SPOTLIGHT 204: A Multicenter, Phase 2b, open-label, non-randomized, clinical trial to evaluate safety, tolerability and preliminary efficacy of intra-lesional BO-112 in patients with resectable primary low and high risk basal cell carcinoma - BOT-112-204

开始日期2024-12-10

申办/合作机构-

NCT06422936

/ Recruiting临床2期

SPOTLIGHT 204: a Multicenter, Phase 2b, Open-label, Non-randomized, Clinical Trial to Evaluate Safety, Tolerability and Preliminary Efficacy of Intra-lesional BO-112 in Patients with Resectable Primary Low and High Risk Basal Cell Carcinoma

This is a multicenter, phase 2b, open-label, non-randomized, clinical trial to evaluate safety, tolerability, pharmacodynamics and preliminary efficacy of intra-lesional BO-112 in patients with resectable primary low and high risk basal cell carcinoma.
* primary endpoint is complete visual and pathological response [at surgery] on patient level assessed by central review
* secondary endpoints are
1. Occurrence of adverse events (AEs), serious adverse events (SAEs), and AEs leading to discontinuation or death on patient level.
2. Pathological response [at surgery] on patient level assessed by the investigator and central review, respectively, and visual response [during the study and at surgery] on patient level assessed by the investigator and central review, respectively.
3. Recurrence [at 12 and 24 months] after surgery on patient level assessed by the investigator.

开始日期2024-05-27

申办/合作机构

Highlight Therapeutics SL

NCT05265650

/ Unknown status临床1/2期IIT

Phase Ib/II Open-label Clinical Study of Intratumoral Administration of BO-112 in Combination With Radiotherapy and Nivolumab in Patients With Metastatic PD- 1/PD-L1 Refractory Non-small Cell Lung Cancer

This is a study of repeated IT administrations of BO-112 in combination with ablative radiotherapy (SABR) and concurrent nivolumab in patients with metastatic PD-1/PD-L1-refractory NSCLC.

开始日期2022-06-13

申办/合作机构

Clínica Universidad de Navarra

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100 项与 BO-112 相关的临床结果

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100 项与 BO-112 相关的转化医学

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100 项与 BO-112 相关的专利（医药）

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项与 BO-112 相关的文献（医药）

2024-04-01·Journal for immunotherapy of cancer

Efficacy of LCMV-based cancer immunotherapies is unleashed by intratumoral injections of polyI:C

Article

作者: Quintero, Marisol ; Russo-Cabrera, Joan Salvador ; Alvarez, Maite ; Gomar, Celia ; Ardaiz, Nuria ; Di Trani, Claudia Augusta ; Berraondo, Pedro ; Lauterbach, Henning ; Gonzalez-Gomariz, Jose ; Aranda, Fernando ; Arrizabalaga, Leire ; Bella, Angela ; Fernandez-Sendin, Myriam ; Orlinger, Klaus K ; Schippers, Timo ; Melero, Ignacio

Background:

Lymphocytic choriomeningitis virus (LCMV) belongs to the Arenavirus family known for inducing strong cytotoxic T-cell responses in both mice and humans. LCMV has been engineered for the development of cancer immunotherapies, currently undergoing evaluation in phase I/II clinical trials. Initial findings have demonstrated safety and an exceptional ability to activate and expand tumor-specific T lymphocytes. Combination strategies to maximize the antitumor effectiveness of LCMV-based immunotherapies are being explored.

Methods:

We assessed the antitumor therapeutic effects of intratumoral administration of polyinosinic:polycytidylic acid (poly(I:C)) and systemic vaccination using an LCMV-vector expressing non-oncogenic versions of the E6 and E7 antigens of human papillomavirus 16 (artLCMV-E7E6) in a bilateral model engrafting TC-1/A9 cells. This cell line, derived from the parental TC-1, exhibits low MHC class I expression and is highly immune-resistant. The mechanisms underlying the combination’s efficacy were investigated through bulk RNA-seq, flow cytometry analyses of the tumor microenvironment, selective depletions using antibodies and clodronate liposomes, Batf3 deficient mice, and in vivo bioluminescence experiments. Finally, we assessed the antitumor effectiveness of the combination of artLCMV-E7E6 with BO-112, a GMP-grade poly(I:C) formulated in polyethyleneimine, currently under evaluation in clinical trials.

Results:

Intratumoral injection of poly(I:C) enhanced the antitumor efficacy of artLCMV-E7E6 in both injected and non-injected tumor lesions. The combined treatment resulted in a significant delay in tumor growth and often complete eradication of several tumor lesions, leading to significantly improved survival compared with monotherapies. While intratumoral administration of poly(I:C) did not impact LCMV vector biodistribution or transgene expression, it significantly modified leucocyte infiltrates within the tumor microenvironment and amplified systemic efficacy through proinflammatory cytokines/chemokines such as CCL3, CCL5, CXCL10, TNF, IFNα, and IL12p70. Upregulation of MHC on tumor cells and a reconfiguration of the gene expression programs related to tumor vasculature, leucocyte migration, and the activation profile of tumor-infiltrating CD8+T lymphocytes were observed. Indeed, the antitumor effect relied on the functions of CD8+T lymphocytes and macrophages. The synergistic efficacy of the combination was further confirmed when BO-112 was included.

Conclusion:

Intratumoral injection of poly(I:C) sensitizes MHClowtumors to the antitumor effects of artLCMV-E7E6, resulting in a potent therapeutic synergy.

2023-12-31·Oncoimmunology

Intratumoral neoadjuvant immunotherapy based on the BO-112 viral RNA mimetic

Article

作者: Glez-Vaz, Javier ; Alvarez, Maite ; Garasa, Saray ; Gomis, Gabriel ; Quintero, Marisol ; Molina, Carmen ; Olivera, Irene ; Berraondo, Pedro ; Cirella, Assunta ; Ochoa, Maria C. ; Gonzalez-Gomariz, Jose ; Bolaños, Elixabet ; azpilikueta, arantza ; luri-Rey, carlos ; Rodriguez-Ruiz, Maria E ; Melero, Ignacio ; Teijeira, Alvaro

BO-112 is a poly I:C-based viral mimetic that exerts anti-tumor efficacy when intratumorally delivered in mouse models. Intratumoral BO-112 synergizes in mice with systemic anti-PD-1 mAbs and this combination has attained efficacy in PD1-refractory melanoma patients. We sought to evaluate the anti-tumor efficacy of BO-112 pre-surgically applied in neoadjuvant settings to mouse models. We have observed that repeated intratumoral injections of BO-112 prior to surgical excision of the primary tumor significantly reduced tumor metastasis from orthotopically implanted 4T1-derived tumors and subcutaneous MC38-derived tumors in mice. Such effects were enhanced when combined with systemic anti-PD-1 mAb. The anti-tumor efficacy of this neoadjuvant immunotherapy approach depended on the presence of antigen-specific effector CD8 T cells and cDC1 antigen-presenting cells. Since BO-112 has been successful in phase-two clinical trials for metastatic melanoma, these results provide a strong rationale for translating this pre-surgical strategy into clinical settings, especially in combination with standard-of-care checkpoint inhibitors.

2023-01-01·Journal for immunotherapy of cancer

Intratumoral BO-112 in combination with radiotherapy synergizes to achieve CD8 T-cell-mediated local tumor control

Article

作者: Barrio-Alonso, Celia ; Quintero, Marisol ; Sánchez-Mateos, Paloma ; Alvarez, Maite ; Rodríguez López, Inmaculada ; Perez-Gracia, Jose Luis ; Escuin-Ordinas, Helena ; Garate-Soraluze, Eneko ; Serrano-Mendioroz, Irantzu ; Arbea Moreno, Leire ; Diaz Pascual, Victor ; Rodriguez-Ruiz, Maria E ; Sanmamed, Miguel F ; Melero, Ignacio

Background:

Radioimmunotherapy combines irradiation of tumor lesions with immunotherapy to achieve local and abscopal control of cancer. Most immunotherapy agents are given systemically, but strategies for delivering immunotherapy locally are under clinical scrutiny to maximize efficacy and avoid toxicity. Local immunotherapy, by injecting various pathogen-associated molecular patterns, has shown efficacy both preclinically and clinically. BO-112 is a viral mimetic based on nanoplexed double-stranded RNA (poly I:C) which exerts immune-mediated antitumor effects in mice and humans on intratumoral delivery. BO-112 and focal irradiation were used to make the proof-of-concept for local immunotherapy plus radiation therapy combinations.

Methods:

Murine transplantable tumor cell lines (TS/A, MC38 and B16-OVA) were used to show increased immunogenic features under irradiation, as well as in bilateral tumor models in which only one of the lesions was irradiated or/and injected with BO-112. Flow cytometry and multiplex tissue immunofluorescence were used to determine the effects on antitumor immunity. Depletions of immune cell populations and knockout mice for the IFNAR and BATF-3 genes were used to delineate the immune system requirements for efficacy.

Results:

In cultures of TS/A breast cancer cells, the combination of irradiation and BO-112 showed more prominent features of immunogenic tumor cell death in terms of calreticulin exposure. Injection of BO-112 into the tumor lesion receiving radiation achieved excellent control of the treated tumor and modest delays in contralateral tumor progression. Local effects were associated with more prominent infiltrates of antitumor cytotoxic tumor lymphocytes (CTLs). Importantly, local irradiation plus BO-112 in one of the tumor lesions that enhanced the therapeutic effects of radiotherapy on distant irradiated lesions that were not injected with BO-112. Hence, this beneficial effect of local irradiation plus BO-112 on a tumor lesion enhanced the therapeutic response to radiotherapy on distant non-injected lesions.

Conclusion:

This study demonstrates that local BO-112 immunotherapy and focal irradiation may act in synergy to achieve local tumor control. Irradiation plus BO-112 in one of the tumor lesions enhanced the therapeutic effects on distant irradiated lesions that were not injected with BO-112, suggesting strategies to treat oligometastatic patients with lesions susceptible to radiotherapy and with at least one tumor accessible for repeated BO-112 intratumoral injections.

项与 BO-112 相关的新闻（医药）

2025-07-04

·癌度

KRAS突变全覆盖？daraxonrasib（RMC-6236）让RAS药物不再挑三拣四！

临床试验入组病友交流群（点击）在过去几十年，KRAS突变一直是癌症精准治疗的难点之一。2021年起，首代KRAS基因的G12C抑制剂的成功上市为患者带来曙光，但也暴露出治疗局限与耐药问题。如今，靶向RAS活跃状态（RAS-ON）的daraxonrasib（代号RMC-6236），或许能实现更大范围的抑制效果，带来新一轮突破。下面是RMC-6236的一篇最新文献综述，癌度为大家整理编译相关内容，希望对大家有所帮助。1、背景：KRAS突变为何难治？RAS家族包括KRAS、NRAS、HRAS，是一类参与细胞生长调控的重要基因。它们的突变被认为是导致肺癌、胰腺癌、结直肠癌等肿瘤发展的“发动机”，其中KRAS是最常见的突变基因，而且突变的位点也很多。过去很长一段时间，科学家们一直将RAS蛋白视为“不可成药”的靶点。原因在于它结构表面光滑，缺乏传统意义上的“药物结合位点”。直到2021年，首款KRAS G12C靶向药索托拉西布（sotorasib，AMG510）获批上市，才揭开了KRAS靶向治疗的新篇章。然而，KRAS基因的G12C突变只占所有RAS突变患者中的一小部分。更令人担忧的是，即便最初有效，患者很快也可能因二次突变或耐药机制失效。因此，开发能同时靶向多个KRAS突变型、甚至包括野生型RAS的广谱药物，成了学界的重要方向。2、研究数据：daraxonrasib能做什么？RMC-6236是由Revolution Medicines公司开发的一款“广谱”RAS(ON)抑制剂，能够靶向RAS蛋白处于活跃状态（GTP结合状态），这一点与现有的KRAS G12C抑制剂不同，后者只对“关闭状态”（KRAS-OFF）有效。RMC-6236的工作机制很特别：它通过与一种名为CypA的伴侣蛋白形成复合体，再一同与RAS蛋白结合，从而破坏RAS与下游信号分子的连接。这种三元复合机制不仅提高了药物的结合力，也拓展了靶点覆盖范围。临床前数据显示，RMC-6236可以有效抑制多种KRAS突变型细胞系的生长，包括G12C、G12D、G12V等。在动物实验中，它在多种肺癌和胰腺癌模型中表现出显著抗肿瘤活性。例如，在胰腺癌MIA PaCa-2模型中，口服给药能显著抑制肿瘤相关信号DUSP6表达，抑制率高达98%，并维持至少48小时以上。此外，RMC-6236的药代动力学也优异，口服生物利用度在多种动物中达到20%–30%，且心脏毒性和脱靶作用较低。目前，RMC-6236已进入两项关键的三期临床试验：NCT06625320：针对已接受治疗的转移性胰腺癌；NCT06881784：用于RAS突变型非小细胞肺癌的治疗。3、RMC-6236为什么值得期待？与以往靶向G12C基因突变的靶向药药物相比，RMC-6236的最大亮点在于它“广谱、可逆、安全”。它能同时抑制多个RAS突变型，甚至包括部分野生型RAS，且不依赖于某个特定位点。这种机制有望解决KRAS抑制剂的耐药问题。更重要的是，RMC-6236靶向的是RAS的“活跃状态”（RAS-ON），这一点是大多数早期药物无法做到的。只要肿瘤依赖于RAS信号通路，即便突变形式不同，理论上都可能从RMC-6236中获益。当然，RMC-6236这款药物仍处于临床试验阶段，真正的数据还需进一步验证。但从目前的实验与临床前研究看，RMC-6236的确代表着一种创新策略：以全新的靶点机制，正面挑战KRAS耐药难题。未来，如果RMC-6236的三期试验成功，它或许将成为治疗KRAS突变肿瘤的“第二代主力军”，让更多患者迎来新的希望。欢迎大家关注癌度，加入临床试验资讯交流群，等待这款药在国内开展临床试验！参考文献：Zonghui Ma，et al., RAS(ON) Therapies on the Horizon to Address KRAS Resistance: Highlight on a Phase III Clinical Candidate Daraxonrasib (RMC-6236), J Med Chem. 2025. 往期推荐溶瘤病毒在第一大癌种获得突破，BRACELET-01研究证实乳腺癌从溶瘤病毒治疗获益！脑转？第三代靶向药 + 新型抗体偶联药，打破EGFR突变肺癌脑转移困局！早期和晚期肠癌接受CIK细胞疗法联合化疗或手术均能获益，而CEA水平是一个能否有效的指示器！挥别“冷肿瘤”困境！瘤内注射BO-112联合PD-1抑制剂让54%的患者活过了2年！

临床3期临床2期临床1期申请上市

2025-07-02

·癌度

脑转？第三代靶向药 + 新型抗体偶联药，打破EGFR突变肺癌脑转移困局！

临床试验入组病友交流群（点击）如果问大家一个问题，有多大概率肺癌患者会出现脑转移，您可能对这个概率不是很了解。其实70%的EGFR基因突变的肺癌患者可能会发生脑转移，也就是患者能从靶向药获益，但是也不得不面对一些麻烦，有强势驱动基因突变的肺癌往往在脑转移、免疫治疗无效存在一些麻烦。下面是一篇最新发布在《肺癌》杂志的综述，讲述肺癌脑转移的治疗措施，癌度为大家做一下编译，希望能给到大家一些启发。本文的参考文献刊例示意图1、EGFR基因突变的肺癌为何容易脑转移非小细胞肺癌（NSCLC）是肺癌中最常见的类型，其中约50%亚洲患者携带EGFR基因突变，常见的突变类型包括19号外显子缺失突变和21号外显子的L858R突变。而令人头疼的是，这类患者中多达70%最终会出现脑转移，大大影响了患者的生活质量与生存时间。也许我们看到检查是脑转移发生了，但是这个情况往往涉及到很复杂的机制，上面的图片展示了脑转移的发生过程，总之脑转移的发生涉及肿瘤细胞侵袭性增强、上皮-间质转化（EMT）、外泌体释放以及血脑屏障（BBB）的破坏等机制，而传统治疗难以穿透屏障到达病灶。在EGFR突变的肺癌患者中，肿瘤生长相对缓慢但更倾向“转战脑中枢”，因此寻找能够穿透血脑屏障且精准打击EGFR突变的药物成为关键。2、三代靶向药+新型ADC：疗效提升、突破耐药目前，第三代EGFR靶向药（如奥希替尼）已成为治疗EGFR基因突变脑转移的一线标准。其不仅能精准抑制常见突变与T790M耐药突变，还能有效穿透血脑屏障，大幅延长患者的无进展生存期（PFS），部分患者甚至出现脑部病灶完全缓解（也就是所有可见病灶消失了）。然而，靶向药的耐药仍然难以避免，最常见的是EGFR基因的C797S突变、绕道通路激活（如MET基因扩增、HER2基因突变）或组织转化为小细胞肺癌。这时，联合治疗和新一代药物成为突破口，最近出现的抗体偶联药ADC就成了一个备受关注的焦点。HER3-DXd（德帕曲妥珠单抗）在HERTHENA-Lung01研究中，对脑转移患者的客观缓解率达33.3%，显示出良好穿脑与疗效。TROP2-DXd（德达博妥单抗）在EGFR基因突变人群中，治疗应答率达43.6%，中位无进展生存时间为5.8个月。Teliso-V（维汀-特立妥珠单抗）联合奥希替尼治疗c-Met过表达患者，治疗应答率达50%，但对脑转移疗效数据尚需扩大样本验证。这些抗体偶联药ADC不仅精准打击肿瘤抗原，有的还能“旁观者效应”杀死邻近未表达靶点的肿瘤细胞，成为耐药后脑转移控制的有力补充。3、未来展望：动态监测与多学科协作是关键随着精准医学的发展，我们已经可以借助血液ctDNA和脑脊液（CSF）的ctDNA来实现“提前发现、提前应对”的分子层级监测。最新的研究表明。脑脊液比血液的ctDNA更能反映脑内真实突变状态，适用于判断是否耐药、转化、或复发。血液和脑脊液的ctDNA突变检测一致率达93%，说明非侵入式检测也正逐渐可靠。此外，除了药物“治疗顺序”和“局部联合”的策略也在优化。例如，放疗+奥希替尼组合，可能进一步提升脑内控制率，延缓疾病进展。而未来的治疗发展则是包含第四代靶向药，通过建立动态治疗地图，根据循环肿瘤DNA（ctDNA）的变化，实时调整治疗的策略。对EGFR基因突变的肺癌患者来说，“脑转移”已不再意味着“无药可救”。从第三代靶向药到新型ADC、从联合方案到ctDNA动态检测，临床正不断探索突破之道。希望随着未来更多临床研究的开展，脑转移治疗能更加精准、更加温柔，真正实现“带瘤长存”的目标。欢迎大家关注癌度，了解全球肿瘤诊疗的最新进展，联系癌度申请临床试验，免费使用抗癌新药。参考文献：H. Wang, et al., Advances in the treatment of brain metastases in EGFR-mutant non-small cell lung cancer, Lung Cancer (2025). 往期推荐早期和晚期肠癌接受CIK细胞疗法联合化疗或手术均能获益，而CEA水平是一个能否有效的指示器！挥别“冷肿瘤”困境！瘤内注射BO-112联合PD-1抑制剂让54%的患者活过了2年！脑转移的小细胞肺癌，伽马刀、全脑放和手术治疗措施那种更好？这里有个新综述告诉您！三颗药夺走她的生命！这项几百元的基因检测，医生没提，家人不知…

免疫疗法抗体药物偶联物临床结果

2025-07-01

·癌度

早期和晚期肠癌接受CIK细胞疗法联合化疗或手术均能获益，而CEA水平是一个能否有效的指示器！

临床试验入组病友交流群（点击）对于细胞治疗我一直没很好的印象，不过还是有不少病人会去自费打。NC/CIK细胞疗法的问题在于回输的免疫细胞不能很好地识别肿瘤细胞，所以这个东西估计用处真不大。这与目前比较火热的TILS（肿瘤浸润淋巴细胞疗法）不同，TILS是通过穿刺肿瘤病灶，将病灶里识别癌细胞的免疫细胞提取、扩增然后回输。我们癌度的所有的内容都是源自参考文献，今天的细胞疗法治疗肠癌也是最新报道的一篇文章，这是在郑州大学第一附属医院开展的研究，这个医院也号称宇宙里最大的医院。研究者发现采用细胞免疫治疗（CIK细胞）联合术后/化疗显著提升结直肠癌患者的无进展生存期和总生存期，术前CEA血清水平可作为疗效预判指标。本文的参考文献刊例示意图1、CIK细胞与结直肠癌治疗结直肠癌是我们国家发病率比较高的恶性肿瘤，一般确诊后会根据基因突变信息进行分类，KRAS、BRAF以及MSI微卫星不稳定型等，不同的分子特征的肠癌治疗存在差异。主要的区别是选择的靶向药不同，尽管治疗的药物也多了，但是患者仍面临复发率高、副作用大等问题。CIK（Cytokine-Induced Killer）细胞来自患者自身的血液，通过进行体外培养，加入特定细胞因子（如抗CD3抗体、IL‑2、IFN‑γ）激活扩增而得。它们具有以下特点：增殖迅速同时具备T细胞和NK细胞的抗肿瘤能力不依赖于单一抗原，适用于多种肿瘤类型在体外实验中，CIK细胞能表达CD107标志，并有效诱导肿瘤细胞凋亡。既往研究也证实CIK对多种实体瘤（如肺癌、黑色素瘤等）安全有效。这里需要说明体外试验将CIK细胞和癌细胞放一块估计管用，但是打入体内的问题还是在有效识别的问题。2、真实世界疗效：CIK联合疗法大幅延长患者生存这是来自郑州大学附属一院的回顾性研究（2008–2020年），共纳入98例结直肠癌患者，对照组患者使用了手术和/或化疗，而CIK治疗组：CIK细胞联合术后/化疗。研究结果显示：无进展生存期（PFS）和总生存期（OS）在CIK细胞治疗联合组均明显优于对照组对于早期和晚期患者，疗效一致特别是在术前CEA < 5 ng/ml患者中，CIK细胞治疗组的效果更亮眼如上面的图示，对于治疗效果的预测，通过简单血液检测即可预测：术前CEA水平低 (<5 ng/ml) 的患者更可能从CIK疗法中获益。3、这个用药策略可以参考吗?由于细胞治疗目前处于比较严密的监管中，而且不是属于已经获批上市的药物，因此大家使用的时候只能通过参加临床试验或自费的方式。当然自费的花费可不便宜，上面的这个研究数据给出了一些启发，尤其是对于化疗后风险高的患者。这项研究的突破之处在于首次揭示血清CEA水平可作为CIK疗效的预测因子，相关的临床试验数据为后面临床试验选择、筛选患者提供重要参考依据。后面CIK细胞疗法将会开展更多的临床试验，探索与放疗、靶向药、PD-1等免疫治疗的搭配联合，进一步验证这个疗法的安全性和有效性。当然鉴于之前细胞疗法的口碑问题，癌度强烈建议大家只参加临床试验免费使用药物，谨慎自费去打细胞疗法，而且该疗法需要与其他治疗搭配。肿瘤靶向药基因检测，临床试验免费用药欢迎联系癌度咨询！参考文献：Jieyao Li et al, Serum carcinoembryonic antigen levels as a predictive biomarker for cytokine-induced killer cell immunotherapy in patients with colorectal cancer, The Journal of Immunology (2025). 往期推荐挥别“冷肿瘤”困境！瘤内注射BO-112联合PD-1抑制剂让54%的患者活过了2年！脑转移的小细胞肺癌，伽马刀、全脑放和手术治疗措施那种更好？这里有个新综述告诉您！三颗药夺走她的生命！这项几百元的基因检测，医生没提，家人不知…“定制疫苗”能预防肿瘤复发？胰腺癌和肾癌这两种高难癌症给出了希望！

细胞疗法免疫疗法临床研究

100 项与 BO-112 相关的药物交易

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研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
基底细胞癌	临床2期	以色列	Highlight Therapeutics SL	2024-05-27
基底细胞癌	临床2期	西班牙	Highlight Therapeutics SL	2024-05-27
转移性非小细胞肺癌	临床2期	西班牙	Highlight Therapeutics SL	2022-06-13
非小细胞肺癌	临床2期	西班牙	Highlight Therapeutics SL	2022-06-13
不可切除的黑色素瘤	临床2期	法国	Highlight Therapeutics SL	2020-12-30
不可切除的黑色素瘤	临床2期	法国	Merck Sharp & Dohme LLC	2020-12-30
不可切除的黑色素瘤	临床2期	西班牙	Highlight Therapeutics SL	2020-12-30
不可切除的黑色素瘤	临床2期	西班牙	Merck Sharp & Dohme LLC	2020-12-30
结直肠癌	临床2期	比利时	Highlight Therapeutics SL	2020-06-17
结直肠癌	临床2期	意大利	Highlight Therapeutics SL	2020-06-17

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临床结果

适应症

分期

评价

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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


NCT04508140 (CTgov)	临床2期	食管癌 \| 胃食管交界处癌 \| 结直肠癌	18	Hepatic Biopsy+BO-112+pembrolizumab (Cohort A)	選範淵鹽齋簾獵鏇願顧 = 範繭襯襯鬱夢艱繭鏇窪鬱衊窪蓋齋築觸鑰鑰遞 (壓製築鑰襯鬱齋構餘蓋, 鏇鹹餘艱襯鏇衊鹽簾鹽 ~ 簾壓範願鑰膚觸齋築淵) 更多	-	2024-11-29
NCT04508140 (CTgov)	临床2期	食管癌 \| 胃食管交界处癌 \| 结直肠癌	18	Hepatic Biopsy+BO-112+pembrolizumab (Cohort B)	選範淵鹽齋簾獵鏇願顧 = 顧淵壓窪繭壓衊簾觸簾鬱衊窪蓋齋築觸鑰鑰遞 (壓製築鑰襯鬱齋構餘蓋, 觸獵壓鏇鹹選衊窪襯選 ~ 窪鑰襯遞糧範獵膚獵範) 更多	-	2024-11-29
NCT04570332 (SPOTLIGHT203, AACR2022) 人工标引	临床2期	局部晚期黑色素瘤	42	Pembrolizumab+BO 112 (Global )	醖鬱獵顧醖憲襯蓋簾築(選夢膚夢淵淵製鑰顧繭) = 願窪壓繭憲衊衊積艱顧齋鬱艱膚窪獵壓糧鬱鹹 (選壓襯醖糧淵網窪觸鑰 ) 更多	积极	2022-06-15
NCT04570332 (SPOTLIGHT203, AACR2022) 人工标引	临床2期	局部晚期黑色素瘤	42	Pembrolizumab+BO 112 (Mucosal)	醖鬱獵顧醖憲襯蓋簾築(選夢膚夢淵淵製鑰顧繭) = 廠鹽鏇製壓網憲窪範製齋鬱艱膚窪獵壓糧鬱鹹 (選壓襯醖糧淵網窪觸鑰 ) 更多	积极	2022-06-15
NCT04570332 (AACR2022)	临床2期	难治性黑色素瘤	42	BO-112 plus pembrolizumab	廠簾鹹壓糧繭壓襯鏇糧(製鹽鏇糧淵顧願選襯願) = 構艱衊積蓋製壓膚憲糧遞獵糧築願願齋範願獵 (餘遞範繭艱餘網選簾糧 ) 更多	-	2022-06-15
AACR2021	临床2期	结肠癌肝转移 \| 胃食管交界处癌	69	BO-112	憲製選願襯憲襯範淵積(選構鏇廠鏇構蓋鏇鑰膚) = 蓋鑰鏇獵構築蓋鹹範積鹽簾膚鏇觸淵構蓋顧遞 (襯齋淵蓋繭選製範網構 )	-	2021-07-01
NCT04570332 (AACR2021)	临床2期	黑色素瘤	40	BO-112 in combination with pembrolizumab	襯網選齋願鏇獵淵繭膚(醖鹹膚範獵網襯願願鏇) = 餘構壓蓋鬱淵蓋衊夢鑰構襯鏇構築範網窪繭夢 (膚鏇顧憲築獵淵壓鏇願 ) 更多	-	2021-07-01
NCT02828098 (ESMO2018)	临床1期	实体瘤	28	BO-112 Monotherapy	願艱衊網膚醖築積繭餘(襯廠願製鏇鹹壓繭築窪) = 膚壓範觸鑰餘襯廠憲膚選網夢廠襯觸窪夢簾餘 (糧顧簾憲衊鑰鹹鹹衊範 ) 更多	积极	2018-10-20
NCT02828098 (ESMO2018)	临床1期	实体瘤	28	Combination BO-112+anti PD-1	願艱衊網膚醖築積繭餘(襯廠願製鏇鹹壓繭築窪) = 積壓艱築鏇獵憲糧鏇觸選網夢廠襯觸窪夢簾餘 (糧顧簾憲衊鑰鹹鹹衊範 )	积极	2018-10-20