预约演示
更新于：2026-05-23
INB-03
更新于：2026-05-23
概要
基本信息
原研机构 |
在研机构 |
最高研发阶段临床2期 |
首次获批日期- |
最高研发阶段(中国)- |
特殊审评快速通道 (美国) |
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结构/序列
Sequence Code 9998254
来源: *****
关联
6
项与 INB-03 相关的临床试验NCT05321498
A Phase 2, Randomized, Placebo-Controlled, Double-Blind Study of XPro1595 in Patients With Mild Cognitive Impairment (MCI) With Biomarkers of Inflammation
NCT05522387
An Open Label Extension of XPro1595 in Patients With Alzheimer's Disease That Have Completed a Phase 1 or Phase 2 Study With XPro1595
NCT05318976
A Randomized, Placebo-Controlled, Double-Blind Study of XPro1595 in Patients With Early Alzheimer's Disease With Biomarkers of Inflammation
100 项与 INB-03 相关的临床结果
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100 项与 INB-03 相关的转化医学
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100 项与 INB-03 相关的专利（医药）
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44
项与 INB-03 相关的文献（医药）2026-02-01JOURNAL OF PHYSIOLOGY-LONDON
Targeting necroptosis protects against astrocyte death and hippocampal sclerosis in experimental temporal lobe epilepsy
Article
作者: Lukas Henning ; Christian Steinhäuser ; Zhou Wu ; Peter Bedner
Abstract:
Temporal lobe epilepsy (TLE) is the most common and severe form of adult focal epilepsy and is frequently associated with hippocampal sclerosis (HS). Accumulating evidence suggests that brain inflammation plays an important pathophysiological role in TLE. A key pro‐inflammatory mediator is tumour necrosis factor α (TNFα), which can trigger necroptosis pathways regulated by RIPK1, RIPK3 and MLKL through binding to the TNF receptor 1 (TNFR1). Previously, we detected activation of RIPK1, RIPK3 and MLKL in hippocampal CA1 astrocytes, along with a reduction in astrocyte density, during the early stages of experimentally induced TLE‐HS, providing strong evidence for necroptotic astrocytic cell death. Using immunohistochemistry, pharmacology and long‐term EEG recording, here we unravel the mechanisms underlying necroptosis induction in astrocytes and its role in epileptogenesis. The results show that pharmacological inhibition of necroptosis using Nec‐1s, a specific inhibitor of RIPK1, or selective inhibition of soluble TNFα by XPro1595, as well as genetic knockout of TNFR1, effectively rescued CA1 astrocyte loss caused by kainate‐induced status epilepticus. Furthermore, targeting necroptosis by Nec‐1s administration attenuated CA1 astrogliosis, degeneration of pyramidal neurons, granular cell dispersion and shrinkage of the CA1 subfield. In contrast, Nec‐1s did not affect acute and chronic epileptic activity in the TLE‐HS model. Our findings demonstrate that TNFα‐induced necroptotic astrocyte death is involved in the pathogenesis of TLE.
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Key points:
In the early stage of experimental temporal lobe epilepsy with hippocampal sclerosis (TLE‐HS), we observed activation of RIPK1, RIPK3 and MLKL in CA1 astrocytes, along with a reduction in astrocyte density, providing evidence for necroptotic cell death.Pharmacological inhibition of necroptosis (Nec‐1s), blockade of soluble tumour necrosis factor α (XPro1595) or genetic knockout of TNFR1 prevented astrocyte loss after status epilepticus.Continuous telemetric EEG recordings showed that Nec‐1s has no effect on acute or chronic epileptic activity in the TLE‐HS model.Immunohistochemical analysis revealed that Nec‐1s treatment reduced the extent of hippocampal sclerosis in experimental TLE‐HS.Our results provide further insights into the molecular mechanisms underlying the development and progression of TLE.
2026-01-01Neurobiology of pain (Cambridge, Mass.)
Xpro®1595 alleviates neuropathic pain by targeting spinal dorsal horn ADAM17-mediated inflammation
Article
作者: Li, Li ; Yao, Wei-Wei ; Sun, Yan-Yan ; Sun, Ling-Ling ; Su, Yidie
A disintegrin and metalloprotease 17 (ADAM17) mediates the shedding of key pro-inflammatory cytokines, yet its specific contribution to neuropathic pain remains elusive. Here, we investigated the role of ADAM17 in the rat spinal nerve ligation (SNL) model. Following nerve injury, ADAM17 expression was significantly upregulated in the spinal dorsal horn (SDH) and dorsal root ganglion (DRG). Specifically, ADAM17 colocalized with TRPV1 and IB4 positive afferents in the superficial SDH, and with IB4, CGRP, and TRPV1 positive neurons in the DRG. Intrathecal administration of exogenous ADAM17 to naive rats recapitulated neuropathic pain behaviors-inducing mechanical and thermal hypersensitivity-and significantly increased the levels of TNF-α, IL-1β, and IL-6 in the SDH. Conversely, therapeutic treatment with Xpro®1595 markedly attenuated SNL-induced pain behaviors. This analgesic effect correlated with the suppression of injury-induced ADAM17 upregulation and a consequent reduction in proinflammatory cytokines. These findings demonstrate that ADAM17 is a critical driver of the neuroinflammatory cascade in neuropathic pain. Moreover, our data suggest that the analgesic efficacy of Xpro®1595 is mediated, at least in part, by disrupting this ADAM17-dependent inflammatory feedback loop.
2025-12-23BIOSCIENCE REPORTS
The effect of the nonselective TNF inhibitor etanercept and of the selective TNF inhibitor XPro1595 on lesioned supraspinatus muscle
Article
作者: Nasseri, Sohail ; Aboo, Christopher ; Jensen, Peter Toft ; Ditzel, Nicholas ; Hejbøl, Eva Kildall ; Ding, Ming ; Stensballe, Allan ; Lambertsen, Kate Lykke ; Schrøder, Henrik Daa ; Frich, Lars Henrik ; Linh Ta, Thi My
The cytokine tumor necrosis factor (TNF), a major regulator of inflammatory responses, exists in both a membrane-bound form and a soluble form. We used the nonselective TNF inhibitor etanercept and the selective inhibitor XPro1595 and compared supraspinatus muscle cytokine levels, histology, and proteomic signatures in mice after supraspinatus tendon tear. The aim was to investigate the effect of anti-TNF treatment on the early inflammatory response in the muscle after tendon tear. In addition, the effect on body composition and bone mineral content was compared in naive mice after 2 months of treatment with either etanercept or XPro1595 using dual-energy X-ray absorptiometry (DEXA) and micro-CT. Inhibition of TNF did not significantly affect DEXA indexes of body composition nor bone microarchitecture, apart from increased structure model index and decreased bone surface density at 14 days, and bone surface to volume ratio at 2 months. Supraspinatus tendon tear caused extensive inflammatory changes in the supraspinatus muscle and initiated a regenerative response. However, TNF inhibition did not significantly affect these processes recorded as density in the lesioned supraspinatus muscle of macrophages and myogenin-positive nuclei. Although both inhibitors had an effect on mitochondrial proteins, particularly etanercept tended to modulate mitochondrial function, and eternacept also influenced NF-κB signaling. Modulation of the mitochondrial proteome and the influence on NF-κB signaling seen after etanercept treatment could correspond with its known effect on apoptosis.
100 项与 INB-03 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 |
|---|---|---|---|---|
| 并发症 | 临床3期 | 美国 | 2020-10-21 | |
| 新型冠状病毒感染 | 临床3期 | 美国 | 2020-10-21 | |
| 阿尔茨海默症 | 临床2期 | 澳大利亚 | 2022-02-28 | |
| 阿尔茨海默症 | 临床2期 | 加拿大 | 2022-02-28 | |
| 阿尔茨海默症 | 临床2期 | 捷克 | 2022-02-28 | |
| 阿尔茨海默症 | 临床2期 | 法国 | 2022-02-28 | |
| 阿尔茨海默症 | 临床2期 | 德国 | 2022-02-28 | |
| 阿尔茨海默症 | 临床2期 | 波兰 | 2022-02-28 | |
| 阿尔茨海默症 | 临床2期 | 西班牙 | 2022-02-28 | |
| 阿尔茨海默症 | 临床2期 | 英国 | 2022-02-28 |
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临床结果
临床结果
适应症
分期
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临床2/3期 | 79 | (INB03 + Standard of Care) | 願醖鬱襯繭齋艱製夢網 = 鏇製鹹觸膚築窪衊壓廠 齋壓簾繭夢繭餘製憲鬱 (遞鬱壓鑰窪膚壓構衊齋, 齋範鏇蓋鏇襯鬱膚艱廠 ~ 襯繭壓鬱廠鹽憲繭鹽簾) 更多 | - | 2026-05-19 | ||
Placebo (Placebo + Standard of Care) | 願醖鬱襯繭齋艱製夢網 = 獵遞繭襯憲觸膚簾獵膚 齋壓簾繭夢繭餘製憲鬱 (遞鬱壓鑰窪膚壓構衊齋, 網製壓憲網糧網築膚構 ~ 築鏇築憲觸製範窪廠鬱) 更多 | ||||||
临床2期 | 208 | 衊夢獵顧艱選選憲構鹹(鹹鹽襯衊網醖夢鏇顧醖) = was not met 膚餘製顧襯壓廠廠獵醖 (壓醖築蓋顧齋窪餘鏇顧 ) 未达到 更多 | 积极 | 2025-07-24 | |||
Placebo | |||||||
临床2期 | 208 | 窪網膚襯遞鑰壓餘醖願(齋衊蓋窪襯遞膚憲衊範) = did not meet the primary cognitive endpoint. 艱廠鑰淵夢構醖遞壓繭 (艱壓壓餘鏇積壓積淵遞 ) 未达到 更多 | 不佳 | 2025-06-30 | |||
Placebo | |||||||
GlobeNewswire 人工标引  | 临床2期 | 7 | 獵鹹鹽窪衊齋壓餘網願(製糧觸憲製夢夢獵鑰製) = statistically significant increase in Alpha wave frequency and power (p<0.05) 築選醖鏇積網製鹽艱鑰 (膚鑰齋願願積衊鏇膚鹹 ) | 积极 | 2024-03-05 | ||
placebo | |||||||
临床1期 | 阿尔茨海默症 inflammation | 3 | 構鹽襯鹽築壓選醖鬱夢(鏇願糧願觸獵網襯積積) = 淵繭鑰膚製製鏇選獵網 衊築網鏇壓築簾憲繭廠 (鹹鬱艱鏇衊齋襯鹽夢蓋 ) | 积极 | 2023-10-24 | ||
临床1期 | 9 | 鏇製構膚壓壓壓廠鏇膚(繭襯簾襯顧遞壓範遞鹽) = 範觸衊糧鑰範齋壓範積 廠醖艱觸製鏇築鏇艱壓 (艱製窪醖繭鹽餘鏇淵襯 ) | 积极 | 2023-10-24 |
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