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更新于：2026-08-10

Clopidogrel Bisulfate

硫酸氢氯吡格雷

更新于：2026-08-10

概要

基本信息

简介Clopidogrel Bisulfate 是一种商标为 Plavix® 的药物，在1997年于美国批准上市，由施贵宝研发。其作用机制是抑制P2Y12受体，从而减少血小板活化和聚集。这随后降低了血栓的风险及其潜在的致命后果。氯吡格雷适用于治疗心肌梗塞、中风、外周血管疾病、冠状动脉疾病和脑血管疾病。由于其作为抗血小板药物的作用，氯吡格雷被证明在预防血栓引起的严重并发症（如心脏病发作、中风甚至死亡）方面具有无可估量的价值。该药物在心血管事件的管理和预防方面显示出疗效，使其成为现代医学的基本药物。

药物类型

小分子化药

别名

clopidogrel、Clopidogrel Bisufate、Clopidogrel bisulfate (USP)

+ [33]

靶点

P2Y12 receptor

作用方式

拮抗剂

作用机制

P2Y12 receptor拮抗剂(嘌呤P2Y12受体拮抗剂)

治疗领域

神经系统疾病心血管疾病其他疾病

在研适应症

动脉粥样硬化缺血稳定型心绞痛+ [15]

非在研适应症

急性心肌梗塞慢性心力衰竭先天性心脏缺损+ [3]

原研机构

Bristol Myers Squibb Co.

在研机构

Taw Pharma (Ireland) Ltd.

Krka dd Novo Mesto

Biogaran SAS

+ [10]

非在研机构

Acino Pharma AGBristol-Myers Squibb Pharma EEIGArchie Samuel Sro

+ [10]

权益机构

Bristol Myers Squibb Co.

Ascendia Pharmaceuticals, Inc.Sanofi-Aventis Korea Co., Ltd.

+ [5]

最高研发阶段批准上市

首次获批日期

美国 (1997-11-17),

心肌梗塞脑卒中

最高研发阶段(中国)批准上市

特殊审评优先审评 (中国)

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结构/序列

分子式C16H18ClNO6S2

InChIKeyFDEODCTUSIWGLK-RSAXXLAASA-N

CAS号120202-66-6

关联

758

项与硫酸氢氯吡格雷相关的临床试验

NCT07720934

/ Not yet recruitingN/AIIT

A Pilot Study to Investigate Platelet Reactivity in Patients With Elevated Lipoprotein(a) and Its Response to Antiplatelet Therapy Randomised, Open-Label, Mechanistic Pilot Study With A Crossover Design

The Lp(a)-PLAT Study is designed to close a critical evidence gap in cardiovascular prevention for the roughly 20% of the population who carry genetically determined elevations in lipoprotein(a) - a recognised pro-thrombotic and pro-atherosclerotic risk factor. Its objective is to delineate the pro-thrombotic platelet phenotype driven by high Lp(a) levels and to evaluate, through pharmacodynamic comparison, how two standard-of-care antiplatelet strategies - clopidogrel, a P2Y12 ADP-receptor inhibitor, and aspirin, a COX-1 inhibitor - differ in their capacity to attenuate this platelet hyperreactivity.
This study will provide the first head-to-head mechanistic comparison of clopidogrel versus aspirin on platelet reactivity in patients with elevated plasma levels of Lp(a).

开始日期2026-11-01

申办/合作机构

Les Hôpitaux Universitaires de Genève

[+1]

NCT07744191

/ Not yet recruiting临床4期IIT

A Randomized, Double-blind, Placebo-controlled Crossover Trial of Antiplatelet Therapies in Psoriasis

The purpose of this study is to determine the effect of antiplatelet therapy on the endovascular phenotype in psoriasis, specifically whether clopidogrel reduces vascular endothelial pro-atherosclerotic transcript expression more than aspirin or placebo. The primary endpoint is mean change in a composite endothelial pro-inflammatory/pro-atherosclerotic transcript expression signature measured from brachial vein endothelial cells.

开始日期2026-09-01

申办/合作机构

NYU Langone Health

[+1]

NCT07604298

/ Not yet recruitingN/AIIT

Efficacy and Safety of Indobufen, Aspirin, Cilostazol, and Clopidogrel in the Treatment of Ischemic Stroke: a Single-center, Retrospective Study

Through a single-center retrospective cohort study of acute ischemic stroke (AIS) patients receiving secondary prevention with indobufen, clopidogrel, cilostazol, or aspirin as monotherapy or dual therapy, we aim to compare the real-world effectiveness and safety of these four antiplatelet regimens. Through closely tracking the recurrence of stroke (including ischemic and hemorrhagic stroke) and bleeding events (GUSTO-defined) within one year of treatment, we evaluate the association between each antiplatelet agent and the risk of stroke recurrence, thereby providing critical evidence to guide individualized antiplatelet therapy in AIS patients.

开始日期2026-07-01

申办/合作机构

南方医科大学南方医院

100 项与硫酸氢氯吡格雷相关的临床结果

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100 项与硫酸氢氯吡格雷相关的转化医学

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100 项与硫酸氢氯吡格雷相关的专利（医药）

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8,266

项与硫酸氢氯吡格雷相关的文献（医药）

2026-07-01·AMERICAN HEART JOURNAL

Design and rationale of the clinical trial to obtain the highest efficacy of dual antiplatelet therapy after carotid artery stenting in high bleeding risk patients (CHET): A multicenter, randomized, open-label, superiority trial

Article

作者: Park, Moo-Seok ; Baek, Jang-Hyun ; Kim, Yong-Won ; Park, Hee-Kwon ; Kim, Bum Joon ; Kim, Joong-Goo ; Song, Tae-Jin ; Lee, Seok-Yoon ; Lee, Seung-Jae ; Lee, Jun ; Lee, Seong-Joon ; Kim, Hyung Jun ; Jeong, Darda ; Yoo, Joonsang ; Kang, Hyun Goo ; Cho, Han-Jin ; Joon An, Sang ; Choi, Kang-Ho ; Woo, Ho Geol ; Kim, Young-Dae ; Eun, Mi-Yeon ; Seo, Woo-Keun ; Jung, Jin-Man ; Seo, Jung-Hwa ; Bang, Oh Young ; Shin, Dong-Woo ; Kim, Jun Yup ; Park, Hyungjong

RATIONALE:

Abbreviated dual antiplatelet therapy (DAPT) strategies effective in percutaneous coronary intervention among patients with high bleeding risk (HBR) may not be applicable to carotid artery stenting (CAS) owing to anatomical and procedural differences.

PRIMARY HYPOTHESIS:

Among patients with HBR undergoing CAS, abbreviated DAPT followed by SAPT will reduce clinically significant bleeding compared to prolonged DAPT, while maintaining noninferiority in net clinical outcomes, including ischemic and major bleeding events.

DESIGN:

CHET trial is a multicenter, randomized, open-label, superiority trial in HBR patients undergoing CAS. Assuming a 38% relative reduction in bleeding (10.4%-6.45%), 1,524 participants (762 per group) provide 80% power with a two-sided alpha of 0.05; the final target is 1,556 (778 per group), allowing 2% dropout. Key HBR criteria include age ≥75 years, ischemic stroke within 6 months, renal insufficiency, anemia, and thrombocytopenia. All patients will receive aspirin and clopidogrel for 30 days after CAS (enrichment period). Event-free patients on day 30 were randomized 1:1 to receive SAPT (aspirin 100 mg daily or clopidogrel 75 mg daily, at the treating physician's discretion) or continued DAPT for 11 months. The primary safety endpoint is clinically significant bleeding (BARC 2, 3, or 5) from day 30 to 12 months post-CAS. The secondary efficacy endpoint is a composite of nonfatal stroke, nonfatal myocardial infarction, cardiovascular death, and major bleeding (BARC 3 or 5).

ENROLLMENT DATES AND CURRENT STATUS:

CHET began enrollment on July 15, 2024. As of February 5, 2026, the trial is currently enrolling, with 328 participants enrolled. Enrollment is expected to be completed by November 2029, and follow-up by December 2030.

CONCLUSIONS:

CHET trial is the first randomized controlled trial to define optimal DAPT duration in HBR patients after CAS.

TRIAL REGISTRATION:

www.

CLINICALTRIALS:

gov (NCT06276374).

2026-06-01·Therapeutic Advances in Neurological Disorders

Residual early neurological deterioration following dual antiplatelet in stroke: post hoc analysis of the ATAMIS trial

Article

作者: Kong, Xiang-Ru ; Chen, Hui-Sheng ; Zhang, Jing ; Cui, Yu

Background::

A clinically significant proportion of patients experience early neurological deterioration (END) despite receiving dual antiplatelet therapy (DAPT) for acute ischemic stroke. It is crucial to identify this specific population for risk stratification and targeted intervention.

Objectives::

To identify predictors for END after DAPT in acute ischemic stroke.

Design::

We performed a post hoc analysis of the antiplatelet therapy in acute mild to moderate ischemic stroke (ATAMIS) trial.

Methods::

Patients who received DAPT (clopidogrel plus aspirin) in the ATAMIS trial were included, and classified into END and Non-END groups according to whether they experienced END. END was defined as an increase of ⩾2 points within 7 days from baseline on the National Institutes of Health Stroke Scale (NIHSS). Independent predictors were identified using multivariable logistic regression.

Results::

Of the 1,122 patients with acute mild-to-moderate ischemic stroke treated with DAPT, 66 (5.9%) developed END within 7 days. Multivariable analysis identified three independent factors associated with increased END risk: a shorter time from symptom onset to antiplatelet initiation (adjusted odds ratio [aOR] per hour, 0.97; 95% CI, 0.95–0.99; p = 0.01), higher admission systolic blood pressure (aOR per mmHg, 1.01; 95% CI, 1.00–1.02; p = 0.047), and a stroke etiology of either small artery occlusion (aOR, 2.24; 95% CI, 1.29–3.89; p = 0.004) or cardioembolism (aOR, 28.36; 95% CI, 1.23–654.11; p = 0.04).

Conclusion::

Among patients with mild-to-moderate ischemic stroke receiving DAPT, key predictors of END include very early presentation, elevated systolic blood pressure at admission, and a nonlarge artery atherosclerosis etiology (small artery occlusion or cardioembolism). These findings highlight subgroups that may require intensified monitoring or adjunctive therapeutic strategies beyond standard DAPT.

Trial registration::

ClinicalTrials.gov Identifier: NCT02869009.

2026-04-01·STROKE

Lp-PLA2 Activity and Genotype-Guided Dual Antiplatelet Therapy in Minor Stroke or Transient Ischemic Attack

Article

作者: Jin, Aoming ; Wang, Yubo ; Zhao, Xingquan ; Wang, Yongjun ; Li, Zixiao ; Zhou, Hongyu ; Xie, Xuewei ; Li, Shangzhi ; Meng, Xia ; Jing, Jing ; Jiang, Yong ; Li, Hao ; Wang, Yilong ; Lin, Jinxi ; Zhang, Ling

BACKGROUND::

Lp-PLA2 (lipoprotein-associated phospholipase A2) is a sensitive biomarker of vascular inflammation and atherosclerosis. This study evaluated the influence of Lp-PLA2 activity on the efficacy and safety of ticagrelor-aspirin versus clopidogrel-aspirin among patients with minor stroke or transient ischemic attack carrying CYP2C19 loss-of-function alleles.

METHODS::

The CHANCE-2 trial (Clopidogrel in High-Risk Patients With Acute Nondisabling Cerebrovascular Events-II) randomized 6412 patients with minor stroke or transient ischemic attack carrying CYP2C19 loss-of-function alleles to receive ticagrelor-aspirin or clopidogrel-aspirin. This subgroup study included patients with available baseline Lp-PLA2 activity measurements, stratified by the median value of 188.4 nmol/min per milliliter. The primary efficacy and safety outcomes were stroke recurrence and severe or moderate bleeding events within 90 days. Associations between treatment and outcomes were assessed using multivariable Cox proportional hazards models, adjusting for a history of hyperlipidemia.

RESULTS::

A total of 5919 patients were included (mean age, 64.4 years; 33.9% female). Among patients with low Lp-PLA2 activity, ticagrelor-aspirin reduced the 90-day risk of recurrent stroke compared with clopidogrel-aspirin (5.4% versus 7.4%; adjusted hazard ratio, 0.72 [95% CI, 0.54–0.97]). In patients with high Lp-PLA2 activity, no significant difference was observed (6.9% versus 8.2%; adjusted hazard ratio, 0.84 [95% CI, 0.65–1.09]). The P value was 0.45 for the treatment × Lp-PLA2 activity interaction effect on stroke recurrence. The risk of bleeding associated with ticagrelor–aspirin did not differ across Lp-PLA2 activity levels.

CONCLUSIONS::

In patients with minor stroke or transient ischemic attack carrying CYP2C19 loss-of-function alleles, elevated Lp-PLA2 activity did not significantly modify the efficacy or safety of dual antiplatelet therapy. Further research is needed to clarify the potential role of Lp-PLA2 in guiding individualized treatment decisions.

REGISTRATION::

URL: https://www.clinicaltrials.gov ; Unique identifier: NCT04078737.

581

项与硫酸氢氯吡格雷相关的新闻（医药）

2026-08-05

·海魂酒酿

集采落标后，谁在院外找到了第二增长曲线

关于集采的讨论，很容易滑向一个圈外人的焦虑：原研药是不是要消失了？每隔几个月，社交媒体上就会出现一波"进口药买不到了"的讨论。患者在医院药房找不到熟悉的蓝色包装，转而在社交平台发帖询问。焦虑沿着信息流扩散，最终汇成一个判断——集采正在"杀死"原研药。但这不是最根本的问题。更深层的问题是：同样是集采落标，为什么有的原研药从此沉沦，有的却在院外活得更好？真正决定一种药物命运的，也许不是是否中标，而是企业是否具备渠道重构和品牌信任的能力。也就是说，集采落标不是原研药的终点，而已经变成其生命周期的分水岭。一、被误读的"原研药退潮" 在讨论落标原研药之前，需要先清理几个常见的认知噪音。第一个误读："集采导致原研药断供"。国家医保局在2025年1月的公开函件中明确表示，集采协议量一般在医疗机构报量的60%-80%，剩余部分由医疗机构自主选择拟采购品牌，无一刀切不允许采购使用进口原研药的制度安排。换言之，落标不等于禁售，医院仍可采购，只是采购的额度降低了。第二个误读："进口药集体撤退"。 2024年10月，国家药监局注销80个药品注册证书，引发"进口药退市潮"的说法。但据中欧国际工商学院的研究分析，其中大多数是已在海外退市的老药、面临激烈竞争的仿制药，或因疗效不佳而被淘汰的"鸡肋"产品。真正因无可替代而令患者陷入困境的药物微乎其微。这更像一场正常的市场自然选择或者企业的主动战略，而非原研药的集体败退。第三个误读："落标就等于死"。截至第十一批国采，集采已覆盖487个品种。在历次集采中，外资原研药的中标率一直偏低，第四批集采中诺华、勃林格殷格翰各5个品种、辉瑞和阿斯利康各3个品种均未中标。但多数落标产品并未消失，而是转向了不同的渠道。排除这些噪音后，真正值得追问的是：为什么有些落标原研药活了下来，活下来之后活的怎么样？二、分水岭：三种命运，三种逻辑代表药物企业集采表现院外表现当前状态立普妥（阿托伐他汀）辉瑞落标零售渠道销量保留率升至280% 院外市场龙头波立维（氯吡格雷）赛诺菲先落标后中标院内份额崩塌，销售额下滑50%+ 边缘化沐舒坦（氨溴索）勃林格殷格翰未中标暂停在华销售 2025年底重返，聚焦OTC 波立达（阿利西尤单抗）赛诺菲非集采品种受国产PCSK9替代冲击退出中国市场这四种命运背后，藏着同一条底层逻辑：落标原研药的去留，取决于三个变量的乘积——品牌信任的厚度、渠道迁移的能力、患者自费的意愿。任何一个变量为零，药物的院外生命就难以延续。三、机制拆解：品牌信任、渠道迁移与患者自费为什么立普妥能在院外翻盘？立普妥是全球销量最高的降脂药之一，2011年专利到期，但在中国市场凭借品牌效应维持着远超欧美的价格。2018年其在华销售额仍高达约100亿元，超过辉瑞中国销售额的三分之一。首轮"4+7"集采中，立普妥落标。根据法伯科技统计，集采执行当年，立普妥在城市医院渠道的销量保留率下降至43%，随后随着市场自然增长回升至近50%。真正的故事发生在院外。立普妥在零售药店渠道的表现可以用"逆势翻盘"来形容。集采执行当年，其零售渠道销量保留率不降反升至180%，后续进一步升至280%以上。虽然价格略有下降，但销售额保留率升至约200%，基本弥补了院内渠道的销量下降。据《E药经理人》此前报道，立普妥落标后，辉瑞心血管团队人数不降反增，扩岗约2000人，主要推广方向是下沉到民营医院和乡镇市场。2019年第一季度，辉瑞普强在新兴市场业务增长25%，核心驱动力正是立普妥、络活喜等过专利期原研药在中国的销量增长。辉瑞甚至将专注于成熟药品的普强全球总部落地上海，姿态非常明确——在中国做深成熟药。为什么波立维的"背水一战"失败？波立维是赛诺菲的拳头产品，全球巅峰年销售额超过100亿美元。2012年专利到期后，赛诺菲并未主动调价，延续高价策略，到2018年仍占据中国氯吡格雷市场近60%的份额。首轮"4+7"集采中，赛诺菲不敌信立泰，未能中标。为挽回失地，赛诺菲在2019年全国扩面集采中选择"背水一战"，以2.54元/片的价格中标，较首轮中标价再降约20%。但"以价换量"未能扭转颓势。赛诺菲2019年第四季度中国市场销售额同比下滑21%，此后财报电话会议中，赛诺菲预计波立维2020年在华销售额将进一步下滑约50%。波立维的失败揭示了一个关键机制：降价不是万能药。当原研药大幅降价后，支撑其高价时代的营销和学术推广费用被削减，品牌护城河随之变薄。与立普妥不同，波立维落标后选择了降价中标而非坚守院外，结果两端失守——院内价格被压低，院外品牌溢价也被削弱。为什么沐舒坦能"走了又回"？沐舒坦（盐酸氨溴索）是祛痰药领域的经典原研品牌。2024年第一季度，因注册证到期叠加集采未中标影响，勃林格殷格翰暂停了沐舒坦在华销售。但不到两年，沐舒坦预计将于2025年12月重返中国市场。其重返后的策略预计绕开院内渠道，聚焦于院外OTC渠道。沐舒坦的"走了又回"说明：对于患者自费意愿强的OTC品类，品牌信任可以穿越政策周期。患者对"沐舒坦"三个字的信任，不会因为药品短暂退出公立医院而消失。只要品类属性适合自费购买，院外OTC就是一个可行的着陆点。为什么波立达连"退"的机会都没有？波立达（阿利西尤单抗）是PCSK9抑制剂，2019年在中国获批，2021年通过医保谈判进入国家医保目录。它的退场不是因为集采，而是因为同类竞品和国产替代的崛起——诺华的Inclisiran每年仅需注射两次，患者依从性更高；信达生物的托莱西单抗已进入医保；恒瑞的瑞卡西单抗实现每12周给药一次。 2025年，赛诺菲正式宣布波立达停止在中国市场推广并逐步退出。同一时期，赛诺菲中国区收入同比仅微增0.1%，远低于其他主要市场。波立达的案例揭示第四个机制：当治疗领域出现真正的临床替代品时，品牌信任不足以续命。与化学药不同，生物制剂领域的患者品牌忠诚度显著更低。一旦国产类似药在疗效和便捷性上追平甚至超越，原研药的品牌溢价就会瓦解。四、方法论：落标原研药的四步生存框架归纳以上案例，可以提炼出一套可操作的判断框架：第一步：判断品类属性——你的药适不适合做院外不是所有落标原研药都能走院外路线。关键判断标准有三个： · 自费意愿强度：慢病用药（如降脂药、降压药）存在一批坚持选择原研药的患者，愿意自费换取品牌保障；而急救用药、住院用药难以在院外承接。 · 品牌认知厚度：立普妥在中国市场经营了20余年，患者认知极深。如果品牌认知薄弱，院外渠道迁移的阻力会大幅增加。 · 处方延续性：慢病用药处方稳定，患者可以带着处方去药店买药；而需要院内配制或注射的药品，院外承接难度极高。第二步：选择渠道策略——保价还是换量落标后只有两条路：要么保价转院外，要么降价争院内。立普妥选择保价转院外——维持价格体系，凭借品牌信任在零售药店承接自费需求。结果是零售渠道销量保留率升至280%以上，基本弥补了院内损失。波立维选择降价争院内——以2.54元/片的价格中标扩面集采。结果是院内份额没有守住，院外品牌溢价也被削弱，销售额下滑超过50%。一位曾在跨国药企工作的人士的分析可以作为参照：“在化学药领域，尤其是慢病用药和肿瘤药，仍存在一批坚持选择原研药的患者群体，愿意自费支付以换取品牌保障。” “相反，在生物类似药领域，一旦技术达标、质量相当，医生和患者对品牌的依赖度显著降低，国产替代的接受度更高。” 第三步：重建渠道能力——团队重构与终端渗透选择院外路线后，企业需要的不是裁人，而是换人。辉瑞在立普妥落标后扩岗2000人，方向是下沉民营医院和乡镇。赛诺菲早在2011年就成立基层医疗事业部，到2018年团队扩至1100人，覆盖全国1600多个县。院外渠道能力的核心不是"卖货"，而是"承接处方"。根据米内网2025年数据，立普妥在零售药店的店均销售金额为7677.1元，同比增长5.13%。但动销铺货率连续多年下降，2025年为56.82%——说明虽然单店产出在增长，但铺货覆盖面在收窄。这是一个信号：院外市场不是自然增长的，需要主动投入渠道建设。第四步：守住品牌信任的底线——质量一致性争议中的差异化集采制度的核心逻辑是通过仿制药一致性评价替代原研药。但"生物等效"不等于"制剂等质"。中欧国际工商学院的研究指出，药品并非仅由有效成分构成，其中80%甚至更多是辅料。辅料的差异会直接影响有效成分在体内的溶解和释放速度，导致临床中患者感到"药劲不足"或"药效不稳定"。同时，压片、包衣等制剂工艺需长期技术积累，制剂工艺精密度不足也可能导致药物在特定患者群体中的疗效稳定性不如原研药。这不是说国产仿制药不好——中国一些领先药企的仿制药质量已接近甚至超越原研药。但这恰恰为落标原研药提供了品牌差异化的空间：在一致性评价解决了"等效"问题但尚未完全解决"等质"问题的阶段，原研药可以通过学术教育、患者服务和真实世界数据，巩固品牌信任。五、从"落标"到"退场"：跨国药企的系统性战略调整把视角从单个药物放大到企业层面，会发现集采落标只是跨国药企在华战略重塑的一个触发点。在战略定位上，中国已从靠专利过期药套利的单纯销售市场，升级为全球创新源头和合作伙伴。具体而言，跨国药企的调整分为三层：第一层是"断舍离"——处置非核心成熟管线。部分跨国药企选择退出集采和公立医院市场，将产品出售或授权给本土药企。例如，罗氏将美罗华的市场推广权授予百洋医药子公司，拜耳将瑞戈非尼片和索拉非尼片的国内推广权交给亿帆医药。赛诺菲在波立达退场的同时，通过收购箕星药业和维亚臻的在研产品，加速布局RNAi等前沿管线。第二层是"深耕本土"——研发与生产本土化。 2024年，礼来、辉瑞、拜耳等8家国际药企在北京新设研发或创新中心。阿斯利康在北京建立第六个全球研发中心，其在华三大生产基地已实现向全球70多个市场供应创新药物。赛诺菲宣布投资10亿欧元在北京新建胰岛素生产基地。诺华在浙江海盐建立首个外资核药生产基地。第三层是"创新同步"——从执行者转向策源者。 2019年，罗氏将上海研发中心升级为中国创新中心，授予其从靶点筛选到临床试验设计的独立决策权。阿斯利康中国研发管线与全球的同步率已达100%。诺华自2022年以来所有新药及新适应症开发也100%实现全球同步。这三层调整指向一个结论：集采落标对跨国药企而言，与其说是打击，不如说是一记闹钟。它提醒企业，依靠过专利期原研药在中国市场维持高利润的时代已经结束，未来只有创新药才有溢价空间。六、对本土企业的启示：原研药退出的空白，谁来填补集采为本土仿制药企业创造了巨大的市场空间，但机会背后也有陷阱。集采节省的医保资金主要用于两个战略领域：一是支付创新药，二是提高医疗服务价格。集采的目的是"腾笼换鸟"，而非强迫高价原研药退出市场。本土企业需要清醒认识到三点：第一，仿制药替代不等于品牌替代。集采给了仿制药进入公立医院的入场券，但品牌信任需要长期积累。在院外市场，患者对原研药的品牌偏好仍然存在，尤其是慢病用药领域。本土企业不能只靠低价抢占院内份额，还需要在院外市场建立自己的品牌认知。第二，"一致性评价"不等于"一次性评价"。国家药监部门已对集采中选产品实行生产企业检查和中选品种抽查100%全覆盖。但市场信任的建立需要时间，一旦出现质量下降的案例，损害的是整个国产仿制药的声誉。第三，创新才是终极出路。中国药品批文中约95%属于仿制药，而美国创新药占据绝对市场份额，销售额占整个市场超过70%。集采正在倒逼中国医药产业从"大而不强、多而不精"的结构性缺陷中转型。那些真正专注于产品质量、效率、成本和合规的企业，以及在创新药领域持续投入的企业，将在这一轮洗牌中胜出。七、回到主命题：落标不是终局，分水岭才是集采落标原研药何去何从？答案不是"消失"，也不是"投降"，而是分道扬镳。品牌信任足够厚、渠道迁移能力足够强的药物，在院外找到了第二增长曲线。立普妥在零售药店的销量保留率从100%升至280%以上，证明了品牌信任穿越政策周期的力量。品牌信任不足、或选择了错误策略的药物，在降价和替代的双重夹击下走向边缘。波立维的"背水一战"以销售额腰斩收场，证明了降价不是万能药。品类属性不适合院外承接的药物，最终退出中国市场。波立达在国产PCSK9抑制剂的围堵下黯然退场，证明了当临床替代品真正出现时，品牌溢价无法续命。但"退"也可以是为了更好的"进"。沐舒坦暂停一年后重返OTC市场，跨国药企在处置成熟管线后加速引入创新药物——2024年中国创新药海外授权交易数量约百起，总交易金额约500亿美元。集采落标不是原研药的终点，而是其生命周期的分水岭。真正决定一种药物命运的，不是招标结果上的一个"未中选"，而是企业是否具备在渠道重构、品牌信任和患者服务上做出系统性投入的能力。对跨国药企而言，过专利期原研药在中国维持高利润的时代已经结束。但这不意味着退场，而是意味着角色的转换——从产品独占者，变为全球创新的共创者。对中国本土企业而言，原研药退出留下的空白既是机会也是考验。低价抢占份额只是第一步，建立真正的品牌信任和创新管线，才是穿越周期的关键。最终，一切回归一个朴素的判断：药品的生命力，不取决于政策给了多少保护，而取决于它在患者心中有多少不可替代的价值。参考资料 1. 国家医保局，《关于请协助做好当面听取集采药品相关意见的函》，2025年1月 2. 法伯科技，立普妥集采后城市医院及零售渠道保留率统计数据 3. 米内网，《从"集采失地"到药店增长引擎：立普妥院外市场消费全景分析》，2026年3月 4. 中欧国际工商学院周东生、阮丽旸，《集采之下，原研药"退场"背后》，2024年 5. 深蓝观/医药魔方ByDrug，《原研药"走了又回"，归来还是王者吗？》，2025年 6. 《E药经理人》，《4+7后的跨国药企转轨：官司、谈判与消失的高溢价》，2019年 7. 动脉新医药，《跨国药企洞察｜从波立维降价到波立达退市，"赛诺菲"们如何转身？》，2025年8月 8. 安永，《中国医药改革背景下，跨国药企的战略应对》研究报告觉得有启发，欢迎转发给需要的朋友。往期推荐东南亚国家的医疗真相：和中国的差距，比你想的大得多手把手搭建院外C端推广体系｜澄清院外：院外不是一件事，而是三件事医药人必备的10个底层思维模型：升级你的决策工具箱你怎么看？评论区聊聊。

2026-08-05

·BioSpace

New 23andMe Research Institute Study First to Identify Association Between Specific Side Effects from Common Antidepressants and Genetics

Study with more than 100,000 consented participants shows CYP2C19 genetic variation is associated with an individual’s risk of side effects and their continued use of serotonin reuptake inhibitors (SSRIs) PALO ALTO, Calif., Aug. 05, 2026 (GLOBE NEWSWIRE) -- 23andMe Research Institute, a nonprofit research organization dedicated to advancing science for the public good, announced the publication of a study demonstrating the impact of genetic variation on risk of specific side effects related to the use of three common selective serotonin reuptake inhibitors (SSRIs) antidepressants, escitalopram (Lexapro®), citalopram (Celexa®), and sertraline (Zoloft®). The CYP2C19 gene was already known to be involved in the processing of these drugs. This large-scale study is the first to link genetic variation in CYP2C19 to a person's risk of specific SSRI side effects such as sexual dysfunction and trouble sleeping. Published today in The Pharmacogenomics Journal , the study investigates the genetic basis of variability in side effects with common SSRI antidepressants. Researchers at the 23andMe Research Institute examined data from more than 114,000 individuals who have used this class of antidepressants and responded to a survey about the effectiveness of the medication(s) and what side effects they experienced. They looked for differences in effectiveness, side effects and reasons for discontinuation when relevant based on the individual’s CYP2C19 genetic variants (i.e. metabolizer status). The findings provide evidence that variation in the CYP2C19 gene is associated with variations in response to SSRI therapies. Specifically, the study included the following key findings: Participants whose CYP2C19 variant results in slower metabolism of SSRIs have significantly increased risk of very specific side effects like tremors, sleep issues and sexual dysfunction. Slower CYP2C19 metabolizers were more likely to discontinue their SSRI medication due to side effects. The study gives researchers a rare, clear picture of how common different side effects are in a large, diverse group of people. Participants reported a range of effects, including anxiety, sleep problems, emotional numbness, sexual problems, gastrointestinal issues, tremors and weight gain, and researchers were able to see how common these side effects were broken down by which drug people were taking as well as their sex and ancestry. Finding the right antidepressant is often a long, frustrating process. Fewer than half of people respond to the first SSRI they try. Within a year of starting treatment, roughly 80% of patients switch medications or stop taking them altogether . And side effects are the most common reason why people switch or stop. ezstandalone.cmd.push(function () { ezstandalone.showAds(131); }); Study participants were sorted into categories of metabolizer types, ranging from poor (slowest) to ultrarapid (fastest) based on which genetic variants they had. For individuals with the version of the CYP2C19 enzyme that works more slowly, the drug lingers in their system at higher concentrations, which raises the likelihood of side effects. Slower metabolizers reported side effects more often than faster metabolizers. But this study was large enough to look at specific side effects and not just side effects as a general category. Among participants taking escitalopram, slower metabolizers were significantly more likely to suffer from sleep and sexual problems compared to faster metabolizers. Similarly, among those taking sertraline, more slower metabolizers reported experiencing tremors than did faster metabolizers. These side effects contributed to slow metabolizers quitting their medication altogether due to side effects (depending on which drug they took, between 25.7% and 29.7% of poor metabolizers stopped compared with 20.2% to 21.6% of ultrarapid metabolizers). Finally, the study highlights why diversity in genetic research matters. Genetic ancestry impacts how common these variants are in a given population. Roughly 17.8% of East Asian-ancestry participants were poor metabolizers, compared with about 2.3% of European-ancestry participants. “Because 23andMe has such a massive community of people choosing to participate in research, we were able to pair genetic data with real, personal experiences on these medications,” noted Dr. Ryanne Wu, M.D., one of the lead authors of the paper and director of genomic medicine at the 23andMe Research Institute. “Earlier studies were too small to spot these patterns and other large genetic databases are only just starting to collect this kind of medication history, which has slowed down progress in the past. This study shows exactly what can happen when millions of people come together to further advance medical science.” For those who are considering an SSRI, or those who have struggled with SSRI side effects in the past, genetics may offer important insights. 23andMe Premium Ancestry + Health members can view their CYP2C19 Drug Metabolism report* and talk with a healthcare professional about how their status may affect their response to certain medications including SSRIs. Giving them one more data point to help find a treatment that fits. About 23andMe Research Institute 23andMe Research Institute is a new nonprofit 501(c)(3) research organization that enables people everywhere to access their genetic information, learn about themselves, and participate in large-scale research for public good. The Institute unites people with the common goal of improving health and deepening our understanding of DNA, the code of life. Media Contact: Aushawna Collins 23andMe Research Institute aushawnac@23andme.com *23andMe PGS Pharmacogenetic reports: The 23andMe test uses qualitative genotyping to detect 3 variants in the CYP2C19 gene in the genomic DNA of adults from saliva for the purpose of reporting and interpreting information about the processing of certain therapeutics to inform discussions with a healthcare professional. It does not describe if a person will or will not respond to a particular therapeutic and does not describe the association between detected variants and any specific therapeutic. Our CYP2C19 Pharmacogenetic report provides certain information about variants associated with metabolism of some therapeutics and provides interpretive drug information regarding the potential effect of citalopram and clopidogrel therapy. Certain CYP2C19 results should be confirmed by an independent genetic test prescribed by your own healthcare provider before taking any medical action. Warning: Test information should not be used to start, stop, or change any course of treatment and does not test for all possible variants that may affect metabolism or protein function. The PGS test is not a substitute for visits to a healthcare professional. Making changes to your current regimen can lead to harmful side effects or reduced intended benefits of your medication, therefore consult with your healthcare professional before taking any medical action. For important information and limitations regarding Pharmacogenetic reports, visit .

临床结果

2026-08-02

·普朗克网络科技

从恒瑞新药获批说起：依达拉奉、自由基与氢分子的二十年科学之路

前两天看到一条行业新闻：恒瑞医药旗下子公司北京盛迪的HRS-8829注射液拿到了国家药监局的临床试验批件，准备做Ib期试验，适应症是急性缺血性卒中，要和依达拉奉联合用药。恒瑞在这款药上已经投了1660万研发费用。这条消息在医药圈不算大新闻，但我读完停了几秒。因为它从一个很有意思的角度，给氢分子医学这十几年的研究做了一个注脚。依达拉奉是干什么的？依达拉奉这个药，对普通人来说可能有点陌生，但在神经内科，它是写进指南的老药。 2001年在日本上市，2003年进入中国，目前是治疗急性缺血性脑卒中——也就是脑梗——为数不多被公认有效的神经保护剂之一。它的核心机制就四个字：清除自由基。脑梗发生时，脑血管堵了，脑细胞缺血缺氧。但这阶段真正致命的，不只是“缺血”本身。更棘手的是，当血管再通、氧气重新灌进来时，会爆发式产生大量自由基——尤其是羟自由基，活性极强，会无差别攻击细胞膜、蛋白质和DNA，造成所谓的缺血再灌注损伤。很多脑梗患者即使溶了栓、通了血管，神经功能依然恢复不好，缺血再灌注损伤是重要原因之一。临床研究也证实，在急诊救治急性缺血性脑卒中时，依达拉奉联合抗血小板药物能显著提高治疗有效率、促进神经功能恢复。依达拉奉的作用，就是在这一阶段清除多余的自由基，给脑细胞争取生存窗口。它的药理机制就是抗氧化、清除自由基、抑制脂质过氧化，从而抑制脑细胞、血管内皮细胞和神经细胞的氧化损伤。临床上，依达拉奉已经过了二十多年的验证。而恒瑞这次做的HRS-8829是要和依达拉奉联用——换句话说，国内头部药企不仅认可“清除自由基保护神经”这个方向，还在加码布局。氢气与依达拉奉的“同一条路” 那这和氢分子有什么关系？关系就在机制上。 2007年，日本医科大学太田成男教授团队在《Nature Medicine》上发表了一篇奠基性论文。他们发现：吸入2%浓度的氢气，能选择性清除羟自由基——恰恰是依达拉奉也在对付的那种危害性最强的自由基。实验显示，氢气能显著减少大鼠脑梗死面积，且不影响那些对身体有用的信号自由基——比如超氧阴离子、过氧化氢，它们在免疫和信号传导中有正常生理功能。这正是传统自由基清除剂的短板。依达拉奉也好，维生素C、维生素E也好，它们多多少少存在一个问题：选择性不够强。用打比方的话，它们是“广谱扫射”，好坏一起清。而氢分子因为小——只有0.289纳米，是自然界最小的分子——能轻松穿过血脑屏障、钻进线粒体，并且化学性质温和。它只跟活性最强的羟自由基和过氧亚硝基阴离子反应，生成水直接排出体外，不碰那些有正常生理功能的自由基。这在理论上，是非常理想的抗氧化策略。氢气对脑损伤的保护：从基础研究到临床探索 2007年之后，氢气在神经系统保护方面的研究快速积累。一篇2024年发表于《International Journal of Molecular Sciences》的综述明确指出：分子氢具有选择性抗氧化、抗炎、细胞保护和信号调节等特性，在脑卒中等缺血再灌注损伤模型中显示出保护效果，作用机制包括抑制氧化应激和炎症、增强ATP生成、减少钙超载、调控细胞死亡等。另一篇2025年发表于《Current Neurovascular Research》的综述则系统总结了氢气在脑损伤中的神经保护作用，包括缺血性脑卒中、创伤性脑损伤、缺氧缺血性脑病、脑出血等。文章特别强调氢气对线粒体质量控制网络的调控能力——包括抗氧化膜保护、线粒体自噬调控、线粒体动力学重塑和代谢重编程，从而改善神经元存活和功能恢复。 2023年的一项临床研究显示，在胶质瘤术后脑水肿患者中，吸入氢气的患者术后脑水肿消退速度显著快于对照组。这项单中心随机对照试验为氢气的临床神经保护作用提供了直接证据。在新生儿缺氧缺血性脑病（HIE）领域，波士顿儿童医院正在开展一项氢气辅助低温治疗的临床试验，计划给患儿吸入2%氢气、持续72小时，评估其安全性和可行性，预计2028年完成。 2025年12月，一篇发表于《Oxygen》的综述甚至探讨了氢氧混合气在癌症治疗中的潜力，指出氢气可通过调控MAPK通路、抑制PI3K/Akt磷酸化级联等方式诱导肿瘤细胞凋亡。 2026年初发表于《European Journal of Pharmacology》的一篇综述则系统阐述了氢气在脓毒症相关脑病中的神经保护机制：氢气通过清除活性氧、抑制星形胶质细胞和小胶质细胞活化、维持血脑屏障完整性、恢复线粒体功能等多重途径发挥保护作用，且耐受性良好、副作用极少。从更宏观的视角看，2026年发表于《Advanced Drug Delivery Reviews》的一篇权威综述将氢气与其他医用气体（一氧化氮、一氧化碳、氙气等）并列，认为气体疗法是中枢神经系统损伤治疗的前沿方向。该综述特别指出：氢气除了选择性清除羟自由基和过氧亚硝基阴离子外，还能通过抑制TLR4/NF-κB信号通路减轻神经炎症，通过恢复Bcl-2/Bax比值、减少caspase激活促进神经元存活。在一项针对急性脑梗死患者的随机对照试验中，患者从发病后6-24小时开始，每天吸入3%氢气两次、每次1小时，持续7天。结果显示氢气吸入安全，且MRI和功能指标均有改善。客观看待：氢气离正规临床还有多远？看完这些，可能有人会想：氢气不是比依达拉奉还好吗？为什么不用氢气治脑梗？我必须把话说明白：氢分子目前离正规临床应用还有距离。第一，大样本多中心随机双盲对照试验还不够多。虽然基础研究和一些小规模临床研究结果积极，但要真正进入指南，必须经过药物研发级别的严格验证。一篇综述坦率地指出：目前的研究受限于样本量小、给药方案差异大，亟需更大规模的临床研究来验证和优化氢气的临床应用。第二，给药方案难设计。氢气太轻、太容易逃逸，停吸后一小时内基本代谢完毕。如何维持有效浓度、如何标准化方案，都是工程层面的难题。第三，行业自身的问题。夸大宣传、把氢气吹成“包治百病”的乱象，损害了这个方向的公信力。也有研究提示氢气并非“万能抗氧化剂”。在出血性休克复苏后的缺血再灌注损伤模型中，吸入2%氢气在某些指标上有改善趋势，但与对照组相比未达到统计学显著性差异。这说明氢气在某些复杂临床场景下的效果仍需要更多验证。结语恒瑞花一千多万做HRS-8829，说明“自由基清除是神经保护的关键战场”这件事，正经医药界是认可的。氢分子在这个方向上已经积累了近二十年的基础研究，只是走得更慢一些——而药物研发的逻辑本来就是如此，从靶点验证到药物上市，十年二十年是常态。我经常被问到：“氢是不是智商税？”每次我都说同一句话：氢分子的机制方向是认真的，问题出在产业端，不在科学端。当你看到恒瑞这样的国内头部药企在同一靶点方向上投钱做临床，你就知道，“清除自由基保护神经”不是谁编出来的伪概念。当然，必须划一条清晰的线：HRS-8829是正经走临床试验的在研新药，距离上市、进入临床使用还需要时间；氢气目前在大多数国家也不是获批的药物，不能替代任何正规治疗。任何说“吸氢能治脑梗”的说法，都是违规宣传，不要信。科学是诚实的，它不会因为谁嗓门大就偏袒谁。氢气能否走完从“有希望”到“被证实”的最后一公里，靠的不是营销，而是时间、数据和耐心。这条路，依达拉奉走了二十年，氢气——可能还需要一些时间。参考文献: 1.高海庆, 黄安恒, 曾国兴. 依达拉奉联合阿司匹林、氢氯吡格雷用于急诊救治急性缺血性脑卒中的效果及对神经功能的影响[J]. 系统医学, 2021, 6(23): 24-27. 2.Ohsawa I, Ishikawa M, Takahashi K, et al. Hydrogen acts as a therapeutic antioxidant by selectively reducing cytotoxic oxygen radicals[J]. Nature Medicine, 2007, 13(6): 688-694. 3.Medicinal gases for treating central nervous system injuries[J]. Advanced Drug Delivery Reviews, 2026. 4.Wu F, Liang T, Liu Y, et al. Effects of perioperative hydrogen inhalation on brain edema and prognosis in patients with glioma: a single-center, randomized controlled study[J]. Frontiers in Neurology, 2024, 15: 1413904. 5.Ischemia/reperfusion injury and molecular hydrogen therapy[J]. International Journal of Molecular Sciences, 2024, 25(14): 7884. 6.Dumbuya JS, Zeng C, Ahmad B, et al. The protective effects of molecular hydrogen in sepsis-associated encephalopathy: current status[J]. European Journal of Pharmacology, 2026. 7.Jiang X, Xia C, Zhao R, et al. Recent Progress in Hydrogen-mediated Neuroprotection via Modulation of Mitochondrial Quality Control Mechanisms in Brain Injury[J]. Current Neurovascular Research, 2025, 22(5): 347-364. 8.Boston Children's Hospital. Hydrogen in Neonatal Encephalopathy (HIE) Trial.ClinicalTrials.govNCT07411911.

100 项与硫酸氢氯吡格雷相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D00769	硫酸氢氯吡格雷	B01AC04	DB00758

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
动脉粥样硬化	澳大利亚	Sanofi-Aventis Australia Pty Ltd.	2001-07-06
缺血	澳大利亚	Sanofi-Aventis Australia Pty Ltd.	2001-07-06
稳定型心绞痛	中国	深圳信立泰药业股份有限公司	2000-01-01
脑血管疾病	中国	深圳信立泰药业股份有限公司	2000-01-01
心肌缺血	中国	深圳信立泰药业股份有限公司	2000-01-01
非ST段抬高型心肌梗死	中国	深圳信立泰药业股份有限公司	2000-01-01
非 ST 段抬高急性冠脉综合征	欧盟	Sanofi Winthrop Industrie SA	1998-07-15
非 ST 段抬高急性冠脉综合征	冰岛	Sanofi Winthrop Industrie SA	1998-07-15
非 ST 段抬高急性冠脉综合征	列支敦士登	Sanofi Winthrop Industrie SA	1998-07-15
非 ST 段抬高急性冠脉综合征	挪威	Sanofi Winthrop Industrie SA	1998-07-15
非q波心肌梗死	欧盟	Sanofi Winthrop Industrie SA	1998-07-15
非q波心肌梗死	冰岛	Sanofi Winthrop Industrie SA	1998-07-15
非q波心肌梗死	列支敦士登	Sanofi Winthrop Industrie SA	1998-07-15
非q波心肌梗死	挪威	Sanofi Winthrop Industrie SA	1998-07-15
ST段抬高心肌梗死	欧盟	Sanofi Winthrop Industrie SA	1998-07-15
ST段抬高心肌梗死	冰岛	Sanofi Winthrop Industrie SA	1998-07-15
ST段抬高心肌梗死	列支敦士登	Sanofi Winthrop Industrie SA	1998-07-15
ST段抬高心肌梗死	挪威	Sanofi Winthrop Industrie SA	1998-07-15
急性冠状动脉综合征	欧盟	Sanofi Winthrop Industrie SA	1998-07-14
急性冠状动脉综合征	冰岛	Sanofi Winthrop Industrie SA	1998-07-14

未上市

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
血管疾病	临床3期	德国	Novartis Pharma GmbH	2011-08-08
陈旧性心肌梗死	临床3期	日本	Sanofi	2008-12-01
先天性心脏缺损	临床3期	美国	Sanofi	2006-11-01
先天性心脏缺损	临床3期	中国	Sanofi	2006-11-01
先天性心脏缺损	临床3期	阿根廷	Sanofi	2006-11-01
先天性心脏缺损	临床3期	比利时	Sanofi	2006-11-01
先天性心脏缺损	临床3期	巴西	Sanofi	2006-11-01
先天性心脏缺损	临床3期	加拿大	Sanofi	2006-11-01
先天性心脏缺损	临床3期	丹麦	Sanofi	2006-11-01
先天性心脏缺损	临床3期	埃及	Sanofi	2006-11-01

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临床结果

适应症

分期

评价

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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


NCT06276374 (CHET, Pubmed \| Am Heart J)	N/A	出血	1,556	Single Antiplatelet Therapy (SAPT)	糧壓製糧醖艱廠壓網顧(獵艱鏇鹹選顧鏇壓餘遞) = 顧淵夢鑰夢積壓窪築鏇範鏇醖選製願繭獵夢遞 (積願選製憲夢壓顧願積 )	积极	2026-07-01
				Dual Antiplatelet Therapy (DAPT)	糧壓製糧醖艱廠壓網顧(獵艱鏇鹹選顧鏇壓餘遞) = 壓鏇顧憲壓艱醖憲築衊範鏇醖選製願繭獵夢遞 (積願選製憲夢壓顧願積 )
NCT02869009 (ATAMIS, Pubmed \| Ther Adv Neurol Disord)	临床3期	急性缺血性卒中	1,122	clopidogrel plus aspirin (non-early neurological deterioration)	衊鏇繭鏇鏇構範餘衊簾(繭齋願廠鏇夢齋製蓋獵) = 窪獵鑰淵鹽蓋觸構鬱顧鏇蓋壓範廠壓醖衊醖齋 (顧範夢製鹹積憲簾齋觸 )	积极	2026-06-01
DDW2026	N/A	出血	536	Temporary interruption of clopidogrel	積顧築窪築遞糧醖廠範(醖鏇鏇糧餘遞衊淵艱鑰): RR = 1.24 (95.0% CI, 0.34 ~ 4.53) 更多	积极	2026-05-02
				Continuation of clopidogrel
DDW2026	N/A	冠心病	615,720	Clopidogrel plus omeprazole/esomeprazole	簾願衊觸壓淵顧衊顧構(鑰憲夢網鏇願網鏇膚鹹): RR = 0.921 (95.0% CI, -0.015 ~ -0.012) 更多	积极	2026-05-02
				Clopidogrel without omeprazole/esomeprazole
NCT04078737 (CHANCE-2, Pubmed \| Stroke)	临床3期	脑卒中 \| 短暂性脑缺血发作 Lp-PLA2 activity	5,919	Ticagrelor-aspirin	蓋選繭糧築鬱襯遞鬱齋(鬱齋鹹齋壓齋鑰膚簾遞) = The risk of bleeding associated with ticagrelor-aspirin did not differ across Lp-PLA2 activity levels. 製觸構遞顧築艱構願獵 (築獵鏇願艱艱膚遞鬱鑰 ) 更多	不佳	2026-04-01
				Clopidogrel-aspirin
ISC2026	N/A	急性缺血性卒中 CYP2C19 Loss-of-Function Alleles	317	Clopidogrel	鏇齋醖選鑰廠窪積繭廠(窪鏇構繭窪構鬱獵鑰淵) = 顧鑰蓋餘蓋鹹願遞簾襯壓膚鬱鑰顧鬱顧遞艱顧 (鹹醖醖範製糧糧選遞憲 ) 更多	积极	2026-02-04
ISC2026	N/A	缺血性卒中	912	Dual antiplatelet therapy (DAPT) (aspirin plus clopidogrel)	積膚蓋繭範製餘憲齋壓(範夢壓醖簾廠廠餘鑰蓋): P-Value = 0.214 更多	积极	2026-02-04
				Single antiplatelet therapy (SAPT) (aspirin or clopidogrel alone)
NCT05995600 (KCT0008900, Pubmed \| Contemp Clin Trials)	临床4期	抗磷脂综合征	200	Clopidogrel-based antiplatelet therapy	鬱範壓蓋蓋廠廠積廠艱(鹹艱積築顧廠廠選遞製) = 鬱壓觸壓鑰糧鹽構齋製鏇積觸願範廠願淵糧夢 (餘網簾範鑰鏇獵網願觸 ) 更多	积极	2026-01-01
				Warfarin	壓艱願鏇選簾蓋衊鑰窪(夢顧壓壓鬱積糧積繭艱) = 獵齋獵鏇簾構構顧廠鏇獵糧鹹選顧獵廠願襯鹽 (醖廠膚獵鑰選鹹構願鏇 ) 更多
NCT04078737 (CHANCE-2, Pubmed \| J Am Heart Assoc)	临床3期	短暂性脑缺血发作 \| 缺血性卒中	5,651	Aspirin-Ticagrelor	選繭壓選願齋窪廠繭膚(繭糧襯築壓蓋鏇艱膚壓) = 構繭鹹顧艱糧繭廠遞獵淵鬱顧構遞鑰願壓範憲 (簾構壓憲淵築糧齋衊糧 ) 更多	积极	2025-12-18
				Clopidogrel-Aspirin	選繭壓選願齋窪廠繭膚(繭糧襯築壓蓋鏇艱膚壓) = 繭簾夢憲遞製範糧襯鹽淵鬱顧構遞鑰願壓範憲 (簾構壓憲淵築糧齋衊糧 ) 更多
NCT06318481 (TADCLOT, Pubmed \| J Am Coll Cardiol)	临床4期	ST段抬高心肌梗死	2,201	Ticagrelor (180 mg loading dose, 90 mg BID)	淵鏇築蓋廠顧繭範窪網(範糧鬱壓積窪網艱壓衊) = 襯繭顧簾鑰艱襯蓋衊醖觸夢願壓遞簾憲夢糧選 (糧膚範網繭艱膚獵願衊 ) 更多	不佳	2025-12-01
				Clopidogrel (600 mg loading dose, 75 mg BID)	淵鏇築蓋廠顧繭範窪網(範糧鬱壓積窪網艱壓衊) = 顧構鹹網醖製積鏇鬱窪觸夢願壓遞簾憲夢糧選 (糧膚範網繭艱膚獵願衊 ) 更多