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更新于：2026-04-03

Ketoconazole

酮康唑

更新于：2026-04-03

概要

基本信息

简介酮康唑是一种小分子化合物，可作为 CYP51A1 的抑制剂。该药物由著名的 Janssen Pharmaceutica NV 开发，于 1981 年 6 月首次获得批准。作为 CYP51A1 的抑制剂，其作用机制取决于抑制真菌酶羊毛甾醇 14α-脱甲基酶。后者在麦角甾醇的合成中起着不可或缺的作用 - 麦角甾醇是真菌细胞膜的基本成分。通过阻止这种关键的酶活性，酮康唑有效地破坏了真菌的生长，最终导致它们的死亡。值得注意的是，酮康唑可作为多种真菌感染的有效治疗选择，涵盖从皮肤感染到全身感染，包括头发和指甲。尽管最近副作用相对较少的抗真菌药物在很大程度上取代了酮康唑，但该药物在某些情况下仍具有重要意义，例如当替代治疗方式失败或存在禁忌症时。最终，酮康唑作为真菌感染管理中的关键治疗干预措施得以持续。

药物类型

小分子化药

别名

KCZ、Ketoconazole (JP17/USP)、Ketoconazole Cream

+ [21]

靶点

C14DM

作用方式

拮抗剂

作用机制

C14DM拮抗剂(C14DM拮抗剂)、咪唑类抗真菌药

治疗领域

感染内分泌与代谢疾病皮肤和肌肉骨骼疾病+ [2]

在研适应症

内源性库欣综合征头皮屑脂溢性皮炎+ [11]

非在研适应症

晚期癌症着色霉菌病转移性肿瘤+ [2]

原研机构

Janssen Pharmaceutica NV

在研机构

Teikoku Seiyaku Co. Ltd.

西安杨森制药有限公司

Iwaki Seiyaku Co., Ltd.

+ [3]

非在研机构

Janssen Pharmaceuticals, Inc.Janssen Research & Development LLCJohnson & Johnson Pharmaceutical Research & Development LLC

+ [2]

权益机构

Janssen Pharmaceuticals, Inc.

STADA Arzneimittel AG

HRA Pharma Development SARL

+ [4]

最高研发阶段批准上市

首次获批日期

美国 (1981-06-12),

着色霉菌病球孢子菌病组织胞浆菌病+ [1]

最高研发阶段(中国)批准上市

特殊审评孤儿药 (美国)、孤儿药 (欧盟)

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结构/序列

分子式C26H28Cl2N4O4

InChIKeyXMAYWYJOQHXEEK-MKNUCDGGSA-N

CAS号65277-42-1

关联

192

项与酮康唑相关的临床试验

ISRCTN15840647

/ Recruiting临床4期

A Phase IV, randomized, single-blinded study to evaluate the efficacy and safety of ketoconazole 2% shampoo + conditioner vs ketoconazole 2% shampoo alone in adults with seborrheic dermatitis

开始日期2026-03-03

申办/合作机构

STADA Arzneimittel AG

NCT07333170

/ Not yet recruiting临床4期IIT

Comparison of the Efficacy of Topical Luliconazole 2% Cream vs Topical Ketoconazole 1% Cream in the Treatment of Pityriasis Versicolor.

Pityriasis versicolor is a common superficial fungal infection caused by Malassezia species, characterized by hypo- or hyper-pigmented scaly patches on the skin. Topical antifungal agents are the mainstay of treatment. Ketoconazole has been widely used; however, newer agents such as luliconazole may offer improved efficacy and shorter treatment duration. This randomized controlled study aims to compare the efficacy and safety of topical luliconazole versus topical ketoconazole in patients with pityriasis versicolor. Treatment response will be assessed clinically and mycologically to determine comparative outcomes.

开始日期2026-02-01

申办/合作机构-

NCT07471178

/ Not yet recruiting临床4期IIT

Mycological Efficacy and Safety of Ketoconazole 2% Shampoo With a Seven-Day Versus Three-Day Treatment Duration in Pityriasis Versicolor: A Double-Blind Randomized Clinical Trial

The goal of this clinical study is to find out whether using ketoconazole 2% shampoo for seven days works better than using it for three days in treating pityriasis versicolor. The study will also evaluate the safety of both treatment durations.
The main questions this study aims to answer are:
* Does treatment with ketoconazole 2% shampoo for seven days result in better mycological efficacy compared with three days of treatment in patients with pityriasis versicolor?
* Does treatment with ketoconazole 2% shampoo for seven days lead to better clinical improvement compared with three days of treatment?
* Are there differences in side effects between the seven-day and three-day ketoconazole 2% shampoo treatment regimens?
* Are there differences in dermoscopic features of pityriasis versicolor before and after treatment with ketoconazole 2% shampoo when used for seven days compared with three days?

开始日期2026-02-01

申办/合作机构

Fakultas Kedokteran, Universitas Indonesia

100 项与酮康唑相关的临床结果

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100 项与酮康唑相关的转化医学

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100 项与酮康唑相关的专利（医药）

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10,547

项与酮康唑相关的文献（医药）

2026-05-01·DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE

Molecular identification and pathogenicity confirmation of multi-azole resistant Malassezia species isolated from dandruff infected individuals prevailing in Mysuru, India

Article

作者: S, Mahadeva Murthy ; C, Sowrabha

Worldwide distribution of dandruff associated scalp infections is caused by lipophilic Malassezia spp. This rationale lead the study to investigate the prevalence and etiologic species in a cross-sectional study involving 300 subjects who visited dermatology hospitals to seek treatment in K.R. Hospital, JSS Hospital and CSI Holdsworth Memorial Mission Hospital, Mysuru region, Karnataka, India. With the consent of participants, dandruff flakes samples were collected. The presence of Malassezia spp. were assessed by morphological and biochemical characterization, where six major yeast groups M. furfur (36%), M. globosa (21%), M. restricta (18%), M. sympodialis (12%), M. japonica (8%) and M. obtusa (5%) causing dandruff were found to be present in 79.6% of collected test samples. High resistant patterns to antimycotic data of minimal inhibitory concentration (MIC90) to Fluconazole, Ketoconazole and Miconazole indicated the emergence of multi azole resistant Malassezia spp. The isolates being pathogenic was hemolysis positive. The dandruff specific isolates M. furfur, M. restricta and M. globosa exhibited typical phospholipase activity indicating the pan-genome attributes for inducing severe itching along with scalp infections in infected individuals. It was evident from SEM data that Malassezia spp. had characteristics of yeast like structure with collarets appearing during blastospore formation. Further with M13RAPD-PCR, ITS-PCR, epidemiological specificity and genotypic relatedness of isolates to Malassezia spp. was confirmed and 18S rDNA sequences were submitted to NCBI database with the accession numbers PP189840 to PP189845. The data acquired during study can be of prime diagnostic method for timely management and accurate analysis of dandruff caused by Malassezia spp. at global settings.

2026-04-01·VETERINARY RESEARCH COMMUNICATIONS

Emergence of Fusarium oxysporum infection in farmed Labeo rohita: Isolation, growth requirements, antifungal response, and pathogenic potential

Article

作者: Dekari, Debojit ; Chouhan, Nayan ; Shah, Tarang Kumar ; Saha, Himadri ; Mohapatra, Subhransu

Fusarium oxysporum, was isolated from a naturally infected captive-reared Labeo rohita in Tripura, India. The infected fish exhibited clinical signs of fungal growth with haemorrhage on the ventral body surface and erosion of the caudal fin. Morphological identification of fungal colony, including microscopic observation of 5-day-old culture, revealed the presence of multi-septate macroconidia and one-septate microconidia. Growth requirement study revealed that the fungus grew best at 30 °C and pH 6.0. In vitro studies revealed that the isolate produced extracellular enzymes such as caseinase, lipase, starch hydrolase and DNase, which contributed to its pathogenicity. The partial 18 S gene sequence was assigned NCBI accession number PQ013739.1 and confirmed its identity as F. oxysporum. Pathogenicity test by intraperitoneal injection of fungal spore suspension in healthy L. rohita fingerlings with fungal growth at the site of injection; LD₅₀ value obtained by probit analysis was 4.85 × 10⁷ spores/ml. Antifungal susceptibility testing indicated that none of amphotericin B, ketoconazole, itraconazole, clotrimazole, and nystatin produced zones of inhibition against the fungal isolate. In contrast, the fungus exhibited sensitivity to sodium chloride and copper sulfate, with reduced radial growth at salinity levels exceeding 0.5% and CuSO₄ concentrations above 25 ppm. Our findings confirm that the F. oxysporum strain is virulent to L. rohita, and highlights the potential utility of salinity and copper sulfate-based management strategies for control of this fungus in aquaculture.

2026-03-01·EUROPEAN JOURNAL OF PHARMACEUTICS AND BIOPHARMACEUTICS

Enhancing bioavailability of a weakly basic drug through cocrystallization: PBPK modeling of ketoconazole–succinic acid

Article

作者: Santos Goes, Ana Karolina ; Oliveira, Paulo Renato ; de Moraes, Natalia Valadares ; Kowthavarapu, Venkata Krishna ; Soliman, Amira

Pharmaceutical cocrystals, formed by combining an active pharmaceutical ingredient (API) with a suitable coformer, offer a promising strategy to enhance drug solubility, stability, and dissolution, thereby improving absorption and bioavailability without altering pharmacological properties. This approach is particularly advantageous for poorly soluble drugs such as ketoconazole (KTZ), a BCS Class II compound characterized by dissolution-limited absorption and variable oral bioavailability. As a weak dibasic drug, KTZ exhibits pH-dependent dissolution, which was favored under acidic gastric conditions. To overcome the pH-dependent dissolution, a cocrystal of KTZ with succinic acid (SA) was developed and a physiologically based pharmacokinetic (PBPK) approach informed by in vitro solubility and dissolution data was used to predict KTZ plasma concentration profiles, following administration of KTZ or KTZ-SA cocrystal. The developed PBPK model was verified, with a predicted/observed AUC ratio within a 2-fold range for KTZ. The model successfully captured the reduced exposure to KTZ when administered with omeprazole. PBPK simulations demonstrated a reduced KTZ exposure following a 200 mg dose under achlorhydric conditions (AUC: 1.1 µg·h·mL-1) or with omeprazole administration (AUC: 3.1 µg·h·mL-1), compared to healthy subjects (AUC: 12.2 µg·h·mL-1). In contrast, KTZ-SA cocrystal achieved consistently similar exposure in healthy subjects (AUC: 17.2 µg·h·mL-1), achlorhydric populations (AUC: 18.6 µg·h·mL-1), or when coadministered with omeprazole (AUC: 16.9 µg·h·mL-1). This model-based approach has demonstrated the potential of KTZ-SA cocrystal to enhance bioavailability in populations with achlorhydria-related disparities, effectively addressing the challenges posed by variable gastric acidity. The findings support the development of pharmaceutical cocrystals to optimize drug delivery and maximize therapeutic outcomes.

383

项与酮康唑相关的新闻（医药）

2026-04-02

·国际糖尿病idiabetes

朱虹教授：异位ACTH综合征的识别与管理

点击“蓝字”关注我们编者按：在库欣综合征（CS）这一充满挑战的课题中，异位促肾上腺皮质激素（ACTH）分泌综合征（EAS）无疑是最为诡谲多变、诊断最为棘手的一类，约占ACTH依赖性库欣综合征病例的10%~20%。其由垂体以外的肿瘤异常分泌ACTH引发，原发灶隐匿多变（从小细胞肺癌到罕见神经内分泌肿瘤），若不及时定位，可致严重并发症甚至危及生命。近日，在2026华东内分泌代谢病学术年会上，来自温州医科大学附属第一医院内分泌科朱虹教授发表了演讲——《异位ACTH综合征的识别与管理》，借助一例极具代表性的病例：一位年轻女性，历经数年高血压、高血糖困扰，最终被确诊为由极罕见的阑尾神经内分泌肿瘤引起的异位ACTH综合征，从筛查、定性、定位到治疗的全流程。本文将为大家深度剖析其诊断迷局与治疗策略。朱虹教授温州医科大学附属第一医院医学博士、主任医师、教授、博士生导师温州医科大学附属第一医院内分泌科主任中华医学会糖尿病学分会委员中华医学会糖尿病学分会糖尿病足与周围血管病变学组委员浙江省预防医学会糖尿病预防与控制专业委员会副主任委员浙江省医学会内分泌学分会常务委员浙江省医师协会内分泌代谢科医师分会常委温州市糖尿病研究重点实验室主任温州市医学会内分泌分会副主任委员主持国家自然科学基金项目、浙江省自然科学基金项目等一什么是EAS？ EAS是指垂体以外的肿瘤自主分泌过量ACTH，刺激肾上腺皮质增生、皮质醇分泌过多，进而引发库欣综合征的疾病[1,2]。其核心病理机制在于：垂体以外的肿瘤组织因POMC基因异常激活，不受高皮质醇血症的负反馈抑制，持续分泌ACTH，打破了正常的下丘脑-垂体-肾上腺轴（HPA轴）调节机制，导致双侧肾上腺皮质增生，皮质醇水平异常升高，引发全身代谢紊乱。与库欣病（垂体源性）不同，库欣病的ACTH来源于垂体且受反馈调节；而EAS的肿瘤来源广泛且不受反馈调节，因此病情往往更为凶险[1,2]。EAS约占ACTH依赖性库欣综合征的10%～20%，是临床中不容忽视的病因[2]。该病好发于40~50岁人群，女性略多于男性（比例约1~2:1）。原发肿瘤类型多样，其中以肺部肿瘤最为常见，包括支气管神经内分泌肿瘤（20%～40%）和小细胞肺癌（10%～40%）；其次为胰腺（10%～20%）和胸腺（5%～10%）神经内分泌肿瘤，以及甲状腺髓样癌、嗜铬细胞瘤等。值得注意的是，EAS的诊断极具挑战性，即便经过全面检查，仍有10%～20%的病例无法定位原发灶，被称为隐匿性EAS[2,3]。二 EAS有什么临床特征？ 1 典型库欣综合征表现[2] 患者通常表现为向心性肥胖、满月脸、水牛背、皮肤菲薄、宽大紫纹、多血质外貌等经典体征。 2 高皮质醇相关并发症[2] 常伴重度高血压、高血糖/糖尿病、低血钾、代谢性碱中毒、骨质疏松、神经精神症状等。 3 EAS的特异性表现[2] 与垂体源性库欣病相比，EAS的症状通常更严重、进展更迅速。肌无力和低血钾的症状尤为突出，部分患者甚至因严重的低钾血症麻痹而首发就诊。体型差异：部分恶性程度高的EAS患者（如小细胞肺癌所致），由于消耗极大，可能无典型库欣体型，反而呈现消瘦状态，极易误导诊断。色素沉着：由于ACTH水平极高，部分患者可出现明显的皮肤黏膜色素沉着。三 EAS如何识别与诊断临床中，EAS的临床筛查流程共分为3步：第一步：怀疑与识别，即对具有典型症状（如向心性肥胖、紫纹）或高危因素的患者保持高度警惕；第二步：通过24小时尿游离皮质醇（UFC）、午夜唾液（或血）皮质醇及1 mg地塞米松抑制试验（LDDST）进行筛查，至少两项阳性方可确诊高皮质醇血症；第三步：明确ACTH依赖性，测定血浆ACTH水平是关键分水岭，若ACTH>20 pg/ml则提示为ACTH依赖性（垂体或异位来源）。在鉴别库欣病与EAS时，《库欣病诊治专家共识（2025）》及2023年《柳叶刀》（The Lancet）发表的《库欣综合征》综述均提供了明确的诊疗流程图（图1），为临床决策提供了重要依据。图1. 诊断及鉴别要点：库欣病 vs. 异位ACTH综合征在肿瘤定位技术中，传统影像学（CT/MRI）筛查作为基础手段，是临床常规检查，设备普及度高，检查流程标准化，结果易于解读，对直径大于1 cm的肿瘤（如支气管或胸腺类癌）检出率高且技术成熟。但在面对直径小于1 cm的微小隐匿灶或位置隐蔽的肿瘤（如胰腺、肠道、卵巢）时，常因敏感性不足而出现假阴性，且对于位置隐蔽的肿瘤（如胰腺、肠道、卵巢等部位），难以通过单纯的形态学特征明确其性质和来源。此时，功能影像学成为破局关键。68Ga- DOTATATE PET-CT通过特异性结合神经内分泌肿瘤高表达的SSTR 2受体，实现靶向显像，具有更高的灵敏度和特异性，能够精准识别微小的肿瘤病灶。有前瞻性研究显示，68Ga-DOTATATE PET-CT和18F-DOPA PET-CT存在互补性，通过增加结构扫描的灵敏度和检测到的病灶的阳性预测值来改善肿瘤检测[4,5]。基于此，朱教授分享了一例典型病例：一位26岁的温州女性，其病程迁延五年且屡遭忽视——早在2019年妊娠期，患者便已出现重度高血压与高血糖，却未引起足够重视。2024年9月再次妊娠时，因严重低钾血症（2.85 mmol/L）及皮质醇、ACTH升高疑诊库欣综合征，虽当时影像学阴性但仍被迫引产，且术后药物控制不佳；2025年曾尝试司美格鲁肽治疗肥胖无效，终因难治性高血压于同年9月再次就诊。入院查体可见典型库欣面容（满月脸、痤疮、多毛、皮肤菲薄、宽大紫纹）及特征性色素沉着，体重指数（BMI）28.4 kg/m2，血压137/100 mmHg。生化检查定性：24小时尿游离皮质醇显著升高（2938.51 nmol），1 mg地塞米松抑制试验不能抑制，基础ACTH水平提示ACTH依赖性，且大剂量地塞米松抑制试验显示皮质醇抑制率<50%。在垂体、肾上腺及腹部常规MRI均呈阴性的困境下，功能影像学实现突破：2025年9月22日的[18F]AlF-NOTA-Octreotide PET-CT清晰地显示阑尾增粗伴结节，SUVmax高达16.7，强烈提示阑尾神经内分泌肿瘤。随后小肠增强三维重建CT进一步证实阑尾区存在24 mm×13 mm明显强化的软组织影，最终成功锁定病灶。四 EAS如何治疗？在库欣综合征诊疗中，核心目标是快速控制高皮质醇血症、根治原发肿瘤及管理并发症，延长生存期以提升生存质量。治疗遵循“先控症、后根治、长随访”的阶梯策略，并依托多学科协作（MDT）制定个体化方案。 1 手术治疗：首选根治手段手术治疗作为EAS的首选根治手段，需根据肿瘤可切除性及患者整体状况进行个体化决策：根治性手术：对于定位明确、体积小且无远处转移的患者，首选胸腔镜或腹腔镜微创手术彻底清除肿瘤，力争生化缓解。术后需严密监测激素水平，警惕肾上腺危象并及时补充糖皮质激素。姑息性干预：若原发灶无法切除或已广泛转移，可选择双侧肾上腺切除术以迅速控制高皮质醇血症（需终生激素替代），或行肿瘤减瘤术（晚期或身体状况较差者）以减轻负荷、缓解症状、改善生活质量。 MDT协同：围手术期由内分泌科评估生化状态，外科主导手术执行，影像科提供精准定位与随访，三方闭环协作确保诊疗安全高效。 2 药物治疗：重要的辅助与桥接[2,6-8] 对于无法手术、肿瘤未定位、术后复发转移或术前需快速控制病情的患者，药物治疗至关重要。根据作用机制不同，主要药物类别包括：类固醇合成抑制剂（如酮康唑、美替拉酮、奥西卓司他）：直接抑制皮质醇合成，快速降低激素水平；其中奥西卓司他为新型11β-羟化酶抑制剂，口服方便、起效快，是EAS推荐的重要选择；糖皮质激素受体拮抗剂（如米非司酮、瑞拉可兰）：阻断皮质醇作用，缓解代谢与精神症状；生长抑素类似物（如奥曲肽、帕瑞肽）：用于异位ACTH综合征，抑制肿瘤分泌与增殖；靶向药（如舒尼替尼、塞普替尼）：针对特定分子靶点，控制肿瘤进展并间接调控激素。 3 其他治疗手段除手术与药物外，放射治疗和核素靶向治疗为特定患者提供重要补充：立体定向放疗（SBRT）：适用于局部晚期或术后残留肿瘤，通过高精度照射有效控制病灶、降低ACTH分泌，尤其适合无法再次手术者；肽受体放射性核素治疗（PRRT）：针对表达生长抑素受体的神经内分泌肿瘤转移灶，用于化疗无效的转移性EAS患者，可实现精准内照射、延缓进展。随后，朱教授详细阐述了患者的后续诊疗经过。患者入院初期血压波动显著，经苯磺酸氨氯地平调控稳定后，于2025年10月16日接受了腹腔镜下回盲部病损切除术。术中探查发现阑尾处有一枚约2 cm×2.5 cm的肿瘤，并伴有侧腹壁粘连。术中冰冻及术后石蜡病理均确诊为阑尾神经内分泌瘤（NET G1），免疫组化结果证实ACTH阳性、Ki67指数约2%，且手术切缘阴性。术后疗效立竿见影，激素水平迅速回落：首日皮质醇即骤降至24.4 nmol/L，ACTH降至<1.5 ng/L，标志着异位库欣综合征实现了生化治愈。在术后糖皮质激素替代治疗的辅助下，患者血压恢复正常并成功停用降压药。截至术后5个月随访，患者体态显著改善，紫纹明显变淡，各项监测指标持续稳定，整体预后良好。五结语朱教授系统阐述了EAS的识别要点与管理策略，并结合一例阑尾神经内分泌瘤致EAS的典型病例，予以生动阐释。该病极为罕见（全球仅报道约十余例），好发于年轻女性，因症状隐蔽极易误诊，需依赖功能显像（如68Ga-SSTR-PET/CT）精准定位[9,10]。其管理核心在于：早期识别提升警觉、精准定位捕捉隐匿灶、多学科协作优化路径、个体化治疗改善预后。未来，液体活检与新型靶向药将带来新突破。唯有践行“早诊、精治、共管”策略，方能显著提升患者生存质量与长期预后。参考文献（上下滑动可查看） 1.Nieman LK, et al. Endocr Rev. 2022 Sep 26;43(5):852-877. 2.Gadelha M, et al. Cushing's syndrome. Lancet. 2023 Dec 9;402(10418):2237-2252. 3.agnarsson O, et al.Trends Endocrinol Metab. 2024 Apr;35(4):347-360. 4.Elenius H, et al. J Clin Endocrinol Metab. 2025 Oct 16;110(11):e3794-e3802. 5.Diwaker C, et al. Clin Nucl Med. 2019 Nov;44(11):881-882. 6.Dillon BR, et al. Drugs. 2025 Oct;85(10):1207-1230. 7.Duggan S. Osilodrostat: First Approval. Drugs. 2020 Apr;80(5):495-500. 8.Feelders RA, et al. Lancet Diabetes Endocrinol. 2019 Apr;7(4):300-312. 9.Zhao YX, et al. Front Endocrinol (Lausanne). 2022 Feb 18;13:808199. 10.Desai R, et al. JCEM Case Rep. 2025 Aug 1;3(9):luaf171. 声明：本文仅供医疗卫生专业人士了解最新医药资讯参考使用，不代表本平台观点。该等信息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，如果该信息被用于资讯以外的目的，本站及作者不承担相关责任。最新《国际糖尿病》读者专属微信交流群建好了，快快加入吧！扫描左边《国际糖尿病》小助手二维码（微信号：guojitnb），回复“国际糖尿病读者”，ta会尽快拉您入群滴！（来源：《国际糖尿病》编辑部）版权声明版权属《国际糖尿病》所有。欢迎个人转发分享。其他任何媒体、网站未经授权，禁止转载。

2026-04-01

·有临医药

药物相互作用（DDI）研究中的临床药理考量

OPINION 有临观点 MEDICAL 药物-药物相互作用（DDI）研究是新药安全性和有效性评价的关键环节，其研究结果直接影响药品说明书中的剂量调整、合并用药禁忌乃至上市决策。临床DDI研究的科学性与试验设计的严谨性、剂量选择的合理性密切相关。有临医药临床药理团队，可在研究启动前基于药物的ADME（吸收、分布、代谢、排泄）特征进行精准的风险评估与模型引导的DDI研究设计，从而确保临床DDI研究既符合监管要求，又兼具科学性与执行效率。本篇将从临床药理角度出发，系统论述了临床DDI研究的总体策略、主要试验设计类型及其适用场景，重点探讨了受试药物和相互作用药物的剂量确定原则，并结合最新研究进展和法规要求，提出了优化DDI研究设计的综合考量。引言在临床实践中，参与者合并使用多种药物的情况极为普遍。当一种药物的药代动力学（PK）或药效学（PD）特征被另一种药物改变时，即发生药物-药物相互作用。这种相互作用可能导致药物暴露量出现数量级的变化，引发严重的毒性反应或治疗失败。经典的案例包括：抗真菌药酮康唑（CYP3A4强抑制剂）与特非那定合用导致的心脏毒性，以及利福平（强诱导剂）导致的口服避孕药失效等。因此，在新药研发过程中，系统评估其作为“受变药”（即被其他药物影响）和促变药（即影响其他药物）的潜力，是临床药理学的核心任务之一。临床DDI研究遵循从体外到体内、从探索到确证的逻辑路径。国际人用药品注册技术协调会（ICH）及相关监管机构（如FDA、EMA、NMPA）发布的指导原则均强调，研究应从体外试验起步，利用人肝细胞、肝微粒体或重组酶等系统，初步判断药物是否为代谢酶（主要是CYP450酶系）或转运体（如P-gp、OATP1B1）的底物、抑制剂或诱导剂。基于体外抑制常数（Ki）与体内游离药物浓度（Imax,u）的比值等基础模型，可预测临床发生DDI的风险。若预测结果显示存在潜在风险（如R值≥1.02），则需要进一步采用静态机理模型、生理药代动力学（PBPK）模型或直接开展临床DDI研究进行评估。临床DDI研究的设计核心在于如何准确、灵敏地量化这种相互作用,涉及试验类型的选择（如交叉设计还是序贯设计）、参与者的选择（通常为健康志愿者以控制变异度）、给药方案的确定（单次还是多次给药）、采血点的设置（需覆盖3-5个半衰期）以及最关键的问题——剂量的选择。本文将围绕这些临床药理考量展开详细论述。临床DDI研究的设计要素临床DDI试验的核心设计要素 1.主要试验设计类型根据药物的PK特性和研究目的，临床DDI研究通常采用以下几种设计：随机交叉研究：这是评估短期半衰期药物与特定抑制剂相互作用的理想设计。试验参与者随机分为两组，一组先接受受试药物（A）单独给药，后接受受试药物联合抑制剂（A+I）；另一组则顺序相反，中间设置足够的清洗期。这种设计的优点是可以减少个体间变异，统计学效能较高。序贯交叉研究（固定序列设计）：这是最常见的设计类型。所有试验参与者先接受受试药物单独给药，经过清洗期后，再接受抑制剂多次给药至稳态，然后再次给予受试药物。该设计适用于大多数半衰期合理（通常≤3天）的药物，操作相对简单。评估诱导剂（如利福平）的研究通常也采用此设计，即先给予受试药物基线，然后给予诱导剂数日（如7-14天），再联合给予受试药物。平行设计：当受试药物或抑制剂的半衰期极长（如抗体偶联药物、某些长效制剂），或清洗期不可行时，需采用平行组设计。一组单独接受受试药物，另一组接受受试药物联合相互作用药物。这种设计需要更大的样本量来克服个体间变异的影响。 2.研究对象与采样策略绝大多数DDI研究在健康志愿者中进行，以排除疾病状态的混杂因素。但对于细胞毒性抗肿瘤药物，有时不得不采用患者人群。血样采集时间点必须足够长，以确保在抑制剂存在（可能延长受试药物半衰期）和不存在的情况下，均能完整描述3-5个半衰期的药时曲线。临床 DDI 研究设计的关键临床药理考量 1.相互作用药物（促变药）方案相互作用药物（促变药）的选择需严格遵循强效性、选择性、临床相关性和安全性。抑制剂需能使目标酶活性降低≥80%（对应底物药AUC增加≥5倍），诱导剂需能使酶活性提升2倍以上（对应底物药AUC降低≥50%），确保充分暴露相互作用潜力；同时需尽量减少对非目标酶/转运体的干扰，避免多靶点作用混淆研究结果；优先选用临床常用、相互作用特征明确的药物（如CYP3A抑制剂首选伊曲康唑，诱导剂首选利福平）。当研究药物涉及多条代谢通路或同时为转运体底物时（如同时经CYP3A4与UGT代谢、或兼具OATP1B1转运体底物属性），单一强抑制剂可能无法完全阻断其清除，此时可选择两种特异性抑制剂分阶段研究，明确各通路的相互作用贡献；或采用“鸡尾酒法”，同时给予多种选择性探针底物（如咪达唑仑用于CYP3A、右美沙芬用于CYP2D6），高效获取药物对不同代谢酶/转运体的抑制或诱导潜力。 2.给药剂量的选择在临床DDI研究中，为精准捕捉药物间相互作用的最大效应幅度，促变药的给药方案设计需以“充分暴露其/诱导潜力”为核心原则。根据ICH M12指导原则要求，促变药应采用临床推荐的最大剂量与最短给药间隔，通过达到稳态时的高暴露浓度，最大化其对目标代谢酶或转运体的调控作用，确保潜在DDI效应被充分表征。如果药物作为受变药是线性PK特征，评估高剂量单独使用的安全性。如果安全性良好，且与促变药药物合用的风险可控，临床高剂量是首选，在DDI研究中可以更灵敏地检测出促变药药物对其代谢或转运的抑制/诱导作用。若药物的治疗指数狭窄（如华法林、他克莫司等），或已有非临床毒性数据提示高剂量下存在安全风险时，选择低剂量（通常为临床拟用剂量的最低有效水平）是稳妥的。此时即使DDI检测灵敏度下降，但研究结果仍能直接反映临床真实用药情境下的风险，避免将试验参与者暴露于不必要的危险中。若为非线性 PK，则需选择最易观察到 DDI 的治疗剂量，若存在安全性隐患，可使用低于治疗剂量的剂量，但需验证低剂量结果可外推至治疗剂量，如通过模型分析（如群体PK模型）或桥接试验验证该剂量下的DDI结果可外推至临床实际治疗剂量，确保研究结果能真实反映临床场景中底物药与促变药合并用药的相互作用程度。 3.单次/多次给药与给药时机促变药通常采用多次给药以达到稳态，若DDI仅发生在吸收环节（如肠道 P-gp 抑制）或促变药单次给药暴露量可代表稳态暴露量，且非时间依赖性抑制剂/诱导剂，可采用单次给药；诱导剂需多次给药以确保达到最大诱导效应，预处理时长通常为7-14天，需结合诱导剂达稳时间、代谢酶 / 转运体的周转时间及底物药半衰期考量。底物药若为线性PK，单次给药即可，其暴露量变化可外推至稳态，若为非线性PK则需多次给药。给药时机需关注促变药兼具抑制和诱导作用的情况，为避免抑制效应掩盖诱导效应，需错时给药；若研究目的为模拟临床联合用药，则需采用临床实际的给药时机。 4.制剂与给药途径研究中药物的给药途径应与临床治疗一致，若药物有多种给药途径，需基于DDI机制选择，例如口服给药需关注肠道代谢酶/转运体的相互作用，静脉给药则重点考察肝脏及全身效应。制剂相关的 DDI需予以关注，不同制剂的吸收速率和程度差异可能影响 DDI 效应，外推不同制剂的DDI结果时，需验证制剂间的PK特征一致性。 5.样本与数据收集 PK 采样时间需足以表征单独给药和合并用药下底物药的完整浓度 - 时间曲线，单剂量研究需确保AUC0-t与AUC0-inf的平均差异小于20%，并考虑DDI可能导致的底物药半衰期延长；多次给药研究需收集稳态下的Cmax、Cmin、AUC0-tau等参数。样本检测除原形药外，若代谢产物对药物安全性 / 有效性有重要贡献或有助于阐释 DDI 机制，需同时检测代谢产物浓度；对于肾脏转运体介导的 DDI，需收集尿液样本评估肾脏清除率变化。若体外数据提示DDI机制无法通过全身暴露量评价（如转运体抑制改变药物组织分布），需同时收集PD数据，以临床疗效或毒性为终点补充评估DDI效应。临床 DDI 研究结果的解读与外推临床 DDI 研究结果的核心评价指标为受变药在合并/不合并促变药时PK参数的几何均值比（GMR）及 90% 置信区间（90% CI），解读需结合无效应界值、促变药分类及临床实际综合判断。默认无效应界值为 80%-125%，若 GMR 的 90% CI落在该范围内，通常认为无临床意义的DDI；若超出该范围，则需结合受变药的暴露 - 效应（E-R）关系、安全性窗宽度进一步分析 —— 对于治疗指数狭窄的药物（如华法林），即使 AUC变化20%-30%也可能引发严重风险，需严格限制合并用药；而安全性窗宽的药物可适当放宽界值。结果外推需遵循 “机制导向” 原则：指针药物研究结果可外推至同代谢酶/转运体介导的其他药物，例如CYP3A强效抑制剂伊曲康唑与咪达唑仑的 DDI 结果，可外推至伊曲康唑与其他CYP3A底物的合并用药风险；CYP抑制剂/诱导剂按强效、中效、弱效分类（如CYP3A强效抑制剂使底物AUC增加≥5 倍，中效 2-5 倍，弱效 1.25-2 倍），同一类别药物的外推性更强。需注意转运体介导的DDI因缺乏特异性指针药物，外推时需谨慎，只有充分了解药物ADME特征时才可以有限推广。结语临床DDI研究是一门融合了试验设计、PK科学和风险评估的学科。成功的DDI研究不仅依赖于严谨的试验设计（如选择交叉/平行设计、确定合理的采样周期），更依赖于科学的剂量选择。对于受试药物，剂量应兼顾安全性与灵敏度；对于相互作用药物，必须确保其暴露水平足以最大程度地抑制或诱导靶点。近年来，随着PBPK模型应用的普及和对转运体认识的加深，DDI研究正从单一的经验性设计向定量预测与验证相结合的模式转变。在新药研发早期充分理解药物的代谢和转运特性，合理利用体外数据指导临床设计，不仅能加速研发进程，更能为临床安全用药提供坚实依据。参考文献： [1] ICH M12 药物相互作用研究, 2024. [2] ICH M12 Drug Interaction Studies: Summary of the Efforts to Achieve Global Convergence[J], Clinical Pharmacology & Therapeutics, 2025. [3] Chen J, Li J, Wu J, et al. An open-label study to explore the optimal design of CYP3A drug–drug interaction clinical trials in healthy Chinese people[J]. Pharmacology Research & Perspectives, 2024, 12(4): e1252. [4] Doses Evaluated in Clinical Pharmacology Studies Investigating the Effect of Intrinsic and Extrinsic Factors on PK and Safety: Case Examples from Approved Drug Development Programs[J]. The AAPS Journal, 2024, 26: 71. 撰写：谢珊珊审核：李瑷宁、佟巍、韩海雄有临医药有临医药创立于2017年，总部设于上海，聚焦肿瘤、自免、神经领域的创新药物临床研究。依托AI赋能的数字化平台、专业临床资源与团队优势，已构建覆盖新药研发全周期的智能化服务体系：从IND策略-NDA申报，提供I期至III期新药临床研究一站式解决方案。服务包括：策略咨询、注册申报、医学事务、临床运营、数据管理与统计、临床药理、药物警戒、独立影像评估、生物分析、SMO及专业化人才派驻等。具备中美双报、创新性试验设计经验、全球多中心临床研究服务能力；引进海外优质产品，推动本土创新产品国际化。拥有500余人服务团队，驻地全国超过100个城市，与2000余名核心领域临床专家及1000余家研究中心建立有效合作。已为400余项新药临床研究项目提供服务。如您有任何需要解答或交流的问题欢迎扫码或致电咨询 TEL: 021-56321338 E-mail: bd@unionclin.com www.unionclin.com 更多精彩推荐欢迎关注“有临医药”订阅号了解更多公司资讯！

2026-03-30

·PRNewswire

Calliditas Therapeutics AB to Present Exploratory Biomarker and Post-Hoc NefIgArd Analyses at the World Congress of Nephrology

Calliditas will present new secondary, biomarker, and mechanistic analyses from the Phase 3 NefIgArd study at the 2026 World Congress of Nephrology. Data further support Nefecon's gut–targeted, disease–modifying mechanism of action in IgA nephropathy. Calliditas to present seven posters and sponsor a scientific symposium highlighting the evolving IgAN treatment paradigm. STOCKHOLM, March 30, 2026 /PRNewswire/ -- Calliditas Therapeutics AB, an Asahi Kasei company, announced today that new data from the Phase 3 NefIgArd study in patients with primary immunoglobulin A nephropathy (IgAN) will be presented at the 2026 World Congress of Nephrology (WCN), taking place from March 28 to 31 in Yokohama, Japan. Nefecon's approval status, labeled indication, and availability vary globally. It is approved in the United States where it is marketed as TARPEYO® (budesonide) delayed-release capsules. It is available in Europe where it is marketed as Kinpeygo® by STADA Arzneimittel AG and in select countries in Asia, including Mainland China, Hong Kong, Macau, Taiwan, Singapore, and South Korea by Everest Medicines. It is also the subject of clinical trials in Japan by Viatris Pharamaceticals Japan Inc. The presentations will highlight secondary analyses from the Phase 3 NefIgArd study evaluating Nefecon, its effects on serum biomarkers associated with gut-associated lymphoid tissue (GALT) activity and the immunological impact of orally administered budesonide on B- and T-cell subsets in murine Peyer's patches following in vivo stimulation. These findings reinforce observations from earlier exploratory biomarker analyses and demonstrate the immunomodulatory effects in the Peyer's patches that underlie Nefecon's mechanism of action in modulating the mucosal immune system in the gut. Collectively, these data support a disease-modifying role for Nefecon in reducing levels of pathogenic galactose-deficient IgA1 in patients with IgAN. In total, 7 abstracts, of which 3 are based on secondary clinical efficacy and safety analyses from the Phase 3 NefIgArd study and 2 on mechanistic/biomarker analyses, will be presented. In addition, the initial demographics of the real-world PERFORM registry will be presented. Calliditas will also sponsor a symposium for educational scientific exchange, highlighting the evolving treatment paradigm in IgA nephropathy. Symposium and Presentation details as follows: Company Sponsored Symposium: Title: "The Evolving IgAN Treatment Paradigm: Why Target the Gut?" Date and time: March 30, 12:50 pm to 13:50 pm JST Presenters: Dr. Yusuke Suzuki, Juntendo University, Tokyo, Japan Dr. Sayna Norouzi, Loma Linda University Medical Center, Loma Linda, California, USA Dr. Chee Kay Cheung, University of Leicester, Leicester, UK Poster Presentations: Abstract No. WCN26-AB-8040 Title: "Impact of treatment with Nefecon on serum biomarkers of gut-associated lymphoid tissue function in patients with immunoglobulin A nephropathy from the Phase 3 NefIgArd trial" Date and time: March 30, 17:00 pm – 18:00 pm JST Presenter: Nadia Nawaz, College of Life Sciences, University of Leicester, Leicester, United Kingdom Abstract No. WCN26-AB-8197 Title: "Budesonide Modulates B- and T-Cell Immunity in Peyer's Patches: Implications for IgA Nephropathy" Date and time: March 28, 17:30 pm – 18:30 pm JST Presenter: Roza Ghotbi, Calliditas Therapeutics AB, Stockholm, Sweden Encore Poster Presentations: Title: "Urine protein–creatinine ratio response at 12 months in patients with immunoglobulin A nephropathy receiving Nefecon vs placebo: Analysis of NefIgArd trial data" Date and time: March 28, 17:30 pm – 18:30 pm JST Presenter: Richard Lafayette, Stanford University, CA Title: "Duration of absolute proteinuria response with Nefecon in patients with primary immunoglobulin A nephropathy: Results from the 2-year NefIgArd trial" Date and time: March 30, 17:00 pm – 18:00 pm JST Presenter: Brad Rovin , The Ohio State University Wexner Medical Center Title: "Absolute proteinuria over time with Nefecon vs placebo in patients with immunoglobulin A nephropathy: Results from the Phase 3 NefIgArd trial" Date and time: March 30, 17:00 pm – 18:00 pm JST Presenter: Heather Reich, University of Toronto Title: "The creation and initial demographics of the PERFORM™ Patient Registry: A novel real-world registry of patients treated for IgA nephropathy in the United States" Date and time: March 29, 17:00 pm – 18:00 pm JST Presenter: Russell Jones, Calliditas Therapeutics AB, Stockholm, Sweden Title: "Safety and preliminary efficacy findings from a Phase 2a randomized, double-blind, placebo-controlled trial of setanaxib in patients with Alport syndrome" Date and time: March 28, 17:30 pm – 18:30 pm JST Presenter: Daniel Gale , University College London The World Congress of Nephrology (WCN) is the flagship scientific, educational, and networking event of the International Society of Nephrology (ISN). Each year, WCN brings together kidney care professionals from around the world to exchange knowledge, showcase groundbreaking research, and participate in regionally-relevant symposia, training programs, and courses. About TARPEYO ® /Kinpeygo® TARPEYO is an oral 4mg delayed-release formulation of budesonide, designed to dissolve in the pH of the distal ileum. Each capsule contains coated beads of budesonide that target mucosal B-cells present in the ileum, including the Peyer's patches, which are responsible for the production of galactose-deficient IgA1 antibodies (Gd-IgA1), causing IgA nephropathy. About Primary Immunoglobulin A Nephropathy Primary immunoglobulin A nephropathy (IgA nephropathy or IgAN or Berger's Disease) is a rare, progressive, chronic immune-mediated disease that attacks the kidneys and occurs when galactose-deficient IgA1 is recognized by autoantibodies, creating IgA1 containing immune complexes that become deposited in the glomerular mesangium of the kidney. This deposition in the kidney can lead to progressive kidney damage, potentially resulting in end-stage kidney disease. IgAN most often develops between late teens and late 30s. IMPORTANT SAFETY INFORMATION FOR US AUDIENCE INDICATION TARPEYO is indicated to reduce the loss of kidney function in adults with primary immunoglobulin A nephropathy (IgAN) who are at risk for disease progression. IMPORTANT SAFETY INFORMATION CONTRAINDICATIONS TARPEYO is contraindicated in patients with hypersensitivity to budesonide or any of the ingredients of TARPEYO. Serious hypersensitivity reactions, including anaphylaxis, have occurred with other budesonide formulations. WARNINGS AND PRECAUTIONS Hypercorticism and adrenal axis suppression: When corticosteroids are used chronically, systemic effects such as hypercorticism and adrenal suppression may occur. Corticosteroids can reduce the response of the hypothalamus-pituitary-adrenal (HPA) axis to stress. In situations where patients are subject to surgery or other stress situations, supplementation with a systemic corticosteroid is recommended. When discontinuing therapy or switching between corticosteroids, monitor for signs of adrenal axis suppression. Patients with moderate to severe hepatic impairment (Child-Pugh Class B and C respectively) could be at an increased risk of hypercorticism and adrenal axis suppression due to an increased systemic exposure to oral budesonide. Avoid use in patients with severe hepatic impairment (Child-Pugh Class C). Monitor for increased signs and/or symptoms of hypercorticism in patients with moderate hepatic impairment (Child-Pugh Class B). Immunosuppression and Increased Risk of Infection: Corticosteroids, including TARPEYO, suppress the immune system and increase the risk of infection with any pathogen, including viral, bacterial, fungal, protozoan, or helminthic pathogens. Corticosteroids can: reduce resistance to new infections, exacerbate existing infections, increase the risk of disseminated infections, increase the risk of reactivation or exacerbation of latent infections, and mask some signs of infection. Corticosteroid-associated infections can sometimes be serious. Monitor for infection and consider TARPEYO withdrawal as needed. Avoid corticosteroid therapy, including TARPEYO, in patients with active or quiescent tuberculosis or hepatitis B infection; untreated fungal, bacterial, systemic viral, or parasitic infections; ocular herpes simplex; or Kaposi's sarcoma. Avoid exposure to active, easily-transmitted infections (e.g., chickenpox, measles). Corticosteroid therapy may decrease the immune response to some vaccines. Other corticosteroid effects: TARPEYO is a systemically available corticosteroid and is expected to cause related adverse reactions. Monitor patients with hypertension, prediabetes, diabetes mellitus, osteoporosis, peptic ulcer, glaucoma or cataracts, or with a family history of diabetes or glaucoma, or with any other condition where corticosteroids may have unwanted effects. ADVERSE REACTIONS In clinical studies, the most common adverse reactions with TARPEYO (occurring in ≥5% of TARPEYO treated patients, and ≥2% higher than placebo) were peripheral edema (17%), hypertension (12%), muscle spasms (12%), acne (11%), headache (10%), upper respiratory tract infection (8%), face edema (8%), weight increased (7%), dyspepsia (7%), dermatitis (6%), arthralgia (6%), and white blood cell count increased (6%). DRUG INTERACTIONS Budesonide is a substrate for CYP3A4. Avoid use with potent CYP3A4 inhibitors, such as ketoconazole, itraconazole, ritonavir, indinavir, saquinavir, erythromycin, and cyclosporine. Avoid ingestion of grapefruit juice with TARPEYO. Intake of grapefruit juice, which inhibits CYP3A4 activity, can increase the systemic exposure to budesonide. USE IN SPECIFIC POPULATIONS Pregnancy: The available data from published case series, epidemiological studies, and reviews with oral budesonide use in pregnant women have not identified a drug-associated risk of major birth defects, miscarriage, or other adverse maternal or fetal outcomes. There are risks to the mother and fetus associated with IgAN. Infants exposed to in-utero corticosteroids, including budesonide, are at risk for hypoadrenalism. Please see Full Prescribing Information About Calliditas Therapeutics Calliditas Therapeutics is a biopharma company with offices in Stockholm, Sweden, focused on identifying, developing, and commercializing novel treatments in orphan indications with significant unmet medical needs. Visit Calliditas.com for further information. About Asahi Kase i Asahi Kasei is a diversified global company that contributes to life and living for people around the world. Since its foundation in 1922, with businesses in ammonia and cellulose fiber, Asahi Kasei has consistently grown through proactive portfolio transformation to meet the evolving needs of every age. With 50,000 employees worldwide, the company contributes to sustainability by providing solutions to the world's challenges across its three business sectors: Healthcare, Homes, and Material. For more information, visit . SOURCE Calliditas Therapeutics 21% more press release views with Request a Demo

临床3期上市批准临床结果临床2期

100 项与酮康唑相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D00351	酮康唑	D01AC08 J02AB02 G01AF11	DB01026

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
内源性库欣综合征	欧盟	Esteve Pharmaceuticals SA	2014-11-18
内源性库欣综合征	冰岛	Esteve Pharmaceuticals SA	2014-11-18
内源性库欣综合征	列支敦士登	Esteve Pharmaceuticals SA	2014-11-18
内源性库欣综合征	挪威	Esteve Pharmaceuticals SA	2014-11-18
头皮屑	美国	Kramer Laboratories	1997-10-10
脂溢性皮炎	日本	Teikoku Seiyaku Co. Ltd.	1997-07-02
皮肤念珠菌病	日本	Teikoku Seiyaku Co. Ltd.	1993-10-01
体癣	日本	Teikoku Seiyaku Co. Ltd.	1993-10-01
股癣	日本	Teikoku Seiyaku Co. Ltd.	1993-10-01
足癣	日本	Teikoku Seiyaku Co. Ltd.	1993-10-01
花斑癣	日本	Teikoku Seiyaku Co. Ltd.	1993-10-01
皮肤真菌病	日本	Janssen Pharmaceutical KK	1993-10-01
着色霉菌病	美国	Janssen Pharmaceuticals, Inc.	1981-06-12
副球菌病	美国	Janssen Pharmaceuticals, Inc.	1981-06-12
球孢子菌病	美国	Janssen Pharmaceuticals, Inc.	1981-06-12
组织胞浆菌病	美国	Janssen Pharmaceuticals, Inc.	1981-06-12
念珠菌病	中国	西安杨森制药有限公司	-
外阴阴道念珠菌病	中国	西安杨森制药有限公司	-
毛囊炎	中国	西安杨森制药有限公司	-

未上市

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适应症	最高研发状态	国家/地区	公司	日期
晚期癌症	临床2期	比利时	Janssen Research & Development LLC	2011-02-01
转移性肿瘤	临床2期	比利时	Janssen Research & Development LLC	2011-02-01
前列腺癌	临床2期	美国	Janssen Pharmaceuticals, Inc.	2000-05-01

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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


NCT00859781 (CTgov)	临床2期	非转移性前列腺癌	55	111In-J591+Ketoconazole+Hydrocortisone	膚餘顧衊製簾製遞憲淵 = 觸淵選廠製廠夢鹽襯網憲壓糧窪願淵壓廠淵顧 (鬱鑰齋獵夢繭範壓網願, 簾艱窪鏇壓鹹襯遞選壓 ~ 選壓觸構願窪膚觸鹹製) 更多	-	2023-07-19
NCT01584297 (GREKO (GRanulosa Et KetOconazole), Pubmed)	临床2期	卵巢颗粒细胞瘤	6	Ketoconazole	構構鹽壓鬱積艱繭醖淵(鬱餘製製築廠築壓鑰膚) = 衊襯壓夢糧糧構餘淵淵齋繭願構網積觸鏇醖網 (鹹鹽觸鏇鏇鏇選簾膚獵, 5.43 ~ 22.69)	-	2023-01-28
NCT03261336 (CTgov)	临床2期	去势抵抗性前列腺癌	1	Calcitriol+Ketoconazole+Hydrocortisone	齋齋鬱製構餘衊憲憲繭 = 構範顧選獵遞鏇糧範獵觸鹹網構鏇壓繭鹹蓋齋 (糧艱獵壓繭醖鏇廠繭鬱, 構鑰遞夢餘鏇夢鹽衊簾 ~ 膚獵繭繭壓鹹壓積憲選) 更多	-	2021-02-08
NCT01036594 (Keto/Dex, CTgov)	临床2期	去势抵抗性前列腺癌	32	Ketoconazole+Hydrocortisone (Ketoconazole + Hydrocortisone)	醖鑰窪鹹糧獵壓衊遞築(積繭築襯齋積鹽網鬱膚) = 壓網觸醖膚繭顧鑰積願顧鏇鹹衊繭齋觸觸淵壓 (繭製淵鑰範艱衊選鏇網, 醖憲衊餘選齋積選鑰襯 ~ 觸觸窪膚選網齋壓窪鬱) 更多	-	2020-06-29
				Dexamethasone+Ketoconazole (Ketoconazole + Dexamethasone)	願淵艱淵夢淵餘憲鬱網 = 顧顧艱醖艱襯鹽鹹膚鹹顧構網糧鏇鹹廠憲構鏇 (齋蓋夢選齋憲蓋廠遞選, 蓋遞鬱憲願餘鹽獵製網 ~ 簾鑰構範憲齋簾憲繭齋) 更多
NCT01576575 (CTgov)	N/A	-	21	buprenorphine (Control (no Pretreatment))	憲築淵鏇齋壓餘蓋壓網(蓋願繭構憲築窪廠鑰淵) = 夢簾積鹹餘製鏇淵夢鹹鹹艱廠範繭艱襯窪壓夢 (網襯顧糧淵醖壓壓鏇窪, 築積蓋獵餘鬱構築夢鬱 ~ 蓋簾範鹽選鏇廠夢蓋鏇) 更多	-	2020-01-22
				buprenorphine+rifampin (Liver and Gut CYP3A Induction)	憲築淵鏇齋壓餘蓋壓網(蓋願繭構憲築窪廠鑰淵) = 選蓋憲壓糧窪鑰艱壓膚鹹艱廠範繭艱襯窪壓夢 (網襯顧糧淵醖壓壓鏇窪, 襯繭膚觸築鹹壓繭觸鏇 ~ 窪顧顧餘壓膚鹽窪顧窪) 更多
NCT03824912 (CTgov)	临床3期	足癣	831	Ketoconazole Cream 2% (Test: Ketoconazole Cream 2%)	觸廠繭鹹鬱網醖窪鏇夢 = 築觸願夢膚壓鑰簾製繭襯顧糧鑰築獵鹽醖網鏇 (範鏇鹹顧鹽鬱鹹膚簾觸, 膚膚憲衊鑰餘壓鑰襯網 ~ 鹹糧餘鏇網鹽網衊窪壓) 更多	-	2019-06-13
				Ketoconazole (Reference: Ketoconazole Cream 2%)	觸廠繭鹹鬱網醖窪鏇夢 = 餘顧鹽鹹窪鑰夢廠繭鹹襯顧糧鑰築獵鹽醖網鏇 (範鏇鹹顧鹽鬱鹹膚簾觸, 鬱廠選鑰繭繭蓋糧鏇憲 ~ 窪衊選鑰糧艱衊糧鏇觸) 更多
NCT00460031 (Pubmed \| Invest New Drugs) 人工标引	临床2期	去势抵抗性前列腺癌	34	Ketoconazole+Lenalidomide	鑰構衊衊淵構網廠願餘(壓築鏇齋淵製襯艱壓觸) = 窪糧選淵壓網廠糧選製選膚鏇鹹繭網獵範窪糧 (糧醖夢鹹淵憲網積鏇顧 ) 更多	不佳	2018-12-01
NCT02494713 (CTgov)	临床2期	前列腺癌 \| 前列腺腺癌	4	Estramustine+Doxorubicin+Degarelix+Ketoconazole+Docetaxel	繭廠襯製蓋廠艱鬱鹽網(鏇構製蓋獵遞鹹選鑰製) = 壓艱衊齋願遞艱糧觸襯糧網憲蓋願齋築衊鬱觸 (餘積廠醖鹹襯構鹹壓膚, 窪鹹襯鹹鹹繭遞簾選製 ~ 簾積夢網窪艱積艱膚遞) 更多	-	2018-11-27
NCT02560051 (CTgov)	临床2期	局部晚期前列腺癌 \| 晚期前列腺癌	19	Estramustine+Doxorubicin+Degarelix+Ketoconazole+Docetaxel (Definitive Local Therapy)	觸鑰鹽蓋壓夢網築餘鑰 = 醖齋艱糧艱構餘鏇醖醖鹹選艱餘製構夢築願憲 (築鬱夢顧壓襯餘遞構夢, 糧構獵淵夢網鬱齋顧衊 ~ 膚鏇鬱範選憲齋齋構窪) 更多	-	2018-10-11
				Estramustine+Doxorubicin+Degarelix+Ketoconazole+Docetaxel (Nodal Only/Low-volume Bone)	觸鑰鹽蓋壓夢網築餘鑰 = 鹹鹹網襯鬱築壓膚廠築鹹選艱餘製構夢築願憲 (築鬱夢顧壓襯餘遞構夢, 遞築製觸壓餘鬱遞壓構 ~ 艱醖壓憲糧觸淵網築淵) 更多
NCT01288521 (CTgov)	临床4期	-	8	Tacrolimus (Tacrolimus Alone)	鏇壓壓膚顧淵鹽簾淵膚(構糧製廠淵觸獵糧壓壓) = 觸獵鹽夢壓廠範艱襯鹹獵鏇簾淵鏇構憲繭廠醖 (餘簾鬱獵製壓構膚網衊, 0.107) 更多	-	2018-03-09
				Tacrolimus+Ketoconazole (Tacrolimus + Ketoconazole)	鏇壓壓膚顧淵鹽簾淵膚(構糧製廠淵觸獵糧壓壓) = 憲觸淵獵窪艱構醖觸顧獵鏇簾淵鏇構憲繭廠醖 (餘簾鬱獵製壓構膚網衊, 0.308) 更多