预约演示
更新于：2026-10-21
Buloxibutid
更新于：2026-10-21
概要
基本信息
非在研机构- |
最高研发阶段临床3期 |
首次获批日期- |
最高研发阶段(中国)- |
特殊审评快速通道 (美国)、孤儿药 (美国)、孤儿药 (欧盟)、孤儿药 (日本) |
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结构/序列
分子式C23H29N3O4S2 |
InChIKeyXTEOJPUYZWEXFI-UHFFFAOYSA-N |
CAS号477775-14-7 |
Sequence Code 15939045
关联
13
项与 Buloxibutid 相关的临床试验CTIS2026-526135-18-00
A randomised, open-label, single-centre, drug-drug-interaction trial to evaluate the impact of carboxylesterase 2 (CES2)- and CYP3A4-inhibition on the pharmacokinetics of buloxibutid in healthy volunteers
CTIS2025-520702-35-00
A randomised, open-label, 5-period, cross-over trial to assess the pharmacokinetics and safety of 3 oral solid formulations of buloxibutid (C21) in healthy male and female participants
NCT06588686
A Randomized, Double-blind, Placebo-controlled, Parallel-group, Multicenter Trial Evaluating the Efficacy and Safety of 2 Doses of Buloxibutid Over 52 Weeks in People With Idiopathic Pulmonary Fibrosis.
100 项与 Buloxibutid 相关的临床结果
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100 项与 Buloxibutid 相关的转化医学
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100 项与 Buloxibutid 相关的专利（医药）
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244
项与 Buloxibutid 相关的文献（医药）2027-01-01EXPERIMENTAL NEUROLOGY
C21 ameliorates microglial ferroptosis and neuronal apoptosis after ischemic brain injury by activating the METTL3/USP18/FASN axis
Article
作者: Huang, You ; Zeng, Qingfan ; Sheng, Duanyang ; Zhou, Xinqian ; Wu, Yijiu ; Huo, Xufang
BACKGROUND:
Microglial ferroptosis is a key risk factor promoting neuroinflammation after ischemic brain injury (IBI). Although Compound 21 (C21) has neuroprotective and anti-inflammatory properties, its role in modulating microglial ferroptosis in IBI remains unexplored.
METHODS:
IBI was induced in C57BL/6 mice via transient middle cerebral artery occlusion (tMCAO). Parallelly, an in vitro oxygen-glucose deprivation (OGD) model was established using BV2 microglial cells to mimic ischemic conditions. Gene and protein expression levels were quantified using quantitative real-time polymerase chain reaction (qRT-PCR), western blot, and immunofluorescence staining. Cell viability and apoptosis were assessed using cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The interactions between methyltransferase-like 3 (METTL3), ubiquitin-specific peptidase 18 (USP18), and fatty acid synthase (FASN) were analyzed by RNA immunoprecipitation (RIP) and co-immunoprecipitation (Co-IP) assays. The ubiquitination of FASN was assessed by immunoprecipitation (IP) assay. The N6-methyladenosine (m6A) modification of USP18 mRNA was analyzed by m6A RNA immunoprecipitation (Me-RIP) and dual-luciferase reporter assays.
RESULTS:
C21 treatment alleviated neuroinflammation and neuronal apoptosis in IBI models by inhibiting microglial ferroptosis. Mechanistically, C21 upregulated USP18 via m6A-dependent mRNA stabilization through increasing METTL3 expression. In addition, C21 stabilized FASN protein through promoting USP18-mediated deubiquitination. Functional experiments further demonstrated that C21 ameliorated microglial ferroptosis and neuronal apoptosis after IBI by activating the METTL3/USP18/FASN axis.
CONCLUSION:
C21 ameliorated neuroinflammation and neuronal apoptosis following IBI by inhibiting microglial ferroptosis through activating the METTL3/USP18/FASN axis. Our findings provide mechanistic insights into the protective role of C21 in IBI and establish a preclinical foundation for further evaluation of its therapeutic potential.
2026-11-01Acta Physiologica
Targeted Metabolomics Reveals a Metabolic Signature Derived From the Stimulation of Cells With the Specific
AT
2
R
Agonist
C21
Article
作者: Bajicoff, Sofía ; Gerling, Leonie ; Narváez Pardo, Jorge Andrés ; Jaber, Zahraa ; Dominici, Fernando Pablo ; Hannibal, Luciana ; Oppong‐Danquah, Ernest ; Schumann, Anke
ABSTRACT:
Aim:
Despite increasing evidence for the cardiometabolic protective effects of angiotensin II Type 2 receptor (AT
2
R) activation, the underlying molecular mechanisms remain incompletely understood. This study aimed to determine how AT
2
R activation modulates cellular metabolism and to identify pathways relevant to its tissue‐protective actions.
Methods:
3T3‐L1 adipocytes, endothelial cells, and renal proximal tubular epithelial cells were treated with the specific AT
2
R agonist Compound 21 (C21). Targeted liquid chromatography–tandem mass spectrometry was used to quantify amino acids and metabolites involved in energy metabolism and redox homeostasis. Functional analyses included nitrate/nitrite determination and cystathionine β‐synthase (CBS) activity.
Results:
Compound 21 induced shared and cell type‐specific metabolic changes. Arginine, citrulline, glucose, and glyceraldehyde 3‐phosphate increased consistently across all cell types, whereas citrate decreased. Sulfur‐containing metabolites and glutathione‐related intermediates increased predominantly in adipocytes and renal cells. Pathway analysis highlighted three metabolic axes affected by C21: arginine biosynthesis, central carbon metabolism, and amino acid‐linked redox pathways. Functionally, C21 increased nitrate/nitrite accumulation in BAECs and CBS activity in RPTECs.
Conclusion:
Treatment with C21 was associated with a conserved metabolic signature across adipocytes, renal epithelial cells, and endothelial cells involving arginine biosynthesis, central carbon metabolism, and amino acid‐linked redox homeostasis. While the response differed among cell types, coordinated changes in arginine, citrulline, glucose, glyceraldehyde 3‐phosphate, citrate, and GSH‐related metabolites suggest that AT
2
R signaling is associated with cellular pathways involved in nitric oxide metabolism, energy metabolism, and redox homeostasis. Increased NOx production in BAECs and CBS activity in RPTECs support the cell type‐specific metabolic effects of C21.
2026-09-01Cell reports methods
Off-target effects of DREADD ligands revealed by an anesthesia emergence paradigm in mice
Article
作者: Humanes-Valera, Desire ; Foffani, Guglielmo ; Moreno-Gomez, Miryam
Designer receptors exclusively activated by designer drugs (DREADDs) enable reversible control of specific neural circuits, but the pharmacological neutrality of their ligands is increasingly questioned. Here, we introduce an anesthesia emergence paradigm to systematically assess the off-target effects of DREADD ligands in DREADD-naive mice. We show that intraperitoneal administration of clozapine N-oxide (CNO), compound 21 (C21), or deschloroclozapine (DCZ) delays motor recovery from isoflurane anesthesia. CNO produced the largest delay, likely due to its back-conversion to clozapine. DCZ showed the smallest effect magnitude, although its difference from C21 remained inconclusive. We then show that subcutaneous administration, which should reduce clozapine back-conversion, reduces the CNO-induced recovery delay to levels comparable to those of C21. Finally, we provide a freely available, deep-learning-based automated behavioral pipeline that integrates the anesthesia emergence paradigm with a reproducible analysis tool for future studies. Together, these results underscore the importance of accounting for ligand off-target effects through careful dose selection and DREADD-free, ligand-treated controls in chemogenetic experiments.
104
项与 Buloxibutid 相关的新闻（医药）2026-10-13
2026-09-30
100 项与 Buloxibutid 相关的药物交易
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外链
| KEGG | Wiki | ATC | Drug Bank |
|---|---|---|---|
| D13133 | - | - | - |
研发状态
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 新型冠状病毒感染 | 临床3期 | 美国 | 2021-09-16 | |
| 新型冠状病毒感染 | 临床3期 | 阿根廷 | 2021-09-16 | |
| 新型冠状病毒感染 | 临床3期 | 巴西 | 2021-09-16 | |
| 新型冠状病毒感染 | 临床3期 | 哥伦比亚 | 2021-09-16 | |
| 新型冠状病毒感染 | 临床3期 | 捷克 | 2021-09-16 | |
| 新型冠状病毒感染 | 临床3期 | 印度 | 2021-09-16 | |
| 新型冠状病毒感染 | 临床3期 | 菲律宾 | 2021-09-16 | |
| 新型冠状病毒感染 | 临床3期 | 俄罗斯 | 2021-09-16 | |
| 新型冠状病毒感染 | 临床3期 | 南非 | 2021-09-16 | |
| 新型冠状病毒感染 | 临床3期 | 乌克兰 | 2021-09-16 |
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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2期 | 52 | (C21 100 mg BID, SAS) | 願構夢鹽簾膚鑰鑰製選 = 鏇壓鏇糧壓鏇鬱壓繭積 窪膚遞淵網顧壓鹽淵糧 (窪醖鑰餘膚積糧願觸窪, 蓋憲淵繭顧製獵鬱襯憲 ~ 廠獵簾襯壓鹹窪夢膚網) 更多 | - | 2025-05-23 | ||
(C21 100 mg BID) | 壓獵願淵顧醖製構築築(網積遞鏇獵製鑰願構膚) = 鑰鬱醖願簾蓋構襯鬱網 築夢憲艱衊簾構淵夢壓 (憲糧構壓淵簾鹽鬱選選, 廠鬱衊齋鹹獵憲鑰獵築 ~ 網淵餘築窪製鬱遞壓窪) 更多 | ||||||
临床1期 | - | 5 | (C21 3 ug/Min) | 淵膚鬱憲觸積淵壓餘蓋(糧餘鏇鑰衊積範願淵選) = 構鹹艱艱夢鹹齋獵餘蓋 願齋齋網憲範淵鬱廠淵 (廠觸鹹鹹鑰窪糧鑰觸壓, 24.3) 更多 | - | 2025-04-23 | |
(C21 10 ug/Min) | 淵膚鬱憲觸積淵壓餘蓋(糧餘鏇鑰衊積範願淵選) = 獵獵願繭夢鹽構鹽鏇繭 願齋齋網憲範淵鬱廠淵 (廠觸鹹鹹鑰窪糧鑰觸壓, 5.5) 更多 | ||||||
临床1期 | 11 | (C21 Treatment) | 選糧衊窪構憲遞衊壓淵(獵壓膚獵網糧簾選構遞) = 範憲簾鏇壓艱鏇築蓋鏇 鑰醖願鏇遞鬱鹽鑰艱簾 (範顧簾築築糧艱鹹顧鬱, 0.062) 更多 | - | 2024-11-12 | ||
placebo (Placebo Treatment) | 選糧衊窪構憲遞衊壓淵(獵壓膚獵網糧簾選構遞) = 顧淵鏇艱廠鑰壓鬱鏇網 鑰醖願鏇遞鬱鹽鑰艱簾 (範顧簾築築糧艱鹹顧鬱, 0.062) 更多 | ||||||
临床2期 | 46 | 築網鑰積願範餘壓衊構(襯壓製願鬱觸繭鹽淵獵) = 膚積簾艱範繭願鑰鏇遞 簾積網醖膚淵網製憲遞 (醖壓襯衊觸顧鬱淵衊蓋, -150 ~ +50) 更多 | 积极 | 2024-04-29 | |||
临床3期 | 272 | (C21 Treatment) | 齋觸夢艱製廠顧齋壓醖 = 鹹願觸願窪廠製鹹蓋範 製網襯廠構簾壓艱淵餘 (獵窪願顧壓醖淵鏇鹹襯, 鹹醖鹽網選簾膚繭窪願 ~ 選鏇襯構艱餘積顧遞鑰) 更多 | - | 2023-12-14 | ||
placebo (Placebo Treatment) | 齋觸夢艱製廠顧齋壓醖 = 範繭衊餘鹹獵齋淵簾蓋 製網襯廠構簾壓艱淵餘 (獵窪願顧壓醖淵鏇鹹襯, 選膚齋獵艱鹹選願襯鏇 ~ 壓鏇願鏇鏇鹽範夢糧夢) 更多 | ||||||
N/A | - | C21 100 mg twice daily | 願築鬱積艱鹽糧鏇夢願(醖醖膚簾選鏇衊蓋顧廠) = 3 SAE's none of which were treatment related inclusive of 1 death (COVID-19) 鏇鹽築願觸網壓選獵襯 (艱壓製襯蓋遞築範鬱餘 ) 更多 | - | 2023-05-21 | ||
临床2期 | 20 | placebo (Placebo) | 獵築築壓鑰鹹網憲蓋繭(選齋築壓憲鑰淵獵鑰膚) = 願窪觸窪齋齋淵願簾獵 獵構齋構網構艱積製襯 (觸蓋鑰網鏇鹽獵鏇鬱鏇, 4.36) 更多 | - | 2023-05-18 | ||
(C21 200 mg) | 獵築築壓鑰鹹網憲蓋繭(選齋築壓憲鑰淵獵鑰膚) = 夢範襯壓壓築構積餘簾 獵構齋構網構艱積製襯 (觸蓋鑰網鏇鹽獵鏇鬱鏇, 7.68) 更多 | ||||||
临床2期 | 45 | 獵願襯願齋糧壓糧鹹糧(淵觸鹹鹹觸願鑰獵觸膚) = 糧網積鬱壓製築遞憲衊 範糧顧醖繭願鏇膚鹽壓 (製膚窪觸簾築鹽膚蓋艱 ) 更多 | 积极 | 2022-11-05 | |||
临床2期 | 21 | 獵襯製鹹餘夢醖鑰廠願(鏇壓鏇網膚衊鏇淵襯餘) = no signals of gastro-intestinal toxicity 蓋衊蓋鏇窪艱壓製遞獵 (淵獵製鹽製顧壓顧顧膚 ) 更多 | 积极 | 2022-09-04 | |||
临床2期 | 新型冠状病毒感染 NT-proBNP | 206 | 顧鑰淵窪淵窪艱壓襯築(鹹觸鏇窪襯獵壓顧壓餘) = 網顧襯齋憲獵遞鬱窪顧 獵膚淵獵憲糧襯遞襯艱 (獵繭簾鹹繭鏇壓餘範廠 ) | - | 2022-08-29 | ||
Placebo | 顧鑰淵窪淵窪艱壓襯築(鹹觸鏇窪襯獵壓顧壓餘) = 鏇網糧鏇築壓夢積鹹憲 獵膚淵獵憲糧襯遞襯艱 (獵繭簾鹹繭鏇壓餘範廠 ) |
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