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更新于：2026-02-28
Cilofexor tromethamine
更新于：2026-02-28
概要
基本信息
最高研发阶段临床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C32H33Cl3N4O8 |
InChIKeyCUWTTWVBVUZPAP-UHFFFAOYSA-N |
CAS号2253764-93-9 |
关联
12
项与 Cilofexor tromethamine 相关的临床试验NCT04060147
A Proof-of-Concept, Open-Label Study Evaluating the Safety and Tolerability of Cilofexor in Subjects With Primary Sclerosing Cholangitis (PSC) and Compensated Cirrhosis
NCT03987074
A Proof of Concept, Open-Label Study Evaluating the Safety, Tolerability, and Efficacy of Monotherapy and Combination Regimens in Subjects With Nonalcoholic Steatohepatitis (NASH)
ACTRN12619000655145
A Phase 1 Open-Label, Parallel-Group, Two-Treatment, Single-Dose Study to Evaluate the Pharmacokinetics of GS-9674 and GS-0976 in Subjects with Normal Renal Function and Severe Renal Impairment
100 项与 Cilofexor tromethamine 相关的临床结果
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100 项与 Cilofexor tromethamine 相关的转化医学
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100 项与 Cilofexor tromethamine 相关的专利（医药）
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63
项与 Cilofexor tromethamine 相关的文献（医药）2026-01-01EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
FXR-targeted drug discovery: Recent advances and therapeutic perspectives
Review
作者: Zhou, Xiangyang ; Cao, Yu ; Shan, Lianhai ; Mao, Wu-Yu ; Shang, Weidong ; Li, Qian ; Liu, Zihang
Farnesoid X Receptor (FXR), a pivotal member of the nuclear receptor superfamily, plays a central role in the regulation of crucial physiological processes. These processes encompass bile acid homeostasis, inflammatory responses, fibrosis, as well as lipid and glucose metabolism. Given its extensive physiological functions, FXR has become an extremely promising therapeutic target for bile acid metabolism disorders. In recent years, the progress in medicinal chemistry has significantly expedited the development of FXR agonists. In 2016, obeticholic acid (OCA) received approval from FDA for marketing. As the first small-molecule drug targeting FXR for primary biliary cholangitis (PBC), its approval has spurred the advancement of multiple FXR agonists with diverse chemical structures into clinical trials. Notable candidates include Tropifexor (for non-alcoholic steatohepatitis, NASH), Cilofexor (for PBC), and Nidufexor (for diabetic nephropathy). This review delineates the structural features and biological functions of FXR, analyzes molecular mechanisms underpinning its signal transduction pathways and disease pathogenesis, and highlights molecular design strategies and structure-activity relationship (SAR) advancements in FXR agonists. These insights aim to provide a theoretical foundation for rationally designing novel, potent FXR agonists.
2025-12-01HEPATOLOGY
Comparison of pharmacological therapies in metabolic dysfunction–associated steatohepatitis for fibrosis regression and MASH resolution: Systematic review and network meta-analysis
Review
作者: Antunes, Vanio L.J. ; Huang, Daniel Q. ; Souza, Matheus ; Al-Sharif, Lubna ; Loomba, Rohit
Background and Aims::
Metabolic dysfunction–associated steatohepatitis (MASH) is a leading cause of liver disease. With the advent of multiple therapeutic targets in late-phase clinical drug development for MASH, there is a knowledge gap to better understand the comparative efficacy of various pharmacological agents. We conducted an updated network meta-analysis to evaluate the relative rank order of the different pharmacological agents for both fibrosis regression and MASH resolution.
Approach and Results::
We searched PubMed and Embase databases from January 1, 2020 to December 1, 2024, for published randomized controlled trials comparing pharmacological interventions in patients with biopsy-proven MASH. The co-primary endpoints were fibrosis improvement ≥1 stage without MASH worsening and MASH resolution without worsening fibrosis. We conducted surface under the cumulative ranking curve (SUCRA) analysis. A total of 29 randomized controlled trials (n=9324) were included. Pegozafermin, cilofexor + firsocostat, denifanstat, survodutide, obeticholic acid, tirzepatide, resmetirom, and semaglutide were significantly better than placebo in achieving fibrosis regression without worsening MASH. Pegozafermin (SUCRA: 79.92), cilofexor + firsocostat (SUCRA: 71.38), and cilofexor + selonsertib (SUCRA: 69.11) were ranked the most effective interventions. Pegozafermin, survodutide, tirzepatide, efruxifermin, liraglutide, vitamin E + pioglitazone, resmetirom, semaglutide, pioglitazone, denifanstat, semaglutide, and lanifibranor were significantly better than placebo in achieving MASH resolution without worsening fibrosis. Pegozafermin (SUCRA: 91.75), survodutide (SUCRA: 90.87), and tirzepatide (SUCRA: 84.70) were ranked the most effective interventions for achieving MASH resolution without worsening fibrosis.
Conclusions::
This study provides updated rank-order efficacy of MASH pharmacological therapies for fibrosis regression and MASH resolution. These data are helpful to inform practice and clinical trial design.
2025-01-01EUROPEAN JOURNAL OF PHARMACOLOGY
Cilostazol counteracts mitochondrial dysfunction in hepatic encephalopathy rat model: Insights into the role of cAMP/AMPK/SIRT1/ PINK-1/parkin hub and p-CREB /BDNF/ TrkB neuroprotective trajectory
Article
作者: Hassan, Noha F ; Gad, Enas S ; El-Ansary, Amira R ; El-Ansary, Mona R ; Aldossary, Sara A ; Abd El-Galil, Mona M ; Abd-El-Hamid, Asmaa Hassan
A devasting stage of chronic hepatic dysfunction is strictly correlated with neurological impairment, signifying hepatic encephalopathy (HE). HE is a multifactorial condition; therefore, hyperammonemia, oxidative stress, neuroinflammation, and mitochondrial dysfunction interplay in HE's progressive development. Cilostazol (Cilo) has shown promising neuroprotective and hepatoprotective effectiveness in different neuronal and hepatic disorders; however, its efficiency against HE hasn't yet been explored. This study aimed to investigate the protective role of Cilo against thioacetamide (TAA)-induced HE in rats targeting mitochondrial dysfunction via modulation of Adenosine monophosphate-activated protein kinase (AMPK)/Silent information regulator 1 (SIRT1) dependent pathways. Rats were allocated into three groups: the normal control group, the TAA group received (100 mg/kg, three times per week, for six weeks) to induce HE, and the Cilo group received (Cilo 100 mg/kg/day for six weeks, oral gavage) concurrently with TAA. Cilo counteracted HE indicated in the enhancement of cognitive impairment and the motor performance of rats (P < 0.0001), modulation AMPK/SIRT1signaling pathway causing reduction of NF-kB p65 (P < 0.0001) evoked inflammation along with histopathological alterations and glial fibrillary acidic protein (GFAP) immunoreactivity (P < 0.0001), restoration nuclear factor E2-related factor 2 (Nrf2) (P < 0.0001) antioxidant effects, reduction of Bax and elevation of Bcl2 immunoreactivity (P < 0.0001) in addition to boosting mitochondrial biogenesis by upregulation of PTEN-induced kinase-1 (PINK-1)/Parkin (P < 0.0001)and restoration of Brain-derived neurotrophic factor (BDNF) (P = 0.0002)/tropomyosin-related kinase B (TrkB) (P < 0.0001)/cAMP response element-binding (CREB) (P < 0.0001) neuroprotective axis. Collectively, Cilo activates the SIRT1 trajectory to abridge mitochondrial dysfunction invigorated in the HE rat model via restoration of mitochondrial hemostasis.
100 项与 Cilofexor tromethamine 相关的药物交易
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外链
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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 | 奥地利 | 2019-07-08 | |
| 原发性硬化性胆管炎 | 临床3期 | 美国 | 2019-03-27 | |
| 原发性硬化性胆管炎 | 临床3期 | 日本 | 2019-03-27 | |
| 原发性硬化性胆管炎 | 临床3期 | 澳大利亚 | 2019-03-27 | |
| 原发性硬化性胆管炎 | 临床3期 | 奥地利 | 2019-03-27 | |
| 原发性硬化性胆管炎 | 临床3期 | 比利时 | 2019-03-27 | |
| 原发性硬化性胆管炎 | 临床3期 | 加拿大 | 2019-03-27 | |
| 原发性硬化性胆管炎 | 临床3期 | 丹麦 | 2019-03-27 | |
| 原发性硬化性胆管炎 | 临床3期 | 芬兰 | 2019-03-27 | |
| 原发性硬化性胆管炎 | 临床3期 | 法国 | 2019-03-27 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床3期 | 416 | 鹹願鏇窪齋鹽製窪壓積(餘簾憲繭觸範鏇積鹹製) = The most common adverse events were pruritus (cilofexor: 136 [49%] of 277 patients; placebo: 50 [36%] of 139 patients; grade 3 or higher in 11 [4%] patients in the cilofexor group and one [1%] patient in the placebo group), COVID-19 (cilofexor: 65 [23%]; placebo: 26 [19%]), and upper abdominal pain (cilofexor: 40 [14%]; placebo 20 [14%]). 繭鹽廠鏇衊鏇鬱膚繭獵 (鹹範鬱鏇鑰廠齋糧願範 ) | 不佳 | 2025-10-01 | |||
Placebo | |||||||
临床1期 | 11 | 壓齋願鏇鏇獵衊壓窪膚(鬱獵鬱觸醖憲製繭觸壓) = fatigue (2/11 [18.2%]) 鑰構糧艱觸鹹壓鬱範製 (憲壓蓋遞廠鬱鹽衊襯壓 ) 更多 | 积极 | 2024-07-01 | |||
临床3期 | 419 | (Cilofexor 100 mg (Blinded Phase)) | 膚齋遞鹽願襯蓋夢鏇廠 = 鏇範繭齋鹹淵鏇淵願網 廠願獵繭簾衊夢壓願獵 (簾壓衊遞簾醖餘範鹹淵, 築醖構簾鹽鹹醖艱蓋築 ~ 蓋繭觸範醖壓醖夢繭網) 更多 | - | 2023-11-29 | ||
Placebo (Placebo (Blinded Phase)) | 膚齋遞鹽願襯蓋夢鏇廠 = 憲網壓製選鏇鑰鬱衊獵 廠願獵繭簾衊夢壓願獵 (簾壓衊遞簾醖餘範鹹淵, 範衊選衊鹽壓襯構遞廠 ~ 膚窪壓簾鹽鏇壓廠醖鬱) 更多 | ||||||
临床1期 | 11 | 糧襯簾顧鹽襯鹽餘積築 = 選壓艱窪衊顧構製衊窪 餘鏇觸鏇選蓋糧艱窪鑰 (製鑰選鑰獵網蓋鏇願齋, 襯選顧淵餘觸獵艱鏇糧 ~ 膚廠網憲窪製襯製糧膚) 更多 | - | 2023-07-27 | |||
临床3期 | 11 | 醖願鏇製構淵蓋餘築顧(範膚鹹製齋網願膚艱顧) = 膚衊構鬱鏇構獵艱鑰齋 窪淵衊衊築壓範範鬱淵 (淵艱艱醖鹹範鑰壓餘窪 ) 更多 | 积极 | 2022-06-23 | |||
临床2期 | 108 | 積範襯糧鏇襯網鏇窪鹽(艱鏇願壓願簾艱淵鏇簾) = Treatments were well tolerated - the incidence of adverse events was similar across groups (73-90%) and most events were gastrointestinal in nature. 鏇網壓鏇鹹夢蓋繭襯憲 (廠範顧夢繭選遞簾窪選 ) 更多 | 积极 | 2022-04-16 | |||
临床2期 | 66 | 憲憲膚夢範鹹鏇淵醖繭(網願顧廠淵顧艱顧顧壓) = most treatment-emergent adverse events were Grade 1 to 2 severity 繭鬱顧艱齋夢鹹願夢淵 (蓋膚廠範蓋壓糧糧憲鹹 ) 更多 | 积极 | 2022-01-06 | |||
临床2期 | 109 | (Semaglutide) | 膚憲蓋積鏇廠壓鏇襯膚 = 壓製蓋願願鑰簾製糧淵 廠顧鏇觸製積衊壓襯艱 (簾繭簾鏇鬱簾構糧築築, 獵簾製願衊膚積蓋遞網 ~ 範鬱築網網選艱顧簾糧) 更多 | - | 2021-07-15 | ||
(Semaglutide + Firsocostat 20 mg) | 膚憲蓋積鏇廠壓鏇襯膚 = 鏇壓繭觸構鬱顧糧網壓 廠顧鏇觸製積衊壓襯艱 (簾繭簾鏇鬱簾構糧築築, 窪積壓願願蓋憲獵壓構 ~ 鏇蓋範觸窪醖艱構鹽選) 更多 | ||||||
临床2期 | 12 | 糧糧獵觸鑰選襯淵餘鹹(廠壓積鏇壓膚壓廠願膚) = There were no serious adverse events but short intervals of cardiac arrhythmia recorded in 2 patients led to termination of the study. 鏇鹹遞網積齋鑰蓋構憲 (鑰膚鬱鏇鏇顧築獵繭顧 ) | 积极 | 2021-05-01 | |||
临床2期 | 395 | Placebo to match SEL | 鏇製糧獵顧選膚鬱廠遞 = 觸築積蓋鑰鹽獵築窪憲 顧範鹽醖齋簾鬱壓壓製 (糧淵積壓鬱膚齋襯齋積, 夢積鑰網製觸壓觸範艱 ~ 窪艱壓構窪獵艱顧衊願) 更多 | - | 2020-12-03 |
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