A Phase 1/2 Open-label, Dose Escalation and Dose Expansion Study Designed to Evaluate the Safety, Tolerability, PharmacoKinetics, Pharmacodynamics and EfficacY of PT217 Bispecific Antibody in Patients With NeuRoendocrIne Carcinomas That May Benefit From Treating Their DLL3 expressinG CancEr.

PT217 is a bispecific antibody (bsAb) against human DLL3 (huDLL3) and human CD47 (huCD47). This is a first-in-human, Phase 1/2, open-label, dose-escalation and expansion study designed to evaluate the safety, tolerability, pharmacokinetics, pharmacodynamics, and preliminary efficacy of PT217 in subjects with neuroendocrine carcinomas.
Patients with the following tumor types will be eligible for screening: small cell lung cancer (SCLC), large cell neuroendocrine carcinoma of the lung (LCNEC), and extrapulmonary neuroendocrine carcinoma (EP-NEC), including but not limited to neuroendocrine prostate cancer (NEPC) and gastroentero-pancreatic neuroendocrine carcinoma (GEP-NEC). Patients must have progressed after standard therapy (platinum-based chemotherapy) or standard therapy has proven to be ineffective, intolerable or is considered inappropriate.

开始日期2023-09-05

申办/合作机构

Phanes Therapeutics, Inc.初创企业

NCT05482893 / Recruiting临床1/2期

A Phase 1/2, Open-Label, Dose Escalation and Expansion Study With PT886 Followed by a Multi-cohorT Study in Patients With Advanced GastrIc, Gastroesophageal JuNction (GEJ), or Pancreatic Ductal AdEnocarcinomas of PT886, in Combination With Either ChemotherApy, and/or the ChecKpoint Inhibitor Pembrolizumab TWINPEAK Study

This is a first-in-human, Phase 1/2, open-label, dose escalation and dose expansion and combination study designed to evaluate the safety, tolerability, pharmacokinetics, pharmacodynamics, and preliminary efficacy of PT886.
Patients with the following tumor types will be eligible for screening: unresectable or metastatic gastric adenocarcinoma, gastroesophageal junction (GEJ) adenocarcinoma, and pancreatic ductal adenocarcinoma (PDAC).

开始日期2023-03-15

申办/合作机构

Phanes Therapeutics, Inc.初创企业

[+1]

NCT05431270 / Recruiting临床1期

A Phase I, First-in-Human, Open-Label, Dose Escalation and Expansion Study of PT199 Administered Alone and in Combination With a PD-1 Inhibitor in Adult Patients With Advanced Solid Tumors.

This is a first-in-human, Phase I, open-label, dose-escalation and expansion study designed to evaluate the safety, tolerability, pharmacokinetics, pharmacodynamics, and preliminary efficacy of PT199 (an Anti-CD73 mAb) alone and in combination with a PD-1 inhibitor, in patients with locally advanced or metastatic solid tumors that have progressed after all available standard therapy or for which standard therapy has proven to be ineffective, intolerable, or is considered inappropriate.

开始日期2022-08-11

申办/合作机构

Phanes Therapeutics, Inc.初创企业

100 项与 Phanes Therapeutics, Inc. 相关的临床结果

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0 项与 Phanes Therapeutics, Inc. 相关的专利（医药）

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项与 Phanes Therapeutics, Inc. 相关的文献（医药）

2023-02-01·Journal of Clinical Oncology

A phase I, first-in-human, open-label, dose escalation and expansion study of PT886 in adult patients with advanced gastric, gastroesophageal junction, and pancreatic adenocarcinomas.

作者: Wright, Harold M ; Melhem, Ramzi ; Perer, Jessica K ; Li, Jack ; Blum-Murphy, Mariela A. ; Wang, Ming ; Petrosyan, Lina ; Ramos, Claudia ; Zou, Hui ; Overman, Michael J.

TPS765 Background: PT886 is a novel bispecific antibody that targets Claudin 18.2 (CLDN18.2) and CD47. CLDN18.2 is overexpressed in a significant proportion of gastric and pancreatic adenocarcinomas and its restricted expression makes it a promising therapeutic target for the treatment of these carcinomas. Moreover, studies have found that immunoglobulin superfamily CD47 is overexpressed widely across tumor types, and CD47 plays an important role in suppressing phagocytes activity through binding to the transmembrane protein SIRPα in phagocytic cells. Hence, by targeting both pathways, one can direct macrophage-mediated phagocytotic activity to tumor cells by blocking the “don’t eat me” signal mediated by CD47/ SIRPα interaction, potentially offering a better safety profile than anti-CD47 monoclonal antibodies. Additionally, PT886 utilizes IgG1 to enhance antibody-dependent cellular cytotoxicity (ADCC) by NK cells and antibody-dependent cellular phagocytosis (ADCP) by macrophages and thus increases the antitumor activity. The combined cancer killing effects by the above mechanisms therefore represent a novel approach in treating CLDN18.2-positive malignancies. Methods: This is an open label, Phase I study to evaluate the safety, tolerability, pharmacokinetics (PK) and preliminary efficacy of PT886 in subjects with unresectable or metastatic gastric adenocarcinoma, gastroesophageal junction adenocarcinoma, and pancreatic ductal adenocarcinoma (PDAC) for which there is no available standard therapy. Approximately 34-58 patients will be enrolled. The study consists of 2 parts: Dose Escalation, and Dose Expansion. The dose escalation study of PT886 will be guided by a standard 3+3 dose escalation study design to determine the maximum tolerated dose (MTD) and/or the optimal biological doses for expansion. The MTD or the optimal biological dose and a lower dose level will be further evaluated in a dose expansion cohort to determine a recommended phase II dose (RP2D). Each enrolled patient will receive PT886 as a monotherapy (0.1, 0.3, 1, 3 or 6 mg/kg QW) as an intravenous infusion continuously (over 60 minutes) in 28-day cycles. The primary endpoints are Dose Limiting Toxicity (DLT) and MTD, if reached, and RP2D of PT886 as a single agent. PD markers of PT886 biological activity will be measured, including T-cell receptor sequencing on circulating T cells, T-cell activation studies, serum cytokines and assessing CLDN18.2 expression in tumor tissues. PT886, which was recently granted orphan drug designation by the FDA for the treatment of pancreatic cancer, has the potential to be a new treatment option for pancreatic and gastric cancer patients whose current standard of care is limited. Preliminary safety and efficacy data are anticipated in the second quarter of 2023. Clinical trial information: NCT02178241 .

2022-06-15·Cancer Research

Abstract 4259: PT199, a next generation anti-CD73 mAb that inhibits both membrane-bound and soluble CD73 activity to completion without “hook effect”

作者: Li, Jack ; Long, Yan ; Zou, Hui ; Pei, Fen ; Chen, Kelan ; Wang, Ming ; Perer, Jessica ; Pejza, Lauren ; Greenwood, Lorraine ; Jia, Haiqun (John)

AbstractCD73, also known as ecto-5’-nucleotidase, is implicated in promoting immunosuppressive tumor microenvironment (TME) through production of adenosine. The first generation of anti-CD73 therapeutic antibodies currently in clinical studies have largely exhibited subdued clinical activities mainly due to several unfavorable characteristics such as incomplete enzyme inhibition and/or “hook effect”. These weaknesses are caused by the unfavorable target binding sites and enzyme inhibition mechanisms, which explains why these molecules do not inhibit soluble CD73 enzyme activity, or why the enzyme inhibition depends on certain stochiometric ratios of CD73 and the antibody and exhibits “hook effect” in dose-response curves. Here we report a next generation humanized monoclonal antibody against human CD73 (hCD73), PT199, which binds to a unique site on human CD73 that confers a different mechanism of enzyme inhibition and consequently does not have the flaws associated with the first generation of anti-CD73 mAbs currently in clinic. By directly binding to an epitope that is in or near the CD73 catalytic domain, PT199 potently inhibits both soluble shed CD73 and membrane-bound CD73 activity to completion without “hook effect”. Enzyme kinetic studies demonstrate that PT199 inhibits CD73 enzyme activity in a noncompetitive manner, allowing complete CD73 inhibition even at high AMP concentrations reported in TME. In a cell-based functional assay, PT199 inhibition of CD73 alleviates the immunosuppression effect of AMP on T cell proliferation. Compared with the first-generation molecules, PT199 completely inhibits CD73 activity in cancer patient serum. Furthermore, when administrated to hCD73 knock-in mice, PT199 greatly elevates endogenous AMP level, demonstrating a robust pharmacodynamic effect in blocking the conversion of AMP to adenosine. Comparative mechanistic studies indicate that PT199 binds to both the “open conformation” (inactive enzyme state) and the “closed conformation” (active enzyme state) with high affinity but with shifted binding curves, suggesting that PT199 may inhibit the CD73 enzyme activity by preventing the transition of the enzyme from the “open conformation” to the “closed conformation”. PT199 did not cause B cell reduction in either acute or repeated dosing studies in NHP. In NHP toxicology studies, PT199 exhibits no clinical observations at up to 300 mg/kg weekly repeated dosing and has an excellent PK profile typical of mAbs. Taken together, our data confirms PT199 as a potential best-in-class anti-hCD73 mAb. Phase 1 clinical trial is planned to start in the first quarter of 2022.Citation Format: Haiqun (John) Jia, Jack Li, Fen Pei, Lorraine Greenwood, Lauren Pejza, Yan Long, Kelan Chen, Jessica Perer, Ming Wang, Hui Zou. PT199, a next generation anti-CD73 mAb that inhibits both membrane-bound and soluble CD73 activity to completion without “hook effect” [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 4259.

2022-06-15·Cancer Research

Abstract 4260: PT886, an anti-claudin18.2/anti-CD47 bispecific antibody constructed with the PACbody࣪ and SPECpair࣪ technology platforms, exhibits robust anti-tumor activity in a pancreatic cancer xenograft model

作者: Zou, Hui ; Ramsey, Erin ; Wang, Ming ; Lam, Albert ; Wu, Huiwen ; Li, Jack ; Chen, Kelan ; Jia, Haiqun ; Long, Yang

AbstractClaudin 18.2 (CLDN18.2) is a surface protein overexpressed in gastric and pancreatic tumors and has been demonstrated to be a clinically validated target for developing mAb and CAR-T therapies for these tumors. CD47 is a well-established “don’t eat me” signal and commonly overexpressed by many types of tumor cells as a mechanism for evading the innate immune system. It has been demonstrated in clinic that blocking CD47 from interacting with its ligand SIRPα leads to reduced growth of certain hematological tumors, presumably by activating the innate immune system against tumor cells. Here we present a therapeutic strategy for targeting both CLDN18.2 and CD47 with a bispecific antibody to achieve cancer killing by two mechanisms: (1) Blocking the CD47-SIRPα interaction and stimulating phagocytosis of tumor cells by macrophages. (2) Delivering robust effector effect (ADCC by NK cells and ADPC by macrophages) mediated by the functional Fc of the bispecific antibody. We report a native IgG-like anti-CLDN18.2/anti-CD47 bispecific antibody, PT886, that was generated using our newly developed PACbody™ and SPECpair™ technology platforms. The PACbody™ and SPECpair™ technologies are designed to allow assembled bispecific antibodies to have excellent biophysical properties and to be manufactured by a conventional three-step platform process commonly used for mAbs. PT886 has high affinity monovalent binding to cell surface CLDN18.2 and low affinity monovalent binding to cell surface CD47. This combination allows for the preferential binding of PT886 to tumor cells which overexpress both CLDN18.2 and CD47, but reduced binding to normal cells that only express CD47. Consequently, PT886 exhibits higher activity toward CLDN18.2-expressing tumor cells and lower to no activity to normal cells that do not express CLDN18.2. This was demonstrated in a phagocytosis assay where PT886 stimulates stronger phagocytosis in the presence of CLDN18.2 binding in vitro. In addition to targeting both CLDN18.2 and CD47, PT886 has a fully functional Fc to directly recruit the tumor cell killing activities of NK cells and macrophages. The potent anti-tumor activity of PT886 was demonstrated in vivo in a pancreatic cancer xenograft model, where PT886 treatment resulted in a complete tumor clearance at doses as low as 1 mg/kg. PT886 also demonstrated a good safety profile in NHP studies and exhibited regular mAb-like manufacturability in process development and CMC. These data support the proof of concept of the PACbody™ and SPECpair™ technology platforms and demonstrate the unique profile of our anti-CD47 arm that’s suitable for the bispecific antibody approach. PT886 is a first-in-class anti-CLDN18.2/anti-CD47 bispecific antibody with native IgG-like structure and phase 1 clinical trial is planned for the first quarter of 2022.Citation Format: Jack Li, Haiqun Jia, Erin Ramsey, Huiwen Wu, Yang Long, Kelan Chen, Albert Lam, Ming Wang, Hui Zou. PT886, an anti-claudin18.2/anti-CD47 bispecific antibody constructed with the PACbody࣪ and SPECpair࣪ technology platforms, exhibits robust anti-tumor activity in a pancreatic cancer xenograft model [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 4260.

1,324

项与 Phanes Therapeutics, Inc. 相关的新闻（医药）

2024-10-31

·医药笔记

安进：第2款实体瘤CD3双抗，Xaluritamig将启动前列腺癌三期临床

▎Armstrong 2024年10月30日，安进发布三季度财报，介绍了研发管线的最新进展，肿瘤业务板块中重点提到STEAP1/CD3双抗Xaluritamig将在本季度启动紫杉醇后线的前列腺癌三期临床试验。 Xaluritamig采用Xencor的XmAb 2+1技术设计，目前处于一期临床阶段，意味着安进将直接推进到三期临床。 Xencor还有其他多款实体瘤CD3双抗在推进中，覆盖靶点包括ENPP3、Claudin6、B7H3等，均采用XmAb 2+1技术。今年AACR会议上，安进披露了Xaluritamig的一期临床数据，PSA和RECIST评估疗效数据如下，PSA50为49%，PSA90为28%。以RECIST评估，高剂量组ORR为41%，DCR为79%。总结作为最老牌的biotech，安进研发管线中还有多哥潜在爆款产品，除了前述两款实体瘤CD3双抗，还有自免领域的OX40抗体Rocatinlimab，代谢领域的GIPR抗体融合GLP-1分子MariTide等。 Armstrong技术全梳理系列 GPRC5D靶点全梳理； CD40靶点全梳理； CD47靶点全梳理；补体靶向药物技术全梳理；补体药物：眼科治疗的重要方向； Claudin 6靶点全梳理； Claudin 18.2靶点全梳理；靶点冷暖，行业自知；中国大分子新药研发格局；被炮轰的“me too”；佐剂百年史；胰岛素百年传奇； CUSBEA：风雨四十载；中国新药研发的焦虑；中国生物医药企业的研发竞争；中国双抗竞争格局；中国ADC竞争格局；中国双抗技术全梳理；中国ADC技术全梳理； Ambrx技术全梳理； Vir Biotech技术全梳理； Immune-Onc技术全梳理；亘喜生物技术全梳理；康哲药业技术全梳理；科济药业技术全梳理；恺佧生物技术全梳理；同宜医药技术全梳理；百奥赛图技术全梳理；腾盛博药技术全梳理；创胜集团技术全梳理；永泰生物技术全梳理；中国抗体技术全梳理；德琪医药技术全梳理；德琪医药技术全梳理2.0；和铂医药技术全梳理；荣昌生物技术全梳理；再鼎医药技术全梳理；药明生物技术全梳理；恒瑞医药技术全梳理；豪森药业技术全梳理；正大天晴技术全梳理；吉凯基因技术全梳理；基石药业技术全梳理；百济神州技术全梳理；百济神州技术全梳理第2版；信达生物技术全梳理；信达生物技术全梳理第2版；中山康方技术全梳理；复宏汉霖技术全梳理；先声药业技术全梳理；君实生物技术全梳理；嘉和生物技术全梳理；志道生物技术全梳理；道尔生物技术全梳理；尚健生物技术全梳理；康宁杰瑞技术全梳理；科望医药技术全梳理；科望医药技术全梳理2.0；岸迈生物技术全梳理；礼进生物技术全梳理；康桥资本技术全梳理；余国良的抗体药布局；荃信生物技术全梳理；安源医药技术全梳理；三生国健技术全梳理；仁会生物技术全梳理；乐普生物技术全梳理；同润生物技术全梳理；宜明昂科技术全梳理；派格生物技术全梳理；迈威生物技术全梳理； Momenta技术全梳理； NGM技术全梳理；普米斯生物技术全梳理；普米斯生物技术全梳理2.0；三叶草生物技术全梳理；贝达药业抗体药全梳理；泽璟制药抗体药全梳理；恒瑞医药抗体药全梳理；齐鲁制药抗体药全梳理；石药集团抗体药全梳理；豪森药业抗体药全梳理；华海药业抗体药全梳理；科伦药业抗体药全梳理；百奥泰技术全梳理；凡恩世技术全梳理。

AACR会议临床3期财报抗体药物偶联物

2024-10-31

·医药笔记

安进：CD3/CD19双抗启动狼疮肾炎二期临床

▎Armstrong 2024年10月30日，安进发布三季度三包，营收81.51亿美元，同比增长23%，扣除收购Horizon的影响，营收增长8%。肿瘤业务板块，CD3/CD19双抗Blincyto三季度销售额3.27亿美元，同比增长49%，小细胞肺癌的DLL3/CD3双抗Imdelltra首季度销售额3600万美元。 Blincyto正在探索皮下剂型，B-ALL的1/2期临床已经完成入组，预计2025年下半年推进到二期注册临床。安进正在积极开拓自免领域，CD3/CD19双抗和CD19单抗已经启动狼疮肾炎的二期临床试验。 2a期临床计划入组50例，其中CD3/CD19双抗采用皮下注射剂型。安全性终点观察52周，疗效终点观察12周和24周。总结 Blincyto为全球首个也是唯一一个获批上市的CD3/CD19双抗，这一波自免浪潮中第一个推进到二期临床。Cullinan刚刚启动1b期临床，计划入组24例狼疮患者。默沙东7亿美元引进了同润生物的CD3/CD19双抗，葛兰素史克8.5亿美元引进恩沐生物的CD3/CD19/CD20双抗。Xencor宣布CD3/CD20双抗、CD3/CD19双抗转战自免领域。Candid收购了嘉和生物的CD3/CD20双抗、岸迈生物的CD3/BCMA双抗。 Armstrong技术全梳理系列 GPRC5D靶点全梳理； CD40靶点全梳理； CD47靶点全梳理；补体靶向药物技术全梳理；补体药物：眼科治疗的重要方向； Claudin 6靶点全梳理； Claudin 18.2靶点全梳理；靶点冷暖，行业自知；中国大分子新药研发格局；被炮轰的“me too”；佐剂百年史；胰岛素百年传奇； CUSBEA：风雨四十载；中国新药研发的焦虑；中国生物医药企业的研发竞争；中国双抗竞争格局；中国ADC竞争格局；中国双抗技术全梳理；中国ADC技术全梳理； Ambrx技术全梳理； Vir Biotech技术全梳理； Immune-Onc技术全梳理；亘喜生物技术全梳理；康哲药业技术全梳理；科济药业技术全梳理；恺佧生物技术全梳理；同宜医药技术全梳理；百奥赛图技术全梳理；腾盛博药技术全梳理；创胜集团技术全梳理；永泰生物技术全梳理；中国抗体技术全梳理；德琪医药技术全梳理；德琪医药技术全梳理2.0；和铂医药技术全梳理；荣昌生物技术全梳理；再鼎医药技术全梳理；药明生物技术全梳理；恒瑞医药技术全梳理；豪森药业技术全梳理；正大天晴技术全梳理；吉凯基因技术全梳理；基石药业技术全梳理；百济神州技术全梳理；百济神州技术全梳理第2版；信达生物技术全梳理；信达生物技术全梳理第2版；中山康方技术全梳理；复宏汉霖技术全梳理；先声药业技术全梳理；君实生物技术全梳理；嘉和生物技术全梳理；志道生物技术全梳理；道尔生物技术全梳理；尚健生物技术全梳理；康宁杰瑞技术全梳理；科望医药技术全梳理；科望医药技术全梳理2.0；岸迈生物技术全梳理；礼进生物技术全梳理；康桥资本技术全梳理；余国良的抗体药布局；荃信生物技术全梳理；安源医药技术全梳理；三生国健技术全梳理；仁会生物技术全梳理；乐普生物技术全梳理；同润生物技术全梳理；宜明昂科技术全梳理；派格生物技术全梳理；迈威生物技术全梳理； Momenta技术全梳理； NGM技术全梳理；普米斯生物技术全梳理；普米斯生物技术全梳理2.0；三叶草生物技术全梳理；贝达药业抗体药全梳理；泽璟制药抗体药全梳理；恒瑞医药抗体药全梳理；齐鲁制药抗体药全梳理；石药集团抗体药全梳理；豪森药业抗体药全梳理；华海药业抗体药全梳理；科伦药业抗体药全梳理；百奥泰技术全梳理；凡恩世技术全梳理。

临床2期并购临床1期抗体药物偶联物

2024-10-30

·Armstrong生物药资讯

礼来：替尔泊肽前三季度大卖110亿美元

▎Armstrong 2024年10月30日，礼来发布三季度财报，前三季度营业收入315亿美元，同比增长27%，净利润61.8亿美元。前三季度，替尔泊肽降糖版Moujaro销售额80.10亿美元，去年同期为29.58亿美元，替尔泊肽减重版Zepbound销售额30.18亿美元。替尔泊肽合计销售额110亿美元，预计全年超过160亿美元。替尔泊肽去年11月份上市以来放量迅速，累计处方患者超过60万人。降糖版Mounjaro三季度与二季度销售额基本持平，美国处方份额约30%。总结诺和诺德司美格鲁肽今年上半年销售额为130亿美元，替尔泊肽正在快速抢占市场，与司美格鲁肽的差距快速缩小。横向对比，Keytruda今年上半年销售额142亿美元，未来新的药王争夺大概率会在司美格鲁肽、替尔泊肽中间产生。 Armstrong技术全梳理系列 GPRC5D靶点全梳理； CD40靶点全梳理； CD47靶点全梳理；补体靶向药物技术全梳理；补体药物：眼科治疗的重要方向； Claudin 6靶点全梳理； Claudin 18.2靶点全梳理；靶点冷暖，行业自知；中国大分子新药研发格局；被炮轰的“me too”；佐剂百年史；胰岛素百年传奇； CUSBEA：风雨四十载；中国新药研发的焦虑；中国生物医药企业的研发竞争；中国双抗竞争格局；中国ADC竞争格局；中国双抗技术全梳理；中国ADC技术全梳理； Ambrx技术全梳理； Vir Biotech技术全梳理； Immune-Onc技术全梳理；亘喜生物技术全梳理；康哲药业技术全梳理；科济药业技术全梳理；恺佧生物技术全梳理；同宜医药技术全梳理；百奥赛图技术全梳理；腾盛博药技术全梳理；创胜集团技术全梳理；永泰生物技术全梳理；中国抗体技术全梳理；德琪医药技术全梳理；德琪医药技术全梳理2.0；和铂医药技术全梳理；荣昌生物技术全梳理；再鼎医药技术全梳理；药明生物技术全梳理；恒瑞医药技术全梳理；豪森药业技术全梳理；正大天晴技术全梳理；吉凯基因技术全梳理；基石药业技术全梳理；百济神州技术全梳理；百济神州技术全梳理第2版；信达生物技术全梳理；信达生物技术全梳理第2版；中山康方技术全梳理；复宏汉霖技术全梳理；先声药业技术全梳理；君实生物技术全梳理；嘉和生物技术全梳理；志道生物技术全梳理；道尔生物技术全梳理；尚健生物技术全梳理；康宁杰瑞技术全梳理；科望医药技术全梳理；科望医药技术全梳理2.0；岸迈生物技术全梳理；礼进生物技术全梳理；康桥资本技术全梳理；余国良的抗体药布局；荃信生物技术全梳理；安源医药技术全梳理；三生国健技术全梳理；仁会生物技术全梳理；乐普生物技术全梳理；同润生物技术全梳理；宜明昂科技术全梳理；派格生物技术全梳理；迈威生物技术全梳理； Momenta技术全梳理； NGM技术全梳理；普米斯生物技术全梳理；普米斯生物技术全梳理2.0；三叶草生物技术全梳理；贝达药业抗体药全梳理；泽璟制药抗体药全梳理；恒瑞医药抗体药全梳理；齐鲁制药抗体药全梳理；石药集团抗体药全梳理；豪森药业抗体药全梳理；华海药业抗体药全梳理；科伦药业抗体药全梳理；百奥泰技术全梳理；凡恩世技术全梳理。

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