regardless of age. Additionally, age progression had a marked impact in ANXA1^-/- mice, with markedly augmented vascular remodeling, impaired vascular distensibility, and body composition. Consistent with vascular dysfunction, cardiac dysfunction, and hypertrophy were also evident, together with markers of senescence and inflammation. These findings suggest that endogenous ANXA1 plays a critical role in regulating BP, cardiovascular function, and remodeling and delays cardiac senescence. Our findings support the development of novel ANXA1-based therapies to prevent age-related cardiovascular pathologies.

项与 ANXA1 相关的新闻（医药）

2024-02-26

·今日头条

用AI指导大肠癌治疗，大型临床研究再添新证

02月26日的《热心肠日报》，我们解读了 15 篇文献，关注：机器学习，大肠癌，预后，癌症筛查，药物研发，治疗靶点，肺腺癌，模拟禁食饮食，迈威生物，JUZTLAB草本未来，Leucine Rich Bio，北极星药业，赛诺菲。该篇日报由R·AI辅助创作生成，人工审核校对。 AI提升结肠癌化疗用药准确性 Journal of Clinical Oncology——[45.3] ① 匹兹堡大学鲁兴华和孙旻教授与团队训练了一个名为COLOXIS的AI模型，用来预测结肠癌患者对奥沙利铂的反应；② 在1065名患者中，有526名被预测为COLOXIS+（奥沙利铂响应者），而539名被预测为COLOXIS-（非响应者），COLOXIS+组的病人显著受益于奥沙利铂，而COLOXIS-组的病人则不受益；③ 建议在结直肠癌辅助治疗中仅对COLOXIS+患者使用奥沙利铂，但需要进一步验证；④ COLOXIS可以让约半数接受辅助治疗的结肠癌患者避免不必要的奥沙利铂诱发的毒副作用，并大幅度提高总体获益风险比；⑤ COLOXIS是目前唯一用逾一千病人的大规模的临床试验数据证明化疗药物疗效可以用AI的方法来推算的模型，证实了用AI指导化疗药物的可行性。【原文信息】 Machine Learning Predicts Oxaliplatin Benefit in Early Colon Cancer 2024-02-05 , doi: 10.1200/JCO.23.01080 Lancet子刊：多靶点粪便免疫化学检测改善结直肠癌筛查效果 The Lancet Oncology——[51.1] ① 这项研究显示相较于传统粪便免疫化学试验（FIT），多靶点粪便免疫化学试验（mtFIT）在检测高级别前癌病变方面具有更高的灵敏度；② 在结直肠癌筛查项目中，15283人提交了同一次排便收集的FIT和mtFIT样本，FIT的阳性率和高级别腺癌检出率分别是4.08%和1.21%，而mtFIT分别是9.11%和2.27%；③ mtFIT和FIT对结直肠癌、高危腺瘤、晚期锯齿状息肉的检出率分别0.20% vs 0.17%、1.64% vs 0.86%、0.43% vs 0.17%；④ 建模显示，基于mtFIT的筛查可将结直肠癌发病率降低21%，并将相关死亡率降低18%，与当前的荷兰结直肠癌筛查计划相比，成本可行；⑤ 在相同的阳性率下，mtFIT在诊断产出方面优于FIT；⑥ 在同样低的阳性率下，基于mtFIT的筛查将使结直肠癌发病率进一步降低5%，相关死亡率降低4%。【原文信息】 The multitarget faecal immunochemical test for improving stool-based colorectal cancer screening programmes: a Dutch population-based, paired-design, intervention study 2024-02-09 , doi: 10.1016/S1470-2045(23)00651-4 Lancet子刊：CD8+细胞和FoxP3+细胞预测结直肠癌患者预后 The Lancet Oncology——[51.1] ① 本研究通过对SCOT和QUASAR 2临床试验中II-III期结直肠癌患者肿瘤样本进行多重免疫荧光染色分析，发现综合评估上皮内CD8（CD8IE）和基质内FoxP3（FoxP3IS）细胞的密度能更精准地进行风险分层；② 在SCOT试验中，CD8IE和FoxP3IS作为连续变量显示出强烈的预后价值，而且与单独标记相比，CD8IE-FoxP3IS复合标记在作为连续变量和分为低、中、高密度组时表现更优越；③ 在QUASAR 2试验中，CD8IE-FoxP3IS的预后价值得到验证，尤其是在将其作为连续变量以及作为低密度与高密度的分类变量；④ CD8IE和FoxP3IS的联合评估有助于在结直肠癌中进行更精细的风险分层，同时也提示了将FoxP3IS细胞作为免疫治疗靶点的可能性。【原文信息】 Multiplex analysis of intratumoural immune infiltrate and prognosis in patients with stage II-III colorectal cancer from the SCOT and QUASAR 2 trials: a retrospective analysis 2024-02-01 , doi: 10.1016/S1470-2045(23)00560-0 Nature子刊：基于通路进行结直肠癌分型，揭示出缓慢增殖的生物学表型与较差的临床预后相关 Nature Genetics——[30.8] ① 本研究基于基因本体（GO分析）和生物激活状态信息对结直肠癌（CRC）进行分类，揭示了结直肠癌中与较差临床结果相关的缓慢增殖的生物表型；② 定义出三种亚型（PDS），PDS1肿瘤——经典/LGR5+干细胞丰富、高增殖并显示良好预后，PDS2肿瘤——再生/ANXA1+干细胞丰富，具有升高的基质和免疫肿瘤微环境谱系和PDS3肿瘤——CMS2中先前被忽视的缓慢增殖的肿瘤亚组，其干细胞数量减少，分化谱系增加，特别是肠细胞和肠内分泌细胞，然而在局部晚期疾病中显示出最差的预后；③ PDS3的表型特征在多个批量和单细胞数据集中均有体现，标志着一系列在临床前模型中尚未充分代表的生物状态，且不能使用现有的亚型分类器进行识别；④ 这些发现强调了使用通路级别信息进行分子分型的重要性，为结直肠癌的个性化治疗提供了新的视角。【原文信息】 Pathway level subtyping identifies a slow-cycling biological phenotype associated with poor clinical outcomes in colorectal cancer 2024-02-13 , doi: 10.1038/s41588-024-01654-5 Nature子刊：多巴胺转运体拮抗剂vanoxerine或可治疗结肠肿瘤 Nature Cancer——[22.7] ① 本研究发现多巴胺转运体（DAT）拮抗剂vanoxerine通过抑制G9a表达，有效阻断结肠癌干细胞（CSCs）的功能，为治疗结肠肿瘤提供了新策略；② 通过基于干细胞的表型药物筛选，确定vanoxerine能特异性降低G9a表达；③ 基因沉默和化学拮抗DAT通过抑制G9a表达以阻碍结肠CSC的功能；④ 拮抗DAT还通过激活内源性转座元件和I型干扰素反应，增强肿瘤淋巴细胞浸润，从而改善抗肿瘤免疫应答；⑤ 本研究揭示了DAT-G9a轴直接参与CSCs的维持，并提出了一种改善结肠肿瘤抗肿瘤免疫应答的新策略。【原文信息】 The dopamine transporter antagonist vanoxerine inhibits G9a and suppresses cancer stem cell functions in colon tumors 2024-02-13 , doi: 10.1038/s43018-024-00727-y 国内团队：脂质纳米粒子传递IFNβ编码质粒，增强结肠癌抗肿瘤免疫 ACS Nano——[17.1] ① 天津大学吕春婉团队发现通过阳离子脂质纳米粒子传递干扰素β（IFNβ）编码质粒，能有效恢复结肠癌中IFNβ的表达，增强抗肿瘤免疫；② IFN-I通过激活Cxcl9和Cxcl10的表达，增强T细胞对肿瘤的浸润；③ 在结肠肿瘤组织中，通过强制表达IFNα13和IFNβ可提高MHC I的表达并抑制肿瘤生长；④ IFNβ表达与患者HLA的表达、与患者对PD-1阻断免疫疗法反应相关的IFN-I信号激活正相关；⑤ 通过1,2-二油酰基-3-三甲基铵丙烷（DOTAP）-胆固醇包裹的IFNβ编码质粒（IFNBCOL01）治疗，可激活MHC I和颗粒酶B的表达，抑制小鼠中的结肠肿瘤生长。【原文信息】 Delivery of Interferon β-Encoding Plasmid via Lipid Nanoparticle Restores Interferon β Expression to Enhance Antitumor Immunity in Colon Cancer 2024-02-06 , doi: 10.1021/acsnano.3c10972 Nature子刊：卡博替尼与杜瓦伦单抗联用或可治疗化疗难治性结直肠癌 Nature Communications——[16.6] ① CAMILLA CRC队列的II期试验结果显示，卡博替尼与杜瓦伦单抗联合治疗化疗耐药的结直肠癌（CRC）患者表现出了抗肿瘤活性和可管理的毒性；② 29名可评估患者中，100%的患者确诊为pMMR/MSS型肿瘤，客观缓解率（ORR）为27.6%，4个月无进展生存率（PFS）为44.83%，中位总生存期（OS）为9.1个月，39%的患者发生≥3级治疗相关副作用；③ 对于RAS野生型肿瘤患者，客观缓解率提高到50%，中位PFS和OS分别为6.3个月和21.5个月；④ 治疗前进行肿瘤空间转录组分析，发现在反应者与非反应者中，VEGF和MET信号通路上调、细胞外基质活性增加以及抗肿瘤免疫反应与免疫抑制特征（如T细胞迁移障碍）共存；⑤ 此项临床试验的结果支持STELLAR-303三期试验的启动。【原文信息】 Clinical and biomarker results from a phase II trial of combined cabozantinib and durvalumab in patients with chemotherapy-refractory colorectal cancer (CRC): CAMILLA CRC cohort 2024-02-20 , doi: 10.1038/s41467-024-45960-2 浙大Cell子刊：巨噬细胞导向模块可作为大肠癌潜在治疗靶点 Cell Reports Medicine——[14.3] ① 浙江大学的赵鹏、阮健、盛剑鹏及包暄文作为共同通讯在Cell Reports Medicine发表最新研究，通过多组学分析辅以深度学习模型，在结直肠癌（CRC）中鉴定出一个以巨噬细胞为中心的模块；② 该CRC免疫模块（CCIM）包括FOLR2+巨噬细胞、耗竭的CD8+ T细胞、耐受的CD8+ T细胞、耗竭的CD4+ T细胞和调节性T细胞等；③ 通过多重免疫组化技术描绘了CCIM，并利用深度学习技术建立了空间交互图以预测化疗反应；④ CCIM-Net展示出良好的化疗反应预测性能，并且通过靶向FOLR2+巨噬细胞的治疗手段在体内打破了免疫抑制的CCIM，增强了化疗反应。【原文信息】 A multiomics analysis-assisted deep learning model identifies a macrophage-oriented module as a potential therapeutic target in colorectal cancer 2024-01-30 , doi: 10.1016/j.xcrm.2024.101399 郑心+黄适等：肠道菌群可介导肺腺癌治疗疗效 Experimental Hematology and Oncology——[10.9] ① 哈佛医学院Zheng Sun、青岛市中医特色卫生院郑心、香港大学黄适与团队发表研究，对携带PC-9肿瘤的小鼠进行不同治疗的肠道菌群变化纵向研究；② 与吉非替尼单独治疗相比，联合使用益生菌或中药的治疗方案能更有效地减小肿瘤体积、改善体重和肿瘤标志物测试结果，而使用抗生素可抑制吉非替尼的抗肿瘤效果；③ 肠道菌群的时间变化与不同治疗强相关；④ 无论何种治疗，13种介质（扩增子序列变体，ASVs）调节吉非替尼的抗肿瘤效果，即肠道菌群与吉非替尼治疗效果之间存在因果关系；⑤ 本研究揭示了肠道菌群在提高肺腺癌靶向治疗（吉非替尼治疗）效果中的重要作用，为抗肿瘤药物开发提供了新策略。【原文信息】 Revealing the role of the gut microbiota in enhancing targeted therapy efficacy for lung adenocarcinoma 2024-02-09 , doi: 10.1186/s40164-024-00478-7 模拟禁食饮食辅助治疗慢性淋巴细胞白血病 Cancer Research——[11.2] ① 周期性模拟禁食饮食（FMD）是一种在实体恶性肿瘤模型中具有强大抗肿瘤活性的实验性营养干预措，这项研究发现FMD联合蛋白酶体抑制剂和抗CD20抗体对慢性淋巴细胞白血病（CLL）具有显著的治疗效果，延缓CLL的进展并显著延长小鼠的生存期；② 2名CLL患者接受FMD，可逆地减少外周血淋巴细胞的数量；③ 小鼠CLL模型中，禁食模拟条件显示轻微的细胞毒性作用，导致胰岛素和IGF-1降低介导的凋亡激活；④ CLL细胞中，禁食促进蛋白酶体活性的增加，添加蛋白酶体抑制剂硼替佐米（BTZ）可显著增强饥饿条件的促凋亡效果；⑤ CLL模型中，FMD/BTZ/利妥昔单抗（RTX，anti-CD20）联用延缓CLL的进展，并显著延长小鼠的存活时间；⑥ 蛋白酶体抑制剂与FMD相结合促进CLL死亡，这为以饥饿逃逸途径为靶点的治疗策略提供新的思路。【原文信息】 Cyclic fasting-mimicking diet plus bortezomib and rituximab is an effective treatment for chronic lymphocytic leukemia 2024-01-19 , doi: 10.1158/0008-5472.CAN-23-0295 迈威生物Nectin-4 ADC新药获FDA快速通道认定 ① 2月25日，迈威生物宣布其自主研发的靶向Nectin-4 ADC创新药（9MW2821）获FDA快速通道认定，用于治疗晚期、复发或转移性食管鳞癌（ESCC）；② 9MW2821为靶向Nectin-4的定点偶联ADC新药，是国内企业同靶点药物中首个开展临床试验的品种；③ 截至2024年2月20日，在2期临床试验1.25mg/kg剂量组下中，9MW2821单药治疗并完成至少一次肿评的30例晚期食管癌患者的ORR和DCR分别为30%和73.3%；④ 9MW2821是全球首款针对食管癌适应症披露临床有效性数据的靶向Nectin-4治疗药物。【原文信息】迈威生物Nectin-4 ADC新药获FDA快速通道认定 2024-02-25 , 医药魔方Info 药食同源品牌JUZTLAB获若羽臣千万级融资 ① 近日，JUZTLAB草本未来获得若羽臣千万元天使轮融资；② 资金将主要用于供应链布局及团队建设；③ JUZTLAB草本未来是基于中医药食同源的高附加值健康养生品牌，以中医草本为核⼼，针对25-34岁年轻人群的生活场景提供养生产品解决方案；④ 品牌由康奈尔大学团队成立于2021年末，携手浙江大学茶叶研究所和浙江中医药大学，致力于发扬中国传统古方；⑤ JUZTLAB草本未来种子轮由小一创投独家投资，当前已建立起多元销售网络，在上线不到一年时间内，销售额突破千万。【原文信息】加码大健康赛道，“新中式”养生品牌JUZTLAB获若羽臣千万级融资 2024-02-23 , FoodTalks Leucine Rich Bio公司公布旗下个性化营养试剂盒BugSpeaks临床积极数据 ① 2月23日，Leucine Rich Bio公司宣布，其微生物组分析试剂盒BugSpeaks在临床试验中取得显著成效，能够有效改善糖尿病患者的血糖、炎症标志物和血压参数；② BugSpeaks是一种肠道微生物组分析试剂盒，可根据个体肠道微生物组提供营养建议；③ 该临床试验招募了42-65岁、患有高血糖和高胆固醇的印度成年男女；④ 受试者被随机分为两组，一组接受基于BugSpeaks的个性化饮食，另一组接受常规饮食，为期3个月；⑤ 结果显示，接受BugSpeaks个性化饮食的患者在研究的第90天显示出优异的结果，受试者的HbA1c水平从8.30降至6.67，收缩压降低了14%，炎症标志物CRP降低了20%。【原文信息】 Leucine Rich Bio announces clinical trial results of microbiome profiling kit on diabetes patients 2024-02-23 , Pharmabiz 强攻减肥药，北极星药业斥资6.7亿元扩厂 ① 2月25日，北极星药业-KY宣布，通过子公司北极星生医以6.7亿元购得约8000平方米的中国台湾竹南厂房，计划改建为GLP-1多肽药物生产基地；② 该厂房预计今年第4季投产，未来可建设三条生产线，年产5亿剂GLP-1多肽药物；③ GLP-1多肽药物主要用于调节2型糖尿病患者血糖，同时具有减重效果；④ 北极星药业锁定的市场包括东南亚、俄罗斯、中东及非洲等国家；⑤ 此外，北极星药业计划在大陆再投资近10亿元扩产，加强其在癌症代谢疗法新药和多肽药物领域的发展。【原文信息】强攻减肥药！北极星药业扩厂 2024-02-25 , GLP减重宝典赛诺菲消费者保健业务或被收购，金额高达200亿美元 ① 近日，据彭博社报道，安宏资本和黑石集团考虑以高达200亿美元收购赛诺菲消费者保健业务；② 贝恩资本、CVC Capital Partners、殷拓和KKR & Co也对收购感兴趣；③ 赛诺菲自2019年12月起，计划分拆消费者保健业务，以专注于原研药和疫苗开发；④ 2023年，赛诺菲消费者保健业务收入增长至51.8亿欧元；⑤ 大型制药公司近年来趋向于剥离消费者保健业务，聚焦创新药物开发。【原文信息】赛诺菲消费者保健业务或被收购，金额高达200亿美元 2024-02-21 , 医药魔方感谢本期日报的审核者：RZN，章台柳，圆圈儿，九卿臣，617 点击阅读过去10天的日报： 0225 | 65分综述详解：超加工食品和食品添加剂如何影响肠道健康？ 0224 | 陈思凡等Cell子刊新发现：促血栓的新型肠菌代谢物 0223 | 膳食纤维怎样影响代谢健康？18页综述一文讲透 0222 | 65分综述详解跨越菌群-肠-脑轴的"通讯之门" 0221 | Cell子刊新发现：肠菌藏身"安全屋"躲避抗生素 0220 | 秦环龙/许谦/李宁Cell子刊：深入探究菌群移植中的供-受体微生物对话 0219 | 如何用菌对抗大肠癌？《自然·综述》发出最新观点 0218 | Cell重磅：某些无糖食品为何让人肠胃不适？菌群给出答案 0209 | 《自然·综述》详解：自身免疫病中，肠道为何关键？ 0208 | 今日Nature双发，肠菌胆汁酸代谢成焦点

2024-01-19

·Science Daily

Targeting annexin-A1 can halt cancer cell growth

A new study highlights the effectiveness of MDX-124, the first therapeutic drug to target annexin-A1, a protein which is overexpressed in several cancer types and promotes tumor progression. A new study published in Nature's cancer journal Oncogene highlights the effectiveness of MDX-124, the first therapeutic drug to target annexin-A1, a protein which is overexpressed in several cancer types and promotes tumour progression. The research was led by Professor Chris Parris and Dr Hussein Al-Ali at Anglia Ruskin University (ARU) in collaboration with Professor Chris Pepper of Brighton and Sussex Medical School and UK biotech company Medannex, which has produced the MDX-124 monoclonal antibody therapy. High annexin-A1 expression levels correlate with poorer overall survival in various cancers that currently have limited treatment options, including triple-negative breast, pancreatic, colorectal and prostate cancers. The new study found that MDX-124, which is being developed for use in immunotherapy, significantly reduces proliferation across a number of human cancer cell lines expressing annexin-A1. This anti-proliferative effect is instigated by stopping cell cycle progression. Additionally, MDX-124 is shown to significantly inhibit tumour growth in in vivo models of triple-negative breast and pancreatic cancer, indicating that annexin-A1-targeted therapy represents a viable and innovative approach to cancer treatment. The phase Ib clinical study of MDX-124, called ATTAINMENT, is currently underway to establish the safety and optimum dose of the novel therapy. Its clinical efficacy will then be evaluated in newly-diagnosed cancer patients, in combination with current appropriate treatments. Professor Chris Parris, Head of School of Life Sciences at Anglia Ruskin University (ARU), said: "We know that the protein annexin-A1 activates formyl peptide receptors to initiate a complex network of intracellular signalling pathways, which can lead to numerous cellular responses, including tumour initiation and progression. "We have demonstrated in this new study that using MDX-124 can reduce cell growth in annexin-A1-expressing cancer cells both in vitro and in vivo, providing further evidence that annexin-A1 is a valid target for therapy in cancer." Medannex Director of Scientific Operations, Dr Fiona Dempsey, who co-authored the paper, said: "We are delighted to publish this work with our collaborators demonstrating the anti-cancer potential of our innovative antibody therapeutic and look forward to the clinical data coming out of the ATTAINMENT study in due course."

免疫疗法临床1期抗体药物偶联物

2023-11-06

·PRNewswire

ResoTher Pharma receives a €2.5 million grant from European Innovation Council (EIC) to support a Phase 2a clinical study of their Lead Candidate RTP-026 for Myocardial Infarction

HOLTE, Denmark, Nov. 6, 2023 /PRNewswire/ -- ResoTher Pharma, a biotech company focused on developing life-saving options for patients suffering from cardiovascular disease, today announced that the company has received a €2.5 million grant from the European Innovation Council (EIC) to support the development of the company's Lead Compound, RTP-026, in a Phase 2a clinical study in Myocardial Infarction. The project focusing on development of Resother Pharmas RTP-026 compound is one of 47 projects selected to receive funding out of 648 full proposals submitted for evaluation to the EIC-accelerator program. The grant given to ResoTher Pharma is defined as a "Grant first," meaning that the project will be considered for further support by the European Investment Bank upon completion of the Phase 2a study supported by the current grant. "The EIC Grant is a major boost to our RTP-026 development program," says Anders Kronborg, CEO of ResoTher Pharma. "It has made it possible to focus entirely on development, thereby accelerating the Phase 2a development path with the aim to initiate dosing in Q1 2024." RTP-026 is developed as a new and innovative way to modulate the inflammatory response that occurs in the heart during the recovery phase of a myocardial infarction. Especially in the subset of patients showing high inflammatory activity, there is a need for novel treatments to reduce the risk of reinfarction and other major cardiovascular events. Following the completion of Phase 1 development, RTP-026 is ready to enter Phase 2a development with the aim of testing the potential of the compounds to modulate the hyperinflammatory response of the heart in patients undergoing percutaneous coronary intervention with the aim to reestablish blood supply in patients with acute myocardial infarction. In Phase 1 development conducted in healthy volunteers, the compound showed a very good safety profile when given as a single dose or in repeated dosing, with very good plasma exposure indicating a good safety profile relative to what is expected to be relevant exposure levels in patients. The RTP-026 compound, an IP-protected analogue of the N-terminus of the Annexin A1 protein, is developed in collaboration with the Faculty of Medicine and Dentistry, Queen Mary University of London. The compound was designed and characterized in Professor Mauro Petretti's laboratory at the William Harvey Research Institute. The continued Phase 2 development, where the first step will be a Phase 2a dose range study to focus on safety and efficacy in a subset of high-risk ST-elevation Myocardial Infarction patients undergoing acute percutaneous coronary intervention will include active recruitment of patients at the Barts Heart Centre at St Bartholomew's Hospital in London, one of Europe's biggest coronary departments in London. "The EIC grant has made it possible to proceed with Phase 2 development at Barts Heart Centre of a compound designed and characterized at Queen Mary. This important partnership demonstrates how our cutting-edge research in translational Pharmacology in the inflammatory and cardiovascular field moves from the lab to improving better health outcomes in East London and beyond," says Professor Sir Mark Caulfield, MD, Vice Principal for Health, Queen Mary University of London, Director of the NIHR Barts Biomedical Research Centre. "Resother Pharma previously received non-diluting funding from the Danish Innovation Fund and from Barts Charity, and continued collaboration with William Harvey Research Institute, a world-leading translational Pharmacology institute at Queen Mary University of London, has been highly valued," says Anders Kronborg, CEO of ResoTher Pharma. About ResoTher Pharma ResoTher Pharma is a Danish privately held clinical-stage biotech company, focusing on the development of compounds that induce inflammatory resolution in cardiovascular diseases. The company was founded in 2016 with the aim of developing compounds with the ability to promote pharmacological resolution in cardiovascular diseases. The company is privately owned by a group of prominent Danish investors. The company was founded by board member Jeppe Øvlesen and the head of the Scientific Advisory Board, Thomas Jonassen, MD. The co-inventor of the company's lead compound, RTP-026, Professor Mauro Perretti, is also a shareholder in the company. Mode of action of RTP-026: Upon formyl peptide type 2 receptor stimulation the RTP-026 compound induces a combination of anti-inflammatory and pre-resolving effects which in experimental models of myocardial infarction has profound effect not only on reducing the infarction size compared to placebo treatment, but importantly to restore cardiac function to a pre-infarction level. For more information, please contact Anders Kronborg, CEO [email protected] +4531516343 Or visit or follow us on LinkedIn. Logo - SOURCE ResoTher Pharma ApS

临床2期临床结果临床1期