The purpose of this study is to evaluate the investigational drug, silmitasertib (a pill taken by mouth), in combination with FDA approved drugs for solid tumors. An investigational drug is one that has not been approved by the U.S. Food & Drug Administration (FDA), or any other regulatory authorities around the world for use alone or in combination with any drug, for the condition or illness it is being used to treat.
The goals of this part of the study are:
* Establish a recommended dose of silmitasertib in combination with chemotherapy
* Test the safety and tolerability of silmitasertib in combination with chemotherapy in subjects with cancer
* To determine the activity of study treatments chosen based on:
* How each subject responds to the study treatment
* How long a subject lives without their disease returning/progressing

开始日期2024-10-30

申办/合作机构

Hershey Medical Center

NCT06202521

/ Recruiting临床2期

Evaluation of the Safety and Efficacy of Silmitasertib (CX-4945) in Combination With Standard of Care (SOC) for Treating Patients With Community-Acquired Pneumonia (CAP) Associated With SARS-CoV-2 and Influenza Viral Infections

This is a Phase II, multi-center, double-blind, randomized, interventional study in approximately 120 subjects to evaluate clinical benefit of CX-4945 in adult outpatients with SARS-CoV-2 and influenza viral infection-associated pneumonia. The subjects will be recruited into two domains, including SARS-CoV-2 and influenza virus domains. The study will compare the efficacy of Standard of Care (SOC) combined with CX-4945 against SOC paired with a placebo, utilizing a 1:1 allocation ratio in each domain.

开始日期2024-02-27

申办/合作机构

生华生物科技股份有限公司

NCT05817708

/ Completed临床1期

A Dose Selection Phase 1 Study Evaluating the Safety and Tolerability of Silmitasertib

This is a Phase I single center, open-label, parallel design in 30 subjects to evaluate safety and tolerability of CX-4945 200mg QD, 200 mg BID and 400mg BID doses (10 subjects in each regimen) for continuously 5 days in healthy subjects for dose selection.

开始日期2022-11-28

申办/合作机构

生华生物科技股份有限公司

100 项与 CK2 相关的临床结果

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100 项与 CK2 相关的转化医学

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0 项与 CK2 相关的专利（医药）

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项与 CK2 相关的文献（医药）

2025-12-31·Cancer Biology & Therapy

Targeting the IKZF1/BCL-2 axis as a novel therapeutic strategy for treating acute T-cell lymphoblastic leukemia

Article

作者: Ye, Chunmei ; Li, Hui ; Li, Juan ; Li, Jun

OBJECTIVESAcute T-cell lymphoblastic leukemia (T-ALL) is a severe hematologic malignancy with limited treatment options and poor long-term survival. This study explores the role of IKZF1 in regulating BCL-2 expression in T-ALL.METHODSCUT&Tag and CUT&Run assays were employed to assess IKZF1 binding to the BCL-2 promoter. IKZF1 overexpression and knockdown experiments were performed in T-ALL cell lines. The effects of CX-4945 and venetoclax, alone and in combination, were evaluated in vitro and in vivo T-ALL models.RESULTSCUT&Tag sequencing identified IKZF1 binding to the BCL-2 promoter, establishing it as a transcriptional repressor. Functional assays demonstrated that IKZF1 overexpression reduced BCL-2 mRNA levels and increased repressive histone marks at the BCL-2 promoter, while IKZF1 knockdown led to elevated BCL-2 expression. CX-4945, a CK2 inhibitor, could reduced BCL-2 levels in T-ALL cells. Notably, knockdown of IKZF1 partially rescued the CX-4945-induced repression of BCL-2. These results underscore the CK2-IKZF1 signaling axis as a key regulator of BCL-2 expression. In vitro, CX-4945 enhanced the cytotoxicity of venetoclax, with the combination showing significant synergistic effects and increased apoptosis in T-ALL cell lines. In vivo studies with cell line-derived xenograft (CDX) and patient-derived xenograft (PDX) models demonstrated that CX-4945 and venetoclax combined therapy provided superior therapeutic efficacy, reducing tumor burden and prolonging survival compared to single-agent treatments.CONCLUSIONSIKZF1 represses BCL-2 in T-ALL, and targeting the CK2-IKZF1 axis with CX-4945 and venetoclax offers a promising therapeutic strategy, showing enhanced efficacy and potential as a novel treatment approach for T-ALL.

2025-07-01·Biochemical Pharmacology

The dual targeting effects of KD025 on casein kinase 2 and ROCK2 in a mouse model of diet-induced obesity

Article

作者: Oh, Byung-Chul ; Jun, Hee-Sook ; Lee, Dae Ho ; Maeng, Han-Joo ; Lee, Jeongmi ; Chun, Kwang-Hoon ; Sactivel, Bathiga ; Oh, Yu Jin ; Tran, Nhu Nguyen Quynh ; Choi, Hojung ; Kim, Young-Bum ; Kim, Min Kyung

KD025(belumosudil), a selective ROCK2 inhibitor, exhibits unique anti-adipogenic activity through inhibition of casein kinase 2 (CK2). This study investigated the dual inhibitory effects of KD025 on metabolism in a diet-induced obese model. C57BL/6 mice on a high fat diet (HFD) were treated with KD025 for 4 weeks, while fasudil (a pan-ROCK inhibitor) and CX-4945 (a CK2-specific inhibitor) served as comparison treatments. KD025 significantly reduced body weight gain without affecting food intake, serum insulin, or fasting blood glucose levels. In contrast, while both CX-4945 and fasudil treatments showed a trend toward weight reduction, these results were not statistically significant. KD025 improved lipid metabolism by significantly lowering LDL cholesterol and triglyceride, although it slightly impaired glucose metabolism, as observed in insulin and glucose tolerance tests. Weight reduction in the KD025- and CX-4945-treated groups was attributed to decreased adipose tissue mass, particularly in inguinal (ingWAT) and epididymal (epiWAT) fat depots. Hematoxylin and eosin (H&E) staining confirmed smaller adipocyte size in these groups. KD025 had no significant effect on serum levels of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), or monocyte chemoattractant protein-1 (MCP-1) with varied inflammatory responses. Furthermore, KD025 and CX-4945 upregulated adipogenic and browning markers, such as Cebpa, Cidea, and Pparg in the epiWAT, though without significant UCP1 expression. Overall, KD025 effectively reduced weight gain in HFD-fed mice through dual inhibition of CK2 and ROCK2, highlighting its potential as a therapeutic agent for obesity-related conditions.

2025-06-01·Redox Biology

Redox signaling modulates axonal microtubule organization and induces a specific phosphorylation signature of microtubule-regulating proteins

Article

作者: Monteiro-Abreu, Nanci ; Brandt, Roland ; Conze, Christian ; Singh, Lisha ; Romero, Daniel Villar ; Wienbeuker, Eike ; Holtmannspötter, Michael ; Bakota, Lidia ; Schwarze, Anna-Sophie ; Trushina, Nataliya I

Many life processes are regulated by physiological redox signaling, but excessive oxidative stress can damage biomolecules and contribute to disease. Neuronal microtubules are critically involved in axon homeostasis, regulation of axonal transport, and neurodegenerative processes. However, whether and how physiological redox signaling affects axonal microtubules is largely unknown. Using live cell imaging and super-resolution microscopy, we show that subtoxic concentrations of the central redox metabolite hydrogen peroxide increase axonal microtubule dynamics, alter the structure of the axonal microtubule array, and affect the efficiency of axonal transport. We report that the mitochondria-targeting antioxidant SkQ1 and the microtubule stabilizer EpoD abolish the increase in microtubule dynamics. We found that hydrogen peroxide specifically modulates the phosphorylation state of microtubule-regulating proteins, which differs from arsenite as an alternative stress inducer, and induces a largely non-overlapping phosphorylation pattern of MAP1B as a main target. Cell-wide phosphoproteome analysis revealed signaling pathways that are inversely activated by hydrogen peroxide and arsenite. In particular, hydrogen peroxide treatment was associated with kinases that suppress apoptosis and regulate brain metabolism (PRKDC, CK2, PDKs), suggesting that these pathways play a central role in physiological redox signaling and modulation of axonal microtubule organization. The results suggest that the redox metabolite and second messenger hydrogen peroxide induces rapid and local reorganization of the microtubule array in response to mitochondrial activity or as a messenger from neighboring cells by activating specific signaling cascades.

项与 CK2 相关的新闻（医药）

2025-02-14

·精准药物

【Drug Discovery Today】陆涛/陈亚东/卢帅：通过双功能分子调控靶蛋白磷酸化——疾病治疗的新范式

蛋白质的磷酸化与去磷酸化是细胞中最为关键的翻译后修饰（PTM）过程之一。这一动态平衡作为一个精密的开关，不仅调控细胞的增殖、分化、迁移和凋亡，还直接影响信号通路的激活与抑制。然而，磷酸化网络的失调与癌症、糖尿病、神经退行性疾病等多种病理状态密切相关。传统的小分子激酶抑制剂或磷酸酶调节剂虽在临床中广泛应用，但其选择性差、耐药性频发等问题亟待突破。近年来，磷酸化调控双功能分子（Phosphorylation-regulating Bifunctional Molecules, PBMs）的兴起，为精准调控靶蛋白磷酸化状态提供了全新策略。近日，中国药科大学陆涛/陈亚东/卢帅团队于药学知名期刊Drug Discovery Today发表了题为“Modulating the phosphorylation status of target proteins through bifunctional molecules ”的文章。文中，作者从机制、应用、优势与挑战等方面，全面解析这一领域的科学进展与未来潜力。一、磷酸化的生物学意义与传统疗法的局限磷酸化调节是指通过激酶（Kinase）向蛋白质添加磷酸基团，或通过磷酸酶（Phosphatase）移除磷酸基团，动态调控蛋白质功能。蛋白质的磷酸化和去磷酸化是细胞调控信号传递、增殖和凋亡的核心机制。当这一过程失衡时，疾病随之而来。例如，表皮生长因子受体（EGFR）蛋白异常磷酸化激活下游RAS-MAPK通路，驱动细胞增殖，促使肿瘤生长；低分子量蛋白酪氨酸磷酸酶（LMPTP）过度活跃导致胰岛素抵抗，这与糖尿病等代谢性疾病密切相关；在阿尔茨海默病中，Tau蛋白的过度磷酸化导致神经纤维缠结，破坏神经元功能。传统药物（如激酶抑制剂）虽有效，却因靶点相似性高、易引发耐药性而受限。例如，ATP竞争性抑制剂因靶向激酶的保守ATP结合口袋，常导致脱靶效应与耐药性的产生，且部分激酶（如BTK）的支架功能独立于催化活性，难以通过抑制剂完全阻断。而激酶变构抑制剂虽选择性高，但发现过程依赖偶然性。除此之外，磷酸酶调节剂磷酸酶活性位点带正电，需带负电的小分子结合，但这类分子往往膜渗透性差（如PTP1B抑制剂的开发困境），成药性不佳。蛋白降解靶向嵌合体 (Proteolysis Targeting Chimera, PROTAC)等基于“化学诱导接近（CIP）”策略的药物范式的出现给科学家们带来了全新的药物研发思路，是否可以通过类似的药物设计从而实现靶蛋白与激酶或磷酸酶空间上的临近，从而调节靶蛋白的磷酸化状态？二、PBMs通过化学诱导接近策略调节靶蛋白的磷酸化状态 PBMs通过双功能设计，一端结合靶蛋白（Protein of Interest, POI），另一端结合激酶或磷酸酶，利用连接链（Linker）拉近两者空间距离，从而诱导靶蛋白的磷酸化或去磷酸化（图1）。这一策略的核心在于“事件驱动”，即PBMs无需高亲和力结合靶点，仅需短暂形成三元复合物即可催化修饰反应。图1：PBMs的作用机制与分类 1. PHICs：从概念验证到临床前突破一般而言，PHICs通常由激酶激活剂与靶蛋白配体通过Linker偶联。在一些PHICs的研究中，其表现出独特的优势。例如，Choudhary团队设计的化合物1在体外实验中显著诱导BRD4的多个丝氨酸/苏氨酸位点的磷酸化（图2A）。尽管BRD4的天然激酶为CK2，PHIC-1通过人工拉近AMPK与BRD4，实现了底物特异性的“重编程”,使AMPK磷酸化非天然底物BRD4，突破了激酶固有的底物限制，体现了PHICs能够重编程激酶底物特异性；化合物5通过招募PKC激酶，诱导BTKS180A突变体的抑制性磷酸化（S310/S378），阻断其Y223自磷酸化，从而抑制耐药性白血病细胞增殖（图2E）。此外，在针对BTKC481S突变（伊布替尼耐药）细胞中，化合物11（伊布替尼作为靶蛋白的配体，图3D）能够与BTK结合并招募ABL激酶，成功诱导BTKC481S抑制性磷酸化（图3C）。体现了PHICs克服激酶耐药的潜力。针对激酶抑制剂无法直接用于PHICs的问题（因其抑制催化活性），CoLDR策略通过可降解连接链将抑制剂转化为“临时配体”。具体而言，对于结合口袋外围具有亲核残基（如半胱氨酸）的功能性激酶，半胱氨酸与PHIC的连接结构形成共价键，抑制剂部分将被释放，这一方面减轻了PHIC对功能性激酶的抑制，另一方面暴露了功能性激酶表面的POI配体，以招募POI并形成蛋白质复合物（图3B）。这种可降解连接体，为基于激酶抑制剂的PHIC设计提供了一种新策略。利用丰富的激酶抑制剂库，可以大大扩展PHICs的设计范围。图2，3：PHICs的结构与作用机制 2. PhORCs/PhosTACs：逆转病理磷酸化的利器 PhORCs/PhosTACs通常由磷酸酶激活剂与靶蛋白配体连接而成。首个PhORC（化合物12）由Staben团队提出，通过将AKT与PP1-HaloTag融合蛋白拉近，显著降低pAKTT308水平（图4A），抑制肿瘤细胞存活信号。后续的研究中，他们使用了短链RVxF肽作为PP1的激活剂（化合物14），成功实现了对天然AKT与PP1的募集与AKT的有效去磷酸化（图4C）。化合物19利用Tau追踪剂PI-2620与FKBP12F36V-PP2A招募配体，以1μM浓度下在表达Tau的HeLa细胞中实现50%的去磷酸化，并促进Tau经蛋白酶体降解（图5C）。后续的动物模型也验证了化合物19的疗效，在Tau368转基因小鼠中，脑室内注射可减少海马区磷酸化Tau沉积，改善突触可塑性，表现出PhosTACs对Tau蛋白去磷酸化的治疗潜力。化合物20（Gefitinib-AP1867嵌合体）通过招募PTPN2磷酸酶，降低EGFRY1068磷酸化水平，并抑制下游SHC和SOS1信号（图5D）。此外，RIPK2是吉非替尼的已知脱靶蛋白，而这种去磷酸化对RIPK2的抑制作用相比于吉非替尼明显减弱，这表明PhosTACs可能增强靶点选择性。图4，5：PhORCs/PhosTACs的结构与作用机制 3. 非小分子PBMs：肽类与抗体系统除了上述提及的小分子PBMs外，一些肽类与抗体类PBMs也陆续报道。DEPTACs是一种38氨基酸的肽类分子，通过招募PP2A，促使神经元中多个AD相关Tau位点和AT8表位的去磷酸化，以及去磷酸化依赖性降解，这些都有助于改善Tau相关疾病（图6A）。Sapkota团队披露了另一种非小分子PBM，即亲和定向磷酸酶（AdPhosphatase）系统。AdPhosphatase系统包括绿色荧光蛋白（GFP）抗体、磷酸酶（如PP1或PP2A）的催化亚基和FLAG标记的报告蛋白。AdPhosphatase与POI-GFP融合蛋白的结合诱导磷酸酶催化亚基与POI的空间接近，从而实现对POI的特异性去磷酸化修饰（图6B）。此外，RIPR-PD1一种由PD-1单抗和CD45单抗组成的异源双特异性二价抗体，它可以同时结合PD-1和CD45的胞外结构域，并通过CD45诱导PD-1胞内区域的去磷酸化，最终激活T细胞的免疫功能（图6C）。图6：一些非小分子PBMs的结构与作用机制三、PBMs的独特优势与核心挑战目前，PBMs已经体现出较传统激酶/磷酸酶调节剂独特的优势，表现出超越传统疗法的潜力。这包括了： 1.高选择性：通过靶向非催化结构域或蛋白互作界面，减少脱靶效应（如化合物20对RIPK2的脱靶抑制率较吉非替尼大大减小）。 2.克服耐药性：使用突变耐药的调节剂作为靶蛋白的配体得到的PBMs，对突变激酶的磷酸化调节（如BTKC481S、EGFRT790M）仍有效。 3.多功能调控：单分子可同时干预多个磷酸化位点（如化合物5诱导BTK多个位点的磷酸化），体现出PBMs可以调节蛋白的多个功能。 4.工具分子：PBMs可以作为分子探针，解析磷酸化网络的功能机制（如AdPhosphatase系统用于ULK1去磷酸化研究）。尽管如此，PBMs的临床运用仍旧面临诸多挑战，是否能真正作为药物仍存在诸多不确定因素： 1.配体匮乏：80%的激酶缺乏非抑制性配体，磷酸酶激活剂（如PP5的P5SA-2）多依赖偶然发现。尽管CoLDR策略通过可降解连接链将抑制剂转化为“临时配体”，但这种策略对激酶结构有一定的要求。 2.药代动力学缺陷：PBMs分子量常超过800 Da，违反类药五规则（Lipinski's Rule），导致口服生物利用度低。 3.复杂性风险：多磷酸化位点调控可能引发不可预见的信号扰动（如化合物5对BTK下游通路的多重影响）。 4. 耐药机制：细胞可能通过上调反向激酶或磷酸酶补偿PBMs的作用，这也许会带来耐药风险。四、未来方向：技术融合与临床转化 PBMs的一大问题是激酶/磷酸酶配体的缺乏，通过计算生物学策略可以驱动配体发现。具体而言，利用AlphaFold等基于AI的蛋白结构预测系统可以实现预测激酶/磷酸酶的隐蔽结合位点与潜在的调控口袋，指导配体设计并加速PBMs开发。对于PBMs的成药性差等问题，通过新型递送系统的设计可以有效解决。这包括了使用纳米载体，即脂质体或外泌体包裹PBMs，增强细胞膜乃至血脑屏障的穿透性。前药的设计也能解决一部分的成药性问题，通过酶敏感连接链设计“隐形PBMs”，在靶组织内激活，实现高效组织穿透。为了实现PBMs的临床转化，亟需对其进行毒理学评估，系统研究PBMs对靶蛋白磷酸化调控后的下游信号转导所产生的生物学效应，同时评估对正常磷酸化网络的影响，避免干扰生理过程。除此之外，药物联用在临床研究中也体现出较高的应用价值，可以增强药物疗效，减少耐药性。例如，PBMs与PROTACs联用，可以实现同时降解异常蛋白并调控其磷酸化状态，增强疗效。五、结语：开启精准磷酸化调控的新纪元 PBMs作为化学生物学与药物设计的交叉产物，正逐步从概念验证迈向临床前研究。其核心价值在于“精准”与“可逆”——既能针对特定磷酸化事件，又可避免PROTACs的不可逆降解风险。尽管当前面临配体发现、药代优化等挑战，但随着计算工具、递送技术和临床转化的协同突破，PBMs有望在癌症、神经退行性疾病、代谢紊乱等领域实现革命性应用。未来十年，这一领域或将成为继PROTACs之后，药物开发的又一黄金赛道。参考文献： He Q, Wang Z, Wang R, Lu T, Chen Y, Lu S. Modulating the phosphorylation status of target proteins through bifunctional molecules. Drug Discovery Today. 2025:104307 声明：发表/转载本文仅仅是出于传播信息的需要，并不意味着代表本公众号观点或证实其内容的真实性。据此内容作出的任何判断，后果自负。若有侵权，告知必删！长按关注本公众号粉丝群/投稿/授权/广告等请联系公众号助手觉得本文好看，请点这里↓

蛋白降解靶向嵌合体

2024-11-07

·Outsourcing Pharma

Senhwa Biosciences starts trial of silmitasertib in children with difficult to treat cancers

Silmitasertib, also known as CX-4945, was originally developed by Cylene Pharmaceuticals, a San Diego-based biotech that ceased operations in 2013. Since then, Senhwa Biosciences, which is headquartered in Taiwan but also has a San Diego base gained the rights to the small molecule, first in class, casein kinase 2 (CK2) inhibitor. CK2 is overexpressed in a number of tumors. Various studies have shown silmitasertib appears to have good anticancer activity. For example , it triggers autophagy and promote apoptosis of cancer cells in pancreatic and lung cancer and also promotes colorectal cancer cell death. Senhwa is currently testing silmitasertib in early human trials for treatment of cholangiocarcinoma, basal cell carcinoma, medulloblastoma and neuroblastoma. In preclinical studies , the small molecule showed good oral bioavailability and was able to effectively inhibit tumor growth in animal studies while being well tolerated. When combined with DNA-damaging chemotherapy drugs such as gemcitabine and cisplatin, the anticancer activity of silmitasertib seems to be enhanced so it is being tested as an add-on therapy in the new trial. The phase 1/2 study will include 114 children and young adults with relapsed or refractory neuroblastoma, Ewing's sarcoma, osteosarcoma, rhabdomyosarcoma, and liposarcoma in the US. "We are thrilled to be able to move this important research forward on a larger scale," said Giselle Sholler, division chief of pediatric hematology/oncology and director of pediatric oncology research at the College of Medicine and chairperson of the Beat Childhood Cancer Research Consortium, which is supporting the study. googletag.cmd.push(function () { googletag.display('text-ad1'); }); “The insights gained from this trial will help not only local patients and their families but can lead to new therapies that can help children throughout the US and internationally.” Additional indication for Covid-19 patients As well as being a promising anti-cancer therapy, silmitasertib is being tested to treat people infected with SARS-CoV-2 who develop serious symptoms that require hospitalization in a phase 2 study. CK2 is involved in regulating signaling pathways important for innate immune responses. Inhibiting this protein kinase can help reduce the excessive cytokine storm immune response often seen in people with severe Covid-19. Studies have shown that silmitasertib and other kinase inhibitors seem to reduce levels of inflammatory biomarkers such as interleukin 6 and tumor necrosis factor-alpha, both of which are high in hospitalized Covid-19 patients. So far results phase 2 results announced by Senhwa have been good with significantly better recovery times observed for Covid-19 patients given silmitasertib versus standard care, with a good safety profile.

临床2期临床结果临床1期

2024-11-06

·PRNewswire

Senhwa Biosciences announces first patient dosed in the Phase I/II study of Silmitasertib in children and young adults with relapsed refractory solid tumors.

TAIPEI and SAN DIEGO, Nov. 6, 2024 /PRNewswire/ -- Senhwa Biosciences, Inc. (TPEx: 6492), a new drug development company focusing on first-in-class therapeutics for oncology, rare diseases, and infectious diseases, today announced that the enrollment of the first patient at Penn State Health Children's Hospital in its Phase I/II clinical study evaluating the efficacy of Silmitasertib (CX-4945) in combination with chemotherapy for children and young adults with relapsed or refractory solid tumors. This innovative trial seeks to establish a recommended dose of Silmitasertib in combination with chemotherapy and assess the safety, tolerability and efficacy in patients with cancer, with a focus on neuroblastoma, Ewing's sarcoma, osteosarcoma, rhabdomyosarcoma, and liposarcoma. "This clinical trial is a critical piece in understanding the mechanism of how the medicine works and develop more precise treatments for our patients," said Dr. Chandrika Behura, study chair and principal investigator, Four Diamonds researcher and associate professor of pediatrics at the College of Medicine. "It's very important to develop the right combination that can be the most toxic to cancer cells, but the least harmful to the normal cells around them." The study is projected to enroll up to 114 participants nationwide through the Beat Childhood Cancer Research Consortium member hospitals. By evaluating the activity of the study treatments based on individual responses and duration of disease control, the trial aims to develop novel therapeutic approaches. "We are thrilled to be able to move this important research forward on a larger scale," said Dr. Giselle Sholler, division chief of pediatric hematology/oncology and director of pediatric oncology research at the College of Medicine and chairperson of the Beat Childhood Cancer Research Consortium. "The insights gained from this trial will help not only local patients and their families but can lead to new therapies that can help children throughout the US and internationally." With the College of Medicine serving as its home, the Beat Childhood Cancer Research Consortium is a worldwide network of more than 50 universities and children's hospitals focused on saving lives and helping the Children's Hospital make a lasting difference around the world. Funding for this clinical trial is provided by the Beat Childhood Cancer Foundation and the Little Warrior Foundation. Funding for Behura's research which led to the clinical trial was provided by Four Diamonds. "This is the culmination of the work of many people over the years," said Suzanne Graney, executive director of Four Diamonds. "Without the dedication of our physician-scientists and the generosity of our donors and community, this kind of essential work to improve treatments with an ultimate goal of curing cancer would not be possible." The pediatric cancer care specialists at Beat Childhood Cancer Research Consortium hospitals and researchers at the College of Medicine are dedicated to turning groundbreaking discoveries into lifesaving treatments for childhood cancer. "By expanding our research and increasing clinical trials, we are exploring immunotherapy, cellular therapy and precision medicine to deliver the most optimized care to each unique patient," said Dr. Dr. Yatin Vyas, pediatrician-in-chief and chair of the Department of Pediatrics at the Children's Hospital. "We are greatly honored to collaborate with the Penn State College of Medicine and Beat Childhood Cancer Research Consortium, which have been diligently fighting childhood cancers by infusing invaluable resources from over 50 universities and children's hospitals across the United States for the clinical study," said Jin-Ding Huang, PhD, CEO of Senhwa Biosciences, Inc. "We appreciate for having the opportunity of providing Silmitasertib as a potential effective treatment and look forward to realizing its therapeutic value in this urgently needed field for childhood cancers though this study". 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

临床研究免疫疗法