更新于：2024-11-01

RAD51

更新于：2024-11-01

基本信息

别名

BRCA1/BRCA2-containing complex, subunit 5、BRCC5、DNA repair protein RAD51 homolog 1

+ [12]

简介

Plays an important role in homologous strand exchange, a key step in DNA repair through homologous recombination (HR) (PubMed:18417535, PubMed:20348101, PubMed:12205100, PubMed:20231364, PubMed:23754376, PubMed:23509288, PubMed:28575658, PubMed:26681308). Binds to single-stranded DNA in an ATP-dependent manner to form nucleoprotein filaments which are essential for the homology search and strand exchange (PubMed:18417535, PubMed:20348101, PubMed:12205100, PubMed:20231364, PubMed:23754376, PubMed:23509288, PubMed:28575658, PubMed:26681308). Catalyzes the recognition of homology and strand exchange between homologous DNA partners to form a joint molecule between a processed DNA break and the repair template (PubMed:18417535, PubMed:20348101, PubMed:12205100, PubMed:20231364, PubMed:23754376, PubMed:23509288, PubMed:28575658, PubMed:26681308). Recruited to resolve stalled replication forks during replication stress (PubMed:27797818, PubMed:31844045). Part of a PALB2-scaffolded HR complex containing BRCA2 and RAD51C and which is thought to play a role in DNA repair by HR (PubMed:24141787, PubMed:12442171). Plays a role in regulating mitochondrial DNA copy number under conditions of oxidative stress in the presence of RAD51C and XRCC3 (PubMed:20413593). Also involved in interstrand cross-link repair (PubMed:26253028).

关联

项与 RAD51 相关的药物

Deoxymab

靶点

RAD51

作用机制

RAD51抑制剂

在研机构

Patrys Ltd. [+2]

原研机构

Yale University

在研适应症

胰腺癌 [+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

STX-100 (SyntheX)

靶点

RAD51

作用机制

RAD51抑制剂

在研机构

SyntheX, Inc.初创企业

原研机构

SyntheX, Inc.初创企业

在研适应症

肿瘤

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

CAM833

靶点

BRCA2 x RAD51

作用机制

BRCA2 inhibitors [+1]

在研机构

University of Cambridge

原研机构

University of Cambridge

在研适应症

肿瘤

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

项与 RAD51 相关的临床试验

NCT03997968 / Active, not recruiting临床1/2期

A Multi-Center, Open Label Phase 1/2 Study of CYT-0851 in Patients With Relapsed/Refractory B-Cell Malignancies and Advanced Solid Tumors

This clinical trial is an interventional, active-treatment, open-label, multi-center, Phase 1/2 study. The study objectives are to assess the safety, tolerability and pharmacokinetics (PK) of CYT-0851 in patients with relapsed/refractory B-cell malignancies and advanced solid tumors and to identify a recommended Phase 2 dose as a monotherapy and in combination with chemotherapy for evaluation in these patients.

开始日期2019-10-09

申办/合作机构

Cyteir Therapeutics, Inc.

100 项与 RAD51 相关的临床结果

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100 项与 RAD51 相关的转化医学

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0 项与 RAD51 相关的专利（医药）

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12,526

项与 RAD51 相关的文献（医药）

2025-01-01·Gene

Identification and expression analysis of dmc1 in Chinese soft-shell turtle (Pelodiscus sinensis) during gametogenesis

Article

作者: Zeng, Linhui ; Chen, Kaili ; Zhan, Zeyu ; Tan, Zhimin ; Tian, Jiamin ; Xu, Hongyan ; Xu, Jianfei ; Ban, Wenzhuo

DNA meiotic recombinase 1 (disrupted meiotic cDNA, Dmc1) protein is homologous to the Escherichia coli RecA protein, was first identified in Saccharomyces cerevisiae. This gene has been well studied as an essential role in meiosis in many species. However, studies on the dmc1 gene in reptiles are limited. In this study, a cDNA fragment of 1,111 bp was obtained from the gonadal tissues of the Chinese soft-shell turtle via RT-PCR, containing a 60 bp 3' UTR, a 22 bp 5' UTR, and an ORF of 1,029 bp encoding 342 amino acids, named Psdmc1. Multiple sequence alignments showed that the deduced protein has high similarity (>95 %) to tetrapod Dmc1 proteins, while being slightly lower (86-88 %) to fish species.Phylogenetic tree analysis showed that PsDmc1 was clustered with the other turtles' Dmc1 and close to the reptiles', but far away from the teleost's. RT-PCR and RT-qPCR analyses showed that the Psdmc1 gene was specifically expressed in the gonads, and much higher in testis than the ovary, especially highest in one year-old testis. In situ hybridization results showed that the Psdmc1 was mainly expressed in the perinuclear cytoplasm of primary and secondary spermatocytes, weakly in spermatogonia of the testes. These results indicated that dmc1 would be majorly involved in the developing testis, and play an essential role in the germ cells' meiosis. The findings of this study will provide a basis for further investigations on the mechanisms behind the germ cells' development and differentiation in Chinese soft-shell turtles, even in the reptiles.

2024-12-31·Epigenetics

GGNBP2 regulates histone ubiquitination and methylation in spermatogenesis

Article

作者: Liu, Lingyun ; Guo, Kaimin ; Cao, Yin ; Zhao, Zhiyi ; Zhao, Jiantao ; Wang, Hongliang

Gametogenetin binding protein 2 (GGNBP2) was indispensable in normal spermatids for transformation into mature spermatozoa in mice, and when Gametogenetin binding protein 2 is bound to BRCC36 and RAD51, the complex participates in repairing DNA double-strand breaks (DSB) during the meiotic progression of spermatocytes. Ggnbp2 knockout resulted in the up-regulation of H2A_K119ubi and down-regulation of H2B_K120ubi in GC-2 cells (mouse spermatogonia-derived cell line) and postnatal day 18 testis lysate. Our results also demonstrated that Gametogenetin binding protein 2 inducedASXL1 to activate the deubiquitinating enzyme BAP1 in deubiquitinating H2A, while Gametogenetin binding protein 2 knockout disrupted the interaction between ASXL1 and BAP1, resulting in BAP1 localization change. Furthermore, the Gametogenetin binding protein 2 deletion reduced H2B ubiquitination by affecting E2 enzymes and E3 ligase binding. Gametogenetin binding protein 2 regulated H2A and H2B ubiquitination levels and controlled H3_K27 and H3_K79 methylation by PRC2 subunits and histone H3K79 methyltransferase. Altogether, our results suggest that Ggnbp2 knockout increased DNA damage response by promoting H2A ubiquitination and H3_K27trimethylation (H3_K27me3) and reduced nucleosome stability by decreasing H2B ubiquitination and H3K79 dimethylation (H3_K79me2), revealing new mechanisms of epigenetic phenomenon during spermatogenesis. Gametogenetin binding protein 2 seems critical in regulating histone modification and chromatin structure in spermatogenesis.

2024-12-01·Molecular Biology Reports

FANCD2 counteracts O6-methylguanine-induced mismatch repair-dependent apoptosis

Article

作者: Fujikane, Ryosuke ; Hidaka, Masumi ; Uechi, Yuka ; Morita, Sho ; Matsuura, Takashi

BACKGROUNDSn1-type alkylating agents methylate the oxygen atom on guanine bases thereby producing O⁶-methylguanine. This modified base could pair with thymine and cytosine, resulting in the formation of O⁶-methylguanine/thymine mismatch during DNA replication, recognized by the mismatch repair (MMR) complex, which then initiates the DNA damage response and subsequent apoptotic processes. In our investigation of the molecular mechanisms underlying MMR-dependent apoptosis, we observed FANCD2 modification upon the activity of alkylating agent N-methyl-N-nitrosourea (MNU). This observation led us to hypothesize a relevant role for FANCD2 in the apoptosis induction process.METHODS AND RESULTSWe generated FANCD2 knockout cells using the CRISPR/Cas9 method in the human cervical cancer cell line HeLa MR. FANCD2-deficient cells exhibited MNU hypersensitivity. Upon MNU exposure, FANCD2 colocalized with the MMR complex. MNU-treated FANCD2 knockout cells displayed severe S phase delay followed by increased G2/M arrest and MMR-dependent apoptotic cell death. Moreover, FANCD2 knockout cells exhibited impaired CtIP and RAD51 recruitment to the damaged chromatin and DNA double-strand break accumulation, indicated by simultaneously observed increased γH2AX signal and 53BP1 foci.CONCLUSIONSOur data suggest that FANCD2 is crucial for recruiting homologous recombination factors to the sites of the MMR-dependent replication stress to resolve the arrested replication fork and counteract O⁶-methylguanine-triggered MMR-dependent apoptosis.

项与 RAD51 相关的新闻（医药）

2024-10-30

·CPHI制药在线

晶锐医药可入脑的BET抑制剂获批临床，拥挤赛道是否还有突围机会

关注并星标CPHI制药在线近日，中国国家药监局药品审评中心（CDE）官网公示，晶锐医药1类新药JRD-018片获批临床，拟开发治疗晚期恶性肿瘤。 JRD-018是一款可入脑的BET抑制剂，今年4月已经获美国FDA批准开展1期临床研究。晶锐医药拟开启1期临床试验并将针对晚期实体瘤患者进行招募，继而扩展到血液瘤、脑转移或原发性脑瘤，旨在探索JRD-018在患者中的安全性、耐受性、药代动力学以及初步抗肿瘤活性。体内药效研究结果表明，JRD-018单独使用在脑胶质瘤模型、小细胞肺癌模型、非小细胞肺癌模型、髓性单核细胞白血病模型以及乳腺癌模型中均表现出良好的抗肿瘤活性。在临床前动物模型研究中，JRD-018已显示出良好的对脑转移或原发性脑瘤、恶性脑肿瘤的抑制效果。表观遗传学靶点之BET 溴结构域和超末端结构域（bromodomain and extra terminal domain，BET）属于溴结构域蛋白家族，BET蛋白家族包含四个异构体BRD2、BRD3、BRD4、BRDT，它们的结构相似，在N端有2个串联的溴结构域（BD1和BD2）以及一个超末端结构域（ET）。BD1和BD2识别并结合乙酰化赖氨酸残基，与染色质重塑和基因转录的调控过程相关；ET结构域与多种转录因子相互作用。BET蛋白家族通过溴结构域与乙酰化的染色质结合，从而实现在表观遗传学水平上对基因表达进行调控。 BET蛋白家族在人体内表达广泛，与多种实体瘤和恶性血液性肿瘤、炎症、肥胖、肺纤维化等多种疾病的发生和发展密切相关。如原癌基因Myc在超过一半的肿瘤中过表达，BET抑制剂通过竞争性结合阻止BRD4与染色质结合，进而抑制Myc的转录，从而实现抑制肿瘤的目的。 BET抑制剂是一类新型抗癌药，这类药物在治疗血液癌症如白血病和淋巴瘤方面具有良好的前景。BET抑制剂能够通过阻断BET蛋白的功能从而抑制肿瘤生长。研发BET蛋白选择性抑制剂是目前的新方向。目前，一系列BET抑制剂正在临床试验中检验它们治疗包括白血病、淋巴瘤、脑瘤和骨髓瘤在内的多种癌症的疗效。 BET抑制剂：诺华高调购入，加思科、正大天晴加速推进 BET被认为是抗肿瘤药物研发潜力靶点。目前，全球药企针对该靶点已开发出多款药物，详见下表。在研BET抑制剂大多为小分子化学药，此外还包括蛋白水解靶向嵌合体（PROTACs）。适应症上，BET抑制剂主要被开发用于实体瘤和血液性肿瘤，其中部分还被开发用于治疗炎症性疾病如白癜风等。全球至今还尚无BET抑制剂获批，进度最快的就是MorphoSys的Pelabresib，是首个三期临床试验取得成功的BET抑制剂。MorphoSys围绕该药物布局了骨髓纤维化、恶性外周神经鞘瘤、多发性骨髓瘤等多项适应症。 Pelabrisib是由MorphoSys AG公司研制的first-in-class BET抑制剂，近期Pelabrisib治疗骨髓纤维化III期达到了主要研究终点SVR35（脾脏缩小超过35%），从214例患者的临床数据来看， Pelabrisib与JAK抑制剂芦可替尼联用24周，有65.9%的患者脾脏缩小超过35%，而对照组（芦可替尼与安慰剂）仅有35.2%的患者达到SVR35，实验组的疗效比对照组高30.4%。今年年初，诺华以29亿美元收购MorphoSys AG从而拥有了pelabresib这款BET抑制剂。诺华将基于III期MANIFEST-2研究的积极数据在今年下半年向FDA和EMA提交pelabresib联合芦可替尼治疗骨髓纤维化的上市申请。 ZEN-3694是一种领先的差异化BET抑制剂，被开发联合免疫检查点抑制剂、PARP抑制剂、MEK抑制剂、CDK4/6抑制剂、HDAC抑制剂治疗多种肿瘤。ZEN-3694可以降低BRCA1/2和RAD51等蛋白的DNA修复活性，以提高肿瘤细胞对PARP抑制的敏感性，当前用以治疗转移性去势抵抗性前列腺癌II期临床正在开展中。2019年8月，Zenith Epigenetics 与恒翼生物就该药签订超7800万美元的许可协议，授权恒翼生物获得ZEN-3694在中国（包括中国香港、中国台湾和中国澳门地区）的权益。 JAB-8263是加科思自主研发、具有全球知识产权的小分子BET抑制剂，临床前研究显示其对多种实体瘤和血液瘤均能发挥抗肿瘤作用。从公开数据来看，JAB-8263是同类临床项目中活性最强的BET抑制剂，有望在极低剂量下有效抑制多种肿瘤生长，和Pelabrisib相比具有巨大的差异化优势。目前，加科思正在中美两地开展JAB-8263的多中心、开放性I/IIa期临床研究，适应症涉及白血病及实体瘤。 TQB3617是正大天晴自主研发的一款具有全新化学结构的BET抑制剂，能够通过抑制BET蛋白功能减少c-Myc、NF-κB、Aurora B和BCL-2等致癌基因的异常表达，进而发挥抗肿瘤作用。临床前研究结果显示，TQB3617对BET家族的BRD2、BRD3、BRD4、BRDT蛋白均具有较强的抑制活性。TQB3617用于晚期恶性肿瘤的I期临床试验显示，2例骨髓纤维化患者在治疗第12周结束时，脾脏体积较基线分别缩小13%和30%，展现出潜在的抗骨髓纤维化疗效。在28例接受疗效评估的淋巴瘤中，总缓解率（ORR）为39.3%（11/28），其中4例CR，7例PR。 Trotabresib（CC-90010）是一种新型、口服、可逆性、小分子BET抑制剂，可穿透高级别胶质瘤患者的脑肿瘤组织，临床前研究显示其可增强替莫唑胺（TMZ）的抗肿瘤作用。已公布的1b/2期开放标签、剂量探索研究结果显示：在长期随访中，新诊断胶质母细胞瘤（GBM）患者接受Trotabresib+TMZ辅助治疗或Trotabresib+TMZ+RT（放疗）同步治疗耐受性良好，未出现新的不良反应。结语整体来看，BET是进展相对较慢的一个表观遗传学药物靶点。BET蛋白家族在人体内表达广泛，与多种实体瘤和恶性血液性肿瘤、炎症、肥胖、肺纤维化等多种疾病的发生和发展密切相关，是非常有潜力的药物靶点，全球首个BET抑制剂pelabresib III期临床试验的成功宣告了该靶点的成效性，目前全球围绕BET靶点研发火热，值得一提的是，随着科学技术的发展，BET抑制剂的研发不再局限于小分子化药，已有多家企业、机构研发出BET靶向PROTACs。目前国内药企也积极布局BET靶点，而布局方式除了自主研发，还从外部企业引进，如恒翼生物。期待在药企的不懈努力下，BET靶点可以早日迎来重大突破。参考来源 1.Raajit Rampal, Sebastian Grosicki, Dominik Chraniuk et al.Updated safety and efficacy data from the phase 3 MANIFEST-2 study of pelabresib in combination with ruxolitinib for JAK inhibitor treatment-na?ve patients with myelofibrosis.?JCO?42,?6502-6502(2024).DOI:10.1200/JCO.2024.42.16_suppl.6502 2.2024 ASCO. Abstract?#6502: Updated safety and efficacy data from the phase 3 MANIFEST-2 study of pelabresib in combination with ruxolitinib for JAK inhibitor treatment-na?ve patients with myelofibrosis. END 来源：CPHI制药在线声明：本文仅代表作者观点，并不代表制药在线立场。本网站内容仅出于传递更多信息之目的。如需转载，请务必注明文章来源和作者。投稿邮箱：Kelly.Xiao@imsinoexpo.com ▼更多制药资讯，请关注CPHI制药在线▼ 点击阅读原文，进入智药研习社~

临床1期临床3期蛋白降解靶向嵌合体临床2期临床结果

2024-10-17

·生物探索

Nature | BRCA1-BARD1蛋白复合体在DNA双链断裂修复中的关键作用

引言 DNA双链断裂（DSB）是细胞分裂过程中最严重的DNA损伤类型之一，如果不及时修复，会导致基因突变和癌症。同源重组（HR）是DSB修复的主要途径之一，HR依赖于同源染色体之间的序列匹配，以修复DSB【1】。HR的启动需要先对DSB末端进行DNA端重组，生成单链DNA模板，以便RAD51重组酶等蛋白组装并执行修复。BRCA1-BARD1复合体是重要的肿瘤抑制因子，在HR中发挥关键作用【2】。它参与多个HR阶段，包括DNA端重组，并已被证明与RAD51重组酶相互作用并增强其活性【3】。尽管BRCA1-BARD1在HR中至关重要，但其直接调节DNA端重组活性的机制尚不清楚。近日，来自美国德克萨斯大学健康科学中心的Patrick Sung，Sandeep Burma研究团队和哥伦比亚大学的Eric C. Greene研究团队合作在Nature杂志上发表题为Promotion of DNA end resection by BRCA1-BARD1 in homologous recombination的研究论文，该研究发现BRCA1-BARD1通过增强关键重组酶的活性，以及与DNA端重组机器的协同作用，在DSB修复中发挥至关重要的作用。首先研究人员利用体外酶促反应，将纯化的BRCA1-BARD1、BLM和DNA2与32P标记的DNA底物混合，并观察DNA解旋和DNA端重组的效率。结果发现BRCA1-BARD1显著增强BLM的解旋酶活性和DNA2的DNA端切割酶活性，并提高BLM-DNA2复合物的进程性和效率。接着通过亲和层析实验，研究人员验证BRCA1-BARD1与BLM和DNA2的相互作用。研究结果表明，BRCA1-BARD1与BLM和DNA2直接相互作用，这导致BLM-DNA2途径的DNA解旋和DNA端重组效率显著提高。BRCA1-BARD1的加入还促进了BLM-DNA2复合物的组装进程和效率，使其在DNA端重组过程中发挥更积极的作用。与BRCA1-BARD1增强BLM-DNA2途径的实验类似，研究人员使用纯化的BRCA1-BARD1、WRN和DNA2与32P标记的DNA底物混合，并观察DNA解旋和DNA端重组的效率。通过亲和层析实验，验证BRCA1-BARD1与WRN的相互作用。结果发现BRCA1-BARD1显著增强WRN的解旋酶活性，并提高WRN-DNA2复合物的进程性和效率。与BLM-DNA2途径类似，BRCA1-BARD1的加入并没有改变WRN-DNA2复合物的组成，而是通过增强其活性来提高端重组的效率。研究还发现，BRCA1-BARD1与EXO1直接相互作用，并显著增强EXO1的5’→3’外切酶活性。这意味着BRCA1-BARD1不仅作用于解旋酶和DNA切割酶，也作用于外切酶，进一步增强了DNA端重组的整体效率。机制解析发现BRCA1-BARD1通过与EXO1的特定结构域相互作用，提供辅助作用，促进DNA端的切割，并提高EXO1在DNA端重组过程中的稳定性和效率。例如，BRCA1-BARD1可能通过稳定EXO1的结构，或通过改变其活性位点的电荷状态，来增强其切割能力。最后，研究发现，BRCA1和BLM1都含有独立的DNA结合模块，它们协同作用以增强DNA端重组的效率。此外，BARD1的DNA结合域对于BRCA1-BARD1促进DNA端重组的能力至关重要。这表明BRCA1-BARD1通过与DNA端的结合，更有效地引导和协调重组酶的活性。同期在Nature杂志上，来自瑞士提契诺大学（USI）生物医学院的Petr Cejka研究团队发表题为Mechanism of BRCA1-BARD1 function in DNA end resection and DNA protection的研究论文，该研究也发现了BRCA1-BARD1在DNA端重组中的重要作用，并阐明了其保护DNA的功能。总之，这两项工作都深入探讨了BRCA1-BARD1在DNA双链断裂修复中的关键作用，特别是它在同源重组过程中的DNA端重组阶段。这些研究不仅加深了我们对BRCA1-BARD1功能和癌症发生的理解，还可能为开发针对BRCA1-BARD1缺陷的癌症治疗方法提供新思路。参考文献 1. Tarsounas, M. & Sung, P. The antitumorigenic roles of BRCA1-BARD1 in DNA repair and replication. Nat. Rev. Mol. Cell Biol. 21, 284-299 (2020). 2. Prakash, R., Zhang, Y., Feng, W. & Jasin, M. Homologous recombination and human health: the roles of BRCA1, BRCA2, and associated proteins. Cold Spring Harb. Perspect. Biol. 7, a016600 (2015). 3. Zhao, W. et al. BRCA1-BARD1 promotes RAD51-mediated homologous DNA pairing. Nature 550, 360-365 (2017). https://doi.org/10.1038/s41586-024-07910-2 https://doi.org/10.1038/s41586-024-07909-9 责编|探索君排版|探索君文章来源|“BioArt” End 往期精选围观一文读透细胞死亡(Cell Death) | 24年Cell重磅综述（长文收藏版）热文 Cell | 是什么决定了细胞的大小？热文 Nature | 2024年值得关注的七项技术热文 Nature | 自身免疫性疾病能被治愈吗？科学家们终于看到了希望热文 CRISPR技术进化史 | 24年Cell综述

临床结果

2024-10-14

·PRNewswire

US FDA issues Study May Proceed letter for the Pilot Study of Pidnarulex Pharmacodynamics in Patients with Advanced Solid Tumors, Sponsored by the US National Cancer Institute

TAIPEI and SAN DIEGO, Oct. 14, 2024 /PRNewswire/ -- Senhwa Biosciences, Inc. (TPEx: 6492), a drug development company focusing on first-in-class therapeutics for oncology, rare diseases, and infectious diseases, today announced that FDA issues Study May Proceed letter for its developing drug Pidnarulex (CX-5461) in trial entitled "Pilot Study of Pidnarulex Pharmacodynamics in Patients with Advanced Solid Tumors" sponsored by the US National Cancer Institute (NCI). The study will assess whether Pidnarulex (CX-5461) induces a Rad51 response, in patients with and without homologous repair deficiency (HRD) genetic mutations. This pilot study also aims to explore potential biomarkers beyond BRCA1/2 and PALB2 that may demonstrate synthetic lethality with Pidnarulex (CX-5461). The findings from this study may identify patients who are more responsive to Pidnarulex (CX-5461) treatment, potentially expanding its therapeutic applications, and may accelerate its path to market approval. In addition to this monotherapy trial, the NCI is considering future clinical trials involving Pidnarulex (CX-5461) in combination with other therapies, such as immunotherapies and antibody-drug conjugates (ADCs). Should these trials proceed as planned, they will be led by the NCI, utilizing its vast medical expertise, scientific resources, and regulatory experience—support that could significantly accelerate the development of Pidnarulex. Pidnarulex (CX-5461), developed by Senhwa, is a first-in-class small-molecule designed to stabilize G-quadruplex (G4) structures, which are frequently observed in promoters of oncogenes. By stalling replication fork progression, Pidnarulex induces DNA damage and promotes cancer cell death. Through this mechanism, Pidnarulex holds great potential as a therapeutic agent for various cancers. In recent years, immunotherapy has been the fastest-growing category in the cancer drug market. According to the 2023 global best-selling drug market analysis, the first PD-1 inhibitor Keytruda(Pembrolizumab), developed by Merck, topped the sales charts with $25.11 billion. Immunotherapy and cancer drugs account for nearly half of the market sales. International clinical research indicates that combined immunotherapy can enhance tumor response rates, reduce mortality, and prolong patient survival. Given that only 20% to 25% of patients benefit from effective immunotherapy, Senhwa expects that in future immuno-combination therapy trials, CX-5461 will change the tumor microenvironment with its innovative mechanism, thereby enhancing the efficacy of immunotherapy, realizing the corporate mission of bringing hope to life. SOURCE Senhwa Biosciences, Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED