A Phase 3, Randomized, Double-blind, Placebo-controlled Study Evaluating the Safety and Efficacy of Denifanstat in Patients With Noncirrhotic Metabolic Dysfunction-associated Steatohepatitis (MASH) and F2/F3 Fibrosis (FASCINATE-3)

A randomized, double-blind, placebo-controlled Phase 3 study to determine if denifanstat 50 mg or 25 mg is effective, as compared to placebo, in resolving MASH without the worsening of fibrosis and/or in fibrosis regression without the worsening of steatohepatitis.

开始日期2025-03-01

申办/合作机构

Sagimet Biosciences, Inc.

NCT06692283

/ Withdrawn临床3期

A Phase 3, Randomized, Double-Blind, Placebo-Controlled Study Evaluating the Safety and Efficacy of Denifanstat in Patients With Metabolic Dysfunction-Associated Steatotic Liver Disease (MALSD)/Metabolic Dysfunction-Associated Steatohepatitis (MASH)

A phase 3, randomized, double-blind, placebo-controlled study evaluating the safety and tolerability of denifanstat 50 mg compared to placebo in patients with metabolic dysfunction-associated steatotic liver disease (MALSD)/metabolic dysfunction-associated steatohepatitis (MASH) after 52 weeks of treatment.

开始日期2025-03-01

申办/合作机构

Sagimet Biosciences, Inc.

NCT06248008

/ Active, not recruiting临床3期

An Open, Multicenter, Phase III Extension Clinical Trial to Evaluate the Long-term Safety of ASC40 (Denifanstat) Tablets in Patients With Moderate to Severe Acne Vulgaris

This is a multicenter, open-label study designed to determine the long-term safety of ASC40 (Denifanstat) tablets in patients with moderate to severe acne vulgaris enrolled in the ASC40-303 Phase III study. All subjects are eligible for study eligibility screening after enrollment in ASC40-303 Phase III study, and all eligible subjects with moderate to severe acne vulgaris will receive ASC40 (Denifanstat) tablets after signing informed consent. The investigational drug will be administered orally once daily (QD) for up to 40 weeks. There will be a total of 7 visits for screening and follow-up. The tests required by the program included routine blood tests, blood biochemistry, lipid profile, pregnancy test and urine routine, etc.

开始日期2024-04-18

申办/合作机构

歌礼药业（浙江）有限公司

100 项与地尼法司他相关的临床结果

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100 项与地尼法司他相关的转化医学

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100 项与地尼法司他相关的专利（医药）

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项与地尼法司他相关的文献（医药）

2025-06-01·METABOLISM-CLINICAL AND EXPERIMENTAL

Pharmacologically targeting fatty acid synthase-mediated de novo lipogenesis alleviates osteolytic bone loss by directly inhibiting osteoclastogenesis through suppression of STAT3 palmitoylation and ROS signaling

Article

作者: Zhang, Yuannan ; He, Guangxu ; Luo, Xi ; Zhang, Ziyi ; Chen, Jianquan ; Zhang, Lei ; Chen, Zhiyuan ; Zhao, Hangkai ; Ji, Kaizhong ; Zhang, Chenxi ; Xiu, Chunmei

Aberrant increases in osteoclast formation and/or activity are the underlying cause of bone loss in a variety of osteolytic diseases. Fatty acid synthase (Fasn)-mediated de novo lipogenesis (DNL) is one of the major lipid metabolic pathways and has been shown to play critical roles in diverse physiological and pathological processes. However, little is known about its role in osteoclastogenesis. Here, we investigate the direct role of DNL in osteoclastogenesis and its therapeutic potential in osteolytic diseases. We found that Fasn expression and DNL levels are upregulated during receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis. Inhibition of Fasn by shRNA knockdown or its pharmacological inhibitors (ASC40 and trans-C75) impairs osteoclast differentiation in vitro. Mechanistically, pharmacological inhibition of Fasn suppresses RANKL-induced c-Fos/NFATc1 expression and thus osteoclastogenesis partly by disrupting STAT3 palmitoylation, while promoting ROS scavenging to impair mitogen-activated protein kinase (MAPK) signaling. Finally, the therapeutic potential of ASC40 for the treatment of osteolytic bone loss is tested in two mouse models of osteolytic diseases, i.e. ovariectomy (OVX)-induced osteoporosis and titanium nanoparticle-induced calvarial osteolysis. The results show that ASC40 significantly attenuates bone loss and osteoclastogenesis in both models. In conclusion, our results demonstrate that Fasn-mediated DNL is a novel positive regulator of osteoclastogenesis and may serve as a promising therapeutic target for the treatment of osteoclast-driven osteolytic bone diseases.

2025-06-01·Translational Oncology

Targeting FASN enhances cisplatin sensitivity via SLC7A11-mediated ferroptosis in cervical cancer

Article

作者: Lin, Xiaoying ; Peng, Zhangqing ; Du, Qiqiao ; Wei, Mengxun ; Chi, Chudan ; Zou, Qiaojian ; Mai, Qiuwen ; Chen, Yili ; Du, Liu ; Wang, Shuyi ; Wang, Xiaojun ; Chen, Qianrun ; Liu, Junxiu ; Abdugheni, Karima ; Yao, Shuzhong

OBJECTIVE:

The cisplatin resistance significantly hinders the prospects for curing patients with advanced, recurrent, and metastatic cervical cancer (CC). Our study aims to clarify the mechanisms underlying cisplatin resistance in CC and provide a novel treatment strategy to overcome the cisplatin resistance of CC patients.

METHODS:

Intracellular levels of reactive oxygen species, glutathione, malondialdehyde and Fe²⁺ were measured as indicators of ferroptosis. Biological information analyses, IC₅₀, immunofluorescence assays, qPCR and western blot analyses were conducted to elucidate the functions of FASN in CC. In vivo studies were conducted to examine the antitumor effects of the combination of TVB-2640 and cisplatin.

RESULTS:

Fatty acid synthase (FASN) was identified as a key driver of cisplatin resistance in CC through transcriptome sequencing and Gene Expression Omnibus (GEO) data analysis. The clinically safe FASN inhibitor TVB-2640 was found to restore cisplatin sensitivity, resulting in synergistic tumor growth attenuation in xenograft models. Mechanistically, FASN downregulation promoted ferroptosis and reduced solute carrier family 7 member 11 (SLC7A11) expression, both in vitro and in vivo models.

CONCLUSION:

Targeting FASN enhances cisplatin sensitivity in CC by promoting SLC7A11-mediated ferroptosis. TVB-2640 combined with cisplatin had superior synergistic antitumor effects in cisplatin-resistant CC models.

2025-04-01·NEOPLASIA

Fatty acid synthase (FASN) inhibition cooperates with BH3 mimetic drugs to overcome resistance to mitochondrial apoptosis in pancreatic cancer

Article

作者: Duran, Cristina ; Lupu, Ruth ; Steen, Travis Vander ; Casadevall, Guillem ; Espinoza, Ingrid ; Kemble, George ; Billadeau, Daniel D ; Verdura, Sara ; Osuna, Sílvia ; Serrano-Hervás, Eila ; McWilliams, Robert ; Menendez, Javier A ; Kaufmann, Scott H ; Cuyàs, Elisabet

Resistance to mitochondrial apoptosis is a major driver of chemoresistance in pancreatic ductal adenocarcinoma (PDAC). However, pharmacological manipulation of the mitochondrial apoptosis threshold in PDAC cells remains an unmet therapeutic goal. We hypothesized that fatty acid synthase inhibitors (FASNis), a family of targeted metabolic therapeutics recently entering the clinic, could lower the apoptotic threshold in chemoresistant PDAC cells and be synergistic with BH3 mimetics that neutralize anti-apoptotic proteins. Computational studies with TVB-3166 and TVB-3664, two analogues of the clinical-grade FASNi TVB-2640 (denifanstat), confirmed their uncompetitive behavior towards NADPH when bound to the FASN ketoacyl reductase domain. The extent of NADPH accumulation, a consequence of FASN inhibition, paralleled the sensitivity of PDAC cells to the apoptotic effects of TVB FASNis in conventional PDAC cell lines that naturally express varying levels of FASN. FASN inhibition dramatically increased the sensitivity of "FASN-high" expressing PDAC cells to the BCL2/BCL-X_L/BCL-W inhibitor ABT-263/navitoclax and the BCL2-selective inhibitor ABT-199/venetoclax, both in vitro and in in vivo xenografted tumors. The ability of TVB FASNis to shift the balance of pro- and anti-apoptotic proteins and thereby push PDAC cells closer to the apoptotic threshold was also observed in cell lines developed from patient-derived xenografts (PDXs) representative of the classical (pancreatic) transcriptomic subtype of PDAC. Experiments in PDAC PDXs in vivo confirmed the synergistic antitumor activity of TVB-3664 with navitoclax and venetoclax, independent of the nature of the replication stress signature of patient-derived PDAC cells. The discovery that targeted inhibition of FASN is a metabolic perturbation that sensitizes PDAC cells to BH3 mimetics warrants further investigation to overcome resistance to mitochondrial apoptosis in PDAC patients.

198

项与地尼法司他相关的新闻（医药）

2025-09-24

·ir.sagimet.com

Sagimet Biosciences Announces Upcoming Panel Participation at Fierce Biotech Week

SAN MATEO, Calif., Sept. 24, 2025 (GLOBE NEWSWIRE) -- Sagimet Biosciences Inc. (Sagimet, Nasdaq: SGMT), a clinical-stage biopharmaceutical company developing novel therapeutics targeting dysfunctional metabolic and fibrotic pathways, today announced its participation in a drug development panel at Fierce Biotech Week taking place October 7-9, 2025 in Boston, MA. Panel Title: How Biotechs are Leveraging Artificial Intelligence (AI)/Machine Learning (ML) to Drive Efficiency and ROI Presenter: Marie O’Farrell, Ph.D., Senior Vice President of Research and Development, Sagimet Biosciences Date and time: Thursday, October 9, 2025, 11.15am ET Panel Overview: Discussion of the use of AI in the drug development space. Sagimet plans to share how it is employing state-of-the-art AI-based digital pathology platforms to complement conventional biopsy approaches in clinical trials. For drug development in metabolic dysfunction associated steatohepatitis (MASH), AI can enable granular objective quantitation of histology and enhance the ability to analyze morphology and spatial configuration of steatosis and fibrosis in liver biopsies. About Sagimet Biosciences Sagimet is a clinical-stage biopharmaceutical company developing novel fatty acid synthase (FASN) inhibitors that are designed to target dysfunctional metabolic and fibrotic pathways in diseases resulting from the overproduction of the fatty acid, palmitate. Sagimet’s lead drug candidate, denifanstat, is an oral, once-daily pill and selective FASN inhibitor in development for the treatment of metabolic dysfunction associated steatohepatitis (MASH). FASCINATE-2, a Phase 2b clinical trial of denifanstat in MASH with liver biopsy-based primary endpoints, was successfully completed with positive results. Denifanstat has been granted Breakthrough Therapy designation by the FDA for the treatment of non-cirrhotic MASH with moderate to advanced liver fibrosis (consistent with stages F2 to F3 fibrosis), and end-of-Phase 2 interactions with the FDA have been successfully completed, supporting the advancement of denifanstat into further development. Sagimet has recently initiated a Phase 1 first-in-human clinical trial with a second oral FASN inhibitor drug candidate, TVB-3567, that is planned to be developed for acne in the U.S. For additional information about Sagimet, please visit www.sagimet.com. Investor Contact: Joyce Allaire LifeSci Advisors JAllaire@LifeSciAdvisors.com Media Contact: Michael Fitzhugh LifeSci Communications mfitzhugh@lifescicomms.com Source: Sagimet Biosciences Inc.

临床2期临床1期突破性疗法临床结果

2025-09-19

·香港证券交易所

自願性公告 - 歌禮在2025年歐洲皮膚病與性病學會(EADV)年會最新突破性研究專場報告了同類首創脂肪酸合成酶(FASN)抑制劑地尼法司他(ASC40)治療痤瘡的III期研究結果

香港交易及結算所有限公司及香港聯合交易所有限公司對本公告的內容概不負責，對其準確性或完整性亦不發表任何聲明，並明確表示，概不就因本公告全部或任何部分內容所產生或因依賴該等內容而引致的任何損失承擔任何責任。（於開曼群島註冊成立的有限公司）（股份代號：1672）自願性公告歌禮在2025年歐洲皮膚病與性病學會(EADV)年會最新突破性研究專場報告了同類首創脂肪酸合成酶(FASN)抑制劑地尼法司他(ASC40) 治療痤瘡的III期研究結果－地尼法司他（denifanstat，ASC40）達到所有主要、關鍵次要及次要療效終點（意向治療集(ITT)分析），與安慰劑相比顯著改善中重度痤瘡。－地尼法司他(ASC40)顯示出了良好的安全性與耐受性特徵。地尼法司他 (ASC40)組和安慰劑組的治療期間發生的不良事件(TEAE)發生率相當： 58.6%對比56.3%。大部分TEAE為輕度（1級）或中度（2級）。－歌禮正與中國國家藥品監督管理局(NMPA)進行地尼法司他(ASC40)的上市申請前(Pre-NDA)溝通，NMPA目前反饋良好。歌禮計劃在完成上市申請前溝通後向NMPA提交地尼法司他(ASC40)用於治療中重度尋常性痤瘡的新藥上市申請(NDA)。本公告乃歌禮製藥有限公司（「本公司」或「歌禮」，連同其附屬公司稱為「本集團」）自願作出，以使本公司股東及潛在投資者了解本集團的最新業務發展。本公司董事（「董事」）會（「董事會」）宣佈，在2025 年9 月17 日於法國巴黎舉行的2025 年歐洲皮膚病與性病學會(EADV)年會最新突破性研究專場上口頭報告了地尼法司他（denifanstat，ASC40）治療中重度尋常性痤瘡的III期研究 (NCT06192264)結果。口頭報告細節標題：同類首創脂肪酸合成酶(FASN)抑制劑地尼法司他治療尋常性痤瘡達到所有終點：一項III期隨機、安慰劑對照試驗的結果報告人：項蕾紅博士，地尼法司他(ASC40) III期研究主要研究者，復旦大學附屬華山醫院皮膚科該項III期臨床試驗是一項在中國開展的隨機、雙盲、安慰劑對照、多中心的臨床試驗，旨在評估地尼法司他(ASC40)每日一次口服片在480例中重度尋常性痤瘡患者中的安全性和療效。患者被按照1:1的比例入組並隨機分至一個活性藥物組和一個安慰劑對照組，接受每日一次50毫克地尼法司他(ASC40)口服片或匹配的安慰劑治療，為期12周。地尼法司他(ASC40)組和安慰劑組基線特徵均衡。主要終點包括治療成功百分比（治療成功的定義為在第12周時，研究者總體評估（Investigator’s Global Assessment，IGA）評分較基線下降至少2分，且IGA分級為0分（光潔）或1分（幾乎光潔））、第12周時總皮損計數(TLC)相對基線百分比下降，以及第12周時炎性皮損計數(ILC)相對基線百分比下降。治療4周後，地尼法司他(ASC40)治療組已在多項療效終點上均顯示出較安慰劑組具有統計學意義的顯著改善(p<0.05)，包括治療成功、TLC、ILC及非炎性皮損計數(NILC)。治療12周後，地尼法司他(ASC40)達到所有主要、關鍵次要及次要療效終點。表1 總結了III期研究對比安慰劑的療效結果（意向治療集(ITT)分析）。表1. III期研究對比安慰劑的療效結果（意向治療集(ITT)分析） |療效終點(1)|50毫克地尼法司他(ASC40)，口服，每日一次（n=240）|安慰劑，口服，每日一次（n=240）|經安慰劑校準|P 值| |---|---|---|---|---| |主要終點||||| |治療成功(2)百分比|33.17|14.58|18.59|<0.0001| |TLC相對基線的百分比下降|57.38|35.42|21.96|<0.0001| |ILC相對基線的百分比下降|63.45|43.21|20.24|<0.0001| |關鍵次要終點||||| |NILC相對基線的百分比下降|51.85|28.94|22.91|<0.0001| |次要終點||||| |TLC相對基線的絕對下降|58.25|36.17|22.08|<0.0001| |ILC相對基線的絕對下降|26.56|18.42|8.14|<0.0001| 註釋： (1) 所有療效終點均為最小二乘均值。 (2) 治療成功的定義為在第12周時，研究者總體評估（Investigator’s Global Assessment，IGA）評分較基線下降至少2分，且IGA分級為0分（光潔）或1分（幾乎光潔）。 (3) TLC：總皮損計數；ILC：炎性皮損計數；NILC：非炎性皮損計數。每日一次口服50 毫克地尼法司他(ASC40)，為期12 周的安全性和耐受性特徵良好。地尼法司他(ASC40)治療組和安慰劑組的治療期間發生的不良事件（treatment-emergent adverse events，TEAE）發生率相當：58.6%對比56.3%。任何類別的與試驗藥物相關的TEAE發生率均不超過10%。僅兩類TEAE的發生率超過5%（皮膚乾燥在地尼法司他(ASC40)治療組和安慰劑組的發生率分別為6.3% 和2.9%，乾眼症在地尼法司他(ASC40)治療組和安慰劑組的發生率分別為5.9%和 3.8%）。大部分TEAE為輕度（1級）或中度（2級）。所有與地尼法司他(ASC40)相關的TEAE均為輕度（1級）或中度（2級）。沒有與地尼法司他(ASC40)相關的3級或4 級TEAE，且沒有與地尼法司他(ASC40)相關的嚴重不良事件(SAE)。未有報告死亡病例。未觀察到與地尼法司他(ASC40)相關的永久性終止治療或退出試驗的情況。在2025年EADV年會上報告的詳細數據見歌禮網站（鏈接）。「地尼法司他(ASC40)是痤瘡治療領域的創新性療法，具有潛在的臨床重要意義。我們非常榮幸能在本屆EADV年會上向皮膚病學界展示這些結果。」歌禮創始人、董事會主席兼首席執行官吳勁梓博士表示，「地尼法司他(ASC40)採用痤瘡治療新作用機制，在III期研究中所有主要和次要終點較安慰劑均顯示出高度具有統計學意義且臨床意義顯著的改善，同時顯示出良好的安全性和耐受性特徵。」歌禮正與中國國家藥品監督管理局(NMPA)進行地尼法司他(ASC40)的上市申請前(Pre-NDA)溝通，NMPA目前反饋良好。歌禮計劃在完成上市申請前溝通後向NMPA提交地尼法司他(ASC40)用於治療中重度尋常性痤瘡的新藥上市申請 (NDA)。歌禮已從Sagimet Biosciences Inc.（納斯達克股票代碼：SGMT）獲得地尼法司他 (ASC40)的大中華區獨家授權。香港聯合交易所有限公司證券上市規則第18A.05條規定的警示聲明：我們無法保證我們將能夠最終令地尼法司他(ASC40)成功開發、銷售及╱或商業化。於本公告日期，本公司董事會包括執行董事吳勁梓博士及何淨島女士；及獨立非執行董事魏以楨博士、顧炯先生及華林女士。

临床3期ASCO会议临床结果临床成功申请上市

2025-09-17

·歌礼

-地尼法司他(denifanstat，ASC40)达到所有主要、关键次要及次要疗效终点(意向治疗集(ITT)分析)，与安慰剂相比显著改善中重度痤疮。 -地尼法司他(ASC40)显示出了良好的安全性与耐受性特征。地尼法司他(ASC40)组和安慰剂组的治疗期间发生的不良事件(TEAE)发生率相当：58.6%对比56.3%。大部分TEAE为轻度(1级)或中度(2级)。 -歌礼正与中国国家药品监督管理局(NMPA)进行地尼法司他(ASC40)的上市申请前(Pre-NDA)沟通，NMPA目前反馈良好。歌礼计划在完成上市申请前沟通后向NMPA提交地尼法司他(ASC40)用于治疗中重度寻常性痤疮的新药上市申请(NDA)。香港，2025年9月18日--歌礼制药有限公司(香港联交所代码：1672，简称“歌礼”)今日宣布，在2025年9月17日于法国巴黎举行的2025年欧洲皮肤病与性病学会(EADV)年会最新突破性研究专场上口头报告了地尼法司他(denifanstat，ASC40)治疗中重度寻常性痤疮的III期研究(NCT06192264)结果。口头报告细节标题：同类首创脂肪酸合成酶(FASN)抑制剂地尼法司他治疗寻常性痤疮达到所有终点：一项III期随机、安慰剂对照试验的结果报告人：项蕾红博士，地尼法司他(ASC40) III期研究主要研究者，复旦大学附属华山医院皮肤科该项III期临床试验是一项在中国开展的随机、双盲、安慰剂对照、多中心的临床试验，旨在评估地尼法司他(ASC40)每日一次口服片在480例中重度寻常性痤疮患者中的安全性和疗效。患者被按照1:1的比例入组并随机分至一个活性药物组和一个安慰剂对照组，接受每日一次50毫克地尼法司他(ASC40)口服片或匹配的安慰剂治疗，为期12周。地尼法司他(ASC40)组和安慰剂组基线特征均衡。主要终点包括治疗成功百分比(治疗成功的定义为在第12周时，研究者总体评估(Investigator's Global Assessment，IGA)评分较基线下降至少2分，且IGA分级为0分(光洁)或1分(几乎光洁)）、第12周时总皮损计数(TLC)相对基线百分比下降，以及第12周时炎性皮损计数(ILC)相对基线百分比下降。治疗4周后，地尼法司他(ASC40)治疗组已在多项疗效终点上均显示出较安慰剂组具有统计学意义的显著改善(p<0.05)，包括治疗成功、TLC、ILC及非炎性皮损计数(NILC)。治疗12周后，地尼法司他(ASC40)达到所有主要、关键次要及次要疗效终点。表1总结了III期研究对比安慰剂的疗效结果(意向治疗集(ITT)分析)。表1. III期研究对比安慰剂的疗效结果(意向治疗集(ITT)分析) 注释：（1）所有疗效终点均为最小二乘均值。（2）治疗成功的定义为在第12周时，研究者总体评估(Investigator's Global Assessment，IGA)评分较基线下降至少2分，且IGA分级为0分(光洁)或1分(几乎光洁)。（3）TLC：总皮损计数；ILC：炎性皮损计数；NILC：非炎性皮损计数。每日一次口服50毫克地尼法司他(ASC40)，为期12周的安全性和耐受性特征良好。地尼法司他(ASC40)治疗组和安慰剂组的治疗期间发生的不良事件(treatment-emergent adverse events，TEAE)发生率相当：58.6%对比56.3%。任何类别的与试验药物相关的TEAE发生率均不超过10%。仅两类TEAE的发生率超过5%(皮肤干燥在地尼法司他(ASC40)治疗组和安慰剂组的发生率分别为6.3%和2.9%，干眼症在地尼法司他(ASC40)治疗组和安慰剂组的发生率分别为5.9%和3.8%)。大部分TEAE为轻度(1级)或中度(2级)。所有与地尼法司他(ASC40)相关的TEAE均为轻度(1级)或中度(2级)。没有与地尼法司他(ASC40)相关的3级或4级TEAE，且没有与地尼法司他(ASC40)相关的严重不良事件(SAE)。未有报告死亡病例。未观察到与地尼法司他(ASC40)相关的永久性终止治疗或退出试验的情况。在2025年EADV年会上报告的详细数据见歌礼网站(“科学研究”栏目下的“拓展性适应症”)。吴劲梓博士歌礼创始人、董事会主席兼首席执行官地尼法司他(ASC40)是痤疮治疗领域的创新性疗法，具有潜在的临床重要意义。我们非常荣幸能在本届EADV年会上向皮肤病学界展示这些结果。地尼法司他(ASC40)采用痤疮治疗新作用机制，在III期研究中所有主要和次要终点较安慰剂均显示出高度具有统计学意义且临床意义显著的改善，同时显示出良好的安全性和耐受性特征。歌礼正与中国国家药品监督管理局(NMPA)进行地尼法司他(ASC40)的上市申请前(Pre-NDA)沟通，NMPA目前反馈良好。歌礼计划在完成上市申请前沟通后向NMPA提交地尼法司他(ASC40)用于治疗中重度寻常性痤疮的新药上市申请(NDA)。歌礼已从Sagimet Biosciences Inc.(纳斯达克股票代码：SGMT)获得地尼法司他(ASC40)的大中华区独家授权。关于歌礼制药有限公司歌礼制药有限公司是一家全价值链整合型生物技术公司，聚焦有望成为治疗代谢疾病同类最佳(best-in-class)和同类首创(first-in-class)药物的开发和商业化。利用公司专有的基于结构的AI辅助药物发现(Artificial Intelligence-Assisted Structure-Based Drug Discovery，AISBDD)平台和超长效药物开发平台(Ultra-Long-Acting Platform，ULAP)，歌礼已自主研发多款候选药物，包括其核心项目：ASC30，一款在研小分子GLP-1受体(GLP-1R)激动剂，既可每日一次口服也可每月一次至每季度一次皮下注射作为减重治疗疗法和减重维持疗法，用于长期体重管理。歌礼已在香港联交所上市(1672.HK)。欲了解更多信息，敬请登录网站：www.ascletis.com。关于该临床试验（NCT06192264），可点击“阅读原文”查看详细信息！

临床3期临床结果ASCO会议突破性疗法申请上市

100 项与地尼法司他相关的药物交易

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研发状态

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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3期	-	Sagimet Biosciences, Inc.	2025-03-01
非酒精性脂肪肝	临床3期	-	Sagimet Biosciences, Inc.	2025-03-01
非酒精性脂肪性肝炎	临床3期	-	Sagimet Biosciences, Inc.	2025-03-01
寻常痤疮	临床3期	中国	歌礼生物科技（杭州）有限公司	2024-01-23
复发性胶质母细胞瘤	临床3期	中国	歌礼药业（浙江）有限公司	2022-01-21
胶质母细胞瘤	临床3期	中国	歌礼生物科技（杭州）有限公司	2021-12-17
KRAS突变非小细胞肺癌	临床2期	美国	Sagimet Biosciences, Inc.	2019-09-11
代谢综合征	临床2期	美国	Sagimet Biosciences, Inc.	2017-02-01
转移性去势抵抗性前列腺癌	临床1期	美国	Sagimet Biosciences, Inc.	2023-11-20
肝损伤	临床1期	美国	Sagimet Biosciences, Inc.	2023-05-01

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临床结果

适应症

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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


NCT06192264 (NEWS) 人工标引	临床3期	寻常痤疮	480	Denifanstat	淵醖襯齋襯鏇獵積齋襯(蓋蓋膚膚膚觸憲艱襯廠) = 鑰積醖膚築艱夢繭夢製廠艱鑰獵範鏇醖齋築鏇 (願憲艱壓鏇鏇獵齋顧窪 ) 达到更多	积极	2025-06-04
				Placebo	淵醖襯齋襯鏇獵積齋襯(蓋蓋膚膚膚觸憲艱襯廠) = 鏇遞憲醖繭繭淵憲糧夢廠艱鑰獵範鏇醖齋築鏇 (願憲艱壓鏇鏇獵齋顧窪 ) 达到更多
NCT03938246 (FASCINATE-1, CTgov)	临床2期	非酒精性脂肪性肝炎	142	TVB-2640 (TVB-2640 25 mg (US))	糧窪蓋鏇網鑰艱鑰衊壓(壓廠鹹構鏇製鬱衊遞襯) = 構遞憲願蓋齋鑰顧網鑰觸壓艱襯範鑰蓋襯鑰簾 (艱衊蓋糧選糧繭遞鑰築, 29.837) 更多	-	2024-12-19
				TVB-2640 (TVB-2640 50 mg (US))	糧窪蓋鏇網鑰艱鑰衊壓(壓廠鹹構鏇製鬱衊遞襯) = 積醖選艱鹽鹹製壓願齋觸壓艱襯範鑰蓋襯鑰簾 (艱衊蓋糧選糧繭遞鑰築, 28.354) 更多
NCT04906421 (FASCINATE-2, Biospace) 人工标引	临床2期	非酒精性脂肪性肝炎	168	Denifanstat	壓襯製顧壓憲糧醖鹹構(製築選觸鏇選簾窪簾餘) = 簾膚餘鹽顧糧襯繭艱願網壓壓觸膚艱鑰糧艱簾 (壓膚鏇餘襯齋鑰築憲憲 ) 更多	积极	2024-10-11
				Placebo	壓襯製顧壓憲糧醖鹹構(製築選觸鏇選簾窪簾餘) = 鹹積壓簾壓廠鑰網衊淵網壓壓觸膚艱鑰糧艱簾 (壓膚鏇餘襯齋鑰築憲憲 ) 更多
NCT04906421 (FASCINATE-2, EASL2024) 人工标引	临床2期	纤维化	168	Denifanstat 50 mg	鑰窪構範範窪餘齋窪蓋(範製艱蓋鹹獵觸遞艱鏇) = 簾構願膚積憲選艱選鑰淵鬱廠鑰鹹襯膚糧糧鬱 (鬱築鹽顧齋獵窪構製鏇 ) 更多	积极	2024-06-01
				Placebo	鑰窪構範範窪餘齋窪蓋(範製艱蓋鹹獵觸遞艱鏇) = 廠淵願壓願積餘憲鹹壓淵鬱廠鑰鹹襯膚糧糧鬱 (鬱築鹽顧齋獵窪構製鏇 ) 更多
NCT05104125 (AAD2024) 人工标引	临床2期	寻常痤疮	180	ASC40 25mg	壓壓鹽鏇衊鏇觸醖艱淵(窪膚壓簾餘願繭遞鏇鹽) = 衊蓋範範淵構淵壓範糧壓製簾淵餘選遞廠網鏇 (遞廠餘顧糧築鬱選憲艱 ) 更多	积极	2024-03-10
				ASC40 50mg	壓壓鹽鏇衊鏇觸醖艱淵(窪膚壓簾餘願繭遞鏇鹽) = 艱憲繭獵積艱顧廠鑰蓋壓製簾淵餘選遞廠網鏇 (遞廠餘顧糧築鬱選憲艱 ) 更多
NCT04906421 (FASCINATE-2, Biospace) 人工标引	临床2期	非酒精性脂肪性肝炎	168	Denifanstat	憲糧鹹鏇艱積選範憲鏇(襯窪衊衊壓艱獵鹽膚積) = 艱鹽膚繭鹽鏇鑰衊醖顧獵製簾窪積衊築憲鏇醖 (衊簾築淵夢壓範鹽醖願 ) 更多	积极	2024-01-22
				Placebo	憲糧鹹鏇艱積選範憲鏇(襯窪衊衊壓艱獵鹽膚積) = 衊窪蓋壓構壓顧構壓積獵製簾窪積衊築憲鏇醖 (衊簾築淵夢壓範鹽醖願 ) 更多
NCT03032484 (CTgov)	临床2期	星形细胞瘤	25	TVB-2640+Bevacizumab	餘夢夢網糧憲衊觸壓顧 = 構廠鏇鏇餘襯鏇壓積築夢獵衊鏇觸積衊壓鬱憲 (膚艱觸艱鬱夢艱憲壓衊, 繭夢選遞築淵顧憲築構 ~ 衊蓋繭餘鹽簾鏇積餘齋) 更多	-	2023-06-15
NCT02948569 (CTgov)	临床1/2期	代谢综合征	12	3-V Bioscience-2640	遞獵齋淵獵顧構廠顧顧(夢鹹窪築糧廠遞醖糧衊) = 膚壓衊鏇獵鏇醖衊顧構襯鑰夢壓積糧壓願鏇醖 (糧積鏇簾鑰憲鹹鹽築積, 1.5) 更多	-	2023-04-20
NCT04906421 (FASCINATE-2, NEWS) 人工标引	临床2期	非酒精性脂肪性肝炎	52	Denifanstat	襯襯築醖鏇鹽顧夢選鹽(網構蓋餘艱網襯範廠蓋) = 鹽夢夢範製築獵觸繭醖網願積鏇積獵壓鏇網選 (鏇獵衊憲鹽膚構夢願壓 ) 更多	积极	2022-11-04
				Placebo	襯襯築醖鏇鹽顧夢選鹽(網構蓋餘艱網襯範廠蓋) = 鑰製鹹衊製蓋選積壓選網願積鏇積獵壓鏇網選 (鏇獵衊憲鹽膚構夢願壓 ) 更多