The study aims to assess safety and tolerability of oral toll-like receptor (TLR) 8 agonist Selgantolimod (SLGN) administered for 24 weeks in participants with both CHB and HIV who have been receiving suppressive antiviral therapy for both viruses for ≥5 years and have qHBsAg level >1000 (3 log10) IU/mL at screening. The study will also evaluate if TLR8 stimulation with SLGN will reduce hepatitis B surface antigen (HBsAg) titers in the blood.

开始日期2023-05-05

申办/合作机构

National Institute of Allergy & Infectious Diseases

NCT05045261

/ Recruiting临床2期IIT

ANRS HB07 IP-Cure-B Proof of Concept (PoC) Clinical Trial. Educating the Liver Immune Environment Through TLR8 Stimulation Followed by NUC Discontinuation

The ANRS HB07 IP-cure-B study is a proof of concept Phase II clinical trial in HBeAg negative virally suppressed non-cirrhotic CHB patients. It will explore whether stopping NUC or stopping NUC after SLGN administration can increase the rate of HBsAg decline compared to standard of care CHB treatment.

开始日期2022-02-01

申办/合作机构

France Recherche Nord & Sud SIDA HIV-Hepatites

NCT04891770

/ Completed临床2期

A Phase 2a, Open-Label Study to Evaluate the Safety and Efficacy of Selgantolimod (SLGN)-Containing Combination Therapies for the Treatment of Chronic Hepatitis B (CHB)

The primary objectives of this study are to evaluate the safety and tolerability of study treatment(s) (selgantolimod-containing combination therapies) and to evaluate the efficacy of study treatment(s) as measured by the proportion of participants who achieve functional cure, defined as hepatitis B surface antigen (HBsAg) loss and hepatitis B virus (HBV)deoxyribonucleic acid (DNA) < lower limit of quantitation (LLOQ) at Follow-up (FU) Week 24 in participants with chronic hepatitis B (CHB).

开始日期2021-08-14

申办/合作机构

Gilead Sciences, Inc.

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100 项与 Selgantolimod 相关的转化医学

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100 项与 Selgantolimod 相关的专利（医药）

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项与 Selgantolimod 相关的文献（医药）

2024-12-01·GUT

TLR8 agonist selgantolimod regulates Kupffer cell differentiation status and impairs HBV entry into hepatocytes via an IL-6-dependent mechanism

Article

作者: Dubois, Anaëlle ; Michelet, Maud ; Fletcher, Simon P ; Saez-Palma, Maria ; Diederichs, Audrey ; Daffis, Stephane ; Wallin, Jeffrey J ; Heintz, Sarah ; Hsu, Yao-Chun ; Grand, Xavier ; Vanwolleghem, Thomas ; Lau, Audrey H ; Plissonnier, Marie-Laure ; Li, Li ; Zoulim, Fabien ; Kolhatkar, Nikita ; Levrero, Massimo ; Giraud, Guillaume ; Van Renne, Nicolaas ; Rivoire, Michel ; Testoni, Barbara ; Roca Suarez, Armando Andres

Objective:

Achieving HBV cure will require novel combination therapies of direct-acting antivirals and immunomodulatory agents. In this context, the toll-like receptor 8 (TLR8) agonist selgantolimod (SLGN) has been investigated in preclinical models and clinical trials for chronic hepatitis B (CHB). However, little is known regarding its action on immune effectors within the liver. Our aim was to characterise the transcriptomic changes and intercellular communication events induced by SLGN in the hepatic microenvironment.

Design:

We identified TLR8 -expressing cell types in the human liver using publicly available single-cell RNA-seq data and established a method to isolate Kupffer cells (KCs). We characterised transcriptomic and cytokine KC profiles in response to SLGN. SLGN’s indirect effect was evaluated by RNA-seq in hepatocytes treated with SLGN-conditioned media (CM) and quantification of HBV parameters following infection. Pathways mediating SLGN’s effect were validated using transcriptomic data from HBV-infected patients.

Results:

Hepatic TLR8 expression takes place in the myeloid compartment. SLGN treatment of KCs upregulated monocyte markers (eg, S100A12 ) and downregulated genes associated with the KC identity (eg, SPIC ). Treatment of hepatocytes with SLGN-CM downregulated NTCP and impaired HBV entry. Cotreatment with an interleukin 6-neutralising antibody reverted the HBV entry inhibition.

Conclusion:

Our transcriptomic characterisation of SLGN sheds light into the programmes regulating KC activation. Furthermore, in addition to its previously described effect on established HBV infection and adaptive immunity, we show that SLGN impairs HBV entry. Altogether, SLGN may contribute through KCs to remodelling the intrahepatic immune microenvironment and may thus represent an important component of future combinations to cure HBV infection.

2024-12-01·GUT

Immunomodulation and entry inhibition: selgantolimod’s double punch against hepatitis B virus

Article

作者: Cornberg, Markus ; Urbanek-Quaing, Melanie ; Baumert, Thomas

2024-02-01·JHEP reports : innovation in hepatology

Safety, pharmacodynamics, and antiviral activity of selgantolimod in viremic patients with chronic hepatitis B virus infection

Article

作者: Yang, Jenny C ; Wallin, Jeffrey J ; Tseng, Cheng-Hao ; Chen, Diana ; Fung, Scott ; Nguyen, Anh-Hoa ; Dunbar, P Rod ; Brainard, Diana M ; Lim, Young-Suk ; Kao, Jia-Horng ; Kim, Yoon Jun ; Ahn, Sang Hoon ; McDonald, Circe ; Brooks, Anna E ; Gaggar, Anuj ; Fletcher, Simon P ; Coffin, Carla S ; Janssen, Harry L ; Elkhashab, Magdy ; Kim, Hyung Joon ; Sowah, Leonard ; Chuang, Wan-Long

Background & Aims:

Novel finite therapies for chronic hepatitis B (CHB) are needed, since lifelong treatment is usually required with current available oral antivirals. This phase II study (NCT03615066) evaluated the safety, pharmacodynamics, and antiviral activity of selgantolimod (a Toll-like receptor 8 agonist [TLR8]) with tenofovir alafenamide (TAF).

Methods:

Viremic patients with CHB not receiving treatment were stratified by HBeAg status and randomized 2:2:1 to TAF 25 mg/day with selgantolimod 3 mg orally once weekly (QW), selgantolimod 1.5 mg QW, or placebo. Combination therapy continued until week (W)24, followed by TAF monotherapy until W48; patients then discontinued TAF and were followed until W96 (treatment-free follow-up [TFFU] period). The primary efficacy endpoint was the proportion with ≥1 log₁₀ IU/ml HBsAg decline at W24.

Results:

Sixty-seven patients received study drug; 27 were followed during TFFU. Nausea, headache, vomiting, fatigue, and dizziness were the most common adverse events. Most adverse events were grade 1. Alanine aminotransferase flares were not observed up to W48. Four patients experienced alanine aminotransferase and hepatitis flares during TFFU; all had HBV DNA increases. Selgantolimod increased serum cytokines and chemokines and redistributed several circulating immune cell subsets. No patients achieved the primary efficacy endpoint. Mean HBsAg changes were -0.12, -0.16, and -0.12 log₁₀ IU/ml in the selgantolimod 3 mg, selgantolimod 1.5 mg, and placebo groups, respectively, at W48; HBV DNA declined in all groups by ≥2 log₁₀ IU/ml as early as W2, with all groups rebounding to baseline during TFFU. No HBsAg or HBeAg loss or seroconversion was observed throughout TFFU.

Conclusions:

Selgantolimod up to 3 mg was safe and well tolerated. Pharmacodynamics and antiviral activity in viremic patients support continued study of selgantolimod in combination CHB therapies.

Impact and implications:

Novel therapeutics for chronic HBV infection are needed to achieve a functional cure. In this study, we confirmed the safety and tolerability of selgantolimod (formerly GS-9688, a TLR8) when administered with tenofovir alafenamide over 24 weeks in viremic patients with chronic HBV infection. Overall, declines in HBsAg levels with selgantolimod treatment were modest; subgroup analysis indicated that patients with alanine aminotransferase levels greater than the upper limit of normal had significantly greater declines compared to those with normal alanine aminotransferase levels (-0.20 vs. -0.03 log₁₀ IU/ml; p <0.001). These findings suggest a potential differential response to selgantolimod based on patients' baseline HBV-specific immune response, which should be considered in future investigations characterizing the underlying mechanisms of selgantolimod treatment and in HBV cure studies using similar immunomodulatory pathways.

Clinical trial number:

NCT03615066 be found at https://www.gileadclinicaltrials.com/transparency-policy/.

项与 Selgantolimod 相关的新闻（医药）

2026-01-08

·Pharmaceutical Technology

GSK to file for approval of twice-yearly hep B drug on positive Phase III data

GSK said that the drug met its primary endpoint, with more patients achieving functional cure with bepirovirsen plus standard of care compared to standard of care alone. Image credit: Magda Wygralak / Shutterstock.com GSK’s six-monthly triple-action investigational antisense oligonucleotide (ASO) candidate has demonstrated a clinically and statistically significant functional cure in chronic hepatitis B in two Phase III trials. The B-Well 1 (NCT05630807) and B-Well 2 (NCT05630820) studies, which enrolled over 1,800 patients from 29 countries, met their primary endpoint, and bepirovirsen demonstrated a statistically significant and clinically meaningful functional cure rate. Functional cure rates were significantly higher with bepirovirsen plus standard of care (SoC) compared with SoC alone. All ranked endpoints were statistically significant, including in patients with baseline surface antigen (HBsAg) <=1000 IU/ml where an even greater effect was demonstrated. The drug also proved to be safe and tolerable in the trials. Based on the Phase III trials, GSK will be filing for regulatory approval of the drug globally. Full data will be presented at an upcoming medical meeting. Tony Wood, chief scientific officer, GSK, said: “Bepirovirsen has the potential to transform treatment goals for people living with CHB by achieving significant functional cure rates – a first for the disease. CHB affects more than 250 million people and leads to approximately 56% of liver cancer cases worldwide. Today’s result supports our plans to progress bepirovirsen as a treatment and also continue its development as a backbone in future sequential therapies.” GlobalData Strategic Intelligence US Tariffs are shifting - will you react or anticipate? Don’t let policy changes catch you off guard. Stay proactive with real-time data and expert analysis. By GlobalData Learn more about Strategic Intelligence Current SoC for hepatitis B is nucleoside and nucleotide analogues, which often require lifelong therapy and the functional cure rates remain low, typically only 1%. Bepirovirsen acts by inhibiting the replication of viral DNA in the body, suppressing the level of hepatitis B surface antigen (HBsAg) in the blood, and stimulating the immune system to increase the chances of a durable and sustained response. GSK licensed the drug from Ionis in 2019, following a positive Phase II trial, and collaborated with the company on its development. The drug gained Fast Track designation from the US Food and Drug Administration (FDA), Breakthrough Therapy designation from the Chinese National Medical Products Administration (NMPA) and SENKU designation from the Japanese Pharmaceuticals and Medical Devices Agency (PMDA). GlobalData predicts the hepatitis B therapeutics market to reach $3.2bn across seven major markets (7MM: the US, France, Germany, Italy, Spain, the UK, and Japan) in 2034. By this year, more than 65% of the market will be attributed to sales from specific functional cure drugs. As well as bepirovirsen, GlobalData also believes that a host of rival drugs will launch before 2034. This includes Gilead Sciences’ toll-like receptor 8 (TLR8) agonist, selgantolimod; GSK’s small interfering ribonucleic acid, daplusiran plus tomligisiran; Aligos Therapeutics’ capsid protein inhibitor, ALG-000184; and Arbutus Biopharma’s hepatitis B virus (HBV) surface antigen inhibitor, imdusiran. Stephanie Kurdach, infectious disease analyst at GlobalData, said: “Functional cure drugs are projected to be more expensive than the currently marketed chronic hepatitis B therapeutics, thereby driving the growth of the market. By 2034, the forecasted functional cure drugs will account for over 65% of the chronic hepatitis B market sales.” GlobalData is the parent company of Clinical Trials Arena .

临床结果临床3期临床2期快速通道突破性疗法

2026-01-07

·今日头条

我国慢乙肝临床治愈的新药即将到来！！我国在慢乙肝临床治愈的新药研发方面进展迅速全球领先地位，已有药物获批上市，更多联合疗法正在临床试验中，为“临床治愈”提供了前所未有的现实路径。当前情况的详细梳理：一、什么是“临床治愈”？首先需要明确，这里说的“临床治愈”不等于“完全根治”。临床治愈（F

我国慢乙肝临床治愈的新药即将到来！！我国在慢乙肝临床治愈的新药研发方面进展迅速全球领先地位，已有药物获批上市，更多联合疗法正在临床试验中，为“临床治愈”提供了前所未有的现实路径。当前情况的详细梳理：一、什么是“临床治愈”？首先需要明确，这里说的“临床治愈”不等于“完全根治”。临床治愈（Functional Cure）：指患者完成有限疗程的治疗后，血清乙肝表面抗原（HBsAg）和乙肝病毒DNA持续检测不到，伴或不伴表面抗体（HBsAb）出现，肝脏炎症和纤维化减轻，疾病进展和肝癌风险大幅降低，停药后不复发。这已是当前治疗的最高目标。完全根治（Complete Cure）：指肝细胞内的乙肝病毒cccDNA被彻底清除。目前所有疗法均无法实现。二、有望实现临床治愈的新药策略与代表药物目前的策略主要是联合治疗：以现有的核苷（酸）类药物（NA，如恩替卡韦、替诺福韦）为基础（强力抑制病毒DNA复制），联合新型药物来清除或抑制HBsAg，从而恢复人体免疫系统功能，最终实现HBsAg清除（血清学转换）。新型药物主要针对以下几个方向，中国药企均有重磅布局： 1. 直接抗病毒药物（DAAs）作用机制：直接靶向病毒生命周期的不同环节。代表药物：核心蛋白变构调节剂（CpAM）：这是目前最热门的赛道之一。戈诺卫（GST-HG141）：福建广生堂药业研发，已进入III期临床。它能破坏病毒衣壳的正常组装，抑制DNA复制和HBsAg产生。 ALG-000184（进口合作）：齐鲁制药引进，效果强劲，国内已进入后期临床。 siRNA（小干扰RNA）：像“基因导弹”一样降解病毒mRNA，从而大幅降低HBsAg等多种病毒蛋白水平。贺普拉肽：上海贺普药业研发，靶向HBV进入受体的抑制剂，联合治疗可显著降低HBsAg。反义寡核苷酸（ASO）：与siRNA类似，通过不同途径阻断病毒蛋白翻译。 2. 免疫调节剂作用机制：唤醒和增强患者自身被病毒抑制的免疫系统，使其重新识别并清除被感染的肝细胞。代表药物：治疗性乙肝疫苗：中国研究历史悠久。艾博卫泰（乙型肝炎治疗性疫苗）：已有多款在研，旨在诱导特异性的T细胞和B细胞免疫反应。免疫检查点抑制剂（如PD-1/L1抑制剂）：在部分研究中与抗病毒药联用，显示出清除HBsAg的潜力，但因安全性问题（可能诱发肝炎急性发作），需非常谨慎地探索。 TLR激动剂：如戈立德西（GS-9688）的类似物，国内有药企在跟进研发。 3. 已获批上市的革命性新药：派安普利单抗（Praperalimab）这是中国首个且目前唯一正式获批用于慢乙肝临床治愈适应症的新药（2024年初获批）。它是什么：一款Fc段改造的PD-1抑制剂（免疫检查点抑制剂）。其结构经过优化，在激活抗病毒T细胞的同时，理论上降低了传统PD-1抑制剂的一些副作用风险。如何用：并非单用，而是与长效干扰素（PEG-IFNα）和核苷（酸）类药物（NA）进行三联治疗，用于特定的经治患者。意义：它的获批标志着“临床治愈”从一个研究概念正式进入了临床实践指南，为医生和患者提供了一个强有力的新武器。大量临床试验数据显示，这种三联方案能显著提高HBsAg清除率。三、现状与展望从“有望”到“已来”：以派安普利单抗三联疗法的获批为标志，对于部分优势人群（如低HBsAg基线水平、经过NA治疗的患者），临床治愈已成为可及的目标。联合治疗是王道：未来的主流方案必然是“NA + 直接抗病毒药（如CpAM或siRNA） + 免疫调节剂（如治疗性疫苗或PD-1）”的强强联合。多种国产新药正在开展“NA+新药A+新药B”的临床试验。追求更高治愈率：研究者们正在不断优化联合方案，寻找最佳药物组合、治疗时机和疗程，旨在将临床治愈率从目前的20%-30%左右（针对优势人群）进一步提升，并惠及更广泛的患者群体。个体化治疗：未来会根据患者的基线特征（HBsAg水平、基因型、免疫状态等）制定个性化的临床治愈方案。建议慢乙肝患者： 1. 夯实基础治疗：坚持服用核苷（酸）类药物，保持病毒DNA不可测，是任何新疗法成功的前提。 2. 定期监测：特别是HBsAg定量，这是评估是否适合接受临床治愈治疗和判断疗效的关键指标。 3. 咨询专业医生：如果HBsAg水平较低（特别是低于1500 IU/mL），可以主动咨询肝病专科医生，评估是否有机会加入现有疗法或合适的临床试验。 4. 通过正规医院和渠道了解新药进展，切勿轻信网络上的“根治”偏方。中国在慢乙肝临床治愈的药物研发上已走在世界前列，从理论到实践均取得了突破性进展。虽然距离普惠所有患者还有一段路要走，但治疗格局已经彻底改变，临床治愈的大门已经打开。

2025-12-31

·四川华西肝病研究所乙肝治愈门诊

2025年全球乙肝新药进展

设为【★星标】⭐了解更多乙肝临床治愈资讯慢性乙型肝炎的治愈之路，正在经历一场从“持久控制”到“有限疗程内实现临床治愈”的深刻范式转变。长期以来，病毒难以清除的“堡垒”——共价闭合环状DNA（cccDNA），以及由此导致的免疫耐受，是横亘在治愈前的两大核心障碍。单一药物，无论是现有的核苷（酸）类似物，还是早期在研的靶向药，往往“独木难支”。正因如此，当前全球乙肝新药研发的主旋律已不再是寻找单一的“神奇子弹”，而是基于对病毒生命周期和宿主免疫系统的深刻理解，精心设计“多兵种协同作战”的联合治疗方案。从直接抑制病毒复制的siRNA、反义寡核苷酸（ASO），到旨在清除或沉默cccDNA的基因编辑、表观遗传调控，再到重建宿主免疫应答的治疗性疫苗、免疫调节剂，各类创新机制药物如雨后春笋般涌现，并在临床试验中积极探索着彼此间的最佳搭配。小编梳理截至2025年底，全球处于活跃研发阶段的各类乙肝新药（包括但不限于 siRNA、ASO、衣壳抑制剂、进入抑制剂、免疫疗法等）的作用机制、最新临床研究阶段。全球乙肝新药进展 siRNAs:干扰和破坏病毒RNA 统计截止至 2025-12 类别/药物名称作用机制美国FDA 批准状态 ALN-HBV02 (VIR-2218) RNAi基因沉默 II期 GSK5637608 (JNJ3989) RNAi基因沉默 IIb期（联合治疗） AB-729 RNAi基因沉默 II期 RBD1016 RNAi基因沉默 II期 HRS-5635 RNAi基因沉默 II期 BW-20507 RNAi基因沉默 II期（联合治疗） HT-101 RNAi基因沉默 II期 TQA3038 RNAi基因沉默 Ib/IIa期 KW-040 RNAi基因沉默 I期 ALG-125755 RNAi基因沉默 I期 SA1211 RNAi基因沉默 I期 YKYY013 RNAi基因沉默 I期 HECN30227 RNAi基因沉默 I期 OLX703A RNAi基因沉默临床前 ALG-072571 RNAi基因沉默临床前 SA011 RNAi基因沉默临床前 SA012 RNAi基因沉默临床前 KC13-M2G2 RNAi基因沉默临床前全球乙肝新药进展进入抑制剂：干扰HBV进入肝细胞统计截止至 2025-12 类别/药物名称作用机制美国FDA 批准状态 Hepcludex(Bulevirtide formerly Myrcludex B) 进入抑制剂 II期（乙肝IIb期；丁肝上市） Hepalatide 进入抑制剂 II期（乙肝II期；丁肝III期） hzVSF(IgG4) 进入抑制剂 II期 A2342 进入抑制剂临床前 PRX-202 进入抑制剂临床前 A7387 进入抑制剂临床前（HBV/HDV） Skimmianine 进入抑制剂临床前 JH-B10 进入抑制剂临床前 HH-1270 进入抑制剂临床前（HBV/HDV） HH-003 单克隆抗体临床前（HBV/HDV） HH-006 单克隆抗体 I期（HBV/HDV） BJT-778 单克隆抗体 I期（HBV/HDV） N6HB426-20 单克隆抗体临床前全球乙肝新药进展衣壳抑制剂：干扰病毒DNA蛋白的形成统计截止至 2025-12 类别/药物名称作用机制美国FDA 批准状态 Morphothiadin, GLS4 衣壳抑制剂 III期 ZM-H1505R 衣壳抑制剂 III期 GST-HG141 衣壳抑制剂 III期 QL-007 衣壳抑制剂 II期 EDP-514 衣壳抑制剂 II期 ALG-000184 衣壳抑制剂 II期 TQA3605 衣壳抑制剂 II期 LW-231 衣壳抑制剂 I/II期 KL060332 衣壳抑制剂 Ib期 HRS5091 衣壳抑制剂 I期 ABI-4334 衣壳抑制剂 I期 HEC121120 衣壳抑制剂 I期 VD1219 衣壳抑制剂 I期 XTYW001 衣壳抑制剂 I期 Freethiadine 衣壳抑制剂 I期 CS-12088 衣壳抑制剂 I期 GLP-26 衣壳抑制剂临床前 ALG-005398 衣壳抑制剂临床前 AMS-I-1274 衣壳抑制剂临床前 BA-53038B 衣壳抑制剂临床前 KW-034 衣壳抑制剂临床前 HEC72702 衣壳抑制剂临床前 SHR5133 衣壳抑制剂临床前 CS-SBA-1 衣壳抑制剂临床前 CDCS12 衣壳抑制剂临床前全球乙肝新药进展 HBsAg抑制剂：干扰HBsAg的产生统计截止至 2025-12 类别/药物名称作用机制美国FDA 批准状态 REP 2139 HBsAg抑制剂 II期（联合治疗） REP 2165 HBsAg抑制剂 II期（联合治疗） GST-HG131 HBsAg抑制剂 II期 GST-HG121 HBsAg抑制剂 I期 LP-128 HBsAg抑制剂 I期全球乙肝新药进展反义RNA:与病毒mRNA结合以防止病毒蛋白形成统计截止至 2025-12 类别/药物名称作用机制美国FDA 批准状态 Bepirovirsen(IONIS-HBVRx或GSK 3228836) 病毒蛋白抑制剂 III期 AHB-137 病毒蛋白抑制剂 III期全球乙肝新药进展基因编辑统计截止至 2025-12 类别/药物名称作用机制美国FDA 批准状态 PBGENE-HBV 病毒基因编辑 (ARCUS) I期 EBT107 病毒基因编辑 (CRISPR/Cas 9) 临床前 CBEs 基因编辑 (胞嘧啶碱基编辑器) 临床前 ABEs 病毒基因编辑 (腺嘌呤碱基编辑器) 临床前全球乙肝新药进展治疗性疫苗：疫苗技术被用作激活人体免疫系统的治疗方法统计截止至 2025-12 类别/药物名称作用机制美国FDA 批准状态 NASVAC 治疗性疫苗 III期（古巴上市；日本研究中；中国退出研究） TVAX-008 治疗性疫苗 III期 CVI-HBV-002 治疗性疫苗 IIb期 GS-4774 治疗性疫苗 II期（联合治疗） VVX001 治疗性疫苗 II期 VBI-2601 (BRII-179) 治疗性疫苗 IIa/IIb期（联合治疗） GSK4388067A 治疗性疫苗 II期（联合治疗） AIC 649 治疗性疫苗 II期 HB-110 治疗性疫苗 II期 VTP-300 治疗性疫苗 IIb期（联合治疗） ISA104 治疗性疫苗 I/II期 TherVacB 治疗性疫苗 Ib/IIa期 VRON-0200 治疗性疫苗 Ib期 JNJ 64300545 治疗性疫苗 I期 CARG-201 治疗性疫苗 I期 GS-2829/6779 (HB-400) 治疗性疫苗 Ia/Ib期 CLB-3000 治疗性疫苗 Ib期 CLB-4000 治疗性疫苗 Ib期 AVX70371 治疗性疫苗 I期 SN2001 治疗性疫苗 I期 WGc-0201 治疗性疫苗 I期 J-51 治疗性疫苗临床前 Chimigen HBV 治疗性疫苗临床前 PRGN-2013 治疗性疫苗临床前 FNX008 治疗性疫苗临床前 Decoy20 治疗性疫苗临床前 ADV-311 治疗性疫苗临床前 AHB-201 治疗性疫苗临床前 AHB-837 治疗性疫苗临床前全球乙肝新药进展先天免疫防御途径：激活先天免疫系统的化合物统计截止至 2025-12 类别/药物名称作用机制美国FDA 批准状态 GS9688 TLR-8激动剂 II期 TQA3334 TLR-7激动剂 II期 TQA3810 TLR-8激动剂 II期 HRS9950 TLR-8激动剂 II期 CB06 TLR-8激动剂 I/II期 YS-HBV-002 TLR3,RIG1,MDA5激活剂 I期 Cavrotolimod TLR-9激动剂 Ib期 SBT 8230 TLR-8激动剂临床前 HEC191834 TLR-8激动剂临床前全球乙肝新药进展宿主作用途径：诱导程序性细胞死亡(凋亡)的化合物统计截止至 2025-12 类别/药物名称作用机制美国FDA 批准状态 APG-1387 凋亡诱导剂 II期（终止） CRV 431 Ciclofillin抑制剂 II期（NASH-Ila期）全球乙肝新药进展单克隆抗体统计截止至 2025-12 类别/药物名称作用机制美国FDA 批准状态 GC1102 HBsAg单克隆抗体 II期 VIR-3434 (BRII-877) 单克隆抗体 II期（联合治疗） HT-102 (BM012) 单克隆抗体 II期 162 单克隆抗体 I期 KW-027 单克隆抗体 I期 HepB mAb19 单克隆抗体 I期 4G2 单克隆抗体临床前全球乙肝新药进展免疫检查点抑制剂统计截止至 2025-12 类别/药物名称作用机制美国FDA 批准状态 TQB2450 PD-L1抑制剂 II期（联合治疗） GS4224 PD-L1抑制剂 I期 AB-101 PD-L1抑制剂 I期 ARB-272572 PD-L1抑制剂临床前 ALG-093453 PD-1/PD-L1抑制剂临床前 ALG-093702 PD-L1抑制剂临床前 ALG-094103 PD-L1抑制剂临床前全球乙肝新药进展其他免疫学物质统计截止至 2025-12 类别/药物名称作用机制美国FDA 批准状态 IMC-I109V T细胞受体 I/II期 SCG101 TCR-T细胞疗法 I期 LioCyx TCR-T细胞疗法 I期 Undisclosed TCR双特异性抗体临床前 ALVR107 同种异体T细胞疗法临床前 AB359 IL-2免疫疗法临床前 Anti-PDL1-IFNα heterodimer PD-L1抑制剂/免疫调节临床前 SCG201 双特异性抗体临床前 SCG211 双特异性抗体临床前 CG-1999 免疫调节剂临床前全球乙肝新药进展其他统计截止至 2025-12 类别/药物名称作用机制美国FDA 批准状态 Hepatect®CP 免疫球蛋白 II期（联合治疗；预防用已上市） Zutectra® 免疫球蛋白 II期（联合治疗；预防用已上市） GSK3965193 PAPD5/7抑制剂 I/II期 CRMA-1001 表观遗传编辑 I/II期 BJT-628 PAPD5/7抑制剂 I期 DF-006 ALPK1激动剂 I期 EPI-003 表观遗传编辑 I期 TUNE-401 表观遗传编辑 Ib期 GIGA-2339 重组多克隆抗体 I期 CB07 HBV RNA去稳定剂临床前 SAG-282 HBV RNA去稳定剂临床前 SAG-524 HBV RNA去稳定剂临床前 HBV MicroRNA 临床前 ENOB-HB-01 控制HBV聚合酶临床前 GV1001 “新型肽段” 临床前 HEC96719 FXR激动剂临床前 UM06 双特异性抗体临床前 ccc_R08 HBV cccDNA抑制剂临床前 BAY87-2243 HBV cccDNA抑制剂临床前 HT-103 基因治疗临床前 HBVZ10 基因治疗临床前全国开设乙肝临床治愈门诊中西医疑难肝病联合诊疗中心全国已有多家医院开设乙肝临床治愈门诊，为患者提供“全病程科学管理”服务。患者应保持信心，积极配合专业医生，选择最适合的个体化治疗方案，拥抱没有乙肝困扰的健康未来。四川华西肝病研究所附属门诊部，凭借 39 年深耕肝病领域的卓越成就，现荣获北京协和医学院的权威指导，并正式成为其“中西医疑难肝病联合诊疗中心”的核心协作单位，已获授官方牌匾。这是对研究所专业实力、科研高度与临床诊疗水平的国家级最高认可，标志着本所将站在国家级权威平台之上，全面升级区域内的疑难肝病诊疗服务。医疗专家资源下沉以人民健康为中心为积极响应国家政策，切实满足人民群众对肝脏健康的需求，四川华西肝病研究所特此免费开放线上问诊通道，为广大市民提供专业、系统的肝健康筛查与咨询服务。为推动慢性肝炎的临床治愈，四川华西肝病研究所附属门诊部成立了乙肝临床治愈门诊。整合多方优势资源为患者带来全方位、个性化优质体验，治疗上依托多学科专家团队协同，整合前沿资源制定精准方案并动态调整；服务上以门诊健康讲座、患者互助为基础，拓展一对一咨询及专业护理康复服务；管理上通过全流程精细化体系实现信息共享、优化诊疗流程并建立随访闭环，全方位保障患者健康。帮助患者更好地了解病情、树立信心、配合治疗。同时，定期举办知识科普、专家会诊、公益补助等活动，为患者营造了一个相互支持、共同康复的温馨环境。希望通过提高诊断率和治疗率，减少肝硬化肝癌的发生。为实现“2030健康中国”贡献力量。有疑问请点击原文链接在线咨询，欢迎大家的评论区留言！声明：本内容仅为医学科普信息，不作为任何医疗指导。请在诊疗过程中务必遵循专业医生的建议和指导！本文部分内容及图片来自网络，如有侵权，请联系删除！了解更多乙肝临床治愈 1 乙肝联合治疗竟与干扰素单药“打平手”？ 2 乙肝抗病毒治疗如何科学选药？医生剖析三大关键，助您找到个体化方案 3 聚焦低病毒血症，干扰素联合疗法为慢乙肝患者带来新突破关注以下平台了解更多资讯点击关注官方微博账号点击了解更多肝病特色治疗点击查看更多肝病科普视频点击下方“阅读原文”了解更多

临床2期核酸药物siRNA临床1期免疫疗法

100 项与 Selgantolimod 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11871	-	-	DB16324

研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
慢性乙型肝炎	临床2期	美国	Gilead Sciences, Inc.	2018-04-06
慢性乙型肝炎	临床2期	新西兰	Gilead Sciences, Inc.	2018-04-06

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临床结果

适应症

分期

评价

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT04891770 (CTgov)	临床2期	慢性乙型肝炎	103	Nivolumab+Tenofovir Alafenamide+Selgantolimod+VIR-2218 (Cohort 1: TAF + VIR-2218 + SLGN + Nivolumab)	範窪鏇衊窪獵鏇遞窪願 = 醖糧艱蓋窪積淵廠觸範獵選鑰窪觸餘壓鑰鹽夢 (襯窪範積壓艱廠製餘築, 鑰觸積築憲糧範積艱餘 ~ 遞鏇餘窪壓築艱構選遞) 更多	-	2025-07-24
				Nivolumab+Tenofovir Alafenamide+Selgantolimod+VIR-2218 (Cohort 2 Group A: VIR-2218 + SLGN + Nivolumab)	範窪鏇衊窪獵鏇遞窪願 = 鑰鏇積願簾網夢廠齋製獵選鑰窪觸餘壓鑰鹽夢 (襯窪範積壓艱廠製餘築, 餘淵製簾簾醖獵製夢構 ~ 鏇選鹹夢衊襯繭鑰齋鏇) 更多
NCT03491553 (Pubmed \| J Hepatol)	临床2期	慢性乙型肝炎	48	Selgantolimod 3 mg	簾選夢齋簾選顧壓顧醖(廠艱繭壓蓋築膚糧願觸) = 46% 衊襯鏇衊鹽鏇蓋蓋選範 (繭膚願鹽鹹膚獵夢夢鹹 ) 更多	积极	2023-03-01
				Selgantolimod 1.5 mg
EASL2021	临床2期	慢性乙型肝炎 \| 病毒血症	67	Selgantolimod 3 mg	艱選齋鏇憲艱淵網鏇淵(選簾鬱夢窪衊製糧範簾) = 11% v 0 築膚膚醖艱範願鏇憲鏇 (窪糧醖鏇鹽憲膚膚選窪 ) 更多	积极	2021-06-23
NCT03615066 (CTgov)	临床2期	慢性乙型肝炎	67	TAF+Selgantolimod (Selgantolimod 3 mg + TAF)	壓壓鬱鏇醖淵願淵獵餘 = 鑰鬱遞築膚憲齋鏇夢壓構繭鬱醖製壓鹽艱簾壓 (醖獵範艱窪鹹蓋蓋鑰襯, 鑰餘顧襯鬱餘鹹淵窪壓 ~ 艱廠淵鏇衊觸繭膚襯範) 更多	-	2021-01-06
				Placebo+TAF+Selgantolimod (Selgantolimod 1.5 mg + TAF)	壓壓鬱鏇醖淵願淵獵餘 = 鬱餘願顧衊鹽簾遞繭鬱構繭鬱醖製壓鹽艱簾壓 (醖獵範艱窪鹹蓋蓋鑰襯, 糧願憲醖願夢壓願觸獵 ~ 願餘顧製淵鑰鑰壓夢鹹) 更多
NCT03491553 (CTgov)	临床2期	慢性乙型肝炎	48	Hepatitis B virus (HBV) OAV Therapy+Selgantolimod (Selgantolimod 3 mg: HBeAg-positive CHB Participants)	繭憲選壓範蓋壓鏇網願 = 廠鹽餘襯鹽齋淵糧窪蓋製鹹廠鑰鬱願淵鑰餘窪 (築壓製顧願獵鏇廠網選, 製鏇壓夢簾鑰積遞蓋選 ~ 齋壓選範製淵鏇遞築獵) 更多	-	2020-04-01
				Hepatitis B virus (HBV) OAV Therapy+Selgantolimod (Selgantolimod 3 mg: HBeAg-negative CHB Participants)	繭憲選壓範蓋壓鏇網願 = 網鏇獵觸淵艱築簾繭夢製鹹廠鑰鬱願淵鑰餘窪 (築壓製顧願獵鏇廠網選, 構廠蓋鹽憲襯襯選蓋夢 ~ 鹹壓鑰鹽窪鹹壓鏇網糧) 更多
EASL2019	临床2期	慢性乙型肝炎	-	GS-9688 1-500 nM	廠廠製範獵構艱醖積夢(鑰構網鏇艱構膚夢餘壓) = 鬱觸壓蓋壓鑰鬱鬱衊醖鹽廠願鹹築顧淵製衊積 (鏇積網願構襯艱獵壓積 )	积极	2019-04-12