Beta Lapachone(Beta Lapachone) - 药物靶点：NQO1_专利_临床

概要

基本信息

药物类型

小分子化药

别名

+ [6]

靶点

NQO1

作用方式

抑制剂

作用机制

NQO1抑制剂(苯醌还原酶-1抑制剂)

治疗领域

肿瘤消化系统疾病内分泌与代谢疾病+ [1]

在研适应症-

非在研适应症

腺癌晚期恶性实体瘤纤维化+ [9]

原研机构

Arisyn Therapeutics Inc

在研机构-

非在研机构

Yungjin Pharm. Co., Ltd.

ArQule, Inc.Arisyn Therapeutics Inc

权益机构-

最高研发阶段终止临床2期

首次获批日期-

最高研发阶段(中国)-

特殊审评-

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结构/序列

分子式C15H14O3

InChIKeyQZPQTZZNNJUOLS-UHFFFAOYSA-N

CAS号4707-32-8

关联

13

项与 Beta Lapachone 相关的临床试验

NCT02338856

/ Completed临床1期

A Phase I Clinical Trial to Evaluate the Pharmacokinetics and Safety of MB12066 in Healthy Male Volunteers

The purpose of this study is to investigate the safety and tolerability of MB12066 after multiple dose and to investigate the pharmacokinetic characteristics of MB12066 after multiple dose.

开始日期2015-01-01

申办/合作机构

Yungjin Pharm. Co., Ltd.

NCT02029586

/ Terminated临床2期

A Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel Group, 12 Weeks, Therapeutic Exploratory Phase 2 Clinical Study to Evaluate the Safety and Efficacy of MB12066 in Patients With Nonalcoholic Fatty Liver Disease (NAFLD) Except Cirrhosis

This is a controlled study to determine the effectiveness and safety of MB12066 in the treatment of adult patients with Nonalcoholic Fatty Liver Disease(NAFLD) except cirrhosis.

开始日期2013-01-01

申办/合作机构

Yungjin Pharm. Co., Ltd.

NCT01444677

/ Completed临床1期

A Dose Block-randomized, Double-blind, Placebo-controlled, Single or Multiple Dosing, Dose-escalation Clinical Trial to Investigate the Safety, Tolerability and Pharmacokinetic Characteristics of MB12066 in Healthy Male Subjects

The purpose of this study is to investigate the safety and tolerability of MB12066 after a single or multiple oral dose and to investigate the pharmacokinetic characteristics of MB12066 after a single or multiple oral dose.

开始日期2011-04-01

申办/合作机构

Yungjin Pharm. Co., Ltd.

[+1]

100 项与 Beta Lapachone 相关的临床结果

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100 项与 Beta Lapachone 相关的转化医学

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100 项与 Beta Lapachone 相关的专利（医药）

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881

项与 Beta Lapachone 相关的文献（医药）

2025-06-01·Biomaterials

Hybrid membrane based biomimetic nanodrug with high-efficient melanoma-homing and NIR-II laser-amplified peroxynitrite boost properties for enhancing antitumor therapy via effective immunoactivation

Article

作者: Zha, Yongchao ; Xue, Wei ; Yu, Siming ; Zeng, Yina ; Lin, Qi ; Zhang, Yu

Owing to the excellent stability, anticancer activity and immunogenicity, peroxynitrite (ONOO^-) has been gained enormous interests in cancer therapy. Nevertheless, precise delivery and control release of ONOO^- in tumors remains a big challenge. Herein, B16F10 cancer cell membrane/liposome hybrid membrane (CM-Lip) based biomimetic nanodrug with high-efficient tumor-homing and NIR-II laser controlled ONOO^- boost properties was designed for melanoma treatment. Briefly, NIR-II molecule IR1061, NO donor BNN6 and β-lapachone (Lapa) were firstly encapsulated in the heat-responsive palmitoyl phosphatidylcholine/cholesterol liposome, followed by fusion with B16F10 cell membrane (CM) to obtain biomimetic CM-Lip@(IR/BNN6/Lapa). The hybrid membrane-based nanodrug displayed excellent biocompatibility and melanoma-targeting efficiency. Upon 1064 nm laser irradiation, the mild photothermal effect of CM-Lip@(IR/BNN6/Lapa) firstly triggered the release of NO and Lapa, which subsequently catalyzed the quinone oxidoreductase 1 (NQO1) overexpressed in tumors to produce O₂^•-, finally caused intraturmal ONOO^- boost via cascade reaction. The boosted ONOO^- could effectively inhibit melanoma by ways of triggering mitochondrion-mediated apoptotic pathway, upregulating 3-nitrotyrosine expression, inducing DNA damage and inhibiting DNA repair enzyme expression of poly (ADP-ribose) polymerase 1 (PARP-1). Moreover, ONOO^- displayed excellent immunoactivation and immunomodulation activities by effectively inducing immunogenic tumor cell death, promoting dendritic cells maturation, increasing cytotoxic T lymphocytes expression and repolarizing M1-phenotype macrophages.

2025-05-01·Chinese Chemical Letters

A β-lapachone-loaded iron-polyphenol nanocomplex enhances chemodynamic therapy through cascade amplification of ROS in tumor

作者: Xu, Xiaodan ; Tang, Jianbin ; Xiao, Bing ; Hu, Hongjie ; Xu, Hongxia ; Shi, Xueying ; Zhang, Wei ; Zhou, Zhuxian ; Shen, Youqing ; Shao, Shiqun ; Zhou, Xiaoxuan

Chemodynamic therapy (CDT), using Fenton agents to generate highly cytotoxic .OH from H2O2 has been demonstrated as a powerful anticancer method.However, the insufficient endogenous H2O2 in tumor cells greatly limited its therapeutic effect.Herein, we prepared a pH-responsive β-lapachone-loaded iron-polyphenol nanocomplex (LIPN) through a one-pot method. β-Lapachone in LIPN selectively enhanced H2O2 concentration in tumor cells, and ferrous ions cascadely generated abundant cytotoxic .OH.Therefore, LIPN with cascade amplification of reactive oxygen species (ROS) showed high chemodynamic cytotoxicity in tumor cells, efficiently improving the expression of damage-associated mol. patterns (DAMPs), and exerting strong immunogenic cell death (ICD).As a result, LIPN exhibited efficient tumor inhibition ability in 4T1 s.c. tumor model in vivo with great biocompatibility.Addnl., the infiltration of cytotoxic CD8+ T lymphocytes and inhibition of regulatory CD4+ FoxP3+ T lymphocytes in tumors demonstrated the activation of immunosuppressive tumor microenvironment by LIPN-induced ICD.Therefore, this work provided a new approach to enhance ICD of chemodynamic therapy through selective cascade amplification of ROS in cancer cells.

2025-05-01·Cell Biology International

Chlorogenic Acid Enhances Beta‐Lapachone‐Induced Cell Death by Suppressing Autophagy in NQO1‐Positive Cancer Cells

Article

作者: Bahar, Md Entaz ; Zada, Sahib ; Kim, Wanil ; Kim, Deok Ryong

ABSTRACTResistance to apoptosis‐inducing drugs frequently occurs in cancer cells, limiting their usefulness in ongoing cancer treatment. Despite ongoing efforts to overcome drug resistance, a definitive solution remains elusive. However, autophagy inhibition has been shown to enhance the effectiveness of some anticancer drugs and is a possible strategy for overcoming drug resistance. In this study, we demonstrate that chlorogenic acid (CGA), a natural antioxidant, significantly enhances beta‐lapachone (β‐Lap)‐induced cell death in cancer cells. The augmented apoptosis induced by CGA is associated with activation of protein kinase A (PKA) in β‐Lap–treated cells, independent of the antioxidant properties of CGA. As a result, PKA activation in cancer cells co‐treated with β‐Lap and CGA effectively inhibits autophagy. Notably, PKA activation leads to phosphorylation of microtubule‐associated protein 1 A/1B‐light chain 3 (LC3) at the serine 12 residue, causing autophagy suppression irrespective of mTORC activity. Importantly, the cell death induced by β‐Lap and CGA in NQO1‐overexpressing breast or lung cancers is closely linked to autophagy inhibition. These findings suggest that combining β‐Lap and CGA might be a novel strategy for cancer therapy, particularly for overcoming drug resistance caused by autophagy induction in cancer cells.

100 项与 Beta Lapachone 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB11948

研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
纤维化	临床2期	美国	Yungjin Pharm. Co., Ltd.	2013-01-01
代谢功能障碍相关的脂肪肝病	临床2期	美国	Yungjin Pharm. Co., Ltd.	2013-01-01
转移性头颈部鳞状细胞癌	临床2期	美国	-	2006-07-01
平滑肌肉瘤	临床2期	美国	-	2006-02-01
腺癌	临床2期	美国	ArQule, Inc.	2005-01-01
转移性胰腺腺癌	临床2期	美国	ArQule, Inc.	2005-01-01
晚期恶性实体瘤	临床2期	美国	-	2003-09-01
头颈部肿瘤	临床2期	-	Arisyn Therapeutics Inc	-
平滑肌瘤	临床2期	-	Arisyn Therapeutics Inc	-
胰腺癌	临床2期	-	Arisyn Therapeutics Inc	-

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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


ASCO2005 人工标引	临床1期	晚期恶性实体瘤	18	ARQ 501	(顧醖襯淵餘範艱獵獵餘) = Up to the 390 mg/m2 dose, ARQ 501 exhibited apparent linear pharmacokinetics, 淵艱襯膚夢繭壓築衊餘 (夢鏇積遞艱鬱窪壓艱範 ) 更多	积极	2005-06-01
ARVO2004	N/A	视网膜母细胞瘤	-	Beta-lapachone	艱膚艱製範遞製遞夢淵(鹹糧蓋選壓鏇積壓窪餘) = 襯鏇齋餘製夢繭憲選憲淵醖夢製鏇醖廠網鑰鹹 (夢鬱簾獵糧網鹹繭製獵 ) 更多	-	2004-05-01
ARVO2004	N/A	视网膜母细胞瘤	-	Etoposide	憲醖憲膚築窪衊鬱鹹鹽(夢廠壓鹹網餘願鏇廠簾) = 衊餘顧蓋鏇願窪觸餘繭網壓膚網醖簾醖築選選 (鬱獵淵鹹範壓鑰範膚衊 )	-	2004-05-01