Phase II Neoadjuvant Trial of Nivolumab in Combination With HF10 Oncolytic Viral Therapy in Resectable Stage IIIB, IIIC, IVM1a Melanoma (Neo-NivoHF10)

This is a single-arm, open label, Phase II study evaluating the safety and efficacy of neoadjuvant Nivolumab and HF10 in resectable stage IIIB, IIIC, and IVM1a melanoma.

开始日期2018-01-03

申办/合作机构

University of Utah

[+2]

ISRCTN87648175 / RecruitingN/A

A multi-center, prospective, pragmatic, randomized, controlled clinical trial to compare HF10 therapy to Conventional Medical Management in the treatment of Non-Surgical Refractory Back Pain

开始日期2017-10-31

申办/合作机构

Nevro Corp.

NCT03252808 / Active, not recruiting临床1期

Phase I Study of Combination With TBI-1401(HF10), a Replication-competent HSV-1 Oncolytic Virus, and Chemotherapy in Patients With Stage III or IV Unresectable Pancreatic Cancer.

The purpose of this study is to determine the recommended dose of TBI-1401(HF10) treatment in combination with chemotherapy (Gemcitabine + Nab-paclitaxel or TS-1) in patients with stage III or IV unresectable pancreatic cancer.

开始日期2017-09-25

申办/合作机构

Takara Bio, Inc.

100 项与 Canerpaturev(University of Utah) 相关的临床结果

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100 项与 Canerpaturev(University of Utah) 相关的转化医学

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100 项与 Canerpaturev(University of Utah) 相关的专利（医药）

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项与 Canerpaturev(University of Utah) 相关的文献（医药）

2023-07-31·Life (Basel, Switzerland)

New Treatment Horizons in Uveal and Cutaneous Melanoma.

Review

作者: Zemba, Mihail ; Nicolescu, Alin Codruț ; Moraru, Andreea Dana ; Brănişteanu, Cătălina Ioana ; Porumb, Vlad ; Brănişteanu, George ; Stărică, Alexandra ; Brănişteanu, Daniel Constantin ; Porumb-Andrese, Elena ; Brănişteanu, Daciana Elena

Melanoma is a complex and heterogeneous malignant tumor with distinct genetic characteristics and therapeutic challenges in both cutaneous melanoma (CM) and uveal melanoma (UM). This review explores the underlying molecular features and genetic alterations in these melanoma subtypes, highlighting the importance of employing specific model systems tailored to their unique profiles for the development of targeted therapies. Over the past decade, significant progress has been made in unraveling the molecular and genetic characteristics of CM and UM, leading to notable advancements in treatment options. Genetic mutations in the mitogen-activated protein kinase (MAPK) pathway drive CM, while UM is characterized by mutations in genes like GNAQ, GNA11, BAP1, EIF1AX, and SF3B1. Chromosomal aberrations, including monosomy 3 in UM and monosomy 10 in CM, play significant roles in tumorigenesis. Immune cell infiltration differs between CM and UM, impacting prognosis. Therapeutic advancements targeting these genetic alterations, including oncolytic viruses and immunotherapies, have shown promise in preclinical and clinical studies. Oncolytic viruses selectively infect malignant cells, inducing oncolysis and activating antitumor immune responses. Talimogene laherparepvec (T-VEC) is an FDA-approved oncolytic virus for CM treatment, and other oncolytic viruses, such as coxsackieviruses and HF-10, are being investigated. Furthermore, combining oncolytic viruses with immunotherapies, such as CAR-T cell therapy, holds great potential. Understanding the intrinsic molecular features of melanoma and their role in shaping novel therapeutic approaches provides insights into targeted interventions and paves the way for more effective treatments for CM and UM.

2021-11-01·Nagoya journal of medical science4区 · 医学

S-1 facilitates canerpaturev (C-REV)-induced antitumor efficacy in a triple-negative breast cancer model.

4区 · 医学

Article

作者: Kasuya, Hideki ; Kikumori, Toyone ; Morimoto, Daishi ; Tanaka, Maki ; Miyajima, Noriyuki ; Mukoyama, Nobuaki ; Matsumura, Shigeru ; Ragab Eissa, Ibrahim ; Bustos-Villalobos, Itzel ; Takeuchi, Dai ; Ichinose, Toru ; Kodera, Yasuhiro ; Tsunoda, Nobuyuki ; Naoe, Yoshinori ; Abdelmoneim, Mohamed ; Shibata, Masahiro

Canerpaturev (C-REV) is a highly attenuated, replication-competent, mutant strain of oncolytic herpes simplex virus type 1 that may be an effective new cancer treatment option. S-1, an oral formulation containing the 5-fluorouracil (5-FU) prodrug tegafur and the two enzyme modulators gimeracil and oteracil, is used as a key chemotherapeutic agent for metastatic recurrent breast cancer. Although the antitumor effects of oncolytic viruses combined with 5-FU in vivo have been reported, the detailed mechanisms are unknown. Here, we investigated the antitumor mechanism of the combination of C-REV and S-1 in triple-negative breast cancer (TNBC) in the context of tumor immunity. The combined effect of C-REV and S-1 was evaluated in a bilateral tumor model of murine TNBC 4T1 in vivo. S-1 enhanced the TNBC growth inhibitory effects of C-REV, and decreased the number of tumor-infiltrating, myeloid-derived suppressor cells (MDSCs), which suppress both innate and adaptive immune responses. Moreover, C-REV alone and in combination with S-1 significantly increased the number of CD8⁺ T cells in the tumor and the production of interferon γ (IFNγ) from these cells. Our findings indicate that C-REV suppresses TNBC tumor growth by inducing the expansion of effector CD8⁺ T cell subsets in tumors in which S-1 can inhibit MDSC function. Our study suggests that MDSCs may be an important cellular target for breast cancer treatment. The combination of C-REV and S-1 is a new approach that might be directly translated into future clinical trials against TNBC.

2021-10-01·Translational cancer research4区 · 医学

The efficacy and safety of oncolytic viruses in the treatment of intermediate to advanced solid tumors: a systematic review and meta-analysis

4区 · 医学

Article

作者: Gao, Peng ; Wang, Lujia ; Ding, Guanxiong

BACKGROUND:

Cancer treatment remains one of the most formidable challenges worldwide. Some novel treatment strategies, including molecularly targeted therapy, gene therapy, and cellular immunotherapy, have also been investigated to improve therapeutic effects for cancer patients and have demonstrated unexpected positive effects. This systematic review and meta-analysis evaluated the efficacy and safety of oncolytic virus (OV) monotherapy or combination therapy for intermediate to advanced solid tumors.

METHODS:

We retrieved articles from PubMed, Embase, Web of Science, CNKI, Wanfang and VIP. The quality of the included studies was assessed by Review Manager Software version 5.3. STATA software was used to perform meta-analyses of efficacy, overall survival (OS) and adverse reactions.

RESULTS:

A total of 22 studies involving 3,996 patients were included in this analysis, including 13 H101 studies, 5 T-VEC studies, 2 Pexa-Vec studies, 1 HF10 study and 1 Reolysin study. Regarding oncolytic adenovirus H101, meta-analysis showed that patients treated with H101 monotherapy or H101 combined with chemotherapy had a significantly higher objective response rate (ORR) than those treated with chemotherapy. Patients in the H101 and T-VEC groups had significantly longer effect size (ES) than the control group patients. The odds ratio (OR) and ES of patients with hepatocellular carcinoma, lung cancer and melanoma treated with OV were analyzed. For the safety profile, the total incidence of adverse reactions was similar in both groups. In terms of the other OVs, according to a systematic review, we found that after Reolysin treatment, the ORR was 26.9% in patients with head and neck cancer. The phase I study of HF10 exhibited some therapeutic potential. The adverse events (AEs) associated with the other OVs mainly included fever, nausea and vomiting, leukopenia, and hypotension.

DISCUSSION:

OVs are effective and well tolerated for the treatment of intermediate to advanced solid cancer and represent a promising therapeutic approach for solid cancers.

项与 Canerpaturev(University of Utah) 相关的新闻（医药）

2022-09-29

·生物制品圈

胰腺癌溶瘤病毒疗法研究综述

胰腺癌属致命恶性肿瘤之一，死亡率居世界第七位，主要分为胰腺导管腺癌（PDAC）和胰腺神经内分泌肿瘤。胰腺癌具有高度转移倾向，大部分患者诊断即为晚期，其化疗耐药性和特殊的肿瘤微环境会影响治疗效果，不可通过手术切除的局部晚期胰腺癌患者（LAPC）生存率小于5%。晚期常出现腹痛、恶心、中背痛、体重减轻、阻塞性黄疸、胃肠道 (GI) 出血、静脉血栓栓塞 (VTE)等相关症状。目前临床上针对LAPC患者常使用放化疗（CRT）结合吉西他滨等药物治疗，而转移性PDAC患者使用FOLFIRINOX（亚叶酸、5-氟尿嘧啶、伊立替康和奥沙利铂）能有效延长生存期。除了常规治疗手段，近来免疫疗法特别是溶瘤病毒疗法备受关注。近日，Frontiers in Oncology杂志刊登了题为《An Extensive Review on Preclinical and Clinical Trials of Oncolytic Viruses Therapy for Pancreatic Cancer》的研究综述，详细阐述了胰腺癌进展的分子机制以及总结了2000年以来已发表的溶瘤病毒疗法临床研究。胰腺癌细胞基因突变及分子机制研究发现，胰腺癌中大量聚集癌症干细胞（CSC），可能导致化疗耐药，肿瘤转移和复发，而产生CSC富集现象与上皮间充质转化（EMT）相关。针对各类胰腺癌进行全基因组测序分析，报告显示平均每个胰腺癌患者有63个突变，相关信号通路在大部分肿瘤中被阻断。“关于EMT-MET上皮细胞由于细胞黏附分子(如E-钙黏蛋白)表达减少、细胞角蛋白细胞骨架转化为波形蛋白（Vimentin）为主的细胞骨架，转变为间充质细胞，获得了较高的迁移与侵袭、抗凋亡和降解细胞外基质等能力。癌细胞在EMT激活后获得侵袭特性，从而导致癌细胞转移。当癌性间充质细胞到达（转移部位）时，会再次经历间充质-上皮转化 (MET)，以恢复上皮表型。miRNA失调MicroRNAs (miRNAs) 是小的非编码RNAs（20-25 nt），可调节靶mRNA的翻译。许多表达失调的miRNA与胰腺癌进展相关，如肿瘤转移、肿瘤耐药、癌症干性。过表达上调：过表达miR-301通过抑制胰腺癌细胞中E-cadherin的表达来调节EMT并导致吉西他滨耐药；过表达miR-296-5p靶向并下调BOK（凋亡调节基因），促进EMT、癌症侵袭和耐药性；过表达miR-103/107、miR-9、miR-181a促进EMT相关信号传导。干扰下调：胰腺癌细胞中Let-7和miR-200家族miRNA表达下调，抑制 Notch信号传导。在发现了 Let-7 和 miR-200 的下调；miR-148a、miR-141、miR-200家族、miR-216a、miR-217和miR-375等其他miRNA在胰腺癌中表达水平降低。K-Ras基因突变K-Ras蛋白是一种小GTPase转导蛋白，通过将外部信号传递到细胞核来调节细胞分裂。其在酪氨酸激酶激活后被激活，表皮生长因子 (EGF)与其受体结合，为表皮生长因子受体 (EGFR)。活化的K-Ras与GTP结合并通过MAPK和P13K/Akt引导的级联将活化信号转导到细胞核，从而调节细胞转化。致癌K-Ras基因突变使K-Ras因GTP水解被抑制而永久激活，导致对化学疗法产生抗性。在胰腺癌患者中，K-Ras基因突变高度发生且参与肿瘤形成发展，可作为重要治疗靶点。近日，一种直接共价靶向G12C突变体KRAS的策略揭示了潜在的动态药物结合位点，其他直接抑制K-Ras的基于结构的药物设计项目正在进行中。P13K信号通路磷脂酰肌醇3-激酶(PI3K)信号级联激活与生长因子刺激和细胞因子有关。细胞因子通过高亲和力细胞表面受体酪氨酸激酶(RTK)进入癌细胞，P13K下游信号通过进一步激活其他信号通路介导各种致癌功能，如癌细胞代谢、生长和运动。在PDAC和K-Ras构建的胰腺癌小鼠模型中P13K/Akt被激活，控制黏蛋白（MUC1）介导的放化疗法抗性。由此，MUC1-P13k信号的调节可作为胰腺癌的有效治疗靶点，使用P13K特异性抑制剂和下游信号分子衰减剂可尝试治疗PDAC患者。MAPK信号通路丝氨酸-苏氨酸激酶（MAPK），参与与各种细胞活动，如增殖、分化、转化和凋亡相关的细胞内信号传导，包括ERK（细胞外信号调节激酶）、JNK（c-Jun NH2-末端激酶）和p38。MAPK信号通路的中断显著加快了胰腺癌的进展。靶向MAPK信号下游基因可能使胰腺癌治疗效果提高。TGF-β信号通路转化生长因子-β（TGF-β）包含TGF- β、骨形态发生蛋白(BMP)和激活素/抑制素，调节细胞迁移、分化、增殖、凋亡和EMT等功能，在胰腺癌癌症初期通过阻止细胞周期进程和促进细胞凋亡表现肿瘤抑制特性，在癌症晚期阶段通过增强转移表达肿瘤促进特性。在靶向TGF-β的临床前试验中，与免疫检查点抑制剂联合使用时，靶向药物疗效改善。缺氧信号通路在各种实体瘤中可以观察到缺氧介导的治疗抗性和生物学变化导致肿瘤转移率增加。肿瘤细胞通过刺激某些对氧敏感的信号通路进行反应，包括缺氧诱导因子1/2 (HIF1/2)信号通路和未折叠蛋白反应(UPR)，缺氧信号级联的变化导致新血管形成，最终导致肿瘤侵袭。胰腺癌中缺氧区域与不良预后和肿瘤发展有关，可作为胰腺癌恶性肿瘤的潜在治疗靶点。Wnt信号通路Wnt信号通路是一种进化保守的调控通路，包括非经典平面细胞极性(PCP)通路、非经典 Wnt/钙通路和经典通路，主要在细胞增殖、分化和存活中起作用。在胰腺癌中，该通路通过调节EMT、血管生成、细胞凋亡、干性和肿瘤微环境来促进癌变，瘤内经典Wnt配体过表达，通路持续激活也与胰腺癌耐药性有关。Notch信号通路Notch信号通过配体与Notch受体的结合而激活，显著促进细胞增殖、存活和分化。在癌症中，通过表达EMT标志物来促进细胞运动和侵袭特性，且会根据细胞环境发挥肿瘤抑制和致癌双重作用。胰腺癌中，Notch过表达，起致癌作用，信号通路的再激活也与胰腺癌的发生和进展有关，因此可作为胰腺癌有效生物标志物和治疗靶点。溶瘤病毒疗法癌症免疫疗法通过增强机体免疫系统识别和破坏癌细胞，溶瘤病毒（OVs）疗法作为一种新型的靶向免疫疗法，通过裂解作用选择性地消灭癌细胞，从而产生抗肿瘤免疫。由于肿瘤细胞内信号通路失调，使得病毒对异常的肿瘤细胞具有靶向选择性，而抗病毒信号传导的主要蛋白质编码基因突变导致的功能不完全丧失，有助于肿瘤细胞中的病毒复制，中断的信号传导也受到抑制以提高溶瘤病毒治疗的效果。研究表明，将相关信号通路抑制剂与溶瘤病毒协同作用，增强了病毒的细胞毒性，在癌症治疗中良好的临床治疗效果。（图为溶瘤病毒设计各通路靶点的应用汇总）腺病毒腺病毒是是非包膜双链DNA病毒，具有二十面体衣壳，55种血清型，通过柯萨奇和腺病毒受体（CAR）进入细胞。设计工程化腺病毒旨在提高抗肿瘤疗效和癌细胞选择性。临床前试验：① 溶瘤腺病毒Ad5/3-E2F-d24-vIL2使用具有携带Ad5型核酸和Ad3-Fiber的病毒基因组骨架，编码vIL-2、IL-2免疫调节变体蛋白。62%的小鼠模型显示出长期存活率以及免疫反应的激活。② 溶瘤腺病毒AdNuPAR-E-miR222-S外包被聚乙二醇化寡肽修饰的聚β-氨基酯，避免中和抗体产生，通过干扰miR-222在胰腺癌细胞中表达，有效控制了PANC-1肿瘤小鼠模型进展。③ 重组腺病毒DNX-2401易在具有缺陷P16 / RB / E2F通路的细胞中复制，有效抑制胰腺癌细胞系中肿瘤细胞的进展。在I期临床试验中显示针对脑癌的有效结果。临床试验：单纯疱疹病毒单纯疱疹病毒是包膜双链DNA病毒，具有二十面体衣壳，通过HVEM、nectin1、nectin2受体进入细胞，常用的工程化疱疹病毒有T-VEC, G207, HF10, HSV1716和OrienX010。临床前试验：① 具有突变ICP6基因的Myb34.5单纯疱疹病毒1型（HSV-1），在过表达β-myb基因的胰腺肿瘤细胞中显示有效的复制，与吉西他滨低剂量组合治疗小鼠模型，能够有效减小肿瘤大小。② 重组单纯疱疹病毒HSVGM-CS缺失3个基因（γ134.5，ICP47和ICP6），过表达GM-CSF。在基于胰腺癌细胞系的测试中发现，甲氨蝶呤（MTX）影响HSV-1在肿瘤细胞中的复制；5-氟尿嘧啶（5-FU），伊立替康（CPT-11），细胞因子如肿瘤坏死因子-α（TNF-α）与HSV-1联合用药改善了病毒复制并增加HSV-1的活性。临床试验：呼肠孤病毒呼肠孤病毒是非包膜分节段双链RNA病毒，对人体具有非致病性，通常选择性感染K-Ras、BRAF、EGFR突变的肿瘤细胞并复制。临床前试验：① 呼肠孤病毒（Reolysin）与硼替佐米（BZ）联合治疗胰腺癌，体外和体内测试发现增强了癌细胞凋亡，抗癌反应水平高。② 重组呼肠孤病毒rS1-mmGMCSF表达小鼠GM-CSF，临床前胰腺癌小鼠模型试验显示改善了免疫细胞（DC、 T细胞）全身抗肿瘤活性。③ 呼肠孤病毒与CD3-双特异性抗体（CD3-bsAbs）分别给药胰腺癌模型，病毒显著增强（CD3-bsAbs）抗肿瘤疗效，诱导了非注射远端病变的消退。临床试验：牛痘病毒牛痘病毒是包膜双链DNA病毒，设计工程化牛痘病毒增强胰腺癌细胞特异性裂解作用。临床前试验：① 牛痘病毒mpJX-594（mpJX）联合抗程序性死亡受体-1抗体（PD1）在小鼠胰腺神经内分泌肿瘤模型中提高抗肿瘤免疫反应，细胞凋亡水平增加，增殖减少。② 重组牛痘病毒VVL-21表达B5R和白细胞介素-21（IL-21）基因，在胰腺癌转移性小鼠和仓鼠模型中全身给药VVl-21与α程序性细胞死亡蛋白1（α-PD1），免疫细胞中CD8+T细胞、自然杀伤细胞和巨噬细胞活性水平增加。③ 重组牛痘病毒VV-ING4表达生长抑制剂ING4基因。在胰腺癌小鼠模型中测试VV-ING4单独使用发现其有效诱导癌细胞毒性和凋亡，与吉西他滨联合治疗中，VV-ING4改善吉西他滨抗癌疗效。④ 重组牛痘病毒vvdd-tdtomato-hGMCSF表达GMCSF基因，在免疫功能正常的仓鼠上测试，表达牛痘病毒的GMCSF有助于通过中性粒细胞和巨噬细胞的激活和侵袭完全清除皮下胰腺病变。临床试验：细小病毒细小病毒是非包膜单链DNA病毒，可降低胰腺癌细胞中IG和HERV的水平，减弱细胞先天免疫。临床前试验：① 腹膜转移的胰腺癌小鼠模型中，在肿瘤内注射H-1PV导致肿瘤减少，同时注射IFNγ，进一步改善了机体免疫反应。② 携带细胞趋化因子IL-2、MCP-3/CCL7和IP-10/CXCL10的细小病毒在胰腺癌异种移植中抗肿瘤疗效显著，表达IL-12的细小病毒比其他两种变体表现出更强的抗肿瘤反应。临床试验：麻疹病毒麻疹病毒是包膜单链负义RNA病毒，通过信号传导淋巴细胞活化分子（SLAM）受体或CD46受体进入细胞。临床前试验：① 重组麻疹病毒MeV-CD-FmiRTS148a表达5-氟胞嘧啶及前体，在胰腺癌异种移植模型中瘤内注射，治疗的小鼠显示出肿瘤大小减小，无进展生存期延长。少量MeV与吉西他滨联合给药，肿瘤体积减小大于50%。② 麻疹病毒MV-EGFPmtd编码miRTS（miR-122，miR-7和miR-148a），在体外和体内测试发现MV-EGFPmtd的高靶向胰腺癌细胞。水疱性口炎病毒水疱性口炎病毒是包膜非分段负义RNA病毒，优先在肿瘤细胞中感染复制。临床前试验：① 混合水疱性口炎病毒（VSV-FH）替换了麻疹病毒包膜蛋白F、H，通过突变K174E和E238K，降低了肿瘤对VSV的耐药性。② 重组VSV-ΔM51变异体通过下调IFN信号传导，并联合小分子抑制剂，显著消除了胰腺癌细胞中VSV耐药性。新城疫病毒新城疫病毒是包膜单链负义RNA病毒，通过病毒内吞作用或质膜融合进入细胞，对人类不具有致病性。因癌细胞过表达I型IFN、Bcl-xL和小GTPase，NDV选择性地在癌细胞中感染和复制。临床前试验：① 在小鼠低表达TGF-β模型中静脉注射NDV，发现肿瘤有效减少，无进展生存期延长。② 在异种移植模型肿瘤内注射rNDV-F3aa，显示肿瘤消退和抗肿瘤细胞毒性。小结溶瘤病毒疗法通过工程化插入外源基因或miRNA提高了胰腺癌治疗的有效性、特异性和安全性，特别是跟吉西他滨联合给药时，能显著降低吉西他滨的高剂量毒性，同时得到有效的临床结果。针对胰腺癌细胞中受损通路的有效靶点，设计特异的溶瘤病毒将是一种安全且有前景的治疗方式。（图为吉西他滨与重组或天然溶瘤病毒联合治疗相关的临床前研究汇总）

抗体免疫疗法放射疗法信使RNA

2021-01-11

·BioSpace

Nevro Announces Preliminary, Unaudited Fourth Quarter and Full-Year 2020 Revenue

REDWOOD CITY, Calif., Jan. 11, 2021 /PRNewswire/ -- Nevro Corp. (NYSE: NVRO), a global medical device company that is providing innovative, evidence-based solutions for the treatment of chronic pain, today announced its preliminary, unaudited revenue for the fourth quarter and full-year ended December 31, 2020. Fourth Quarter 2020 Preliminary, unaudited fourth quarter 2020 worldwide revenue is expected to be $109.7 million, compared to $114.4 million in the fourth quarter in the prior year period. Preliminary, unaudited fourth quarter 2020 U.S. revenue is expected to be $94.6 million, compared to $97.9 million in the prior year period. Preliminary, unaudited fourth quarter 2020 international revenue is expected to be $15.1 million, compared to $16.5 million in the prior year period. Fourth quarter U.S. trial procedures were down approximately 8% versus prior year. Full-Year 2020 Nevro's preliminary, unaudited full year 2020 worldwide revenue is expected to be $362.0 million, compared to $390.3 million in the prior year period. Preliminary, unaudited full year U.S. revenue is expected to be $311.9 million, compared to $326.0 million in the prior year period. Preliminary, unaudited full year international revenue is expected to be $50.2 million, compared to $64.3 million in the prior year period. "Despite the challenges created by the COVID-19 pandemic in 2020, I am extremely proud of the significant efforts of the Nevro team to serve our customers and patients, and execute on our plans for the future," said D. Keith Grossman, Chairman, CEO and President of Nevro. "In the second half of the fourth quarter, the increase in COVID activity negatively affected both trial and permanent implant volumes. Even with the pandemic challenges throughout the year, we continued to capture share in the core lower back and leg pain market with our best-in-class SCS technology, superior clinical data and sharpened execution. I believe we are well positioned for attractive growth when the pressure of COVID on our business subsides. In addition, we are excited about expanded growth opportunities to treat Painful Diabetic Neuropathy and Non-Surgical Refractory Back Pain, which will bring our HF10 therapy to the many patients who are unable to find relief with currently available treatment options." Nevro plans to report its full financial results and provide more detail for its fourth quarter and full-year 2020 financial results after the market closes on Wednesday, February 24, 2021, to be followed by its quarterly conference call at 1:30 pm Pacific Time that day. Nevro to Present at J.P. Morgan Healthcare Conference D. Keith Grossman, Chairman, CEO and President of Nevro, will present at the J.P. Morgan Healthcare Conference on Tuesday, January 12, 2021, at 4:30 pm Eastern Time / 1:30 pm Pacific Time. A live webcast of this event, as well as an archived recording, will be available in the Investors section of Nevro's website at . Internet Posting of Information Nevro routinely posts information that may be important to investors in the "Investor Relations" section of its website at . The company encourages investors and potential investors to consult the Nevro website regularly for important information about Nevro. About Nevro Corp. Headquartered in Redwood City, California, Nevro is a global medical device company focused on providing innovative products that improve the quality of life of patients suffering from debilitating chronic pain. Nevro has developed and commercialized the Senza spinal cord stimulation (SCS) system, an evidence-based, non-pharmacologic neuromodulation platform for the treatment of chronic pain. HF10 therapy has demonstrated the ability to reduce or eliminate opioids in ≥65% of patients across six peer-reviewed clinical studies. The Senza® System, Senza II™ System, and the Senza® Omnia™ System are the only SCS systems that deliver Nevro's proprietary HF10® therapy. Senza, Senza II, Senza Omnia, HF10, Nevro and the Nevro logo are trademarks of Nevro Corp. To learn more about Nevro, connect with us on LinkedIn, Twitter, Facebook and Instagram. Forward-Looking Statements In addition to historical information, this press release contains forward-looking statements reflecting the current beliefs and expectations of management made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995, including: the company's expectations for its fourth quarter and full year 2020 worldwide, U.S. and international revenue; our belief that we are well positioned for attractive growth when the pressure of COVID on our business subsides; and our excitement about expanded growth opportunities to treat Painful Diabetic Neuropathy and Non-Surgical Refractory Back Pain. These forward-looking statements are based upon information that is currently available to us or our current expectations, speak only as of the date hereof, and are subject to numerous risks and uncertainties, including our ability to successfully commercialize our products; our ability to manufacture our products to meet demand; the level and availability of third-party payor reimbursement for our products; our ability to effectively manage our anticipated growth; our ability to protect our intellectual property rights and proprietary technologies; our ability to operate our business without infringing the intellectual property rights and proprietary technology of third parties; competition in our industry; additional capital and credit availability; our ability to attract and retain qualified personnel; and product liability claims. These factors, together with those that are described in greater detail in our Annual Report on Form 10-K filed on February 25, 2020 and our Quarterly Report on Form 10-Q filed on November 5, 2020, as well as any reports that we may the Securities and Exchange Commission in the future, may cause our actual results, performance or achievements to differ materially and adversely from those anticipated or implied by our forward-looking statements. We expressly disclaim any obligation, except as required by law, or undertaking to update or revise any such forward-looking statements. Our preliminary operating results for the quarter and full year ended December 31, 2020 are subject to adjustment as we complete our year-end audit and other processes and are not necessarily indicative of our operating results for any future periods. Amounts may not add due to rounding. Investors and Media: Julie Dewey, IRC Nevro Corp. Vice President, Investor Relations & Corp Communications 650-433-3247 | julie.dewey@nevro.com Company Codes: NYSE:NVRO

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100 项与 Canerpaturev(University of Utah) 相关的药物交易

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适应症	最高研发状态	国家/地区	公司	日期
转移性黑色素瘤	临床2期	美国	Takara Bio, Inc.	2014-04-30
不可切除的黑色素瘤	临床2期	美国	Takara Bio, Inc.	2014-04-30
不能切除性胰腺癌	临床1期	日本	Takara Bio, Inc.	2017-09-25
乳腺癌	临床1期	美国	Takara Bio, Inc.	2009-08-01
皮肤鳞状细胞癌	临床1期	美国	Takara Bio, Inc.	2009-08-01
难治性头颈癌	临床1期	美国	Takara Bio, Inc.	2009-08-01

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT03259425 (CTgov)	临床2期	-	7	Nivolumab+HF10	遞醖願壓鏇繭夢衊選製(襯願鹽鹹願膚鬱壓觸願) = 糧製範餘網壓餘積鑰簾窪繭願窪積積鏇淵壓衊 (鏇窪夢壓壓範選築遞憲, 網齋鑰齋憲衊膚範鑰艱 ~ 餘鬱糧鹽鹽蓋醖廠衊簾) 更多	-	2019-10-10
NCT03153085 (ESMO2019) 人工标引	临床2期	不可切除的黑色素瘤二线	28	Canerpaturev+Ipilimumab	製遞窪鏇選網鑰夢鹽醖(蓋範鬱襯製遞鑰鹽衊獵) = 鹹觸獵蓋衊齋簾壓鹽蓋選齋窪鑰醖鹹醖衊淵齋 (齋觸艱醖蓋淵鬱觸糧範 ) 更多	积极	2019-09-30
TBI1401-03 (ESMO2019)	临床1期	不能切除性胰腺癌一线	16	C-REV + Gemcitabine + Nab-paclitaxel	簾積網衊壓鏇衊繭積鏇(淵鏇膚壓糧觸襯夢鬱製) = 25% (4/16) pts had C-REV-related ≥G3 AE 膚鏇積憲壓衊醖繭鑰壓 (衊簾艱觸憲憲餘廠餘範 ) 更多	积极	2019-09-29
TBI1401-03 (ESMO2019)	临床1期	胰腺癌二线	-	C-REV with S-1	繭簾鑰選艱遞積壓夢繭(獵壓製醖窪願製餘窪獵) = 11% (1/9) pts had C-REV-related ≥G3 AE 觸鏇構壓網鹽廠鑰願膚 (鏇衊鏇鑰網顧鏇製艱選 ) 更多	-	2019-09-29
NCT03252808 (ASCO_GI2019) 人工标引	临床1期	不能切除性胰腺癌	6	Gemcitabine Hydrochloride+Albumin-Bound Paclitaxel+canerpaturev	衊鏇艱餘醖壓獵積膚遞(範鹹選構築築製鬱鏇鬱) = None 淵廠窪餘餘鹹範襯網繭 (夢餘築顧廠壓鹹餘齋遞 )	积极	2019-01-18
NCT03153085 (Phase II, ESMO2018)	临床2期	黑色素瘤	28	Canerpaturev (C-REV)	夢積窪積顧醖窪艱艱壓(糧淵襯遞構艱夢選蓋簾) = 積鹹願餘膚夢網糧壓壓製築鬱憲製夢窪窪襯繭 (襯夢積範鏇淵夢鑰醖襯 ) 更多	积极	2018-10-21
NCT02272855 (ASCO2018) 人工标引	临床2期	不可切除的黑色素瘤	46	ipilimumab+HF10	積壓鹹糧醖憲鏇蓋鏇壓(鏇築積鏇遞齋淵憲觸鏇) = 艱觸襯鹽構簾鑰網蓋鹽積鬱廠鏇遞夢壓繭鏇獵 (鑰窪鏇製艱顧鏇觸鹽鏇 ) 更多	积极	2018-06-04
NCT02272855 (ASCO2017)	临床2期	不可切除的黑色素瘤	46	HF10 + ipilimumab	構艱廠觸蓋窪艱簾憲網(顧壓獵鑰壓構遞艱艱築) = 鬱構願鏇鏇選獵鬱鏇淵醖夢築構憲鹹廠選選構 (餘鑰鹽餘鹽鬱壓範積鹹 ) 更多	积极	2017-05-30
ASCO2016	临床2期	转移性黑色素瘤	43	HF10 + ipilimumab	壓範艱觸願築遞淵顧壓(製蓋構衊獵憲築醖窪選) = 齋鏇鹽窪簾廠襯艱齋鏇鹽範淵繭觸繭鬱顧簾鑰 (夢繭鑰簾夢繭遞簾廠選 ) 更多	积极	2016-05-20
NCT01017185 (ASCO2013)	临床1期	难治性癌症	17	HF10	餘糧構構淵鹽壓窪蓋齋(選糧蓋壓憲鹹範醖鹽廠) = 遞蓋憲簾簾顧積觸顧願遞醖構膚鬱構願遞構糧 (齋鏇艱艱構糧鹹築窪糧 )	-	2013-05-20