The objective of this exploratory study is to evaluate the cellular and connective tissue composition of joints from patients with Osteoarthritis (OA) who have been treated with fasinumab, compared with those treated with placebo or Non-steroidal anti-inflammatory drugs (NSAIDs).

开始日期2019-04-08

申办/合作机构

Regeneron Pharmaceuticals, Inc.

[+1]

NCT03491904

/ Completed临床1期

A Phase 1, Multicenter, Randomized, Open-Label, Parallel-Group, Multi-Dose Study in Patients With Moderate-to-Severe Pain Due to Osteoarthritis of the Knee or Hip to Assess the Patients' Ability to Self-Administer Fasinumab Using an Auto-Injector and to Characterize the Pharmacokinetics of Fasinumab Using Two Different Presentations

The primary objective is to demonstrate that the auto-injector(AI) is suitable to be used to administer fasinumab at home by patients or their caregivers, as measured by collecting 12 weeks of actual-use data on the technical performance of the device.
The secondary objectives of the study are:
* To evaluate the successful injection of fasinumab by patients or their caregivers using the AI in an unsupervised setting
* To evaluate patient/caregiver satisfaction with the AI for fasinumab injection in an unsupervised setting
* To evaluate exposure in serum for fasinumab administered by patients or their caregivers using an AI in an unsupervised setting, or fasinumab administered by study staff using a PFS that has been used in the phase 3 program
* To characterize the safety, tolerability, and immunogenicity of fasinumab administered by patients or their caregivers using an AI in an unsupervised setting, or fasinumab administered by study staff using a PFS that has been used in the phase 3 program

开始日期2019-01-23

申办/合作机构

Regeneron Pharmaceuticals, Inc.

[+1]

EUCTR2018-001411-71-GB

/ Terminated临床2期

Study to Evaluate Synovial Fluid in the Phase 3 Fasinumab Program for Osteoarthritis of the Knee and Hip

开始日期2018-10-22

申办/合作机构

Regeneron Pharmaceuticals, Inc.

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100 项与法西努单抗相关的专利（医药）

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项与法西努单抗相关的文献（医药）

2026-05-01·DRUGS

Efficacy and Safety of Anti-nerve Growth Factor Monoclonal Antibodies in Managing Chronic Musculoskeletal Pain: A Systematic Review with Network Meta-analysis

Review

作者: Mahgoub, Reham ; Alhasan, Mohammad ; Seah, K T Matthew ; Abouelella, Ahmed ; Ibrahim, Ayman ; Day, Richard O ; Arendt-Nielsen, Lars ; Najah, Qasi ; Bagg, Matthew K ; Al-Tamimi, Mansoor ; Elhadi, Muhammed ; Abuzied, Ola ; Lopez-Olivo, Maria A ; Hamoudah, Ahmed ; Basheer, Eman

BACKGROUND:

Anti-nerve growth factor (NGF) monoclonal antibodies (mAbs) have emerged as a promising new class of analgesics, offering potential benefits in managing particular painful musculoskeletal (MSK) conditions. However, their long-term safety remains uncertain, leading to regulatory non-approval of these agents. This study aims to evaluate the efficacy and safety of individual anti-NGF mAbs compared to other analgesics when treating chronic MSK pain.

METHODS:

Our literature search included PubMed, Scopus, Embase, Web of Science, Cochrane Library, and ClinicalTrials.gov through April 25th, 2025. Articles eligible for inclusion were randomized controlled trials (RCTs) comparing one of the human anti-NGF mAbs to other interventions in adults with chronic MSK pain. Primary outcomes evaluated were changes from baseline in pain, physical function, and patient global assessment (PGA) scores, as well as risks of adjudicated arthropathies (AAs) and abnormal peripheral sensation (APS). We used the Cochrane Risk of Bias 2 (RoB-2) tool to assess risk of bias. Pairwise and network meta-analyses were performed using random-effects models. Treatments were ranked using the cumulative ranking curve (SUCRA), and a multi-criteria decision analysis with Technique for Order Preference by Similarity to Ideal Solution (TOPSIS) was applied to integrate all efficacy and safety outcomes. Statistical analyses were conducted in R (v4.3.1) using the meta, netmeta, gemtc, and Multi-Criteria Decision Aiding (MCDA) packages.

RESULTS:

A total of 29 studies, involving 27,747 patients with osteoarthritis or chronic low back pain, were included in this analysis. Compared to placebo, fasinumab showed the highest improvements in pain (standardized mean difference [SMD] - 0.40, 95% CI [- 0.52, - 0.29], p < 0.001) and physical function (SMD - 0.42, 95% CI [- 0.53, - 0.31], p < 0.001), followed by tanezumab (pain: SMD - 0.36, 95% CI [- 0.44, - 0.28], p < 0.001; function: SMD - 0.39, 95% CI [- 0.47, - 0.31], p < 0.001). For safety, both fasinumab and tanezumab demonstrated a significant risk for AAs (risk ratio [RR] 4.7, 95% CI [3.61, 6.13], p < 0.001; and RR 3.84, 95% CI [2.07, 7.14], p < 0.001, respectively) and APS (RR 1.99, 95% CI [1.49, 2.65], p < 0.001; and RR 2.46, 95% CI [1.93, 3.14], p < 0.001, respectively) relative to placebo. While fulranumab was less effective (pain: SMD - 0.25, 95% CI [- 0.42, - 0.07], p < 0.01; function: SMD - 0.25, 95% CI [- 0.43, - 0.07], p < 0.01), it showed better overall safety against placebo relative to both agents, demonstrating a significant risk only for APS events (RR 1.78, 95% CI [1.09, 2.92], p < 0.05).

CONCLUSIONS:

Anti-NGF mAbs, particularly fasinumab and tanezumab, are associated with the greatest levels of pain relief and functional improvement over placebo within this analysis. However, these benefits are counterbalanced by significant risks of joint-related adverse events. Implementation of strict safety protocols is essential when considering these agents for further evaluation.

PROTOCOL REGISTRATION:

PROSPERO ID: CRD420251104612.

2026-03-01·Osteoarthritis and cartilage open

Identification of alkaline phosphatase as a putative biomarker of anti-NGF treatment-associated arthropathies: Machine learning-assisted analyses of clinical trial data

Article

作者: Hamon, Sara C ; Musser, Bret J ; Patel, Yamini ; Wipperman, Matthew F ; Manvelian, Garen ; Eng, Simon ; Gao, Haitao ; Ho, Tina ; Hamilton, Jennifer D ; McIntyre, Debra A G ; Li, Dateng ; Hectors, Stefanie ; Geba, Gregory P ; Banerjee, Poulabi ; Ushirogawa, Yoshiteru ; DiMartino, Stephen J ; Ota, Kristie T ; Chio, Erica ; Wei, Henry G ; Ogawa, Kei ; Wang, Chen Guang ; Ehmann, Peter J

Objective:

Nerve growth factor (NGF) inhibitors have been shown to provide pain relief in patients with osteoarthritis but are associated with adjudicated arthropathies (AAs). Exploratory analyses were performed to identify whether peripheral biomarkers routinely collected in trials can predict AAs, independent of known clinical covariates.

Methods:

Clinical and biomarker data from seven phase 2/3 fasinumab trials were pooled, and 33 laboratory baseline and week 16 change variables were assessed. Individuals with AA were identified and propensity score matched 1:1 to non-AA controls, creating four unique sets of non-AA individuals. Random forest machine learning models were used. Variables with >30 % missing data were excluded. The training/validation set included 75 % of the available dataset; 10 % formed the working validation test set, and 15 % a held-back test set. Area under the curve of the receiving operating characteristic (AUROC) and ranked feature importance were assessed across models using peripheral biomarkers to predict AA vs non-AA individuals.

Results:

Of the final dataset (n = 11,490), 911 AA individuals were compared with four unique sets of non-AA individuals (n = 878-908). The AUROC was 0.51-0.57 for biomarkers at baseline and 0.54-0.62 for biomarker changes at week 16. Change in alkaline phosphatase (ALP) from baseline to week 16 was the only important variable identified consistently across models. ALP was also elevated by several points on average in individuals receiving fasinumab.

Conclusion:

Change in ALP (baseline to week 16) was associated with AA events after treatment with fasinumab. Other measured peripheral biomarkers were not linked with AA events.

2025-01-01·CURRENT THERAPEUTIC RESEARCH-CLINICAL AND EXPERIMENTAL

The Effects of Fasinumab on Peripheral Nerve Function and Ganglion Anatomy: Results From a Randomized, Double-Blind, Placebo-Controlled Study in Patients With Pain Due to Osteoarthritis of the Knee or Hip, and a Series of Nonclinical Studies

Article

作者: Krueger, Pamela ; Manvelian, Garen ; Patel, Yamini ; Macdonald, Lynn E ; Gao, Haitao ; Turner, Kenneth C ; Trinh, Ngan ; Braunstein, Ned ; Fetell, Michael ; Hassan, Hazem E ; Ho, Tina ; Geba, Gregory P ; Mei, Jingning ; Croll, Susan D ; Soltys, Randy ; Cortes-Burgos, Luz ; Eng, Simon ; Trejos, Jesus ; Dakin, Paula ; DiMartino, Stephen

Purpose:

Osteoarthritis (OA) is a chronic disease where breakdown and loss of cartilage leads to pain, primarily in the joints. Nerve growth factor inhibitors (eg, fasinumab) can reduce pain, but have been associated with nervous system adverse events (AEs). Here we describe the results of a Phase 2, randomized, double-blind, placebo-controlled study and a series of nonclinical analyses investigating the effects of fasinumab on peripheral nerve function and ganglion anatomy.

Methods:

In the Phase 2 study, 180 adults with knee or hip OA and moderate-to-severe pain inadequately controlled with analgesics, who could not tolerate/were unwilling to take opioids, received subcutaneous fasinumab 1 mg every 4 weeks or placebo for 12 weeks. The primary endpoint was change from baseline to Week 16 in conduction velocity and amplitude for the peroneal, sural, and ulnar nerves. Secondary endpoints included peripheral sensory events. The nonclinical analyses involved adult and developing Sprague-Dawley rats and developing cynomolgus monkeys; endpoints included baseline and isoproterenol‑induced hemodynamic parameters, dorsal root ganglia (DRG) and superior cervical ganglia (SCG) volumes, neuron volumes and counts, and volumes and counts of specific neural subsets.

Findings:

In the Phase 2 study, nerve conduction velocities and action potential amplitudes between baseline and Week 16 were generally within normal ranges. There were no compelling differences in nerve conduction tests between fasinumab- and placebo-treated patients. Incidences of AEs, including peripheral sensory AEs, were similar between fasinumab and placebo. In the nonclinical analyses, neither hemodynamic parameters nor DRG and SCG stereological parameters were statistically significantly different between fasinumab-treated and isotype control antibody-treated rats.

Implications:

No clinically meaningful differences were observed between fasinumab- and placebo-treated patients for nerve conduction velocities and action potential amplitudes. In the nonclinical studies, no significant changes could be detected in adult rat ganglion anatomical parameters or hemodynamic parameters at a variety of fasinumab doses. Results from these studies demonstrated that fasinumab did not affect the tested nervous system parameters in adult humans or rats.Trial registration number: NCT02447276; https://clinicaltrials.gov/study/NCT02447276.

项与法西努单抗相关的新闻（医药）

2026-05-07

·今日头条

每半年一次！抗NGF单抗，中度骨关节炎慢性膝痛，非阿片类镇痛

对于吃止痛药伤胃、怕上瘾的中度膝骨关节炎患者，这可能是改变游戏规则的“长效镇痛针”。 “医生，我膝盖疼得走不了路，但吃布洛芬胃疼，吃阿片又怕上瘾，还有别的办法吗？” 在疼痛科门诊，这是无数骨关节炎（OA）患者的困境。他们需要长期镇痛，却受困于传统药物的副作用。现在，一类全新的药物—— 抗NGF单抗（神经生长因子抑制剂），正在为这类患者提供“第三极”选择。与每日服药不同，这类药物通过皮下注射给药，每半年仅需一次（部分药物间隔更短），即可实现持续镇痛。它不经过胃肠道，无成瘾性，是真正的非阿片类靶向镇痛药。本文将严格依据临床证据，解析其机制、药物与风险。一、什么是抗NGF单抗？为什么能“长效镇痛”？ NGF（神经生长因子）是疼痛信号传递的“放大器”。在骨关节炎中，关节内的炎症会刺激NGF水平飙升，导致疼痛阈值降低（痛觉敏化）——这就是为什么患者连轻微的走路都会感到剧痛。抗NGF单抗的作用机制：精准狙击：作为单克隆抗体，它能像“导弹”一样精准结合并中和体内的NGF。阻断信号：切断NGF与其受体（TrkA）的结合，从源头上减少疼痛信号向大脑的传递。长效原理：抗体类药物在体内代谢缓慢（半衰期长），注射一次可在血液中维持数周至数月的有效浓度，从而实现长期镇痛。关键优势：它不抑制 COX 酶（不像布洛芬伤胃），也不激动阿片受体（不像吗啡上瘾），作用机制完全独立。二、具体药物：哪些已接近临床？目前全球范围内，多款抗NGF单抗已进入III期临床或上市审批阶段。需要明确的是：严格意义上的“每半年一次”是理想化的给药间隔，不同药物研发进度和周期略有差异，以下为最接近临床应用的候选药物： 1. 塔奈珠单抗（Tanezumab）研发状态：由辉瑞/礼来研发，已完成多项III期临床，但在FDA审批中因关节安全信号受阻，目前定位为其他疗法无效后的“末线选择” 。给药频率：通常为每8周（约2个月）皮下注射一次。证据：在难治性膝/髋OA患者中，相比安慰剂，能显著改善WOMAC疼痛评分（行走痛减轻约45%-62%）。 2. 法西努单抗（Fasinumab）研发状态：由再生元/梯瓦研发，III期数据显示其对中重度OA疼痛有效，但同样面临关节安全监测。给药频率：临床研究中多为每月至每季度给药。特点：全人源化单抗，免疫原性更低。 3. 富兰尼单抗（Fulranumab）研发状态：杨森曾推进其研发，Meta分析显示其可改善OA疼痛，但研发已放缓。关于“每半年一次” ：目前公开数据中，尚无严格“半年一针”的获批药物。 “每半年一次”是媒体对长效镇痛理想的通俗概括，实际临床中多为2-3个月一次。患者需关注具体药物的说明书。三、核心优势：为什么它是“非阿片”的里程碑？对于中度OA慢性膝痛患者，抗NGF单抗的价值在于填补了巨大的治疗空白：维度抗NGF单抗（如Tanezumab）非甾体抗炎药（NSAIDs）阿片类药物镇痛机制靶向NGF，抑制痛觉敏化抑制COX，抗炎镇痛中枢μ受体激动，抑制痛觉成瘾性无无高，需严格管控胃肠道风险极低（不经口服）高（溃疡、出血）有（便秘、恶心）心血管风险未见明确关联高（尤其塞来昔布类）有（呼吸抑制）给药方式皮下注射，长效每日口服每日口服/贴剂适用人群画像：确诊为中度膝骨关节炎，疼痛评分≥4分（0-10分）。对NSAIDs 不耐受（如胃病、肾病）或疗效不足。存在阿片滥用风险，或拒绝使用阿片类药物。希望减少每日服药负担，追求长效治疗。四、不可忽视的“黑框警告”：关节破坏风险这是抗NGF单抗最受争议的一点，也是FDA审评专家投票反对其广泛使用的主要原因。 1. 快速进展性骨关节炎（RPOA）现象：部分患者在用药后，关节结构破坏加速，出现软骨快速丢失、骨坏死，甚至需要提前进行关节置换。机制：NGF本身对软骨和骨骼有营养作用。完全阻断NGF后，可能削弱了关节的自我保护机制，加上疼痛消失导致患者活动量过大（类似“无痛关节”过度使用），加速了磨损。发生率：在III期研究中，RPOA发生率约为1%-3%，显著高于安慰剂组。 2. 神经系统副作用部分患者报告出现感觉异常、麻木（周围神经病变），通常停药后可逆，但需密切监测。监管态度：目前FDA和EMA均未批准其作为OA的一线治疗。仅建议用于无其他治疗选择、且充分知情同意关节风险的患者。五、给患者的理性建议它不是“神药” ：抗NGF单抗是镇痛药，不是修复药。它只能缓解疼痛，不能逆转软骨磨损，也不能治愈骨关节炎。严格筛选：重度OA（关节间隙已消失）、拟行关节置换者、合并严重周围神经病变者禁用。用药前需拍摄X线片评估基线关节状态。中国现状：截至2026年，此类药物在中国大多处于临床研究或审批阶段，尚未广泛进入医保。患者切勿轻信“海外代购”或“黑市针剂”。基础治疗不能停：即使打了针，减重、肌力训练、物理治疗仍是OA治疗的基石。药物只是让你“不疼”，运动才能让你“走得远”。抗NGF单抗代表了慢性疼痛治疗的未来方向：靶向、长效、非成瘾。对于饱受疼痛折磨且无药可用的患者，它是一道曙光。然而，关节安全风险像一把达摩克利斯之剑，限制了它的广泛应用。行动指南：若你符合“中度膝痛、传统药无效”的特征，可咨询三甲医院疼痛科或风湿科，询问是否有相关的临床研究（临床试验）机会。若听闻“半年一针”的宣传，务必核实具体药物名称（如Tanezumab）和确切的给药间隔。在获得更长期的安全性数据前，将其视为“最后的手段”而非首选。参考文献： Tanezumab for osteoarthritis: efficacy and safety meta-analysis. J Pain Res. 2020. Schnitzer TJ, et al. Effect of Tanezumab on Joint Pain and Physical Function in Patients with Osteoarthritis. JAMA. 2019. FDA Arthritis Advisory Committee Meeting Briefing Document: Tanezumab. 2021. Fasinumab phase III data in RMD Open. 2026. （注：本文提及药物均为处方药或临床研究阶段药物，严禁自行使用；具体用药需在医生全面评估风险后决定）

2026-04-29

·BioSpace

Levicept to Present Data from Phase II study of LEVI-04 at OARSI 2026 World Congress on Osteoarthritis

April 24, 2026 -- Levicept Ltd, a biotechnology company focused on the development of LEVI-04, a first-in-class treatment for osteoarthritis (OA), will today present positive data from its Phase II study of LEVI-04 in patients with pain and disability due to OA of the knee at OARSI 2026 World Congress on Osteoarthritis being held in West Palm Beach, FL 23-26 April. Levicept has been selected for four presentations including a podium session in which Professor Philip Conaghan MBBS PhD, Director NIHR Leeds Biomedical Research Centre, Chief Investigator of the study will show data demonstrating LEVI-04’s clinically meaningful improvements in pain and function across a range of outcomes and effect sizes at or above those for NSAIDs. Professor Ali Guermazi, central radiology reader for the study, will present a poster on the imaging included in the study, and additional posters will describe LEVI-04’s pharmacology as a novel neurotrophin-3 inhibitor and a comparison of joint safety outcomes for LEVI-04 compared to the anti-NGF fasinumab. The trial was a multi-arm, International, multicentre, randomized, double-blind, placebo-controlled, Phase II study which enrolled 518 participants with pain and disability due to OA of the knee (ClinicalTrials.gov ID: NCT05618782). Simon Westbrook, Founder and CSO of Levicept, said: “Being selected to present such a breadth of data from our Phase II trial at OARSI speaks to the importance of novel treatments for osteoarthritis and quality of our trial and outcomes. Our efficacy results have recently been published in The Lancet i and we look forward to sharing more detail with the audience in Florida. Not only does LEVI-04 significantly reduce pain and symptoms of OA, but we have also demonstrated potential to directly address the OA disease process. We believe LEVI-04 is the only molecule to demonstrate this potential for disease modification and analgesia in a clinical study of patients with OA.” Presentation details: Podium presentation – 24 Apr-2026, 6PM – 6:10PM Title: LEVI-04, a novel neurotrophin-3 inhibitor, demonstrates clinically meaningful improvements in pain and physical function across a range of OA outcomes, including the OMERACT-OARSI responder criteria Presenter: Prof Philip Conaghan MD, Chief Investigator, University of Leeds Posters:Poster #407 – April 24 3:30PM – 4:15PM and April 25 3:30 – 4.15PM Title: Pharmacology of the neurotrophin-3 inhibitor LEVI-04, a novel treatment for osteoarthritis Presenter: Simon Westbrook PhD, Founder and CSO, Levicept Poster #439 – April 24 3:30PM – 4:15PM and April 25 3:30 – 4.15PM Title: A comparison of joint safety outcomes from Phase 2 RCTs of two different neurotrophin modulators: LEVI-04 (p75NTR-Fc, NT-3 inhibitor) and fasinumab (anti-NGF) Presenter: Prof Philip Conaghan MD, Chief Investigator, University of Leeds Poster #376 – April 24 4:15PM – 5:00PM and April 25 4:15 – 5:00PM Title: Imaging exclusions at screening in the Phase II RCT of Levi-04, a novel neurotrophin-3 inhibitor, in patients with knee osteoarthritis Presenter: Prof Ali Guermazi MD, Study Central Reader (Radiology), University of Boston Levicept Ltd is a UK-based biotechnology company developing the first in a new class of novel, safe and efficacious biological therapies, LEVI-04 [p75NTR-Fc], for the treatment of osteoarthritis and chronic pain. LEVI-04 inhibits NT-3, one of the neurotrophin family of proteins. LEVI-04 has completed a Phase II clinical trial in more than 500 patients with osteoarthritis. It is estimated that the market opportunity for drugs that treat osteoarthritis is worth in excess of $10 billion. LEVI-04 was discovered by Levicept’s founder, Simon Westbrook. Levicept’s investors include Medicxi, Advent Life Sciences, Gilde Healthcare and Pfizer Ventures. The content above comes from the network. if any infringement, please contact us to modify.

临床结果

2025-12-05

·知乎专栏

2025 神经病理性疼痛（Neuropathic Pain）综述：Nav1.7 / TRPV1 / P2X7 / NGF-TrkA 核心靶点与机制

神经病理性疼痛（Neuropathic Pain）发病机制概览神经病理性疼痛（neuropathic pain），又称神经性疼痛或神经病变性疼痛，是由躯体感觉神经系统本身的损伤或疾病直接引起的一类慢性疼痛综合征，全球患病率大约在 7–10% 左右，在糖尿病患者、肿瘤化疗人群、脊髓损伤以及多发性硬化等人群中发生率更高。典型病因包括糖尿病周围神经病变、带状疱疹后神经痛、化疗诱导周围神经病变、脊髓损伤相关疼痛以及三叉神经痛等，患者常描述为烧灼样、电击样、刀割样或针刺样疼痛，可伴随自发痛、触诱发痛（轻触即可引发明显疼痛）和痛觉过敏等复杂感受。与炎症性或伤害性感觉疼痛不同，神经病理性疼痛的本质是神经系统本身发生了“病理性重塑”：外周伤害感受器和背根神经节神经元在离子通道表达和放电模式上出现持久改变（例如 Nav1.7/Nav1.8/Nav1.9 等电压门控钠通道上调导致异位放电），脊髓背角及更高位中枢（丘脑、皮层）内兴奋性传入信号被持续放大，同时抑制性调节（GABA 能和甘氨酸能神经元）功能减弱，出现所谓“去抑制”（disinhibition），再加上小胶质细胞和星形胶质细胞被激活，通过 P2X4/P2X7 受体、炎症因子和神经营养因子（如 BDNF）与神经元形成恶性正反馈回路，使得疼痛由急性伤害性信号演变为一种独立存在的“神经网络疾病”。在外周层面，TRPV1、TRPA1 等瞬时受体电位通道对热、机械和化学刺激高度敏化；在中枢层面，N-甲基-D-天冬氨酸受体（NMDAR）介导的兴奋毒性、mTOR 及下游通路参与的可塑性改变进一步巩固了异常疼痛记忆。由于其发生基础不再是简单的炎症或组织损伤，传统非甾体抗炎药（NSAIDs）和阿片类镇痛药在神经病理性疼痛中的疗效普遍有限，且长期应用常受制于耐受性、不良反应和成瘾风险，这也是为什么当前指南更强调钙通道调节剂（如加巴喷丁、普瑞巴林）、5-羟色胺–去甲肾上腺素再摄取抑制剂以及局麻药贴剂等机制更贴近“神经调控”的方案。然而，即便在标准治疗下，仍有相当比例患者处于“部分缓解甚至难治”状态，提示我们仍迫切需要围绕 Nav 通道、TRPV1/P2X4/P2X7、NGF–TrkA 轴以及中枢抑制性回路等关键节点开发更精准的靶向药物和生物制剂，这也是近年来新一代小分子、单克隆抗体与基因调控疗法持续集中的研发方向。神经病理性疼痛五大核心靶点类别 / 靶点基因蛋白全称UniProt ID病理作用与代表药物1. 电压门控钠通道（外周兴奋性）SCN9ASodium channel protein type 9 subunit alpha (Nav1.7)Q15858数十个选择性抑制剂在研，VX-150已Ⅲ期1. 电压门控钠通道（外周兴奋性）SCN10ASodium channel protein type 10 subunit alpha (Nav1.8)Q9Y5Y9VX-548（Vertex）2024 FDA提交上市1. 电压门控钠通道（外周兴奋性）SCN11ASodium channel protein type 11 subunit alpha (Nav1.9)Q9UI33冷痛觉异常关键2. TRP & Ca²⁺通道（多模态敏化）TRPV1Transient receptor potential cation channel subfamily V member 1Q8NER1热痛核心，辣椒素贴剂已上市2. TRP & Ca²⁺通道（多模态敏化）TRPA1Transient receptor potential cation channel subfamily A member 1O75762冷痛、化学刺激2. TRP & Ca²⁺通道（多模态敏化）TRPM8Transient receptor potential cation channel subfamily M member 8Q7Z2W7冷超敏2. TRP & Ca²⁺通道（多模态敏化）CACNA2D1Voltage-dependent calcium channel subunit alpha-2/delta-1 (α2δ-1)P54289普瑞巴林、加巴喷丁直接靶点3. 神经-免疫接口（小胶质激活）P2RX4P2X purinoceptor 4Q99571最早激活标志物3. 神经-免疫接口（小胶质激活）P2RX7P2X purinoceptor 7Q99572多个脑渗透抑制剂Ⅱ期3. 神经-免疫接口（小胶质激活）CCR2C-C chemokine receptor type 2P41597单核细胞浸润3. 神经-免疫接口（小胶质激活）CX3CR1CX3C chemokine receptor 1 (Fractalkine receptor)P49238小胶质-神经元串话4. 神经营养因子轴NGFBeta-nerve growth factorP01138Tanezumab、Fasinumab抗体4. 神经营养因子轴NTRK1High affinity nerve growth factor receptor (TrkA)P04629高选择性小分子在研4. 神经营养因子轴BDNFBrain-derived neurotrophic factorP23560脊髓中枢敏化4. 神经营养因子轴NTRK2BDNF/NT-3 growth factors receptor (TrkB)Q16620选择性拮抗剂临床前5. 中枢调制受体OPRM1Mu-type opioid receptorP35372经典强效镇痛5. 中枢调制受体OPRD1Delta-type opioid receptorP41143无成瘾风险5. 中枢调制受体OPRK1Kappa-type opioid receptorP41145外周限制性激动剂5. 中枢调制受体CNR1Cannabinoid receptor 1 (CB1)P21554医用大麻主要靶点治疗启示（2025）：Nav1.7/1.8选择性小分子、抗NGF单抗、P2X7脑渗透抑制剂、α2δ新一代配体已成为最有希望的疾病修饰策略；联合外周+中枢双靶点是未来趋势。对实验设计的启示：体外模型中，可通过调节 Nav1.7 / Nav1.8、TRPV1 或 P2X7 的表达与功能，模拟外周神经元兴奋性与神经炎症。在体模型中，可联合检测 NGF/BDNF-Trk 轴与小胶质激活标志物（如 P2X4、CX3CR1），构建从外周到中枢敏化的完整 readout 体系。想要了解其他神经系统疾病的相关靶点（如阿尔茨海默病、、、亨廷顿病等），可参考。Fig 1. 神经病理性疼痛核心通路(PMID: 39996814）神经病理性疼痛最新研究进展以下表格总结了神经病理性疼痛领域的关键临床与基础研究突破，数据来源于顶级期刊、临床试验注册与权威机构。进展主题关键发现/试验结果发表/更新时间潜在影响引用来源VX-548（Vertex，Nav1.8）两项Ⅲ期急性痛试验达标，2024年底向FDA提交NDA，神经病理性疼痛适应症扩展试验启动；Phase 2显示在糖尿病周围神经痛中显著降低痛感评分2024 NEJM + Vertex公告首个非阿片类、高选择性Nav抑制剂有望打破30年镇痛药空白[1]抗NGF抗体长期安全性Tanezumab骨关节炎痛Ⅲ期联合NSAIDs安全性可控，某些抗NGF抗体在特定适应症与给药方案下，安全性信号逐步明确，相关临床限制有所调整2024 Ann Rheum Dis重启神经病理性疼痛适应症开发[2]P2X7脑渗透抑制剂JNJ-55308942等多个候选药在糖尿病神经痛Ⅱ期显示剂量依赖镇痛；2025年系列论文证实P2X7在小胶质激活中的核心作用2024-2025临床更新 + Pain期刊神经炎症-疼痛轴首款潜在疾病修饰药[3]NGF-TrkA轴机制综述NGF通过激活TrkA增强Nav1.7表达，促进外周敏化；抑制NGF可逆转TRPV1转导2025 Curr Issues Mol Biol支持抗NGF单抗在神经病变性疼痛的应用[4]小胶质激活综述P2X4/P2X7介导ATP驱动的IL-1β释放，是神经炎症-神经病理痛典型靶点2022 Int J Mol Sci指导小胶质模型实验设计[5]Nav1.7/1.8交互作用Nav1.8与Nav1.7协同驱动神经元过度兴奋；在神经病理性疼痛模型中双敲除显著缓解痛敏2024 J Gen Physiol支持联合Nav抑制策略[6]TRPV1双向作用TRPV1敏化导致热痛觉过敏，脱敏（如高浓度辣椒素）则产生镇痛2024 Front Mol Neurosci解释辣椒素贴剂临床疗效[7]纳米材料慢性疼痛治疗新型纳米递送系统可靶向DRG或脊髓，实现精准镇痛2025 J Headache Pain跨疾病慢性疼痛新策略[8]abinScience 神经病理性疼痛研究重组蛋白与抗体产品清单以下为 abinScience 针对神经病理性疼痛核心靶点的全部102款产品，已按类别分组并默认折叠（点击“展开”即可查看完整清单）。对合作伙伴与经销商意味着：一个覆盖 Nav1.7、TRPV1、P2X7、NGF-TrkA、α2δ-1、阿片受体、大麻素受体等全通路的完整产品矩阵，支持从体外筛选到在体模型的全流程实验。统一批次质控与详尽技术资料，方便快速向客户推荐。货号品名（英文全称）HC047012Recombinant Human Delta-type opioid receptor (OPRD1) Protein, N-His-KSIHX943012Recombinant Human Voltage-dependent calcium channel subunit alpha-2/delta-1 (CACNA2D1) Protein, N-HisHY107012Recombinant Human High affinity nerve growth factor receptor (NTRK1) Protein, N-HisHW331012Recombinant Human CX3C chemokine receptor 1 (CX3CR1) Protein, N-GST & C-HisHS929022Recombinant Human Sodium channel protein type 9 subunit alpha (SCN9A) Protein, N-GST & C-HisHB935022Recombinant Human Brain-derived neurotrophic factor (BDNF) Protein, N-HisMB935012Recombinant Human Brain-derived neurotrophic factor (BDNF) Protein, N-HisHB822012Recombinant Human Cannabinoid receptor 1 (CNR1) Protein, N-GST & C-HisHS929012Recombinant Human Sodium channel protein type 9 subunit alpha (SCN9A) Protein, N-HisHP943012Recombinant Human P2X purinoceptor 4 (P2RX4) Protein, N-GST & C-HisHP943022Recombinant Human P2X purinoceptor 4 (P2RX4) Protein, N-HisHB935011Recombinant Human Brain-derived neurotrophic factor (BDNF) Protein, C-HisHV713012Recombinant Human P2X purinoceptor 7 (P2RX7) Protein, N-HisHV711012Recombinant Human Transient receptor potential cation channel subfamily V member 1 (TRPV1) Protein, N-HisHS892012Recombinant Human BDNF/NT-3 growth factors receptor (NTRK2) Protein, N-HisHB935012Recombinant Human Brain-derived neurotrophic factor (BDNF) Protein, N-HisHF909012Recombinant Human Beta-nerve growth factor (NGF) Protein, N-HisHF909011Recombinant Human Beta-nerve growth factor (NGF) Protein, C-FcHF525012Recombinant Human Transient receptor potential cation channel subfamily A member 1 (TRPA1) Protein, N-His货号品名（英文全称）HC047012Recombinant Human Delta-type opioid receptor (OPRD1) Protein, N-His-KSIHX943012Recombinant Human Voltage-dependent calcium channel subunit alpha-2/delta-1 (CACNA2D1) Protein, N-HisHY107012Recombinant Human High affinity nerve growth factor receptor (NTRK1) Protein, N-HisHW331012Recombinant Human CX3C chemokine receptor 1 (CX3CR1) Protein, N-GST & C-HisHS929022Recombinant Human Sodium channel protein type 9 subunit alpha (SCN9A) Protein, N-GST & C-HisHB935022Recombinant Human Brain-derived neurotrophic factor (BDNF) Protein, N-HisMB935012Recombinant Human Brain-derived neurotrophic factor (BDNF) Protein, N-HisHB822012Recombinant Human Cannabinoid receptor 1 (CNR1) Protein, N-GST & C-HisHS929012Recombinant Human Sodium channel protein type 9 subunit alpha (SCN9A) Protein, N-HisHP943012Recombinant Human P2X purinoceptor 4 (P2RX4) Protein, N-GST & C-HisHP943022Recombinant Human P2X purinoceptor 4 (P2RX4) Protein, N-HisHB935011Recombinant Human Brain-derived neurotrophic factor (BDNF) Protein, C-HisHV713012Recombinant Human P2X purinoceptor 7 (P2RX7) Protein, N-HisHV711012Recombinant Human Transient receptor potential cation channel subfamily V member 1 (TRPV1) Protein, N-HisHS892012Recombinant Human BDNF/NT-3 growth factors receptor (NTRK2) Protein, N-HisHB935012Recombinant Human Brain-derived neurotrophic factor (BDNF) Protein, N-HisHF909012Recombinant Human Beta-nerve growth factor (NGF) Protein, N-HisHF909011Recombinant Human Beta-nerve growth factor (NGF) Protein, C-FcHF525012Recombinant Human Transient receptor potential cation channel subfamily A member 1 (TRPA1) Protein, N-His货号品名（英文全称）HW331033Anti-Human CX3C chemokine receptor 1 (CX3CR1) Antibody (SAA2443)HF909013Anti-Human Beta-nerve growth factor (NGF) Antibody (PG110)HF909116Research Grade povovetugHA561013Anti-Human Mu-type opioid receptor (OPRM1) Antibody (BMS986122)HC047014Anti-Human Delta-type opioid receptor (OPRD1) Polyclonal AntibodyHX943014Anti-Human Voltage-dependent calcium channel subunit alpha-2/delta-1 (CACNA2D1) Polyclonal AntibodyHY107014Anti-Human High affinity nerve growth factor receptor (NTRK1) Polyclonal AntibodyHW331014Anti-Human CX3C chemokine receptor 1 (CX3CR1) Polyclonal AntibodyHW331023Anti-Human CX3C chemokine receptor 1 (CX3CR1) Nanobody (11H11)HB822043Anti-Cannabinoid receptor 1 (CNR1) Antibody (L112/22)HB822023Anti-Cannabinoid receptor 1 (CNR1) Antibody (L112/26)HB822033Anti-Cannabinoid receptor 1 (CNR1) Antibody (L112/49)HB822010InVivoMAb Anti-Human Cannabinoid receptor 1 (CNR1) Nanobody (5D12)HB822020InVivoMAb Anti-Human Cannabinoid receptor 1 (CNR1) Nanobody (5G11)HB822030InVivoMAb Anti-Human Cannabinoid receptor 1 (CNR1) Nanobody (6B7)HS929013Anti-Human Sodium channel protein type 9 subunit alpha (SCN9A) Antibody (SAA1834)HA935013Anti-Human Sodium channel protein type 11 subunit alpha (SCN11A) Antibody (SAA1857)HW331013Anti-Human CX3C chemokine receptor 1 (CX3CR1) Antibody (SAA1640)HX943013Anti-Human Voltage-dependent calcium channel subunit alpha-2/delta-1 (CACNA2D1) Antibody (SAA1645)HV711013Anti-Human Transient receptor potential cation channel subfamily V member 1 (TRPV1) Antibody (SAA1705)HW387013Anti-Human Kappa-type opioid receptor (OPRK1) Nanobody (SAA1169)HB822013Anti-Human Cannabinoid receptor 1 (CNR1) Nanobody (SAA1274)HB935010InVivoMAb Anti-Human Brain-derived neurotrophic factor (BDNF) (Iv0093)HF909010InVivoMAb Anti-Human Beta-nerve growth factor (NGF) (Iv0066)HB822014Anti-Human Cannabinoid receptor 1 (CNR1) Polyclonal AntibodyHF525014Anti-Human Transient receptor potential cation channel subfamily A member 1 (TRPA1) Polyclonal AntibodyHV711014Anti-Human Transient receptor potential cation channel subfamily V member 1 (TRPV1) Polyclonal AntibodyHS929014Anti-Human Sodium channel protein type 9 subunit alpha (SCN9A) Polyclonal AntibodyHP943014Anti-Human P2X purinoceptor 4 (P2RX4) Polyclonal AntibodyHP943024Anti-Human P2X purinoceptor 4 (P2RX4) Polyclonal AntibodyHV713014Anti-Human P2X purinoceptor 7 (P2RX7) Polyclonal AntibodyHS892014Anti-Human BDNF/NT-3 growth factors receptor (NTRK2) Polyclonal AntibodyHB935014Anti-Human Brain-derived neurotrophic factor (BDNF) Polyclonal AntibodyHF909014Anti-Human Beta-nerve growth factor (NGF) Polyclonal AntibodyDF909018Tanezumab ELISA KitHF909016Research Grade TanezumabHF909026Research Grade FasinumabHF909036Research Grade Fulranumab货号品名（英文全称）HW331033Anti-Human CX3C chemokine receptor 1 (CX3CR1) Antibody (SAA2443)HF909013Anti-Human Beta-nerve growth factor (NGF) Antibody (PG110)HF909116Research Grade povovetugHA561013Anti-Human Mu-type opioid receptor (OPRM1) Antibody (BMS986122)HC047014Anti-Human Delta-type opioid receptor (OPRD1) Polyclonal AntibodyHX943014Anti-Human Voltage-dependent calcium channel subunit alpha-2/delta-1 (CACNA2D1) Polyclonal AntibodyHY107014Anti-Human High affinity nerve growth factor receptor (NTRK1) Polyclonal AntibodyHW331014Anti-Human CX3C chemokine receptor 1 (CX3CR1) Polyclonal AntibodyHW331023Anti-Human CX3C chemokine receptor 1 (CX3CR1) Nanobody (11H11)HB822043Anti-Cannabinoid receptor 1 (CNR1) Antibody (L112/22)HB822023Anti-Cannabinoid receptor 1 (CNR1) Antibody (L112/26)HB822033Anti-Cannabinoid receptor 1 (CNR1) Antibody (L112/49)HB822010InVivoMAb Anti-Human Cannabinoid receptor 1 (CNR1) Nanobody (5D12)HB822020InVivoMAb Anti-Human Cannabinoid receptor 1 (CNR1) Nanobody (5G11)HB822030InVivoMAb Anti-Human Cannabinoid receptor 1 (CNR1) Nanobody (6B7)HS929013Anti-Human Sodium channel protein type 9 subunit alpha (SCN9A) Antibody (SAA1834)HA935013Anti-Human Sodium channel protein type 11 subunit alpha (SCN11A) Antibody (SAA1857)HW331013Anti-Human CX3C chemokine receptor 1 (CX3CR1) Antibody (SAA1640)HX943013Anti-Human Voltage-dependent calcium channel subunit alpha-2/delta-1 (CACNA2D1) Antibody (SAA1645)HV711013Anti-Human Transient receptor potential cation channel subfamily V member 1 (TRPV1) Antibody (SAA1705)HW387013Anti-Human Kappa-type opioid receptor (OPRK1) Nanobody (SAA1169)HB822013Anti-Human Cannabinoid receptor 1 (CNR1) Nanobody (SAA1274)HB935010InVivoMAb Anti-Human Brain-derived neurotrophic factor (BDNF) (Iv0093)HF909010InVivoMAb Anti-Human Beta-nerve growth factor (NGF) (Iv0066)HB822014Anti-Human Cannabinoid receptor 1 (CNR1) Polyclonal AntibodyHF525014Anti-Human Transient receptor potential cation channel subfamily A member 1 (TRPA1) Polyclonal AntibodyHV711014Anti-Human Transient receptor potential cation channel subfamily V member 1 (TRPV1) Polyclonal AntibodyHS929014Anti-Human Sodium channel protein type 9 subunit alpha (SCN9A) Polyclonal AntibodyHP943014Anti-Human P2X purinoceptor 4 (P2RX4) Polyclonal AntibodyHP943024Anti-Human P2X purinoceptor 4 (P2RX4) Polyclonal AntibodyHV713014Anti-Human P2X purinoceptor 7 (P2RX7) Polyclonal AntibodyHS892014Anti-Human BDNF/NT-3 growth factors receptor (NTRK2) Polyclonal AntibodyHB935014Anti-Human Brain-derived neurotrophic factor (BDNF) Polyclonal AntibodyHF909014Anti-Human Beta-nerve growth factor (NGF) Polyclonal AntibodyDF909018Tanezumab ELISA KitHF909016Research Grade TanezumabHF909026Research Grade FasinumabHF909036Research Grade FulranumababinScience：以高品质重组蛋白与精准抗体，赋能神经病理性疼痛机制研究与药物开发。如需根据课题或在研管线定制靶点 panel，欢迎与 abinScience 技术支持support@abinscience.com。参考文献Khalil MW, et al. Selective inhibition of NaV1.8 with VX-548 for acute pain: results from randomized clinical trials. N Engl J Med. 2023.Hochberg MC, et al. Long-term safety and efficacy of subcutaneous tanezumab versus nonsteroidal anti-inflammatory drugs for hip or knee osteoarthritis: a randomized trial. Arthritis Rheumatol. 2021;73(5):859–871.Ursu D, et al. Gain and loss of function of P2X7 receptors: mechanisms, pharmacology and relevance to diabetic neuropathic pain. Mol Pain. 2014;10:37. doi:10.1186/1744-8069-10-37.García-Domínguez M. NGF in neuropathic pain: understanding its role and therapeutic opportunities. Curr Issues Mol Biol. 2025;47(2):93. doi:10.3390/cimb47020093.Chen T, et al. Silencing P2X7R alleviates diabetic neuropathic pain via inhibition of TRPV1 in dorsal root ganglia. Int J Mol Sci. 2022;23(14):7799. doi:10.3390/ijms23147799.Vasylyev DV, et al. Interplay of Nav1.8 and Nav1.7 channels drives neuronal hyperexcitability in neuropathic pain. J Gen Physiol. 2024;156(11):e202413596. doi:10.1085/jgp.202413596.Gao N, et al. The dual role of TRPV1 in peripheral neuropathic pain: pain switches caused by its sensitization or desensitization. Front Mol Neurosci. 2024;17:1400118. doi:10.3389/fnmol.2024.1400118.Sun R, et al. Emerging treatments for chronic neuropathic pain from a cross-disease perspective: developments and applications of nanomaterials. J Headache Pain. 2025;26:143. doi:10.1186/s10194-025-02081-5.仅限科研使用。不得用于诊断或治疗。

100 项与法西努单抗相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D10337	法西努单抗	-	DB12157

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
髋关节炎	临床3期	美国	Regeneron Pharmaceuticals, Inc.	2017-08-17
髋关节炎	临床3期	丹麦	Regeneron Pharmaceuticals, Inc.	2017-08-17
髋关节炎	临床3期	德国	Regeneron Pharmaceuticals, Inc.	2017-08-17
髋关节炎	临床3期	匈牙利	Regeneron Pharmaceuticals, Inc.	2017-08-17
髋关节炎	临床3期	立陶宛	Regeneron Pharmaceuticals, Inc.	2017-08-17
髋关节炎	临床3期	波兰	Regeneron Pharmaceuticals, Inc.	2017-08-17
髋关节炎	临床3期	罗马尼亚	Regeneron Pharmaceuticals, Inc.	2017-08-17
髋关节炎	临床3期	俄罗斯	Regeneron Pharmaceuticals, Inc.	2017-08-17
髋关节炎	临床3期	南非	Regeneron Pharmaceuticals, Inc.	2017-08-17
髋关节炎	临床3期	西班牙	Regeneron Pharmaceuticals, Inc.	2017-08-17

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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


NCT03161093 (Pubmed \| RMD Open)	临床3期	髋关节炎 \| 膝关节炎	1,801	Fasinumab 1 mg Q4W	齋選範夢範膚選網鹹獵(鏇遞餘憲齋夢製齋築壓) = 築廠蓋醖築夢鏇艱簾築醖遞獵蓋膚鑰壓獵膚襯 (夢觸獵獵廠觸淵製簾願 ) 更多	积极	2026-01-01
				Fasinumab 1 mg Q8W	齋選範夢範膚選網鹹獵(鏇遞餘憲齋夢製齋築壓) = 壓簾顧餘範膚遞築鬱簾醖遞獵蓋膚鑰壓獵膚襯 (夢觸獵獵廠觸淵製簾願 ) 更多
NCT02683239 (FACT LTS & OA, CTgov)	临床3期	疼痛 \| 骨关节炎	5,331	Placebo+Fasinumab (Fasinumab-matching Placebo Q4W/Q8W)	範範壓壓製衊憲鹹觸鹹 = 鑰願壓鏇簾蓋鏇繭鑰膚築範顧醖遞選餘淵簾積 (衊餘積顧窪築願艱製觸, 觸繭襯餘築餘築鏇鏇範 ~ 憲遞鑰廠鹽鹽願醖築顧) 更多	-	2023-10-13
				Fasinumab (Fasinumab 1 mg SC Q8W)	範範壓壓製衊憲鹹觸鹹 = 淵壓夢顧願壓衊鏇膚衊築範顧醖遞選餘淵簾積 (衊餘積顧窪築願艱製觸, 齋鹽廠襯繭鹽網積鑰鬱 ~ 觸憲窪獵齋壓艱廠製築) 更多
NCT03691974 (CTgov)	临床2期	疼痛 \| 髋关节炎 \| 膝关节炎	180	Placebo	繭製觸鬱鹽範壓襯範選 = 範醖衊襯糧糧構網製製鹽鹽齋願淵積觸膚窪鹽 (鏇繭鏇顧襯顧鏇鑰觸憲, 範構蓋壓廠夢鹽艱壓網 ~ 鬱築構鏇選蓋糧鑰鬱構)	-	2023-03-01
NCT03304379 (FACT OA2, CTgov)	临床3期	疼痛 \| 髋关节炎 \| 膝关节炎	1,650	placebo+Fasinumab (Placebo)	齋淵製廠積遞範鬱積選(製鹽夢築糧繭構顧蓋鏇) = 選窪網簾鑰鹽鑰糧淵廠窪窪醖繭憲獵淵衊範願 (繭獵網憲憲艱糧蓋鹹壓, 0.165) 更多	-	2023-02-24
				Fasinumab (Fasinumab 1 mg)	齋淵製廠積遞範鬱積選(製鹽夢築糧繭構顧蓋鏇) = 網製糧蓋窪艱觸選襯繭窪窪醖繭憲獵淵衊範願 (繭獵網憲憲艱糧蓋鹹壓, 0.127) 更多
NCT03285646 (FACT CLBP 1, CTgov)	临床3期	腰痛 \| 膝关节炎	63	Placebo+Fasinumab (Fasinumab-matching Placebo)	獵襯鏇繭獵鹹鏇鑰網鹽(鏇壓壓築繭獵衊觸衊夢) = 艱醖淵窪鏇構鹹壓積齋憲窪糧鏇範簾淵願範鏇 (積觸願憲廠積艱製艱醖, 1.424) 更多	-	2021-06-30
				Fasinumab (Fasinumab 3 mg SC Q4W)	獵襯鏇繭獵鹹鏇鑰網鹽(鏇壓壓築繭獵衊觸衊夢) = 淵築齋選壓壓願鏇鹽艱憲窪糧鏇範簾淵願範鏇 (積觸願憲廠積艱製艱醖, 2.037) 更多
NCT02620020 (Pubmed \| Arthritis Rheumatol) 人工标引	临床2/3期	腰痛	-	Fasinumab	鏇齋憲廠夢壓鏇淵艱遞(鏇範蓋顧壓糧選製窪窪) = 齋鹽製蓋衊糧獵窪蓋獵獵顧襯壓艱餘簾衊淵願 (鹹積鏇願鹽廠憲顧構獵 )	积极	2020-11-16
				Placebo	廠鹽艱積憲衊鹹醖鹽選(鏇齋繭願壓積窪窪範簾) = 窪網夢膚觸淵淵壓構膚鬱顧憲構艱廠鹹積齋壓 (膚壓築艱壓壓憲醖獵窪, 0.3) 更多
NCT02620020 (CTgov)	临床2/3期	腰痛	563	placebo (Placebo SC Q4W and Placebo IV Q8W)	夢廠鹹餘願廠衊艱鑰糧(鹽鹹鹹鏇繭餘構膚壓鑰) = 遞構糧淵膚壓鏇窪簾壓蓋鑰築顧餘壓襯繭簾積 (獵構廠蓋積構繭壓蓋鏇, 0.23) 更多	-	2019-08-01
				placebo+Fasinumab (Fasinumab 6 mg SC Q4W and Placebo IV Q8W)	夢廠鹹餘願廠衊艱鑰糧(鹽鹹鹹鏇繭餘構膚壓鑰) = 衊膚構製範壓蓋網齋願蓋鑰築顧餘壓襯繭簾積 (獵構廠蓋積構繭壓蓋鏇, 0.23) 更多