预约演示

更新于：2025-05-07

TNSALP

更新于：2025-05-07

基本信息

别名

Alkaline phosphatase liver/bone/kidney isozyme、alkaline phosphatase, biomineralization associated、alkaline phosphatase, liver/bone/kidney

+ [11]

简介

Alkaline phosphatase that metabolizes various phosphate compounds and plays a key role in skeletal mineralization and adaptive thermogenesis (PubMed:12162492, PubMed:23688511, PubMed:25982064). Has broad substrate specificity and can hydrolyze a considerable variety of compounds: however, only a few substrates, such as diphosphate (inorganic pyrophosphate; PPi), pyridoxal 5'-phosphate (PLP) and N-phosphocreatine are natural substrates (PubMed:12162492, PubMed:2220817). Plays an essential role in skeletal and dental mineralization via its ability to hydrolyze extracellular diphosphate, a potent mineralization inhibitor, to phosphate: it thereby promotes hydroxyapatite crystal formation and increases inorganic phosphate concentration (PubMed:23688511, PubMed:25982064). Acts in a non-redundant manner with PHOSPHO1 in skeletal mineralization: while PHOSPHO1 mediates the initiation of hydroxyapatite crystallization in the matrix vesicles (MVs), ALPL/TNAP catalyzes the spread of hydroxyapatite crystallization in the extracellular matrix (By similarity). Also promotes dephosphorylation of osteopontin (SSP1), an inhibitor of hydroxyapatite crystallization in its phosphorylated state; it is however unclear whether ALPL/TNAP mediates SSP1 dephosphorylation via a direct or indirect manner (By similarity). Catalyzes dephosphorylation of PLP to pyridoxal (PL), the transportable form of vitamin B6, in order to provide a sufficient amount of PLP in the brain, an essential cofactor for enzymes catalyzing the synthesis of diverse neurotransmitters (PubMed:20049532, PubMed:2220817). Additionally, also able to mediate ATP degradation in a stepwise manner to adenosine, thereby regulating the availability of ligands for purinergic receptors (By similarity). Also capable of dephosphorylating microbial products, such as lipopolysaccharides (LPS) as well as other phosphorylated small-molecules, such as poly-inosine:cytosine (poly I:C) (PubMed:28448526). Acts as a key regulator of adaptive thermogenesis as part of the futile creatine cycle: localizes to the mitochondria of thermogenic fat cells and acts by mediating hydrolysis of N-phosphocreatine to initiate a futile cycle of creatine dephosphorylation and phosphorylation (By similarity). During the futile creatine cycle, creatine and N-phosphocreatine are in a futile cycle, which dissipates the high energy charge of N-phosphocreatine as heat without performing any mechanical or chemical work (By similarity).

关联

项与 TNSALP 相关的药物

Amifostine

氨磷汀

靶点

TNSALP

作用机制

TNSALP调节剂

在研机构

Links Medical Products, Inc. [+2]

原研机构

MedImmune LLC

在研适应症

细胞保护佐剂 [+2]

非在研适应症

急性髓性白血病 [+12]

最高研发阶段批准上市

首次获批国家/地区

美国

首次获批日期1995-12-08

Efzimfotase alfa

靶点

TNSALP

作用机制

TNSALP刺激剂

在研机构

阿斯利康全球研发（中国）有限公司 [+2]

原研机构

Alexion Pharmaceuticals, Inc.

在研适应症

低碱性磷酸酶血症 [+1]

非在研适应症-

最高研发阶段临床3期

首次获批国家/地区-

首次获批日期1800-01-20

DS-1211

靶点

TNSALP

作用机制

TNSALP抑制剂

在研机构

Daiichi Sankyo Co., Ltd. [+1]

原研机构

Sanford Burnham Prebys Medical Discovery Institute

在研适应症

弹性假黄瘤 [+1]

非在研适应症-

最高研发阶段临床2期

首次获批国家/地区-

首次获批日期1800-01-20

项与 TNSALP 相关的临床试验

CTIS2023-505675-73-00

/ Recruiting临床3期

A Phase 3, Randomized, Double-blinded, Placebo-controlled, Multicenter Study to Evaluate Efficacy and Safety of ALXN1850 Versus Placebo Administered Subcutaneously in Pediatric (2 to < 12 years of age) Participants with Hypophosphatasia Who Have Not Received Previous Treatment with Asfotase Alfa - ALXN1850-HPP-305

开始日期2024-10-07

申办/合作机构

Alexion Pharmaceuticals, Inc.

CTIS2023-505673-32-00

/ Recruiting临床3期

A Phase 3, Randomized, Double-blinded, Placebo-controlled, Multicenter Study to Evaluate Efficacy and Safety of ALXN1850 (Recombinant Alkaline Phosphatase) Administered Subcutaneously in Adolescent (12 to < 18 years of age) and Adult Participants with Hypophosphatasia Who Have Not Previously Been Treated with Asfotase Alfa (Hickory) - ALXN1850-HPP-301

开始日期2024-08-12

申办/合作机构

Alexion Pharmaceuticals, Inc.

NCT06079359

/ Recruiting临床3期

A Phase 3, Randomized, Double-blinded, Placebo-controlled, Multicenter Study to Evaluate Efficacy and Safety of ALXN1850 Versus Placebo Administered Subcutaneously in Pediatric (2 to < 12 Years of Age) Participants With Hypophosphatasia Who Have Not Received Previous Treatment With Asfotase Alfa

The primary purpose of this study is to evaluate the efficacy of ALXN1850 versus placebo on radiographic outcomes in pediatric participants with HPP who have not previously been treated with asfotase alfa.

开始日期2024-05-14

申办/合作机构

Alexion Pharmaceuticals, Inc.

100 项与 TNSALP 相关的临床结果

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100 项与 TNSALP 相关的转化医学

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0 项与 TNSALP 相关的专利（医药）

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1,647

项与 TNSALP 相关的文献（医药）

2025-06-01·Regenerative Therapy

Selective effects of collagen-derived peptides Pro-Hyp and Hyp-Gly on the proliferation and differentiation of SSEA3-positive human dental pulp stem cells

Article

作者: Ntege, Edward Hosea ; Nakamura, Hiroyuki ; Isa, Mikana ; Suzuki, Risako ; Murahashi, Makoto ; Ide, Kentaro ; Tokuchi, Shusuke ; Kawano, Toshihiro ; Shimizu, Yusuke ; Sunami, Hiroshi

IntroductionCollagen-derived peptides demonstrate diverse biological activities, but their effects on human dental pulp stem cells (hDPSCs) remain unclear. This study investigated the influence of prolyl-hydroxyproline (Pro-Hyp) and hydroxyproline-glycine (Hyp-Gly) on stage-specific embryonic antigen 3 (SSEA3)-positive hDPSCs.MethodsSSEA3-positive and SSEA3-negative hDPSCs were isolated and cultured with Pro-Hyp or Hyp-Gly (200 μg/ml) under stem cell medium or differentiation-inducing conditions. Cell proliferation was assessed using the MTT assay. The expression of the chondrogenic and osteogenic markers was analyzed by real-time PCR. Matrix production was evaluated using Alcian blue and Alizarin red S staining.ResultsPro-Hyp and Hyp-Gly enhanced the proliferation of SSEA3-positive hDPSCs compared with SSEA3-negative cells. Pro-Hyp promoted chondrogenic differentiation through early upregulation of Col II followed by sustained SOX9 expression, with enhanced matrix production after 2 weeks in chondrogenic medium. Hyp-Gly specifically enhanced the osteogenic differentiation of SSEA3-positive cells through the temporal regulation of gene expression, progressing from early transcription factors (RUNX2 and RANKL) to matrix proteins (ALPL, Col I, BSP, and OCN), resulting in increased mineralization under osteogenic conditions.ConclusionsThis study demonstrated that Pro-Hyp and Hyp-Gly selectively influenced SSEA3-positive hDPSC fate through the distinct temporal regulation of differentiation pathways. These findings provide new insights into the development of targeted regenerative strategies using collagen-derived peptides in dental tissue engineering.

2025-06-01·Vascular Pharmacology

TNAP expressing adventitial pericytes contribute to myogenesis during foetal development

Article

作者: Santoleri, S ; Fancello, I ; Amer, S ; Bragg, L ; Cossu, G ; Willett, S ; Galli, F ; Castiglioni, C

OBJECTIVEDuring growth and differentiation of skeletal muscle, cell types other than canonical myoblasts can be recruited to a myogenic fate. Among these, TNAP+ pericytes can differentiate into skeletal or smooth muscle cells during postnatal growth and contribute to muscle regeneration. However, their role in muscle development has not been investigated. This study aims to characterise pericyte fate choices during embryonic and foetal myogenesis, occurring in the second half of gestation.APPROACH AND RESULTSUsing Cre-loxP lineage tracing with multiple reporters including the multifluorescent Confetti, we labelled TNAP+ precursors in vivo and assessed the smooth or skeletal muscle differentiation in their lineage at a perinatal stage. We found that TNAP+ cells contribute in vivo to skeletal and smooth muscle cells, as well as other pericytes, also during pre-natal muscle development. The resulting clones showed that such fate choices are likely to depend on distinct unipotent progenitors rather than multipotent progenitors. In addition, we isolated and differentiated in vitro foetal cells derived from TNAP+ precursors, which showed that they are not spontaneously myogenic unless co-cultured with other skeletal muscle cells.CONCLUSIONSThis work extends our understanding of the differentiative potency of these non- canonical skeletal muscle progenitors during prenatal life, with a view to a future application of this knowledge to optimise cell therapies for muscle wasting disorders.

2025-05-01·Acta Obstetricia et Gynecologica Scandinavica

Sequential prenatal diagnosis of fetal skeletal dysplasia: A cohort study

Article

作者: Wang, Jing ; Yu, Bin ; Jiang, Mengting ; Zhang, Bin ; Qiao, Wei ; Mao, Xiuzhen

AbstractIntroductionGenetic factors are considered to be the main factors leading to fetal skeletal dysplasia (SD), and chromosomal microarray analysis (CMA) has been used clinically for the detection of SD fetuses. At present, whole exome sequencing (WES) has been applied in SD fetuses, but there is still a lack of data accumulation. The aim of this study is to perform sequential prenatal diagnosis for fetuses with SD indicated by ultrasound and to explore the clinical value of CMA followed by WES.Material and MethodsFrom January 2019 to May 2024, 147 fetuses with SD were detected by prenatal ultrasound screening. After the collection of amniotic fluid or abortive tissue, CMA was performed first, then WES was performed in the cases with a negative CMA result.Results147 cases accepted the prenatal CMA test, and 23 cases were reported to have chromosomal abnormalities, including 9 cases of chromosomal aneuploidies, 11 cases of pathogenic copy number variants, and 3 cases of likely pathogenic copy number variants. The detection rate of chromosomal abnormalities by the prenatal CMA test was 15.6% (23/147). 58 cases with negative results of CMA underwent WES, and 21 genes with pathogenic/likely pathogenic variants were detected in 21 cases, including FGFR3, COL2A1, COL1A1, COL1A2, RUNX2, LMX1B, GLI3, SHOX, ALPL, and DYNC2H1. The rate of abnormal prenatal WES was 36.2% (21/58). In the subgroup analysis of the SD phenotype, the detection rate of chromosomal abnormalities in isolated SD fetuses was 7.7% (7/91), which was significantly lower than that in SD fetuses combined with other system abnormalities (28.6%, 16/56) (p = 0.001). The detection rate of monogenic abnormalities in short long bones with other skeletal abnormalities was 62.5% (10/16), which was higher than that in short long bones with non‐skeletal abnormalities 10.5% (2/19), and the difference was statistically significant (p = 0.003).ConclusionsSD is mostly caused by monogenic abnormalities, and prenatal WES has significantly improved the detection rate of SD fetuses. The prenatal WES can be used as an important molecular genetic testing method combined with CMA in the sequential prenatal diagnosis of SD fetuses.

项与 TNSALP 相关的新闻（医药）

2025-03-11

·派真生物PackGene

客户文献解读 | 新研究揭示糖尿病性骨质疏松症的潜在治疗靶点

2型糖尿病（T2DM）是一种全球范围内高发的代谢性疾病，其患者常伴随骨质疏松（diabetic osteoporosis），表现为骨量减少、骨微结构破坏以及骨折风险增加。这种骨质疏松的主要原因是成骨细胞功能受损。然而，T2DM导致成骨细胞功能障碍的分子机制尚未完全阐明，这阻碍了有效治疗策略的开发。图片来源：https://news.qq.com/rain/a/20211104A0AEO200 近日，南京大学鼓楼医院骨科蒋青/郭保生团队在《Bone Research》（IF=14.3）杂志发表了题为“Enhanced SIRT3 expression restores mitochondrial quality control mechanism to reverse osteogenic impairment in type 2 diabetes mellitus”的研究论文，系统地阐明了SIRT3通过调节线粒体质量控制逆转2型糖尿病骨质疏松的机制，并探索了基于此机制的新型治疗策略。一、研究背景 2型糖尿病（T2DM）患者常伴有骨质疏松，表现为骨微结构破坏和骨形成受损。近年来的研究发现线粒体功能障碍与糖尿病及其并发症（如骨质疏松）的发展密切相关。线粒体自噬（Mitophagy）是细胞内选择性清除损伤或衰老线粒体的自噬过程，以维持线粒体稳态并防止细胞受到损害。当线粒体受到应激（如氧化应激、膜电位丧失或蛋白损伤）时，细胞会激活线粒体自噬，将受损的线粒体包裹进自噬小体（autophagosome），再运送至溶酶体（lysosome）进行降解，从而防止有害的活性氧（ROS）积累和线粒体功能异常。 PINK1（PTEN-induced kinase 1）/PRKN（E3 ubiquitin-protein ligase parkin，泛素连接酶）通路是经典的线粒体自噬调控通路，主要负责识别并标记受损线粒体，促进其降解。当线粒体受损时，PINK1在线粒体外膜上积累，随后招募并激活PRKN，从而启动线粒体自噬。 SIRT3是一种主要的线粒体去乙酰化酶，它影响能量代谢、抗氧化防御和线粒体动态变化。既往研究表明，SIRT3通过调节FOXO3的去乙酰化影响线粒体自噬，并在多种疾病中发挥重要作用。二、研究亮点首次揭示了SIRT3在T2DM相关骨质疏松中的关键作用，阐明了其通过FOXO3/PINK1/PRKN轴调控线粒体自噬的分子机制，为理解T2DM导致的成骨细胞功能障碍提供了新视角。三、主要研究结果 1. T2DM环境下成骨细胞功能障碍与线粒体自噬抑制：在通过高脂饮食（HFD）联合链脲佐菌素（STZ）诱导T2DM小鼠模型中，观察到显著的骨量减少和骨微结构破坏（BV/TV、Tb.N下降，Tb.Sp增加）。在T2DM小鼠和HGPA处理的成骨细胞中，成骨标志物（如RUNX2、COL1A1）表达显著下调，矿化能力降低。透射电镜（TEM）显示T2DM小鼠成骨细胞中线粒体结构异常，伴随膜电位下降和活性氧（ROS）积累。进一步研究发现，PINK1/PRKN介导的线粒体自噬显著受抑。 2. SIRT3激活改善骨质疏松：在体外实验中，使用SIRT3激动剂Honokiol（HKL）或SIRT3过表达（Lv-Sirt3）可显著恢复HGPA诱导的线粒体自噬抑制，改善成骨细胞分化和矿化能力。MitoTracker染色显示线粒体碎片化减少，PINK1、PRKN和LC3表达显著上调（文章图5）。文章图5 激活SIRT3可促进线粒体自噬，并改善MC3T3-E1细胞的成骨细胞功能障碍。a. 转染Lv-Ctrl和Lv-Sirt3的MC3T3-E1细胞中SIRT3的相对蛋白和mRNA表达水平。b, c. Lv-Ctrl、Lv-Sirt3、HGPA+Lv-Ctrl和HGPA+Lv-Sirt3组的线粒体代表性图像及定量分析。d. MitoTracker标记的线粒体（深红色）、Mtphagy Dye标记的线粒体自噬（红色）和Lyso Dye标记的溶酶体（绿色）的代表性图像，其中共定位表明线粒体自噬的发生。e. HGPA+Lv-Ctrl和HGPA+Lv-Sirt3组的MC3T3-E1细胞经CCCP刺激6小时后，TOM20（红色）、PRKN（绿色）和MitoTracker（深红色）的代表性免疫荧光染色图像。f, g. 上述各组中线粒体自噬相关蛋白（包括PINK1、PRKN、LC3和SQSTM1）的Western blot图像及定量分析。h. 3次独立重复实验中Alpl、Runx2、Col1a1和Ibsp基因的qPCR分析。i. 上述四组MC3T3-E1细胞的ALP（7天）和ARS（21天）染色的代表性图像及定量分析。j, k. MC3T3-E1细胞中RUNX2、ALP和COL1A1的Western blot结果及定量分析。l, n. 经HGPA、HGPA+HKL和HGPA+mdivi-1处理的MC3T3-E1细胞的ALP染色代表性图像及定量分析。o, m. 不同干预下MC3T3-E1细胞中RUNX2和ALP的Western blot分析。在体内实验中，通过AAV介导的SIRT3过表达可显著改善T2DM小鼠的骨量和骨微结构，恢复成骨细胞功能（文章图7）。双标记实验显示骨形成速率（MAR）显著提高。文章图7 Sirt3过表达可拯救HFD&STZ诱导的线粒体自噬缺陷。a. T2DM模型构建示意图。b. 对正常饮食（CTRL）和Sirt3过表达（Sirt3OE）组小鼠的骨切片进行SIRT3免疫组化染色。c. 骨切片的免疫荧光图。d. 对上述各组小鼠的原代成骨细胞进行MitoTracker Green染色，观察线粒体的代表性图像及定量分析。e. 来自CTRL、Sirt3OE、HFD&STZ和HFD&STZ+Sirt3OE小鼠的原代成骨细胞中PINK1和PRKN与线粒体的共定位免疫荧光图。f. 骨组织中PINK1和PRKN的免疫荧光图。g, h. 对各组小鼠骨组织中线粒体自噬标志物的Western blot图像及定量分析。 3. SIRT3通过FOXO3调控线粒体自噬：SIRT3通过去乙酰化FOXO3促进其核转位，增强其对Prkn基因启动子的结合能力，从而上调PRKN表达，恢复线粒体自噬。四、研究结论 SIRT3在T2DM相关骨质疏松症中起关键调节作用，其通过去乙酰化FOXO3恢复PINK1/PRKN介导的线粒体自噬，从而改善成骨细胞功能和骨质疏松症状。 SIRT3/FOXO3轴是调节成骨细胞线粒体稳态的重要机制，可能成为治疗糖尿病性骨质疏松症的潜在靶点。本研究用到的病毒载体如下：派真生物有幸为以上研究提供慢病毒包装服务。点击文末“阅读原文/Read more”，即可查阅原文，了解更多实验细节与数据支持。参考文献 Xian Y, Liu B, Shen T, et al. Enhanced SIRT3 expression restores mitochondrial quality control mechanism to reverse osteogenic impairment in type 2 diabetes mellitus. Bone Research. 2025;13:30. DOI: 10.1038/s41413-024-00399-5 关于派真生物

蛋白降解靶向嵌合体

2025-01-08

·PRNewswire

1cBio and Alesta Therapeutics Announce Exclusive Global Licensing Agreement for a Novel Potentially First-in-Class Small Molecule for Hypophosphatasia

SAN FRANCISCO and LEIDEN, Netherlands, Jan. 8, 2025 /PRNewswire/ -- 1cBio, Inc. ("1cBio") an emerging biotech company developing precision medicines for significant unmet needs, and Alesta Pharmaceuticals ("Alesta") a leader in developing first-in-class small molecules for rare diseases, announced an exclusive worldwide licensing agreement. Under this agreement, Alesta will develop, commercialize, and manufacture OC-1(also known as ALE1), an orally active therapeutic candidate for hypophosphatasia (HPP). HPP is a rare genetic disorder caused by mutations in the ALPL gene, leading to defective bone and tooth mineralization. This results in skeletal abnormalities, fragile bones, early tooth loss, and, in older patients, significant muscle weakness, fatigue, and pain. Affecting tens of thousands of patients worldwide, HPP is believed to be underdiagnosed, particularly in older populations. OC-1 is a novel oral therapeutic that inhibits a novel target to reduce levels of inorganic pyrophosphate (PPi), a key metabolite driving disease pathology. Currently progressing through GLP toxicology studies, OC-1 is expected to enter clinical trials in the second half of 2025. OC-1 was developed by combining 1cBio's expertise in medicinal chemistry and translational sciences with thought partners in clinical and basic sciences to guide its innovation. "We are excited to partner with Alesta Therapeutics, who is pioneering the development of transformative medicines for rare disease and can help us to reach HPP patients more rapidly," said Andrew Wong, Chief Executive Officer at 1cBio. "OC-1 is another example of the 1cBio team's capabilities to identify white spaces in disease treatments and develop highly differentiated molecules for precision medicine. We look forward to collaborating with Alesta's innovative development team to efficiently progress a potentially first-in-class, oral therapy for HPP patients." "With the support of 1cBio, the expertise and commitment of our team, and collaborations with leading academics and disease advocacy groups, we are poised to make significant strides in addressing the unmet needs of HPP patients," said Ilan Ganot, Chief Executive Officer of Alesta Therapeutics. "We look forward to advancing OC-1 toward clinical proof of concept and bringing us closer to delivering this transformative therapy to address the entire spectrum of HPP in this underserved disease." Under the terms of the agreement, Alesta will assume responsibility for Phase I preparation activities, including submission of the Clinical Trial Application (CTA) and Investigational New Drug (IND) application, and all subsequent clinical-development activities and global commercialization activities. 1cBio is eligible to receive potential development, regulatory and commercial milestone payments, including an equity investment, and tiered royalties on global sales, contingent upon successful development and commercialization. About 1cBio 1cBio is an emerging biotechnology company which strives to identify white spaces in cancer therapies and develop molecules that can serve as precision medicines. The company's programs are geared to treat the disease and preemptively counter mechanisms for acquired or intrinsic resistance. Core expertise in medicinal chemistry and translational sciences along with thought partners in clinical and basic sciences guides 1cBio's innovation. 1cBio's second lead program is OC-3, a selective-PARP1 inhibitor with the potential to be best-in-class for HR-deficient and HR-proficient tumors when combined with approved targeted therapies. For more information, visit . About Alesta Therapeutics Alesta Therapeutics is a Netherlands-based biotechnology company committed to developing novel oral small molecule therapies for underserved rare diseases. The company's lead asset, ALE1, is being developed for hypophosphatasia (HPP), a rare genetic disorder with significant unmet needs. Alesta is also advancing ALE2, a promising candidate to treat Charcot-Marie-Tooth (CMT) disease. In January 2025 Alesta announced a €65 million Series A financing supported by leading biotech and life science investors. For more information, visit . SOURCE 1cBio WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

引进/卖出临床1期

2024-10-22

·药明康德

潜在“first-in-class”B细胞疗法进入临床开发，有望变革血友病治疗

▎药明康德内容团队编辑今日，致力于开发B细胞疗法的Be Biopharma宣布达到多个关键里程碑。用于治疗血友病B的主打项目BE-101进入临床开发阶段；同时该公司宣布选定第二个候选药物，用于治疗低磷酸酶症（HPP）。这两个项目均基于Be Biopharma公司强大且高效的B细胞药物（BCM）平台，该平台利用基因编辑技术改造B细胞，使其能够持续产生治疗性蛋白质，最终开发出具有持久性、可滴定且可重复给药的候选药物，无需预处理，具有成为潜在“best-in-class”基因疗法的潜力。该公司最近达到的里程碑包括： 2024年5月，Be Biopharma宣布其潜在“first-in-class”B细胞疗法BE-101的IND申请获得FDA的许可。BE-101的设计目的是无需预处理，即可让B细胞持续产生恒定水平的凝血因子IX，具有持久性、可重复给药性及可滴定性。首个人体临床试验BeCoMe-9已开始招募患者，这是一项多中心的人体剂量递增研究，旨在评估BE-101在中度至重度血友病B成人患者中的安全性和初步疗效。FDA最近已授予BE-101快速通道资格。该公司宣布BE-102已被选为治疗HPP的候选药物，HPP是一种严重的遗传疾病，具有极高的未满足医疗需求。它的特征是由于ALPL基因的功能缺失突变，导致碱性磷酸酶（ALP）活性不足，从而引起骨骼和牙齿的发育不良和脆弱。现有的获批疗法需要每周多次注射，且仅限于儿科发病的形式。此前展示的数据表明，BE-102有潜力在体内生成活性ALP并且持续维持ALP水平。该公司还宣布已完成8200万美元的融资，得到了多家风险投资公司和医药公司的支持，包括ARCH Venture Partners、Atlas Venture、RA Capital Management、Alta Partners、Longwood Fund、百时美施贵宝和武田创投。获得资金将用于实现BE-101的临床概念验证，并推进BE-102的开发。 ▲欲了解更多前沿技术在生物医药产业中的应用，请长按扫描上方二维码，即可访问“药明直播间”，观看相关话题的直播讨论与精彩回放参考资料： [1] Be Bio Announces $82 Million Financing and Transition to Clinical Stage Company. Retrieved October 22, 2024, from https://www.businesswire.com/news/home/20241022283327/en 免责声明：药明康德内容团队专注介绍全球生物医药健康研究进展。本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。版权说明：本文来自药明康德内容团队，欢迎个人转发至朋友圈，谢绝媒体或机构未经授权以任何形式转载至其他平台。转载授权请在「药明康德」微信公众号回复“转载”，获取转载须知。分享，点赞，在看，聚焦全球生物医药健康创新

细胞疗法快速通道临床申请临床1期