作者: Tumber, Anthony ; Brewitz, Lennart ; Salah, Eidarus ; Corner, Thomas P. ; Alshref, Faisal M. ; Nakashima, Yu ; Jabbary, Mohammadparsa ; Basak, Shyam ; Schnaubelt, Lara I. ; Schofield, Christopher J.

The 2-oxoglutarate (2OG)/Fe(II)-dependent γ-butyrobetaine hydroxylase (BBOX) catalyzes the final step in l-carnitine biosynthesis, i.e., stereoselective C-3 oxidation of γ-butyrobetaine (GBB). BBOX inhibition is a validated clinical strategy to modulate l-carnitine levels and to enhance cardiovascular efficiency. Reported BBOX inhibitors, including the clinically used cardioprotective agent Mildronate, manifest moderate inhibitory activity in vitro, limited selectivity, and/or unfavorable physicochemical properties, indicating a need for improved BBOX inhibitors. We report that the clinically used hypoxia-inducible factor-α prolyl residue hydroxylase (PHD) inhibitors Desidustat, Enarodustat, and Vadadustat efficiently inhibit isolated recombinant BBOX, suggesting that BBOX inhibition by clinically used PHD inhibitors should be considered as a possible off-target effect. Structure-activity relationship studies on the Desidustat scaffold enabled development of potent BBOX inhibitors that manifest high levels of selectivity for BBOX inhibition over representative human 2OG oxygenases, including PHD2. The Desidustat derivatives will help to enable investigations into the biological roles of l-carnitine and the therapeutic potential of BBOX inhibition.

2025-04-01·EXPERIMENTAL NEUROLOGY

Prolyl hydroxylase inhibitor desidustat improves stroke outcomes via enhancing efferocytosis in mice with chronic kidney disease

Article

作者: Pandey, Nilesh ; Frausto, Louise ; Yurdagul, Arif ; Magdy, Tarek ; Kidder, Evan ; Kaur, Harpreet ; Das, Sandeep ; Vikram, Ajit ; Martinez, Alexa ; Parmar, Deven V ; Jain, Mukul R ; Anand, Sumit Kumar ; Kansagra, Kevinkumar ; Richard, Koral S E ; Chandaluri, Lakshmi ; Trivedi, Ravi Kumar ; Patel, Vishal J ; Orr, A Wayne ; Shaaban, Nirvana ; Joharapurkar, Amit A ; Kumar, Dhananjay ; Patel, Harilal ; Rom, Oren ; Pandit, Rajan ; Dhanesha, Nirav ; Lu, Xiao-Hong ; Kshirsagar, Samadhan G

Patients with chronic kidney disease (CKD) are at a significantly increased risk of stroke and experience worse stroke outcomes and higher mortality. CKD exacerbates stroke risk and severity through a complex interplay of systemic inflammation, oxidative stress, and impaired clearance of uremic toxins, leading to neuroinflammation and microglial activation. Current acute ischemic stroke treatments, while effective in the general population, do not adequately address CKD-specific mechanisms, limiting their efficacy in this high-risk population. Prolyl hydroxylase domain (PHD) inhibitors have shown promise in treating anemia associated with CKD and may offer cerebroprotective benefits. However, the effects of PHD2 inhibition on long-term sensorimotor outcomes and the underlying mechanisms in mice with CKD remain largely unknown. Here, we investigated the impact of CKD on stroke severity and assessed the therapeutic potential of desidustat, a PHD inhibitor, in improving stroke outcomes. Using an adenine-induced CKD mouse model, we demonstrated that CKD exacerbated stroke-induced long-term sensorimotor deficits, increased neuroinflammation, and impaired microglial efferocytosis via dysregulation of the ADAM17-MerTK axis. Desidustat treatment in mice with CKD significantly improved long-term sensorimotor functional outcomes and reduced post-stroke neuroinflammation while enhancing microglial efferocytosis by reducing ADAM17 and enhancing microglial MerTK expression. In vitro studies using human-induced microglia-like cells further confirmed the ability of desidustat to enhance efferocytosis of apoptotic neurons by reducing the cleavage of MerTK. These findings suggest that desidustat may serve as a novel therapeutic strategy for improving stroke outcomes in patients with CKD, a population at high risk for stroke and poor functional recovery.

2025-04-01·DRUG DEVELOPMENT RESEARCH

HIF–Prolyl Hydroxylase Inhibitor Desidustat Increases Pyruvate Kinase Activity and Reduces Oxidative Stress in Red Blood Cells, Causes Erythrocytosis in Thalassaemic Mice, and Reduces Sickling in Sickle Cell Patient's Blood

Article

作者: Kshirsagar, Samadhan G. ; Savsani, Hardikkumar H. ; Patel, Maulik S. ; Rakhasiya, Milan H. ; Dodiya, Harshad S. ; Jain, Mukul R. ; Joharapurkar, Amit A. ; Patel, Vishal J.

ABSTRACT:

Sickle cell anemia and beta‐thalassemia are the major hemoglobinopathies associated with anemia. Bone marrow transplants or blood transfusion are frequently employed as treatment for these diseases, and erythropoietin analogues are sometimes used to boost erythropoiesis to compensate the destruction of RBCs. RBCs of hemoglobinopathy patients have reduced pyruvate kinase activity and increased oxidative stress, which makes the RBCs prone to destruction and precipitate vaso‐occlusive crises and pain. The objective of this study was to evaluate desidustat, a hypoxia inducible factor (HIF) stabilizer in beta thalassemic mice (B6.D2‐Hbbd3th/BrkJ) model, phenylhydrazine‐induced acute hemolysis in C57 mice model, and sodium metabisulfite‐induced sickling in sickle cell disease patient's blood. Desidustat treatment increased hemoglobin, RBCs, and hematocrit in both mice models. Desidustat treatment decreased iron overload, splenomegaly, and oxidative stress in phenylhydrazine‐induced hemolytic anemia in mice. Desidustat treatment increased pyruvate kinase activity in RBCs of human, mice, and rats in a dose‐dependent manner, and reduced sickling in SCD patients' RBCs. These data indicate that desidustat stimulates pyruvate kinase and attenuates oxidative stress in red blood cells, causes erythrocytosis in thalassemic mice, and reduces sickling in sickle cell patient's blood.

项与德度司他相关的新闻（医药）

2025-11-08

·ETPharma

Zydus gets USFDA's orphan drug designation for beta-thalassemia product

New Delhi: Zydus Lifesciences on Thursday said the US health regulator has granted Orphan Drug Designation ( ODD ) to Desidustat , a novel product for the treatment of beta-thalassemia. The US Food and Drug Administration ( USFDA ) grants orphan status to support development of medicines for the treatment of rare diseases that affect fewer than 2 lakh people in the US. "This Orphan Drug Designation from the USFDA underlines the urgent medical need to develop Desidustat to address beta-thalassemia," Zydus Lifesciences MD Sharvil Patel said in a regulatory filing. Beta thalassaemia patients have low levels of haemoglobin, which results in a lack of oxygen in many parts of the body, leading to weakness, fatigue and more serious complications. Treatment for people with beta thalassaemia often requires lifelong regimens of chronic blood transfusions for survival and treatment for iron overload due to the transfusions. Desidustat is a hypoxia inducible factor (HIF)-prolyl hydroxylase inhibitor (PHI) and has the potential to increase haemoglobin and red blood cell counts. This ODD provides eligibility for certain development incentives, including tax credits for qualified clinical testing, prescription drug user fee exemptions and a potential seven-year marketing exclusivity upon the USFDA approval. Zydus Lifesciences shares were trading 0.71 per cent down at Rs 965.95 apiece on BSE.

孤儿药

2025-09-29

·医脉通

NDD-CKD患者贫血治疗，新证据如何优化新策略？

贫血在慢性肾脏病（CKD）患者中很常见，而与透析依赖的CKD（DD-CKD）患者相比，非透析依赖的CKD（-CKD）患者的贫血风险更不容小觑，其患病率会随着CKD病程进展而逐渐升高。近年来，随着更多循证研究的发布，-CKD贫血患者的优化治疗策略也有许多可探讨之处。 -CKD患者贫血治疗任重道远，早诊早治不容忽视贫血严重影响-CKD患者的预后，是患者死亡的独立危险因素[1]。研究提示，我国-CKD患者贫血患病率为28.5%~94.9%[1]。其贫血并发症表现为“一高三低”的态势，即患病率高、知晓率低、治疗率低、达标率低。我国多中心横断面调查显示，随着CKD进展，贫血的知晓率逐渐增加，CKD 1~5期贫血知晓率分别为43.9%、55.2%、61.4%、73.2%和82.4%，贫血治疗率分别为19.4%、11.4%、26.9%、46.3%和73.0%[2]。如将血红蛋白（Hb）靶目标值定为110~120g/L，则仅有8.2%的患者达标，如果将Hb靶目标值定为100~120g/L，也仅有26.4%的患者达标[2]。因此，有必要加强肾性贫血的认知和宣传，提高公众对肾性贫血的认知水平，达到早诊早治的目的。立足循证，看-CKD肾性贫血治疗策略目前，我国近50%的-CKD患者在Hb<80g/L时才启动贫血治疗，近30%的患者甚至在Hb<70g/L时才开始干预[2]。有研究显示，与Hb水平在100-110g/L的患者相比，Hb<90g/L的患者发生肾脏事件*的风险显著升高（风险比2.52），90-100g/L的患者差异虽不显著但也呈风险更高趋势（风险比1.48），提示-CKD患者需尽早接受贫血治疗（表1）[3]。表1 开始接受贫血治疗的-CKD患者根据Hb水平分组后的肾脏事件*风险对比对于-CKD患者的贫血起始药物选择，权威指南给出了新建议。2024年ERA发布的HIF-PHI临床应用专家共识指出：低氧诱导因子-脯氨酰羟化酶抑制剂（HIF-PHI）可能更适用于和腹膜透析（PD）贫血患者起始治疗[4]，具体包括以下情况（图1）： ① 患者偏向于口服给药(可及性、便利性、易于管理、储存要求较低) ② 无法接受ESAs治疗(针头恐惧症、依从性较低) ③ 在使用铁剂或需要增加铁剂用量时，存在挑战 ④ ESA低反应或治疗不耐受 ⑤ 慢性炎症状态(CRP≥3mg/dL) 图1 对于-CKD或PD患者，可考虑使用HIF-PHI作为起始治疗的情况从循证证据来看，口服给药的HIF-PHI更易被患者接受。一项日本研究显示，在治疗开始后6个月停药的累计发生率来看，相较于ESA（91.8%）和静脉铁剂（97.5%）等治疗，HIF-PHI的停药发生率在数值上更低（46.4%），HIF-PHI组患者的平均Hb水平数值上更高[5]。近期也有研究提示，对于-CKD患者，HIF-PHI在降低铁调素方面比红细胞生成刺激剂（ESA）和安慰剂更具优势，可以通过改善铁代谢的机制综合改善贫血[6]。从药物机制来看，HIF-PHI通过抑制脯氨酰羟化酶（PH）的活性来抑制HIF的降解，稳定HIF-1α和HIF-2α的水平，增加促红细胞生成素（EPO）及其受体的产生和调节铁稳态，从而促进红细胞生成，同时还具有改善铁转运和铁利用率的作用，已被多项研究证实具有明确的贫血持续改善作用和治疗安全性[7]。 HIF-PHI和ESA之间或不同类型HIF-PHI之间对铁调素的影响是否具有差异，目前尚缺乏头对头研究数据。我国一项荟萃分析比较了五种HIF-PHI**、两种ESA和安慰剂对-CKD贫血患者中铁代谢的影响[6]，结果提示，与安慰剂相比，4种HIF-PHI可显著降低铁调素水平，且该4种HIF-PHI之间降低铁调素水平没有统计学差异（图2）。图2 不同干预措施中降低铁调素和提高Hb的有效性的成对比较下三角区域显示八种干预措施在降低铁调素有效性方面的两两比较结果，上三角区域显示八种干预措施在升高血红蛋白有效性方面的两两比较结果。当均数差的95%CI不包含0时，认为两种干预措施之间的差异具有统计学显著性。#，表示与安慰剂相比有显著差异。*，表示与ESA相比有显著差异。总结 -CKD患者接受贫血治疗的获益毋容置疑，然而其诊治现状仍有许多可改善之处，HIF-PHI因其口服优势、确切的疗效和安全性证据，通过多途径改善贫血，给患者带来生理和心理上的多种获益。希望通过合理应用此类药物，给-CKD贫血患者的治疗带来更有力的促进作用。 * 肾脏事件定义：开始肾脏替代治疗、血清肌酐水平翻倍，以及估算的肾小球滤过率低于6.0mL/min/1.73m²。 ** 包括罗沙司他、恩那度司他、达普度司他（Daprodustat）、伐达度司他（Vadadustat）、德度司他（Desidustat），后三者目前系中国大陆地区未获批产品。参考文献 1.金海姣,王琴,倪兆慧.非透析慢性肾脏病患者贫血长期管理的探索.中国实用内科杂志, 2023, 43(07): 556-559+566. 2.Li Y，Shi H，Wang WM，et al. Prevalence，awareness，and treatment of anemia in Chinese patients with nondialysis chronic kidney disease：First multicenter，cross- sectional study. Medicine（Baltimore），2016，95（24）：e3872. 3.Akizawa T, Tsubakihara Y, Hirakata H, et al. A prospective observational study of early intervention with erythropoietin therapy and renal survival in non-dialysis chronic kidney disease patients with anemia: JET-STREAM Study. Clin Exp Nephrol. 2016 Dec;20(6):885-895. 4.Stoumpos S, Crowe K, Sarafidis P, et al. Hypoxia-inducible factor prolyl hydroxylase inhibitors for anaemia in chronic kidney disease: a document by the European Renal Best Practice board of the European Renal Association. Nephrol Dial Transplant. 2024 Apr 4:gfae075. 5.Kuragano T, Okami S, Tanaka-Mizuno S, et al. Anemia Treatment, Hemoglobin Variability, and Clinical Events in Patients With Nondialysis-Dependent CKD in Japan. Kidney360. 2023 Sep 1;4(9):e1223-e1235. 6.Yang J, Xing J, Zhu X, et al. Effects of hypoxia-inducible factor-prolyl hydroxylase inhibitors vs. erythropoiesis-stimulating agents on iron metabolism in non-dialysis-dependent anemic patients with CKD: A network meta-analysis. Front Endocrinol (Lausanne). 2023 Mar 16;14:1131516. 7.中国医师协会肾脏内科医师分会肾性贫血指南工作组. 中国肾性贫血诊治临床实践指南[J]. 中华医学杂志,2021,101(20):1463-1502. 本材料由阿斯利康(中国)提供，仅供医疗卫生专业人士参考。审批编号CN-168752 过期日期：2025-12-24 撰写：ZCJ 审校：ZCJ 排版：Shelly 执行：Zelda 本平台旨在为医疗卫生专业人士传递更多医学信息。本平台发布的内容，不能以任何方式取代专业的医疗指导，也不应被视为诊疗建议。如该等信息被用于了解医学信息以外的目的，本平台不承担相关责任。本平台对发布的内容，并不代表同意其描述和观点。若涉及版权问题，烦请权利人与我们联系，我们将尽快处理。

临床终止临床结果临床研究CSCO会议

2025-09-26

·医脉通

DD-CKD患者贫血治疗新变革，HIF-PHI的应用探讨

我国透析患者总数近年增长迅速，依据中国大陆地区的最新透析数据统计结果：截至2024年12月，中国大陆地区登记的透析总人数已突破118万[1]。贫血是透析依赖的慢性肾脏病（DD-CKD）患者的常见并发症，数据提示，透析患者贫血患病率高达91.6%~98.2%[2]，其治疗仍有很大可改进之处。 Hb达标率，从现状到策略目前，肾性贫血的临床控制水平尚有很大改善空间。研究提示，在接受红细胞生成刺激剂（ESA）治疗的腹膜透析患者中，较低的血红蛋白水平与更高的全因死亡率显著相关。与血红蛋白（Hb）水平在110~120g/L的血液透析患者相比，Hb水平为100~＜110g/L、90~＜100g/L、≤90g/L的患者，其时间依赖性死亡风险分别升高12%、30%及38%，心血管死亡风险分别增加11%、37%和12%[3]。MAR研究[4]进一步提示，Hb水平可预测血液透析患者生存率和住院率：Hb<100g/L、100~110g/L、110~120g/L组的一年生存率相对风险（RR）依次为0.77、0.82和0.89，一年未住院RR分别为0.34、0.47和0.54；在多因素调整后该关联仍然显著。 ESA和铁剂治疗是肾性贫血常用治疗手段。ESAs可缓解慢性肾脏病（CKD）患者促红细胞生成素（EPO）缺乏，促进红细胞生成。近年来，长效ESAs在肾性贫血治疗中的临床应用取得了一定进展，但国内应用还处于起步阶段，临床证据较为有限[5]。口服铁剂适用于轻度肾性贫血或贫血纠正后的维持治疗；静脉铁剂因其高吸收率，可快速提升Hb水平，减少EPO用量和输血需求，并避免口服铁剂的胃肠道不良反应和吸收问题。透析患者往往存在ESA抵抗、功能性铁缺乏、微炎症等临床状态，增加贫血纠正难度。数据显示，约12.5%的DD-CKD贫血患者存在ESA低反应[6]，主要影响因素包括铁绝对/功能性缺乏、感染及微炎症状态、透析状态等，次要因素包括严重的继发性甲状旁腺功能亢进、抗体介导的纯红细胞再生障碍性贫血、合并肿瘤、应用血管紧张素转化酶抑制剂等。此时盲目增加ESA剂量并非优选策略，研究显示透析前3个月内ESA剂量＞10000 IU/周是中国血透患者全因死亡率的独立预测因子[7]。铁剂治疗亦存在局限：口服铁剂因吸收较差及胃肠道刺激性等，导致依从性低。静脉补铁则易造成铁超载、氧化损伤、增加感染风险等。因此，在贫血治疗中应注重基础疾病处理与病理状态纠正，避免盲目加药，需综合评估获益与风险，制定个体化方案。合理应用低氧诱导因子脯氨酰羟化酶抑制剂（HIF‐PHI）类药物可以更综合地改善铁代谢和铁利用，增加机体内源性EPO水平，多方面调控改善肾性贫血。多项证据提示，HIF-PHI有益于肾性贫血高效管理从首个HIF‐PHI在国内上市到目前已应用七年，已得到了较为广泛的临床应用。此类药物的优势主要集中于两大方面： ① 改善贫血机制 HIF‐PHI通过抑制PHD（脯氨酰羟化酶），稳定体内HIF水平，促进造血相关基因的转录及表达，从而提升机体内源性EPO生成及受体表达，促进与铁代谢相关蛋白的表达，同时降低铁调素水平，综合调控机体促进红细胞的生成[2]。 ② 用药方式 HIF‐PHI通过口服给药，避免了皮下或静脉注射，无需冷藏保存，使用更便利，可极大改善患者依从性。已有研究提示，在血液透析和腹膜透析患者中，HIF‐PHI均被证实可有效改善贫血，患者耐受性好[2,8]。此外，HIF-PHI疗效不受微炎症状态影响。荟萃分析[9]显示，在使用ESA的患者中，C反应蛋白（CRP）升高者的Hb应答率较低，且所需ESA剂量更高。包含7项随机对照研究的荟萃分析[10]显示：无论患者基线CRP水平如何，HIF-PHI均可有效改善贫血，且用药剂量并未因炎症状态而增加（图1）。另一项前瞻性研究的亚组分析则提示，在CRP升高（>4.9mg/L）的患者中，HIF-PHI组Hb升高幅度显著优于ESA组（0.9±1.0g/dl vs 0.3±1.1g/dl）[8]。安全性方面，一项同时涵盖透析和非透析人群的荟萃分析显示，HIF-PHI*与ESA的安全性相当，均可有效CKD患者Hb水平，降低铁调素并促进铁代谢[11]。图1：森林图显示CRP水平对HIF-PHI疗效的影响，按透析类型分组：对于透析和非透析患者，无论基线CRP水平高低，在Hb距基线变化（ΔHb）方面均无显著差异。总结中国DD-CKD患者的贫血治疗任重道远，在目前ESA及铁剂已充分应用的基础上，肾性贫血达标率仍有进一步的空间。HIF-PHI因其综合机制和口服便利性，成为改善肾性贫血的优选。基于不同药物的具体差异，仍需要综合考虑药物获批适应证、患者病情、治疗目标和相关循证证据等因素，做出个体化的治疗决策。 * 文章中纳入的HIF-PHI包括罗沙司他、恩那度司他、达普度司他（Daprodustat）、伐达度司他（Vadadustat）、德度司他（Desidustat），莫立司他（Molidustat），后四者目前系中国未获批产品。参考文献 1.2024CCBPC大会报道 2.中国医师协会肾脏内科医师分会肾性贫血指南工作组. 中华医学杂志,2021,101(20):1463-1502. 3.Molnar MZ, Mehrotra R, Duong U, et al.Clin J Am Soc Nephrol. 2011, 6(8): 1973-81. 4.Portolés J, López-Gómez JM, Aljama P. Nephrol Dial Transplant. 2007; 22(2): 500-7. 5. 中国非公立医院协会肾病透析专业委员会共识专家组. 中华肾脏病杂志, 2024, 40(2): 146-157. DOI: 10.3760/cma.j.cn441217-20231025-01037. 6.Luo J, Jensen DE, Maroni BJ, et al. Am J Kidney Dis. 2016 Nov;68(5):763-771. 7.Pan S, Zhao DL, Li P, et al. Blood Purif. 2022;51(2):171-181. 8.Chen N, Hao C, Liu BC, et al. N Engl J Med. 2019; 381(11): 1011-1022. 9.Zheng Q, Zhang P, Yang H, et al. Heliyon. 2023, 9(4): e15310. 10.Xiaoyu Luo,et al.BMC Nephrol.2024Feb5:25(1):47. 11.Ren S, Yao X, Li Y, Zhang Y, Tong C, Feng Y. Front Pharmacol. 2023 Nov 30;14:1296702. 本材料由阿斯利康(中国)提供，仅供医疗卫生专业人士参考。审批编号：CN-168751 过期日期：2025-12-24 撰写：ZCJ 审校：ZCJ 排版：Shelly 执行：Zelda 本平台旨在为医疗卫生专业人士传递更多医学信息。本平台发布的内容，不能以任何方式取代专业的医疗指导，也不应被视为诊疗建议。如该等信息被用于了解医学信息以外的目的，本平台不承担相关责任。本平台对发布的内容，并不代表同意其描述和观点。若涉及版权问题，烦请权利人与我们联系，我们将尽快处理。

临床研究临床结果

100 项与德度司他相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	德度司他	-	DB16135

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
慢性肾衰竭贫血	印度	Zydus Lifesciences Ltd.	2022-03-07

未上市

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适应症	最高研发状态	国家/地区	公司	日期
慢性肾病	申请上市	中国	康哲（湖南）制药有限公司	2024-04-23
新型冠状病毒感染	临床2期	墨西哥	Zydus Lifesciences Ltd.	2020-07-25
贫血	临床1期	美国	Zydus Lifesciences Ltd.	2022-04-25

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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


ASN2024	N/A	-	65	Desidustat	網艱繭築齋製鬱鬱憲壓(簾壓醖鹹簾鹹夢鑰艱築) = There were no major adverse events during the follow-up duration. 鏇製網鏇鑰構遞壓範廠 (窪構積廠鹽觸鹹遞顧簾 )	积极	2024-10-24
ASN2024	N/A	伴随慢性肾病的贫血	64	Desidustat 100 mg	淵顧夢憲鹹鹽壓廠艱築(獵糧鹽鹹艱鑰憲鑰範鹹) = There was statistically significant improvement in mean Hb (figure 1). In different category of EpO naïve Switched from EpO, DD vs ND rise of Hb was comparable. 齋構膚觸顧襯構遞衊艱 (鹽築繭鹹壓觸膚衊壓糧 )	积极	2024-10-24
ISN WCN2019	临床1/2期	慢性肾病	-	Desidustat 100 mg	顧夢築積膚醖構齋範壓(鏇廠窪壓構憲網遞簾齋) = 膚範製築艱鹽鏇觸淵夢艱顧觸顧膚膚遞繭鹽選 (淵憲齋糧醖廠膚遞鹽製, 170449.605) 更多	-	2019-07-01
				Desidustat 150 mg	顧夢築積膚醖構齋範壓(鏇廠窪壓構憲網遞簾齋) = 餘範餘鑰淵艱築夢憲積艱顧觸顧膚膚遞繭鹽選 (淵憲齋糧醖廠膚遞鹽製, 3358.696) 更多
CTRI/2017/05/008534 (Pubmed \| Am J Nephrol)	临床2期	贫血 \| 慢性肾病	117	Desidustat 100 mg	膚觸艱築積艱窪選網繭(鹹範願鑰夢壓艱製願糧) = 鹽築簾鬱範夢憲艱壓艱淵觸醖艱蓋製衊構壓淵 (願遞糧醖遞膚膚遞選蓋 )	-	2019-01-01
				Desidustat 150 mg	膚觸艱築積艱窪選網繭(鹹範願鑰夢壓艱製願糧) = 壓獵廠鑰顧選繭憲構窪淵觸醖艱蓋製衊構壓淵 (願遞糧醖遞膚膚遞選蓋 )
ACTRN12614001240639 (Pubmed \| Clin Pharmacokinet)	临床1期	-	100	ZYAN1 10 mg	觸選憲獵夢獵齋選鹽鏇(餘窪齋鑰淵積選壓繭築) = 夢積壓淵製蓋壓衊齋遞選淵鬱繭網積觸鏇襯觸 (積顧鹽餘鑰憲構範壓築 ) 更多	-	2018-01-01
				ZYAN1 25 mg	觸選憲獵夢獵齋選鹽鏇(餘窪齋鑰淵積選壓繭築) = 繭繭繭繭構遞築鏇鏇獵選淵鬱繭網積觸鏇襯觸 (積顧鹽餘鑰憲構範壓築 )