A Phase 2, Randomized, Open-Label Study to Assess the Safety and Efficacy of GPC 100 and Propranolol With and Without G-CSF for the Mobilization of Stem Cells in Patients With Multiple Myeloma Undergoing Autologous Stem Cell Transplant

This is a randomized, open-label study. Patients will be screened within 28 days prior to the study drug administration. Patients will be randomly assigned to 1 of 2 treatment arms prior to study drug administration.
Approximately 40 patients will be randomized in a 1:1 ratio to the following treatment arms:
* GPC-100 in combination with propranolol; or
* GPC-100 in combination with propranolol and G-CSF. To characterize the safety and clinical activity of GPC-100, the study will employ a Bayesian Optimal Phase II (BOP2) design to enroll patients for each arm.
All patients will receive via IV 3.14 mg/kg GPC-100 (Burixafor) at least 2 hours prior to leukapheresis sessions from Days 7-8 (Days 9-11 optional) and 30 mg propranolol (3 x 10 mg tablets) twice daily at 8:30 AM (+/- 1 hr) and 4:00 PM (+/- 1 hr) local time from Days 1 to 8 (and on Days 9-11, if applicable). Patients will administer the first dose of propranolol onsite on Day 1. Patients will be provided with doses of propranolol for self-administration at time points when they are not otherwise required to be onsite. Sites should contact patients via telephone to confirm propranolol administration for doses administered outside of clinic.

开始日期2023-02-13

申办/合作机构

GPCR Therapeutics, Inc.

CTR20130291

/ Completed临床1期

评估布利沙福并用阿糖胞苷及氟达拉滨治疗复发或难治性急性髓系白血病成人患者安全性及有效性的I期临床研究

1.确定本品并用阿糖胞苷及氟达拉滨来治疗复发或难治性急性髓系白血病成人患者的最高耐受剂量。评估患者的安全性及耐受性；完全缓解率（包括CR和CRi）;无病生存期、总生存期和造血恢复时间。 2.评估布利沙福对急性髓系白血病细胞的动员特征。 3.评估布利沙福的药代动力学特征。

开始日期2015-07-28

申办/合作机构

太景医药研发（北京）有限公司

NCT02104427

/ Completed临床2期

A Phase II, Open-Label Study to Evaluate the Hematopoietic Stem Cell Mobilization of TG-0054 Combined With G-CSF in Patients With Multiple Myeloma, Non-Hodgkin Lymphoma or Hodgkin Disease

This is a phase II study to evaluate the efficacy and safety of TG-0054 combined with G-CSF in mobilizing hematopoietic stem cells in patients with multiple myeloma, non-Hodgkin lymphoma or Hodgkin disease.

开始日期2015-02-01

申办/合作机构

GPCR Therapeutics, Inc.

100 项与氢溴酸布利沙福相关的临床结果

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100 项与氢溴酸布利沙福相关的转化医学

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100 项与氢溴酸布利沙福相关的专利（医药）

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项与氢溴酸布利沙福相关的文献（医药）

2026-01-01·JOURNAL OF CONTROLLED RELEASE

Structure-guided design and clinical evaluation of 68Ga-GP01 for FAP-targeted PET imaging in solid tumors

Article

作者: Chen, Zihao ; Li, Jian ; Li, Jingze ; Mo, Yufeng ; Shi, Yaxin ; Zhang, Xin ; Cui, Mutian ; Tam, Kam Pui ; Zhang, Lei ; Liang, Shuheng ; Chow, Hoi Yee ; Tang, Ganghua ; Chong, Weixia ; Li, Xuechen ; Tang, Weikun ; Fu, Wei ; Mu, Xingyu ; Huang, Wentao

Fibroblast activation protein (FAP)-targeted radioligands have shown superior performance in detecting FAP-expressing cancers. However, the quinoline-based agent ⁶⁸Ga-FAPI-46 exhibits only moderate in vivo stability and suboptimal pharmacokinetics. To overcome these limitations, a FAP inhibitor, GP01 was designed by introducing N-methyl-benzenesulfonic acid side chain on FAPI-46 with enhanced binding affinity and improved in vivo stability. ⁶⁸Ga-GP01 demonstrated high radiochemical purity, favorable binding energy, and excellent in vitro stability. It specifically bound to FAP on A549-hFAP and U87MG cells, exhibiting greater uptake, enhanced internalization, and slower efflux compared to ⁶⁸Ga-FAPI-46. In vivo PET/CT imaging revealed that ⁶⁸Ga-GP01 accumulated specifically in FAP-positive tumor models, with improved pharmacokinetic behavior and a higher tumor-to-background ratio than ⁶⁸Ga-FAPI-46. Tumor uptake correlated significantly with both ex vivo biodistribution and immunohistochemical FAP expression. Clinical evaluation in 35 patients with solid tumors revealed that ⁶⁸Ga-GP01 has optimal pharmacokinetics, persistent target engagement and promising lesion detection, delivering a low effective dose with no adverse events within 6 h post-injection. Furthermore, in a direct comparison with ¹⁸F-FDG, ⁶⁸Ga-GP01 detected more lesions and achieved higher uptake and tumor-to-background ratios. These data support ⁶⁸Ga-GP01 as a clinically translatable FAP-targeted PET tracer and motivate prospective trials in indications where stromal imaging augments or surpasses metabolic imaging.

2025-04-01·MOLECULAR PHARMACOLOGY

Pharmacological characterization of a clinical candidate, TG-0054, a small molecule inverse agonist targeting CXCR4

Article

作者: Mobach, Simon ; Annibale, Paolo ; Wang, Ziming ; Pan, Kylie S ; Zimmermann, Mirjam ; Siderius, Marco ; Rizk, Aurélien ; Pfeil, Cy ; Bergkamp, Nick D ; Roth, Susanne ; Bosma, Reggie ; Smit, Martine J ; Lohse, Martin J

CXCR4 is an important therapeutic target for hematopoietic stem cell mobilization, which enhances the success of autologous stem cell transplantation for treating blood cancers such as lymphomas and myeloma. As CXCR4 has been shown to be involved in various inflammatory diseases, cancer progression, and cell entry by the human immunodeficiency virus, understanding the molecular mechanism of CXCR4 inhibitors has potential implications in a wide area of diseases. Here, we present an exploratory study which involves the molecular pharmacological characterization of TG-0054 (burixafor, GPC-100), a clinical candidate for hematopoietic stem cell mobilization. TG-0054 inhibited CXCL12 binding at CXCR4, and antagonized both Gα_i and β-arrestin2 recruitment as well as the downstream Gα_i-attenuation of cAMP signaling pathway, with pIC₅₀ of 7.7, 8.0, and 7.9, respectively. Compared with the clinically used antagonist AMD3100 and the prototypical inverse agonist Isothiourea-1t (IT1t), TG-0054 displayed a unique pharmacological profile. Like IT1t, TG-0054 inhibited the constitutive Gα_i signaling of CXCR4. However, in contrast to IT1t and other reported inverse agonists, TG-0054 was not able to induce monomerization of CXCR4 oligomeric complexes. Considering the unique properties of TG-0054 on CXCR4, TG-0054 is an interesting tool compound for studying the relevance of inverse agonism as well as CXCR4 monomerization in various pathologies. SIGNIFICANCE STATEMENT: CXCR4-targeted therapeutics hold important potential for the treatment of blood cancers. TG-0054 has inverse agonistic properties and is a non-CXCR4-monomerizing small molecule antagonist, unlike other well studied CXCR4 small molecule antagonists.

2023-11-01·Clinical pharmacology in drug development

Pharmacokinetics and Pharmacodynamics of Burixafor Hydrobromide (GPC‐100), a Novel C‐X‐C Chemokine Receptor 4 Antagonist and Mobilizer of Hematopoietic Stem/Progenitor Cells, in Mice and Healthy Subjects

Article

作者: Caculitan, Niña G. ; Chang, Li‐wen ; Tsai, Cheng‐yuan ; Cardarelli, Pina M. ; Sukhtankar, Devki D.

Abstract:

Adequate mobilization of hematopoietic stem cells (HSCs), especially CD34+ cells, is necessary for stem cell transplantation in patients with hematological malignancies or autoimmune diseases. Burixafor is an inhibitor of the C‐X‐C Chemokine Receptor 4 that disrupts the C‐X‐C motif chemokine 12 (CXCL12)/CXCR4 axis in the bone marrow, releasing HSCs into circulation. In mice, a single intravenous dose of burixafor was rapidly absorbed (time to maximum concentration, 5 minutes) and increased peripheral white blood cell counts within 30 minutes. Additionally, burixafor was administered to 64 healthy subjects in a randomized, double‐blind, placebo‐controlled, single‐ascending‐dose study to evaluate safety, pharmacokinetics, and pharmacodynamics. Subjects received burixafor intravenous doses ranging from 0.10 to 4.40 mg/kg in 8 cohorts. Single doses were generally safe and well tolerated. Gastrointestinal events were reported at doses of 2.24 mg/kg or greater. Exposure (maximum concentration and area under the concentration–time curve) increased in an approximately dose‐proportional manner. Time to maximum concentration occurred with a median of 0.26–0.30 hours that was not dose proportional. As expected, white blood cell, CD133+ cell, and CD34+ cell concentrations generally increased with the increases in burixafor dose from 0.10 to 3.14 mg/kg. At maximal levels, the CD34+ cell counts increased 3‐ to 14‐fold from baseline levels. These results provide support for continued clinical development of burixafor.

项与氢溴酸布利沙福相关的新闻（医药）

2026-08-03

·GlobeNewswire-Health Care

Exicure to Settle GPCR Therapeutics Clinical Milestone Payment Through Equity Issuance

WILMINGTON, Del., Aug. 03, 2026 (GLOBE NEWSWIRE) -- Exicure, Inc. (Nasdaq: XCUR) (“Exicure” or the “Company”) today announced that it expects to issue 172,058 shares of its common stock to GPCR Therapeutics, Inc. (“GPCR Therapeutics”) during August 2026 in settlement of a $1.0 million clinical milestone payment obligation under the parties’ License and Collaboration Agreement. The milestone payment was triggered by the completion of the Phase 2 clinical trial of Burixafor (GPC-100), including the formal submission of the Clinical Study Report to the U.S. Food and Drug Administration on January 16, 2026. The shares are expected to be issued at a deemed value of $5.81 per share, based on applicable Nasdaq trading data, representing an aggregate deemed value of approximately $1.0 million. On July 31, 2026, the Company submitted a Listing of Additional Shares Notification to The Nasdaq Stock Market in connection with the equity issuance. The Company also completed and delivered the applicable treasury issuance instructions to its transfer agent, Equiniti Trust Company, LLC. The Company expects the issuance to be completed during August 2026, subject to the completion of customary Nasdaq and transfer agent review and processing procedures. Exicure intends to provide an additional update following completion of the issuance. “Settling this milestone payment through the issuance of common stock will allow Exicure to preserve cash and maintain financial flexibility as we continue to pursue our operational and strategic priorities,” said Jung Soo Kim, Chief Executive Officer of Exicure. About Exicure, Inc. Exicure, Inc. (Nasdaq: XCUR) has historically been an early-stage biotechnology company focused on developing nucleic acid therapies targeting ribonucleic acid against validated targets. Following its restructuring and suspension of clinical and development activities, the Company is exploring strategic alternatives to maximize stockholder value. In January 2025, it acquired a clinical-stage biotechnology company developing therapeutics for hematologic diseases. The Company’s lead program is being evaluated for its ability to improve stem cell mobilization in multiple myeloma, sickle cell disease, and in support of cell and gene therapy. Forward-Looking Statements This press release contains forward-looking statements within the meaning of applicable federal securities laws, including statements regarding the anticipated issuance of shares to GPCR Therapeutics, the expected timing and completion of the issuance, the settlement of the Company’s milestone payment obligation, and the Company’s strategic direction. Forward-looking statements are based on management’s current expectations and assumptions and are subject to risks and uncertainties that could cause actual results to differ materially from those expressed or implied by such statements. The Company undertakes no obligation to update any forward-looking statements except as required by applicable law. Media Contact Exicure, Inc.pr@exicuretx.com

临床2期引进/卖出并购

2026-07-01

·南模生物SMOC

CXCR4：从趋化因子受体到肿瘤微环境调控核心——靶向药物与临床前研究进展

C-X-C趋化因子受体4（CXCR4）因其在肿瘤进展和转移中通过维持干细胞样表型的关键作用，已成为癌症治疗的重要分子生物标志物。该受体在20余种癌症中过表达，包括实体瘤和血液系统恶性肿瘤，且常与肿瘤侵袭性强和预后不良相关。CXCR4最初被认为是HIV感染的共受体，过去数十年间已发现了大量靶向CXCR4的配体和拮抗剂，涵盖小分子、多肽和生物制剂。尽管目前仅少数应用于癌症治疗领域，但近期以CXCR4为分子靶点的生物技术进展显示出革新未来癌症治疗的巨大潜力。 CXCR4的靶点生物学基础分子结构与信号转导机制 CXCR4属于G蛋白偶联受体超家族中的趋化因子受体亚类，由352个氨基酸组成，具有典型的七次跨膜螺旋结构。其唯一内源性配体CXCL12，又称基质细胞衍生因子1（SDF-1），是一种由68个氨基酸构成的趋化因子。当CXCL12与CXCR4结合后，受体构象发生改变，进而激活多种下游信号通路，包括磷脂酰肌醇3-激酶（PI3K）通路、磷脂酶C（PLC）通路、Janus激酶/信号转导与转录激活因子（JAK/STAT）通路以及丝裂原活化蛋白激酶（MAPK）通路。图1. CXCR4在生理及病理过程中的信号转导[1] 生理与病理功能 CXCR4及其配体CXCL12构成的信号轴在机体正常生理过程中不可或缺。在胚胎发育阶段，该信号轴参与心血管系统形成、神经嵴细胞定向迁移及肾脏器官发生。在成体造血系统中，CXCR4是造血干细胞归巢至骨髓微环境的关键分子，维持造血稳态，同时参与B细胞发育成熟及淋巴细胞再循环。在组织损伤修复中，CXCR4介导间充质干细胞向损伤部位募集并促进血管新生。然而，当CXCR4信号轴调控失衡时，其病理效应同样显著。在血液系统恶性肿瘤中，白血病细胞和多发性骨髓瘤细胞高表达CXCR4，沿CXCL12浓度梯度归巢至骨髓保护性微环境，逃避化疗杀伤，是耐药和复发的重要机制。在实体瘤转移中，肿瘤细胞上调CXCR4使其能够识别远处器官（如骨骼、肺、肝脏和淋巴结）中CXCL12富集区域，实现定向转移。此外，CXCL12梯度可招募调节性T细胞和髓源性抑制细胞至肿瘤微环境，参与免疫抑制。在罕见遗传病WHIM综合征中，CXCR4基因C端功能获得性突变导致受体脱敏障碍，引起白细胞骨髓滞留，临床表现为疣、低丙种球蛋白血症、感染和骨髓粒细胞缺乏。肿瘤微环境中的核心角色 CXCR4在癌症进展中发挥多重关键作用。其过度表达通过激活MAPK、PI3K/Akt和PLC信号通路促进肿瘤细胞增殖，同时通过JAK/STAT通路诱导药物耐药性和复发，具体机制包括上调抗凋亡信号、下调细胞死亡受体表达，以及协同免疫检查点（CTLA-4、PD-L1等）帮助癌细胞逃避免疫监视。在转移方面，CXCR4+癌干细胞通过激活Rac1和MMP-2/MMP-14增强肿瘤侵袭与迁移能力，并通过促进癌细胞对内皮细胞的黏附及VEGF/VEGFR上调加速血管生成，使癌细胞具备进入循环系统、归巢至CXCL12/SDF-1分泌器官并定植转移的能力。此外，CXCR4+上皮癌细胞通过调控肿瘤微环境促进恶性进展。肿瘤相关间质细胞分泌的高水平CXCL12以旁分泌方式刺激细胞增殖、诱导上皮间充质转化（EMT），并增强肿瘤边缘的迁移与侵袭。同时，CXCL12招募调节性T细胞、肿瘤相关巨噬细胞和髓系来源抑制细胞等免疫抑制性群体浸润肿瘤，形成免疫豁免屏障，阻断抗肿瘤免疫应答。图2. CXCR4在癌症中的作用[1] CXCR4靶向治疗的临床应用现状已获批上市药物全球已获批上市的CXCR4靶向药物目前共有3款：2008年，双环胺类小分子Plerixafor（普乐沙福）获FDA批准，联合G-CSF用于多发性骨髓瘤和非霍奇金淋巴瘤患者的造血干细胞动员，首次验证了CXCR4作为可成药靶点的可行性；2023年9月，环肽类拮抗剂Motixafortide（Aphexda/莫替福肽）获批同适应症，以更长的受体占位时间和更优的动员效率成为该领域十年来首个新药，目前还在探索联合PD-1抑制剂用于胰腺癌等实体瘤治疗；2024年4月，口服小分子Mavorixafor获批用于罕见遗传病WHIM综合征，通过抑制CXCR4的过度激活信号恢复白细胞正常分布，成为该病史上首个靶向治疗药物——三款药物从干细胞动员到罕见病，逐次拓宽了CXCR4靶点的临床边界。诊断显像探针在诊断领域，以环肽类分子 Pentixafor 为配体的放射性核素标记探针实现了重要突破。作为首个进入临床研究的 CXCR4 靶向 PET 探针，镓-68 标记的 Pentixafor（[⁶⁸Ga]Pentixafor）具有三大核心优势：对人CXCR4 的低纳摩尔级亲和力、快速的肾脏清除动力学，以及由此带来的低背景信号。目前，该探针已在德国等欧洲国家以医院豁免或临床试验形式开展应用。在肿瘤诊断中，[⁶⁸Ga]Pentixafor PET 已成功用于多发性骨髓瘤、淋巴瘤等血液肿瘤及胶质母细胞瘤等部分实体瘤的 CXCR4 表达可视化。在心血管领域，该探针可无创评估动脉粥样硬化斑块的 CXCR4 阳性炎症细胞浸润，既能识别易损斑块，又能评价他汀类药物等抗炎干预的疗效。此外，心肌梗死后梗死区 CXCR4 在炎症修复期显著上调，PET成像可据此追踪炎症消退与组织修复的动态过程。在神经炎症方面，[⁶⁸Ga]Pentixafor 已用于多发性硬化等疾病的脑内炎症负荷定量评估。在治疗端，与诊断探针配对的治疗型配体 [¹⁷⁷Lu]Pentixather 和 [⁹⁰Y]Pentixather 已进入临床研究。二者通过 CXCR4 靶向内照射杀伤高表达病灶，与 [⁶⁸Ga]Pentixafor PET 共同构成诊疗一体化闭环。临床在研药物盘点 CXCR4在20余种癌症类型中过表达，多种拮抗剂（主要为小分子、多肽和抗体）已被开发用于靶向该受体，其中多项已进入临床试验阶段。表1. 靶向CXCR4已上市或进入临床研究阶段药物研发管线（数据来源于智慧芽）小分子拮抗剂 Plerixafor（普乐沙福）是最经典的CXCR4小分子拮抗剂，2008年获FDA批准联合G-CSF动员造血干细胞用于淋巴瘤和骨髓瘤患者自体移植，兼具化疗增敏作用，目前已注册超过150项临床试验。Mavorixafor为口服CXCR4拮抗剂，可增强CD8+ T细胞浸润、减少免疫抑制细胞，联合免疫检查点抑制剂在肾细胞癌和黑色素瘤中安全性良好，近期获FDA批准用于WHIM综合征。Burixafor联合G-CSF及普萘洛尔的三联方案较标准动员方案效果更优，II期试验正在进行。GMI-1359为CXCR4/E-selectin双靶点抑制剂，临床前显示促白血病细胞动员和骨转移抗肿瘤活性，联合多西他赛增敏效果优于单一CXCR4拮抗剂。Burixafor（GPC-100）可动员造血干细胞，联合G-CSF在NHL、霍奇金淋巴瘤和MM中成功实现干细胞动员。其与普萘洛尔及G-CSF的三联方案较标准普乐沙福联合G-CSF方案显示出更优动员效果，相关II期试验正在进行。GMI-1359为CXCR4和E-selectin双靶点抑制剂，临床前在AML和MM模型中促进白血病细胞动员并延长生存，且具有骨转移抗肿瘤活性，联合多西他赛增敏效果优于单靶点CXCR4拮抗剂。目前正在HR⁺转移性乳腺癌患者中评估其靶点结合效应。多肽多肽类CXCR4拮抗剂是肿瘤治疗中另一类重要方向。其中进展最快的是Motixafortide（BL-8040），已获FDA批准（商品名Aphexda），联合G-CSF用于多发性骨髓瘤患者的造血干细胞动员和自体移植，III期GENESIS试验安全性良好。目前其联合阿糖胞苷治疗复发/难治AML、联合PD-1抑制剂及化疗用于转移性胰腺癌等多项研究正在推进，并探索用于镰状细胞病的基因治疗干细胞动员。Balixafortide联合艾日布林未能在HER2阴性转移性乳腺癌中增效，但可单独动员造血干细胞。CTCE-9908（PTX-9908）在多种肿瘤模型中抑制生长和转移，目前已进入肝癌I/II期临床，评估其在肝动脉化疗栓塞后预防肝细胞癌复发的作用。抗体类药物 Ulocuplumab（BMS-936564）是百时美施贵宝开发的全人源IgG4抗CXCR4单克隆抗体。临床前研究显示，其在AML、非霍奇金淋巴瘤和多发性骨髓瘤等血液肿瘤中通过非caspase依赖的活性氧产生途径诱导凋亡，发挥抗肿瘤效应。临床方面，Ulocuplumab联合来那度胺和硼替佐米在复发/难治多发性骨髓瘤患者中表现出高反应率，包括既往重度治疗人群，安全性可接受；联合伊布替尼治疗Waldenström巨球蛋白血症同样安全。然而，其联合阿糖胞苷治疗AML的I/II期试验因入组缓慢及商业目标变更而终止，胰腺癌和小细胞肺癌试验也因疗效不足终止。 LY2624587是礼来开发的全人源化单抗，通过受体内化下调细胞表面CXCR4，临床前模型中促进凋亡，但其造血干细胞动员能力明显弱于同类多肽拮抗剂LY2510924。PF-06747143为辉瑞的人源化IgG1抗体，区别于Ulocuplumab，其具备抗体依赖性细胞毒性（ADCC）和补体依赖性细胞毒性（CDC）双重效应机制，临床前在AML和多发性骨髓瘤模型中与化疗显著协同，但I期AML试验因战略优先调整终止。F50067同样依赖ADCC和CDC机制，但因血小板减少等血液学毒性在复发/难治骨髓瘤试验中终止。此外，双表位纳米抗体ALX-0651亦未能在临床试验中优于现有标准治疗。寡核苷酸类药物已发现多种调控CXCR4的miRNA具有肿瘤治疗潜力：miR-146、miR-193-5p可抑制结直肠癌增殖并增强化疗敏感性；miR-139可降低乳腺癌干细胞侵袭能力；miR-613能抑制骨肉瘤转移。然而，这些miRNA的临床应用受限于血液降解和脱靶毒性，目前研究正聚焦于开发纳米载体等递送系统以提高稳定性与靶向性。放射性核素治疗放射性核素治疗是CXCR4靶向药物最具前景的发展方向之一，其核心在于将高亲和力CXCR4配体与治疗性核素偶联，实现肿瘤精准内照射。钇-90和镥-177标记的Pentixather均已进入临床研究：90Y-Pentixather在多发性骨髓瘤的首次人体试验及CNS淋巴瘤的临床试验中展现出治疗潜力；177Lu-Pentixather因β粒子射程较短（约2 mm）、半衰期更长，对微小病灶更具剂量学优势，正在神经内分泌肿瘤等适应症中开展I/II期评估。两者与诊断探针[⁶⁸Ga]Pentixafor配对，构成显像筛选—精准治疗的诊疗一体化闭环。在临床前研究中，锕-225等α粒子发射体标记的环肽配体正被积极探索。α粒子具有高传能线密度，短射程内释放巨大能量，对微转移灶和单个肿瘤细胞杀伤力极强，有望弥补常规β粒子治疗对微小病灶效果不佳的短板。南模生物CXCR4相关小鼠模型南模生物长期致力于各种小鼠模型的开发，可以提供多种CXCR4靶点相关小鼠，例如人源化CXCR4小鼠，为相关药物的临床前药理药效评估和安全性评价提供强有力的工具。表2. 南模生物CXCR4靶点相关小鼠品系 hCXCR4(2), 目录号：NM-HU-251443 图3. 通过流式细胞术检测WT C57BL/6小鼠与HO hCXCR4(2)小鼠脾脏中T细胞、B细胞及CD11b+细胞表面的CXCR4表达。hCXCR4仅在HO hCXCR4(2)小鼠中检出，WT小鼠中未检测到。图4. 通过流式细胞术检测WT C57BL/6小鼠与HO hCXCR4(2)小鼠骨髓中T细胞、B细胞及CD11b+细胞表面的CXCR4表达。hCXCR4仅在HO hCXCR4(2)小鼠中检出，WT小鼠中未检测到。全人源抗hCXCR4抗体ulocuplumab的体内靶点结合验证图5. 通过流式细胞术检测WT C57BL/6小鼠与HO hCXCR4(2)小鼠骨髓中T细胞、B细胞及CD11b+细胞表面ulocuplumab的结合。ulocuplumab仅和HO hCXCR4(2)小鼠的细胞结合，不与WT小鼠的细胞结合。相关阅读 ASCO 2026炸场！94项口头报告+12项LBA，这些模型与服务成研发硬核助攻从ASCO 2026爆款PD-1/VEGF双抗，看人源化小鼠模型如何支撑临床前研发细说肝癌治疗潜力靶点--GPC3 做ADC项目，这些模型和服务可能正是你需要的！人源化小鼠模型：CAR-T疗法临床前验证的关键工具与转化桥梁从ex vivo到in vivo：CAR-T细胞治疗的第二次革命世界癌症日｜“以人为本，携手抗癌”，南模肿瘤平台驱动新药突破 >>> 点击进入药靶百科合集 Reference： [1] Rueda, A., Serna, N., Mangues, R. et al. Targeting the chemokine receptor CXCR4 for cancer therapies. Biomark Res 13, 68 (2025). [2] Yang, B., Hu, W., Zhang, X., Gai, Y., An, R., Qin, C., Li, M., Lan, X. (2026). The CXCR4-targeted theranostics era: a comprehensive review of a decade of progress (2015–2025). Theranostics, 16(12), 6576-6599. 关于我们上海南方模式生物科技股份有限公司（Shanghai Model Organisms Center, Inc.，简称"南模生物"），成立于2000年9月，是一家上交所科创板上市高科技生物公司（股票代码：688265），始终以编辑基因、解码生命为己任，专注于模式生物领域，打造了以基因修饰动物模型研发为核心，涵盖多物种模型构建、饲养繁育、表型分析、药物临床前评价等多个技术平台，致力于为全球高校、科研院所、制药企业等客户提供全方位、一体化的基因修饰动物模型产品解决方案。欢迎通过以下方式联系我们： 💬 微信公众号「南模生物SMOC」在线咨询 📞 拨打400-728-0660 📧 发送邮件至marketing@modelorg.com 🔗 点击文末「阅读原文」即可查看更多数据

2026-04-23

·BioSpace

Exicure Announces Co-Development Agreement with Adbiotech for Burixafor (GPC-100)

CHICAGO, April 22, 2026 (GLOBE NEWSWIRE) -- Exicure, Inc. (Nasdaq: XCUR) today announced that it has entered into a co-development agreement with Adbiotech Co., Ltd. (KOSDAQ: 179530), a Korea-based biotechnology company, to explore combination therapies based on Burixafor (GPC-100) across multiple therapeutic areas. The collaboration will focus on evaluating combination strategies involving Burixafor (GPC-100) in indications including sickle cell disease (SCD), acute myeloid leukemia (AML), and solid tumors. Under the agreement, Adbiotech will conduct in vivo studies and support preclinical validation and translational research, while Exicure will provide Burixafor and lead clinical and regulatory strategy. Burixafor successfully completed a Phase 2 clinical trial in multiple myeloma last year, providing a foundation for further evaluation in hematologic indications such as AML and SCD. Based on its clinical pro date, Burixafor may have potential applicability in additional hematologic indications. The parties intend to conduct in vivo validation studies and, subject to further agreement, may advance selected programs into IND-enabling studies and clinical trials. The parties also intend to secure funding to support the advancement of future clinical development. Further details regarding development plans, budget, intellectual property, and commercialization will be determined in a subsequent definitive agreement. A representative of Exicure commented, “This agreement represents an important step in expanding the evaluation of Burixafor in combination approaches across multiple indications.” About Exicure, Inc. Exicure, Inc. (Nasdaq: XCUR) has historically been an early-stage biotechnology company focused on developing nucleic acid therapies targeting ribonucleic acid against validated targets. Following its restructuring and suspension of clinical and development activities, the Company is exploring strategic alternatives to maximize stockholder value. In January 2025, it acquired a clinical-stage biotechnology company developing therapeutics for hematologic diseases. The Company’s lead program in development is being evaluated for its ability to improve stem cell mobilization in multiple myeloma, sickle cell disease, and in support of cell and gene therapy. For more information, visit . Forward-Looking Statements This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. All statements in this press release other than statements of historical fact may be deemed forward looking including, but not limited to, statements regarding: the Company’s current business plans and objectives, including the pursuit of strategic alternatives to maximize stockholder value, the timing of the equity investment closing and potential additional equity investment and the Nasdaq Hearings Panel process and potential results. Words such as “plans,” “expects,” “will,” “anticipates,” “continue,” “advance,” “believes,” “target,” “may,” “intend,” “could,” and other words and terms of similar meaning and expression are intended to identify forward-looking statements, although not all forward-looking statements contain such terms. Forward-looking statements are based on management’s current beliefs and assumptions that are subject to risks and uncertainties and are not guarantees of future performance. For a discussion of other risks and uncertainties, and other important factors, any of which could cause the Company’s actual results to differ from those contained in the forward-looking statements, see the section titled “Risk Factors” in the Company’s Annual Report on Form 10-K for the year ended December 31, 2025 filed with the Securities and Exchange Commission in connection with this press release, as updated by the Company’s subsequent filings with the Securities and Exchange Commission. All information in this press release is as of the date of the release, and the Company undertakes no duty to update this information or to publicly announce the results of any revisions to any of such statements to reflect future events or developments, except as required by law. Media Contact Exicure, Inc. pr@exicuretx.com

临床2期引进/卖出并购基因疗法

100 项与氢溴酸布利沙福相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB11970

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
霍奇金淋巴瘤	临床2期	中国台湾	GPCR Therapeutics, Inc.	2010-02-01
多发性骨髓瘤	临床2期	中国台湾	GPCR Therapeutics, Inc.	2010-02-01
急性髓性白血病	临床1期	中国	太景医药研发（北京）有限公司	2015-07-28

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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


NCT05561751 (ASH2025)	临床2期	多发性骨髓瘤	10	Burixafor (GPC-100) + Propranolol + G-CSF	範鏇構顧齋鑰鏇鑰獵鹹(淵膚糧製鑰鑰積廠遞獵) = 餘淵鹹製鑰獵餘襯遞鹽遞選網鏇夢糧網夢範餘 (窪選觸觸鹹築顧膚衊襯 ) 更多	积极	2025-12-06
NCT05561751 (ASH2024) 人工标引	临床2期	多发性骨髓瘤 CD34+	20	Propranolol+G-CSF+ Burixafor	鹽遞糧餘鑰蓋餘獵齋夢(淵觸繭蓋齋積窪顧積齋) = 構鹹壓觸顧艱廠築淵獵壓鹽構簾顧顧鬱選網積 (網願鹹壓夢窪鹹衊夢繭 )	积极	2024-12-09
NCT01458288 (CTgov)	临床2期	霍奇金淋巴瘤 \| 多发性骨髓瘤	12	TG-0054	廠襯遞願網蓋鑰醖鏇襯 = 範積獵膚壓衊選艱網觸鹽壓齋範簾鑰廠鑰壓遞 (醖艱窪鏇遞齋顧構構鹽, 淵顧築憲獵襯積膚鹹繭 ~ 襯襯淵夢艱簾齋積選獵) 更多	-	2015-01-08