The purpose of this research study is to study the effect of giving nivolumab with CCR2/5-inhibitor or anti-IL-8 before surgery, and after surgery, with the goal of determining if this medicine results in:
1. A significant immune response against their tumor (which the study team will see in the tumor that is taken out at the time of surgery)
2. Improvement in long term survival rates

开始日期2020-03-05

申办/合作机构

Icahn School of Medicine at Mount Sinai

[+1]

NCT03767582

/ Completed临床1/2期IIT

A Phase I/II Trial of Combination Immunotherapy With Nivolumab and a CCR2/CCR5 Dual Antagonist (BMS-813160) With or Without GVAX Following Chemotherapy and Radiotherapy for Locally Advanced Pancreatic Ductal Adenocarcinomas (PDACs).

The purpose of this study is to evaluate if the combination of nivolumab and a CCR2/CCR5 dual antagonist (BMS-813160) with GVAX is safe in patients with locally advanced pancreatic cancer (LAPC) who have received chemotherapy and radiotherapy, and to see if this combination therapy enhances the infiltration of CD8+CD137+ cells in PDACs .

开始日期2019-12-12

申办/合作机构

The Sidney Kimmel Comprehensive Cancer Center

[+1]

NCT03496662

/ Completed临床1/2期IIT

A Phase I/II Study to Evaluate the Tolerability and Efficacy of BMS-813160 (CCR2/5 Inhibitor) With Nivolumab and Gemcitabine and Nab-paclitaxel in Borderline Resectable and Locally Advanced Pancreatic Ductal Adenocarcinoma (PDAC)

The purpose of this research study is to learn more about a new combination of drugs being given to treat pancreatic cancer. The drugs being tested are BMS-813160, nivolumab, gemcitabine, and nab-paclitaxel. The investigators will be looking at both the side effects and the way the disease responds to treatment.

开始日期2018-08-31

申办/合作机构

Washington University School of Medicine

[+4]

100 项与 BMS-813160 相关的临床结果

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100 项与 BMS-813160 相关的转化医学

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100 项与 BMS-813160 相关的专利（医药）

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项与 BMS-813160 相关的文献（医药）

2026-01-01·Journal for ImmunoTherapy of Cancer

Phase 1b/2 study of BMS-813160, a CCR2/5 dual antagonist, in combination with chemotherapy or nivolumab in patients with advanced pancreatic or colorectal cancer

Article

作者: BasuMallick, Atrayee ; Ma, Wen Wee ; Twyman Saint Victor, Christina ; Garrido-Laguna, Ignacio ; Davis, S Lindsey ; Gutierrez, Martin ; O’Brien, Shaun ; Folprecht, Gunnar ; Osawa, Mayu ; Dutta, Santanu ; Xu, Ke ; Chen, Eric ; Lenz, Heinz-Josef ; Le, Dung T ; Novosiadly, Ruslan D ; Varghese, Anna M ; Noel, Marcus ; Greenawalt, Danielle M ; Dayyani, Farshid ; Trikalinos, Nikolaos A

Background:

Cysteine–cysteine chemokine receptors 2 (CCR2) and 5 (CCR5) contribute to immune suppression in tumor microenvironments. CCR2 and CCR5 antagonists have demonstrated antitumor activity in pancreatic ductal adenocarcinoma (PDAC) and colorectal cancer (CRC), respectively. This phase 1b/2, open-label study evaluated BMS-813160, a CCR2/5 dual antagonist, in combination with chemotherapy±nivolumab in advanced PDAC or metastatic CRC.

Methods:

Part 1 included patients with metastatic untreated (first-line (1L)) PDAC, 1L CRC, or previously treated (second or third line (2/3L)) microsatellite stable (MSS) CRC. Patients received 2 weeks of BMS-813160 monotherapy (300 mg two times a day, 600 mg once daily, 300 mg once daily, or 150 mg once daily) and then BMS-813160+chemotherapy (gemcitabine+nab-paclitaxel (gem/nabP; 1L PDAC), 5-fluorouracil+leucovorin+irinotecan (FOLFIRI; 1L CRC)), or nivolumab (2/3L MSS CRC).Part 2 included patients with metastatic 1L PDAC or 2L CRC. Patients received BMS-813160 300 mg two times a day+gem/nabP±nivolumab (1L PDAC), BMS-813160 300 mg two times a day or 150 mg once daily+FOLFIRI (2L CRC), or chemotherapy alone. Primary endpoints were safety and pharmacodynamics (Part 1) and efficacy (Part 2).

Results:

In Part 1, 22 of 75 (29%) and 54 of 72 (72%) patients experienced a treatment-related adverse event during monotherapy lead-in and overall, respectively. Two dose-limiting toxicities (rash and pericardial effusion with pericarditis, both grade 3) occurred. In Part 2, patients with 1L PDAC who received BMS-813160 300 mg two times a day+gem/nabP+nivolumab achieved an overall response rate (ORR) of 37% (13/35); the median duration of response (DOR) was 45 weeks (95% CI 26.1 to not evaluable). ORRs with BMS-813160 300 mg two times a day+gem/nabP and gem/nabP alone were 26% (9/35) and 28% (9/32), respectively; median DORs were 121 and 31 weeks, respectively. Progression-free survival rates at 24 weeks were 56% (BMS-813160 300 mg two times a day+gem/nabP+nivolumab), 56% (BMS-813160 300 mg two times a day+gem/nabP), and 50% (gem/nabP). ORRs in 2L CRC were 19% (6/32; BMS-813160 300 mg two times a day+FOLFIRI), 13% (4/32; BMS-813160 150 mg once daily+FOLFIRI), and 27% (7/26; FOLFIRI).

Conclusions:

In 1L PDAC, BMS-813160 300 two times a day+gem/nabP±nivolumab demonstrated durable antitumor response and was well tolerated. BMS-813160 combination regimens were tolerable in other cohorts, but clinical efficacy was not demonstrated.

Trial registration number:

NCT03184870 .

2023-01-01·Advanced biology

Macrophages in Tumor‐Associated Adipose Microenvironment Accelerate Tumor Progression

Article

作者: Qi Wu ; Juan Wu ; Bei Li ; Si Sun ; Qian Yang ; Zhiyu Li ; Juanjuan Li ; Shengrong Sun ; Siqing Liu ; Zhiliang Xu

Abstract:

Adipose‐tissue macrophages (ATMs), a complex ensemble of diverse macrophage subtypes, are prevalent in the tumor‐adipose microenvironment (TAME) and facilitate tumor growth. However, the mechanisms in which the tumor‐adipocyte crosstalk may enable the properties and plasticity of macrophages remain unclear. The single‐cell RNA‐sequence profiling reveals that a subset of macrophages expressed CD163, CCL2, and CCL5 in TAME, exhibiting an immunosuppressive subtype. It is demonstrated that CD163+ macrophages aggregate to surround adipocytes in breast cancer tissues. The expressions of CCL2 and CCL5 are also elevated in TAME and enable the recruitment and polarize macrophages. Mechanically, the level of exosomal miRNA‐155 increased in the coculture of tumor cells and adipocytes, and then it promoted the generation and release of CCL2 and CCL5 from adipocytes by targeting the SOCS6/STAT3 pathway. Inhibition of exosomal miRNA‐155 in tumor cells reduced the CCL2 and CCL5 levels in tumor‐adipocytes coculture and further retarded tumor growth. Finally, the deletion of macrophages partially inhibited adipocyte‐induced tumor proliferation. Likewise, inhibiting chemokines and their receptors or suppressing the phosphorylation of STAT3 decreased tumor burden in preclinical models. These results demonstrate that the niche factors in TAME, such as exosomal miRNA‐155, regulate the function and polarity of macrophages to facilitate tumor progression.

2022-11-01·TETRAHEDRON LETTERS

An azirine solid-state photodegradant of the CCR2/CCR5 dual antagonist BMS-813160

作者: Fenster, Michael D. B. ; Zang, Jia ; Hritzko, Benjamin ; Yuill, Elizabeth M. ; La Cruz, Thomas ; Sarjeant, Amy ; Ayers, Sloan ; Lin, Ziqing ; Park, Hyunsoo ; Zaretsky, Serge ; Huang, Yande ; Ramirez, Antonio

The synthesis of the CCR2/5 dual chemokine antagonist BMS-813160 (1) presented a number of interesting impurity and degradant structure elucidation challenges.This publication will focus on the structure elucidation of the solid-state photodegradant of 1 which produced an unexpected stable azirine species.The structure was elucidated by mass spectrometry and NMR, with confirmation by single-crystal X-ray crystallog.

项与 BMS-813160 相关的新闻（医药）

2026-02-22

·优在生物

JITC | 约翰霍普金斯大学Le团队评估CCR2/5双拮抗剂联合治疗晚期胰腺癌/结直肠癌疗效

点击上方 [优在生物] 关注我们导语 CCR2和CCR5通路介导免疫抑制性细胞向肿瘤微环境募集，促进胰腺癌和结直肠癌进展。单一CCR2或CCR5拮抗剂已显示初步抗肿瘤活性，但双拮抗剂BMS-813160联合化疗或免疫治疗的临床效果尚未明确。晚期胰腺癌和结直肠癌治疗手段有限，胰腺癌对免疫治疗响应差，结直肠癌二线治疗疗效不佳。亟需探索安全有效的联合治疗方案，明确BMS-813160的临床定位、适用人群及疗效预测标志物。 2026年1月22日，美国约翰霍普金斯大学西德尼・金梅尔癌症中心Dung T Le 团队在国际期刊Journal for ImmunoTherapy of Cancer上发表了题为Phase 1b/2 study of BMS-813160, a CCR2/5 dual antagonist, in combination with chemotherapy or nivolumab in patients with advanced pancreatic or colorectal cancer的研究论文。该研究通过1b/2期临床试验，证实BMS-813160联合吉西他滨/白蛋白紫杉醇±纳武利尤单抗治疗一线胰腺癌耐受性良好，客观缓解率达37%，应答持续时间显著延长；二线结直肠癌队列未显示额外获益。基线低RANTES和IL-8水平可预测胰腺癌患者的治疗响应，为晚期胰腺癌提供了新的治疗选择，也为肿瘤微环境靶向治疗提供了临床依据。正文研究人员首先开展多中心、开放标签的1b/2期临床试验，分为两部分探索BMS-813160的联合治疗潜力。Part1纳入75例患者，涵盖一线胰腺癌、一线结直肠癌及二/三线微卫星稳定结直肠癌，患者先接受2周BMS-813160单药导入（测试300mg每日两次、600mg每日一次等4种剂量），再联合对应化疗（胰腺癌用吉西他滨+白蛋白紫杉醇，结直肠癌用FOLFIRI）或纳武利尤单抗，主要评估安全性和药效学。Part2纳入205例患者，聚焦一线胰腺癌和二线结直肠癌，患者随机分配至BMS-813160联合治疗组或化疗单独组，主要评估客观缓解率、应答持续时间和无进展生存率。Part1结果显示BMS-813160耐受性良好，仅出现2例剂量限制性毒性（3级皮疹和心包积液合并心包炎），72%的患者发生治疗相关不良事件，以恶心、疲劳等轻度反应为主。为验证联合方案的疗效和安全性，Part2进一步扩大样本量并优化治疗方案。一线胰腺癌队列中，102例患者分为三组：BMS-813160300mg每日两次+吉西他滨/白蛋白紫杉醇+纳武利尤单抗（35例）、BMS-813160300mg每日两次+吉西他滨/白蛋白紫杉醇（35例）、吉西他滨/白蛋白紫杉醇单独（32例）。二线结直肠癌队列中，90例患者分为三组：BMS-813160300mg每日两次+FOLFIRI（32例）、BMS-813160150mg每日一次+FOLFIRI（32例）、FOLFIRI单独（26例）。研究同时检测外周血CCL2、CCL4等细胞因子水平和单核细胞来源抑制细胞比例，分析肿瘤组织中CD8+T细胞浸润及干扰素-γ通路基因表达。一线胰腺癌中，三药联合组客观缓解率达37%（13/35），应答持续时间中位数45周，24周无进展生存率56%；双药联合组客观缓解率26%，应答持续时间121周，均优于化疗单独组（客观缓解率28%，应答持续时间31周）。研究人员进一步分析疗效差异的机制及预测标志物，发现BMS-813160治疗后外周血CCL2和CCL4水平显著升高，提示靶点有效结合；三药联合组肿瘤组织中CD8+T细胞浸润增加，干扰素-γ通路和免疫炎症基因表达上调。探索性生物标志物分析显示，基线血清低RANTES（CCL5）和IL-8水平的胰腺癌患者，接受BMS-813160联合治疗后客观缓解率和无进展生存率显著更高。而二线结直肠癌队列中，BMS-813160联合FOLFIRI的客观缓解率仅13%-19%，低于化疗单独组的27%，未显示协同效应。最终证实BMS-813160联合吉西他滨/白蛋白紫杉醇±纳武利尤单抗是一线胰腺癌的有效治疗方案，其疗效与肿瘤类型、基线免疫炎症状态相关，结直肠癌患者未从联合治疗中获益。 C1D28时治疗特异性肿瘤药效动力学变化总结总的来说，该1b/2期临床试验系统评估了CCR2/5双拮抗剂BMS-813160的联合治疗价值，证实其联合吉西他滨/白蛋白紫杉醇±纳武利尤单抗治疗一线胰腺癌耐受性良好，可显著延长应答持续时间，基线低RANTES和IL-8水平是潜在疗效预测标志物；但在二线结直肠癌中未显示额外获益，提示治疗效果具有肿瘤特异性。该研究为晚期胰腺癌提供了新的联合治疗策略，首次证实CCR2/5双靶点抑制可改善胰腺癌肿瘤微环境，增强化疗和免疫治疗的协同作用。其发现不仅推动了BMS-813160的临床转化，也为肿瘤微环境靶向治疗的患者分层和方案优化提供了关键依据，对后续同类药物研发具有重要参考价值。论文链接： https://jitc.bmj.com/content/14/1/e011284 END 内容为【优在生物】公众号原创，转载请写明来源于【优在生物】版权声明：本公众号标注原创的文章系作者个人学习心得，若有版权争议或标注差错，请联系我们。免责声明：本文内容仅供学术交流参考，不构成任何建议或承诺，优在生物不对因使用本文信息导致的任何后果负责。

临床结果免疫疗法临床2期临床申请临床1期

2025-09-29

·闲谈 Immunology

10个自免致病细胞因子

自身免疫性疾病的核心病理机制是免疫系统过度激活，致病细胞因子作为免疫细胞间的 “信号分子”，会持续放大炎症反应、破坏自身组织。 Cytokines in pathogenesis of psoriasis，10.1093/intimm/dxv0631. 肿瘤坏死因子 -α（TNF-α）核心关联疾病类风湿关节炎（RA）、强直性脊柱炎（AS）、银屑病（PsO）、银屑病关节炎（PsA）、溃疡性结肠炎（UC）、克罗恩病（CD）致病机制促进巨噬细胞、中性粒细胞等炎症细胞向病变部位浸润；诱导滑膜细胞、成纤维细胞释放蛋白酶，破坏关节软骨和骨组织；激活血管内皮细胞，加重组织水肿和炎症。靶向治疗药物药物名称药物类别靶点特性主要适应症依那西普 TNF 受体融合蛋白竞争性结合 TNF-α/β RA、AS、PsO、PsA 阿达木单抗抗 TNF-α 单克隆抗体（全人源）直接中和 TNF-α 活性 RA、AS、PsO、PsA、UC、CD 英夫利西单抗抗 TNF-α 单克隆抗体（嵌合）直接中和 TNF-α 活性 RA、AS、PsO、PsA、UC、CD 戈利木单抗抗 TNF-α 单克隆抗体（全人源）直接中和 TNF-α 活性 RA、AS、PsA、UC2. 白细胞介素 - 6（IL-6）核心关联疾病 RA、AS、系统性红斑狼疮（SLE）、巨细胞动脉炎（GCA）、Castleman 病致病机制调控 “急性期反应”（如 C 反应蛋白升高、血沉加快）；促进 B 细胞活化分化为浆细胞，产生自身抗体（如抗环瓜氨酸肽抗体）；刺激 T 细胞增殖，加重关节滑膜炎症和血管炎。靶向治疗药物药物名称药物类别靶点特性主要适应症托珠单抗抗 IL-6 受体单克隆抗体（人源化）阻断 IL-6 与受体结合 RA、GCA、SLE（合并肾炎 / 血小板减少）司妥昔单抗抗 IL-6 单克隆抗体（人源化）直接中和 IL-6 活性多中心 Castleman 病、RA（难治性）3. 白细胞介素 - 1（IL-1，含 IL-1α/IL-1β）核心关联疾病痛风性关节炎（急性发作）、幼年特发性关节炎（JIA）、成人 Still 病、强直性脊柱炎致病机制启动早期炎症反应，诱导发热、疼痛和组织损伤；促进滑膜细胞释放前列腺素 E2（PGE2），加重关节疼痛和肿胀；参与痛风石形成（IL-1β 激活中性粒细胞吞噬尿酸盐结晶）。靶向治疗药物药物名称药物类别靶点特性主要适应症阿那白滞素 IL-1 受体拮抗剂（重组人源）阻断 IL-1 与受体结合 RA（对 TNF 拮抗剂无效者）、JIA 卡那单抗抗 IL-1β 单克隆抗体（全人源）直接中和 IL-1β 活性急性痛风性关节炎、成人 Still 病利纳西普 IL-1 受体融合蛋白竞争性结合 IL-1α/β 家族性寒冷型自身炎症综合征4. 白细胞介素 - 17A（IL-17A）核心关联疾病银屑病（PsO）、银屑病关节炎（PsA）、强直性脊柱炎（AS）、化脓性汗腺炎致病机制招募中性粒细胞至皮肤 / 关节病灶，诱导角质形成细胞过度增殖（银屑病皮损）；促进滑膜细胞释放 IL-6、TNF-α，放大关节炎症；参与肌腱端炎（AS 特征性病变）的发生。靶向治疗药物药物名称药物类别靶点特性主要适应症司库奇尤单抗抗 IL-17A 单克隆抗体（全人源）直接中和 IL-17A 活性 PsO、PsA、AS 依奇珠单抗抗 IL-17A 单克隆抗体（人源化）直接中和 IL-17A 活性 PsO、PsA、AS 布罗利尤单抗抗 IL-17 受体 A 单克隆抗体（全人源）阻断 IL-17A/F 与受体结合 PsO、PsA5. 白细胞介素 - 23（IL-23）核心关联疾病银屑病（PsO）、银屑病关节炎（PsA）、克罗恩病（CD）、溃疡性结肠炎（UC）致病机制维持 Th17 细胞（分泌 IL-17 的关键 T 细胞）的存活和功能，间接促进 IL-17 释放；诱导肠道固有层免疫细胞活化，加重肠道黏膜炎症（IBD）；参与银屑病皮损中角质形成细胞的异常增殖。靶向治疗药物药物名称药物类别靶点特性主要适应症古塞奇尤单抗抗 IL-23 p19 单克隆抗体（全人源）阻断 IL-23 活性（不影响 IL-12） PsO、PsA、CD 乌司奴单抗抗 IL-12/23 p40 单克隆抗体（全人源）同时阻断 IL-12 和 IL-23 PsO、PsA、CD、UC Risankizumab 抗 IL-23 p19 单克隆抗体（全人源）阻断 IL-23 活性 PsO、PsA、CD、UC6. 转化生长因子 -β（TGF-β）核心关联疾病系统性硬化症（SSc）、类风湿关节炎（RA，晚期纤维化）、特发性肺纤维化（IPF，自身免疫相关）致病机制过度激活成纤维细胞，促进胶原蛋白合成，导致皮肤 / 肺脏纤维化（SSc 特征）；调控免疫细胞分化，失衡时加重自身免疫反应和组织修复异常。靶向治疗药物药物名称药物类别靶点特性主要适应症 Fresolimumab 抗 TGF-β 单克隆抗体（全人源）直接中和 TGF-β1/2/3 活性系统性硬化症（临床阶段）、IPF Galunisertib TGF-β 受体 I 激酶抑制剂阻断 TGF-β 信号通路肝癌（合并自身免疫相关纤维化，临床阶段）7. 白细胞介素 - 36（IL-36，含 IL-36α/β/γ）核心关联疾病泛发性脓疱型银屑病（GPP）、斑块型银屑病（PsO）、掌跖脓疱病致病机制激活角质形成细胞和巨噬细胞，释放促炎因子（如 IL-8），诱发脓疱形成；放大皮肤局部炎症反应，加重银屑病皮损。靶向治疗药物药物名称药物类别靶点特性主要适应症 Spesolimab 抗 IL-36 受体单克隆抗体（全人源）阻断 IL-36 与受体结合泛发性脓疱型银屑病（GPP）、PsO8. 白细胞介素 - 21（IL-21）核心关联疾病系统性红斑狼疮（SLE）、类风湿关节炎（RA）、干燥综合征（pSS）致病机制促进 B 细胞活化、分化为浆细胞，产生抗核抗体（ANA）、抗双链 DNA 抗体（dsDNA）等自身抗体（SLE 核心病理）；激活 Tfh 细胞（滤泡辅助 T 细胞），加重体液免疫紊乱。靶向治疗药物药物名称药物类别靶点特性主要适应症 Blisibimod IL-21 受体融合蛋白竞争性结合 IL-21 SLE（临床阶段，针对肾炎）、RA Mimfilia（Anifrolumab）抗 I 型干扰素受体抗体（全人源）间接抑制 IL-21 下游信号（SLE 中 I 型干扰素与 IL-21 协同作用） SLE（获批）9. 干扰素 -γ（IFN-γ）核心关联疾病多发性硬化症（MS）、系统性红斑狼疮（SLE）、结节病致病机制激活巨噬细胞，释放促炎因子（如 TNF-α、IL-1），加重中枢神经系统炎症（MS 脱髓鞘病变）；调控 T 细胞分化为 Th1 细胞，失衡时诱发自身免疫攻击。靶向治疗药物药物名称药物类别靶点特性主要适应症 Fontolizumab 抗 IFN-γ 单克隆抗体（人源化）直接中和 IFN-γ 活性结节病（临床阶段）、MS（临床阶段） Natalizumab 抗 α4 整合素抗体间接抑制 IFN-γ 介导的 T 细胞迁移 MS、CD（减少炎症细胞浸润）10. 趋化因子 CCL2（MCP-1，单核细胞趋化蛋白 - 1）核心关联疾病类风湿关节炎（RA）、系统性硬化症（SSc）、糖尿病肾病（自身免疫相关）致病机制特异性招募单核细胞、巨噬细胞至关节滑膜或肾脏，分化为破骨细胞（RA 骨破坏）或促进纤维化（SSc / 肾病）；加重局部炎症细胞聚集，放大组织损伤。靶向治疗药物药物名称药物类别靶点特性主要适应症 Carmustine CCL2 受体（CCR2）拮抗剂阻断 CCL2-CCR2 信号通路 RA（临床阶段）、糖尿病肾病（临床阶段） BMS-813160 CCR2 拮抗剂阻断单核细胞迁移 RA（临床阶段）参考资料 Yuping Lai and Chen Dong，Therapeutic antibodies that target inflammatory cytokines in autoimmune diseases，International Immunology, Vol. 28, No. 4, pp. 181–188 doi:10.1093/intimm/dxv063 Type I Interferons in Autoimmunity，J Invest Dermatol. 2022 Mar;142(3 Pt B):793-803. doi: 10.1016/j.jid.2021.11.031. Grebenciucova E and VanHaerents S (2023) Interleukin 6: at the interface of human health and disease. Front. Immunol. 14:1255533. doi: 10.3389/fimmu.2023.1255533

免疫疗法

2023-05-08

·PRNewswire

Global Pancreatic Cancer Competitive Landscape Report 2023: Comprehensive Insights about 250+ Companies and 300+ Drugs

DUBLIN, May 8, 2023 /PRNewswire/ -- The "Pancreatic Cancer - Competitive landscape, 2023" report has been added to ResearchAndMarkets.com's offering. This "Pancreatic Cancer- Competitive landscape, 2023" report provides comprehensive insights about 250+ companies and 300+ drugs in Pancreatic Cancer Competitive landscape. It covers the therapeutics assessment by product type, stage, route of administration, and molecule type. It further highlights the inactive pipeline products in this space. In March 2023, Adaptimmune Therapeutics plc. and TCR Therapeutics Inc. (NASDAQ: TCRR), announced entry into a definitive agreement under which Adaptimmune will combine with TCR in an all-stock transaction to create a preeminent cell therapy company focused on treating solid tumors. The combination provides extensive benefits for clinical development and product delivery supported by complementary technology platforms. As a result, and following the closing of the transaction, it is anticipated that the combined company's cash runway will extend into 2026. In February 2023, Akamis Bio, announced an expansion of its ongoing partnership with the Parker Institute for Cancer Immunotherapy (PICI) to include a clinical collaboration with the Cancer Research Institute (CRI) that will focus on advancing novel treatments for pancreatic cancer. As part of the Akamis Bio, PICI, and CRI partnership, NG-350A, an immuno-stimulatory tumor gene therapy driving intratumoral expression of a CD40 agonist monoclonal antibody, will be evaluated in combination with standard-of-care chemotherapy and the CTLA-4 inhibitor ipilimumab (YERVOY). In February 2023, Gritstone bio, Inc. announced that it has entered into a clinical trial agreement with the National Cancer Institute (NCI), an institute of the National Institutes of Health, to evaluate an autologous T cell therapy expressing a T cell receptor targeting mutated KRAS in combination with Gritstone's KRAS-directed vaccine candidate, SLATE-KRAS, in a Phase 1 study. Under the terms of the agreement, NCI will identify patients with metastatic cancer that are eligible for adoptive cell transfer based on the presence of a G12V or G12D KRAS mutation (KRASmut). In February 2023, Keymed Biosciences Inc., jointly announced a global exclusive license agreement with AstraZeneca for CMG901, a potential first-in-class Claudin 18.2 antibody drug conjugate (ADC). Under the license agreement, AstraZeneca will be responsible for the research, development, manufacture and commercialization of CMG901 globally. CMG901 is currently in a Phase I clinical trial for the treatment of Claudin 18.2-positive solid tumors. In January 2023, AIM ImmunoTech Inc. announced it has entered into an external sponsored collaborative clinical research agreement with Erasmus MC and AstraZeneca. Under the agreement, Erasmus MC is planning to perform an investigator-initiated clinical study, entitled "Combining anti-PD-L1 immune checkpoint inhibitor durvalumab with TLR-3 agonist rintatolimod in patients with metastatic pancreatic ductal adenocarcinoma for therapy effect. DURIPANC Study," in which it will use both Study Drugs provided by AstraZeneca and AIM ImmunoTech. Pancreatic Cancer Analytical Perspective In-depth Commercial Assessment: Pancreatic Cancer Collaboration Analysis by Companies The Report provides in-depth commercial assessment of drugs that have been included, which comprises collaboration, agreement, licensing and acquisition - deals values trends. The sub-segmentation is described in the report which provide company-company collaboration (licensing/partnering), company academic collaboration and acquisition analysis in tabulated form. Key Questions Answered Current Treatment Scenario and Emerging Therapies: How many companies are developing Pancreatic Cancer drugs? How many Pancreatic Cancer drugs are developed by each company? How many emerging drugs are in mid-stage, and late-stage of development for the treatment of Pancreatic Cancer? What are the key collaborations (Industry-Industry, Industry-Academia), Mergers and acquisitions, licensing activities related to the Pancreatic Cancer therapeutics? What are the recent trends, drug types and novel technologies developed to overcome the limitation of existing therapies? What are the clinical studies going on for Pancreatic Cancer and their status? What are the key designations that have been granted to the emerging and approved drugs? Key Players Panbela Therapeutics ERYtech Pharma Jiangsu HengRui Medicine Co., Ltd. FibroGen Novartis AG AB Science TME Pharma AG Intensity Therapeutics Silenseed LTD SynerGene Therapeutics Elevation oncology Salspera LLC Redx Pharma Plc AIM ImmunoTech Inc. Rain Oncology Jazz Pharmaceuticals Invyte Corporation Immodulon Therapeutics Ltd GSK plc Merck Sharp & Dohme LLC Roche Helsinn Healthcare SA Argenus Inc. Actuate Therapeutics OSE Immunotherapeutics Incyte Corporation Galera Therapeutics CSPC ZhongQi Pharmaceutical Technology Astellas Pharma Global Development, Inc. NanOlogy Theriva Biologics AstraZeneca Berg, LLC Agenus ABVC BioPharma, Inc. Boehringer Ingelheim Alligator Bioscience CARsgenTherapeutics Co.,Ltd Purple Biotech Ltd. Lisata Therapeutics Chongqing Precision Biotech Co., Ltd Cybrexa Therapeutics Bold Therapeutics BioNTech SE Bristol-Myers Squibb DEKA Biosciences Senhwa Biosciences Cue Biopharma Carisma Therapeutics Inc Key Products Olaptesed pegol INT230-6 SBP-101 Masitinib NIS793 siG12D LODER SGT-53 Seribantumab Salmonella-IL2 RXC004 Rintatolimod RAIN-32 Lurbinectedin Retifanlimab IMM-101 GSK2256098 Belzutifan Atezolizumab Anamorelin AGEN1423 Elraglusib OSE2101 Epacadostat GC4711 Docetaxel Zolbetuximab NanoPac VCN-01 Danvatirsen BPM31510 Botensilimab ABV-1703 BI 907828 Mitazalimab CT041 CM24 CEND-1 CEA-targeted CAR-T cells CBX-12 BOLD-100 BNT141 BMS-813160 DK210 CX-5461 CUE-102 CT-0508 For more information about this report visit About ResearchAndMarkets.com ResearchAndMarkets.com is the world's leading source for international market research reports and market data. We provide you with the latest data on international and regional markets, key industries, the top companies, new products and the latest trends. Media Contact: Research and Markets Laura Wood, Senior Manager [email protected] For E.S.T Office Hours Call +1-917-300-0470 For U.S./CAN Toll Free Call +1-800-526-8630 For GMT Office Hours Call +353-1-416-8900 U.S. Fax: 646-607-1907 Fax (outside U.S.): +353-1-481-1716 Logo: SOURCE Research and Markets

免疫疗法引进/卖出疫苗临床1期抗体药物偶联物

100 项与 BMS-813160 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB16240

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
肝细胞癌	临床2期	美国	Bristol Myers Squibb Co.	2020-03-05
非小细胞肺癌	临床2期	美国	Bristol Myers Squibb Co.	2020-03-05
晚期胰腺导管腺癌	临床2期	美国	Bristol Myers Squibb Co.	2019-12-12
局部晚期胰腺腺癌	临床2期	美国	Bristol Myers Squibb Co.	2019-12-12
晚期恶性实体瘤	临床2期	美国	Bristol Myers Squibb Co.	2017-08-08
晚期恶性实体瘤	临床2期	澳大利亚	Bristol Myers Squibb Co.	2017-08-08
晚期恶性实体瘤	临床2期	比利时	Bristol Myers Squibb Co.	2017-08-08
晚期恶性实体瘤	临床2期	加拿大	Bristol Myers Squibb Co.	2017-08-08
晚期恶性实体瘤	临床2期	德国	Bristol Myers Squibb Co.	2017-08-08
晚期恶性实体瘤	临床2期	西班牙	Bristol Myers Squibb Co.	2017-08-08

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临床结果

适应症

分期

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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


NCT03184870 (Pubmed \| J Immunother Cancer)	临床1/2期	晚期结直肠腺癌 \| 胰腺癌一线 \| 二线	222	BMS-813160 300 mg two times a day+gem/nabP+nivolumab	築衊醖觸顧鏇蓋選構願(顧齋淵鹹鏇醖壓築膚膚) = Two dose-limiting toxicities (rash and pericardial effusion with pericarditis, both grade 3) occurred 顧獵繭蓋襯網鏇淵繭願 (網築衊醖觸鏇鹹網鏇選 ) 更多	积极	2026-01-01
				BMS-813160 300 mg two times a day+gem/nabP
ESMO_IO2023	临床2期	肝细胞癌 \| 非小细胞肺癌	36	Nivolumab + BMS-813160 (CCR2/5i)	憲夢鹹襯夢餘壓選積鑰(繭積憲壓繭鏇廠窪齋蓋) = 網範繭獵鹹衊衊遞醖蓋鑰網餘遞築醖積範憲願 (觸選衊顧願淵窪醖夢範 )	-	2023-12-07
NCT03767582 (ASCO_GI2023) 人工标引	临床1期	胰腺导管腺癌	13	Nivolumab 480mg+BMS-813160 150mg/300mg+GVAX 5x108 cells	夢淵選窪襯憲築衊選膚(網艱餘繭選鑰製鬱鑰壓) = 顧夢網鬱簾選範鬱鑰鏇夢繭製壓窪餘觸鏇糧鏇 (壓構鑰鬱鏇觸憲壓醖餘 ) 更多	积极	2023-01-24
NCT03496662 (CTgov)	临床1/2期	胰腺导管腺癌	40	Peripheral blood+Nivolumab+Nab-paclitaxel+Gemcitabine+BMS-813160 (Part A - Experimental Dose Level 0)	遞網遞淵構簾壓齋艱淵 = 鹽膚餘選選淵蓋壓蓋獵獵襯繭襯範憲觸選範醖 (範鬱鏇觸鑰築壓鹽鏇鬱, 壓構衊蓋製網蓋淵艱壓 ~ 觸觸艱範網構鹽鹹憲鏇) 更多	-	2022-11-30
				Peripheral blood+Nab-paclitaxel+Gemcitabine (Part A - Control (Chemotherapy Only))	構壓簾鹹網醖餘獵製廠(鑰憲願襯顧蓋襯鹹製淵) = 範網選膚糧壓窪餘獵廠選構艱構醖膚簾鏇積鬱 (廠製艱糧鹹壓遞製鹽淵, 窪鬱遞壓網鏇選遞壓衊 ~ 衊壓製顧窪鏇構鬱築鏇) 更多
NCT01752985 (CTgov)	临床2期	2型糖尿病 \| 糖尿病肾病	319	BMS-813160 (BMS-813160 150 mg QD)	構鹹衊繭廠製襯糧鬱構(簾淵繭觸製廠淵構積衊) = 遞積繭衊選糧壓網膚鏇醖獵餘廠積壓壓夢艱憲 (淵醖衊艱壓製遞餘網範, 48.994) 更多	-	2019-06-25
				BMS-813160 (BMS-813160 300 mg BID)	構鹹衊繭廠製襯糧鬱構(簾淵繭觸製廠淵構積衊) = 遞廠夢糧鑰鹹艱壓積製醖獵餘廠積壓壓夢艱憲 (淵醖衊艱壓製遞餘網範, 62.795) 更多