A Phase 3, Randomized, Open-Label Study Comparing the Efficacy and Safety of the Combination of Beleodaq-CHOP or Folotyn-COP to the CHOP Regimen Alone in Newly Diagnosed Patients With Peripheral T-Cell Lymphoma

Part 1: This is a 5 Arm study primarily to determine the best dose out of the two dose levels of Belinostat and Pralatrexate combined with CHOP/COP in newly diagnosed PTCL patients based on Safety for part 2 study.
Part 2 (Efficacy and Safety): This is a 3 Arm study. Patients with previously untreated PTCL will be randomized 1:1:1 into 1 of 3 treatment groups: 2 experimental treatment groups (Bel-CHOP or Fol-COP) or 1 active comparator treatment group (CHOP). Patients will be treated for up to 6 cycles. The primary objective is to compare the Progression Free Survival of patients with newly diagnosed PTCL treated for up to 6 cycles with Beleodaq (belinostat) in combination with CHOP (Bel-CHOP) or Folotyn (pralatrexate injection) in combination with COP (Fol-COP) to CHOP alone.

开始日期2023-10-04

申办/合作机构

Acrotech Biopharma LLC初创企业

NCT05627245 / Recruiting临床1期IIT

Phase 1/Expansion Study of Tazemetostat Plus Belinostat for the Treatment of Relapsed or Refractory Lymphoma

This phase I trial tests the safety, side effects, and best dose of combination therapy with tazemetostat and belinostat in treating patients with lymphomas that have returned (relapsed) or resisted treatment (refractory). Tazemetostat is in a class of medications called EZH2 inhibitors. The EZH2 gene provides instructions for making a type of enzyme called histone methyltransferase which is involved in gene expression and cell division. Blocking EZH2 may help keep cancer cells from growing. Belinostat is in a class of medications called histone deacetylase inhibitors. Histone deacetylases are enzymes needed for cell division. Belinostat may kill cancer cells by blocking histone deacetylase. It may also prevent the growth of new blood vessels that tumors need to grow and may help make cancer cells easier to kill with other anticancer drugs. There is some evidence in animals and in living human cells that combination therapy with tazemetostat and belinostat can shrink or stabilize cancer, but it is not known whether this will happen in people. This trial may help doctors learn more about treatment of patients with relapsed or refractory lymphoma.

开始日期2023-03-01

申办/合作机构

National Cancer Institute

NCT05154994 / Recruiting临床1期IIT

RESOLVE : A Phase I Trial of Tremelimumab + Durvalumab(MEDI4736)+ Belinostat in ARID1A Mutated Cancers With Focus on Urothelial Carcinoma

This phase I trial studies the side effects and best dose of belinostat when given together with durvalumab in treating patients with urothelial cancer that has spread to other places in the body (metastatic) or cannot be removed by surgery (unresectable) and has spread to nearby tissue or lymph nodes (locally advanced). Immunotherapy with monoclonal antibodies, such as durvalumab, may help the body's immune system attack the cancer, and may interfere with the ability of tumor cells to grow and spread. Belinostat is a potential anti-cancer drug, known as a histone deacetylase (HDAC) inhibitor, which means that belinostat stops the activity of HDAC enzymes (an enzyme is a protein that in small amounts can speed up a biological reaction). HDAC enzymes play an important role in cell growth and cell death. Giving durvalumab and belinostat may improve the body's ability to fight cancer.

开始日期2022-01-14

申办/合作机构

University of Utah

[+1]

100 项与贝林司他相关的临床结果

登录后查看更多信息

100 项与贝林司他相关的转化医学

登录后查看更多信息

100 项与贝林司他相关的专利（医药）

登录后查看更多信息

297

项与贝林司他相关的文献（医药）

2024-02-01·Saudi medical journal

Investigation of the effect of belinostat on MCF-7 breast cancer stem cells via the Wnt, Notch, and Hedgehog signaling pathway.

Article

作者: Zeliha Tuncer ; Ercan Kurar ; Tugçe Duran

OBJECTIVES:

To evaluate belinostat's (PXD101) activity on MCF-7 breast cancer stem cells (CSCs) via Wnt, Notch, and Hedgehog.

METHODS:

This research study was carried out at the Department of Medical Biology, Necmettin Erbakan University, Konya, Turkey, from June 2017 to July 2019. The effect of PXD101 on MCF-7 cell viability was determined by cell proliferation kit (XTT). Following belinostat treatment, CD44+/CD24- MCF-7 CSCs were isolated by FACS. Ribonucleic acid isolation and copy-deoxyribonucleic acid synthesis were carried out using HEK-293 cells, MCF-7 cells, and MCF-7 CSCs. Expression changes of metastasis-related genes, Wnt, Hedgehog, Notch, and stem cell markers were analysed by quantitative polymerase chain reaction. The IC50 in MCF-7 cancer cells was 5 μM for 48 hours. The FACS analysis indicated that 2% of the MCF-7 cancer cells were CSCs. Following belinostat treatment, the MCF-7 cell count decreased by 44%, and the MCF-7 CD44+/CD24- CSC count decreased by 66%.

RESULTS:

Belinostat treatment reduced the expression of metastasis, Wnt, Notch, Hedgehog, and stem cell marker genes.

CONCLUSION:

Belinostat has a potential effect on the differentiation and self-renewal of breast CSCs.

2024-01-01·PloS one

Integrated drug response prediction models pinpoint repurposed drugs with effectiveness against rhabdomyosarcoma.

Article

作者: Bin Baek ; Eunmi Jang ; Sejin Park ; Sung-Hye Park ; Darren Reece Williams ; Da-Woon Jung ; Hyunju Lee

Targeted therapies for inhibiting the growth of cancer cells or inducing apoptosis are urgently needed for effective rhabdomyosarcoma (RMS) treatment. However, identifying cancer-targeting compounds with few side effects, among the many potential compounds, is expensive and time-consuming. A computational approach to reduce the number of potential candidate drugs can facilitate the discovery of attractive lead compounds. To address this and obtain reliable predictions of novel cell-line-specific drugs, we apply prediction models that have the potential to improve drug discovery approaches for RMS treatment. The results of two prediction models were ensemble and validated via in vitro experiments. The computational models were trained using data extracted from the Genomics of Drug Sensitivity in Cancer database and tested on two RMS cell lines to select potential RMS drug candidates. Among 235 candidate drugs, 22 were selected following the result of the computational approach, and three candidate drugs were identified (NSC207895, vorinostat, and belinostat) that showed selective effectiveness in RMS cell lines in vitro via the induction of apoptosis. Our in vitro experiments have demonstrated that our proposed methods can effectively identify and repurpose drugs for treating RMS.

2023-12-28·Molecular cancer therapeutics

The methyltransferases METTL7A and METTL7B confer resistance to thiol-based histone deacetylase inhibitors.

Article

作者: Robert W Robey ; Christina M Fitzsimmons ; Wilfried M Guiblet ; William J E Frye ; José M González Dalmasy ; Li Wang ; Drake A Russell ; Lyn M Huff ; Andrew J Perciaccante ; Fatima Ali-Rahmani ; Crystal C Lipsey ; Heidi M Wade ; Allison V Mitchell ; Siddhardha S Maligireddy ; David Terrero ; Donna Butcher ; Elijah F Edmondson ; Lisa M Jenkins ; Tatiana Nikitina ; Victor B Zhurkin ; Amit K Tiwari ; Anthony D Piscopio ; Rheem A Totah ; Susan E Bates ; H Efsun Arda ; Michael M Gottesman ; Pedro J Batista

Histone deacetylase inhibitors (HDACis) are part of a growing class of epigenetic therapies used for the treatment of cancer. Although HDACis are effective in the treatment of T-cell lymphomas, treatment of solid tumors with this class of drugs has not been successful. Overexpression of the multidrug resistance protein P-glycoprotein (P-gp), encoded by ABCB1, is known to confer resistance to the HDACi romidepsin in vitro, yet increased ABCB1 expression has not been associated with resistance in patients, suggesting that other mechanisms of resistance arise in the clinic. To identify alternative mechanisms of resistance to romidepsin, we selected MCF-7 breast cancer cells with romidepsin in the presence of the P-gp inhibitor verapamil to reduce the likelihood of P-gp-mediated resistance. The resulting cell line, MCF-7 DpVp300, does not express P-gp and was found to be selectively resistant to romidepsin but not to other HDACis such as belinostat, panobinostat, or vorinostat. RNA sequencing analysis revealed upregulation of the mRNA coding for the putative methyltransferase, METTL7A, whose paralog, METTL7B, was previously shown to methylate thiol groups on hydrogen sulfide and captopril. As romidepsin has a thiol as the zinc-binding moiety, we hypothesized that METTL7A could inactivate romidepsin and other thiol-based HDACis via methylation of the thiol group. We demonstrate that expression of METTL7A or METTL7B confers resistance to thiol-based HDACis and that both enzymes are capable of methylating thiol-containing HDACis. We thus propose that METTL7A and METTL7B confer resistance to thiol-based HDACis by methylating and inactivating the zinc-binding thiol.

项与贝林司他相关的新闻（医药）

2024-04-01

·FierceBiotech

'One-two punch' of epigenetic cancer drugs could knock out colorectal cancer cells

An upcoming trial in patients with colorectal cancer will be the first to test an DNMT inhibitor and an EZH2 inhibitor together in any type of cancer. A pair of epigenetic cancer drugs packs a “one-two punch” against colorectal tumors to knock them out more effectively than either medication alone, a new study in cells suggests. In a journal article published March 27 in Science Advances, a team of researchers led by scientists from the Van Andel Institute in Grand Rapids, Michigan showed that a low dose of the DNA methyltransferase (DNMT) inhibitor decitabine combined with Tithe EZH2 inhibitor tazemetostat successfully induced changes that would make cancer cells more vulnerable to destruction by the immune system. The chemotherapy decitabine is commercialized by Eisai as Inqovi; tazemetostat is commercialized by Ipsen as Tazverik. Neither company was involved in the study. While agents in both classes of drugs are FDA approved to treat blood cancer, they haven't had much success in solid tumors such as colorectal cancer, Scott Rothbart, Ph.D., the study’s corresponding author, said in a press release. “Our findings highlight the promise of combination cancer therapies by revealing how these two medications interact, with the DNMT inhibitor priming cancer cells in a way that makes the EZH2 inhibitor more effective.” “Epigenetic” is a term that refers to typically reversible modifications made to genes that do not directly alter the genes themselves, but rather affect their expression. Cancer progression involves many epigenetic changes both to the cancer cells themselves and to the immune cells that would otherwise destroy them. Scientists have attempted to destroy cancer by countering these changes pharmacologically and restoring the expression of anti-cancer genes. The most established means of doing so is with histone deacetylase inhibitors, or HDAC inhibitors, such as Merck’s Zolinza (vorinostat) for lymphoma and Acrotech Biopharma’s Beleodaq (belinostat) for myeloma. The only other FDA-approved DNMT inhibitor besides Inquovi is Celgene’s acute myeloid leukemia drug Vidaza (azacitidine). Tazverik is the sole EZH2 inhibitor with FDA approval. Earlier work by Van Andel Institute researchers showed that DNMT inhibitors cause cancer cells to act as though they’ve been infected by a virus, making them more vulnerable to one’s immune system. For the new study, the researchers hypothesized that because DNMT inhibitors alter the cells in a way that could make EZH2 inhibitors more effective, they would work better together than separately. To see whether this was the case, the researchers started by testing them against different types of colorectal cancer cells on their own, then looked at them in combination. The results backed up their rationale: EZH2 inhibitors compounded the changes initiated by the DNMT inhibitors, boosting the duo’s effectiveness. The findings are the basis for an upcoming clinical trial that will evaluate the pair against colorectal cancer in patients. Combinations of DNMT inhibitors and HDAC inhibitors have been tested in clinical trials to mixed results, the study noted. The new trial will be the first to evaluate a DNMT inhibitor and an EZH2 inhibitor. Future studies should evaluate the pair with immunotherapies, too, Rothbart noted in the release. There’s evidence in preclinical models that the viruslike changes the drugs make in the cells could lead to a better response to drugs that boost the immune system. “These data suggest future directions for testing whether DAC and TAZ treatments might improve tumor response to immunomodulating agents,” the researchers wrote in the study.

上市批准免疫疗法临床研究

2024-03-10

·药渡

舒沃哲上市四个月卖9128 万，迪哲医药做对了什么？

来源：药渡撰文：四月的雨编辑：维他命近日，迪哲医药披露了2023年度业绩快报，2023年度实现营收9128.86万元。此外据报告显示，其2022年营收为零元，2021年度营收为1028.54万元，收入来源为向阿斯利康收取的技术支持服务费。迪哲医药在2023年业绩快报中表示，报告期内，公司首次实现产品销售收入，营收全部由其核心产品舒沃哲在上市后四个月的销售额贡献。舒沃哲的上市，开启了迪哲医药收入结构根本性转变之路。PART.01上市即王炸舒沃哲放量迅速舒沃哲（舒沃替尼）是迪哲医药首款进入商业化的源头创新产品。作为首款针对EGFR 20号外显子插入（exon20ins）突变型晚期非小细胞肺癌（NSCLC）的国创新药，舒沃哲于2023年8月23日通过优先审评程序在中国通过获批上市。图1. 舒沃替尼知识图谱，来源：药渡数据近20年来，EGFR Exon20ins突变一直缺乏安全有效的靶向治疗手段，患者生存获益短，是亟需解决的临床痛点。针对经治EGFR exon20ins突变型晚期NSCLC的中国注册临床研究显示，舒沃哲具有高效低毒、同类潜在最佳等优势，其主要研究终点独立影像评估委员会（IRC）确认的客观缓解率（ORR）达61%，突破现有治疗瓶颈（既往药物ORR均未达50%）。舒沃哲是肺癌领域首个获中、美双“突破性疗法认定”的国创新药，也是目前全球唯一获批上市的靶向EGFR exon20ins突变型NSCLC的小分子药物。上市首个季度，舒沃哲就取得了耀眼的商业化成绩。据迪哲医药披露的2023年第三季度季报显示，截至2023年9月30日舒沃哲已经拿下4010万元的销售收入，此时距离上市仅40天。如此耀眼的商业化表现很难不让资本市场掀起波澜，在披露三季报后的第二个交易日（2023年10月30日），迪哲医药股价涨幅超过10%。如今上市四个月卖出9128万销售额，更是引发了行业的广泛关注。与此同时，不禁要问，迪哲医药对舒沃哲做了怎样的“包装”？0124小时无缝接力，强大供应链显“神威”在舒沃哲获批的那一刻，迪哲就全面开启了“24小时不间断”商业化上市推进。在短短4天内，从定稿说明书、包材印刷、生产、包装、检验、质量放行、全国配送、上架、开单，公司和外部合作伙伴日夜兼程无缝接力，将舒沃哲送达全国各地。2023年8月26日上午11点23分，首批舒沃哲到达南京医药第一药店，门店第一时间完成验收入库、上架。获批后第4天正式开始面向全国各医院和药房供药，刷新非自有工厂（由药明康德旗下的合全药业代工）发货最快行业纪录，迪哲医药在供应链上下足了功夫。02销售市场持续投入，商业化团队成熟供应链的优势还不足以带动舒沃哲销售额飙涨，还需商业化团队“给力”。据其业绩预告称，为产品市场覆盖做好充分准备，自舒沃哲上市以来迪哲医药商业化团队不断扩大，在产品上市后的销售渠道部署以及市场推广等方面不断增加投入。迪哲医药是由阿斯利康（持股41.50%）与国投创新（持股41.50%）在2017年合资建立，可谓一出生就含着“金汤匙”。而迪哲医药营销负责人吴清漪于2019年6月加入百济神州，并于2021年9月离职后加入迪哲医药。迪哲医药的董事、监事、高级管理人员及核心技术人员中，多人有阿斯利康任职经历，吴清漪也有多年阿斯利康任职经历。论营销能力，阿斯利康在业内是“顶流”般的存在。03疗效——最好的营销强大的商业化团队和卓越的团队领导者，对于舒沃哲的加速放量起到了加持作用。但打铁还需自身硬，疗效才是最好的营销模式。在疗效方面，舒沃哲展示了卓越的实力：主要终点由独立影像评估委员会（IRC）根据RECIST 1.1评估确认的肿瘤缓解率（cORR）为60.8%，针对基线伴有经治且稳定的脑转移患者cORR达48.4%。抗肿瘤疗效覆盖多种突变亚型，无论Exon20ins突变亚型和插入位点如何，对在近环端（ORR=62%）、远环端（ORR=54%）和C-螺旋发生的插入突变（ORR=100%），均显示良好的抗肿瘤活性。治疗期间绝大多数患者出现的不良事件（AE）为CTCAE 1级或2级，可通过安全性管理进行恢复。半衰期更长（~50h），药物峰值和谷底浓度差更小（~2倍），有利于对靶点的持续抑制，且降低由于药物峰值浓度过高带来的不良事件发生。舒沃哲从国内首例临床研究受试者入组到获批上市，用时不到4年，建立肺癌靶向药临床推进速度新标准；从获批到首方，仅用4天，迪哲速度再创行业纪录。凭借扎实的源头创新和高效的商业运营，迪哲医药拿到了一张战力值超强的王牌。但迪哲医药的王牌远不止舒沃哲。PART.02王牌不止舒沃哲潜力管线加速集结迪哲医药以治疗肿瘤和免疫性疾病为目标，保持在转化科学及药化和分子设计领域的竞争优势。其以自主研发为主，着眼全球市场为发展战略。基于行业领先的转化科学和新药分子设计与筛选技术平台，迪哲医药已建立了五款具备全球竞争力的产品管线，除已获批上市的舒沃哲外，还有处于全球关键性临床试验阶段的戈利昔替尼。图2. 迪哲医药管线，来源：迪哲医药官网01JAK1抑制剂：戈利昔替尼戈利昔替尼是迪哲医药自主研发的新一代、强效且高选择性JAK1抑制剂，其首个申报上市的适应症为复发/难治性（r/r）外周T细胞淋巴瘤（PTCL），于2023年9月获药品监督管理局（NMPA）受理并纳入优先审评，此外正在中国、美国、韩国和澳大利亚等国家开展关键性临床试验。2022年2月，戈利昔替尼获FDA“快速通道认定”（Fast Track Designation），成为首个且唯一获FDA“快速通道认定”的PTCL国创新药，也是全球首个且唯一针对PTCL的高选择性JAK1抑制剂。JAK抑制剂自上市以来因其独特的作用机制，安全性和耐受性一直备受质疑，美国FDA已多次作出审查延迟的决定，并就多家药企研发的多款相关药物给出了黑框警告，有着JAK抑制剂“开山鼻祖”之称的辉瑞便是其中一员。据辉瑞长达6年的研究表明，作为自免领域全球首款JAK抑制剂的Tofacitinib会显著增加心脏相关副作用和致癌风险。基于这项研究结果，FDA对Tofacitinib添加“黑框警告”警示心脏安全和致癌风险。同一时间，收到FDA“红牌警告”的还有礼来的Baricitinib和艾伯维的Upadacitinib。此次风波，对JAK抑制剂的声誉和使用都造成了不小的打击。而戈利昔替尼是一种新一代、口服、强效、高选择性JAK1抑制剂，相比其他JAK抑制剂，对JAK1具有更高的选择性，有效地降低了泛JAK抑制导致的药物安全性风险。以此同时，戈利昔替尼还具备较好的药代动力学特征，因此可实现对JAK/STAT通路的持续有效抑制，同时确保临床安全性。国际多中心关键临床研究（JACKPOT8的B部分）中，戈利昔替尼单药显示出强效持久的抗肿瘤活性，客观缓解率（ORR）达44.3%，且其中一半以上肿瘤缓解的受试者达到了完全缓解（CR），CR率达23.9%，经独立影像评估委员会（IRC）评估的中位缓解持续时间（DoR）长达20.7个月。此外，临床试验研究也已证实戈利昔替尼与已获批用于治疗r/r PTCL的普拉曲沙、罗米地辛、贝林司他和西达本胺等药物相比，在疗效性和安全性上均具有明显优势。其实JAK1抑制剂最扎堆的适应症并不是肿瘤领域，而是自免领域，在迪哲医药筹划IPO上市之时（截至2021年8月），全球已获批上市的7款JAK1抑制剂中，只有诺华的芦可替尼获批了骨髓纤维化/真性红细胞增多症肿瘤相关适应症，而在研的JAK1抑制剂中，自免适应症也多过于肿瘤。据统计，2019年全球JAK1抑制剂市场规模约为55亿美元，预计到2030年将达305亿美元，可以说自免领域对JAK1抑制剂市场规模的贡献要大于肿瘤领域，或许是出于抢占市场的考虑，迪哲医药在开发戈利昔替尼的策略上，选择了先肿瘤后自免的思路。02LYN/BTK双靶点抑制剂：DZD8586除了戈利昔替尼外，另一款抗肿瘤药，即LYN/BTK双靶点抑制剂DZD8586也来头不小。DZD8586是迪哲自主研发的一款针对B细胞非霍奇金淋巴瘤（B-NHL）的非共价LYN/BTK双靶点抑制剂，可完全穿透血脑屏障。在现有的B-NHL治疗药物中，BTK抑制剂的耐药问题仍是全球性挑战。临床前研究表明，DZD8586可同时阻断BTK依赖性和非依赖性BCR信号通路，有效抑制多种B-NHL亚型细胞的生长，有望克服BTK抑制剂的耐药问题。前有舒沃哲在NSCLC领域大展拳脚，后有戈利昔替尼和DZD8586接力，共同打造差异化竞争优势的肿瘤和免疫产品矩阵，能取得这样的“突飞猛进”，离不开迪哲的重金研发。而又正是因为在研发上的大手笔投入，使得迪哲医药被退市争议缠身。PART.03亏损并不等于退市兑现期正在路上2023年度迪哲医药归属于母公司所有者的扣除非经常性损益后的净亏损达117,300 万元左右，比上年同期增加亏损38,800万元左右，同比亏损增加49%左右。亏损增大主要是因为公司各在研产品在稳步推进研发过程中，整体研发投入仍维持在较高水平。2023年，迪哲医药研发费用为81000万元左右，比上年同期增加14500万元左右，同比增加22%左右。在2023年9月7日的投资者关系活动会议上，有投资者担心迪哲医药是否会因为长期亏损退市，吕洪斌则表示：根据科创板上市规则，公司目前没有退市风险。据悉，根据上交所的规定，科创版带U的股票上市第四年起才会存在退市的风险，但是上交所可以根据实际情况调整退市指标，甚至对财务也没有考核。距离迪哲医药2021年12月在科创板鸣锣上市仅有两年之余，留给迪哲医药自证的时间还有两年。而这两年，正是舒沃哲销售额增长爆发期，加之戈利昔替尼获批在即，商业化产品矩阵将迎来新成员，或许属于迪哲医药的收获期才刚开始。参考资料：1、迪哲医药官网2、迪哲医药的野心：IPO的钱还没用完，还要融资？；华博商业评论3、迪哲医药顺利摘U已不远？；药渡Daily*声明：本文仅是介绍医药疾病领域研究进展或简述研究概况或分享医药相关讯息，并非也不会进行治疗或诊断方案推荐，也不对相关投资构成任何建议。内容如有疏漏，欢迎沟通指出！商业化权益收回——开始独当一面的中国创新药企利润飙升408.11%！微芯生物“两驾马车”驱动，研发之路高歌猛进这十款药物，今年有望获FDA批准！

优先审批上市批准财报突破性疗法临床研究

2023-12-21

·BioSpace

SELLAS Receives FDA Orphan Drug Designation for SLS009 for Treatment of Peripheral T-cell Lymphomas

- SLS009 Demonstrated Promising Efficacy in Phase 1 Study with 36.4% Clinical Response (ORR) in r/r Peripheral T-cell Lymphomas (PTCL); ORR in r/r PTCL Patients with Standard of Care is 25.8% - - One Patient with Complete Metabolic Response Continuing Treatment for over 62 weeks and another patient with Complete Response by CT Continuing Treatment for over 24 weeks - - Phase 1b/2 Study in PTCL Ongoing with top line data expected in 1H 2024 - NEW YORK, Dec. 21, 2023 (GLOBE NEWSWIRE) -- SELLAS Life Sciences Group, Inc. (NASDAQ: SLS) (“SELLAS’’ or the “Company”), a late-stage clinical biopharmaceutical company focused on the development of novel therapies for a broad range of cancer indications, today announced that the U.S. Food and Drug Administration (FDA) has granted Orphan Drug Designation (ODD) for SLS009, the Company’s novel and highly selective CDK9 inhibitor, for the treatment of relapsed/refractory (r/r) Peripheral T-cell Lymphomas (PTCL). “We are delighted to announce the FDA’s granting of ODD for SLS009, marking another significant milestone following the recent Fast Track Designation by the FDA for PTCL,” said Angelos Stergiou, MD, ScD h.c., President and Chief Executive Officer of SELLAS. “In the recently completed dose-escalation portion of the Phase 1 trial in r/r hematological malignancies, SLS009 achieved clinical responses in PTCL including two patients reaching complete response. We are excited to see a favorable safety profile, strong initial efficacy signals, and evidence of anti-tumor activity across the Phase 1 study as well as the ongoing Phase 2 studies. With both designations in hand, we look forward to advancing the development of SLS009 and continuing to work closely with regulators with the goal of delivering this treatment to those who may benefit from it.” As it relates to PTCL, SLS009 is currently being evaluated in a Phase 1b/2 trial in patients with r/r PTCL. The open-label, single-arm study will enroll up to 95 patients to evaluate safety and efficacy and, based on the results, may serve as a registrational study. This initial PTCL study is fully funded by GenFleet Therapeutics, Inc. and is being conducted in China. In the recently completed dose-escalation portion of the Phase 1 trial in r/r hematological malignancies, SLS009 demonstrated a favorable safety pro promising clinical efficacy. Complete or partial responses were observed in patients with acute myeloid leukemia as well as lymphoma, including four PTCL patients (36.4%) who achieved clinical responses with one patient with complete metabolic response who is continuing treatment for over 62 weeks, and another patient with complete response by CT scan who is continuing treatment for over 24 weeks. The current standard of care for r/r PTCL, belinostat, an HDAC inhibitor, showed in its pivotal Phase 2 study a 25.8% response rate in a similar patient population to that in the SLS009 Phase 1 clinical trial. The patients who achieved complete response in the SLS009 study were previously treated with regimens containing an HDAC inhibitor. The FDA’s Office of Orphan Products Development grants ODD status to drugs and biologics intended for the safe and effective treatment, diagnosis or prevention of rare diseases or conditions affecting fewer than 200,000 people in the United States. ODD provides benefits to drug developers designed to support the development of drugs and biologics for small patient populations with unmet medical needs. These benefits include assistance in the drug development process, tax credits for qualified clinical costs, exemptions from certain FDA fees and seven years of marketing exclusivity. About SELLAS Life Sciences Group, Inc. SELLAS is a late-stage clinical biopharmaceutical company focused on the development of novel therapeutics for a broad range of cancer indications. SELLAS’ lead product candidate, galinpepimut-S (GPS), is licensed from Memorial Sloan Kettering Cancer Center and targets the WT1 protein, which is present in an array of tumor types. GPS has potential as a monotherapy and combination with other therapies to address a broad spectrum of hematologic malignancies and solid tumor indications. The Company is also developing SLS009 (formerly GFH009), a small molecule, highly selective CDK9 inhibitor, which is licensed from GenFleet Therapeutics (Shanghai), Inc., for all therapeutic and diagnostic uses in the world outside of Greater China. For more information on SELLAS, please visit Forward-Looking Statements This press release contains forward-looking statements. All statements other than statements of historical facts are “forward-looking statements,” including those relating to future events. In some cases, forward-looking statements can be identified by terminology such as “plan,” “expect,” “anticipate,” “may,” “might,” “will,” “should,” “project,” “believe,” “estimate,” “predict,” “potential,” “intend,” or “continue” and other words or terms of similar meaning. These statements include, without limitation, statements related to the SLS009 clinical development program, including data therefrom, and regulatory strategy. These forward-looking statements are based on current plans, objectives, estimates, expectations and intentions, and inherently involve significant risks and uncertainties. Actual results and the timing of events could differ materially from those anticipated in such forward-looking statements as a result of these risks and uncertainties, which include, without limitation, risks and uncertainties with oncology product development and clinical success thereof, the uncertainty of regulatory approval, and other risks and uncertainties affecting SELLAS and its development programs as set forth under the caption “Risk Factors” in SELLAS’ Annual Report on Form 10-K filed on March 16, 2023 and in its other SEC filings. Other risks and uncertainties of which SELLAS is not currently aware may also affect SELLAS’ forward-looking statements and may cause actual results and the timing of events to differ materially from those anticipated. The forward-looking statements herein are made only as of the date hereof. SELLAS undertakes no obligation to update or supplement any forward-looking statements to reflect actual results, new information, future events, changes in its expectations or other circumstances that exist after the date as of which the forward-looking statements were made. Investor Contact Bruce Mackle Managing Director LifeSci Advisors, LLC SELLAS@lifesciadvisors.com

临床结果孤儿药临床1期临床2期快速通道

100 项与贝林司他相关的药物交易

登录后查看更多信息

外链

KEGG	Wiki	ATC	Drug Bank
D08870	贝林司他	L01XX49	DB05015

研发状态

适应症	最高研发状态	国家/地区	公司
外周T细胞淋巴瘤	批准上市	美国更多	Acrotech Biopharma LLC初创企业更多
复发型外周T细胞淋巴瘤	临床1期	中国更多	盛世泰科生物医药技术（苏州）有限公司更多
难治性外周T细胞不明淋巴瘤	临床1期	中国更多	盛世泰科生物医药技术（苏州）有限公司更多
多发性骨髓瘤	终止	美国更多	Topotarget A/S 更多
皮肤T细胞淋巴瘤	终止	泰国更多	Valerio Therapeutics SA 更多

登录后查看更多信息

临床结果

适应症

分期

评价

查看全部结果

研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT03772925 (ASCO2023) 人工标引	临床1期	复发性急性髓细胞白血病 \| 难治性急性髓细胞白血病 \| 骨髓增生异常综合征	18	Belinostat+Pevonedistat	(積蓋廠憲淵構壓繭製繭) = MTD was not reached in this study. 網淵鏇膚構遞膚製願糧 (襯齋夢範積糧鑰積獵窪 ) 更多	积极	2023-05-31
Pubmed 人工标引	临床2期	肉瘤	41	Doxorubicin+PXD101	(獵糧繭鬱鏇繭築衊構齋) = 網顧願憲鏇觸衊範憲壓鹹窪憲餘積憲築夢淵膚 (廠廠觸遞衊鹽選夢夢積 ) 更多	积极	2016-01-01
NCT00303953 (SWOG S0520, Pubmed \| Leukemia) 人工标引	临床2期	弥漫性大B细胞淋巴瘤	22	belinostat	(範觸鏇繭淵獵築製壓觸) = 襯廠網顧窪鏇壓鹽獵鏇窪夢鏇壓襯願範簾觸選 (願願願淵艱膚觸淵醖衊, 1.3 ~ 33.1) 更多	积极	2016-10-01
NCT00926640 (Pubmed \| Anticancer Drugs) 人工标引	临床1期	HR阳性/HER2低表达实体瘤	28	Belinostat+cisplatin+etoposide	(淵鹹願壓顧鏇願築糧醖) = Hematologic toxicities 製齋廠衊糧繭鑰構積範 (窪顧構醖餘蓋壓淵廠積 ) 更多	积极	2018-06-01
NCT02137759 (Pubmed) 人工标引	临床2期	胶质母细胞瘤一线	13	Belinostat	(壓願醖獵蓋淵壓膚鏇製) = 觸選齋鹹糧遞醖觸繭鹽顧鏇鏇壓簾夢獵選齋鹹 (獵範膚積齋艱壓窪簾觸 )	积极	2022-03-03
NCT02137759 (Pubmed) 人工标引	临床2期	胶质母细胞瘤一线	13	Chemoradiotherapy	(壓願醖獵蓋淵壓膚鏇製) = 鑰獵醖獵艱積獵淵構鏇顧鏇鏇壓簾夢獵選齋鹹 (獵範膚積齋艱壓窪簾觸 )	积极	2022-03-03
NCT01839097 (Pubmed \| Exp Hematol Oncol) 人工标引	临床1期	外周T细胞淋巴瘤一线	23	CHOP+Belinostat	(壓獵醖憲選鹽蓋夢鬱繭) = Day 1-5 schedule with 1000 mg/m2 糧簾鑰鏇選糧顧製觸顧 (夢鹹糧選衊醖遞糧鹹觸 ) 更多	积极	2021-02-18
NCT01273155 (Pubmed \| Br J Clin Pharmacol) 人工标引	临床1期	Gilbert病 \| 肿瘤	72	Belinostat	(醖鏇顧襯艱願醖積選窪) = 鹹繭鏇衊網糧網夢餘廠範獵鏇壓鬱齋糧製遞廠 (選壓衊製觸廠窪築積鬱 ) 更多	积极	2019-11-01
NCT01317927 (Pubmed \| Cancer Chemother Pharmacol) 人工标引	临床1期	肿瘤	18	warfarin+belinostat	(願獵蓋廠觸齋襯願艱窪) = diarrhea 5.6 %, nausea 5.6 %, and vomiting 5.6 % 鹹淵製獵廠鏇鑰齋膚醖 (觸鏇製範遞鑰膚構願艱 ) 更多	积极	2016-02-01
NCT00873119 (Pubmed \| Cancer) 人工标引	临床2期	原发部位不明恶性肿瘤一线	89	paclitaxel or carboplatin+belinostat	(淵範觸遞願夢餘夢積淵) = 簾壓顧窪糧選齋遞顧壓糧淵鏇顧構齋蓋蓋餘築 (鏇蓋築蓋壓廠壓製積餘, 3.0 ~ 6.0) 更多	不佳	2015-05-15
NCT00873119 (Pubmed \| Cancer) 人工标引	临床2期	原发部位不明恶性肿瘤一线	89	paclitaxel or carboplatin	(淵範觸遞願夢餘夢積淵) = 鬱夢蓋選願窪鏇鏇糧淵糧淵鏇顧構齋蓋蓋餘築 (鏇蓋築蓋壓廠壓製積餘, 2.8 ~ 6.6) 更多	不佳	2015-05-15
NCT00865969 (CLN-19 \| BELIEF, Pubmed \| J Urol) 人工标引	临床2期	外周T细胞淋巴瘤二线	129	belinostat	(積淵餘膚夢願鹽襯鏇觸) = 獵膚壓壓淵積鏇簾鹹壓淵築構鹹壓鬱膚窪積夢 (繭選觸壓夢齋網膚齋鑰 ) 更多	积极	2015-08-10