更新于：2024-11-01

CD160

更新于：2024-11-01

基本信息

别名

BY55、CD160、CD160 antigen

+ [5]

简介

Receptor on immune cells capable to deliver stimulatory or inhibitory signals that regulate cell activation and differentiation. Exists as a GPI-anchored and as a transmembrane form, each likely initiating distinct signaling pathways via phosphoinositol 3-kinase in activated NK cells and via LCK and CD247/CD3 zeta chain in activated T cells (PubMed:19109136, PubMed:11978774, PubMed:17307798). Receptor for both classical and non-classical MHC class I molecules (PubMed:9973372, PubMed:12486241). In the context of acute viral infection, recognizes HLA-C and triggers NK cell cytotoxic activity, likely playing a role in anti-viral innate immune response (PubMed:12486241). On CD8+ T cells, binds HLA-A2-B2M in complex with a viral peptide and provides a costimulatory signal to activated/memory T cells (PubMed:9973372). Upon persistent antigen stimulation, such as occurs during chronic viral infection, may progressively inhibit TCR signaling in memory CD8+ T cells, contributing to T cell exhaustion (PubMed:25255144). On endothelial cells, recognizes HLA-G and controls angiogenesis in immune privileged sites (PubMed:16809620). Receptor or ligand for TNF superfamily member TNFRSF14, participating in bidirectional cell-cell contact signaling between antigen presenting cells and lymphocytes. Upon ligation of TNFRSF14, provides stimulatory signal to NK cells enhancing IFNG production and anti-tumor immune response (By similarity). On activated CD4+ T cells, interacts with TNFRSF14 and down-regulates CD28 costimulatory signaling, restricting memory and alloantigen-specific immune response (PubMed:18193050). In the context of bacterial infection, acts as a ligand for TNFRSF14 on epithelial cells, triggering the production of antimicrobial proteins and pro-inflammatory cytokines (By similarity). The soluble GPI-cleaved form, usually released by activated lymphocytes, might play an immune regulatory role by limiting lymphocyte effector functions.

关联

项与 CD160 相关的药物

ELB011

靶点

CD160

作用机制

CD160抑制剂

在研机构

ElsaLys Biotech SAS

原研机构

ElsaLys Biotech SAS

在研适应症

眼部疾病

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

CD160-TM(Alderaan)

靶点

CD160

作用机制

CD160抑制剂

在研机构

Alderaan Biotechnology SAS初创企业

原研机构

Alderaan Biotechnology SAS初创企业

在研适应症

三阴性乳腺癌

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

ELB-012

靶点

CD160

作用机制

CD160抑制剂

在研机构

ElsaLys Biotech SAS

原研机构

ElsaLys Biotech SAS

在研适应症

青光眼 [+1]

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 CD160 相关的临床结果

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100 项与 CD160 相关的转化医学

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0 项与 CD160 相关的专利（医药）

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419

项与 CD160 相关的文献（医药）

2025-01-01·Journal of Pharmaceutical and Biomedical Analysis

A study of the association of vitamin D receptor (VDR) as a predictive biomarker for immune checkpoint inhibitor therapy with immune invasion in colon adenocarcinoma

Article

作者: Lin, Ailing ; Chao, Guanqun ; Bao, Yang

Colon adenocarcinoma(COAD) is a primary and aggressive malignancy with the fifth highest mortality rate among cancers, and it is important to discover new strategies. The online database was used to analyze the correlation between Vitamin D receptor (VDR) and COAD, and further explore the immune infiltration and related gene networks.The expression and methylation levels of VDR was analyzed by using Timer database, GEPIA platform and UALCAN database. GeneMANIA database was used to analyze and obtain gene networks that are closely linked to VDR. UALCAN database was used to score the gene effects of VDR in colorectal cancer cell lines. The cBioPortal database was used for the detection of gene mutations. The survival curve analysis was carried out using the GEPIA database. The relationship between VDR expression and immune cell infiltration was analyzed by using the timer database and TISIDB database. TISIDB database was used to obtain VDR-related drug targets.The expression of VDR was significantly lower in COAD(p<0.05). The methylation level of VDR was significantly higher in COAD (p<0.05). The gene mutation rate of VDR in COAD was 2 %. OS and DFS were not associated with changes in the VDR gene in patients with COAD. VDR expression was correlated with CD4+T cell infiltration, macrophage infiltration, neutrophil infiltration, and dendritic cell infiltration. VDR has a clear correlation with ADORA2A, BTLA, CD160, CD244, CD274, CD96, CSF1R, CTLA4, HAVCR2, IL10, IDO1, LAG3, LGALS9, PDCD1, PDCD1LG2, PVRL2, TGFB1, TGFBR1, TIGIT and VTCN1.The expression of VDR is associated with immune infiltration in patients with COAD. VDR may be a new candidate biomarker for determining the level of immune infiltration and predicting immune checkpoint inhibitor therapy.

2024-12-01·Journal of Infection

CD151 identifies an NK cell subset that is enriched in COVID-19 patients and correlates with disease severity

Article

作者: Pérez-Garay, Raquel ; Sevilla, Arrate ; Amo, Laura ; Meijide, Susana ; Arana-Arri, Eunate ; Astarloa-Pando, Gabirel ; Sandá, Víctor ; Amarilla-Irusta, Ainhoa ; Zenarruzabeitia, Olatz ; Pérez-Fernández, Silvia ; Lopez-Pardo, Ainara ; Borrego, Francisco ; Imaz-Ayo, Natale

Severe coronavirus disease 2019 (COVID-19) often lead to acute respiratory distress syndrome and multi-organ dysfunction, driven by a dysregulated immune response, including a cytokine storm with elevated proinflammatory cytokine levels. Natural killer (NK) cells are part of the innate immune system with a fundamental role in the defense against viral infections. However, during COVID-19 acute infection, they exhibit an altered phenotype and impaired functionality contributing to the immunopathogenesis of the disease. In this work, we have studied a cohort of patients with COVID-19 (ranging from mild to severe) by analyzing IL-15, TGF-β, PlGF and GDF-15 plasma levels and performing multiparametric flow cytometry studies. Our results revealed that severe COVID-19 patients exhibited high levels of IL-15, PlGF and GDF-15, along with an enrichment of a NK cell subset expressing the CD151 tetraspanin, which correlated with IL-15 plasma levels and disease severity. In patients, these CD151+ NK cells displayed a more activated phenotype characterized by an increased expression of HLA-DR, CD38 and granzyme B, a distinct receptor repertoire, with lower levels of CD160 and CD31 and higher levels of CD55 and, remarkably, a higher expression of tissue-resident markers CD103 and the NK cell decidual marker CD9. Last of all, in individuals with severe disease, we identified an expansion of a CD151^brightCD9+ NK cell subset, suggesting that these cells play a specific role in COVID-19. Altogether, our findings suggest that CD151+ NK cells may have a relevant role in COVID-19 immunopathogenesis.

2024-11-01·Pflügers Archiv - European Journal of Physiology

Central and peripheral mechanisms underlying respiratory deficits in a mouse model of accelerated senescence

Article

作者: Maia, Octavio A C ; Takakura, Ana C ; Moreira, Thiago S ; Moriya, Henrique T ; Tavares-Lima, Wothan ; Lino-Alvarado, Alembert ; Oliveira, Maria Aparecida

Aging invariably decreases sensory and motor stimuli and affects several neuronal systems and their connectivity to key brain regions, including those involved in breathing. Nevertheless, further investigation is needed to fully comprehend the link between senescence and respiratory function. Here, we investigate whether a mouse model of accelerated senescence could develop central and peripheral respiratory abnormalities. Adult male Senescence Accelerated Mouse Prone 8 (SAMP8) and the control SAMR1 mice (10 months old) were used. Ventilatory parameters were assessed by whole-body plethysmography, and measurements of respiratory input impedance were performed. SAMP8 mice exhibited a reduction in the density of neurokinin-1 receptor immunoreactivity in the entire ventral respiratory column. Physiological experiments showed that SAMP8 mice exhibited a decreased tachypneic response to hypoxia (FiO2 = 0.08; 10 min) or hypercapnia (FiCO2 = 0.07; 10 min). Additionally, the ventilatory response to hypercapnia increased further due to higher tidal volume. Measurements of respiratory mechanics in SAMP8 mice showed decreased static compliance (Cstat), inspiratory capacity (IC), resistance (Rn), and elastance (H) at different ages (3, 6, and 10 months old). SAMP8 mice also have a decrease in contractile response to methacholine compared to SAMR1. In conclusion, our findings indicate that SAMP8 mice display a loss of the NK1-expressing neurons in the respiratory brainstem centers, along with impairments in both central and peripheral respiratory mechanisms. These observations suggest a potential impact on breathing in a senescence animal model.

项与 CD160 相关的新闻（医药）

2024-10-29

·生物探索

Nat Immunol | 淋巴结兼具效应和干性SIV特异性TOX+TCF1+CD39+CD8+T细胞与SIV限制相关

引言在人类免疫缺陷病毒（human immunodeficiency virus，HIV）感染中，CD8+T细胞对于病毒的清除至关重要【1】。因此，CD8+T细胞生物学动态与HIV感染患者息息相关。在慢性感染和肿瘤中，持续的抗原刺激诱导耗竭性T细胞（exhausted T cell，Tx）的产生【2】。TX的典型特征是由TOX等转录因子驱动的转录组和表观组重塑介导的效应功能减弱和抑制性受体的高表达【2】。值得注意的是，TOX不仅表达于Tx，也会表达于部分多功能效应记忆性T细胞，有时甚至与TCF-1共表达【3,4】，呈现干细胞样特性。研究表明，在大多数HIV感染患者中，HIV-特异性CD8+T细胞耗竭分子表达增加与高病毒载量和疾病进展相关【3,5】。在HIV感染患者外周血中，部分HIV-特异性CD8+T细胞中检测到TCF-1和TOX共表达【4】。作为HIV病毒存在和复制的主要位点，淋巴结内CD8+T细胞的表型和功能状态对于治疗策略的改善和设计至关重要。近日，美国埃默里大学国家灵长动物研究中心微生物与免疫学部Mirko Paiardini研究团队在Nature Immunology杂志发表了题为Distinct SIV-specific CD8+ T cells in the lymph node exhibit simultaneous effector and stem-like profiles and are associated with limited SIV persistence的研究文章。这项研究通过流式、质谱、scRNA-seq和TCR-seq等分析在淋巴结内鉴定一群具有干细胞特性中间效应功能的SIV-特异性TOXhiTCF1+CD39+CD8+T细胞，该细胞倾向于淋巴滤泡定居并与靶细胞靠近，且能分化为终末效应细胞参与SIV病毒控制，为SIV/HIV感染提供新的免疫治疗靶点。作者首先在恒河猴中建立猴免疫缺陷病毒（simian immunodefciency virus，SIVmac239）早期（42天）和晚期（17个月）感染模型。流式分析表明淋巴结CD8+T细胞内TOX表达随SIV感染时间延长而显著增加，尤其在CD95+记忆性CD8T细胞（memory CD8+T，TM）。与此同时，流式分析进一步发现淋巴结内 TOX+CD8+TM呈现GzmB+TCF-1-CD39+PD-1+TIGIT+TIM3+CD101+（传统效应T细胞，effector T, TEFF）和GzmK+GzmBlowTCF-1highCD39+PD-1+TIGIT+TIM3+CD101+两种。在未感染恒河猴中，淋巴结CD8+TM主要是TCF1+CD39-（占87%），而TCF1+CD39+只占6%；而在SIV早期感染淋巴结CD8+TM中，TCF1+CD39-占60%，TCF1+CD39+增加至27%；在晚期感染中，TCF1+CD39-降低至30%，而TCF1-CD39+TEFF占30%，TCF1+CD39+增加至40%。尽管TCF1+CD39+细胞群低表达细胞毒GzmB分子，但其与传统TCF1-CD39+TEFF细胞群有相似地活化脱颗粒能力。总之，这些数据表明SIV感染促进淋巴结CD8+T细胞TCF1-CD39+和TCF1+CD39+两种细胞群中TOX表达，虽然TCF1+CD39+细胞低表达细胞毒分子，但表现中间效应功能。为了深入探究TCF1+CD39+CD8+TM功能，作者分离SIV感染恒河猴淋巴结内TCF1+CD39-、TCF1+CD39+和TCF1-CD39+CD8+TM并行质谱分析。结果证实TCF1+CD39+低表达细胞毒分子，包括perforin、GzmB和GzmA。此外，TCF1+CD39+细胞群高表达CD62L（T细胞迁移和淋巴结驻留相关）、CRTAM（淋巴结驻留）、DAP10、EOMES和IFNAR2（抗病毒相关）、NKG2C、NKG2D、CD94、CD160和GzmM（NK细胞毒相关以及T细胞增殖、扩增和功能相关）、CCL5（限制HIV感染）、ZHX3和PLK1（促增殖）和Bcl6（维持CD8细胞干性）。随后，作者分离早期SIV感染淋巴结中SIV特异性CD8+TM并行scRNA-seq分析，发现细胞分为C1（效应）、C2（干细胞样）、C3（增殖）、C4（IFN）和C5（其他）群。值得注意的是，TCF1+CD39+主要富集在C2群，表明干细胞样特性。TCR-seq分析指出TCF1+CD39+细胞群TCR克隆扩增，且主要克隆型与C1群重叠，表明TCF1+CD39+细胞群与TEFF存在线性关系。研究报道PD-1阻断促进干细胞样CD8+T细胞增殖和向TEFF分化【6】。作者发现PD-1抑制剂确实显著增加TCF1+CD39+CD8+TM和TCF1-CD39+TEFF比例，但Ki-67的增加仅在TCF1+CD39+CD8+TM细胞。这些结果表明TCF1+CD39+CD8+TM是一种有干细胞特性的中间效应细胞群，且具有向TEFF分化的能力。随后，作者在SIV感染恒河猴中发现TCF1+CD39+CD8+TM的比例与血浆病毒载量以及淋巴结SIV DNA库呈负相关，表明其可以控制病毒和疾病进展。考虑到CD8+T细胞归巢至淋巴结滤泡与低病毒载量有关【7-9】，作者检测TCF+CD39+CD8+T细胞向淋巴结滤泡的迁移能力。首先，相比于TCF-CD8+T细胞，TCF-CD39+和TCF+CD39+CD8+T细胞CXCR5（滤泡归巢受体）表达显著增加，且TCF1+CD39+CD8+TM中CXCR5的表达同样与血浆病毒载量以及淋巴结SIV DNA库呈负相关，表明CXCR5对于TCF1+CD39+CD8+TM抗SIV的重要作用。其次，免疫荧光证实相比于TCF-CD8+T细胞，更多的TCF1+CD39+CD8+TM定位于B淋巴滤泡区，且与病毒RNA+CD4+靶细胞距离更近，表明TCF1+CD39+CD8+TM细胞具有更好的能力与感染CD4+靶细胞相遇以控制病毒。最后，作者在人HIV淋巴结样本中同样检测到TCF1+CD39+CD8+T细胞的存在。虽然低表达GzmB，但抗原刺激同样诱导脱颗粒和IFNγ表达，表明人HIV感染中TCF1+CD39+CD8+TM细胞可能具有类似的抗病毒能力。综上所述，这项研究在猴和人缺陷免疫病毒感染淋巴结中鉴定一群具有干细胞样中间效应功能的TCF1+CD39+CD8+T细胞群，该细胞尽管缺乏经典细胞毒分子表达，但可以通过CXCR5定位于淋巴结滤泡区并与病毒感染CD4+T细胞作用，并继续分化为终末效应T细胞控制病毒载量，为促进TCF1+CD39+CD8+T扩增介导的病毒控制免疫治疗提供理论基础。参考文献 1. David R, Collins., Gaurav D, Gaiha., Bruce D, Walker.(2020). CD8+ T cells in HIV control, cure and prevention. Nat Rev Immunol, 20(8), 0. doi:10.1038/s41577-020-0274-9 2. Christian U, Blank., W Nicholas, Haining., Werner, Held., Patrick G, Hogan., Axel, Kallies., Enrico, Lugli., et al. (2019). Defining 'T cell exhaustion'. Nat Rev Immunol, 19(11), 0. doi:10.1038/s41577-019-0221-9 3. Jean-Christophe, Beltra., Sasikanth, Manne., Mohamed S, Abdel-Hakeem., Makoto, Kurachi., et al. (2020). Developmental Relationships of Four Exhausted CD8+ T Cell Subsets Reveals Underlying Transcriptional and Epigenetic Landscape Control Mechanisms. Immunity, 52(5), 0. doi:10.1016/j.immuni.2020.04.014 4. Takuya, Sekine., André, Perez-Potti., Son, Nguyen., Jean-Baptiste, Gorin., Vincent H, Wu., Emma, et al. (2020). TOX is expressed by exhausted and polyfunctional human effector memory CD8+ T cells. Sci Immunol, 5(49), 0. doi:10.1126/sciimmunol.aba7918 5. David R, Collins., Jonathan M, Urbach., Zachary J, Racenet., Umar, Arshad., Karen A, Power., et al. (2021). Functional impairment of HIV-specific CD8+ T cells precedes aborted spontaneous control of viremia. Immunity, 54(10), 0. doi:10.1016/j.immuni.2021.08.007 6. Se Jin, Im., Masao, Hashimoto., Michael Y, Gerner., Junghwa, Lee., Haydn T, Kissick., Matheus C, et al. (2016). Defining CD8+ T cells that provide the proliferative burst after PD-1 therapy. Nature, 537(7620), 0. doi:10.1038/nature19330 7. Morgan A, Reuter., Perla M, Del Rio Estrada., Marcus, Buggert., Constantinos, Petrovas., Sara, et al. (2017). HIV-Specific CD8(+) T Cells Exhibit Reduced and Differentially Regulated Cytolytic Activity in Lymphoid Tissue. Cell Rep, 21(12), 0. doi:10.1016/j.celrep.2017.11.075 8. Son, Nguyen., Claire, Deleage., Samuel, Darko., Amy, Ransier., Duc P, Truong., Divyansh, Agarwal., et al. (2019). Elite control of HIV is associated with distinct functional and transcriptional signatures in lymphoid tissue CD8(+) T cells. Sci Transl Med, 11(523), 0. doi:10.1126/scitranslmed.aax4077 9. Constantinos, Petrovas., Sara, Ferrando-Martinez., Michael Y, Gerner., Joseph P, Casazza., Amarendra, et al. (2017). Follicular CD8 T cells accumulate in HIV infection and can kill infected cells in vitro via bispecific antibodies. Sci Transl Med, 9(373), 0. doi:10.1126/scitranslmed.aag2285 https://doi-org.libproxy1.nus.edu.sg/10.1038/s41590-024-01875-0 责编|探索君排版|探索君来源|BioArt End 往期精选围观一文读透细胞死亡(Cell Death) | 24年Cell重磅综述（长文收藏版）热文 Cell | 是什么决定了细胞的大小？热文 Nature | 2024年值得关注的七项技术热文 Nature | 自身免疫性疾病能被治愈吗？科学家们终于看到了希望热文 CRISPR技术进化史 | 24年Cell综述

免疫疗法细胞疗法

2024-10-10

·echemi

Bayer's New Drug Elinzanetant Faces FDA Scrutiny: Safety Concerns Draw Attention, Menopausal Women Should Choose Cautiously!

On October 9, Bayer officially announced that its New Drug Marketing Application (NDA) has been accepted by the US Food and Drug Administration (FDA). The application is for Elinzanetant (Elinetant), a dual NK-1/NK-3 receptor antagonist, indicated for moderate to severe vasomotor symptoms (VMS) associated with menopause, commonly known as menopausal hot flashes. The application is based on the positive results of three Phase III clinical studies, OASIS 1, OASIS 2, and OASIS 3. These studies were designed to comprehensively evaluate the efficacy and safety of Elinzanetant in the treatment of menopausal associated VMS. The results of the study showed that Elinzanetant (120mg orally once daily) was excellent in reducing the frequency and severity of moderate-to severe VMS and demonstrated a good safety profile. In the Elinzanetant treatment group, headache and fatigue were the most common adverse events. In addition, the OASIS 1 and OASIS 2 studies observed sustained improvements across three key secondary endpoints, including a significant reduction in VMS frequency at week 1, improvements in sleep disturbances, and improvements in menopause-related quality of life. Elinzanetant is an innovative dual NK-1 and NK-3 receptor antagonist whose unique mechanism of action lies in the regulation of a group of estrogen-sensitive neurons within the hypothalamus in the brain (KNDy neurons). During menopause, KNDy neurons become hypertrophic due to decreased estrogen levels and lead to overactivation of the thermoregulatory pathway, which in turn disrupts the body temperature control mechanism and triggers VMS. Hot flashes, one of the most common symptoms of menopause, have a significant negative impact on women's quality of life. It is predicted that by 2030, 1.2 billion women worldwide will be affected by menopausal hot flashes. In addition to the OASIS project, Bayer is actively advancing the NIRVANA (NCT06112756) study, which aims to further evaluate Elinzanetant in the treatment of menopausal related sleep disorders.

临床结果临床3期申请上市

2024-09-10

·恒瑞医药

2024WCLC口头报告︱恒瑞创新药HR20013预防以顺铂为基础的化疗所致恶心呕吐主要终点结果发布

2024年世界肺癌大会（WCLC）于当地时间9月7日至10日在美国圣地亚哥召开，期间，由中山大学肿瘤防治中心张力教授牵头，全国68家研究中心共同参与的“HR20013预防以顺铂为基础的化疗导致的恶心、呕吐Ⅲ期研究（PROFIT研究）”主要研究终点结果以口头报告形式公布（摘要号：OA07.05）[1]。研究结果显示，HR20013预防以顺铂为基础的高致吐化疗导致的恶心、呕吐（HEC-CINV）显示出具有前景的临床疗效及可控的安全性，有望为此类患者提供治疗新选择。 PROFIT研究入选2024 年WCLC 口头报告（OA07.05）研究背景最新数据显示，我国恶性肿瘤年新发患者482.47万人，死亡患者257.42万人[2]。对于恶性肿瘤的治疗，化疗仍是基础。化疗相关性恶心呕吐（CINV）是化疗过程中最常见的不良反应之一。CINV会使患者对化疗产生恐惧，降低患者依从性，进而影响患者的生存获益。在CINV发病机制中，5-羟色胺3受体（5-HT3RA）和神经激肽受体1（NK-1RA）起到关键作用[3]。研究表明，对于未进行预防性止吐治疗的化疗患者，恶心和呕吐的发生率超过70％。以顺铂为代表的高致吐性化疗（HEC）可使急性恶心呕吐的发生率超过90%，延迟性恶心呕吐的发生率超过50%[4-5]。目前，国内外指南针对高致吐性化疗（HEC）以及中致吐性化疗（MEC）合并高危风险因素相关CINV的预防，推荐的是以5-羟色胺3受体拮抗剂（5-HT3 RA）和神经激肽受体1拮抗剂（NK-1 RA）为基础的三联/四联方案[6]。临床上使用的止吐药大多是半衰期较短的药物，需要长期、重复多次给药，并且多药联合使用较为复杂，导致临床医生用药实际执行困难且患者的依从性较低。因此，如何简化临床用药，提高患者的用药依从性和临床中指南的遵循度，一次性更加全面的控制肿瘤患者急性期、延迟期甚至是超延迟期的CINV，仍然是亟待解决的临床问题。 HR20013是恒瑞医药自主研发的Ⅰ类新药，目前首个适应症上市申请已被CDE受理。HR20013是由Fosrolapitant（新型NK-1受体拮抗剂，218mg）和帕洛诺司琼（5-HT3 受体拮抗剂，0.25mg）组成的复方注射剂，是一款新型超长效止吐药物，可同时拮抗NK-1和5-HT3受体，从而发挥止吐作用。HR20013仅需每个周期用药一次，即可覆盖急性期，延迟期以及超延迟期，简化了用药管理，兼顾了安全有效性和依从性。研究设计本研究是一项多中心、随机、双盲、双模拟、阳性对照的III期临床研究（NCT05509634），共入组754例未经历化疗的恶性实体瘤患者（750例接受药物治疗），随机分为两组，在每周期给与顺铂为基础的高致吐性化疗（顺铂剂量≥60mg /m2, IV, D1, Q3W，共2个周期）前，分别接受HR20013或福沙匹坦+帕洛诺司琼（FAPR+PALO）治疗，同时口服地塞米松（DEX）（D1-D4），连续观察两个化疗周期。主要终点：第1个化疗周期总体期（0-120h）完全缓解（CR）率。关键次要终点：第1个化疗周期给药后超延迟期（120-168h） CR率。（图1）图1. 研究设计研究结果患者基线治疗组和对照组分别有373例和377例患者接受治疗。两组间基线特征具有可比性（表1）。表1. 患者基线特征临床疗效第一周期总体期（0-120h）的CR率分别为77.7% vs 78.2%（D=-0.9%[95% CI:-6.7,5.0]; 单侧 P<0.01）, 显示主要终点达到非劣效性。同时，该Ⅲ期临床研究数据显示出了HR20013在超延迟期的疗效，无论是第一周期还是第二周期，HR20013超延迟期（BDP；120-168h）CR率数值均高于FAPR+PALO（第1周期：90.3% vs 86.5%；第2周期：92.7% vs 87.8%）。（图2）图2. 第一周期和第二周期CR率在超延迟期（120-168h）阶段，HR20013+DEX组的完全保护（CP；无呕吐/无挽救治疗/无显著恶心[视觉模拟量表得分<25 mm]）和完全控制（TC；无呕吐/无挽救治疗/无恶心[视觉模拟量表得分<5 mm]）数值上优于对照组，尤其是在第2周期（CP：90.8% vs 86.3%；TC：83.8% vs 78.6%）（图3）。在第一周期和第二周期中，无显著恶心、无呕吐和无抢救治疗的患者比例相当（图4、图5）。图3. 完全保护与总控制率图4. 无显著恶心和无恶心率图5. 无呕吐和无抢救治疗率安全性两组的安全性相似。整体研究期间发生的不良事件（TEAE）和治疗相关的不良事件（TRAE）发生率相似。研究结论 HR20013预防以顺铂为基础的高致吐化疗导致的恶心、呕吐显示出具有前景的临床疗效及可控的安全性，有望为此类患者提供治疗新选择。本次WCLC大会，恒瑞医药共有10款创新药的12项研究成果入围[7]，其中4项研究入选口头报告（Oral），8项研究接收为壁报，涉及小细胞肺癌治疗、早期非小细胞肺癌治疗、晚期非小细胞肺癌免疫和靶向治疗以及肿瘤支持治疗等领域，既是国际学术界对恒瑞医药自主创新实力的认可，也是中国医药研发创新力量的展现。未来，恒瑞医药将继续坚持“以患者为中心”的理念，重创新，强研发，力争研制出更多的新药、好药，服务“健康中国”，惠及全球患者。参考文献： 1.Zhang Li, et al. Phase 3 Study of HR20013 for Prevention of Cisplatin-based Chemotherapy-induced Nausea and Vomiting (PROFIT Study). 2024WCLC, OA07.05. 2.Zheng RS,Chen R,Han BF,et al.[Cancer incidence and mortality in China, 2022]. Zhonghua Zhong Liu Za Zhi.2024 Mar 23;46(3):221-231. 3. Antiemesis,NCCN Guidelines,2024 V1. 4.中国药学会医院药学专业委员会，化疗所致恶心呕吐的药物防治指南[J]. 中国医院药学杂志, 2022, 42(5): 457-473. 5.中国抗癌协会肿瘤支持治疗专业委员会，延迟性恶心呕吐防治中国专家共识[J]. 临床肿瘤学杂志, 2023, 28(5): 442-458. 6.China Anti-Cancer Association Committee of Rehabilitation and Palliative Care; China Anti-Cancer Association Committee of Tumor Clinical Chemotherapy; China Anti-Cancer Association Committee of Neoplastic Supportive-Care; Chinese Society of Clinical Oncology Committee of Supportive and Rehabilitative Care. [China guidelines on prevention and treatment of nausea and vomiting caused by antitumor therapies (2023 edition)].Zhonghua Zhong Liu Za Zhi. 2024 Jun 23;46(6):481-501. 7.https://cattendee.abstractsonline.com/meeting/20598?view=appendToCards&initialSearchId=1&searchId=21. 声明： 1. 本新闻旨在分享研发前沿资讯，仅供医疗卫生专业人士基于学术目的参阅，非广告用途。 2. 恒瑞医药不推荐任何未被批准的药品、适应症的使用。撰稿：中央医学事务部排版：程梦真责编：李玉莹往期精选 | 研发创新 | 慢病创新里程碑！恒瑞首个自免创新药夫那奇珠单抗获批上市恒瑞医药新突破！中国首个自研阿片类镇痛创新药富马酸泰吉利定获批上市 | 国际化 | 海外BD再传捷报！恒瑞医药GLP-1类创新药组合实现海外许可恒瑞医药与默克达成合作，携手推进癌症创新疗法 | 重磅奖项 | 喜报！恒瑞医药荣获2023年度国家科技进步奖恒瑞医药连续六年入选全球制药企业50强榜单！ | 社会公益 | “健康中国行·重走长征路”项目启动仪式圆满举行！恒瑞提供公益支持，助力健康中国恒瑞医药集团向中国扶贫基金会捐赠3000万设立“健康帮扶基金”

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