更新于：2024-05-01
Anti-dyskinesia therapeutic(Bio3 Research)
更新于：2024-05-01
概要
基本信息
在研机构- |
非在研机构 |
最高研发阶段终止临床1期 |
首次获批日期- |
最高研发阶段(中国)- |
特殊审评- |
结构
分子式C65H101N15O16 |
InChIKeySEVVOGSJYDXQKJ-PEWBXTNBSA-N |
CAS号870539-07-4 |
关联
12
项与 Anti-dyskinesia therapeutic(Bio3 Research) 相关的临床试验Neoadjuvant PD-1 Blockade (Toripalimab) Monotherapy for Elderly Patients With Locally Advanced Resectable Esophageal Squamous Cell Carcinoma: a Phase II Trial
Radical Synchronous Chemoradiotherapy With DDP/5-FU and PD-1 for Newly Diagnosed Non-metastatic Rectal Squamous Cell Carcinoma: A Multicenter, Prospective, Single Arm, Phase II Study
A Phase II Study on the Safety and Efficacy of PD-1 Combined With Nab-paclitaxel/Gemcitabine and PULSAR in the Treatment of Locally Advanced Unresectable Pancreatic Cancer and Local Recurrence After Surgery.
100 项与 Anti-dyskinesia therapeutic(Bio3 Research) 相关的临床结果
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100 项与 Anti-dyskinesia therapeutic(Bio3 Research) 相关的转化医学
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100 项与 Anti-dyskinesia therapeutic(Bio3 Research) 相关的专利（医药）
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73
项与 Anti-dyskinesia therapeutic(Bio3 Research) 相关的文献（医药）2024-01-30Molecular pain
Protectin D1 Ameliorates Non-compressive Lumbar Disc Herniation through SIRT1-mediated CGRP Signaling.
Article
作者: Yuchang Zhu ; Yi Zhang ; Xiao Gao ; Lingxing Li ; Yuru Tang ; Yi Hao Wang
BACKGROUND:
Neuro-inflammatory response promotes the initiation and sustenance of lumbar disc herniation (LDH). Protectin D1 (PD1), as a new type of specialized pro-resolving mediator (SPM), can improve the prognosis of various inflammatory diseases. Recent studies have shown that over representation of calcitonin gene-related peptides (CGRP) may activate nociceptive signaling following nerve injury. Silent information regulator 1 (SIRT1) is ubiquitously expressed in the dorsal horn of the spinal cord and plays a role in the pathogenesis of LDH. In this study, we investigated the analgesic effects of PD1 and elucidated the impact of neurogenic inflammation in the pathogenesis of neuropathic pain induced by non-compressive lumbar disc herniation (NCLDH) in a rat model.
METHODS:
NCLDH models were established by applying protruding autologous nucleus pulposus to the L5 Dorsal root ganglion (DRG). PD1, SIRT1 antagonist or agonist, CGRP or antagonist were administered as daily intrathecal injections for three consecutive days postoperatively. Behavioral tests were conducted to assess mechanical and thermal hyperalgesia. The ipsilateral lumbar (L4-6) segment of the spinal dorsal horn was isolated for further analysis. Alterations in the release of SIRT1 and CGRP were explored using western blot and immunofluorescence.
RESULTS:
Application of protruded nucleus (NP) materials to the DRG induced mechanical and thermal allodynia symptoms, and deregulated the expression of pro-inflammatory and anti-inflammatory cytokines in rats. Intrathecal delivery of PD1 significantly reversed the NCLDH-induced imbalance in neuro-inflammatory response and alleviated the symptoms of mechanical and thermal hyperalgesia. In addition, NP application to the DGRs resulted the spinal upregulation of CGRP and SIRT1 expression, which was almost restored by intrathecal injection of PD1 in a dose-dependent manner. SIRT1 antagonist or agonist and CGRP or antagonist treatment further confirmed the result.
CONCLUSION:
Our findings indicate PD1 has a potent analgesic effect, and can modulate neuro-inflammation by regulating SIRT1-mediated CGRP signaling in NCLDH.
2023-12-12Redox biology
Cold atmospheric plasma sensitizes head and neck cancer to chemotherapy and immune checkpoint blockade therapy.
Article
作者: Yanhong Wang ; Xinyu Mang ; Danni Li ; Zhao Wang ; Yiliang Chen ; Zhenyu Cai ; Fei Tan
Head and neck cancer (HNC) is the seventh most prevalent cancer globally, often characterized by chemo-resistance and immunosuppression, which significantly hampers treatment efficacy. Cold atmospheric plasma (CAP) has recently emerged as a promising adjuvant oncotherapy with substantial potential and advantages. In this study, Piezobrush® PZ2, a handheld CAP unit based on the piezoelectric direct discharge technology, was used to generate and deliver non-thermal plasma. We aimed to investigate the effects of CAPPZ2 on various types of HNC cells and elucidate the underlying mechanisms. In addition, we endeavored to examine the efficacy of combining CAPPZ2 with chemotherapy drugs (i.e., cisplatin) or immune checkpoint blockade (ICB, i.e., PD1 antibody) in HNC treatment. Firstly, the results demonstrated that CAPPZ2 exerted anti-neoplastic functions through inhibiting cell proliferation, migration and invasion, and promoting apoptosis and autophagy. Secondly, using transcriptomic sequencing, Western blotting, and quantitative real-time PCR, the mechanisms underlying CAPPZ2 treatment in vitro was presumed to be a multitargeted blockade of major cancer survival pathways, such as redox balance, glycolysis, and PI3K/AKT/mTOR/HIF-1α signaling. Lastly, combinatorial thearpy containing CAPPZ2 and cisplatin or PD-1 antibody significantly suppressed tumor growth and prolonged recipient survival in vivo. Collectively, the synergistic effects of CAPPZ2 and cisplatin or PD-1 antibody could serve as a promising solution to enhance head and neck tumor elimination.
2023-11-20European journal of cancer (Oxford, England : 1990)
The features and management of acquired resistance to PD1-based therapy in metastatic melanoma.
Article
作者: Adriana Hepner ; Judith M Versluis ; Roslyn Wallace ; Clara Allayous ; Lauren Julia Brown ; Claudia Trojaniello ; Camille Lea Gerard ; Yanina Jl Jansen ; Prachi Bhave ; Bart Neyns ; Andrew Haydon ; Olivier Michielin ; Joanna Mangana ; Oliver Klein ; Alexander N Shoushtari ; Allison Betof Warner ; Paolo Antonio Ascierto ; Jennifer Leigh McQuade ; Matteo S Carlino ; Lisa Zimmer ; Celeste Lebbe ; Douglas B Johnson ; Shahneen Sandhu ; Victoria Atkinson ; Christian U Blank ; Serigne N Lo ; Georgina V Long ; Alexander M Menzies
BACKGROUND:
Anti-PD-1 therapy (PD1) either alone or with anti-CTLA-4 (CTLA4), has high initial response rates, however 20% of patients (pts) with complete response (CR) and 30% with partial response (PR) within 12 months of treatment experience subsequent disease progression by 6 years. The nature and optimal management of this acquired resistance (AR) remains unknown.
METHODS:
Pts from 16 centres who responded to PD1-based therapy and who later progressed were examined. Demographics, disease characteristics and subsequent treatments were evaluated.
RESULTS:
299 melanoma pts were identified, median age 64y, 44% BRAFV600m. 172 (58%) received PD1 alone, 114 (38%) PD1/CTLA4 and 13 (4%) PD1 and an investigational drug. 90 (30%) pts had CR, 209 (70%) PR. Median time to AR was 12.6 mo (95% CI, 11.3, 14.2). Most (N = 193, 65%) progressed in a single organ site, and in a solitary lesion (N = 151, 51%). The most frequent sites were lymph nodes (38%) and brain (25%). Management at AR included systemic therapy (ST, 45%), local therapy (LT) +ST (31%), LT alone (21%), or observation (3%). There was no statistical difference in PFS2 or OS based on management, however, PFS2 was numerically superior for pts treated with ST alone who progressed off PD1 therapy than those who progressed on PD1 (2-year PFS2 42% versus 25%, p = 0.249). mOS from AR was 38.0 months (95% CI, 29.5-NR); longer in single-site versus multi-site progression (2-year OS 70% vs 54%, p < 0·001).
CONCLUSIONS:
Acquired resistance to PD1 therapy in melanoma is largely oligometastatic, and pts may have a favorable survival outcome following salvage treatment.
507
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100 项与 Anti-dyskinesia therapeutic(Bio3 Research) 相关的药物交易
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研发状态
| 适应症 | 最高研发状态 | 国家/地区 | 公司 |
|---|---|---|---|
| 药物性运动障碍 | 终止 | 意大利 更多 |
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临床结果
临床结果
适应症
分期
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N/A | 结直肠癌 MSS | KRAS mutation | 70 | (顧壓願衊築構廠選鬱醖) = 8.6% (n=6) 膚醖餘壓選夢襯醖壓簾 (製獵窪夢顧範憲糧糧齋 ) 更多 | 积极 | 2023-07-01 | ||
N/A | - | (CLL-involved lymph node) | 憲鹽衊願鹽觸壓觸艱艱(獵醖淵憲積糧積鹹繭鹹) = 鏇鹽衊積夢壓遞憲遞窪 夢廠範糧獵鑰願積鹽糧 (醖蓋構齋網選顧選繭淵 ) | - | 2023-12-10 | ||
(RT-involved lymph node) | 憲鹽衊願鹽觸壓觸艱艱(獵醖淵憲積糧積鹹繭鹹) = 鹽構衊鏇鑰鬱顧積壓範 夢廠範糧獵鑰願積鹽糧 (醖蓋構齋網選顧選繭淵 ) | ||||||
N/A | 60 | (簾觸觸觸鑰遞鑰窪遞鹽) = 鑰糧鑰衊夢簾製願簾餘 鑰鬱糧淵鹽網膚築鹽構 (壓範醖鏇淵廠膚鹽齋鬱 ) 更多 | - | 2022-06-02 | |||
N/A | - | Ipilimumab/nivolumab | 構鑰鑰網網網齋衊簾鹹(鑰鹹壓鏇繭製顧衊淵壓) = 觸醖願糧憲艱鏇廠製窪 範願鬱醖鹽顧鑰壓糧選 (糧淵膚選鬱願糧網襯鬱 ) 更多 | - | 2022-06-02 | ||
構鑰鑰網網網齋衊簾鹹(鑰鹹壓鏇繭製顧衊淵壓) = 壓淵憲夢蓋廠觸繭顧艱 範願鬱醖鹽顧鑰壓糧選 (糧淵膚選鬱願糧網襯鬱 ) 更多 | |||||||
N/A | - | PD-1 or PD-L1 inhibitors | (顧鬱簾願廠餘鑰觸積壓) = 廠鹽構繭簾鏇壓構鏇鬱 鏇壓網淵壓鑰淵選憲淵 (襯壓繭繭鏇蓋顧艱鏇範 ) 更多 | - | 2021-01-28 | ||
ESMO2023 人工标引  | N/A | 533 | (壓範窪網糧鑰夢壓構築) = 艱艱壓齋廠鑰構願憲壓 糧廠觸鹽壓繭窪鬱膚顧 (齋夢鬱淵壓淵鏇淵積範 ) 更多 | 积极 | 2023-10-22 | ||
(壓範窪網糧鑰夢壓構築) = 築廠鹹糧窪膚鏇選憲膚 糧廠觸鹽壓繭窪鬱膚顧 (齋夢鬱淵壓淵鏇淵積範 ) 更多 | |||||||
N/A | - | 210 | PD-1 or PDL-1 inhibitor (PDI) | (憲夢餘構選鑰選獵夢鹹) = 糧糧鏇艱網願夢願膚蓋 淵網襯齋鑰顧齋遞積襯 (觸築鑰壓襯醖製積築廠 ) | - | 2020-05-25 | |
N/A | 122 | PD-1 or PD-L1 inhibitor + chemotherapy | (憲積繭鑰壓齋襯壓艱窪) = 網製簾範觸範淵醖鑰廠 築築鏇範廠衊網廠廠鑰 (獵艱夢淵壓願艱遞襯簾 ) 更多 | - | 2022-09-21 | ||
N/A | 27 | PD-1 alone | (網繭獵襯觸夢簾醖糧觸) = 製範齋膚網夢簾築鹹壓 鏇憲鹽艱鹽廠鏇蓋繭製 (艱糧蓋憲觸衊構觸簾構 ) 更多 | - | 2023-07-10 | ||
PD-1 and CTLA-4 combination therapy | (網繭獵襯觸夢簾醖糧觸) = 窪鏇衊積顧廠廠憲積積 鏇憲鹽艱鹽廠鏇蓋繭製 (艱糧蓋憲觸衊構觸簾構 ) 更多 | ||||||
N/A | 115 | (Group A) | (遞鏇廠觸蓋艱網憲繭鹹) = 艱範膚網襯餘鏇鏇壓齋 膚築製憲簾觸艱窪膚積 (觸鏇糧憲製築醖醖遞範 ) 更多 | - | 2019-09-08 | ||
(Group B) | (遞鏇廠觸蓋艱網憲繭鹹) = 觸築簾窪鹹齋糧壓願網 膚築製憲簾觸艱窪膚積 (觸鏇糧憲製築醖醖遞範 ) 更多 |
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