The primary purpose of this study is to evaluate the pharmacokinetics (PK) and pharmacodynamics (PD) of ublituximab in participants ages 10 to less than (<)18 years and body weight greater than or equal to (≥)25 kilograms (kg) to less than or equal to (≤)40 kg with RMS (Part A) and to evaluate the non-inferiority of ublituximab compared with fingolimod in pediatric RMS participants with body weight ≥ 25 kg (Part B). The study will further evaluate long-term safety and efficacy of ublituximab in RMS in pediatric participants during its extension period (Part C).

开始日期2025-12-01

申办/合作机构

TG Therapeutics, Inc.

NCT06424067

/ Recruiting临床2期

A Phase II Study of Fingolimod in Patients With Non-Small Cell and Small Cell Lung Cancer

This is a single-institution, open-labeled study using fingolimod (FTY720/Gilenya) in patients with non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) who have progressed on chemo-immunotherapy. The study design will be a 6 patient safety lead-in with 2 cohorts of patients for efficacy analysis where fingolimod 0.5 mg will be taken orally once daily.

开始日期2025-05-01

申办/合作机构

The Medical University of South Carolina

IRCT20240701062291N1

/ Recruiting临床2期IIT

The efficacy of fingolimod in enhancing neurological recovery after traumatic spinal cord injury

开始日期2024-08-22

申办/合作机构

Mashhad University of Medical Sciences

100 项与盐酸芬戈莫德相关的临床结果

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100 项与盐酸芬戈莫德相关的转化医学

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100 项与盐酸芬戈莫德相关的专利（医药）

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4,662

项与盐酸芬戈莫德相关的文献（医药）

2025-12-31·Virulence

Ponatinib and other clinically approved inhibitors of Src and Rho-A kinases abrogate dengue virus serotype 2- induced endothelial permeability

Article

作者: Awasthi, Mansi ; Modak, Ayan ; Sobha, Archana ; Sreekumar, Easwaran ; Mishra, Srishti Rajkumar

Severe dengue often presents as shock syndrome with enhanced vascular permeability and plasma leakage into tissue spaces. In vitro studies have documented the role of Src family kinases (SFKs) and RhoA-kinases (ROCK) in dengue virus serotype 2 (DENV2)-induced endothelial permeability. Here, we show that the FDA-approved SFK inhibitors Bosutinib, Vandetanib and Ponatinib, as well as the ROCK inhibitors, Netarsudil and Ripasudil significantly inhibit DENV2-induced endothelial permeability. In cultured telomerase immortalized human microvascular endothelial cells (HMEC-1), treatment with these inhibitors reduced the phosphorylation of VE-Cadherin, Src and myosin light chain 2 (MLC2) proteins that were upregulated during DENV2 infection. It also prevented the loss of VE-Cadherin from the inter-endothelial cell junctions induced by viral infection. In in-vivo studies using DENV2-infected AG129 IFN receptor-α/β/γ deficient mice, ponatinib, when administered 24 h post-infection onwards, demonstrated significant benefits in improving body weight, clinical outcomes, and survival rates. While all virus-infected, untreated mice died by day-10 post-infection, 80% of the ponatinib-treated mice survived, and approximately 60% were still alive at the end of the 15-day observation period. The treatment also significantly reduced disease severity factors such as vascular leakage, thrombocytopenia; mRNA transcript levels of proinflammatory cytokines such as IL-1β and TNF-α; and restored liver function. Comparable effects were observed even when ponatinib treatment was initiated after symptom onset. The results highlight ponatinib as an effective therapeutic option in severe dengue; and also a similar potential for other FDA- approved SFK and ROCK inhibitors.

2025-12-01·MOLECULAR BIOLOGY REPORTS

Lysophosphatidylcholine induces ceramide synthase-2 expression in primary culture model of astrocytopathy: potential therapeutic target in multiple sclerosis

Article

作者: Amarjeet ; Pancholi, Bhaskaranand ; Abate, Selamu Kebamo ; Mohapatra, Abhipsa ; Babu, Raja ; Garabadu, Debapriya

BACKGROUND:

Multiple sclerosis (MS) is a chronic autoimmune condition that damages the myelin sheath of neurons in the central nervous system, resulting in compromised nerve transmission and motor impairment. The astrocytopathy is considered one of the prominent etiological factor in the pathophysiology of demyelination in MS. The expression level of ceramide synthase-2 (CS-2) is yet to be established in the pathophysiology of astrocytopathy although the derailed ceramide biosynthetic pathways is well demonstrated in the pathophysiology of demyelination. Therefore, in the present study, the expression level of CS-2 has been evaluated in lysophosphatidylcholine (LPC)-challenged primary astrocytes in the presence of anti-demyelinating agents such as Fingolimod, a clinically approved anti-demyelinating drug, and Ursolic Acid (UA), an experimentally accepted anti-demyelinating agent, in MS.

METHODS AND RESULTS:

LPC (150 µg/ml) caused astrocytopathy evident by decrease in percentage of viable astrocytes, increase in percentage of apoptotic astrocytes, increase in the level of reactive oxygen species (ROS), and increase in the level of activated astrocytes. Interestingly, LPC significantly increased the expression level of CS-2 in the primary culture of astrocytes where as fingolimod and UA (1, 10, and 100 µM) were able to attenuate the extent of LPC-induced astrocytopathy in the primary culture model of MS. Further, both the drugs drastically reduced the LPC-induced increase in the level of expression of CS-2 in the astrocytes.

CONCLUSIONS:

These observations indicate the fact that CS-2 could be a potential target in the management of astrocytopathy and astrocytopathy-related neurological disorders including MS. In conclusion, CS-2-targeted drugs could be potential therapeutic options in the management of MS.

2025-12-01·Lancet Regional Health-Europe

The effect of disease-modifying therapies on brain volume loss and disability accumulation in multiple sclerosis: a systematic review and network meta-analysis

Article

作者: Cagol, Alessandro ; Schaedelin, Sabine ; Sormani, Maria Pia ; Pretzsch, Roxanne ; Granziera, Cristina ; Kappos, Ludwig

Background:

Multiple treatments have demonstrated efficacy in preventing brain volume loss (BVL) in randomized controlled trials (RCTs) for multiple sclerosis (MS). However, assessing their relative effectiveness remains challenging due to limited head-to-head comparisons. Additionally, the relationship between treatment effects on BVL and disability accumulation is not established for newer therapies. This study aimed to compare the efficacy of approved disease-modifying therapies (DMTs) in reducing BVL in MS and to investigate the association between treatment effects on BVL and disability accumulation.

Methods:

In this systematic review and network meta-analysis, we included all RCTs enrolling adults with MS that evaluated FDA-approved DMTs and reported BVL outcomes over at least one year. We searched PubMed, Embase, and Cochrane from inception to September 2024. Following PRISMA guidelines, two reviewers independently extracted data on BVL, MRI lesion activity, and disability progression. We conducted a mixed-effects network meta-analysis with placebo as the reference group. Meta-regression analyses examined the association between treatment effects on BVL and disability progression, adjusting for MRI lesion activity.The primary outcome was BVL. Secondary outcomes included MRI lesion accumulation and risk of confirmed disability progression. Effect sizes were reported as the ratio of means (ROM) and hazard ratios (HRs), with 95% confidence intervals (CIs). This study is registered with PROSPERO (CRD420251034936).

Findings:

We included 33 RCTs evaluating 16 DMTs and 26,247 patients. Eight DMTs significantly reduced BVL compared to placebo, including ponesimod (ROM = 0.52; 95%-CI: 0.35-0.77), ofatumumab (ROM = 0.58; 95%-CI: 0.40-0.83), alemtuzumab (ROM = 0.63; 95%-CI: 0.49-0.83), teriflunomide (ROM = 0.71; 95%-CI: 0.52-0.97), ozanimod (ROM = 0.74; 95%-CI: 0.56-0.98), natalizumab (ROM = 0.77; 95%-CI: 0.61-0.96), siponimod (ROM = 0.77; 95%-CI: 0.60-0.98), and fingolimod (ROM = 0.83; 95%-CI: 0.71-0.96). The treatment effect on BVL was associated with the treatment effect on disability accumulation (β = 0.466; p = 0.008), and this association remained significant independently of the treatment effect on MRI activity (β = 0.422; p = 0.005).

Interpretation:

Several DMTs-including newer therapies-significantly reduce BVL, and this effect correlates with reduced disability accumulation. These findings support BVL as a meaningful treatment target in MS.

Funding:

None.

172

项与盐酸芬戈莫德相关的新闻（医药）

2025-10-22

·药明康德

致敬时代丨输1次液就能管半年，11年后92%的患者不靠助行器仍能自己走路！多款新疗法为数百万患者打开希望之门

编者按：2025年，药明康德迎来创立25周年的重要里程碑。值此契机，我们向所有与我们共同书写产业变革篇章的科学家、医药人和投资者致以衷心感谢与诚挚敬意，也特别推出“致敬时代”系列，回顾全球同仁如何借助科学与合作的力量，不断拓展治疗边界、改善患者命运。四分之一个世纪的坚守，只为加速每一款新药的诞生。下一个25年，我们将继续心怀感恩与敬畏，依托独特的CRDMO模式，与全球伙伴携手同行，共赴健康未来。多发性硬化（MS）是一种伴随终生的进展性自身免疫性中枢神经系统疾病，也是相对“没那么罕见”的一种罕见病，目前在全球约有300万患者，迄今仍无法治愈。这个病好发于29~39岁的青壮年，女性更为多见。患者的免疫系统会攻击保护神经纤维的髓鞘（类似于电线外层的“绝缘保护套”），导致神经髓鞘不断破损与脱落，并逐步造成患者脊髓、大脑以及视神经功能受损，导致身体机能（如步行）和认知功能（如记忆力）逐渐下降。图片来源：123RF 根据病程，多发性硬化可分为4型——复发缓解型（RRMS）、继发进展型（SPMS）、原发进展型（PPMS）和进展复发型（PRMS），其中复发缓解型多发性硬化是最常见的类型，表现为疾病周期性地复发和缓解，这些缓解可能并不完全，导致患者仍然存在一定程度上的残留疾病。而随着疾病的进展，在确诊后10年、20年和30年内，分别有约25%、50%和75%以上的RRMS患者会发展成为更严重的类型——SPMS。在这类患者中，残疾的进展不再能够得到缓解，他们只能任由症状一次次来袭、不断加重，最终丧失自理能力、失明甚至失去生命。最早关于疑似多发性硬化的案例记载可以追溯到14世纪末。1868年，神经学家让-马丁·沙科（Jean-Martin Charcot）将这类疾病正式命名为“多发性硬化”。从19世纪到20世纪上半叶，人类尝试了数百种疗法都没能成功，但多发性硬化的神经病学特征正逐步被揭开，它与异常免疫反应的关系也浮出水面。20世纪50年代，糖皮质激素可的松被发现可以用于治疗多发性硬化症的复发（也称“发作”或“恶化”），它能在急性期减轻恶化症状并缩短病程，但无法长期控制病情的进展。直到90年代，首批在缓解期也能有效控制疾病进展的免疫调节疗法问世，后续又诞生了多款不同机制的免疫调节疗法，这些药物被统称为“疾病修正疗法（DMT）”，已成为多发性硬化治疗的中流砥柱。近十多年来，更多创新疗法接连问世，极大改善了患者的生存状况。作为全球医药及生命科学行业值得信赖的合作伙伴和重要贡献者，药明康德在过去25年发展历程中，很荣幸见证了多款多发性硬化创新疗法从实验室到临床的突破历程，更通过提供一体化、端到端的新药研发和生产服务，助力全球合作伙伴加速多款多发性硬化创新疗法的研发进程、造福病患。今天这篇文章将回望近25年来多发性硬化创新疗法的发展历程，向那些帮助广大患者挣脱疾病桎梏的英雄们致敬。传统免疫调节注射疗法，开启“疾病修正治疗”时代 20世纪80年代后期，越来越多科学家意识到，异常的自身免疫反应在多发性硬化恶化过程中扮演着重要角色，并开始尝试挖掘多种免疫调节疗法的治疗潜力。几年后，重组人干扰素-β-1b（IFN-β-1b）脱颖而出，成为首个被证明能有效延缓RRMS自然病程的疗法，能让RRMS患者在2年内的年复发次数减少34%。1993年7月，IFN-β-1b获FDA批准上市（商品名：Betaseron），用于RRMS门诊患者，以减少临床恶化的频率。随后，同属此类药物的IFN-β-1a（商品名：Rebif）也于2002年获FDA批准用于RRMS患者，除了减少复发频率，它还能明显延缓患者持续残疾的进展时间。2014年，它的升级版——聚乙二醇化干扰素-β-1a（peginterferon-β-1a，商品名：Plegridy）获FDA批准上市，经过聚乙二醇化，可以让药物在体内维持更长的作用时间，从而减少给药频率，有助于提高患者的依从性。在上述多款干扰素之外，1996年获FDA批准用于RRMS的格拉替雷（glatiramer，商品名：Copaxone）也是早期获批的注射疗法之一。这款药物是由4种氨基酸组成的多肽类混合物，这些肽被认为能竞争性地抑制免疫细胞和髓磷脂之间的相互作用。首批注射疗法的成功，让多发性硬化告别了只能缓解疾病症状的时代，从此进入了可用药物控制病情进展的“疾病修正治疗”时代。由于安全性很强，这些疗法经久不衰，直到今天仍然是多发性硬化治疗方案的重要组成部分。多款生物制剂类靶向疗法诞生，改写更多患者命运不过问题来了——只有约三分之二的患者对上述疗法有应答，且只能达到中等疗效（即让年复发率降低约30%）。此外还有约三分之一的患者对它们几乎没有应答。为了开发出更有效的疗法、让更多患者有药可用，医药企业与科学家们又踏上了探索之路，并由此催生出多款靶向疗法。图片来源：123RF 其中，由Athena Neuroscience、Elan公司与渤健共同开发的natalizumab，是首个获批用于MS的生物制剂类靶向疗法。它的诞生，还要从一次“无心插柳”的意外发现说起。 20世纪90年代，斯坦福大学斯坦曼实验室（Steinman Laboratory）和来自Athena Neuroscience的科学家泰德·耶德诺克博士（Ted Yednock）等人开展了合作，原本是想探究IFN-β能否阻止淋巴细胞异常地穿透血脑屏障（这是多发性硬化的始动环节）、从而减少炎症性脑损伤。令人意外的是，耶德诺克和同事们在大鼠模型中找到了协助淋巴细胞越界而入的“帮凶”——α4β1整合素，并进一步发现，这个“帮凶”能被相应抗体所抑制，从而抑制大脑中淋巴细胞的积累与炎症性脑损伤的发生。耶德诺克博士和同事们马上意识到，这是个令人惊喜的全新发现。于是他们及时调整课题方向，全力以赴设计出了一款针对α4β1整合素的人源化单克隆抗体——natalizumab。后续的临床试验中，这款药一路过关斩将。终于，在目标分子被初次发现的12年后，2004年，natalizumab获FDA批准上市（商品名：Tysabri），用于RRMS患者的治疗。FDA指出，在医疗需求高度未满足的该疾病领域，这款全新机制的药物与当时已有的药物相比具有显著优势。可好事多磨，这款新药在上市第二年就遇到了问题——有几名患者在接受natalizumab治疗时发生了进行性多灶性脑白质病（PML），这款新药一时退出市场。好在，经过安全性审查并增加严格用药的限制后，2006年，natalizumab得以重新回到市场。同样在2006年，natalizumab在长期临床试验中再次证明了自己的实力——与安慰剂组相比，患者在使用natalizumab治疗的2年期间，残疾持续进展的风险降低了42%-54%，年复发率降低了68%。后来的6年里，研发团队一直致力于揪出PML发生的原因。他们发现，用药2年后，每500名患者中有超过1名患者可能会发展为脑部机会性感染，从而出现PML；还找到了预测风险患者的生物标志物——约翰坎宁安病毒（导致PML的病原体）的抗体，这有助于帮医生排查出有PML风险的患者。 2014年，还有一款“老药”获FDA批准用于多发性硬化的新适应症，那就是此前已在慢性淋巴细胞白血病患者中应用了十余年、由拜耳与赛诺菲旗下健赞（Genzyme）共同开发、靶向CD52的阿仑珠单抗（alemtuzumab，商品名：Lemtrada）。虽然早在20世纪90年代末，当时来自剑桥大学的科学家们就已在少数患者中证实，阿仑珠单抗能阻止多发性硬化患者大脑中新出现的炎症反应，并减少新的发作次数，可奇怪的是，虽然不再出现炎症了，大多数患者的病情却仍在继续进展。经过不懈探索，研究团队揭开了谜底——原来，在多发性硬化症的病程中，“炎症”和“退行性病变”是两个各自独立的过程。炎症会引起RRMS的发作，但也会引发神经变性；发作次数多了以后，即使没有炎症了，这种疾病的退行性病变依然会继续发展。就像在雪坡上滚雪球一般，起初给了向下的推力，它就会自动持续朝前翻滚。因此，疾病仍在缓慢进展，此前日积月累的残疾也不会好转。图片来源：123RF 由此，科学家们推断，要让阿仑珠单抗更好地发挥作用，就必须让患者在发作次数还不多的患病初期趁早用上这款药。经过多年潜心研究，2008年，阿仑珠单抗在初步临床试验中交出了惊艳的成绩单：经过长达3年的治疗，与接受传统免疫调节药物治疗的患者相比，接受阿仑珠单抗治疗的患者年复发率降低了74%，持续残疾累积风险降低了71%，残疾评分也得到改善。2014年，阿仑珠单抗获FDA批准用于RRMS患者，历时二十多年的漫漫征程终于开花结果。从2016年至今，还有多款单克隆抗体靶向疗法已陆续获FDA批准用于多发性硬化患者，包括靶向B细胞表面CD20抗原的奥瑞利珠单抗（ocrelizumab，商品名：Ocrevus）、奥法妥木单抗（ofatumumab，商品名：Kesimpta）以及ublituximab（商品名：Briumvi）。其中，奥瑞利珠单抗是FDA批准针对PPMS患者的首个创新疗法。PPMS约占MS的10%，这一类型没有缓解期，疾病进展更快且持续加重、严重程度更高，生活质量也更差。长期随访研究显示，接受奥瑞利珠单抗治疗11年后，在复发性MS患者中，80%的患者无残疾进展，多达92%的人仍能独立行走、不需要包括轮椅在内的各种助行器；即使是更严重的PPMS患者，也有33%的患者无残疾进展、80%的人无需依赖轮椅（部分患者可能需要比轮椅更简单的助行器）。同时，虽然是一种注射疗法，但相比大多数MS生物制剂每月1次的用药频率，这款药物只需半年输注1次，有助于让患者的依从性大大提高。百花齐放的小分子疗法：MS进入口服靶向治疗新时代在相当长的时间内，获得FDA上市的MS疗法都需要注射治疗。因此，科学家们也在寻找用药更便捷的小分子口服药物，由此诞生了作用机制各异的小分子疗法，包括达伐吡啶（dalfampridine，商品名：Ampyra）、特立氟胺（teriflunomide，商品名：Aubagio）、富马酸二甲酯（dimethyl fumarate，商品名：Tecfidera）及其升级版本富马酸地洛西美（diroximel fumarate，商品名：Vumerity），还有以芬戈莫德（fingolimod，商品名：Gilenya）为代表的多款神经鞘氨醇-1-磷酸（S1P）受体调节剂类口服靶向疗法。 2010年1月，达伐吡啶获FDA批准上市，成为全球首款MS口服疗法。这是一款钾离子通道阻滞剂，可恢复脱髓鞘神经纤维的信号传导，从而改善MS患者的运动功能障碍，尤其是步行障碍。据统计，超过90%的MS患者存在行走困难（步行障碍），约半数患者在发病15年内需要辅助行走。而临床研究证实，达伐吡啶能让约三分之一的患者步行速度明显提升，有的患者甚至能基本恢复正常行走能力。图片来源：123RF 特立氟胺是类风湿关节炎“老药”来氟米特的活性代谢物，通过阻断嘧啶的合成途径、可逆性抑制二氢乳清酸脱氢酶，进而抑制活化的T、B淋巴细胞增殖，同时保留保护性免疫应答；富马酸二甲酯和富马酸地洛西美则是通过激活Nrf2通路、发挥免疫调节和细胞保护作用，后者相比前者具有更好的胃肠道耐受性。在这几款药物之外，目前MS的其他小分子疗法都属于“S1P受体调节剂类”这个大家族，它们靶点更明确、疗效也更加突出。2010年9月，芬戈莫德获FDA批准上市，成为全球首个可降低MS复发频率的口服疗法。作为一款S1P受体调节剂，它通过与淋巴细胞表面的S1P受体结合、使其保留于淋巴结而发挥作用。芬戈莫德的诞生，是受到另一款免疫抑制剂“老药”环孢素A的启发。环孢素A早在上世纪80年代就已获批上市，是从一种真菌中分离出的代谢产物。科学家们由此打开了思路——能不能从其他真菌中找到更多的免疫抑制剂呢？经过多番尝试，90年代初，日本京都大学药学院的科学家们在虫草科棒束孢属真菌Isaria sinclairii的培养液中分离出了一种具有免疫抑制作用的天然氨基酸ISP-I。但它在水中溶解度很低，还具有较高的毒性，于是科学家们又对其结构进行简化、修饰，最终得到了具有更强的免疫抑制活性、安全性更高的小分子药物芬戈莫德。长期临床试验表明，使用芬戈莫德治疗10年后，46%的患者无复发，96%和68%的患者的扩展残疾功能量表（EDSS）评分分别维持在7分和4分以下（得分越低，说明残疾进展的程度越轻）。而后，芬戈莫德的升级产品、第二代选择性S1P受体调节剂西尼莫德（siponimod）开始向MS中相对更严重的类型——SPMS发起挑战。如前所述，SPMS通常由RRMS在几次复发后逐渐发展形成。此前的疾病修正疗法对它一般无效，治疗方法十分有限，预后不佳。西尼莫德对S1P受体中的特定亚型S1P1、S1P5具有高度的选择性，通过与二者的结合，它既能阻止淋巴细胞进入中枢神经系统、降低炎症反应，还能穿透血脑屏障、促进髓鞘再生，起到神经修复作用。在临床试验中，即使在患病近16年的SPMS患者中，这款药物仍能显著降低3个月、6个月后的确认残疾进展风险，并将年复发率降低了55%。2019年，西尼莫德获FDA批准上市（商品名：Mayzent），用于治疗复发型多发性硬化（RMS）成年患者，包括活跃的SPMS、RRMS和临床孤立综合征（CIS）。 2020年到2021年，还有两款第二代选择性S1P受体调节剂类口服疗法获FDA批准用于复发型MS患者，分别是奥扎莫德（ozanimod，商品名：Zeposia）与Ponesimod（商品名：Ponvory）。探索仍在继续过去25年间，FDA共批准了至少15款治疗多发性硬化的新疗法。作为全球领先的新药研发一体化赋能平台，药明康德很荣幸能为其中多款疗法提供赋能、助力合作伙伴的这些创新疗法来到全球患者身边。尽管这些年来MS治疗取得显著进展，但由于疾病的高度异质性和血脑屏障的存在，现有疗法在疾病长期控制和神经保护方面仍面临诸多挑战。因此，产业界仍在不断探索，致力于为患者带来更安全、有效、便利的治疗选择。当前还有近80款针对多发性硬化的新疗法正处于积极的临床研究中，其中数款疗法已进入3期临床阶段，涵盖布鲁顿酪氨酸激酶（BTK）抑制剂、CD40L靶向单抗、CD19靶向双抗等等。以fenebrutinib为例，这是一种在研的口服、可逆性BTK抑制剂，能阻断BTK在B细胞发育及活化中的关键作用，同时调控巨噬细胞和小胶质细胞等髓系免疫细胞的活化；同时，该药对BTK的抑制选择性高出其他激酶130倍，有望降低脱靶效应，提升长期使用的安全性。此前公布的2期临床研究96周数据显示，接受fenebrutinib治疗的RMS患者中，患者用药近2年后的年复发率很低（6%），且脑部无活动性病灶、在此期间没发生残疾进展。目前，该药用于复发型和原发进展型多发性硬化的3期研究正在进行中，预计将在今年年底公布结果。在这场攻克多发性硬化的漫漫征途中，正是科学家们数十年如一日的追寻，还有广大患者及其家庭的信赖与支持，才让这一顽疾有了一款又一款突破性疗法，并在治疗效果等方面实现质的飞跃。最后，让我们再次向那些迎难而上、解开多发性硬化治疗难题的英雄们致以崇高的敬意。药明康德也期待与业界同仁继续携手同行，见证更多创新疗法的问世，帮助更多患者“步”入生命的新篇章。参考资料： [1] Atlas-3rd-Edition-Epidemiology-report-EN-updated-30-9-20.pdf. Retrieved Oct 20, 2025 from https://www.msif.org/wp-content/uploads/2020/10/Atlas-3rd-Edition-Epidemiology-report-EN-updated-30-9-20.pdf [2] History of Multiple Sclerosis | MSAA. Retrieved Oct 20, 2025 from https://mymsaa.org/ms-information/overview/history/ [3] Ransohoff, R. M., Hafler, D. A., & Lucchinetti, C. F. (2015). Multiple sclerosis—a quiet revolution. Nature Reviews Neurology, 11(3), 134-142. doi: 10.1038 / nrneurol.2015.14 [4] Lublin, F. (2005). History of modern multiple sclerosis therapy. Journal of Neurology, 252(Suppl 3), iii3-iii9. https://doi.org/10.1007/s00415-005-2010-6 [5] Treatment of Multiple Sclerosis. Retrieved Oct 20, 2025 from https://www.nature.com/collections/whyfzwfvvr/timeline/ [6] 中华医学会神经病学分会神经免疫学组. (2024). 多发性硬化诊断与治疗中国指南(2023版). 中华神经科杂志, 57(01), 10-23. doi: 10.3760/cma.j.cn113694-20230918-00173 [7] Jankovic, S. M. (2010). Injectable interferon beta-1b for the treatment of relapsing forms of multiple sclerosis. Journal of inflammation research, 25-31. doi: 10.2147/jir.s9480 [8] Rudick, R., Polman, C., Clifford, D., Miller, D., & Steinman, L. (2013). Natalizumab: bench to bedside and beyond. JAMA neurology, 70(2), 172-182. doi:10.1001/jamaneurol.2013.598 [9] Steinman, L. (2012). The discovery of natalizumab, a potent therapeutic for multiple sclerosis. J Cell Biol，199(3):413-6. doi: 10.1083/jcb.201207175. [10] 10th anniversary story: Campath – Cambridge Enterprise. Retrieved Oct 20, 2025 from https://www.enterprise.cam.ac.uk/10th-anniversary-storycampath/ [11] Brinkmann, V., Billich, A., Baumruker, T., Heining, P., Schmouder, R., Francis, G., ... & Burtin, P. (2010). Fingolimod (FTY720): discovery and development of an oral drug to treat multiple sclerosis. Nature reviews Drug discovery, 9(11), 883-897. [12] 诺华多发性硬化症新药「芬戈莫德」在中国获批上市. Retrieved Oct 20, 2025 from https://www.phirda.com/about_20417.html [13] Adachi, K., & Chiba, K. (2007). FTY720 story. Its discovery and the following accelerated development of sphingosine 1-phosphate receptor agonists as immunomodulators based on reverse pharmacology. Perspectives in medicinal chemistry, 1, 1177391X0700100002. [14] New Oral Medications for MS Are on the Horizon. Retrieved Oct 20, 2025 from https://www.brainandlife.org/articles/oral-drugs-for-ms [15] Lamore III, R., Jacob, E., Jacob, S. C., & Hilas, O. (2010). Dalfampridine (Ampyra): An aid to walking in patients with multiple sclerosis. Pharmacy and Therapeutics, 35(12), 665. [16] Novartis receives FDA approval for Mayzent® (siponimod), the first oral drug to treat secondary progressive MS with active disease. Retrieved Oct 20, 2025 from https://www.novartis.com/news/media-releases/novartis-receives-fda-approval-mayzent-siponimod-first-oral-drug-treat-secondary-progressive-ms-active-disease [17] A Study to Evaluate the Efficacy and Safety of Fenebrutinib Compared With Teriflunomide in Relapsing Multiple Sclerosis (RMS) (FENhance). Retrieved . Oct 20, 2025 from https://clinicaltrials.gov/study/NCT04586010?term=NCT04586010&rank=1 [18] Study to Evaluate the Efficacy and Safety of Fenebrutinib Compared With Teriflunomide in Relapsing Multiple Sclerosis (RMS) (FENhance 2). . Retrieved Oct 20, 2025 from https://clinicaltrials.gov/study/NCT04586023 [19] Roche’s fenebrutinib maintains near-complete suppression of disease activity and disability progression for up to two years in people with relapsing multiple sclerosis. Retrieved Oct 20, 2025 from https://www.roche.com/media/releases/med-cor-2025-05-30 [20] Rudick, R., Polman, C., Clifford, D., Miller, D., & Steinman, L. (2013). Natalizumab: bench to bedside and beyond. JAMA neurology, 70(2), 172-182. doi:10.1001/jamaneurol.2013.598 [21] Rudick, R. A., & Panzara, M. A. (2008). Natalizumab for the treatment of relapsing multiple sclerosis. Biologics: Targets and Therapy, 2(2), 189-199. doi: 10.2147/btt.s1956 [22] CAMMS223 Trial Investigators. (2008). Alemtuzumab vs. interferon beta-1a in early multiple sclerosis. New England Journal of Medicine, 359(17), 1786-1801. DOI: 10.1056/NEJMoa0802670 [23] 奥瑞利珠单抗注射液（罗可适® ）. Retrieved Oct 20, 2025 from https://www.nhsa.gov.cn/attach/Ypsn2025/YPSW202500367/YPSW202500367(ppt).pdf [24] The patient impact of 11 years of ocrelizumab treatment in multiple sclerosis: long-term data from the Phase III OPERA and ORATORIO studies - ECTRIMS-2024-poster-hauser-the-patient-impact-of-11-years-of-ocrelizumab.pdf. Retrieved Oct 20, 2025 from https://medically.gene.com/global/en/unrestricted/neuroscience/ECTRIMS-2024/ectrims-2024-poster-hauser-the-patient-impact-of-11-yea.html [25] Pikoulas, T. E., & Fuller, M. A. (2012). Dalfampridine: a medication to improve walking in patients with multiple sclerosis. Annals of Pharmacotherapy, 46(7-8), 1010-1015. doi: 10.1345/aph.1Q714. [26] Furthering MS Treatment Selection: A Comparative Study of Peginterferon Beta-1a vs Interferon Beta-1a | NeurologyLive - Clinical Neurology News and Neurology Expert Insights. Retrieved Oct 20, 2025 from Furthering MS Treatment Selection: A Comparative Study of Peginterferon Beta-1a vs Interferon Beta-1a | NeurologyLive - Clinical Neurology News and Neurology Expert Insights 免责声明：本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。版权说明：欢迎个人转发至朋友圈，谢绝媒体或机构未经授权以任何形式转载至其他平台。转载授权请在「药明康德」微信公众号回复“转载”，获取转载须知。分享，点赞，在看，聚焦全球生物医药健康创新

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2025-10-16

·Business Wire

Cycle Pharmaceuticals Launches Its First Oncology Product, PHYRAGO™ (dasatinib) Tablets, in the US

DETROIT--(BUSINESS WIRE)--Cycle Pharmaceuticals announces the launch of PHYRAGO, its first oncology product in the US. PHYRAGO is launched in partnership with Handa Therapeutics, LLC, and will be exclusively available through specialty pharmacy Onco360® with a specialty distribution network from McKesson, Cencora, and Cardinal Health. Cycle Pharmaceuticals launches its first oncology product, PHYRAGO™ (dasatinib) tablets, in the US PHYRAGO is a tyrosine kinase inhibitor indicated for the treatment of adult patients with Philadelphia chromosome-positive chronic myeloid leukemia (Ph+ CML), adult patients with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), and pediatric patients 1 year of age and older with Ph+ CML in chronic phase, and newly diagnosed Ph+ ALL.1 PHYRAGO is bioequivalent to Sprycel® (dasatinib) tablets,2 and has the unique clinical benefit of allowing patients to take proton pump inhibitors (PPIs) and H2 receptor antagonists (H2RAs) concomitantly to help manage gastric acid disorders.1 To help patients with medication access, financial savings, and clinical support, Cycle Vita™ will be available to eligible* patients taking PHYRAGO.† “We are honored to introduce PHYRAGO as a new treatment option for people living with Ph+ leukemia,” said Steve Fuller, Chief Strategy Officer at Cycle Pharmaceuticals. “We understand the daily challenges that come with managing Ph+ CML and Ph+ ALL, and our goal is to ease that burden, not just with an improved formulation of dasatinib, but through the individualized care and hands on support offered by our Cycle Vita program. By enabling more flexibility in co-medication and providing a dedicated support team, we’re committed to helping patients and their families navigate treatment with greater confidence and peace of mind.” Cycle Pharmaceuticals has been empowering patients with rare diseases through its products and support hub since 2017. NITYR ® (nitisinone) Tablets in 2017 SAJAZIR™ (icatibant) Injection in 2021 JAVYGTOR™ (sapropterin dihydrochloride) Tablets for Oral Use and Powder for Oral Solution in 2022 TASCENSO ODT ® (fingolimod) in 2023 ORMALVI™ (dichlorphenamide) tablets in 2024 VENXXIVA™ (tiopronin) Delayed-Release Tablets in 2025 BAFIERTAM ® (monomethyl fumarate) Delayed-Release Capsules in 2025 HARLIKU™ (nitisinone) Tablets in 2025 Indications PHYRAGO™ is a kinase inhibitor indicated for the treatment of: Newly diagnosed adults with Philadelphia chromosome-positive (Ph+) chronic myeloid leukemia (CML) in chronic phase. Adults with chronic, accelerated, or myeloid or lymphoid blast phase Ph+ CML with resistance / intolerance to prior therapy including imatinib. Adults with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph + ALL) with resistance / intolerance to prior therapy. Pediatric patients 1 year of age and older with Ph+ CML in chronic phase. Pediatric patients 1 year of age and older with newly diagnosed Ph+ ALL in combination with chemotherapy. Important Safety Information Warnings and Precautions: Myelosuppression and Bleeding Events: Severe thrombocytopenia, neutropenia and anemia may occur. Use caution if used concomitantly with medication that inhibits platelet function or anticoagulants. Monitor blood counts. Transfuse and interrupt PHYRAGO when indicated. Fluid Retention: Fluid retention, including pleural effusions. Manage with supportive care and/or dose modification. Cardiovascular Toxicity: Monitor for signs or symptoms and treat appropriately. Pulmonary Arterial Hypertension (PAH): PHYRAGO may increase the risk of developing PAH which may be reversible on discontinuation. Consider baseline risk and evaluate patients for signs and symptoms of PAH during treatment. Stop PHYRAGO if PAH is confirmed. QT Prolongation: Use PHYRAGO with caution in patients who have / may develop prolongation of the QT interval. Severe Dermatologic Reactions: Severe mucocutaneous dermatologic reactions have been reported. Tumor Lysis Syndrome: Tumor lysis syndrome has been reported. Maintain hydration and correct uric acid levels prior to initiating treatment. Embryo-Fetal Toxicity: Can cause fetal harm. Advise patients of reproductive potential, of potential risk to fetus and to use effective contraception. Effects on Growth and Development in Pediatric Patients: Epiphyses delayed fusion, osteopenia, growth retardation, and gynecomastia have been reported. Monitor bone growth and development. Hepatotoxicity: Assess liver function before treatment, monthly thereafter or as clinically indicated. Monitor liver function when combined with chemotherapy. Adverse Reactions: Common adverse reactions in adults include myelosuppression, fluid retention events, diarrhea, headache, skin rash, hemorrhage, dyspnea, fatigue, nausea, and musculoskeletal pain. Common adverse reactions in pediatric patients include mucositis, febrile neutropenia, pyrexia, diarrhea, nausea, vomiting, musculoskeletal pain, abdominal pain, cough, headache, rash, fatigue, constipation, arrhythmia, hypertension, edema, infections (bacterial, viral and fungal), hypotension, decreased appetite, hypersensitivity, dyspnea, epistaxis, peripheral neuropathy, and altered state of consciousness. Postmarketing Experience: Post approval adverse reactions: Hepatitis B virus reactivation, atrial fibrillation/atrial flutter, interstitial lung disease, chylothorax, Stevens-Johnson syndrome, nephrotic syndrome, thrombotic microangiopathy, hepatotoxicity. Drug Interactions: Strong CYP3A4 Inhibitors and Strong CYP3A4 Inducers: Dose reduction may be necessary. Antacids: Avoid concomitant use. Use in Specific Populations: Pregnancy: PHYRAGO can cause fetal harm. Advise a pregnant woman of the potential risk to a fetus. Contraception: Should be used during treatment and for 30 days after the last dose. Lactation: Breastfeeding is not recommended during treatment and for 2 weeks after the last dose. Pediatric Use: There is no data in children under 1 year of age. Adverse reactions associated with bone growth and development were reported and should be monitored closely. Refer to the full USPI for pediatric patients with difficulty swallowing tablets. Geriatric Use: Patients over 65 and older may experience: fatigue, pleural effusion, diarrhea, dyspnea, cough, lower gastrointestinal hemorrhage, appetite disturbance, abdominal distention, dizziness, pericardial effusion, congestive heart failure, hypertension, pulmonary Cinzia, and weight decrease. Monitor closely. For more detailed information, please refer to the full Prescribing Information at phyrago.com/PI/. To report SUSPECTED ADVERSE REACTIONS, contact Cycle Pharmaceuticals at 1-844-784-1807, or the FDA at: 1-800-FDA-1088 or www.fda.gov/medwatch. US-DAS-2500114 (October 2025) References PHYRAGO™ (dasatinib). Prescribing Information. Handa Therapeutics, LLC. Study NC9013-002. Center for Drug Evaluation and Research – Clinical Pharmacology Review(s). 2022. [online]. Available at: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2024/216099Orig1s000ClinPharmR.pdf . [Accessed May 21 2025]. *Some areas of support may not be accessible to all patients. Eligibility criteria may apply to ensure compliance with all applicable federal and state requirements, and benefits may be limited to commercially insured patients only. For more detailed information about eligibility, terms and conditions, please contact the Cycle Vita team at 888-360-8482. †Patients who do not wish to have Cycle Vita hub support may be eligible for Co-Pay. -ENDS- ©2025 Cycle Pharmaceuticals Limited. All rights reserved. PHYRAGO™ is a trademark of Handa Therapeutics, LLC. Sprycel® is a registered trademark of Bristol-Myers Squibb Company. NITYR® and TASCENSO ODT® are registered trademarks of Cycle Pharmaceuticals Ltd. in the United States. Cycle Vita™, SAJAZIR™, JAVYGTOR™, and HARLIKU™ are trademarks of Cycle Pharmaceuticals Ltd. in the United States. ORMALVI™ and VENXXIVA™ are trademarks of Torrent Pharma Inc. in the United States. BAFIERTAM® is a registered trademark of Banner Life Sciences, LLC, a company of Cycle Pharmaceuticals. About Cycle Pharmaceuticals Cycle Pharmaceuticals was founded in 2012 with the sole aim of delivering drug treatments and product support to the underserved rare disease community. Cycle Pharma focuses on rare genetic conditions in metabolic, immunology, urology, and oncology. In neurology, we focus on multiple sclerosis. Cycle Pharma is headquartered in Cambridge, UK and has offices in Detroit, Michigan and Boston, Massachusetts. For more information, please visit www.cyclepharma.com and follow us on X, LinkedIn and Facebook. About Handa Pharmaceuticals, Inc. Handa is a specialty pharmaceutical company that focuses on developing high-quality medications that address significant unmet medical needs in oncology and neurology. Handa’s leadership has a proven track record of building effective teams, high quality product portfolios and successful pharmaceutical businesses. For more information, please visit www.handapharma.com. About Onco360 Oncology Pharmacy Onco360 is the nation’s largest independent Oncology Pharmacy and clinical support services company. Onco360 was founded in 2003 to bring together the stakeholders involved in the cancer treatment process and serve the specialized needs of oncologists, patients, hospitals, cancer centers of excellence, manufacturers, health plans, and payers. It dispenses nationally through its network of URAC-, and ACHC-accredited Oncology Pharmacies. Onco360 is headquartered in Louisville, Kentucky, and is a flagship specialty pharmacy brand of PharMerica Corporation, a leading institutional pharmacy, specialty infusion, and hospital services company servicing healthcare facilities in the United States. For more information about Onco360, please visit Onco360.com.

上市批准

2025-10-13

·米内网

【重磅】东阳光药发威，夺$30亿明星药国内首仿

精彩内容近日，东阳光药的盐酸芬戈莫德胶囊成功获批，为国内首仿。芬戈莫德是全球首个治疗多发性硬化症（MS）的口服药物，其全球销售额曾在2016-2020年均超过30亿美元。东阳光药是芬戈莫德首家申报仿制上市并获批的国内药企，同时该产品也是公司首款口服免疫抑制剂。图1：东阳光药最新获批的产品来源：国家药监局官网图2：2016-2020年芬戈莫德的全球销售情况来源：米内网跨国上市公司数据库芬戈莫德是全球首个治疗多发性硬化症（MS）的口服药物，由诺华和日本三菱制药共同开发，2010年获美国FDA批准上市，全球销售额在2016-2020年保持在30亿美元以上。图3：申报芬戈莫德上市的企业情况来源：米内网中国申报进度（MED）数据库原研的盐酸芬戈莫德胶囊在2019年获批进入中国市场，随后在2020年进入国家医保谈判目录，现为2024版国家医保常规目录品种，限10岁及以上患者复发型多发性硬化(RMS)的患者。仿制药方面，广东东阳光药业在2020年首家申报仿制上市，并在近期获批国内首仿+首家过评，北京康蒂尼药业的受理号并未获批，印度瑞迪博士实验室的进口5.2类正在审评审批中。米内网数据显示，在免疫抑制剂市场，东阳光药在2008年获批了注射用吗替麦考酚酯，本次获批的盐酸芬戈莫德胶囊是公司第二款免疫抑制剂。表1：东阳光药今年以来获批的新品来源：米内网中国申报进度（MED）数据库今年以来，东阳光药已累计获批了2个化药1类新药、2个高端仿制药。磷酸萘坦司韦胶囊与艾考磷布韦片联用，治疗初治或干扰素经治的基因1、2、3、6型成人慢性丙型肝炎病毒（HCV）感染，可合并或不合并代偿性肝硬化。舒更葡糖钠注射液是公司首款其它所有治疗用药品，盐酸芬戈莫德胶囊是公司首款口服免疫抑制剂。资料来源：国家药监局官网、米内网数据库免责声明：本文仅作医药信息传播分享，并不构成投资或决策建议。本文为原创稿件，转载文章或引用数据请注明来源和作者，否则将追究侵权责任。投稿及报料请发邮件到872470254@qq.com稿件要求详询米内微信首页菜单栏商务及内容合作可联系QQ：412539092 【分享、点赞、在看】点一点不失联哦

上市批准专利侵权

100 项与盐酸芬戈莫德相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D04187	盐酸芬戈莫德	L04AA27	DB08868

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
复发-缓解型多发性硬化	欧盟	Novartis Europharm Ltd.	2011-03-17
复发-缓解型多发性硬化	冰岛	Novartis Europharm Ltd.	2011-03-17
复发-缓解型多发性硬化	列支敦士登	Novartis Europharm Ltd.	2011-03-17
复发-缓解型多发性硬化	挪威	Novartis Europharm Ltd.	2011-03-17
多发性硬化症	澳大利亚	Novartis AG	2011-02-01
复发性多发性硬化	美国	Novartis Pharmaceuticals Corp.	2010-09-21

未上市

10 条进展最快的记录,

后查看更多信息

适应症	最高研发状态	国家/地区	公司	日期
多灶性获得性脱髓鞘性感觉和运动神经病	临床3期	美国	Mitsubishi Tanabe Pharma Corp.	2012-12-22
多灶性获得性脱髓鞘性感觉和运动神经病	临床3期	美国	Novartis Pharmaceuticals Corp.	2012-12-22
多灶性获得性脱髓鞘性感觉和运动神经病	临床3期	日本	Mitsubishi Tanabe Pharma Corp.	2012-12-22
多灶性获得性脱髓鞘性感觉和运动神经病	临床3期	日本	Novartis Pharmaceuticals Corp.	2012-12-22
多灶性获得性脱髓鞘性感觉和运动神经病	临床3期	澳大利亚	Mitsubishi Tanabe Pharma Corp.	2012-12-22
多灶性获得性脱髓鞘性感觉和运动神经病	临床3期	澳大利亚	Novartis Pharmaceuticals Corp.	2012-12-22
多灶性获得性脱髓鞘性感觉和运动神经病	临床3期	比利时	Mitsubishi Tanabe Pharma Corp.	2012-12-22
多灶性获得性脱髓鞘性感觉和运动神经病	临床3期	比利时	Novartis Pharmaceuticals Corp.	2012-12-22
多灶性获得性脱髓鞘性感觉和运动神经病	临床3期	加拿大	Novartis Pharmaceuticals Corp.	2012-12-22
多灶性获得性脱髓鞘性感觉和运动神经病	临床3期	加拿大	Mitsubishi Tanabe Pharma Corp.	2012-12-22

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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


NCT04088630 (FITCH, CTgov)	早期临床1期	脑出血 \| 脑水肿 \| 出血性卒中	28	Fingolimod (Fingolimod)	夢顧鹽選顧獵繭齋鬱鏇 = 淵積蓋繭壓衊範遞遞構選獵鑰淵醖願鹹廠選衊 (齋製顧壓齋鏇醖獵壓夢, 艱齋構願膚網餘蓋夢築 ~ 築製蓋糧窪蓋獵壓鏇衊) 更多	-	2025-01-14
				Fingolimod (Open-label Fingolimod)	夢顧鹽選顧獵繭齋鬱鏇 = 選憲衊夢醖積淵築糧鏇選獵鑰淵醖願鹹廠選衊 (齋製顧壓齋鏇醖獵壓夢, 簾壓艱顧蓋願製淵範繭 ~ 網積齋觸齋範襯壓艱鏇) 更多
EAN2024	N/A	lymphopenia \| hypertransaminasemia	50	Fingolimod	鏇製觸遞鏇衊築艱淵獵(鬱壓簾繭範糧淵簾選廠) = 夢獵襯糧願簾壓築膚鬱積衊簾遞鹽膚顧願窪夢 (糧餘窪鬱艱獵衊繭繭製 ) 更多	积极	2024-06-28
				Ozanimod	鬱蓋構壓鹹鏇醖觸淵窪(糧鏇選獵夢鏇選簾遞獵) = 鹽範網繭艱襯艱衊壓糧衊廠窪簾糧襯鹹夢夢簾 (艱構網獵簾顧蓋憲壓醖 ) 更多
S31.010 (AAN2024)	N/A	多发性硬化症	930	Fingolimod	顧淵膚選壓網範醖積廠(齋淵鹽鏇構鏇夢鹽餘襯) = 憲憲憲選鏇製糧觸鹽淵製築願齋醖簾窪淵繭醖 (製積構鑰獵製憲淵襯願 )	不佳	2024-04-09
				Natalizumab	顧淵膚選壓網範醖積廠(齋淵鹽鏇構鏇夢鹽餘襯) = 膚築壓繭遞蓋糧遞遞蓋製築願齋醖簾窪淵繭醖 (製積構鑰獵製憲淵襯願 )
ACTRIMS2024	N/A	药物不良反应	350	Fingolimod	遞淵簾選繭繭壓觸壓糧(醖簾觸壓壓願窪襯網鏇) = A 39-year-old woman with RRMS since 2003 presented changes in a nevus on her right foot sole in July 2018. It was excised in November 2018, with a report indicating melanocytic proliferation with atypia. Fingolimod was discontinued, and an autologous bone marrow transplant was performed in 2019. She is currently free of disease activity and skin lesions. A 32-year-old man with RRMS since 2010 reported heartburn and regurgitation in November 2018. Laboratory tests showed aspartate aminotransferase at 19, alanine aminotransferase at 42, and gamma-glutamyl transferase at 97, with no other abnormalities. An endoscopy and biopsy revealed a 2.8 cm subepithelial lesion in the cardia, consistent with leiomyoma. He is currently asymptomatic and continues fingolimod therapy. A 35-year-old woman with Diabetes Mellitus and RRMS since 2015, treated with fingolimod since 2018, developed a skin lesion in 2022. Histopathological examination confirmed cutaneous tuberculosis. Antimicrobial management was initiated without discontinuing fingolimod. The skin lesion has resolved, and there is no RRMS activity. A 38-year-old woman with RRMS since 2016, treated with fingolimod since 2018, developed an axillary lymph node in 2022, which was diagnosed as breast cancer. She is currently undergoing chemotherapy for oncology, with no RRMS activity. 餘蓋膚範糧範製鹽膚鑰 (遞遞膚鏇願壓構壓選齋 )	积极	2024-02-29
NCT00731692 (INFORMS, Pubmed \| Eur J Neurol)	临床3期	多发性硬化症	324	Fingolimod	艱鹹鬱齋齋餘艱網醖襯(鏇簾網範築醖選鹽鹽鏇) = 襯繭鏇遞壓蓋衊願艱鑰膚窪選淵鹽鏇鏇廠簾製 (壓網顧鑰鹹糧獵鏇襯鬱 )	积极	2024-01-01
				Placebo	艱鹹鬱齋齋餘艱網醖襯(鏇簾網範築醖選鹽鹽鏇) = 廠鏇餘積獵範築膚網顧膚窪選淵鹽鏇鏇廠簾製 (壓網顧鑰鹹糧獵鏇襯鬱 )
NCT00355134 (FREEDOMS II, Pubmed)	临床3期	慢性进行性多发性硬化 retinal nerve fiber layer thickness	885	Fingolimod 0.5 mg	願構築願選蓋艱鑰窪選(壓繭繭積蓋壓醖顧餘顧) = 齋選衊製廠憲觸鑰遞醖選醖蓋憲選觸齋範壓鑰 (醖窪蓋廠膚觸蓋壓構顧 )	-	2023-02-01
				Fingolimod 1.25 mg	願構築願選蓋艱鑰窪選(壓繭繭積蓋壓醖顧餘顧) = 襯襯淵餘積築餘蓋獵淵選醖蓋憲選觸齋範壓鑰 (醖窪蓋廠膚觸蓋壓構顧 )
ECTRIMS2022	N/A	-	3,840	fingolimod (Patients with FTY rebound)	壓淵艱積繭鬱獵繭糧構(膚遞簾糧顧蓋願蓋壓顧) = 鑰衊簾簾顧醖糧壓鑰鏇廠觸繭繭積襯鏇膚襯襯 (蓋鬱範簾遞餘積淵糧憲 )	-	2022-10-12
ECTRIMS2022	N/A	新型冠状病毒感染	-	Fingolimod	簾簾艱鏇淵糧鬱鏇構齋(構築鏇廠獵選範顧憲醖) = 淵遞窪齋餘廠膚鏇餘衊願願簾製繭鬱淵壓網觸 (願遞繭製簾築鬱願範繭 ) 更多	-	2022-10-12
				Siponimod	簾簾艱鏇淵糧鬱鏇構齋(構築鏇廠獵選範顧憲醖) = 繭憲淵膚襯衊鑰廠構醖願願簾製繭鬱淵壓網觸 (願遞繭製簾築鬱願範繭 ) 更多
NCT01665144 \| NCT00731692 (Pubmed \| Neurology)	临床3期	慢性进行性多发性硬化 plasma neurofilament light	-	Siponimod	構廠廠遞廠廠網淵蓋顧(艱構窪蓋顧鏇艱選憲夢) = 齋鏇鹽醖選淵夢製醖積衊夢網憲構築鹽鏇窪鹽 (鏇顧鏇繭醖襯窪製鹹襯 ) 更多	积极	2022-05-24
				Fingolimod	-
CLARION (ECTRIMS2021)	临床3期	多发性硬化症	762	Cladribine tablets 10 mg	獵簾簾鬱願築窪範廠醖(衊夢窪窪繭遞衊顧選鑰) = 鏇窪衊淵夢醖製願鹹獵鏇網鑰醖築鬱顧製醖憲 (鑰選壓夢蓋鹹夢鹹蓋繭, 1.3 ~ 21.1) 更多	积极	2021-10-12
				Fingolimod	獵簾簾鬱願築窪範廠醖(衊夢窪窪繭遞衊顧選鑰) = 選繭鹽築遞繭蓋鏇餘齋鏇網鑰醖築鬱顧製醖憲 (鑰選壓夢蓋鹹夢鹹蓋繭, 1.3 ~ 21.4) 更多