Ia 期的目的是评估BBP-398 联合奥希替尼治疗在既往接受第三代EGFR TKIs后出现EGFR 突变的局部晚期或转移性非小细胞肺癌受试者的安全性、耐受性、药代动力学和抗癌活性。 Ib 的目的是研究BBP-398 联合奥希替尼治疗伴有EGFR突变的局部晚期或转移性NSCLC 受试者的疗效和安全性。

开始日期2023-07-12

申办/合作机构

上海联拓生物科技有限公司

[+2]

NCT05375084 / Recruiting临床1期

A Phase 1 Study of the SHP2 Inhibitor BBP-398 (Formerly Known as IACS-15509) in Combination With the Programmed Death Receptor-1 Blocking Antibody Nivolumab in Patients With Advanced Non-Small Cell Lung Cancer With a KRAS Mutation

This is a Phase 1 study of BBP-398, a SHP2 inhibitor, in combination with nivolumab, a PD-1 antibody, in patients with NSCLC with a KRAS mutation. The study involves 2 parts: Phase 1a Dose Escalation and Phase 1b Dose Expansion.

开始日期2022-10-20

申办/合作机构

Navire Pharma, Inc.初创企业

[+1]

CTR20222749 / Terminated临床1期

评价BBP-398 在中国晚期实体瘤受试者中的安全性、耐受性、药代动力学和初步抗肿瘤活性的I 期临床试验

主要目的： -A部分（剂量递增）：评估BBP-398（SHP2抑制剂）在中国晚期实体瘤受试者中的安全性和耐受性；评估BBP-398在中国晚期实体瘤受试者中的最大耐受剂量（MTD）和/或II期推荐剂量（RP2D）。 -B部分（剂量扩展）：评估BBP-398（MTD或RP2D）在NSCLC受试者中的初步抗肿瘤活性。次要目的： -A部分（剂量递增）：评估中国晚期实体瘤受试者接受单/多次BBP-398给药后血浆和尿液的药代动力学（PK）特征；研究者评估BBP-398在中国晚期实体瘤受试者中的初步抗肿瘤活性。 -B部分（剂量扩展）：TEAE和SAE的发生率及严重程度；

开始日期2022-10-18

申办/合作机构

上海联拓生物科技有限公司

[+2]

100 项与 Navire Pharma, Inc. 相关的临床结果

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项与 Navire Pharma, Inc. 相关的文献（医药）

2021-12-01·Molecular Cancer Therapeutics

Abstract P207: BBP-398, a potent, small molecule inhibitor of SHP2, enhances the response of established NSCLC xenografts to KRASG12C and mutEGFR inhibitors

作者: Wade, Anna ; Czako, Barbara ; Beltran, Pedro ; Kohl, Nancy ; Leonard, Paul ; Sun, Yuting ; Jones, Phil ; Donovan, Sofia ; Stice, James P. ; Sinkevicius, Kerstin ; Mseeh, Faika ; Wallace, Eli ; Lim, Justin

AbstractSrc homology 2 domain-containing phosphatase (SHP2), a ubiquitously expressed non-receptor tyrosine phosphatase, plays a critical role in the regulation of the MAPK signaling pathway and cellular proliferation. Activating mutations in SHP2 are associated with the development of multiple malignancies including leukemia, lung cancer and neuroblastoma. In addition, SHP2 promotes the conversion of oncogenic KRAS to its active GTP-bound state and it’s inhibition can enhance efficacy of GDP-KRASG12C inhibitors as well as other MAPK pathway inhibitors (RAF, MEK and ERK) which have suboptimal clinical efficacy as single agents. As a result, inhibition of SHP2 through genetic manipulation or pharmacological means has been shown to suppress tumor growth and presents an attractive potential avenue for the treatment of malignancies as monotherapy or in combination with other MAPK/PI3K inhibitors. Here we describe BBP-398, a potent, orally bioavailable allosteric small molecule inhibitor of SHP2. BBP-398 displays high selectivity against other phosphatases, kinases, GPCRs, transporters and hERG. Predicted human PK properties show good oral bioavailability with half-life of ~12-16 hours enabling continuous daily dosing and optimal therapeutic index in combination with other targeted therapeutics. In cellular assays, BBP-398 demonstrates potent pERK/DUSP6 inhibition and loss of viability across a panel of cell lines with active MAPK signaling, such as mutant EGFR and KRASG12C. In vivo, BBP-398 strongly suppresses RAS-ERK signaling in RTK- or RAS-driven xenografts. In the EGFR-dependent non-small cell lung cancer (NSCLC) HCC827 and esophageal squamous cell carcinoma KYSE-520 xenograft models, BBP-398 drives dose dependent efficacy consistent with the level of target inhibition. Detailed analysis of tumor response shows that efficacy is driven by maintaining better than 50% inhibition of pERK for most of the dosing interval. In addition to its strong single agent activity, BBP-398 also leads to enhanced efficacy in vitro and in vivo when used in combination with targeted therapeutics against driver MAPK genetic alterations, such as KRAS, EGFR or MET. Combination targeting, such as with the GDP-KRASG12C inhibitor sotorasib in the NSCLC NCI-H358 xenograft model, or with the mutant EGFR inhibitor osimertinib in the HCC827 erlotinib resistant (ER) xenograft model, drives strong suppression of MAPK activity and results in tumor regressions. Collectively, these findings highlight that SHP2 inhibition is a promising molecular therapeutic strategy in cancer which can potentially strongly suppress tumor growth as a single agent or in combination with other MAPK pathway inhibitors. Given its preclinical properties and projected favorable clinical pharmacokinetic profile, BBP-398 is currently being evaluated in a Phase 1/1b trial in patients with advanced solid tumors (NCT04528836).Citation Format: James P. Stice, Sofia Donovan, Yuting Sun, Nancy Kohl, Barbara Czako, Faika Mseeh, Paul Leonard, Anna Wade, Justin Lim, Phil Jones, Eli Wallace, Kerstin Sinkevicius, Pedro Beltran. BBP-398, a potent, small molecule inhibitor of SHP2, enhances the response of established NSCLC xenografts to KRASG12C and mutEGFR inhibitors [abstract]. In: Proceedings of the AACR-NCI-EORTC Virtual International Conference on Molecular Targets and Cancer Therapeutics; 2021 Oct 7-10. Philadelphia (PA): AACR; Mol Cancer Ther 2021;20(12 Suppl):Abstract nr P207.

2020-11-01·Cancer Research1区 · 医学

Allosteric SHP2 Inhibitor, IACS-13909, Overcomes EGFR-Dependent and EGFR-Independent Resistance Mechanisms toward Osimertinib

1区 · 医学

Article

作者: Gera, Sonal ; Draetta, Giulio F. ; Jiang, Yongying ; Heffernan, Timothy P. ; Peoples, Michael ; Di Francesco, Maria Emilia ; Mseeh, Faika ; Kohl, Nancy E. ; Leonard, Paul ; Harris, Angela L. ; Johnson, Sarah ; Mandal, Pijus K. ; Chang, Qing ; Parker, Connor A. ; Gao, Guang ; Kovacs, Jeffrey J. ; Lopez, Anastasia M. ; Liu, Chiu-Yi ; Yu, Simon S. ; Kang, Zhijun ; McAfoos, Timothy ; Carrillo, Caroline C. ; Sun, Yuting ; Ramamoorthy, Vandhana ; Carroll, Christopher L. ; Bristow, Christopher A. ; Bivona, Benjamin J. ; Ma, Xiaoyan ; Miller, Meredith A. ; Seth, Sahil ; Marszalek, Joseph R. ; Spencer, Nakia D. ; Zuniga, Andy M. ; Mullinax, Robert A. ; Feng, Ningping ; Wu, Qi ; Williams, Christopher C. ; Jones, Philip ; Czako, Barbara ; Huang, Justin K. ; Meyers, Brooke A. ; Burke, Jason P. ; Cross, Jason B. ; Giuliani, Virginia ; Suzuki, Erika

AbstractSrc homology 2 domain-containing phosphatase (SHP2) is a phosphatase that mediates signaling downstream of multiple receptor tyrosine kinases (RTK) and is required for full activation of the MAPK pathway. SHP2 inhibition has demonstrated tumor growth inhibition in RTK-activated cancers in preclinical studies. The long-term effectiveness of tyrosine kinase inhibitors such as the EGFR inhibitor (EGFRi), osimertinib, in non–small cell lung cancer (NSCLC) is limited by acquired resistance. Multiple clinically identified mechanisms underlie resistance to osimertinib, including mutations in EGFR that preclude drug binding as well as EGFR-independent activation of the MAPK pathway through alternate RTK (RTK-bypass). It has also been noted that frequently a tumor from a single patient harbors more than one resistance mechanism, and the plasticity between multiple resistance mechanisms could restrict the effectiveness of therapies targeting a single node of the oncogenic signaling network. Here, we report the discovery of IACS-13909, a specific and potent allosteric inhibitor of SHP2, that suppresses signaling through the MAPK pathway. IACS-13909 potently impeded proliferation of tumors harboring a broad spectrum of activated RTKs as the oncogenic driver. In EGFR-mutant osimertinib-resistant NSCLC models with EGFR-dependent and EGFR-independent resistance mechanisms, IACS-13909, administered as a single agent or in combination with osimertinib, potently suppressed tumor cell proliferation in vitro and caused tumor regression in vivo. Together, our findings provide preclinical evidence for using a SHP2 inhibitor as a therapeutic strategy in acquired EGFRi-resistant NSCLC.Significance:These findings highlight the discovery of IACS-13909 as a potent, selective inhibitor of SHP2 with drug-like properties, and targeting SHP2 may serve as a therapeutic strategy to overcome tumor resistance to osimertinib.

2019-12-01·Molecular Cancer Therapeutics

Abstract C036: Discovery of IACS-13909, an allosteric SHP2 inhibitor that overcomes multiple mechanisms underlying osimertinib resistance

作者: Kovacs, Jeffrey J ; Draetta, Giulio F ; Johnson, Sarah B ; Feng, Ningping ; Marszalek, Joseph R ; Czako, Barbara ; Parker, Connor A ; Chang, Qing ; Zuniga, Andy M ; Jones, Philip ; Guang, Gao ; Ma, Xiaoyan ; Ramamoorthy, Vandhana ; Seth, Sahil ; Leonard, Paul G ; Huang, Justin Kwang-Lay ; Meyers, Brooke A ; Sun, Yuting ; Peoples, Michael D ; Francesco, Maria E Di ; Carrillo, Caroline C ; Heffernan, Timothy P ; Yu, Simon S ; Suzuki, Erika ; Burke, Jason P ; Williams, Christopher Conrad ; Mseeh, Faika ; Kohl, Nancy E ; McAfoos, Timothy ; Jiang, Yongying ; Wu, Qi ; Carroll, Christopher L ; Gera, Sonal ; Bristow, Christopher A ; Kang, Zhijun ; Mandal, Pijus K ; Mullinax, Robert A ; Cross, Jason B ; Harris, Angela L

AbstractOsimertinib, a third generation EGFR inhibitor, is a front-line therapy for EGFR mutated non-small lung cancer (NSCLC). The long-term effectiveness of osimertinib is limited by acquired resistance. Clinically identified resistance mechanisms include EGFR-dependent mechanisms such as mutations on EGFR that preclude drug binding, and EGFR-independent activation of the MAPK pathway, for instance via activation of alternate RTKs. It has also been noted that frequently a tumor from a single patient harbors more than one resistance mechanism, and the plasticity between the multiple resistance mechanisms will restrict the effectiveness of therapies targeting a single node of the oncogenic signaling network. SHP2 (Src homology 2 domain-containing phosphatase) is a phosphatase that mediates the signaling of multiple RTKs and is required for full activation of the MAPK pathway. Here we report IACS-13909 - a specific and potent allosteric inhibitor of SHP2 - suppresses the signaling of RTK/MAPK pathway. IACS-13909 potently impedes the proliferation of tumors with a broad spectrum of RTKs as the oncogenic driver. Importantly, in NSCLC models with acquired resistance to osimertinib, IACS-13909 administered as a single agent or in combination with osimertinib potently reduces tumor cell proliferation in vitro and in vivo. Together, our findings provide preclinical evidence for using a SHP2 inhibitor as a therapeutic strategy in acquired EGFR inhibitor-resistant NSCLC. Currently, a compound that potently inhibits SHP2 has been selected as the clinical development candidate and is undergoing IND-enabling studies with a projected first-in-human target of early 2020.Citation Format: Yuting Sun, Brooke A Meyers, Sarah B Johnson, Angela L Harris, Barbara Czako, Jason B Cross, Paul G Leonard, Faika Mseeh, Maria E Di Francesco, Connor A Parker, Qi Wu, Christopher A Bristow, Jason P Burke, Caroline C Carrillo, Christopher L Carroll, Qing Chang, Ningping Feng, Sonal Gera, Gao Guang, Justin Kwang-Lay Huang, Yongying Jiang, Zhijun Kang, Jeffrey J Kovacs, Xiaoyan Ma, Pijus K Mandal, Timothy McAfoos, Robert A Mullinax, Michael D Peoples, Vandhana Ramamoorthy, Sahil Seth, Erika Suzuki, Christopher Conrad Williams, Simon S Yu, Andy M Zuniga, Giulio F Draetta, Joseph R Marszalek, Timothy P Heffernan, Nancy E Kohl, Philip Jones. Discovery of IACS-13909, an allosteric SHP2 inhibitor that overcomes multiple mechanisms underlying osimertinib resistance [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; 2019 Oct 26-30; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2019;18(12 Suppl):Abstract nr C036. doi:10.1158/1535-7163.TARG-19-C036

项与 Navire Pharma, Inc. 相关的新闻（医药）

2024-02-14

·同写意

拒绝卖身的“倒爷”Biotech，转眼进入关停倒计时

为打造全球ADC/RDC未来产业高地，成都医学城拟于2024年4月18日-19日举办首届未来XDC新药大会！大会以“共创偶联药物产业未来”为主题，由同写意策划，安排一场主论坛和九场主题论坛，邀请“政、产、学、研、金、媒”各领域专家，通过“成果发布、主题演讲、热点对话、表彰颁奖、展览展示”五位一体的多元化的组织形式，迸发更多XDC产业新科技、新业态、新模式，构建XDC产业全新生态，触摸医药产业未来脉动。2月13日，一则重磅消息刷爆了各位医药人的朋友圈——联拓生物已宣布，其董事会已完成对公司的全面战略审查，决定开始逐步缩减其业务。换句话说，这家致力License-in商业模式的“倒爷”将按计划逐步走向“消亡”。决定从纳斯达克摘牌、注销并暂停其在交易所法案下的报告义务，以减轻运营作为上市公司的负担。此外，公司宣布逐步停止在进行的临床试验，同时决定发放4.8美元/股的特别股息，总计金额约5.28亿美元。与此同时，联拓生物计划在第一季度将裁员50%的员工，并在2024年全年继续进行裁员。预计到2024年底，公司的业务将停止运营。在剩余资产出售或许可终止以及员工裁员基本完成后，联拓生物预计将在2027年上半年完全解散。值得一提的是，联拓生物在资本市场表现依旧稳健。消息公布第二天，公司股票不跌反增，涨幅超过18%。1“倒爷”的生意经众所周知，新药研发是一个极度“烧钱”的高风险项目，早期我国药企研发、创新的能力比较差，研发资金也不充裕，License-in模式凭借其优势乘风而起，该模式一度被视为颇适合中国创新药发展的产业模式。成立于2020年8月的联拓生物，得益于Perceptive Advisors创新药孵化公司的帮助，其公司业务范围已跨越大洋。公司将美国和欧洲的新药和试验性药物引入中国，在中国完成临床研究，以获得批准，并建立销售该药物所需的商业化团队。2021年11月，联拓生物成功登陆纳斯达克市场后，更是创下数项“之最”记录。统公开数据显示，截至去年8月，中国药企的海外License-in项目共计45项。从交易数量来看，联拓生物以5项创新药的License-in项目数量居于国内药企之首。而随着行业发展，在License-in模式中，另一种盈利模式“转卖”，开始进入联拓生物的视野。去年10月24日，联拓生物宣布与BMS达成协议，通过“低买高卖”创新药权益赚了3.5亿美元，就给了行业不小的震撼。根据协议条款，联拓生物授予后者Mavacamten在中国大陆、香港、澳门、台湾以及新加坡、泰国等地进行开发和商业化的权益，而联拓生物将获得3.5亿美元的一次性付款。往前推三年，联拓生物以4000万美元首付款、1.475亿美元潜在里程碑付款，从MyoKardia引进Mavacamten在上述市场的权益。这一波操作下来，联拓生物到账约25亿元。此外，2022年12月，联拓生物还与辉瑞就RSV药物Sisunatovir达成协议，辉瑞将退回联拓生物此前付出的2000万美元首付款，同时，由辉瑞负责这款药物的后续开发和商业化，而联拓生物还可获得1.35亿美元的商业里程碑付款以及销售分成。此番不仅让联拓生物收回首付款，亦有后续销售分成可以拿，成就了联拓通过转卖赚到的第一桶金。2基本盘尚可一观可以肯定的是，做“倒爷”的这几年，联拓生物手里攒下了不少“好货”。（联拓生物部分License-in项目图源：猎药人俱乐部）联拓生物的管线分别来自BridgeBio和MyoKardia的子公司Navire Pharma和QED Therapeutics的多种FIC产品，涵盖心血管肾脏、肿瘤、眼科、炎症疫病和呼吸系统适应症，且大部分已处于后期阶段并已得到临床验证。其中，TP-03、NBTXR3、infigratini和为主要候选产品。 TP-03拟开发用于治疗蠕形螨睑缘炎和睑板腺功能障碍两种眼科疾病。NBTXR3是肿瘤领域一款潜在“first-in-class”放射增强剂，潜在适应症包括头颈癌、实体瘤，是联拓生物与Nanobiotix达成开发和商业化合作的创新疗法。在肿瘤领域，还有FGFR抑制剂infigratinib （BGJ398）、SHP2抑制剂BBP-398。Infigratinib是一种口服FGFR1-3选择性抑制剂，拟开发治疗胆管癌、胃癌、以及其他因FGFR基因变异导致的肿瘤；BBP-398是一种SHP2抑制剂，拟开发用于治疗耐药性和其他难治性肿瘤。上述两款产品均为联拓生物与BridgeBio合作研发的产品，根据协议条款，联拓生物将获得中国及指定亚洲市场的商业化权益，并参与infigratinib与BBP-398的临床研发。除上述几款合作战略产品之外，联拓生物还引进了三款炎症领域的创新药omilancor、NX-13、LYR-210。其中，联拓生物与Landos Biopharma达成了新药Omilancor（BT-11）和NX-13的合作协议。 2020年，联拓生物还与BridgeBio达成战略合作，借此优先获得BridgeBio的20多种管线产品，包括已许可和已收购的产品，为期四年。联拓生物的合作伙伴包括Nanobiotix、Landos Biopharma以及Lyra Therapeutics。（联拓生物达成的BD交易（单位：亿美元）图源：细胞与基因治疗领域）3拒绝“卖身”，高管出走彼时的联拓生物就像风浪之中，没有舵手的孤舟。更糟糕的是，其丰厚的“家产”已经引起了同行的觊觎。去年12月初，Tang Capital Partners旗下的Concentra Biosciences向联拓生物提出了生物技术收购要约，提议以每股4.30美元的现金交易抄底收购后者。Concentra在收购邀约中表示，公司可以为联拓生物股东实现价值最大化，并将管理或过渡任何剩余的临床研究活动。不过，交易完成时联拓生物需要至少拥有5.15亿美元的现金和现金等价物。Concentra还紧迫地要求联拓生物，在12月8日下午就做出回应，否则届时收购邀约将失效。如果联拓生物接受收购要约，Concentra将在12月22日前就最终协议进行谈判，并在2024年2月22日前完成交易。但在联拓生物眼里，Concentra并非“拯救者”。显然，以联拓生物如今的现金流状况无法满足这一要求，截至2023年9月30日，该公司拥有现金、现金等价物、有价证券及限制性现金合计2.522亿美元。12月7日，联拓生物拒绝邀约，认为其“低估了公司的价值，不符合联拓生物和其股东的最佳利益”。颇为棘手的是，在该决定后，接连两日，联拓生物人事还发生了重大变动：两位公司高管相继宣布离职。先是首席执行官王轶喆从公司离职，第二天，公司的首席财务官Yi Larson也宣布了离职。或许是与初心相违，王轶喆曾表示，“联拓生物的License-in不是只把产品买进来，开发之后就结束了，而是要把商业化理念贯穿整个医药生命周期。因为只有最终将创新药物推向市场，才能让患者真正获益”。与此同时，公司的资本结构和偿债能力还引发了投资市场对该公司的关注。财报数据显示，截至2023年三季度末，联拓生物年内净亏损为6970万美元，2022年同期为净亏损9200万美元。现金流方面，截至去年三季度末，其现金、现金等价物、有价证券和限制性现金总额为2.522亿美元。与大多Biotech的命运一样，联拓生物至今仍未有一款产品成功商业化盈利。对此，有行业人士解释称“不是它不想做，而是没有足够的腾挪空间”。说到底，License-in模式最后拼的还是钱，公司管线需要大量的资金储备孵化——反观联拓生物在研管线却还有8条，光支撑研发都可能很难维持两年，更不要提自建商业化团队了。如今来看，联拓生物的“硬骨气”抉择有迹可循。在公司关闭程序中，联拓生物还将立即启动资产出售的动作，一旦出售完成，公司将获得的现金分配给股东。参考资料：1.联拓生物官网2.联拓生物：CEO和CFO离任；细胞基因治疗前沿3.标志性事件：联拓生物将关闭；医药笔记更多优质内容，欢迎关注↓↓↓

引进/卖出抗体药物偶联物医药出海

2023-12-04

·E药经理人

今年两次抄底Biotech的投资大佬，看上联拓生物哪一点？

从成立到收到收购要约，不满4年时间，联拓生物为何能“坐火箭”？日前，联拓生物宣布收到Tang Capital Partners控股的Concentra Biosciences的收购要约，包括以每股4.30美元的现金交易收购联拓生物、Concentra有权获得美国和中国联拓生物公司任何项目净收益的80%等。自2020年成立到如今收到收购要约，联拓生物一路以来的发展都在带给行业“惊喜”。开局拉满的License-in典型与其它Biotech仍在对授权引进讳莫如深的时候，联拓生物自成立之初，就明确了它授权引进的使命。2020年8月，作为美国生物医药投资基金PerceptiveAdvisors进入中国市场的触角，联拓生物成立，主要专注于将欧美市场突破性疗法引入中国及亚洲主要市场。一年之后，2021年10月，联拓生物在纳斯达克上市。事实证明，联拓生物确实是授权引进的高手。从成立伊始，联拓生物就找到了两个固定合作伙伴，分别是美国罕见病治疗公司BridgeBio（BBIO.O）以及美国临床阶段生物医药公司MyoKardia。一年时间通过License-in构建了拥有4个临床阶段候选产品的管线。此外，联拓生物还与BridgeBio达成战略合作，借此优先获得BridgeBio的20多种管线产品，包括已许可和已收购的产品，为期四年。联拓生物的合作伙伴包括Nanobiotix、Landos Biopharma以及Lyra Therapeutics。联拓生物发展节奏之快，其CEO王轶喆此前接受E药经理人采访时，曾表示，“每三个月你就会觉得像到了一家新公司”。与很多主打License-in模式的公司只注重聚焦在某一个领域不同，联拓生物则是在心血管、眼科以及肿瘤等几个不同领域均有布局，“多样化”是联拓生物产品管线的一大特点。联拓生物的管线分别来自BridgeBio和MyoKardia的子公司Navire Pharma和QED Therapeutics的多种FIC产品。手握多款重磅产品的联拓生物，“与众不同”之处还体现在开始通过转卖产品权益而获益，一度被产业称为“倒爷”。今年10月24日，联拓生物与BMS达成协议，以3.5亿美元的一次性付款，以及高达1.275亿美元的剩余里程碑付款，授予BMS在中国大陆、香港、澳门、台湾、新加坡和泰国等市场的mavacamten开发和商业化独家权利，同时终止联拓生物之前与MyoKardia签订的独家许可协议。三年前，联拓生物仅仅以4000万美元首付款，1.475亿美元潜在里程碑付款从MyoKardia引进了这款药物。这笔划算的交易让联拓生物的股票涨幅单日暴涨117.27%。这不是联拓生物第一次通过“倒手”尝到甜头。2021年3月，联拓生物以1400万美元首付款，1.05亿美元里程碑付款，获得RSV药物Sisunatovir在中国大陆、香港、澳门和新加坡地区共同开发和商业化权益。不到两年后，去年12月，双方达成新的协议，辉瑞退回联拓生物此前付出的2000万美元首付款，同时，由辉瑞负责这款药物的后续开发和商业化，而联拓生物还可获得1.35亿美元的商业里程碑付款以及销售分成。显然，联拓给产业带来的“震慑”远未结束。如今，4年未满，联拓生物便收到了收购要约。年内第三次对Biotech出手收购方何许人也？在收购要约中，Concentra和Tang Capital表示，他们认为可以为联拓生物股东实现价值最大化，并将管理或过渡任何剩余的临床研究活动。不过，Concentra的收购要约取决于交易完成时联拓生物需要至少拥有5.15亿美元的现金和现金等价物。从时间节点来看，Concentra要求联拓生物在美国东部时间12月8日下午5点之前做出回应，届时收购要约将失效。如果联拓生物接受收购要约，Concentra将在12月22日前就最终协议进行谈判，并在2024年2月22日前完成交易。Tang Capital上一次受到普遍关注，是今年10月20日宣布收购了一家市值不足1亿美元的Biotech Rain Oncology。再早一些，今年3月，另一家明星Biotech公司Jounce Therapeutics也曾宣布Concentra 提出了一项未经请求的非约束性提案，以收购其100%股权。收购联拓，是Tang Capital今年第三次出手了。Tang Capital是近两年Biotech领域的活跃投资人，尤其擅长低市值医药企业的困境反转投资。Tang Capital是由一名叫唐庆年的（Kevin Tang）人创立，据悉，唐庆年祖上是江苏无锡名门望族，而唐庆年本人是一名商业精英，此次做过好几家公司，大多跟生物科技相关，有的通过出售卖了几笔好价钱。从2020年欲收购市值不足1亿美元、连续亏损好几年的Aptevo Therapeutics却因“价值低估”被拒绝，到2023年频繁提出收购Biotech计划，Tang Capital的举动曾被戏称，“Kevin Tang是经常捡垃圾药股的人。”但与此前的收购邀约不同，从联拓生物目前的经营状况来看，却并非那些处于危机中的小型上市公司。Tang Capital与联拓之间的收购能达成吗？相信不久后将会有答案。登记邮箱信息订阅E药经理人信息服务扫描二维码精彩推荐CM10 | 集采 | 国谈 | 医保动态 | 药审 | 人才 | 薪资 | 榜单 | CAR-T | PD-1 | mRNA | 单抗 | 商业化 | 国际化｜猎药人系列专题启思会 | 声音·责任 | 创百汇 | E药经理人理事会 | 微解药直播 | 大国新药 | 营销硬观点 | 投资人去哪儿 | 分析师看赛道 | 药事每周谈 | 医药界·E药经理人 | 中国医药手册创新100强榜单 | 恒瑞 | 中国生物制药 | 百济 | 石药 | 信达 | 君实 | 复宏汉霖｜翰森 | 康方生物 | 上海医药 | 和黄医药 | 东阳光药 | 荣昌 | 亚盛医药 | 齐鲁制药 | 康宁杰瑞 | 贝达药业 | 微芯生物 | 复星医药｜再鼎医药｜亚虹医药跨国药企50强榜单 | 辉瑞 | 艾伯维 | 诺华 | 强生 | 罗氏 | BMS | 默克 | 赛诺菲 | AZ | GSK | 武田 | 吉利德科学 | 礼来 | 安进 | 诺和诺德 | 拜耳 | 莫德纳 | BI | 晖致 | 再生元

引进/卖出并购突破性疗法

2023-08-22

·PRNewswire

Analysis of the Global Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS)-inhibitors Market 2023-2032: Rapid Evolution of Therapies for KRAS Mutations Presents New Opportunities

DUBLIN, Aug. 22, 2023 /PRNewswire/ -- The "Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS)-inhibitors - Market Insights, Epidemiology and Market Forecast - 2032" report has been added to ResearchAndMarkets.com's offering. The report provides an in-depth analysis of the KRAS inhibitors market, epidemiology, and market trends in the United States, EU4 (Germany, Spain, Italy, and France), the United Kingdom, and Japan. Key Highlights: KRAS mutations contribute less to cancer in Japan compared to Western countries like the United States and Europe. In the United States, KRASG12C is present in approximately 37% of non-small cell lung cancer (NSCLC) cases, while KRASG12D is prevalent in about 42% of pancreatic cancer cases and 30% of colorectal cancer (CRC) cases. Among the approved therapies, LUMAKRAS (sotorasib) is expected to generate more revenue than KRAZATI (adagrasib) in the United States during the study period (2019-2032). The United States is expected to hold the highest market share for KRAS inhibitors in 2022, followed by the EU4 countries, with Germany having the highest share and Spain the lowest. KRAZATI has been added as a therapeutic option after first-line treatment for NSCLC in the latest NCCN guidelines published in December 2022. There is an opportunity for emerging KRAS key players focusing on safer combinations with less toxicity. LUMAKRAS witnessed a decrease in sales after the launch of KRAZATI, primarily due to a price adjustment implemented as part of a reimbursement agreement in Germany. Several companies are developing candidates for pan-KRAS inhibition, which has the potential to create a positive shift in the KRAS-inhibitors market. The report covers the epidemiology of KRAS inhibitors in NSCLC, CRC, and pancreatic cancer, as well as the total KRAS-mutated cases in the 7MM (United States, EU4, UK, and Japan). The total KRAS-mutated cases in the 7MM were over 450,000 in 2022 and are projected to increase during the forecast period. LUMAKRAS (sotorasib) by Amgen and KRAZATI (adagrasib) by Mirati Therapeutics are the approved drugs targeting KRAS G12C mutations. LUMAKRAS received accelerated approval in May 2021 and is marketed as LUMYKRAS in the European Union, UK, and Switzerland. KRAZATI received approval from the FDA in December 2022 and has a Marketing Authorization Application submitted to the EMA. Emerging drugs include JDQ443 by Novartis and divarasib by Roche/Genentech, among others. JDQ443 is in a Phase III trial for NSCLC, while divarasib is being investigated in solid tumors, including NSCLC, CRC, and other cancer types. The United States is expected to have the highest market share among the 7MM in 2022 for KRAS inhibitors. LUMAKRAS is anticipated to capture more market share compared to KRAZATI throughout the study period. The report also includes insights from key opinion leaders (KOLs) and industry experts working in the domain to understand current treatment patterns and market trends. Overall, the KRAS inhibitors market is evolving rapidly with recent approvals and ongoing research for new therapies targeting different KRAS mutations and multiple cancer types. The market holds significant potential for growth as more effective and safer treatments are developed to address various KRAS variants. Key Topics Covered 1. Key Insights 2. Report Introduction 3. Executive Summary of KRAS Inhibitors 4. Key Events 5. Epidemiology and Market Forecast Methodology 6. Disease Background and Overview 7. Treatment 8. Guidelines 9. Epidemiology and Patient Population 10. Marketed Drugs 11. Emerging Drugs 12. Unmet Needs 13. SWOT Analysis 14. KOL Views 15. Market Access and Reimbursement 16. KRAS-inhibitors Market Access and Reimbursement 17. Appendix A selection of companies mentioned in this report includes: Novartis Roche Genentech Verastem Oncology Revolution Medicines Cardiff Oncology Immuneering Corporation Jacobio Pharmaceuticals BridgeBio Pharma (Navire Pharma) Mirati Therapeutics Deciphera Pharmaceuticals Elicio Therapeutics InventisBio Gritstone Bio D3 Bio 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

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100 项与 Navire Pharma, Inc. 相关的药物交易

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100 项与 Navire Pharma, Inc. 相关的转化医学

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管线布局中药物为当前组织机构及其子机构作为药物机构进行统计，早期临床1期并入临床1期，临床1/2期并入临床2期，临床2/3期并入临床3期

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药物(靶点)	适应症	全球最高研发状态

BBP-398 ( SHP2 )	晚期恶性实体瘤更多	临床1期
索托拉西布 ( KRAS G12C )	非小细胞肺癌更多	临床1期
纳武利尤单抗 ( PD-1 )	晚期非小细胞肺癌更多	临床1期