An Open-Label, Multicenter, Randomized, Non-Inferiority Pharmacokinetic and Safety/Tolerability Study of Two Different Weekly Doses of Alpha1-Proteinase Inhibitor Subcutaneous (Human) 15% in Patients With Alpha1-Antitrypsin Deficiency Compared to Corresponding Standard 60 mg/kg/Week and 120 mg/kg/Week Doses of Intravenous Alpha1-Proteinase Inhibitor (5%)

This study is designed to compare two different weekly doses of a medicine called Alpha1-Proteinase Inhibitor given by injection under the skin with the standard doses of the same medicine given through a vein.
Adults with Alpha-1 Antitrypsin Deficiency will take part. Participants will be randomly assigned to one of the treatment groups, and both the study doctors and participants will know which treatment is being given.
The main goals of the study are to understand how the body processes the medicine (pharmacokinetics) and to assess how safe and well tolerated the different weekly doses are.

开始日期2026-05-05

申办/合作机构

Grifols Therapeutics LLC

CTIS2024-517613-33-00

/ Recruiting临床2期IIT

A two-center, randomized, double-blind, placebo-controlled study of intravenous plasma-purified alpha-1 antitrypsin for hospitalized patients with COPD exacerbations (AECOPD study)

开始日期2025-10-16

申办/合作机构

Fondazione IRCCS Policlinico San Matteo

NCT07125664

/ Not yet recruiting临床2期IIT

A Two-center, Randomized, Double-blind, Placebo-controlled Study of Intravenous Plasma-purified Alpha-1 Antitrypsin for Hospitalized Patients With COPD Exacerbations (AECOPD Study)

Intravenous augmentation therapy with purified preparations of AAT (Alpha1-antitrypsin) derived from human plasma is a well consolidated specific therapeutic option to treat the severe deficient state of AAT. Prolastin is used to restore the balance between AAT and elastases in the lung and consequently to prevent a further deterioration in the pulmonary emphysema. Recently, in patients with COVID-19, without genetically lowered AAT levels with moderate to severe ARDS, treatment with AAT was demonstrated to be safe, feasible, and biochemically efficacious as an anti-inflammatory therapeutic therapy.
The aim of the study, based on biological plausibility, is to evaluate the safety and efficacy (from a biological perspective) of the administration of intravenous plasma-purified AAT as an anti-inflammatory treatment for patients admitted to hospital because of a COPD exacerbation leading to an acute or an acute on chronic respiratory failure.
Thirty-six adult patients hospitalized because of a COPD exacerbation leading to an acute or an acute on chronic respiratory failure will be enrolled by the two sites involved in the study, the Pneumology Unit of Fondazione IRCCS Policlinico San Matteo (Pavia, Italy) and the Pneumology Unit of IRCCS Istituto Clinico Humanitas, Rozzano (Milano, Italy).
Participants will be randomized 2:1 in the active treatment group (standard treatment + IV administration of Prolastin) or in the placebo group (standard treatment+ IV administration of 0.9% sodium chloride).
To address the clinical question from a biological perspective, we will investigate the decrease in inflammatory markers in the active treated group in comparison with the placebo group.
The primary objective is to demonstrate a significant reduction in systemic inflammation by IV Prolastin administered once at 120 mg per kilogram of body weight in patients with moderate to severe AECOPD, as assessed by the change in plasma concentration of IL6 at 7 days after randomization, in the active treatment group with respect to placebo group.
Secondary outcomes are:
1. Difference in change in plasma concentration of IL-1b, IL-5, IL-8, IL-10, and soluble TNF receptor 1 (sTNFR1), CRP at 7 days after randomization.
2. Differences in AAT antielastase activity, the amount of active elastase, the AAT levels in serum at baseline and at 7 days after randomization.
3. Difference in treatment failure rate. Treatment failure is a composite endpoint of need for either NIV or CPAP or need of ETI or need of transfer to ICU or in-hospital death after randomization
4. Impact of AECOPD on overall health, daily life, and perceived well-being in patients with obstructive airways disease by the change of St. George's Respiratory Questionnaire (SGRQ) score from Day 7 to follow-up (30 days after hospital discharge).
5. Differences in type and number of AEs and SAEs in the two groups
The expected duration of subject participation is from randomization to 30 days after hospital discharge, with a follow up phone contact.

开始日期2025-10-01

申办/合作机构-

100 项与 Alpha1-proteinase inhibitor(Grifols SA) 相关的临床结果

登录后查看更多信息

100 项与 Alpha1-proteinase inhibitor(Grifols SA) 相关的转化医学

登录后查看更多信息

100 项与 Alpha1-proteinase inhibitor(Grifols SA) 相关的专利（医药）

登录后查看更多信息

1,168

项与 Alpha1-proteinase inhibitor(Grifols SA) 相关的文献（医药）

2026-12-01·MOLECULAR BIOLOGY REPORTS

The role of nitric oxide and connexin 43 in the cardioprotective effects of apigenin against doxorubicin-induced cardiotoxicity in male rats

Article

作者: Dehpour, Ahmad Reza ; Azizi, Yaser ; Goudarzi, Mina ; Safaei, Atlasi ; Fallah, Masoud ; Sheibani, Mohammad

BACKGROUND:

Doxorubicin (DOX) is one of the most widespread antibiotics used in the treatment of malignancies. Cardiotoxicity is the main side effect of DOX. Although the protective effects of apigenin have been shown, its mechanisms are still unknown. This study aimed to assess the role of nitric oxide (NO) in the protective effects of apigenin, particularly by altering the expression of connexin 43 (CX43) in the heart tissue.

METHODS AND RESULTS:

In this study, 60 male Wistar rats were divided into six equal groups: control (normal), DOX (2 mg/kg every 48 h for 12 days i.p.), apigenin (Api, 50 mg/kg oral administration), DOX + Api, DOX + L-NAME (Nitro-L-arginine methyl ester) (30 mg/kg i.p.), and DOX + Api + L-NAME. Our study assessed alterations in the heart weight and body weight, markers of cardiac function via echocardiography Ejection Fraction (%EF), Fractional Shortening (%FS), Left Ventricular Internal Diameter in Systole (LVIDs), and Left Ventricular Internal Diameter in Diastole (LVIDd), cardiac oxidative stress factors Superoxide Dismutase (SOD), Reduced Glutathione (GSH), Malondialdehyde (MDA), Catalase (CAT), cardiac injury markers Lactate Dehydrogenase (LDH), Creatine Kinase-MB (CK-MB), and Cardiac Troponin I (cTn-I), cardiac fibrosis, and CX43 expression (immunohistochemistry). Apigenin improved cardiac tissue damage and functional parameters such as left ventricular EF. Furthermore, treatment with apigenin, but not DOX, caused a significant reduction in the percentage of cardiac fibrosis and oxidative stress activity. Apigenin can also elevate the cardiac CX43 expression in the DOX + Api compared to the DOX group. NOS inhibition by L-NAME attenuates the protective effects of apigenin in DOX-induced cardiotoxicity COCCLUSION: Apigenin could exert its cardioprotective effects through an NO-dependent mechanism and elevation of CX43 expression.

2026-10-01·BIOTECHNOLOGY AND BIOENGINEERING

Glycoengineered Recombinant Alpha1‐Antitrypsin Results in Comparable In Vitro and In Vivo Activities to Human Plasma‐Derived Protein

Article

作者: Rocamora, Frances ; McElvaney, Noel G ; Schoffelen, Sanne ; Fuerst, Thomas R ; Arnsdorf, Johnny ; Voldborg, Bjørn Gunnar Rude ; Wu, Mina Ying Min ; Yunus, Abdul S ; Bjørn, Sara Petersen ; Lewis, Nathan E ; Toth, Eric A ; Cleveland, Thomas E ; Hsieh, Chen-Lin

ABSTRACT:

Alpha‐1‐antitrypsin (A1AT) is a multifunctional, clinically important, high‐value therapeutic glycoprotein that can be used for the treatment of many diseases, such as A1AT deficiency, diabetes, graft‐versus‐host disease, cystic fibrosis, and various viral infections. Currently, the only U.S. food and drug administration‐approved treatment for A1AT disorders is intravenous augmentation therapy with human plasma‐derived A1AT (pdA1AT). In addition to its limited supply, this approach poses a risk of infection transmission, since it uses therapeutic A1AT harvested from donors. To address these issues, we sought to generate recombinant human A1AT (rhA1AT) that is comparable to its plasma‐derived counterpart using glycoengineered Chinese Hamster Ovary (geCHO‐L) cells. By perturbing nine key genes that are part of the CHO glycosylation machinery and expressing the human ST6GAL1 and A1AT genes, we obtained stable, high producing geCHO‐L lines that produced rhA1AT having a highly similar glycoprofile to pdA1AT. Additionally, the rhA1AT demonstrated in vitro activity and in vivo half‐life comparable to commercial pdA1AT. Thus, we anticipate that this platform will help produce human‐like recombinant plasma proteins, thereby providing a more sustainable and reliable source of therapeutics that are cost‐effective and better‐controlled regarding purity, clinical safety, and quality.

2026-10-01·BIOCHEMICAL PHARMACOLOGY

Apigenin restores macrophage homeostasis and angiogenesis via Fgr/IL10 axis in recurrent spontaneous abortion

Article

作者: Li, Ming-Qing ; Li, Meng-Ying ; Yang, Yi-Xing ; Liu, Song-Ping ; Liu, Nan ; Cao, Xiao-Yan ; Chen, Si-Man ; Xie, Feng ; Huang, Xu

Recurrent spontaneous abortion (RSA) is closely associated with disruption of both immune homeostasis and vascular development at the maternal-fetal interface. To decode the underlying cellular defects, we performed single-cell RNA sequencing (scRNA-seq) on human decidual tissues, revealing a profound imbalance in macrophage polarization and impaired efferocytosis in RSA patients. Through transcriptomic screening and clinical validation, we pinpointed the Fgr proto-oncogene, Src family tyrosine kinase (Fgr) as a key pathological driver overexpressed in RSA macrophages, acting as a molecular brake on the pro-healing M2 phenotype. Seeking a targeted intervention, we demonstrated that the natural flavonoid Apigenin (Api) directly binds and inhibits the Fgr kinase domain, which essentially triggers robust Interleukin 10 (IL10) secretion. Crucially, this Api-mediated Fgr/IL10 signaling axis not only restores M2 polarization and enhances apoptotic cell clearance, but also rescues pro-angiogenic crosstalk with endothelial cells in a vascular endothelial growth factor (VEGF) -dependent manner. Furthermore, in a lipopolysaccharide (LPS)-induced murine miscarriage model, Api administration effectively reduced embryo resorption and rescued pregnancy loss. Collectively, our study highlights the Fgr/IL10 axis as a critical determinant of decidual homeostasis and establishes Api as a promising therapeutic strategy for RSA.

项与 Alpha1-proteinase inhibitor(Grifols SA) 相关的新闻（医药）

2026-09-08

·岭南心血管病杂志

【综述】系统性炎症在急性心肌梗死发病中的作用研究进展

版权声明：本平台致力分享好文精选、精读。部分文章推送时未能与原作者取得联系。若涉及版权问题，敬请原作者在本公号留言删除！ 32本文刊于：岭南心血管病杂志，2026，32（03）：327-332 作者：李尚辰，刘东霞通信作者：刘东霞提要本文旨在通过综合分析现有的研究结果，探讨系统性炎症如何影响急性心肌梗死的发生和发展，进一步阐明炎症标志物在急性心肌梗死发病中的潜在作用，并探讨可能的防治策略，以期为改善患者预后提供参考。本综述将重点阐述系统性炎症在急性心肌梗死发生、发展中的作用机制，结合相关的临床研究，为心肌梗死的防治提出新的思路。急性心肌梗死（acute myocardial infarction, AMI）被公认为是导致心血管疾病相关死亡的重要因素之一，每年在全球范围内有数百万例的心肌梗死发生，而其较高的死亡率及不良结局令人堪忧[1]。心肌梗死的发生通常涉及多种复杂的因素，其中系统性炎症反应被广泛认为在该病的发病机制中发挥着至关重要的作用。近期的研究也表明，炎症不仅是心肌梗死的一个显著诱因，同时它还可能对心肌梗死的临床表现以及患者的预后产生深远的影响[2]。研究表明，在心肌梗死发生后，机体会通过多种生物途径激活炎症反应，包括细胞因子的释放、白细胞的动员等，这些反应可能导致心肌细胞进一步的损伤和功能障碍[3]。如，AMI患者的血清中炎症标志物的升高与不良临床结局之间存在着密切的相关性，这提示系统性炎症可能会加重心肌损伤，并严重影响患者的远期预后[4]。因此，深入研究AMI的发病机制与炎症反应之间的复杂关系，对于改善患者临床症状、提升患者的预后具有重要的意义。未来的研究应当进一步探索炎症在心肌梗死中的具体作用机制，并寻找有效的干预措施，以期降低心肌梗死的发病率和死亡率[5]。 1 系统性炎症与急性心肌梗死的病理生理机制 1.1 炎症在动脉粥样硬化中的作用炎症在动脉粥样硬化的发生、发展中起着核心作用，尤其是在病理生理机制上。动脉粥样硬化被视为一种慢性炎症性疾病，其特征是动脉壁内脂质的积累和炎症细胞的浸润。研究表明，炎症细胞如单核细胞和巨噬细胞在动脉粥样硬化斑块的形成和发展中扮演着重要角色，这些细胞通过分泌多种炎症因子促进斑块的增长和不稳定性。此外，慢性、持续存在的炎症与动脉粥样硬化的危险因素，如原发性高血压（高血压）、糖尿病和高胆固醇浓度密切相关，这些因素可通过激活内皮细胞及促进炎症反应加速动脉粥样硬化的进程[6]。总之，炎症在动脉粥样硬化的发展中不仅是一个重要的病理特征，同时也是潜在的治疗靶点。 1.2 炎症与血栓形成的关系炎症与血栓形成之间存在复杂的相互作用，特别是在急性心肌梗死（AMI）的情况下。炎症反应的激活可导致血小板活化和凝血因子的增加，从而促进血栓的形成[7]。如炎症介质如肿瘤坏死因子α（tumor necrosis factor, TNF-α）和白细胞介素（interleukin, IL）-6能够增强血小板的聚集能力，增加凝血活性，从而增加血栓形成的风险[8]。此外，动脉粥样硬化斑块的不稳定性往往伴随着局部炎症的加重，这进一步增加了斑块破裂和血栓形成的风险[9]。因此，控制炎症反应可能成为降低AMI风险和改善预后的重要策略。 1.3 炎症介质在急性心肌梗死中的角色在AMI发生时，炎症介质的释放是心肌损伤和后续反应的关键因素。AMI诱发的炎症反应通常分为三个阶段：急性炎症阶段、修复阶段和成熟阶段。在急性炎症阶段，损伤相关分子模式（DAMPs）被释放，诱导炎症介质，如IL-1β和IL-6的产生，这些因子进一步招募免疫细胞到达受损区域，清除坏死细胞和组织[10]。在修复阶段，抗炎信号开始占主导地位，促进瘢痕组织的形成和心肌的再生。然而，炎症反应的持续存在可能导致心肌重构和功能障碍[10-11]。因此，针对炎症介质的干预可能有助于改善AMI患者的预后，降低心肌重构的风险，成为未来治疗的重要方向。图1的左图显示细胞因子T 细胞、NK 细胞和巨噬细胞在心肌保护和修复中的有益作用。IL-10 和 IL-2 减少促炎信号（如 TNFα、MCP-1、IL-8）和细胞外基质重塑（下调 MMP），同时促进 Treg、Th2 和 NK 细胞活化，进而促使巨噬细胞向 M2 表型极化。图1的中图代表 AMI后晚期持续存在的低度炎症状态。主要致病细胞包括M1型巨噬细胞、泡沫细胞和 PMN。NLRP3 炎症小体的激活增强 IL-1α 和 IL-1β 的产生和分泌，通过 IL-6 的产生进一步放大炎症信号，形成持续的 “余烬” 炎症，是影响患者预后的残余炎症风险（RIR）。图1的右图聚焦于 AMI 早期爆发的过度炎症。斑块破裂和血栓形成触发PMN 活化和单核细胞募集，NET 形成进一步加剧这一过程。随后的氧化爆发在早期阶段加剧心肌损伤。与中图中相同的细胞因子（IL-1 和 IL-6）在 AMI 早期出现特别剧烈的激增，其破坏特性在此阶段被放大。 2 炎症标志物在急性心肌梗死诊断中的应用 2.1 常见炎症标志物在AMI的诊断中，炎症标志物的检测具有重要的临床意义。C-反应蛋白（C-reactive protein, CRP）和白细胞计数（WBC）是常见的炎症标志物。CRP是一种急性期反应蛋白，其浓度在感染或组织损伤时显著升高，能够反映体内的炎症状态。研究表明，CRP的浓度升高与AMI的发生和预后密切相关，且其作为标志物的敏感性和特异性在AMI的早期诊断中具有重要价值[12]。此外，白细胞计数的增加通常与炎症反应强度相关，AMI患者的白细胞计数常常显著高于健康对照组，提示存在系统性炎症反应[12]。虽然这些传统标志物在临床上广泛应用，但它们的特异性不强，常常受到其他病理状态的影响，因此需要结合其他新型标志物进行综合评估，以提高AMI的诊断准确性。 2.2 新型炎症标志物的研究进展近年来，随着对AMI病理机制的深入研究，新型炎症标志物的发现为AMI的早期诊断提供了新的可能性，如研究发现与铜死亡（cuproptosis）和铁死亡（ferroptosis）相关的基因在AMI患者中表达显著变化，这些基因可能成为新的诊断标志物[13]。此外，XPNPEP3被认为与AMI的发生和发展密切相关，其在AMI患者中的表达水平显著升高，且可以作为潜在的诊断标志物[14]。这些新型标志物的研究进展表明，结合传统标志物与新型炎症标志物的联合检测可能会显著提高AMI的诊断能力。 2.3 炎症标志物在急性心肌梗死早期诊断中的价值炎症标志物在AMI早期诊断中的重要性不可小觑。实际上，它们在临床应用中展现出了极其重要的价值和意义。大量研究结果表明，及时检测这些炎症标志物不仅能够有效帮助识别处于危险中的AMI患者，还能为临床医生在制定治疗决策时提供至关重要的指导，如CRP以及白细胞计数在早期出现的上升趋势，往往是心肌损伤的早期信号，并且可能暗示着患者病情的严重程度[12]。进一步结合新型炎症标志物的检测，如趋化因子受体4（CXCR4）等，能够显著提高急性心肌梗死的诊断敏感度和特异度[15]。在实际的临床操作中，采用多种标志物联合检测的方法，不仅能更加全面地评估患者的炎症状态，还有助于大幅度提高对AMI的早期识别率，进而改善患者的整体预后[15]。因此，监测炎症标志物的意义不仅在于为AMI的早期诊断提供支持，更为个体化治疗方案的制定奠定了重要的基础。 3 炎症与急性心肌梗死的预后关系 3.1 炎症标志物与急性心肌梗死患者预后的相关性炎症在AMI的发病机制中扮演着至关重要的角色，成为了研究者们关注的焦点。大量研究表明，炎症标志物浓度的升高与AMI患者的预后之间存在密切的关联。在AMI患者群体中，系统性炎症反应指数（SII）和系统性炎症反应指数（SIRI）也被发现与主要不良心血管事件（major adverse cardiovascular events, MACE）的发生风险显著相关，这一发现提示，这些炎症标志物能够作为预测AMI患者预后的潜在生物标志物[16]。此外，研究还揭示了炎症标志物的变化不仅能够反映心肌损伤的严重程度，还可能显著影响患者的生存率以及心功能的恢复情况[17]。因此，定期监测这些炎症标志物的变化，不仅有助于评估AMI的严重程度，还能够为临床评价干预措施的效果提供宝贵的依据。 3.2 炎症反应对急性心肌梗死后心脏重构的影响在AMI发生后，心脏的重构过程是导致心力衰竭的重要因素，而在这一复杂的病理机制中，炎症反应扮演着至关重要的角色。众多研究表明，AMI后出现的急性炎症反应不仅会加速心肌细胞的凋亡和纤维化，还会进一步导致心室重构以及心脏功能的显著降低。然而，有些因子在心脏重构过程中起到保护作用。此外，还有研究显示自然免疫细胞，特别是巨噬细胞，在心脏重构过程中发挥着复杂的双重作用：一方面，它们能够促进炎症反应，另一方面，通过分泌抗炎因子，又能促进心脏的修复过程[17]。因此，针对AMI后的炎症反应进行调控，可能成为改善心脏重构过程和有效预防心力衰竭的一种有效策略。 3.3 炎症与急性心肌梗死后心力衰竭的关系心力衰竭这一严重的临床症状，常常被视为AMI后的一种常见并发症。而在这一复杂的病理生理过程中，炎症的作用显得尤为重要，发挥着举足轻重的作用。大量研究结果表明，AMI后炎症反应的持续存在与心力衰竭的发生、发展有着密切的关联，高水平的炎症因子，如TNF-α和IL-6，已被证实与心力衰竭的进展密切相关。这些炎症因子不仅会加重心肌细胞的损伤，而且还会对心脏的重构过程产生重大的影响[17]。因此，针对急性心肌梗死后所引发的炎症反应展开治疗，如使用抗炎药物，可能会成为改善心力衰竭患者预后的一种有效手段，从而显著降低心力衰竭的发生率[18]。 4 抗炎治疗在急性心肌梗死中的应用 4.1 传统抗炎药物传统的抗炎药物，如非甾体抗炎药（nonsteroidal anti-inflammatory, NSAIDs），在AMI患者中的应用存在显著局限性。这些药物在抑制炎症方面的效果虽然明确，但由于其非特异性的作用机制，可能导致一系列不良反应。此外，研究表明，使用传统抗炎药物的患者在AMI后，可能会出现心功能不全的加重和不良临床结局[18]。因此，尽管NSAIDs在炎症管理中具有一定的效果，但其潜在的危害性使得其在AMI患者中的应用受到限制。特别是在AMI后期，炎症反应的复杂性和多样性使得单一的抗炎策略难以有效控制炎症并改善预后[19]。因此，迫切需要开发更为特异和安全的抗炎治疗策略，以控制AMI患者的炎症反应。 4.2 新型抗炎药物的研究进展近年来，针对AMI的抗炎治疗研究逐渐向新型抗炎药物转移，特别是针对特定炎症通路的药物，如针对IL-1的抑制剂（如阿那白滞素）和基质金属蛋白酶抑制剂（如多西环素）在临床试验中显示出改善AMI患者临床结局的潜力[18]。此外，研究还表明，抗炎药物，如秋水仙碱和氟比洛芬在AMI患者中的应用可能有效降低MACE的发生率，尤其是伴随高炎症负荷的患者[19]。新型抗炎药物的研究不仅关注其对炎症的抑制作用，还强调了其在改善心肌重构和心脏功能方面的潜在益处。然而，这些新药物的临床应用仍需在大规模随机对照试验中进一步验证其安全性和有效性，以便为临床实践提供坚实的基础。 4.2.1 针对白细胞介素-1治疗的研究针对IL-1β治疗的AMI患者抗炎治疗的临床研究结果并不一致。CANTOS是一项大型（超过10 000例患者）随机、双盲、安慰剂对照试验，招募了既往心肌梗死且超敏C反应蛋白（high-sensitivity CRP, hsCRP）浓度≥2 mg/L的患者，研究证实了针对IL-1β的治疗的药物canakinumab能够显著降低MACE的发生率[20]。然而，CANTOS的结果无法应用于临床实践，因为与安慰剂相比，接受canakinumab治疗的患者致命感染的风险显著升高。低剂量秋水仙碱心血管结局试验（COLCOT）及低剂量秋水仙碱（LoDoCo）研究也表明，低剂量秋水仙碱在MACE的二级预防中具有积极的作用。尽管秋水仙碱主要通过抑制微管蛋白聚合和微管形成来发挥其抗炎作用，但也已证明其抑制包括IL-1在内的炎症趋化因子[19]。值得注意的是，在接受低剂量秋水仙碱的患者组中，主要终点事件发生率的降低主要是由心绞痛和卒中风险降低驱动的。与CANTOS中观察到的致命感染风险增加不同，COLCOT中两组不良事件的总体发生率相似。尽管结果令人放心，但秋水仙碱在临床实践中用于MACE二级预防的常规使用尚未被广泛采用，因为主要终点事件发生率的降低是由心绞痛的减少和由于本研究两组中约20%的早期停药率导致的结果模糊性。 4.2.2 针对白细胞介素-6治疗的研究 IL-6是一种多效性促炎细胞因子，与hs-CRP产生增加相关。它通过纤维帽的降解促进斑块不稳定性，并导致动脉粥样硬化的进展[21]。FAMI（首次AMI研究）表明，与对照组相比，ST段抬高型心肌梗死（ST-segment elevated myocardial infarction, STEMI）患者IL-6的表达增加了4倍[22]。对于各种刺激的反应，如IL-1 β与IL-1R1的结合，次级细胞因子之一IL-6在IL-1下游被激活[23]。IL-6与其受体IL-6R的结合导致受体亚基糖蛋白(Glycoprotein, GP) 130的同源二聚化，随后导致IL-6、IL-6R和GP130之间的高亲和力结合，形成复合物，该复合物有助于下游通过CRP介导的炎症反应。在比较ACS患者与对照组基因差异表达的大型微阵列分析中，发现IL-6在急性冠状动脉综合征（acute coronary syndrome，ACS）进展中起关键作用。它是ACS中蛋白质间相互作用的关键介质，因此，预示着它是一个潜在的治疗靶点[24]。托珠单抗是一种人源化抗IL-6R抗体，传统上用于治疗类风湿性关节炎，在过去5年中也是与AMI相关的多项临床研究的中心。 Kleveland等[25]在他们的双盲、随机、安慰剂对照、2期试验中，招募了117例非ST段抬高型心肌梗死（NSTEMI）患者，并在第1天至第3天的不同时间评估了hsCRP和高敏肌钙蛋白T（high-sensitivity Troponin T, hsTNT）的曲线下面积（area under curve, AUC）。研究人员证明，与接受托珠单抗治疗的患者相比，接受安慰剂治疗的患者hsCRP的AUC高2.1倍（4.2 mg·L-1·h-1vs. 2.0 mg·L-1·h-1，P<0.001），hsTnT的AUC高1.5倍（234 ng·L-1·h-1 vs. 159 ng·L-1·h-1，P =0.007）。更重要的是，在6个月的适度随访期间，安全性终点严重不良事件和MACE没有显著差异[25]。在没有??STAT-MI和Kleveland等证明的安全性问题的情况下，IL-6抑制途径仍然值得未来的研究，如正在进行的ASSAILMI研究[26]。 4.2.3 针对肿瘤坏死因子-α治疗的研究鉴于在患有各种炎性疾病的患者中已知的作用机制和疗效，还在AMI患者中评估了TNF-α抑制剂的使用。尽管最初的临床前研究出现了相互矛盾的结果，引发了一些争议，但Padfield等[27]提供的临床数据表明，其可使全身炎症减少（中性粒细胞计数和IL-6浓度降低），但是增加了血小板活化。然而，考虑到在心力衰竭患者中使用TNF-α抑制剂的数据，显示MACE呈剂量依赖性增加，AMI患者中进一步研究该途径的总体兴趣已经减弱。 4.2.4 针对基质金属蛋白酶治疗的研究基质金属蛋白酶（MMPs）在细胞外基质代谢中起着重要作用，并有助于梗死边缘区的胶原降解和疤痕变薄。因此，已经研究了MMPs作为减少心肌梗死后不良心肌重构的治疗途径。针对该途径的临床试验评估了多西环素（一种非选择性MMP抑制剂）[18]和prolastin C（一种血浆衍生的α1抗胰蛋白酶[AAT]）[19]。虽然是一项开放标签的研究，但TIPTOP研究0是一项2期随机对照研究，评估多西环素（100 mg，2次/d，持续7 d）与安慰剂在通过直接经皮冠状动脉介入治疗进行再灌注且左心室功能低于40%的STEMI患者中的疗效。在6个月随访时评估了基于超声心动图的左心室舒张末期容积指数（LVEDVi）和基于单光子发射计算机断层成像（SPECT）的梗死面积和严重程度。与安慰剂组相比，多西环素组左心室舒张末期容积指数百分比变化的主要终点显著降低（0.4% vs. 13.4%，P=0.012）。类似地，Abbate等[18]最近的一项在10例STEMI患者中的初步临床研究证明了prolastin C的显著抗炎作用。尽管在没有发生重大安全问题的情况下提供了令人放心的抗炎结果，但这两项研究都受到样本量小、开放标签设计和缺乏临床结局评价的限制。今后，针对MMP通路抑制的研究仍然是进一步临床研究的主题。 5 展望炎症在许多疾病的发生和发展中起着关键作用，因此，针对炎症的干预措施在临床应用中具有广阔前景，如研究表明，针对心肌缺血再灌注损伤的炎症反应进行干预，可以显著改善患者的心脏功能和预后[28]。在自身免疫性疾病的治疗中，工程化外泌体的应用也展现出良好的抗炎和免疫调节能力，为临床治疗提供了新的思路。这些研究表明，炎症干预措施不仅可以改善患者的临床症状，还可能改变疾病的进程，提升患者的生活质量。 6 小结综上所述，系统性炎症在AMI的发病机制中扮演着至关重要的角色。大量研究揭示，炎症反应不仅是心肌损伤的主要推动力，还在心肌的修复与再生过程中发挥着复杂的双重作用。这一发现促使我们重新审视炎症在心血管疾病中的角色，从而为临床治疗提供新的视角。在众多的研究中，不同的观点和发现交织在一起，展现了炎症反应的多样性和复杂性，如一些研究指出，炎症介质如细胞因子和趋化因子在心肌细胞的死亡和心肌组织的损伤中起着关键作用，而其他研究则强调适度的炎症反应对于心肌的修复和再生是必要的。这种相互矛盾的证据要求我们在解释炎症与急性心肌梗死之间的关系时，必须保持谨慎，并考虑到个体差异、疾病阶段及其他潜在因素的影响。未来，针对炎症的干预措施可能为改善AMI患者的预后提供新的机遇。通过应用调节炎症反应的药物，如抗炎药物或生物制剂，可能会减轻心肌损伤并促进心肌修复。然而，这些干预措施的临床应用还需要大量的随机对照试验来验证其有效性和安全性。深入研究系统性炎症在AMI中的作用，不仅有助于我们掌握该疾病的发病机制，还可以为开展新的治疗策略奠定基础。未来的研究应继续探索炎症与心血管疾病之间的关系，针对影响预后关键的靶点进行干预，以期为心肌梗死患者获得良好的预后提供更为有效的治疗方案。编辑：陈延峰校对：陈宇审核：莫雅贞参考文献（略）敬请关注岭南心血管病杂志微信公众号，关注心血管领域最新动态微信号：lingnanxxgzz 登录http://jcd.org.cn在线投稿

2026-08-15

·BioSpace

Grifols Announces Last Patient Last Visit in SPARTA, its Phase 3 Outcomes Study of Prolastin®-C in Patients With Emphysema Due to Alpha-1 Antitrypsin Deficiency

Grifols’ SPARTA phase 3 trial is designed to evaluate the clinical efficacy and safety of two separate weekly dose regimens of Grifols’ Prolastin ®-C (Alpha1-Proteinase Inhibitor [Human] modified process) in patients with emphysema due to alpha-1 antitrypsin (AAT) deficiency (known as alpha-1) The trial is the largest randomized, double-blind, placebo-controlled study on alpha-1 and augmentation therapy to-date and has the potential to provide clinical evidence on slowing progression of lung tissue loss in this patient group This milestone marks the completion of follow-up for all 345 participants enrolled across 37 sites in 16 countries Top line results expected by the end of 2026 Grifols continues to advance scientific innovation in alpha-1 through a comprehensive approach that includes disease awareness, genetic testing, clinical research and treatment Aug. 10, 2026 -- Grifols (MCE:GRF, MCE:GRF.P, NASDAQ:GRFS), a global healthcare company and leading producer of plasma-derived medicines, today announced the completion of the clinical portion of SPARTA (Study of ProlAstin-C Randomized Therapy with Alpha-1 augmentation; NCT01983241), its phase 3 outcomes study evaluating the clinical efficacy and safety of two dose regimens of Prolastin®-C (Alpha1-Proteinase Inhibitor [Human] modified process) in patients with emphysema associated with alpha-1 antitrypsin deficiency (AATD), also known as alpha-1. The last patient in the trial completed their final study visit last week. This milestone, known as “last patient, last visit” (LPLV) signifies completion of follow-up for all 345 enrolled participants. Topline results are expected by the end of this year. Alpha-1 is a genetic disorder that can result in chronic obstructive pulmonary disease (COPD), a group of respiratory diseases that include emphysema, which can occur when a patient has low levels of AAT, a protective protein that safeguards the lungs. Alpha-1 remains significantly underdiagnosed1 worldwide despite being the most common known genetic risk factor for COPD.】】 SPARTA is the largest randomized, double-blind, placebo-controlled study conducted to date in augmentation therapy for alpha-1 patients with emphysema. The trial was designed to evaluate the efficacy and safety of weekly administration of two active dose levels of Prolastin-C (60 mg/kg and 120 mg/kg) compared with placebo over a three-year treatment period. The study was conducted across 37 clinical sites in 16 countries and used whole-lung computed tomography (CT) densitometry as its primary efficacy endpoint. CT densitometry is considered the most sensitive method for detecting emphysema progression and quantifying lung tissue loss in patients with AATD2, making SPARTA the first and only three-year study in AATD to generate longitudinal clinical evidence using this biomarker. “The completion of patient follow-up in SPARTA marks a significant milestone for Grifols and the alpha-1 community,” said Eduardo Herrero, Grifols’ Executive Vice President Biopharma Industrial and Scientific Innovation. “We are deeply grateful to the patients, investigators and study teams whose dedication made this achievement possible. As the first and only prospective, double-blind, placebo-controlled three-year CT densitometry study in alpha-1-related emphysema, SPARTA reflects our long-standing commitment to people living with alpha-1 through innovation in testing, diagnosis and treatment.” In addition to the SPARTA study, Grifols recently began the SWIFT-SC trial (NCT07555483), the first Phase 3 trial evaluating a weekly subcutaneous alpha1-proteinase inhibitor for the treatment of AATD. These clinical trials demonstrate the company’s ongoing commitment to innovation and to improving therapeutic options and long-term outcomes for patients with alpha-1. Alpha-1-antitrypsin deficiency, also known as alpha-1, is a rarely diagnosed genetic disease that can result in chronic obstructive pulmonary disease (COPD), a group of respiratory diseases that includes emphysema, a lung condition that causes shortness of breath. Patients who have alpha-1 have a genetic deficiency of alpha-1 antitrypsin, a protective plasma protein that safeguards the lungs from inflammation caused by infection and inhaled irritants such as tobacco smoke. Alpha-1 is the major known genetic risk factor for COPD3. PROLASTIN®-C is an alpha1-proteinase inhibitor (human) (alpha1-PI) indicated for chronic augmentation and maintenance therapy in adults with clinical evidence of emphysema due to severe hereditary deficiency of alpha1-PI (alpha-1-antitrypsin deficiency). The effect of augmentation therapy with any alpha1-PI, including PROLASTIN-C LIQUID, on pulmonary exacerbations and on the progression of emphysema in alpha1-PI deficiency has not been conclusively demonstrated in randomized, controlled clinical trials Clinical data demonstrating the long-term effects of chronic augmentation or maintenance therapy with PROLASTIN-C LIQUID are not available PROLASTIN-C LIQUID is not indicated as therapy for lung disease in patients in whom severe alpha1-PI deficiency has not been established PROLASTIN-C is contraindicated in immunoglobulin A (IgA)-deficient patients with antibodies against IgA or patients with a history of anaphylaxis or other severe systemic reaction to alpha1-PI products. Hypersensitivity reactions, including anaphylaxis, may occur. Monitor vital signs and observe the patient carefully throughout the infusion. If hypersensitivity symptoms occur, promptly stop PROLASTIN-C infusion and begin appropriate therapy. Because PROLASTIN-C is made from human plasma, it may carry a risk of transmitting infectious agents, e.g., viruses, the variant Creutzfeldt-Jakob disease (vCJD) agent, and, theoretically, the Creutzfeldt-Jakob disease (CJD) agent. This also applies to unknown or emerging viruses and other pathogens. The most common adverse reaction during clinical trials in > 5% of subjects was upper respiratory tract infection. The most serious adverse reaction observed during clinical trials with PROLASTIN-C was an abdominal and extremity rash in 1 subject. for Prolastin-C. Always refer to the Summary of Product Characteristics (SmPC) and the local prescribing information of your country. Grifols is a global healthcare company founded in Barcelona in 1909 committed to improving the health and well-being of people around the world. A leader in essential plasma-derived medicines and transfusion medicine, the company develops, produces and provides innovative healthcare services and solutions in more than 110 countries. Patient needs and Grifols’ ever-growing knowledge of many chronic, rare and prevalent conditions, at times life-threatening, drive the company’s innovation in both plasma and other biopharmaceuticals to enhance quality of life. Grifols focuses on treating conditions centered on six core therapeutic areas: immunology, neurology, pulmonology, hematology, hepatology and intensive care. A pioneer in the plasma industry, Grifols continues to grow its network of donation centers, the world’s most diversified with more than 400 across North America, Europe, Africa and the Middle East, and China. The content above comes from the network. if any infringement, please contact us to modify. As a recognized leader in transfusion medicine, Grifols offers a comprehensive portfolio of solutions designed to enhance safety from donation to transfusion, in addition to clinical diagnostic technologies. It provides high-quality biological supplies for life-science research, clinical trials and for manufacturing pharmaceutical and diagnostic products. The company also supplies tools, information and services that enable hospitals, pharmacies and healthcare professionals to efficiently deliver expert medical care. Grifols, with more than 25,000 employees in more than 30 countries and regions, is committed to a sustainable business model that sets the standard for continuous innovation, quality, safety and ethical leadership. The company’s class A shares are listed on the Spanish Stock Exchange, where they are part of the IBEX-35 (MCE:GRF). Grifols non- voting class B shares are listed on the Mercado Continuo (MCE:GRF.P) and on the U.S. NASDAQ through ADRs (NASDAQ:GRFS). _______________ 1 American Thoracic Society; European Respiratory Society. American Thoracic Society/European Respiratory Society statement: standards for the diagnosis and management of individuals with alpha-1 antitrypsin deficiency. Am J Respir Crit Care Med. 2003;168(7):818-900. doi:10.1164/rccm.168.7.818 2 Miravitlles M et al.European Respiratory Society statement: diagnosis and treatment of pulmonary disease in alpha-1 antitrypsin deficiency. Eur Respir J. 2017 3 Sandhaus RA, Turino G, Brantly ML, et al. The Diagnosis and Management of Alpha-1 Antitrypsin Deficiency in the Adult. J COPD Foundation. 2016;3(3):668-682. The content above comes from the network. if any infringement, please contact us to modify.

临床研究

2026-08-10

·grifols.com

Grifols announces Last Patient Last Visit in SPARTA, its Phase 3 Outcomes Study of Prolastin®-C in patients with emphysema due to alpha-1 antitrypsin deficiency

The information is aimed exclusively at authorized healthcare professionals to prescribe or supply medical products and its correct interpretation requires specialized training. Are you a healthcare professional? Grifols’ SPARTA phase 3 trial is designed to evaluate the clinical efficacy and safety of two separate weekly dose regimens of Grifols’ Prolastin®-C (Alpha1-Proteinase Inhibitor [Human] modified process) in patients with emphysema due to alpha-1 antitrypsin (AAT) deficiency (known as alpha-1) The trial is the largest randomized, double-blind, placebo-controlled study on alpha-1 and augmentation therapy to-date and has the potential to provide clinical evidence on slowing progression of lung tissue loss in this patient group This milestone marks the completion of follow-up for all 345 participants enrolled across 37 sites in 16 countries Top line results expected by the end of 2026 Grifols continues to advance scientific innovation in alpha-1 through a comprehensive approach that includes disease awareness, genetic testing, clinical research and treatment Barcelona, Spain, August 10, 2026 – Grifols (MCE:GRF, MCE:GRF.P, NASDAQ:GRFS), a global healthcare company and leading producer of plasma-derived medicines, today announced the completion of the clinical portion of SPARTA (Study of ProlAstin-C Randomized Therapy with Alpha-1 augmentation; NCT01983241), its phase 3 outcomes study evaluating the clinical efficacy and safety of two dose regimens of Prolastin®-C (Alpha1-Proteinase Inhibitor [Human] modified process) in patients with emphysema associated with alpha-1 antitrypsin deficiency (AATD), also known as alpha-1. The last patient in the trial completed their final study visit last week. This milestone, known as “last patient, last visit” (LPLV) signifies completion of follow-up for all 345 enrolled participants. Topline results are expected by the end of this year. Alpha-1 is a genetic disorder that can result in chronic obstructive pulmonary disease (COPD), a group of respiratory diseases that include emphysema, which can occur when a patient has low levels of AAT, a protective protein that safeguards the lungs. Alpha-1 remains significantly underdiagnosed[1] worldwide despite being the most common known genetic risk factor for COPD. SPARTA is the largest randomized, double-blind, placebo-controlled study conducted to date in augmentation therapy for alpha-1 patients with emphysema. The trial was designed to evaluate the efficacy and safety of weekly administration of two active dose levels of Prolastin-C (60 mg/kg and 120 mg/kg) compared with placebo over a three-year treatment period. The study was conducted across 37 clinical sites in 16 countries and used whole-lung computed tomography (CT) densitometry as its primary efficacy endpoint. CT densitometry is considered the most sensitive method for detecting emphysema progression and quantifying lung tissue loss in patients with AATD[2], making SPARTA the first and only three-year study in AATD to generate longitudinal clinical evidence using this biomarker. “The completion of patient follow-up in SPARTA marks a significant milestone for Grifols and the alpha-1 community,” said Eduardo Herrero, Grifols’ Executive Vice President Biopharma Industrial and Scientific Innovation. “We are deeply grateful to the patients, investigators and study teams whose dedication made this achievement possible. As the first and only prospective, double-blind, placebo-controlled three-year CT densitometry study in alpha-1-related emphysema, SPARTA reflects our long-standing commitment to people living with alpha-1 through innovation in testing, diagnosis and treatment.” In addition to the SPARTA study, Grifols recently began the SWIFT-SC trial (NCT07555483), the first Phase 3 trial evaluating a weekly subcutaneous alpha1-proteinase inhibitor for the treatment of AATD. These clinical trials demonstrate the company’s ongoing commitment to innovation and to improving therapeutic options and long-term outcomes for patients with alpha-1. About Alpha-1 and COPD Alpha-1-antitrypsin deficiency, also known as alpha-1, is a rarely diagnosed genetic disease that can result in chronic obstructive pulmonary disease (COPD), a group of respiratory diseases that includes emphysema, a lung condition that causes shortness of breath. Patients who have alpha-1 have a genetic deficiency of alpha-1 antitrypsin, a protective plasma protein that safeguards the lungs from inflammation caused by infection and inhaled irritants such as tobacco smoke. Alpha-1 is the major known genetic risk factor for COPD[3]. About Prolastin®-C PROLASTIN®-C is an alpha1-proteinase inhibitor (human) (alpha1-PI) indicated for chronic augmentation and maintenance therapy in adults with clinical evidence of emphysema due to severe hereditary deficiency of alpha1-PI (alpha-1-antitrypsin deficiency). Limitations of Use The effect of augmentation therapy with any alpha1-PI, including PROLASTIN-C LIQUID, on pulmonary exacerbations and on the progression of emphysema in alpha1-PI deficiency has not been conclusively demonstrated in randomized, controlled clinical trials Clinical data demonstrating the long-term effects of chronic augmentation or maintenance therapy with PROLASTIN-C LIQUID are not available PROLASTIN-C LIQUID is not indicated as therapy for lung disease in patients in whom severe alpha1-PI deficiency has not been established PROLASTIN-C is contraindicated in immunoglobulin A (IgA)-deficient patients with antibodies against IgA or patients with a history of anaphylaxis or other severe systemic reaction to alpha1-PI products. Hypersensitivity reactions, including anaphylaxis, may occur. Monitor vital signs and observe the patient carefully throughout the infusion. If hypersensitivity symptoms occur, promptly stop PROLASTIN-C infusion and begin appropriate therapy. Because PROLASTIN-C is made from human plasma, it may carry a risk of transmitting infectious agents, e.g., viruses, the variant Creutzfeldt-Jakob disease (vCJD) agent, and, theoretically, the Creutzfeldt-Jakob disease (CJD) agent. This also applies to unknown or emerging viruses and other pathogens. The most common adverse reaction during clinical trials in > 5% of subjects was upper respiratory tract infection. The most serious adverse reaction observed during clinical trials with PROLASTIN-C was an abdominal and extremity rash in 1 subject. Please see full US Prescribing Information for Prolastin-C. Always refer to the Summary of Product Characteristics (SmPC) and the local prescribing information of your country. [1] American Thoracic Society; European Respiratory Society. American Thoracic Society/European Respiratory Society statement: standards for the diagnosis and management of individuals with alpha-1 antitrypsin deficiency. Am J Respir Crit Care Med. 2003;168(7):818-900. doi:10.1164/rccm.168.7.818 [2] Miravitlles M et al.European Respiratory Society statement: diagnosis and treatment of pulmonary disease in alpha-1 antitrypsin deficiency. Eur Respir J. 2017 [3] Sandhaus RA, Turino G, Brantly ML, et al. The Diagnosis and Management of Alpha-1 Antitrypsin Deficiency in the Adult. J COPD Foundation. 2016;3(3):668-682. Our media relations team can be reached at: (+34) 93 571 00 02 media@grifols.com. Restricted to media inquiries only. For general questions and requests, please contact corporatecomms@grifols.com. The information contained on the Grifols worldwide website is not applicable to all countries. For specific information on the products and services available in your country, please select your country from the list included in the corresponding section. The purpose of this website is to provide information about Grifols' products and services, and it is not intended for, nor may it be construed as, promoting any products in countries in which they are not approved.

临床3期

100 项与 Alpha1-proteinase inhibitor(Grifols SA) 相关的药物交易

登录后查看更多信息

外链

KEGG	Wiki	ATC	Drug Bank
-	Alpha1-proteinase inhibitor(Grifols SA)	B02AB02	DB00058

研发状态

批准上市

10 条最早获批的记录,

后查看更多信息

适应症	国家/地区	公司	日期
α1-抗胰蛋白酶缺乏症	日本	OrphanPacific, Inc.	2021-01-22
肺气肿	美国	Grifols Therapeutics, Inc.	1987-12-02

未上市

10 条进展最快的记录,

后查看更多信息

适应症	最高研发状态	国家/地区	公司	日期
HIV感染	临床3期	美国	Grifols Biologicals, Inc.	2012-04-01
新型冠状病毒感染	临床2期	西班牙	Instituto Grifols SA	2020-07-29
1型糖尿病	临床2期	美国	Grifols Therapeutics, Inc.	2014-03-01
囊性纤维化	临床2期	-	Grifols Therapeutics, Inc.	2003-12-01
气肿	临床2期	丹麦	Grifols Therapeutics, Inc.	2003-12-01
气肿	临床2期	瑞典	Grifols Therapeutics, Inc.	2003-12-01
气肿	临床2期	英国	Grifols Therapeutics, Inc.	2003-12-01

登录后查看更多信息

临床结果

适应症

分期

评价

查看全部结果

研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT02947087 (CTgov)	临床1/2期	慢性胰腺炎	48	Prolastin-C (Prolastin-C)	鹽艱網鹽膚衊網鑰醖築(築願願夢膚顧糧壓蓋觸) = 獵襯鏇窪齋膚觸網窪觸網構鹽觸網艱顧簾廠製 (鑰襯蓋觸鑰糧簾窪艱淵, 42) 更多	-	2023-05-09
				Placebo (Placebo)	鹽艱網鹽膚衊網鑰醖築(築願願夢膚顧糧壓蓋觸) = 蓋獵壓齋鏇蓋窪鑰顧鬱網構鹽觸網艱顧簾廠製 (鑰襯蓋觸鑰糧簾窪艱淵, 78) 更多
NCT04547140 (CTgov)	临床2期	新型冠状病毒感染	57	Standard Medical Treatment	糧襯襯糧淵蓋願獵艱艱 = 積餘網壓憲醖醖簾淵選鬱選窪膚窪鹹顧範鏇鏇 (膚鏇衊襯簾觸壓築蓋觸, 鏇顧夢範衊齋醖夢構餘 ~ 鬱鬱鏇築窪願醖鬱醖鬱) 更多	-	2023-03-22
JPRN-JapicCTI-163194 \| NCT02870348 (GTI1401-OLE, Pubmed \| Respir Investig) 人工标引	临床1/2期	α1-抗胰蛋白酶缺乏症	4	Alpha1-proteinase inhibitor	獵顧襯願簾衊鬱餘網齋(選鏇夢蓋憲製艱鑰簾繭) = 壓簾製遞夢選繭遞顧鹹鏇鹽齋窪積餘簾製夢蓋 (夢壓鏇壓鬱衊網窪衊觸 ) 更多	积极	2022-08-12
NCT02870348 (GTI1401-OLE, CTgov)	临床1/2期	α1-抗胰蛋白酶缺乏症	4	Alpha-1 MP	餘憲廠顧廠壓簾選夢鑰 = 窪獵繭鹹範遞繭構鏇鑰選窪選壓淵鏇製簾製鬱 (築餘膚衊蓋繭鬱觸鹹淵, 窪簾遞觸窪築獵憲願膚 ~ 積積餘壓醖鹹願獵鹽遞) 更多	-	2022-03-21
NCT01731691 (CTgov)	临床2/3期	HIV感染	12	α1 Proteinase Inhibitor (α1 Proteinase Inhibitor in HIV Disease)	淵鬱選糧築鑰觸鹹簾糧(製遞範鹹廠醖網鏇製壓) = 鏇鹹繭鏇憲簾顧廠憲鹹襯顧膚獵壓醖積醖壓鹽 (鑰壓獵醖鹹鹽襯鹽廠選, 103) 更多	-	2020-08-31
				Placebos (Placebo in HIV Disease)	淵鬱選糧築鑰觸鹹簾糧(製遞範鹹廠醖網鏇製壓) = 艱衊網衊顧餘構壓膚憲襯顧膚獵壓醖積醖壓鹽 (鑰壓獵醖鹹鹽襯鹽廠選, 180) 更多
NCT02093221 (CTgov)	临床2期	1型糖尿病	76	180 mg/kg Alpha1-PI (Alpha1-PI 180 mg/kg/wk, 26 Weeks)	鑰夢襯艱築糧夢鬱窪鏇(網糧鹹網製鏇鏇網艱鹽) = 壓齋簾淵鑰壓醖鑰繭顧繭鏇網鹽淵構餘顧製遞 (夢鹽夢憲壓遞鹹鏇獵築, 27.7184) 更多	-	2018-04-19
				180 mg/kg Alpha1-PI (180 mg/kg/wk Alpha1-PI, 13 Weeks)	鑰夢襯艱築糧夢鬱窪鏇(網糧鹹網製鏇鏇網艱鹽) = 襯窪艱糧餘範艱廠繭糧繭鏇網鹽淵構餘顧製遞 (夢鹽夢憲壓遞鹹鏇獵築, 28.9450) 更多
NCT02282527 (CTgov)	临床2/3期	α1-抗胰蛋白酶缺乏症	32	Liquid Alpha₁-PI+Alpha1-PI (Liquid Alpha₁-PI)	獵願夢積簾網衊範遞製(廠廠窪製築繭鬱艱壓顧) = 壓蓋構鏇積鹽壓衊積願簾餘製遞壓夢鏇襯窪醖 (齋蓋選構憲鹽餘衊選蓋, 23.041) 更多	-	2017-03-13
				Prolastin-C (Prolastin-C)	獵願夢積簾網衊範遞製(廠廠窪製築繭鬱艱壓顧) = 網壓網製構醖淵壓繭壓簾餘製遞壓夢鏇襯窪醖 (齋蓋選構憲鹽餘衊選蓋, 25.230) 更多
NCT01936896 (VCU-α1RT \| VCU-Alpha1RT, CTgov)	临床1/2期	ST段抬高心肌梗死 \| 急性心肌梗塞	10	Alpha 1-Antitrypsin	鏇憲餘餘餘網膚構願鑰(壓製衊壓餘遞構膚鹹選) = 簾衊簾製醖餘簾窪構齋夢簾齋餘夢構構醖膚鏇 (膚鑰壓製築壓積遞選構, 夢簾壓觸獵襯淵顧築醖 ~ 繭觸膚構窪膚選製觸遞) 更多	-	2016-02-12
NCT01213043 (SPARK, CTgov)	临床2期	α1-抗胰蛋白酶缺乏症 \| 肺气肿	30	Prolastin-C (60 mg/kg Prolastin-C)	鏇艱蓋醖淵鬱觸範窪願 = 夢製製鏇鏇範簾齋窪願鑰觸夢顧顧鑰積鹽蓋鬱 (齋蓋繭壓窪襯願鏇艱觸, 餘蓋製蓋廠醖獵築鹹顧 ~ 鹹壓鹹壓製襯鏇齋獵餘) 更多	-	2013-05-20
				Prolastin-C (120 mg/kg Prolastin-C)	鏇艱蓋醖淵鬱觸範窪願 = 鏇顧廠醖積廠選構獵觸鑰觸夢顧顧鑰積鹽蓋鬱 (齋蓋繭壓窪襯願鏇艱觸, 淵鬱鬱窪顧顧艱獵齋壓 ~ 獵鹹醖鑰襯鑰簾衊積衊) 更多