A Phase I Study Investigating the Combination of Cladribine, Low Dose Cytarabine and Sorafenib Alternating With Decitabine in Pediatric Relapsed and Refractory Acute Leukemias

To find the recommended dose of the drug combination cladribine, cytarabine, decitabine, and sorafenib in participants with relapsed/refractory AML, MPAL, and ALAL.

开始日期2025-12-31

申办/合作机构

The University of Texas MD Anderson Cancer Center

NCT05944783

/ Not yet recruiting临床4期

Bioequivalence Studies of Dasatinib 100 Mg Tablets in Healthy Colombian Subjects in Postprandial Condition

A bioequivalence study of Dasatinib will be carried out in 46 healthy subjects, in fed condition, following the complete replicated design, randomized, comparative of 2 sequences, 2 study formulations, in a single dose of 100 mg of Dasatinib tablets / coated tablets, 4 periods. , with a washout time of 7 days between each dose

开始日期2025-09-01

申办/合作机构-

NCT06940297

/ Not yet recruiting临床2期IIT

DART: Phase II Study of Dasatinib and Quercetin in Patients With Relapsed, Refractory Multiple Myeloma Receiving CAR-T Therapy

This phase II trial tests how well giving dasatinib and quercetin with cyclophosphamide, fludarabine and chimeric antigen receptor (CAR)-T cell therapy works in treating patients with multiple myeloma that has come back after a period of improvement (relapsed) or that has not responded to previous treatment (refractory). Dasatinib is in a class of medications called tyrosine kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply, which may help keep cancer cells from growing. Quercetin is a compound found in plants that may prevent multiple myeloma from forming. Chemotherapy such as cyclophosphamide and fludarabine are given to help kill any remaining cancer cells in the body and to prepare the bone marrow for CAR-T therapy. Chimeric antigen receptor T-cell Therapy is a type of treatment in which a patient's T cells (a type of immune system cell) are changed in the laboratory so they will attack cancer cells. T cells are taken from a patient's blood. Then the gene for a special receptor that binds to a certain protein on the patient's cancer cells is added to the T cells in the laboratory. The special receptor is called a chimeric antigen receptor. Large numbers of the CAR T cells are grown in the laboratory and given to the patient by infusion for treatment of certain cancers. Giving dasatinib and quercetin with cyclophosphamide, fludarabine and CAR-T cell therapy may kill more cancer cells in patients with relapsed or refractory multiple myeloma.

开始日期2025-08-15

申办/合作机构

Mayo Clinic

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100 项与 PDGFRβ x RTKs 相关的临床结果

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100 项与 PDGFRβ x RTKs 相关的转化医学

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0 项与 PDGFRβ x RTKs 相关的专利（医药）

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项与 PDGFRβ x RTKs 相关的文献（医药）

2025-12-31·RENAL FAILURE

Role of microvascular pericyte dysfunction in antibody-mediated rejection following kidney transplantation

Article

作者: Ju, Xiaobing ; Xu, Jie ; Tan, Ruoyun ; Han, Zhijian ; Chen, Hao ; Sun, Li ; Fei, Shuang ; Pu, Junyan ; Tao, Jun ; Wang, Zijie ; Gu, Min

OBJECTIVE:

To investigate the role of microvascular pericyte dysfunction in antibody-mediated rejection (ABMR) of transplanted kidneys.

METHODS:

A total of 160 patients who underwent kidney transplantation in our hospital from 2004 to 2020 were enrolled, divided into 4 groups: ABMR group (n = 79), TCMR group (n = 20), mixed rejection group (n = 25) and control group (n = 36). Postoperative renal function indicators were compared, and immunohistochemical and immunofluorescence staining was performed on graft tissues and mice models using the pericyte marker PDGFR-β. An in vitro pericyte dysfunction model was co-cultured with vascular endothelial cells for functional assessment through Western blotting, PCR, and wound healing tests. KEGG pathway analysis from the GEO database identified gene expression changes in pericytes, which were further analyzed using electron microscopy and Western blot techniques.

RESULTS:

There were statistically significant differences in creatinine, urea nitrogen, urine protein, and eGFR among the groups over time, with ABMR displaying the poorest outcomes. Immunohistochemistry revealed lower pericyte expression in ABMR, which was confirmed in mouse model studies showing reduced PDGFR-β expression in ABMR. KEGG analysis highlighted decreased autophagy in pericyte dysfunction, supported by electron microscopy and Western blot findings indicating reduced autophagy and pericyte damage, which could be reversed by chloroquine.

CONCLUSION:

ABMR episodes worsened the long-term prognosis of transplanted kidneys. pericyte dysfunction appears to be one of the crucial causes of poor prognosis in ABMR patients. In vitro studies demonstrated that dysfunction of microvascular pericytes can result in damage to vascular endothelial cells, with autophagy impairment being a significant mechanism contributing to pericyte dysfunction.

2025-10-01·BRAIN BEHAVIOR AND IMMUNITY

A role for fibroblast and mural cell subsets in a nerve ligation model of neuropathic pain?

Article

作者: Villa-Hernandez, Sara ; Walker, Julia Vlachaki ; Hore, Zoe ; Taams, Leonie S ; Shimizu, Fumitaka ; Davis, Harvey ; Denk, Franziska ; Li, Yuening ; Fedele, Laura ; Kanda, Takashi ; Zebochin, Irene

Neuropathic pain is a particularly intractable type of chronic pain that can result from physical nerve damage due to surgery or entrapment. Here, we present data which suggest that a particular subclass of fibroblast and mural cells may be implicated in the sensory neuron dysfunction that is characteristic of this pain state. In a mouse model of traumatic painful neuropathy, we used cell sorting, nerve tissue clearing and RNA sequencing to study stromal cells. With cell sorting (n = 4 mouse nerves) and tissue clearing (n = 5), we show that fibroblasts and mural cells positive for the platelet-derived growth factor receptor beta (Pdgfrb) gene are increased in number for at least two months post-nerve damage. Moreover, single cell RNA sequencing data (n = 4) from our own lab and those of three other laboratories reveal that Pdgfrb+ cells express high levels of known and putative pro-algesic mediators. Bulk sequencing of sorted Pdgfrb+ fibroblasts (n = 10) and Pdgfrb+/Cd146+ mural cells (n = 11) further indicate that many of these mediators are upregulated in neuropathy. We go on to demonstrate that a human nerve pericyte line releases a selection of these pro-algesic mediators at protein level. Moreover, conditioned media from stimulated human pericytes induces intra-cellular changes in human induced pluripotent stem cell derived sensory neurons (n = 5 independent differentiations); these changes (phosphorylation of the transcription factor signal transducer and activator of transcription 3, STAT3) have been previously linked to sensory neuron activation. In summary, our data indicate that stromal cell abnormalities should be considered when developing novel strategies to tackle neuropathic pain.

2025-10-01·BIOMATERIALS

Modification of MSCs with aHSCs-targeting peptide pPB for enhanced therapeutic efficacy in liver fibrosis

Article

作者: Jiang, Yingan ; Yin, Zhengrong ; Chen, Ping ; Shu, Kan ; Xiong, Zhiyu ; Liu, Pingji ; Sun, Muhua ; Wang, Zheng ; Yuan, Mengqin ; Yao, Lichao ; Li, Lanjuan

Mesenchymal stem cells (MSCs) hold significant therapeutic potential for liver fibrosis but face translational challenges due to suboptimal homing efficiency and poor retention at injury sites. Activated hepatic stellate cells (aHSCs), the primary drivers of fibrogenesis, overexpress platelet-derived growth factor receptor-beta (PDGFRB), a validated therapeutic target in liver fibrosis. Here, we engineered pPB peptide-functionalized MSCs (pPB-MSCs) via hydrophobic insertion of DMPE-PEG-pPB (DPP) into the MSC membrane, creating a targeted "MSC-pPB-aHSC" delivery system. Our findings demonstrated that pPB modification preserved MSC viability, differentiation potential, and paracrine functions. pPB-MSCs exhibited higher binding affinity to TGF-β1-activated HSCs in vitro and greater hepatic accumulation in TAA-induced fibrotic mice, as quantified by in vivo imaging. Moreover, pPB-MSCs attenuated collagen deposition, suppressed α-SMA⁺ HSCs, and restored serum ALT/AST levels to near-normal ranges. Mechanistically, pPB-MSCs promoted hepatocyte regeneration via HGF upregulation, inhibited epithelial-mesenchymal transition through TGF-β/Smad pathway suppression, and polarized macrophages toward an M2 phenotype, reducing pro-inflammatory IL-6/TNF-α while elevating anti-inflammatory IL-10. Overall, our study raised a non-genetic MSC surface engineering strategy that synergizes PDGFRB-targeted homing with multifactorial tissue repair, addressing critical barriers in cell therapy for liver fibrosis. By achieving enhanced spatial delivery without compromising MSC functionality, our approach provides a clinically translatable platform for enhancing regenerative medicine outcomes.

项与 PDGFRβ x RTKs 相关的新闻（医药）

2025-06-20

·GlobeNewswire-Health Care

Onco360 Has Been Selected as a National Specialty Pharmacy Partner for QINLOCK® (ripretinib)

LOUISVILLE, Ky., June 20, 2025 (GLOBE NEWSWIRE) -- Onco360®, the nation’s leading independent specialty pharmacy, has been selected as a pharmacy partner by Deciphera Pharmaceuticals, LLC for QINLOCK® (ripretinib), which has been approved by the U.S. Food and Drug Administration for the treatment of adult patients with advanced gastrointestinal stromal tumors (GIST) who have received prior treatment with 3 or more kinase inhibitors, including imatinib.1 This indication was approved based on the Phase III INVICTUS study of QINLOCK in patients with advanced GIST.2 “Onco360 is grateful for the opportunity to partner with the team at Deciphera and become a specialty pharmacy provider for QINLOCK,” said Benito Fernandez, Chief Commercial Officer. “With the addition of QINLOCK to our portfolio, we are continuing to build on our mission of improving the lives of patients battling cancer, rare, and complex disease.” Ripretinib is a tyrosine kinase inhibitor that inhibits KIT proto-oncogene receptor tyrosine kinase (KIT) and platelet derived growth factor receptor A (PDGFRA) kinase, including wild type, primary, and secondary mutations. Ripretinib also inhibits other kinases in vitro, such as PDGFRB, TIE2, VEGFR2, and BRAF.1 The FDA approved QINLOCK based on the results of 129 patients with relapsed or refractory GIST who were treated with ripretinib or placebo in the INVICTUS trial. The primary endpoint was progression free survival (PFS). The median progression free survival (mPFS) was 6.3 months (95% CI 4.6-6.9) for the ripretinib group vs 1.0 months (95% CI 0.9-1.7) for placebo.1 Ripretinib was generally well tolerated in the INVICTUS trial. The most common adverse reactions occurring in ≥ 20% of patients consisted of alopecia, fatigue, nausea, abdominal pain, constipation, myalgia, diarrhea, decreased appetite, palmar-plantar erythrodysesthesia, and vomiting. The most common Grade 3 or 4 laboratory abnormalities (≥4%) were increased lipase and decreased phosphate.1 Please see the full Prescribing Information for QINLOCK®. About Onco360 Oncology Pharmacy:Onco360 is the nation’s largest independent Oncology Pharmacy and clinical support services company. Onco360 was founded in 2003 to bring together the stakeholders involved in the cancer treatment process and serve the specialized needs of oncologists, patients, hospitals, cancer centers of excellence, manufacturers, health plans, and payers. It dispenses nationally through its network of URAC-, and ACHC-accredited Oncology Pharmacies. Onco360 is headquartered in Louisville, Kentucky, and is a flagship specialty pharmacy brand of PharMerica Corporation, a leading institutional pharmacy, specialty infusion, and hospital services company servicing healthcare facilities in the United States. For more information about Onco360, please visit Onco360.com. Media Contact: Benito Fernandez, Chief Commercial OfficerBenito.Fernandez@Onco360.com516-640-1332 References: 1Qinlock (Ripretinib) [Package Insert]. Waltham, MA. Deciphera Pharmaceuticals. 2025. 2Ripretinib in patients with advanced gastrointestinal stromal tumors (INVICTUS): a double-blind, randomized, placebo-controlled, phase 3 trial. Blay, Jean-Yves et al. The Lancet Oncology, Volume 21, Issue 7, 923 – 934.

临床3期临床结果上市批准

2025-06-15

·精准药物

药物筛选中心（暨南大学）对外提供新药筛选服务

咨询合作药物筛选中心（暨南大学），隶属于暨南大学药学院公共科研平台。中心拥有Echo550微量液体超声转移工作站等先进的自动化药物筛选仪器，前期支撑的多个激酶抑制剂已经产业转化及发表JMC等高水平论文。目前，筛选中心建有激酶、蛋白酶、HDAC、COX、GPCR、报告基因、病毒、细菌等筛选模型，能够开展肿瘤、神经系统疾病、心脑血管病、糖尿病、病毒和细菌感染性疾病等领域相关靶标、细胞、机制的筛选和研究，每天能够完成数万次的新药筛选反应。已建立的药物筛选模型1）激酶：Abl, ABL(M351T), ABL(H396P), ABL(Y253F), ABL1 (E255K), ABL1 (G250E), ABL(Q252H), AKT1, AKT2, AKT3, ALK, ALK5, AuroraA, AuroraB, AXL, BRAF, BRAF(V599E), BTK, DDR1, DDR2, EGFR, EGFR (T790M), EGFR(L858R), EGFR(L861Q), EGFR(T790ML858R), EGFR(D746-750), EGFR(D746-750/T790M), Flt3, FLT3(D835Y), FGFR1, FGFR2, FGFR3, FGFR4, Her2, Her4, KIT, MET, IGF-1R, FGFR1, JAK1, JAK2, JAK3, MAPK10, MAPK14, mTOR, TrkA, TrkB, TrkC,TYK2, KDR, SRC, PDGFRa, PDGFRA(D842V), PDGFRb, RET, ZAK。2）肿瘤细胞模型：近500种肿瘤细胞系和基于Ba/F3的耐药模型。3）抗病毒药物筛选：包括抗EV71和HSV病毒活性筛选模型；4）抗细菌药物的筛选模型：包括金黄色葡萄球菌、大肠杆菌和沙门氏杆菌等。5）肿瘤移植瘤模型体内药效。6) 抗重力作用机制。咨询合作

2025-06-13

·恒瑞医药

恒瑞医药创新药苹果酸法米替尼胶囊全国首批发货

2025年6月13日，恒瑞医药1类新药苹果酸法米替尼胶囊（艾比特®）首批发货仪式正式举行。当天，一辆装载法米替尼的运输车从江苏连云港恒瑞医药国际化制剂生产基地发往全国，标志着该产品正式投入临床使用，将为复发或转移性宫颈癌患者提供新的治疗选择。法米替尼于2025年5月在国内获批上市，联合注射用卡瑞利珠单抗（商品名：艾瑞卡®）用于既往接受含铂化疗治疗失败但未接受过贝伐珠单抗治疗的复发或转移性宫颈癌患者。该产品是一种能够靶向PDGFR-β、VEGFR和c-Kit等多个靶点的小分子酪氨酸激酶抑制剂（TKI）。当药物与胞内段酪氨酸激酶功能域发生竞争性结合后，能够抑制其磷酸化，从而阻断细胞下游信号通路的激活，最终实现对肿瘤血管新生的抑制作用1。卡瑞利珠单抗是恒瑞医药自主研发的人源化PD-1单克隆抗体，通过与法米替尼联合使用，可以重塑肿瘤血管和免疫微环境，发挥协同增效的抗肿瘤作用。此次法米替尼获批是基于一项随机、开放、对照、多中心的II期临床研究（SHR-1210-II-217），研究结果表明：法米替尼联合卡瑞利珠单抗可显著提高患者的客观缓解率（ORR）和无疾病进展时间（PFS），并且可延长复发或转移性宫颈癌患者的总生存期（OS）2,3。作为创新型国际化制药企业，恒瑞医药始终践行“科技为本，为人类创造健康生活”的使命，深耕肿瘤药物等高品质创新药研发，目前已在中国获批上市23款新分子实体药物（1类创新药），其中抗肿瘤药占比过半。另有90多个自主创新产品正在临床开发，约400项临床试验在国内外开展。未来，恒瑞医药将持续“以患者为中心”加速创新研发步伐，致力于推出更多新药好药，服务健康中国，造福全球患者。参考文献：1. 子宫颈癌抗血管生成药物临床应用指南(2023年版). 中国实用妇科与产科杂志,2023,39(12):1201-1209.2.Xiaohua Wu. Camrelizumab plus famitinib versus camrelizumab alone and investigator’s choice of chemotherapy in women with recurrent or metastatic cervical cancer. ESMO 2023. LBA44.3.Xiaohua Wu, et al. Overall survival with camrelizumab plus famitinib versus camrelizumab alone and investigator's choice of chemotherapy for recurrent or metastatic cervical cancer. SGO 2024. LBA44.声明：1.本新闻旨在分享医药前沿资讯，仅供医疗卫生专业人士参阅，非广告用途。2.恒瑞医药不对任何药品和/或适应症作推荐。3.本新闻中涉及的信息仅供参考，请遵从医生或其他医疗卫生专业人士的意见或指导。医疗卫生专业人士作出的任何与治疗有关的决定应根据患者的具体情况并遵照药品说明书。排版：程梦真责编：李玉莹往期精选| 研发创新 |恒瑞创新药瑞坦宁®获批，用于预防成人高度致吐性化疗引起的急性和迟发性恶心呕吐| 国际化 |恒瑞医药再次与德国默克集团达成合作，推进辅助生殖领域口服GnRH拮抗剂商业化落地恒瑞医药与默沙东就Lp(a)抑制剂HRS-5346签订独家许可协议| 重磅奖项 |捷报！恒瑞医药创新药海曲泊帕乙醇胺片（恒曲®）专利荣获中国专利金奖喜报！恒瑞医药荣获2023年度国家科技进步奖| 社会公益 |“健康中国行·重走长征路”项目启动仪式圆满举行！恒瑞提供公益支持，助力健康中国恒瑞医药集团向中国扶贫基金会捐赠3000万设立“健康帮扶基金”

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