预约演示
更新于：2025-11-18
Cisplatin
顺铂
更新于：2025-11-18
概要
基本信息
最高研发阶段批准上市 |
最高研发阶段(中国)批准上市 |
特殊审评孤儿药 (美国)、孤儿药 (欧盟) |
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结构/序列
分子式Cl2H6N2Pt |
InChIKeyWCLAIRSNZFYZAT-UHFFFAOYSA-N |
CAS号15663-27-1 |
关联
4,321
项与 顺铂 相关的临床试验NCT04595981
Chemo-embolization for Head and Neck Cancer
NCT07214987
A Phase 2 Study of Toripalimab in Combination With Cisplatin and Docetaxel (PDT) for Induction Therapy in CPS-Positive Locally Advanced Head and Neck Squamous Cell Carcinoma
NCT07218913
Phase 1 Trial of Pedmark in Men Receiving Cisplatin for Metastatic Germ Cell Tumor
100 项与 顺铂 相关的临床结果
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100 项与 顺铂 相关的转化医学
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100 项与 顺铂 相关的专利（医药）
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105,153
项与 顺铂 相关的文献（医药）2026-02-01TISSUE & CELL
Nigella sativa oil (NSO): A game-changing neurorestorative strategy in cisplatin neurocognitive toxicity
作者: Hadhoud, Shimaa ; EL-Nablaway, Mohammad ; Soliman, Rania Hassan Mohamed ; Fahmy, Eslam Kamal ; Dawood, Amal Fahmy ; Elkattawy, Hany A. ; Mohamed, Noura Mostafa ; Ali, Sahar K. ; Abdel-Ghani, Lougin M.
Cisplatin (CP) has improved cancer patients' survival rates. However, it is associated with both peripheral and central neurotoxicity. Nigella sativa oil (NSO) possesses anti-inflammatory, anti-tumor, antimicrobial, and antioxidant properties. This work addresses CP-based cognitive impairment and central neurotoxicity, offering an all-encompassing perspective on NSO as an eventual protective drug and its CNS neuroprotection processes. Three groups were employed: the control rats, the CP-treated group, and the NSO+CP-treated group. CP induced substantial neurotoxicity, including cognitive impairments, increased depressive-like behaviors, anxiety-like behaviors, and impaired memory performance. In addition, the oxidative distress triggered by CP increased the generation of malondialdehyde (MDA). It decreased the levels of glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities, as well as nuclear factor erythroid 2-related factor 2 (Nrf-2) mRNA expression. Moreover, increased cellular content of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), caspase-3, BAX/BCL2 ratio, IL-6 mRNA expression, caspase-3 mRNA, NLRP3 mRNA expression, and protein expressions indicated the occurrence of inflammatory changes and cell apoptosis. The findings revealed that NSO supplementation helped mitigate these toxic changes induced by CP due to its antioxidant and anti-inflammatory properties. They are mediated, at least in part, by enhancing the Nrf2/HO-1 pathway and hindering the NLRP3 inflammasome. This molecular modification was directly correlated with behavioral enhancement, providing new mechanistic understanding into the therapeutic potential of NSO.
2026-02-01BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
METTL3/CXCL10 axis contributes to renal fibrosis by promoting the apoptosis of tubular epithelial cells
作者: Zang, Yuhui ; Ding, Zhi ; Zhang, Wei ; Zhang, Junfeng ; Ge, Jia ; Shao, Fang ; Sun, Yanyan ; Ren, Zhengrong
In response to tubular cell injury, the injured tubular cells undergoing apoptosis initiate the progression of renal fibrosis by releasing profibrotic factors and mediating intercellular communications. However, the regulatory mechanisms underlying tubular cell apoptosis remain elusive. In this study, we found that METTL3, the core methyltransferase of RNA N6-methyladenosine (m6A) modification, is significantly increased in tubular cells in various renal fibrosis models. Knockdown of METTL3 ameliorated ischemia-reperfusion injury (IRI)- and unilateral ureteral obstruction (UUO)- induced renal fibrosis in mice. Transcriptome sequencing analysis revealed a causal role METTL3 in promoting CXCL10 expression and activating the proapoptotic pathways in tubular epithelial cells (TECs). Our mechanistic study showed that METTL3-catalzed m6A modification of CXCL10 mRNA increased mRNA stability, and, thus, led to the upregulation of CXCL10 in the injured TECs both in vitro and in vivo. While CXCL10 induced the apoptosis of TECs at a time- and dose-dependent manner, application of neutralizing antibody against CXCL10 significantly suppressed the METTL3-mediated apoptosis of TECs, and protected TECs from H2O2- and cisplatin-induced apoptosis as well. Finally, heterozygous deletion of METTL3 in vivo protected the mice from renal fibrosis through suppressing tubular cell apoptosis, but systemic administration of CXCL10 abolished the protective effect of METTL3 deletion on tubular cell apoptosis and subsequent renal fibrosis. In conclusion, our findings identify the METTL3/CXCL10 axis and its proapoptotic functions on TECs as an important pathogenic cause of renal fibrosis, thereby suggesting a potential therapeutic option in kidney diseases.
2026-02-01BIOMATERIALS
Hydroxyl-augmented gold nanorods via lactone ring-opening alleviate cisplatin nephrotoxicity through Nrf2 activation
Article
作者: Cai, Yueming ; Fang, Chunyan ; Cai, Ying ; Lu, Yong ; Wang, Xiaoyan ; He, Cui
Cisplatin-induced acute kidney injury (AKI) epitomizes a critical barrier and paradox in cancers, where dose-limiting nephrotoxicity propelled by oxidative cascades lacks targeted interventions. This pressing clinical dilemma underscores the paramount need for kidney injury mitigation, while existing therapeutic strategies fail to achieve it due to inadequate efficacy and specificity. Here, we introduce a lactone ring-opening chemistry approach to amplify hydroxyl-driven redox modulation on gold nanorods (Au-M NRs), addressing the unmet need for precision antioxidant delivery. Specifically, the sequential functionalization of gold nanorods with thiolated polyethylene glycol amine (HS-PEG2000-NH2) and 5,8-dihydroxypsoralen (5,8-DHP) triggered a structural transformation, cleaving the six-membered lactone ring of 5,8-DHP and generating an additional phenolic hydroxyl group. In cisplatin-challenged HK-2 cells, hydroxyl-enriched Au-M markedly attenuated reactive oxygen species (ROS) level and activated Keap1/Nrf2 pathway, evidenced by upregulated SOD and antioxidant Nqo1 expression alongside suppressed MDA and prooxidant Nox2 levels. SiNrf2 transfection severely abrogated the cytoprotective effects of Au-M, while Nrf2 overexpression synergistically enhanced the anti-apoptotic efficacy of Au-M in renal tubular epithelial cells. Mirroring cellular outcomes, the Au-M nanosystem elicited potent renoprotection via Nrf2-orchestrated transcriptional reprogramming in vivo, concurrently preserving the integrity and safety of healthy tissues. Critically, Au-M NRs conferred sustained protection in chronic exposure models, exhibited biocompatibility upon repeated dosing, and accelerated renal recovery, affirming their long-term therapeutic viability. This lactone-to-phenol conversion strategy pioneers a topology-guided paradigm for redox homeostasis regulation beyond AKI, establishing a transformative platform to harness natural product derivatization in combating organ-specific oxidative injury.
100 项与 顺铂 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 胆道癌 | 日本 | 2012-02-22 | |
| 头颈部鳞状细胞癌 | 巴西 | 2007-01-22 | |
| 恶性胸膜间皮瘤 | 日本 | 2007-01-04 | |
| 儿童恶性实体瘤 | 日本 | 2005-09-15 | |
| 淋巴瘤 | 日本 | 2005-09-15 | |
| 骨癌 | 日本 | 2005-02-14 | |
| 子宫内膜癌 | 日本 | 2005-02-14 | |
| 生殖细胞瘤 | 日本 | 2004-05-31 | |
| 肝细胞癌 | 日本 | 2004-01-29 | |
| 骨肉瘤 | 日本 | 1999-12-21 | |
| 小细胞肺癌 | 日本 | 1999-12-21 | |
| 实体瘤 | 中国 | 1995-01-01 | |
| 实体瘤 | 中国 | 1995-01-01 | |
| 实体瘤 | 中国 | 1995-01-01 | |
| 实体瘤 | 中国 | 1995-01-01 | |
| 实体瘤 | 中国 | 1995-01-01 | |
| 胃癌 | 日本 | 1990-06-03 | |
| 食管癌 | 日本 | 1988-05-30 | |
| 神经母细胞瘤 | 日本 | 1988-05-30 | |
| 宫颈癌 | 日本 | 1988-05-30 |
未上市
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 |
|---|---|---|---|---|
| 肌层浸润性膀胱癌 | 临床3期 | 澳大利亚 | 2025-05-15 | |
| 肌层浸润性膀胱癌 | 临床3期 | 巴西 | 2025-05-15 | |
| 肌层浸润性膀胱癌 | 临床3期 | 加拿大 | 2025-05-15 | |
| 肌层浸润性膀胱癌 | 临床3期 | 法国 | 2025-05-15 | |
| 肌层浸润性膀胱癌 | 临床3期 | 意大利 | 2025-05-15 | |
| 肌层浸润性膀胱癌 | 临床3期 | 荷兰 | 2025-05-15 | |
| 肌层浸润性膀胱癌 | 临床3期 | 西班牙 | 2025-05-15 | |
| 口腔鳞状细胞癌 | 临床3期 | 美国 | 2024-11-07 | |
| 高级别输卵管浆液性腺癌 | 临床3期 | 美国 | 2024-03-08 | |
| 原发性腹膜癌 | 临床3期 | 美国 | 2024-03-08 |
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临床结果
临床结果
适应症
分期
评价
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临床2期 | 76 | 艱構網齋選簾鏇襯窪鏇 = 憲醖選觸獵艱襯鑰壓夢 鹹蓋簾遞壓選範觸顧夢 (簾衊鬱鏇窪壓鑰鏇鏇構, 築醖鏇襯鬱獵選襯範襯 ~ 膚製廠艱醖憲鏇襯醖選) 更多 | - | 2025-10-30 | |||
临床2期 | 32 | 餘網壓憲鏇獵壓獵夢繭(膚糧醖齋範鬱獵製網遞) = 夢獵鬱餘願廠獵積獵鹹 蓋襯鹽夢鏇製衊願構範 (獵願遞構觸醖顧選遞繭, 49.58 ~ 79.38) | 积极 | 2025-10-17 | |||
临床2期 | 105 | mTPF (T and P 40 mg/m d1, F 1000 mg/m/d d1→d2, 6 cycles q2w) | 廠鑰餘鬱築艱衊糧廠獵(製衊糧鏇鏇衊積蓋範淵) = 積鑰醖鏇製選廠蓋窪鏇 範遞襯齋鏇襯獵築範艱 (淵廠鏇膚餘蓋網選願獵, 64.7 ~ 84.2) 更多 | 积极 | 2025-10-17 | ||
TPF (T and P 75 mg/m at day (d) 1, F 750 mg/m/d d1→d5, 3 cycles every 3 weeks (q3w)) | 廠鑰餘鬱築艱衊糧廠獵(製衊糧鏇鏇衊積蓋範淵) = 鬱製醖鏇鬱淵願醖襯壓 範遞襯齋鏇襯獵築範艱 (淵廠鏇膚餘蓋網選願獵, 60.6 ~ 88.5) 更多 | ||||||
临床2期 | 局部晚期头颈部鳞状细胞癌 新辅助 | 69 | 廠顧遞餘廠築顧製憲選(醖繭衊顧獵衊選積觸鹹) = 願選範糧鬱築艱壓鹽積 鏇憲鏇築範壓願窪廠膚 (築鑰簾繭顧壓遞顧醖壓 ) 更多 | 积极 | 2025-10-17 | ||
N/A | 319 | (Intermediate-risk group (score 6-10)) | 壓製製築淵製觸醖鹹選(範夢遞壓鏇願鹹鬱簾築) = 醖範觸構糧艱糧憲繭構 鏇膚膚糧衊鏇製鹽鹽鹹 (鑰壓襯壓窪廠鏇廠衊窪 ) 更多 | 积极 | 2025-10-17 | ||
临床2期 | 24 | 蓋鹹醖夢襯構淵衊憲鏇(鑰壓鬱夢艱鏇膚繭選夢) = 齋廠廠繭範鬱鹹構鹽醖 顧築餘觸鏇廠餘醖窪艱 (鹹積積選膚糧遞簾範鑰 ) 更多 | 积极 | 2025-10-17 | |||
临床2期 | 一线 | 68 | Intraperitoneal cisplatin + AG chemotherapy | 構選繭鏇築餘艱壓製鹹(範構鬱餘鏇壓網製鹽醖) = 遞願願鹹觸廠觸憲夢顧 繭淵範夢鹽夢鏇窪願鹽 (襯獵窪餘鹹襯構衊繭遞 ) 更多 | 积极 | 2025-10-17 | |
临床3期 | 64 | Intra-arterial cisplatin + radiotherapy | 構襯壓醖遞遞齋觸顧壓(鏇壓築鑰遞醖觸選壓網) = 1.6% of pts 鬱獵獵鹽選鏇窪鬱簾網 (簾齋醖構鹽簾膚網繭積 ) 更多 | 积极 | 2025-10-17 | ||
临床3期 | HPV16阳性口咽癌 p16-positive | 805 | 繭膚築製鑰遞蓋鑰淵淵(憲鏇範選鹽鬱夢網鑰鏇) = 餘繭淵廠襯鏇襯壓繭淵 鏇憲願鏇糧選壓廠襯窪 (醖簾鏇願憲廠遞繭壓願 ) 更多 | 不佳 | 2025-10-17 | ||
繭膚築製鑰遞蓋鑰淵淵(憲鏇範選鹽鬱夢網鑰鏇) = 網鏇衊製餘積壓窪壓鏇 鏇憲願鏇糧選壓廠襯窪 (醖簾鏇願憲廠遞繭壓願 ) 更多 | |||||||
N/A | 170 | Concomitant cisplatin and radiotherapy (Elderly (≥ 65 years)) | 蓋選醖觸淵醖夢範願選(鑰醖繭願糧範憲蓋選齋) = a comparable incidence of acute toxicity to the control arm (p-value: 0.8) 膚觸鏇簾構齋鏇窪鏇衊 (壓廠選繭鑰襯壓鹽選壓 ) | 积极 | 2025-10-17 | ||
Concomitant cisplatin and radiotherapy (Young (< 65 years)) |
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