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更新于：2026-10-23
Evofosfamide
艾伏磷酰胺
更新于：2026-10-23
概要
基本信息
原研机构 |
最高研发阶段临床2期 |
首次获批日期- |
最高研发阶段(中国)终止 |
特殊审评- |
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结构/序列
分子式C9H16Br2N5O4P |
InChIKeyUGJWRPJDTDGERK-UHFFFAOYSA-N |
CAS号918633-87-1 |
关联
27
项与 艾伏磷酰胺 相关的临床试验NCT06836726
Phase II Clinical Trial to Test Efficacy of Targeting Hypoxia Combined With ARSI After First-line ARSI Therapy for Castrate Resistant Prostate Cancer
NCT06782555
A Phase 1/2 Immunotherapy Study of Evofosfamide in Combination with Zalifrelimab and Balstilimab in Patients with Advanced Solid Malignancies
NCT03098160
A Phase 1 Immunotherapy Study of Evofosfamide in Combination With Ipilimumab in Patients With Advanced Solid Malignancies
100 项与 艾伏磷酰胺 相关的临床结果
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100 项与 艾伏磷酰胺 相关的转化医学
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100 项与 艾伏磷酰胺 相关的专利（医药）
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142
项与 艾伏磷酰胺 相关的文献（医药）2027-01-01JOURNAL OF COLLOID AND INTERFACE SCIENCE
A biomimetic nanozyme platform for spatiotemporally programmed cascade catalysis and potentiated chemodynamic immunotherapy
Article
作者: Wang, Runwei ; Qiu, Shilun ; Sun, Beibei ; Yan, Fei ; Wan, Ruoxi
Metal-nanozyme-mediated chemodynamic therapy (CDT) has emerged as a promising strategy for the treatment of deep-seated tumors; however, its therapeutic efficacy is often limited by insufficient reactive oxygen species (ROS) generation and poor spatiotemporal control of enzyme-like activity within the tumor microenvironment (TME). Here, we report a biomimetic nanoplatform, CuO@MSN/TH302@GOx@CM (CMTGM), which integrates a programmed multi-enzyme cascade consisting of a copper oxide (CuO) core, a dendritic mesoporous silica (MSN) intermediate shell, the hypoxia-activated prodrug TH302, and surface-conjugated glucose oxidase (GOx). This hierarchical architecture enables stepwise activation and release of distinct enzyme-mimetic functions. Furthermore, CMTGM is cloaked with a homologous tumor cell membrane to enhance tumor-targeting capability. Following internalization of CMTGM into the tumor cells, GOx catalyzes glucose oxidation to generate H2O2 and gluconic acid, thereby disrupting tumor metabolism and acidifying the microenvironment, which accelerates MSN degradation and promotes the release of Evofosfamide (TH302) while exposing the CuO core. The Cu2+ ions released from the core exert glutathione peroxidase-like activity, depleting intracellular glutathione, and peroxidase-like activity, converting H2O2 into highly cytotoxic hydroxyl radicals, thereby amplifying CDT. Meanwhile, GOx-mediated oxygen consumption aggravates hypoxia and activates TH302, which further enhances therapeutic efficacy. This spatiotemporally programmed cascade involving substrate self-supply, responsive degradation, catalytic amplification, and prodrug activation eventually triggers multiple programmed cell death pathways and enhances immunogenic cell death, ultimately eliciting systemic anti-tumor immunity. In both in vitro and in vivo studies, CMTGM demonstrated efficient tumor targeting, robust tumor suppression, and favorable biosafety of in a 4 T1 breast cancer model. This study provides a generalizable strategy for the rational design of programmable catalytic nanomedicines with integrated multifunctionality.
2026-07-01CANCER LETTERS
Lactylation of HIF-1α at K172 drives HIF-1 complex assembly to promote hypoxia-induced immune evasion in esophageal squamous cell carcinoma
Article
作者: Li, Yi ; Liu, Zhihua ; Zheng, Sujuan ; Zhang, Haonan ; Cong, Ji
Hypoxia is a hallmark of the tumor microenvironment, but its role in immune evasion in esophageal squamous cell carcinoma (ESCC) remains to be fully elucidated. Here, we demonstrate hypoxia inversely correlated with anti-tumor immune signatures and CD8+ T cell infiltration in clinical samples and murine models. Functionally, reducing hypoxia with the agents TH-302 or PX-478 in the AKR model enhanced intratumoral CD8+ T cell infiltration and increased their expression of Granzyme B, IFNγ, and TNFα. Mechanistically, hypoxia-induced immune suppression was dependent on protein lactylation. Inhibiting lactylation reversed the hypoxic suppression of CD8+ T cell function and abrogated the hypoxia-driven transcriptional program, which involved pathways like glycolysis, TGFβ, and Notch signaling. This lactylation-dependent regulation operated by facilitating the formation of the HIF-1 transcription complex. Specifically, mass spectrometry identified lactylation at the K172 site of HIF-1α, which was crucial for its binding to HIF-1β and subsequent target gene activation. Furthermore, in a preclinical ESCC model, pharmacological inhibition of HIF-1α with PX-478 synergized with anti-PD-1 therapy, leading to superior tumor control and enhanced CD8+ T cell cytotoxicity. Our study identifies HIF-1α K172 lactylation as a pivotal mechanism of hypoxia-mediated immune escape in ESCC, suggesting a therapeutic strategy to improve immunotherapy.
2026-03-01JOURNAL OF COLLOID AND INTERFACE SCIENCE
Self-amplifying hypoxia cascade in covalent organic framework/metal organic framework nanoreactors for synergistic cancer therapy
Article
作者: Lin, Yulong ; Li, Meng ; Liu, Xiaozhen ; Yu, Chengmu ; Zhao, Lianmei ; Lv, Jie ; He, Chengcai ; Zhang, Ye
Tumor hypoxia, a hallmark of the tumor microenvironment (TME), drives malignancy and therapeutic resistance but also offers a target for selective therapy. Hypoxia-activated prodrugs (HAPs) like TH-302 exploit this niche, yet their efficacy is often limited by insufficient hypoxia levels. To overcome this limitation, a hypoxia-responsive nanoplatform COF@MOF/TH-302@HA was designed to intensify tumor hypoxia and trigger a self-amplifying therapeutic cascade. The platform was constructed by growing a hypoxia-sensitive copper-based metal-organic framework (Cu-MOFs) on a nitrogen-rich porphyrinic covalent organic framework (p-COFs) core, followed by loading of the HAP TH-302 and coating with hyaluronic acid for tumor targeting. Upon accumulation in the tumor, the degradation of the Cu-MOFs shell in the hypoxic microenvironment released Cu2+ ions and TH-302. The p-COFs core enabled near-infrared laser-triggered photothermal and photodynamic therapy (PDT). Crucially, the oxygen consumption during PDT further aggravated hypoxia, which in turn accelerated the degradation of the Cu-MOFs, establishing a feedback loop that amplified the release and efficacy of both TH-302 and Cu2+. Simultaneously, photothermal therapy (PTT) enhanced the Cu2+-mediated Fenton-like reaction. This coordinated action of chemodynamic therapy, photothermal therapy, PDT, and hypoxia-activated chemotherapy resulted in effective tumor suppression both in vitro and in vivo with minimal systemic toxicity. This work presents a novel strategy for leveraging the TME to achieve self-enhanced synergistic therapy.
28
项与 艾伏磷酰胺 相关的新闻（医药）2026-10-19
2026-10-14
2026-10-12
100 项与 艾伏磷酰胺 相关的药物交易
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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 |
|---|---|---|---|---|
| 胰腺导管腺癌 | 临床3期 | 美国 | 2012-12-01 | |
| 胰腺导管腺癌 | 临床3期 | 德国 | 2012-12-01 | |
| 胰腺癌 | 临床3期 | 美国 | 2012-12-01 | |
| 转移性软组织肉瘤 | 临床3期 | 美国 | 2011-09-01 | |
| 转移性软组织肉瘤 | 临床3期 | 奥地利 | 2011-09-01 | |
| 转移性软组织肉瘤 | 临床3期 | 比利时 | 2011-09-01 | |
| 转移性软组织肉瘤 | 临床3期 | 加拿大 | 2011-09-01 | |
| 转移性软组织肉瘤 | 临床3期 | 丹麦 | 2011-09-01 | |
| 转移性软组织肉瘤 | 临床3期 | 法国 | 2011-09-01 | |
| 转移性软组织肉瘤 | 临床3期 | 德国 | 2011-09-01 |
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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1期 | 18 | 簾簾築蓋憲醖顧鹹糧醖(簾獵艱廠鑰憲糧齋餘願) = Grade 3 rash(1 pt） 憲襯願選鏇淵淵獵醖製 (蓋蓋築衊網糧淵鬱醖獵 ) 更多 | 积极 | 2021-08-01 | |||
临床1期 | 21 | 膚遞積夢簾選積膚壓鏇(選獵廠構糧壓衊築築廠) = 淵簾艱鹹憲窪顧鹹廠襯 廠餘餘艱醖鹹餘襯蓋選 (鏇觸鏇鹽艱獵艱簾鬱憲 ) 更多 | 积极 | 2021-06-01 | |||
Pubmed | Sci Rep 人工标引  | 临床2期 | 33 | 構簾壓鬱襯鏇願遞遞觸(選築齋餘糧夢選壓夢鹹) = 齋築膚壓憲願鹽製衊醖 簾膚膚糧顧壓鑰獵糧築 (窪獵網觸願衊遞蓋夢獵 ) 更多 | 积极 | 2021-01-27 | ||
临床2期 | 17 | 襯襯鹽遞齋齋簾遞夢顧(餘願憲鹹簾蓋鬱選獵鹹) = 衊夢壓獵窪鏇齋齋淵廠 構鑰觸廠窪鹽淵壓鏇獵 (醖廠餘構鏇製製壓淵顧, 壓憲鏇網糧鏇築簾餘鹹 ~ 糧積壓遞蓋鬱繭蓋醖遞) 更多 | - | 2020-07-27 | |||
临床2期 | 35 | 繭選構鹽廠鬱觸淵鑰糧 = 積遞齋網顧憲淵衊範積 鑰憲顧衊齋憲構艱觸選 (願築繭壓憲鹽鏇簾艱鬱, 壓憲繭膚顧網遞鹽構繭 ~ 鑰艱築襯壓鹽夢簾繭壓) 更多 | - | 2020-04-10 | |||
临床1期 | 21 | 襯築餘觸壓餘夢壓襯願(觸顧網餘廠壓壓願衊簾) = n=16 獵獵顧構築繭鏇簾襯糧 (繭壓膚積衊築廠鹽壓鏇 ) 更多 | 积极 | 2019-11-01 | |||
临床2期 | 28 | Placebo+TH-302 (Cohort 1) | 製鹹鹹範網憲鑰醖齋蓋(餘艱憲淵壓繭築糧願簾) = 衊鑰願淵鏇鹹窪選襯壓 艱蓋願糧觸廠醖製願醖 (蓋餘選衊繭簾鑰夢廠範, 選膚築艱遞襯顧築壓獵 ~ 憲鬱窪鏇選淵繭餘淵艱) 更多 | - | 2019-07-24 | ||
(Cohort 2) | 製鹹鹹範網憲鑰醖齋蓋(餘艱憲淵壓繭築糧願簾) = 夢觸淵觸觸醖淵鹹鑰憲 艱蓋願糧觸廠醖製願醖 (蓋餘選衊繭簾鑰夢廠範, 構鏇壓觸簾鏇繭願夢糧 ~ 膚鹹廠夢鹹築鏇憲積醖) 更多 | ||||||
临床2期 | 17 | 淵鹽糧願憲簾網襯艱鏇(鏇築繭繭蓋廠顧襯膚網) = 顧獵構廠醖觸醖憲鏇鹹 鏇鹽選鏇蓋簾構夢憲夢 (範憲餘築網製鏇築顧遞 ) 更多 | 不佳 | 2019-06-03 | |||
临床1/2期 | 59 | dexamethasone+evofosfamide | 鹽襯衊觸襯齋網膚淵鏇(襯願鬱鹹襯鑰鹹簾選選) = 窪範鏇齋蓋積淵蓋築網 壓壓鑰繭鹹衊獵製範淵 (憲願簾淵選鬱網襯鹹糧 ) 更多 | 积极 | 2019-01-15 | ||
選鏇觸鏇衊夢壓網獵積(積鏇製顧齋齋鹽鬱憲衊) = 簾艱憲選獵餘網壓構鏇 選齋餘淵餘壓窪選範糧 (簾糧觸艱廠鑰觸鹹鑰獵 ) 更多 | |||||||
临床2期 | 6 | 衊繭網構艱憲淵衊餘鬱 = 壓蓋窪夢廠製築醖餘顧 夢壓衊繭製網構膚選廠 (廠憲鬱獵製夢顧淵壓夢, 築積蓋窪顧餘積壓壓鑰 ~ 淵築醖簾獵觸壓艱鹽鹽) 更多 | - | 2018-12-14 |
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