Clinical research advances in the treatment of immune thrombocytopenia with hetrombopag in combination therapy

doi:10.12092/j.issn.1009-2501.2026.03.010

Abstract

Abstract:

Immune thrombocytopenia (ITP) is an acquired autoimmune disease involving multiple mechanisms, which leads to platelet destruction and macrocytosis and impaired platelet production, mainly manifested as decreased platelet levels and a tendency to bleed, which seriously affects the quality of life and prognosis of patients. Treatment of ITP aims to increase platelet count (PLT), reduce the incidence of fatal bleeding, and improve quality of life. To improve efficacy, reduce adverse reactions and the advent of thrombopoietin receptor agonists (TPO-RAs) prompted a shift in ITP treatment to combination therapy. Hetrombopag is a novel oral second generation small molecule, non-peptide TPO-RAs that binds to the transmembrane domain of thrombopoietin receptor (TPO-R), stimulates megakaryocyte proliferation and differentiation, and promotes platelet production. Hetrombopag combined with other drugs (glucocorticoid, rhTPO and cyclosporine A) in the treatment of ITP can achieve multi-target treatment, through the integration of different drug mechanisms of action, can more comprehensively intervene in the pathogenesis of ITP, so as to improve the therapeutic effect, so this article reviews the clinical research progress of hetrombopag combination in the treatment of ITP.

Key words: hetrombopag, immune thrombocytopenia, combination drug, glucocorticoids, rhTPO, cyclosporine A

CLC Number:

R558.2

Shuangmiao JIANG, Huaijun ZHU, Danying LI. Clinical research advances in the treatment of immune thrombocytopenia with hetrombopag in combination therapy[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2026, 31(3): 382-391.

Figures/Tables 2

References 41

1	Colunga-Pedraza PR, Peña-Lozano SP, Sánchez-Rendón E, et al. Oseltamivir as rescue therapy for persistent, chronic, or refractory immune thrombocytopenia: a case series and review of the literature[J]. J Thromb Thrombolysis, 2022, 54 (2): 360- 366. doi: 10.1007/s11239-022-02651-3
2	李昕雨, 何杨, 阮长耿. 原发免疫性血小板减少症的治疗进展[J]. 中国实验血液学杂志, 2021, 29 (3): 983- 987. doi: 10.14033/j.cnki.cfmr.2026.01.047
3	LeVine DN, Brooks MB. Immune thrombocytopenia (ITP): Pathophysiology update and diagnostic dilemmas [J]. Vet Clin Pathol, 2019, 48 (Suppl 1): 17-28.
4	Witkowski M, Witkowska M, Robak T. Autoimmune thrombocytopenia: Current treatment options in adults with a focus on novel drugs[J]. Eur J Haematol, 2019, 103 (6): 531- 541. doi: 10.1111/ejh.13319
5	杨璐, 邹清梅. 糖皮质激素在临床应用中的不良反应及预防策略[J]. 世界临床药物, 2024, 45 (5): 449- 453. doi: 10.13683/j.wph.2024.05.001
6	Mititelu A, Onisâi MC, Roșca A, et al. Current understanding of immune thrombocytopenia: A review of pathogenesis and treatment options[J]. Int J Mol Sci, 2024, 25 (4): 2163. doi: 10.3390/ijms25042163
7	潘惠敏, 文瑞婷, 杨志刚. 激素耐药及复发免疫性血小板减少症的治疗进展[J]. 中国实验血液学杂志, 2023, 31 (2): 616- 620. doi: 10.19746/j.cnki.issn1009-2137.2023.02.047
8	中华医学会血液学分会血栓与止血学组. 成人原发免疫性血小板减少症诊断与治疗中国指南(2020年版)[J]. 中华血液学杂志, 2020, 41 (8): 617- 623. doi: 10.3760/cma.j.cn121090-20251031-00494
9	Neunert C, Terrell DR, Arnold DM, et al. American society of hematology 2019 guidelines for immune thrombocytopenia[J]. Blood Adv, 2019, 3 (23): 3829- 3866. doi: 10.1182/bloodadvances.2019000966
10	Ghanima W, Cooper N, Rodeghiero F, et al. Thrombopoietin receptor agonists: ten years later[J]. Haematologica, 2019, 104 (6): 1112- 1123. doi: 10.3324/haematol.2018.212845
11	Di Buduo CA, Currao M, Pecci A, et al. Revealing eltrombopag's promotion of human megakaryopoiesis through AKT/ERK-dependent pathway activation[J]. Haematologica, 2016, 101 (12): 1479- 1488. doi: 10.3324/haematol.2016.146746
12	Cooper N, Kruse A, Bussel JB. Thrombopoietin receptor agonists in ITP: a 20-year perspective[J]. Blood Reviews, 2023, 61, 101108.
13	Li T, Liu Q, Pu T, et al. Efficacy and safety of thrombopoietin receptor agonists in children and adults with persistent and chronic immune thrombocytopenia: a meta-analysis[J]. Expert Opin Pharmacother, 2023, 24 (6): 763- 774. doi: 10.1080/14656566.2023.2198089
14	Xie C, Zhao H, Bao X, et al. Pharmacological characterization of hetrombopag, a novel orally active human thrombopoietin receptor agonist[J]. J Cell Mol Med, 2018, 22 (11): 5367- 5377. doi: 10.1111/jcmm.13809
15	Li Q, Marcoux G, Hu Y, et al. Autoimmune effector mechanisms associated with a defective immunosuppressive axis in immune thrombocytopenia (ITP)[J]. Autoimmun Rev, 2024, 23 (12): 103677- 103677. doi: 10.1016/j.autrev.2024.103677
16	中国临床肿瘤学会(CSCO)抗肿瘤药物治疗安全管理专家委员会. 海曲泊帕临床应用指导原则[J]. 白血病·淋巴瘤, 2022, 31 (10): 577- 582. doi: 10.3760/cma.j.cn115356-20220809-00229
17	Ezumi Y, Takayama H, Okuma M. Thrombopoietin, c-Mpl ligand, induces tyrosine phosphorylation of Tyk2, JAK2, and STAT3, and enhances agonists-induced aggregation in platelets in vitro[J]. FEBS Lett, 1995, 374 (1): 48- 52. doi: 10.1016/0014-5793(95)01072-M
18	Drachman JG, Millett KM, Kaushansky K. Thrombopoietin signal transduction requires functional JAK2, not TYK2[J]. J Biol Chem, 1999, 274 (19): 13480- 13484. doi: 10.1074/jbc.274.19.13480
19	Rojnuckarin P, Drachman JG, Kaushansky K. Thrombopoietin-induced activation of the mitogen-activated protein kinase (MAPK) pathway in normal megakaryocytes: role in endomitosis[J]. Blood, 1999, 94 (4): 1273- 1282. doi: 10.1182/blood.V94.4.1273
20	Peng G, He G, Chang H, et al. A multicenter phase II study on the efficacy and safety of hetrombopag in patients with severe aplastic anemia refractory to immunosuppressive therapy [J]. Ther Adv Hematol, 2022, 13(12): 20406207221085197.
21	Zheng L, Liang MZ, Zeng XL, et al. Safety, pharmacokinetics and pharmacodynamics of hetrombopag olamine, a novel TPO-R agonist, in healthy individuals[J]. Basic Clin Pharmacol Toxicol, 2017, 121 (5): 414- 422. doi: 10.1111/bcpt.12815
22	张子颖, 吴灵芝, 印妮, 等. 海曲泊帕在血小板减少症中的临床研究进展[J]. 中国药学杂志, 2024, 59 (15): 1361- 1365. doi: 10.11669/cpj.2024.15.001
23	Yang G, Huang R, Yang S, et al. Effect of postdose fasting duration on hetrombopag olamine pharmacokinetics and pharmacodynamics in healthy volunteers[J]. Br J Clin Pharmacol, 2020, 86 (8): 1528- 1536. doi: 10.1111/bcp.14259
24	Syed YY. Hetrombopag: first approval[J]. Drugs, 2021, 81 (13): 1581- 1585. doi: 10.1007/s40265-021-01575-1
25	Wang Z, Chen L, Zhang F, et al. First-in-patient study of hetrombopag in patients with chronic idiopathic thrombocytopenic purpura[J]. J Thromb Haemost, 2020, 18 (11): 3053- 3060. doi: 10.1111/jth.15078
26	Mei H, Liu X, Li Y, et al. A multicenter, randomized phase III trial of hetrombopag: a novel thrombopoietin receptor agonist for the treatment of immune thrombocytopenia[J]. J Hematol Oncol, 2021, 14 (1): 1756- 8722.
27	Gilreath J, Lo M, Bubalo J. Thrombopoietin receptor agonists (TPO-RAs): drug class considerations for pharmacists[J]. Drugs, 2021, 81 (11): 1285- 1305. doi: 10.1007/s40265-021-01553-7
28	曾巧珠, 张晓辉. 成人原发免疫性血小板减少症诊治建议[J]. 中华内科杂志, 2021, 60 (6): 501- 505. doi: 10.3760/cma.j.cn112138-20200714-00670
29	中华医学会血液学分会血栓与止血学组. 促血小板生成药物临床应用管理中国专家共识(2023年版)[J]. 中华血液学杂志, 2023, 44 (7): 535- 542. doi: 10.3760/cma.j.issn.0253-2727.2023.07.002
30	Jurczak W, Chojnowski K, Mayer J, et al. Phase 3 randomised study of avatrombopag, a novel thrombopoietin receptor agonist for the treatment of chronic immune thrombocytopenia[J]. Br J Haematol, 2018, 183 (3): 479- 490. doi: 10.1111/bjh.15573
31	中国临床肿瘤学会(CSCO)淋巴瘤专家委员会, 中国临床肿瘤学会(CSCO)白血病专家委员会. 罗普司亭临床合理应用专家共识(2024年版)[J]. 白血病·淋巴瘤, 2024, 33 (9): 519- 527.
32	Hu Z, Bingjie D, Liu L, et al. PB2621: Treatment of immune thrombocytopenia with hetrombopag—a single-center retrospective, observationa study[J]. HemaSphere, 2023, 7 (S3): e7586119. doi: 10.1097/01.hs9.0000977172.75861.19
33	Yimei F, Ting C, Han Y, et al. PB2606: Real-world experience of hetrombopag in relapse and refractory immune thrombocytopenia [J]. HemaSphere, 2023, 7(S3): e18152a18155.
34	Mei H, Liu X, Li Y, et al. Switching from eltrombopag to hetrombopag in patients with primary immune thrombocytopenia: a post-hoc analysis of a multicenter, randomized phase III trial[J]. Ann Hematol, 2024, 103 (7): 2273- 2281. doi: 10.1007/s00277-024-05826-5
35	Pulanić D, Bátorová A, Bodó I, et al. Use of thrombopoietin receptor agonists in adults with immune thrombocytopenia: a systematic review and Central European expert consensus[J]. Ann Hematol, 2023, 102 (4): 715- 727. doi: 10.1007/s00277-023-05114-8
36	刘菲, 黄秀娟, 魏小芳, 等. 海曲泊帕联合泼尼松治疗原发免疫性血小板减少症的疗效分析[J]. 中国现代应用药学, 2024, 41 (4): 533- 538. doi: 10.13748/j.cnki.issn1007-7693.20231759
37	芮明忠, 黄义军. 海曲泊帕联合泼尼松治疗原发免疫性血小板减少症临床疗效分析[J]. 天津药学, 2024, 36 (4): 45- 49. doi: 10.3969/j.issn.1006-5687.2024.04.010
38	汤丽, 周丽, 范江砂, 等. 地塞米松联合TPO-RA治疗难治性免疫性血小板减少症的临床价值[J]. 医药前沿, 2023, 13 (35): 44- 46. doi: 10.3969/j.issn.2095-1752.2023.35.012
39	Yin J, Tian H, Lv X, et al. Effect of hetrombopag combined with rhtpo in patients with severe immUne thrombocytopenia[J]. Blood, 2023, 142 (S1): 1216- 1216. doi: 10.1182/blood-2023-182691
40	郭星, 赵丹, 左金曼. 海曲泊帕联合重组人血小板生成素治疗原发免疫性血小板减少症的临床观察[J]. 中国药房, 2023, 34 (23): 2910- 2914. doi: 10.6039/j.issn.1001-0408.2023.23.17
41	李亮, 卞建军, 苏玉璇, 等. 海曲泊帕乙醇胺片联合环孢素A治疗难治性免疫性血小板减少症的临床疗效及安全性[J]. 现代生物医学进展, 2024, 24 (24): 4695- 4699. doi: 10.13241/j.cnki.pmb.2024.24.021

Drug		Hetrombopag ^{[16, 26]}	Eltrombopag ^[27-28]	Avatrombopag ^{[27, 29, 30]}	Romiplostim ^{[27, 29, 31]}
TPO receptor binding form		Transmembrane	Transmembrane	Transmembrane	Intracellular
Main mechanism of action		Binds to the transmembrane domain of the TPO receptor, activates the signaling pathway, and promotes the proliferation and differentiation of megakaryocytes.			Fc peptide fusion protein, simulates TPO binding to receptors to activate signaling pathways
Dietary Influence		Yes	Yes	No	No
Method of administration		Oral	Oral	Oral	Intravenous/subcutaneous injection
Drug transformation/metabolism		Mainly metabolized through multiple glucuronide transferases.	Mainly metabolized by CYP1A2, CYP2C8, UGT1A1 and UGT1A3.	Mainly metabolized by CYP2C9 and CYP3A.	Cleared by the reticuloendothelial system via neonatal Fc receptors on endothelial cells.
ITP efficacy	Effectiveness	The efficiency of HETROM-2.5 is 58.9%, and the efficiency of HETROM-5 is 64.3%.	The response rate for patients with newly diagnosed or persistent ITP is 90%, the complete response rate is 75.9%, and the overall response rate for chronic ITP is about 50%-88%.	Compared with placebo, the platelet response rate of avatrombopag (20 mg/d) on day 8 was 65.63%.	Romiplostim can rapidly improve PLT, with an effective rate of 74%-93%. After the third week, about 62% of patients were still effective.
ITP efficacy	Median Time to onset	1-2 weeks	1-2 weeks	1-2 weeks	1-2 weeks
Adverse events	Thrombotic events	0.6%	6%	7%	5.9%
	Myelofibrosis risk	0.6%	The incidence was 6% during the two-year follow-up.	-	About 6.9% of patients with myelofibrosis grade 2 or higher.
	Elevated liver enzymes (≥3 grades)	0.4%	2%	-	-
	Pigmentation	-	3%-5%	-	-
	Cataract	0.4%	7%	-	The incidence was 9% at 8-year follow-up.

Drug		Hetrombopag ^{[16, 26]}	Eltrombopag ^[27-28]	Avatrombopag ^{[27, 29, 30]}	Romiplostim ^{[27, 29, 31]}
TPO receptor binding form		Transmembrane	Transmembrane	Transmembrane	Intracellular
Main mechanism of action		Binds to the transmembrane domain of the TPO receptor, activates the signaling pathway, and promotes the proliferation and differentiation of megakaryocytes.			Fc peptide fusion protein, simulates TPO binding to receptors to activate signaling pathways
Dietary Influence		Yes	Yes	No	No
Method of administration		Oral	Oral	Oral	Intravenous/subcutaneous injection
Drug transformation/metabolism		Mainly metabolized through multiple glucuronide transferases.	Mainly metabolized by CYP1A2, CYP2C8, UGT1A1 and UGT1A3.	Mainly metabolized by CYP2C9 and CYP3A.	Cleared by the reticuloendothelial system via neonatal Fc receptors on endothelial cells.
ITP efficacy	Effectiveness	The efficiency of HETROM-2.5 is 58.9%, and the efficiency of HETROM-5 is 64.3%.	The response rate for patients with newly diagnosed or persistent ITP is 90%, the complete response rate is 75.9%, and the overall response rate for chronic ITP is about 50%-88%.	Compared with placebo, the platelet response rate of avatrombopag (20 mg/d) on day 8 was 65.63%.	Romiplostim can rapidly improve PLT, with an effective rate of 74%-93%. After the third week, about 62% of patients were still effective.
ITP efficacy	Median Time to onset	1-2 weeks	1-2 weeks	1-2 weeks	1-2 weeks
Adverse events	Thrombotic events	0.6%	6%	7%	5.9%
	Myelofibrosis risk	0.6%	The incidence was 6% during the two-year follow-up.	-	About 6.9% of patients with myelofibrosis grade 2 or higher.
	Elevated liver enzymes (≥3 grades)	0.4%	2%	-	-
	Pigmentation	-	3%-5%	-	-
	Cataract	0.4%	7%	-	The incidence was 9% at 8-year follow-up.

Drugs	Year of publication	Number of patients (observation/control group)	Treatment regimen/dose	Duration of treatment	ITP efficacy	Adverse events
Hetrombopag	2021^[26]	424 (168/171/85)	Observation group: HETROM-2.5/5, which can be gradually adjusted to a maximum of 7.5 mg/d according to PLT. Control group: Treatment with placebo.	44 weeks	After 8 weeks of treatment, the effective rate of the three groups was 58.9% vs.64.3% vs.5.9%. Patients had a sustainable platelet response through 24 weeks, with a response rate of 39.9% at ≥75% visits and a median duration of overall response of 49.7%.	Adverse event rates were 91.7% vs. 94.7% vs. 95.3%.
Hetrombopag	2023^[32]	29	Hetrombopag 2.5-7.5 mg was subsequently adjusted to the maximum dose of 7.5 mg/d according to PLT.	1 month	The total effective rate was 79.3%, and the median onset time of hetrombopag was 9 (3-15) days. For patients with severe ITP, the overall response rate was 75%.	One case of elevated transaminase occurred during the treatment, and the overall adverse reactions were safe and controllable.
Hetrombopag	2024^[34]	63	The dose of eltrombopag before conversion was 25-75 mg/d, and the dose of hetrombopag was 2.5-7.5 mg/d after conversion.	24 weeks	After switching to hetrombopag, 88.9% (56/63) of patients achieved platelet response. Before switching, the platelet response rates for patients with platelet counts below 30×10?/L and between 30×10?/L and 50×10?/L were 66.7% (8/12) and 88.9% (8/9), respectively.	Treatment-related adverse events occurred in 50.8% of patients during eltrombopag treatment and 38.1% during hetrombopag treatment.
Hetrombopag +prednisone	2024^[36]	40 (20/20)	Observation group: hetrombopag (2.5 mg/d) combined with prednisone (0.5 mg/d) Control group: prednisone (0.5 mg/d)	6 weeks	The proportions of patients with PLT≥50×10?/L and ≥30×10?/L were 90% vs. 50% and 90% vs. 65%, respectively.	Adverse event rate was 50% vs. 60%.
Hetrombopag +prednisone	2024^[37]	82 (41/41)	Observation group: hetrombopag (2.5 mg/d) combined with prednisone (60 mg/d) Control group: prednisone (60 mg/d)	3 months	The total effective rate of the two groups was 95.12% vs. 80.49%.	Adverse event rate was 14.64% vs. 7.32%.
Hetrombopag+dexamethasone	2023^[38]	60 (30/30)	Observation group: hetrombopag (2.5-5 mg/d) combined with dexamethasone (20 mg/d, ivgtt). Control group: dexamethasone (20 mg/d, ivgtt).	12 weeks	The total efficiency of the two groups: 93.33% vs. 73.33%.	Adverse event rate was 20.00% vs. 16.67%.
Hetrombopag+rhTPO	2023^[39]	20	Hetrombopag (5 mg/d) combined with rhTPO (300 U·kg^-1·d^-1)	28 days	15% of patients had a partial platelet response, and 85% had a complete platelet response. The median time to reach PLT levels of 30×10?/ L, 50×10?/L, and 100×10?/ L was 4.5, 6 and 7 days, respectively.	Two patients had abnormal liver function, all grade 1-2.
Hetrombopag+rhTPO	2023^[40]	255 (98/157)	Observation group: hetrombopag (2.5 mg/d) combined with rhTPO (300 U·kg^-1·d^-1) Control group: rhTPO (300 U·kg^-1·d^-1)	21 days	The total efficiency of the two groups was 79.59% vs. 66.88%, the cumulative endpoint rate was 81.32% vs. 68.68%, and the median effective time was 8 d vs. 10 d.	Adverse event rate was 11.22% vs. 9.55%.
Hetrombopag+CsA	2024^[41]	52 (26/26)	Observation group: hetrombopag (7.5 mg/d) combined with CsA (3-5 mg/kg, bid) Control group: dexamethasone (40 mg/d) combined with rhTPO (15000 U)	2-20 months	The total effective rate was 73% in both groups. At 14 and 28 days of treatment, PLT in the observation group was significantly higher than that in the control group.	Adverse event rate was 35% vs. 46 %.

Drugs	Year of publication	Number of patients (observation/control group)	Treatment regimen/dose	Duration of treatment	ITP efficacy	Adverse events
Hetrombopag	2021^[26]	424 (168/171/85)	Observation group: HETROM-2.5/5, which can be gradually adjusted to a maximum of 7.5 mg/d according to PLT. Control group: Treatment with placebo.	44 weeks	After 8 weeks of treatment, the effective rate of the three groups was 58.9% vs.64.3% vs.5.9%. Patients had a sustainable platelet response through 24 weeks, with a response rate of 39.9% at ≥75% visits and a median duration of overall response of 49.7%.	Adverse event rates were 91.7% vs. 94.7% vs. 95.3%.
Hetrombopag	2023^[32]	29	Hetrombopag 2.5-7.5 mg was subsequently adjusted to the maximum dose of 7.5 mg/d according to PLT.	1 month	The total effective rate was 79.3%, and the median onset time of hetrombopag was 9 (3-15) days. For patients with severe ITP, the overall response rate was 75%.	One case of elevated transaminase occurred during the treatment, and the overall adverse reactions were safe and controllable.
Hetrombopag	2024^[34]	63	The dose of eltrombopag before conversion was 25-75 mg/d, and the dose of hetrombopag was 2.5-7.5 mg/d after conversion.	24 weeks	After switching to hetrombopag, 88.9% (56/63) of patients achieved platelet response. Before switching, the platelet response rates for patients with platelet counts below 30×10?/L and between 30×10?/L and 50×10?/L were 66.7% (8/12) and 88.9% (8/9), respectively.	Treatment-related adverse events occurred in 50.8% of patients during eltrombopag treatment and 38.1% during hetrombopag treatment.
Hetrombopag +prednisone	2024^[36]	40 (20/20)	Observation group: hetrombopag (2.5 mg/d) combined with prednisone (0.5 mg/d) Control group: prednisone (0.5 mg/d)	6 weeks	The proportions of patients with PLT≥50×10?/L and ≥30×10?/L were 90% vs. 50% and 90% vs. 65%, respectively.	Adverse event rate was 50% vs. 60%.
Hetrombopag +prednisone	2024^[37]	82 (41/41)	Observation group: hetrombopag (2.5 mg/d) combined with prednisone (60 mg/d) Control group: prednisone (60 mg/d)	3 months	The total effective rate of the two groups was 95.12% vs. 80.49%.	Adverse event rate was 14.64% vs. 7.32%.
Hetrombopag+dexamethasone	2023^[38]	60 (30/30)	Observation group: hetrombopag (2.5-5 mg/d) combined with dexamethasone (20 mg/d, ivgtt). Control group: dexamethasone (20 mg/d, ivgtt).	12 weeks	The total efficiency of the two groups: 93.33% vs. 73.33%.	Adverse event rate was 20.00% vs. 16.67%.
Hetrombopag+rhTPO	2023^[39]	20	Hetrombopag (5 mg/d) combined with rhTPO (300 U·kg^-1·d^-1)	28 days	15% of patients had a partial platelet response, and 85% had a complete platelet response. The median time to reach PLT levels of 30×10?/ L, 50×10?/L, and 100×10?/ L was 4.5, 6 and 7 days, respectively.	Two patients had abnormal liver function, all grade 1-2.
Hetrombopag+rhTPO	2023^[40]	255 (98/157)	Observation group: hetrombopag (2.5 mg/d) combined with rhTPO (300 U·kg^-1·d^-1) Control group: rhTPO (300 U·kg^-1·d^-1)	21 days	The total efficiency of the two groups was 79.59% vs. 66.88%, the cumulative endpoint rate was 81.32% vs. 68.68%, and the median effective time was 8 d vs. 10 d.	Adverse event rate was 11.22% vs. 9.55%.
Hetrombopag+CsA	2024^[41]	52 (26/26)	Observation group: hetrombopag (7.5 mg/d) combined with CsA (3-5 mg/kg, bid) Control group: dexamethasone (40 mg/d) combined with rhTPO (15000 U)	2-20 months	The total effective rate was 73% in both groups. At 14 and 28 days of treatment, PLT in the observation group was significantly higher than that in the control group.	Adverse event rate was 35% vs. 46 %.

[1]	YUE Zhaorong, XIE Fei, WANG Xin, LI Hongyu. Effect of lienal polypeptide injection on primary immune thrombocytopenia [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2021, 26(11): 1229-1236.
[2]	LI Jing, Ma Lijuan, YUAN Yuan, WANG Jie, YU Changzhi, ZHAO Jun. Relationship between gene polymorphism of inhaled glucocorticosteroids budesonide and efficacy in asthma [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2021, 26(11): 1250-1258.
[3]	LU Xiaohong，WANG Peiguang. Progress in the treatment of dermatomyositis [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2018, 23(7): 836-840.
[4]	ZHANG Zhe, SUN Li, YUAN Sheng-tao. Progress on researches for topotecan in combination drug therapy [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2015, 20(1): 106-111.
[5]	MENG Xiang-guang, NI Wen-qiong, WANG Chao, MA Deng-xuan, LI Zhi, ZHOU Hong-hao. Advances in pharmacogenetics of systemic therapies for psoriasis [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2012, 17(11): 1307-1313.
[6]	LI Dan-dan, LU Jin-ming. Advances of study on glucocorticoids in the treatment of rheumatoid arthritis [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2012, 17(1): 116-120.
[7]	WU Li-ping, LI Qi-xiong. Protective effects of quercetin on nephrotoxicity induced by cyclosporine A in rats [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2007, 12(6): 659-667.
[8]	ZHANG Ya-tong, YANG Li-ping, SHAO Hong, LI Ke-xin, SUN Chun-hua, SHI Lu-wen. Effects of different formulations of cyclosporine A on trough blood concentration in patients with myasthenia gravis [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2005, 10(8): 871-875.
[9]	YU Xi-chong, CHEN Xian-yan, ZHOU Hong-yu, LIN Dan, ZHU Tong-jun. Effects of combination of ketamine and N-acetylcysteine on brain damage following cerebral ischemia /reperfusion in mice [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2005, 10(4): 428-431.
[10]	ZHANG Ya-tong, YANG Li-ping, SHAO Hong, Li Ke-xin, SUN Chun-hua, SHI Lu-wen. Effects of MDR1 gene C3435T polymorphism on pharmacokinetics of cyclosporine A in myasthenia gravis patients [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2005, 10(2): 133-136.
[11]	CHAI Dong, WANG Rui,PEI Fei, FANG Yi, ZHUMan, WANG Zhong-Xiao. Combined effects of clarithromycin and gatifloxacin on experimentalPneumonia withPseudomonas aeruginosa in rats as a model for biofilm-associated infection [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2003, 8(6): 618-620.
[12]	GE Lin-Tong, LIN Li, ZHANG Jin. Analysis of the effect of the combination of radix salviae miltiorrhizaenovol-ten, diclofenac and soldium aescinate in treatment of severe migraine [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2002, 7(3): 250-251.
[13]	ZHENG Qing-Shan, SUN Rui-Yuan. Methods in analysis of the dynamics of drug interaction and its software CoDrug [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2002, 7(1): 81-85.
[14]	SONG Yi-Min, LI Xue-Kun, TAN Jan-Min, LI Zeng-Xi, SHI Shan. Effects of aspirin and verapamil alone or in combination on mesenteric microcirculation of rats¹ [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2001, 6(1): 31-34.
[15]	SONG Yi-Min, ZHOU Li, GAO Er. Effects of aspirin in combination with captopril on hemodynamics in anesthetized open chest dogs [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2000, 5(4): 320-322.