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A Multi-center, Randomized, Double-blind, Placebo-controlled, Phase IIa Clinical Trial to Evaluate the Safety and Explore the Efficacy of J2H-1702 for Non-alcoholic Steatohepatitis

开始日期2023-02-15

申办/合作机构

J2H Biotech, Inc.

NCT06297434

/ Recruiting临床2期

A Multi-center, Randomized, Double-blind, Placebo-controlled, Phase IIa Clinical Trial to Evaluate the Safety and Explore the Efficacy of J2H-1702 for Non-alcoholic Steatohepatitis

The study aims to evaluate the safety of J2H-1702 compared to the placebo and explore the efficacy of J2H-1702 at Week 12 timepoint after administration compared to baseline in patients with NASH.

开始日期2023-02-15

申办/合作机构

J2H Biotech, Inc.

KCT0008007

/ Completed临床1期

A Double-Blind, Placebo Controlled, Single Dosing, Dose-Escalation Phase 1 Clinical Trial to Investigate the Safety, Tolerability, Pharmacokinetics/Pharmacodynamics Characteristics of J2H-1702 (Nonalcoholic Steatohepatitis Treatment Candidate) after Oral Administration in Healthy Female Subjects

开始日期2023-01-02

申办/合作机构

J2H Biotech, Inc.

100 项与 J2H Biotech, Inc. 相关的临床结果

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0 项与 J2H Biotech, Inc. 相关的专利（医药）

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2

项与 J2H Biotech, Inc. 相关的文献（医药）

Cell Death & Disease

Inhibition of 11β-hydroxysteroid dehydrogenase 1 relieves fibrosis through depolarizing of hepatic stellate cell in NASH

Article

作者: Ryu, Hyung Chul ; Kim, Namjeong ; Choi, Inhee ; Kim, Jason ; Lim, Jee Woong ; Seo, Haeng Ran ; Kim, Sanghwa ; Kang, Hyo Jin ; Lee, Su-Yeon ; Song, Yeonhwa

Abstract11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) is a key enzyme that catalyzes the intracellular conversion of cortisone to physiologically active cortisol. Although 11βHSD1 has been implicated in numerous metabolic syndromes, such as obesity and diabetes, the functional roles of 11βHSD1 during progression of nonalcoholic steatohepatitis (NASH) and consequent fibrosis have not been fully elucidated. We found that pharmacological and genetic inhibition of 11βHSD1 resulted in reprogramming of hepatic stellate cell (HSC) activation via inhibition of p-SMAD3, α-SMA, Snail, and Col1A1 in a fibrotic environment and in multicellular hepatic spheroids (MCHSs). We also determined that 11βHSD1 contributes to the maintenance of NF-κB signaling through modulation of TNF, TLR7, ITGB3, and TWIST, as well as regulating PPARα signaling and extracellular matrix accumulation in activated HSCs during advanced fibrogenesis in MCHSs. Of great interest, the 11βHSD1 inhibitor J2H-1702 significantly attenuated hepatic lipid accumulation and ameliorated liver fibrosis in diet- and toxicity-induced NASH mouse models. Together, our data indicate that J2H-1702 is a promising new clinical candidate for the treatment of NASH.

Cell Death & Disease

Inhibition of 11β-hydroxysteroid dehydrogenase 1 alleviates pulmonary fibrosis through inhibition of endothelial-to-mesenchymal transition and M2 macrophage polarization by upregulating heme oxygenase-1

Article

作者: Song, Yeonhwa ; Kim, Sanghwa ; Kang, Hyo Jin ; Seo, Haeng Ran ; Lee, Yoon-Jin ; Kim, Ji-Hee ; Lee, Su-Yeon ; Kim, Jason

AbstractThe intracellular enzyme 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) catalyzes the interconversion of active glucocorticoid (cortisol) and its intrinsically inert form (cortisone) in metabolic tissues. Although 11βHSD1 is considered a promising therapeutic target in metabolic disorders such as type 2 diabetes, obesity, and nonalcoholic steatohepatitis because of its hepatic functions, its roles in other tissues have received less attention. In this study, we show that the 11βHSD1-specific inhibitor J2H-1702 facilitates the reversion of endothelial-to-mesenchymal transition in multicellular lung spheroid models encapsulating the complex crosstalk among lung cancer cells, vascular endothelial cells, and macrophages. In vascular endothelial cells, J2H-1702 not only suppressed interleukin-1α (IL-1α) expression but also attenuated reactive oxygen species-induced DNA damage by upregulating heme oxygenase-1. Additionally, in macrophages, which are key regulators of fibrogenesis, inhibition of 11βHSD1 markedly reduced IL-1β expression, thereby modulating the pro-inflammatory phenotype of activated macrophages. In mouse models of pulmonary fibrosis, including a bleomycin-induced idiopathic model and a radiation-induced model, J2H-1702 alleviated pulmonary fibrosis and markedly improved the efficacy of nintedanib. Collectively, our data suggest that J2H-1702 holds promise as a clinical candidate for the treatment of pulmonary fibrosis associated with reactive oxygen species-induced DNA damage, endothelial-to-mesenchymal transition, and inflammatory responses.

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100 项与 J2H Biotech, Inc. 相关的转化医学

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药物(靶点)	适应症	全球最高研发状态

J2H-1702 ( 11β-HSD )	非酒精性脂肪性肝炎更多	临床2期
J2H-1701	丙型肝炎更多	临床1期
J2H-P1905	特发性肺纤维化更多	临床前
J2H-1802	银屑病更多	临床前
J2H-1803	杜氏肌营养不良症更多	临床前