Evidence-based progress and future therapeutic directions of myosin inhibitor aficamten—from mechanistic exploration to clinical practice

doi:10.12092/j.issn.1009-2501.2026.09.011

Abstract

Abstract:

Hypertrophic cardiomyopathy (HCM) is a common inherited cardiomyopathy, in which patients with the obstructive form (oHCM) face an elevated risk of heart failure and arrhythmias due to left ventricular outflow tract (LVOT) obstruction. Traditional drug therapies primarily aim to alleviate symptoms and are often unable to reverse the pathophysiological progression of the disease. The advent of cardiac myosin inhibitors (CMIs) marks the entry of HCM treatment into a new era of targeted intervention addressing the core disease mechanism. With its unique pharmacokinetic profile—such as a short half-life and low risk of drug-drug interactions—along with outstanding efficacy and safety, Aficamten has been demonstrated in multiple key clinical trials to significantly improve exercise capacity, symptoms, and quality of life in patients with oHCM, while also showing potential for reversing cardiac remodeling. This article systematically reviews the mechanism of action, pharmacological properties, clinical development history of Aficamten, and its position within the HCM treatment landscape, and offers perspectives on future research directions for personalized therapy and disease-modifying effects.

Key words: Aficamten, cardiac myosin inhibitors, hypertrophic cardiomyopathy, left ventricular outflow tract obstruction, targeted therapy

CLC Number:

R542.2

Qi WANG, Yunzeng ZOU. Evidence-based progress and future therapeutic directions of myosin inhibitor aficamten—from mechanistic exploration to clinical practice[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2026, 31(9): 1249-1255.

Figures/Tables 3

References 36

1	Pagel PS, Hang D, Freed JK, et al. Advances in cardiovascular pharmacotherapy I cardiac myosin inhibitors[J]. J Cardiothorac Vasc Anesth, 2025, 39 (5): 1287- 1305. doi: 10.1053/j.jvca.2025.02.009
2	Abunada A, Shah M, Kumar A, et al. Efficacy and safety of cardiac myosin inhibitors for symptomatic hypertrophic cardiomyopathy: a meta-analysis of randomized controlled trials[J]. Front Cardiovasc Med, 2025, 11, 1477487. doi: 10.3389/fcvm.2024.1477487
3	Gollapudi SK, Ma W, Chakravarthy S, et al. Two classes of myosin inhibitors, para-nitroblebbistatin and mavacamten, stabilize β-cardiac myosin in different structural and functional states[J]. J Mol Biol, 2021, 433 (23): 167295. doi: 10.1016/j.jmb.2021.167295
4	唐媛媛, 唐博謇, 严晓伟, 等. 肥厚梗阻型与非梗阻型心肌病的临床特点和预后分析[J]. 中国临床药理学与治疗学, 2009, 14 (2): 195- 198.
5	Olivotto I, Udelson JE, Pieroni M, et al. Genetic causes of heart failure with preserved ejection fraction: emerging pharmacological treatments[J]. Eur Heart J, 2023, 44 (8): 656- 667. doi: 10.1093/eurheartj/ehac764
6	Ogieuhi IJ, Ajekiigbe VO, Adeyemi BA, et al. Cardiac myosin inhibitors: efficacy, safety and future directions of aficamten in hypertrophic obstructive cardiomyopathy[J]. Egypt Heart J, 2025, 77 (1): 61. doi: 10.1186/s43044-025-00652-0
7	Mohran S, Kooiker KB, Naim A, et al. Myosin modulator Aficamten inhibits force in cardiac muscle by altering myosin's biochemical activity without changing thick filament structure[J]. JACC Basic Transl Sci, 2026, 11 (1): 101449. doi: 10.1016/j.jacbts.2025.101449
8	Coats CJ, Masri A, Nassif ME, et al. Dosing and safety profile of aficamten in symptomatic obstructive hypertrophic cardiomyopathy: results from SEQUOIA-HCM[J]. J Am Heart Assoc, 2024, 13 (15): e035993. doi: 10.1161/JAHA.124.035993
9	Pugsley MK, Hwee DT, Winters BR, et al. A characterization of the nonclinical pharmacology and toxicology of aficamten, a reversible allosteric inhibitor of cardiac myosin[J]. Int J Toxicol, 2025, 44 (3): 211- 234. doi: 10.1177/10915818251326466
10	Lim J, Kim HK. Cardiac myosin inhibitors in hypertrophic cardiomyopathy[J]. J Cardiovasc Imaging, 2025, 33 (1): 7. doi: 10.1186/s44348-025-00052-7
11	Ramadan MM, Al-Najjar RA, Abady RS, et al. Mavacamten cardiac myosin inhibitor: clinical applications and future perspectives[J]. Cureus, 2025, 17 (4): e82722. doi: 10.7759/cureus.82722
12	Dalo JD, Weisman ND, White CM. Mavacamten, a first-in-class cardiac myosin inhibitor for obstructive hypertrophic cardiomyopathy[J]. Ann Pharmacother, 2023, 57 (4): 489- 502. doi: 10.1177/10600280221117812
13	Malik FI, Robertson LA, Armas DR, et al. A Phase 1 dose-escalation study of the cardiac myosin inhibitor aficamten in healthy participants[J]. JACC Basic Transl Sci, 2022, 7 (8): 763- 775. doi: 10.1016/j.jacbts.2022.04.008
14	Chuang C, Collibee S, Ashcraft L, et al. Discovery of aficamten (CK-274), a next-generation cardiac myosin inhibitor for the treatment of hypertrophic cardiomyopathy[J]. J Med Chem, 2021, 64 (19): 14142- 14152. doi: 10.1021/acs.jmedchem.1c01290
15	Zhao X, Liu H, Tian W, et al. Safety, tolerability, pharmacokinetics, and pharmacodynamics of single and multiple doses of aficamten in healthy Chinese participants: a randomized, double-blind, placebo-controlled, phase 1 study[J]. Front Pharmacol, 2023, 14, 1227470. doi: 10.3389/fphar.2023.1227470
16	Xu D, Divanji P, Griffith A, et al. Pharmacokinetics, disposition, and biotransformation of the cardiac myosin inhibitor aficamten in humans[J]. Pharmacol Res Perspect, 2024, 12 (5): e70006. doi: 10.1002/prp2.70006
17	Maron MS, Masri A, Choudhury L, et al. Phase 2 study of aficamten in patients with obstructive hypertrophic cardiomyopathy[J]. Am Coll Cardiol, 2023, 81 (1): 34- 45. doi: 10.1016/j.jacc.2022.10.020
18	Owens AT, Masri A, Abraham TP, et al. Aficamten for drug-refractory severe obstructive hypertrophic cardiomyopathy in patients receiving disopyramide: REDWOOD-HCM Cohort 3[J]. J Card Fail, 2023, 29 (11): 1576- 1582. doi: 10.1016/j.cardfail.2023.07.003
19	Masri A, Sherrid MV, Abraham TP, et al. Efficacy and safety of aficamten in symptomatic nonobstructive hypertrophic cardiomyopathy: results from the REDWOOD-HCM Trial, Cohort 4[J]. J Card Fail, 2024, 30 (11): 1439- 1448. doi: 10.1016/j.cardfail.2024.02.020
20	Saleh D, Eskandari M, Choudhury L. Aficamten in the treatment of obstructive hypertrophic cardiomyopathy[J]. Future Cardiol, 2025, 21 (9): 685- 691. doi: 10.1080/14796678.2025.2521183
21	Garcia-Pavia P, Maron MS, Masri A, et al. Aficamten or metoprolol monotherapy for obstructive hypertrophic cardiomyopathy[J]. N Engl J Med, 2025, 393 (10): 949- 960. doi: 10.1056/NEJMoa2504654
22	Saberi S, Abraham TP, Choudhury L, et al. Aficamten treatment for symptomatic obstructive hypertrophic cardiomyopathy: 48-week results from FOREST-HCM[J]. JACC Heart Fail, 2025, 13 (8): 102496. doi: 10.1016/j.jchf.2025.03.040
23	Sebastian SA, Padda I, Lehr EJ, et al. Aficamten: a breakthrough therapy for symptomatic obstructive hypertrophic cardiomyopathy[J]. Am J Cardiovasc Drugs, 2023, 23 (5): 519- 532. doi: 10.1007/s40256-023-00599-0
24	Kukowka A, Droździk M. Cardiac myosin inhibitors in the treatment of hypertrophic cardiomyopathy: clinical trials and future challenges[J]. Biomolecules, 2025, 15 (8): 1098. doi: 10.3390/biom15081098
25	Davis BJ, Volk H, Nguyen O, et al. Safety and efficacy of mavacamten and aficamten in patients with hypertrophic cardiomyopathy[J]. J Am Heart Assoc, 2025, 14 (6): e038758.
26	Hasana U, Korpal M, Haider F, et al. Cardiac myosin inhibitors for hypertrophic cardiomyopathy: a systematic review and meta-analysis of randomized controlled trials[J]. Ann Med Surg (Lond), 2025, 87 (6): 3810- 3818. doi: 10.1097/MS9.0000000000003326
27	《心肌肌球蛋白抑制剂药物治疗专家共识》工作组, 张志玲. 心肌肌球蛋白抑制剂药物治疗专家共识[J]. 临床药物治疗杂志, 2026, 24 (3): 1- 13. doi: 10.3969/j.issn.1672-3384.2026.03.001
28	Masri A, Cardoso RN, Abraham TP, et al. Effect of aficamten on cardiac structure and function in obstructive hypertrophic cardiomyopathy: SEQUOIA-HCM CMR Substudy[J]. J Am Coll Cardiol, 2024, 84 (19): 1806- 1817. doi: 10.1016/j.jacc.2024.08.015
29	Cytokinetics. Cytokinetics announces NMPA approval of MYQORZO® (aficamten) in China for patients with obstructive hypertrophic cardiomyopathy [EB/OL]. (2025-12-17) [2026-09-17]. https://ir.cytokinetics.com/press-releases/press-release-details/2025/Cytokinetics-Announces-NMPA-Approval-of-MYQORZO-aficamten-in-China--for-Patients-with-Obstructive-Hypertrophic-Cardiomyopathy/default.aspx.
30	US FDA. Myqorzo (aficamten): NDA approval [EB/OL] (2025-03-09) [2026-09-17]. https://www.accessdata.fda.gov/drugsatfda_docs/appleletter/2025/219083Orig1s000ltr.pdf.
31	Cytokinetics. Cytokinetics announces European Commission approval of MYQORZO® (aficamten) for the treatment of adults with symptomatic obstructive hypertrophic cardiomyopathy [EB/OL]. (2026-02-17) [2026-09-17]. https://ir.cytokinetics.com/press-releases/press-release-details/2026/Cytokinetics-Announces-European-Commission-Approval-of-MYQORZO-aficamten-for-the-Treatment-of-Adults-with-Symptomatic-Obstructive-Hypertrophic-Cardiomyopathy/default.aspx.
32	Masri A, Maron MS, Abraham TP, et al. Concomitant Aficamten and disopyramide in symptomatic obstructive hypertrophic cardiomyopathy[J]. JACC Heart Fail, 2026, 14 (2): 102441. doi: 10.1016/j.jchf.2025.03.008
33	Ho CY, Olivotto I, Jacoby D, et al. Study design and rationale of EXPLORER-HCM: evaluation of mavacamten in adults with symptomatic obstructive hypertrophic cardiomyopathy[J]. Circ Heart Fail, 2020, 13 (6): e006853. doi: 10.1161/CIRCHEARTFAILURE.120.006853
34	Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC Guideline for the diagnosis and treatment of patients with hypertrophic cardiomyopathy: executive summary: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines[J]. Circulation, 2020, 142 (25): e533- 557. doi: 10.1161/cir.0000000000000945
35	彭娟, 范琳琳, 李然宜, 等. 心力衰竭药物治疗的研究进展[J]. 中国临床药理学与治疗学, 2022, 27 (4): 373- 381.
36	Hegde SM, Wang X, Garcia-Pavia P, et al. Effect of aficamten compared with metoprolol on echocardiographic measures in symptomatic obstructive hypertrophic cardiomyopathy: MAPLE-HCM[J]. J Am Coll Cardiol, 2025, 86 (24): 2452- 2467. doi: 10.1016/j.jacc.2025.08.022

研究名称（阶段）	核心设计与目的	标准给药方案	主要结果（对照组vs. 基线）	安全性概要	临床意义与定位
REDWOOD-HCM（Ⅱ期）	多中心、随机、双盲、安慰剂对照；分4个队列（3个梗阻性+ 1 个nHCM探索不同人群的疗效与安全性	剂量递增探索个体化滴定至目标 LVOT-G	疗效：治疗10周后，显著降低静息及Valsalva后LVOT压差，改善NYHA分级和NT-proBNP水平	不良事件与安慰剂相当无药物相关严重不良事件无治疗中断	全球首个概念验证研究首次证实对nHCM有效支持进入Ⅲ期临床试验
SEQUOIA-HCM （Ⅲ 期）	全球多中心、随机、双盲、安慰剂对照；282例症状性梗阻性 HCM（含46例中国患者）确证 24周治疗的疗效与安全性	起始 5 mg qd；每2周递增5 mg；最高20 mg qd；根据 LVOT-G和LVEF 调整	主要终点：峰值摄氧量（pVO₂）显著改善次要终点：全部10个预设终点均显著改善，包括KCCQ-CSS、NYHA分级、LVOT压差等	安全性良好，不良事件与安慰剂相当；Aficamten组有3.5%患者出现无症状、可逆的LVEF<50%，无相关心衰或停药事件	核心注册研究确立阿非卡坦在症状性梗阻性HCM 中的标准治疗地位
MAPLE-HCM （Ⅲ期）	国际多中心、双盲、双模拟、头对头；175例症状性梗阻性HCM（含22例中国患者）对比阿非卡坦与美托洛尔的优效性	阿非卡坦：起始 5 mg qd，每2 周+ 5 mg，最高20 mg qd；美托洛尔：起始 50 mg qd，每2 周 + 50 mg，最高 200 mg qd	主要终点：pVO₂改善显著优于美托洛尔全面获益：在NYHA分级改善、KCCQ-CSS、LVOT压差、NT-proBNP、LAVI等方面均更优	两组总体不良事件发生率相似；Aficamten组剂量调整需求（5%）远低于美托洛尔组（30%）	全球首个CMI与β受体阻滞剂头对头研究证实阿非卡坦单药疗效显著优于美托洛尔推动HCM治疗从“对症”向“对因”转变
FOREST-HCM （Ⅱ/Ⅲ期）	开放标签延续性研究；296例完成前期试验的梗阻性HCM患者；评估长期（平均62周）疗效与安全性	延续前期个体化给药方案	疗效持久：LVOT压差降低、NYHA分级和KCCQ评分改善在长期随访中早期出现并持续维持生物标志物：NT-proBNP和肌钙蛋白Ⅰ持续显著降低	长期耐受性良好；严重不良事件发生率低，极少患者因LVEF<50%需减量（10例，3.4%）或停药（1例）	证实长期治疗的疗效持续性和良好安全性支持临床长期应用

研究名称（阶段）	核心设计与目的	标准给药方案	主要结果（对照组vs. 基线）	安全性概要	临床意义与定位
REDWOOD-HCM（Ⅱ期）	多中心、随机、双盲、安慰剂对照；分4个队列（3个梗阻性+ 1 个nHCM探索不同人群的疗效与安全性	剂量递增探索个体化滴定至目标 LVOT-G	疗效：治疗10周后，显著降低静息及Valsalva后LVOT压差，改善NYHA分级和NT-proBNP水平	不良事件与安慰剂相当无药物相关严重不良事件无治疗中断	全球首个概念验证研究首次证实对nHCM有效支持进入Ⅲ期临床试验
SEQUOIA-HCM （Ⅲ 期）	全球多中心、随机、双盲、安慰剂对照；282例症状性梗阻性 HCM（含46例中国患者）确证 24周治疗的疗效与安全性	起始 5 mg qd；每2周递增5 mg；最高20 mg qd；根据 LVOT-G和LVEF 调整	主要终点：峰值摄氧量（pVO₂）显著改善次要终点：全部10个预设终点均显著改善，包括KCCQ-CSS、NYHA分级、LVOT压差等	安全性良好，不良事件与安慰剂相当；Aficamten组有3.5%患者出现无症状、可逆的LVEF<50%，无相关心衰或停药事件	核心注册研究确立阿非卡坦在症状性梗阻性HCM 中的标准治疗地位
MAPLE-HCM （Ⅲ期）	国际多中心、双盲、双模拟、头对头；175例症状性梗阻性HCM（含22例中国患者）对比阿非卡坦与美托洛尔的优效性	阿非卡坦：起始 5 mg qd，每2 周+ 5 mg，最高20 mg qd；美托洛尔：起始 50 mg qd，每2 周 + 50 mg，最高 200 mg qd	主要终点：pVO₂改善显著优于美托洛尔全面获益：在NYHA分级改善、KCCQ-CSS、LVOT压差、NT-proBNP、LAVI等方面均更优	两组总体不良事件发生率相似；Aficamten组剂量调整需求（5%）远低于美托洛尔组（30%）	全球首个CMI与β受体阻滞剂头对头研究证实阿非卡坦单药疗效显著优于美托洛尔推动HCM治疗从“对症”向“对因”转变
FOREST-HCM （Ⅱ/Ⅲ期）	开放标签延续性研究；296例完成前期试验的梗阻性HCM患者；评估长期（平均62周）疗效与安全性	延续前期个体化给药方案	疗效持久：LVOT压差降低、NYHA分级和KCCQ评分改善在长期随访中早期出现并持续维持生物标志物：NT-proBNP和肌钙蛋白Ⅰ持续显著降低	长期耐受性良好；严重不良事件发生率低，极少患者因LVEF<50%需减量（10例，3.4%）或停药（1例）	证实长期治疗的疗效持续性和良好安全性支持临床长期应用

对比维度	传统药物治疗（β受体阻滞剂/钙通道阻滞剂/丙吡胺）	Aficamten	介入/外科治疗（室间隔减容术）
核心作用机制	间接对症：通过降低心率、减弱心肌收缩力、改善舒张功能减轻 LVOT梗阻不直接干预疾病分子基础	直接对因：心肌肌球蛋白抑制剂，结合肌球蛋白S1结构域别构位点减慢磷酸盐释放，减少肌球蛋白-肌动蛋白横桥形成，从根本上纠正心肌高收缩状态	物理解除：通过外科切除或酒精消融肥厚室间隔直接解决解剖学梗阻问题
疗效特点	仅部分缓解症状；对运动耐量改善有限（甚至可能降低，如美托洛尔）；对长期预后无明确获益；约30%～50%患者疗效不佳或出现耐受	全面改善：显著降低LVOT梯度、提升运动耐量（pVO₂）、改善NYHA分级和生活质量，降低心衰生物标志物（NT-proBNP、肌钙蛋白），疗效早期出现且长期持续，对梗阻性和nHCM均有效	能快速、显著降低LVOT梯度；可有效改善严重症状；对心肌本身的高收缩性病理基础无作用；对nHCM无效
适用人群	所有症状性HCM患者的一线基础治疗；轻中度症状患者；作为联合治疗的基础	传统药物疗效不佳或不耐受的症状性HCM 患者，oHCM和nHCM均适用，不适合手术的高龄或多共病患者，希望避免有创操作的患者	药物治疗无效的严重症状性 oHCM（NYHA Ⅲ-Ⅳ级）、静息/激发LVOT-G≥50 mmHg、无手术禁忌证的患者
主要局限性	仅对症治疗，无法阻止疾病进展，疗效个体差异大，存在心率、血压过度降低等剂量限制性副作用，丙吡胺有抗心律失常副作用，儿童使用受限	长期（5年）预后和安全性数据仍在积累，治疗费用较高，需定期监测LVEF调整剂量	有创操作，存在手术风险；并发症发生率较高；对高龄或伴多种共病患者适应性差；无法解决心肌舒张功能异常和非梗阻性病变
安全性与风险	β受体阻滞剂：心动过缓、低血压、乏力、支气管痉挛。钙通道阻滞剂：房室传导阻滞、低血压、便秘。丙吡胺：口干、尿潴留、QT间期延长、致心律失常	总体耐受性极佳，不良事件发生率与安慰剂相似；主要风险：一过性无症状LVEF降低（3%～5%），可通过减量或停药恢复；无严重药物相关死亡或永久停药事件	外科肌束切除：死亡率约 1%～ 2%，并发症包括传导阻滞（需永久起搏器）、室间隔穿孔、主动脉瓣损伤；酒精消融：死亡率约1%，并发症包括房室传导阻滞（10%～15%）、心肌梗死、残余梗阻
临床治疗定位	HCM治疗的基础一线用药，用于症状控制和基础管理	传统药物的升级替代选择；有望成为症状性 oHCM的首选一线治疗；可替代约30%～50% 原本需要手术的患者；可作为手术前的桥接治疗优化心功能	药物治疗完全无效后的最后防线，仅用于严重梗阻且药物难治的患者
对治疗格局的影响	传统对症治疗模式的代表，已应用数十年	推动HCM治疗从“对症管理”向“分子靶向对因治疗”转变，重塑治疗流程	地位逐渐从“主要治疗”向 “补救性治疗”转变，适用人群范围缩小

对比维度	传统药物治疗（β受体阻滞剂/钙通道阻滞剂/丙吡胺）	Aficamten	介入/外科治疗（室间隔减容术）
核心作用机制	间接对症：通过降低心率、减弱心肌收缩力、改善舒张功能减轻 LVOT梗阻不直接干预疾病分子基础	直接对因：心肌肌球蛋白抑制剂，结合肌球蛋白S1结构域别构位点减慢磷酸盐释放，减少肌球蛋白-肌动蛋白横桥形成，从根本上纠正心肌高收缩状态	物理解除：通过外科切除或酒精消融肥厚室间隔直接解决解剖学梗阻问题
疗效特点	仅部分缓解症状；对运动耐量改善有限（甚至可能降低，如美托洛尔）；对长期预后无明确获益；约30%～50%患者疗效不佳或出现耐受	全面改善：显著降低LVOT梯度、提升运动耐量（pVO₂）、改善NYHA分级和生活质量，降低心衰生物标志物（NT-proBNP、肌钙蛋白），疗效早期出现且长期持续，对梗阻性和nHCM均有效	能快速、显著降低LVOT梯度；可有效改善严重症状；对心肌本身的高收缩性病理基础无作用；对nHCM无效
适用人群	所有症状性HCM患者的一线基础治疗；轻中度症状患者；作为联合治疗的基础	传统药物疗效不佳或不耐受的症状性HCM 患者，oHCM和nHCM均适用，不适合手术的高龄或多共病患者，希望避免有创操作的患者	药物治疗无效的严重症状性 oHCM（NYHA Ⅲ-Ⅳ级）、静息/激发LVOT-G≥50 mmHg、无手术禁忌证的患者
主要局限性	仅对症治疗，无法阻止疾病进展，疗效个体差异大，存在心率、血压过度降低等剂量限制性副作用，丙吡胺有抗心律失常副作用，儿童使用受限	长期（5年）预后和安全性数据仍在积累，治疗费用较高，需定期监测LVEF调整剂量	有创操作，存在手术风险；并发症发生率较高；对高龄或伴多种共病患者适应性差；无法解决心肌舒张功能异常和非梗阻性病变
安全性与风险	β受体阻滞剂：心动过缓、低血压、乏力、支气管痉挛。钙通道阻滞剂：房室传导阻滞、低血压、便秘。丙吡胺：口干、尿潴留、QT间期延长、致心律失常	总体耐受性极佳，不良事件发生率与安慰剂相似；主要风险：一过性无症状LVEF降低（3%～5%），可通过减量或停药恢复；无严重药物相关死亡或永久停药事件	外科肌束切除：死亡率约 1%～ 2%，并发症包括传导阻滞（需永久起搏器）、室间隔穿孔、主动脉瓣损伤；酒精消融：死亡率约1%，并发症包括房室传导阻滞（10%～15%）、心肌梗死、残余梗阻
临床治疗定位	HCM治疗的基础一线用药，用于症状控制和基础管理	传统药物的升级替代选择；有望成为症状性 oHCM的首选一线治疗；可替代约30%～50% 原本需要手术的患者；可作为手术前的桥接治疗优化心功能	药物治疗完全无效后的最后防线，仅用于严重梗阻且药物难治的患者
对治疗格局的影响	传统对症治疗模式的代表，已应用数十年	推动HCM治疗从“对症管理”向“分子靶向对因治疗”转变，重塑治疗流程	地位逐渐从“主要治疗”向 “补救性治疗”转变，适用人群范围缩小

[1]	Fan HUANG, Ziyan DING, Qian ZHOU, Dingyuan HU, Xiaoyan NIE, Rui DING, Yi FANG. Research advances in targeting OX40/OX40L monoclonal antibodies for the treatment of atopic dermatitis [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2026, 31(5): 649-657.
[2]	Yuxiu ZHANG, Bo HE, Lijun ZHANG, Le JI, Zhuang MA, Hongxing ZHENG, Shanshan QI. Research progress on pathogenesis and drug intervention of alcoholic liver disease [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2026, 31(3): 409-419.
[3]	ZHU Xianjun, ZHANG Danni, LUO Xijun, LIANG Junjie, LI Tao, TANG Xingkui, HE Jialin, LI Wei. Reversal of trastuzumab resistance in gastric cancer cells by targeting GPRC5A with miR-195-5p [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2025, 30(7): 929-934.
[4]	CHEN Hongdan, HUANG Yinde, LI Chong. Research progress on advanced therapeutic approaches and emerging technologies in the drug treatment of refractory thyroid cancer [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2025, 30(3): 325-331.
[5]	WU Yuanyuan, LI Chenlu, CHEN Yan, CAO Mengda, SHAO Hua. Clinical efficacy of Tirellizumab combined with lenvatinib in the treatment of advanced liver cancer [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2025, 30(3): 392-397.
[6]	NIE Yang, WANG Yue, WEI Jia. Research progress on targeted therapy combined with immune-activating strategies in CLDN18.2-positive gastric cancer [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2025, 30(2): 146-158.
[7]	CHEN Zhenmei, CHEN Jinhong. Advances in precision diagnosis and treatment of cholangiocarcinoma [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2025, 30(2): 159-170.
[8]	DU Nan, WEI Miaoyan, XU Jin. Advancements and frontiers in targeted therapy for pancreatic cancer [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2025, 30(2): 183-192.
[9]	JIANG Haitao, XU Yangxian . Research progress on the resistance mechanism of anti-angiogenesis targeted drugs in the treatment of colorectal cancer [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2025, 30(2): 193-199.
[10]	BAI Haodong, SHA Bingxian, Ambedkar Kumar Yadav, XU Xianghuai, YU Li . Targeted biotherapy for chronic obstructive pulmonary disease [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2024, 29(4): 377-382.
[11]	ZHANG Huyunlong, ZHU Xiuzhi, JIN Xi, SHAO Zhimin. Mechanisms of endocrine-resistance and therapeutic breakthroughs in hormone receptor-positive, HER2-negative breast cancer [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2023, 28(8): 854-865.
[12]	LUO Shiping, ZHANG Jie, YU Yushuai, SONG Chuangui. Advances in targeted therapy for HER2-positive breast cancer [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2023, 28(8): 876-886.
[13]	XIANG Yimei, ZHANG Ningning, HUANG Yuxin, ZENG Xiaohua. Research progress of biomarkers related to the efficacy of HER2 positive breast cancer [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2023, 28(8): 887-897.
[14]	CHEN Manxin, ZHANG Bingyu, DAI Min. Clinical efficacy of intracoronally targeted recombinant human urokinase combined with percutaneous coronary intervention (PCI) in acute myocardial infarction (AMI) with high thrombus burden [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2023, 28(5): 544-549.
[15]	CHEN Wenjie, WANG Yabing, CHEN Xiaolin, REN Junling, ZHAO Wanjun, CHEN bin. Advances in the study of iodine-resistant differentiated thyroid cancer [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2022, 27(1): 116-120.