桦木三萜(Birch triterpenes) - 在研适应症：营养不良性大疱性表皮松解，交界型大疱性表皮松解，大疱性表皮松解_专利_临床

概要

基本信息

药物类型

小分子化药

别名

Birch bark extract、Oleogel-S10、AP-101

+ [3]

靶点-

作用方式-

作用机制-

治疗领域

免疫系统疾病遗传病与畸形皮肤和肌肉骨骼疾病+ [1]

在研适应症

营养不良性大疱性表皮松解交界型大疱性表皮松解大疱性表皮松解

非在研适应症

遗传性黄斑型大疱性营养不良创伤和损伤

原研机构

Amryt Pharma Holdings Ltd.

在研机构

CHIESI Farmaceutici SpA

Chiesi Ltd.Amryt Pharmaceuticals DAC

+ [1]

非在研机构

Amryt Research Ltd.

权益机构

Kwangdong Pharmaceutical Co., Ltd.Amryt Pharmaceuticals DAC

CHIESI Farmaceutici SpA

最高研发阶段批准上市

首次获批日期

欧盟 (2016-01-14),

创伤和损伤

最高研发阶段(中国)-

特殊审评孤儿药 (美国)、孤儿药 (欧盟)、优先审评 (美国)

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关联

11

项与桦木三萜相关的临床试验

NCT06917690

/ Recruiting临床3期

Multi-centeR, Open-label Study to EValuate the Safety, Efficacy, and Pharmacokinetics of FIlsuVEz (Oleogel-S10) in Japanese Subjects With Epidermolysis Bullosa (REVIVE)

The goal of this clinical trial is to learn if Oleogel-S10 gel works to treat skin wounds from two types of inherited epidermolysis bullosa (EB): junctional EB (JEB) or dystrophic EB (DEB) in the Japanese population. Children and adults may participate. The trial also looks at the safety of Oleogel-S10 gel. The main questions it will answer are:
* Does Oleogel-S10 gel close wounds from JEB or DEB within 45 days or reduce the size of the wounds?
* Are there any medical problems when using Oleogel-S10 gel?
* How much of the drug ends up in your blood?
The study has 2 parts. In Part 1, participants will:
* Apply Oleogel-S10 gel to the EB wound dressings at least once every 4 days for 45 days.
* Visit the clinic once every 2 weeks for checkups and tests. If participants complete Part 1, they may participate in Part 2 if they choose to. In Part 2, participants will continue to receive Oleogel-S10 gel until the product is available to buy in Japan or until the trial is stopped by the company.

开始日期2025-04-18

申办/合作机构

CHIESI Farmaceutici SpA

NCT06423573

/ RecruitingN/A

A Long-term Non-interventional Study to Assess the Incidence of Skin Malignancies in Patients With Dystrophic and Junctional Epidermolysis Bullosa Receiving Treatment With Filsuvez

In patients with epidermolysis bullosa (EB), collagen does not form properly, so their skin is very fragile and blisters easily. Such patients are also at greatly increased risk of developing skin cancers. Filsuvez is a topical gel used to promote healing of skin lesions in patients with certain types of EB. In this observational study, patients with either dystrophic EB (DEB) or junctional EB (JEB) will receive standard of care treatment, whether Filsuvez or something else, and will be followed for up to 5 years. The main purpose is to see if the use of Filsuvez affects the likelihood of developing skin malignancies in these patient populations.

开始日期2024-12-18

申办/合作机构

Amryt Pharma Holdings Ltd.

[+1]

NCT05190770

/ Completed临床2期IIT

A Randomized Phase II Double-Blinded Study of The Efficacy of Oleogel-S10 (AP101) Gel for the Treatment of Grade 2/3 Radiation Dermatitis in Breast Cancer Patients

The purpose of this study is find out whether Oleogel-S10 is an effective treatment for radiation dermatitis when it is used in combination with a standard wound treatment cream called triamcinolone. Oleogel-S10 has shortened the healing time for other types of skin wounds such as burns. Triamcinolone is a cream that is frequently used to treat moderate to severe skin conditions such as skin irritation caused by poison ivy, eczema, sunburn, and rashes.

开始日期2021-12-15

申办/合作机构

Memorial Sloan Kettering Cancer Center

100 项与桦木三萜相关的临床结果

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100 项与桦木三萜相关的转化医学

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100 项与桦木三萜相关的专利（医药）

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24

项与桦木三萜相关的文献（医药）

2026-01-06·BRITISH JOURNAL OF DERMATOLOGY

Methodological concerns in the EASE study of Oleogel-S10 for epidermolysis bullosa: reply from authors

Article

作者: Torres-Pradilla, Mauricio ; Fernández, Mariá Florencia ; Maher, Laura ; Bruckner, Anna L ; Kiritsi, Dimitra ; Sprecher, Eli ; Kern, Johannes S ; Murrell, Dédée F ; Bodemer, Christine ; Cunningham, Tracy ; Davis, Charles

Authors’ response to ‘Methodological concerns in the EASE study of Oleogel-S10 for epidermolysis bullosa’ by Cao et al.

2026-01-06·BRITISH JOURNAL OF DERMATOLOGY

Methodological concerns in the EASE study of Oleogel-S10 for epidermolysis bullosa

Article

作者: He, Xiafei ; Cao, Qing ; Yang, Lutao

Response to the article ‘Long-term safety and efficacy of Oleogel-S10 in epidermolysis bullosa: 24-month results from the phase III EASE study’ by Murrell et al.

2025-09-01·JOURNAL OF DERMATOLOGY

Reduction in Dressing Change Burden in Patients With Epidermolysis Bullosa—Impact of Oleogel‐S10

Article

作者: Maher, Laura ; Donovan, Maryanne ; Sprecher, Eli ; Kiritsi, Dimitra ; Kern, Johannes S. ; Lee, Lara Wine ; Murrell, Dédée ; Bruckner, Anna L. ; Löwe, Sandra

ABSTRACT:

Epidermolysis bullosa (EB) is a severe genetic disorder marked by skin fragility and blistering from minimal trauma. Management relies on frequent and painful dressing changes. The EASE study (NCT03068780), the largest to date in EB, previously demonstrated accelerated wound healing and reduced wound burden for Oleogel‐S10 (birch triterpenes) versus control gel. This post hoc analysis focused on dressing change frequency and related time and cost savings among patients with daily dressing changes at baseline (Oleogel‐S10 n = 47, control gel n = 53). By Day 90, 35.6% of Oleogel‐S10 patients required fewer daily changes versus 10.6% in the control group (p = 0.005). Weekly dressing changes reduced by 1.36 ± 0.24 with Oleogel‐S10 compared to 0.41 ± 0.23 for control (difference −0.95 ± 0.33; p = 0.005). This translated to almost three fewer dressing changes every 2 weeks for Oleogel‐S10 versus nearly one change for the control gel. The estimated time saved per week was 10.7 h with Oleogel‐S10 (6.4 h patient, 4.3 h caregiver) versus 4.0 h with control (2.4 h patient, 1.6 h caregiver). Estimated dressing costs reduced by 59%, from $63.4 k to $25.9 k per patient over 27 months. Oleogel‐S10 significantly reduced dressing frequency and time burden, with potential to ease the intensive demands of EB wound care.

80

项与桦木三萜相关的新闻（医药）

2026-01-08

·今日头条

渐冻症的研究进展如何？

肌萎缩侧索硬化（Amyotrophic Lateral Sclerosis, ALS），又称渐冻症或运动神经元病（MND），是一种致命的进行性神经退行性疾病，主要累及上、下运动神经元，导致肌肉无力、萎缩、瘫痪，最终呼吸衰竭。全球发病率约1/3万，年新发病例2–3/10万，平均生存期仅3–5年。约90%为散发性，10%为家族性。几乎所有ALS病例（约97%）的病理金标准是TDP-43蛋白的细胞质异常聚集与核内清除。 Fig 1. 不同国家肌萎缩侧索硬化症（ALS）平均发病年龄 ALS研究的关键靶点过去十余年，遗传学与病理学研究已明确多个核心致病基因与蛋白。其中， TDP-43蛋白病被公认为几乎所有ALS病例的共同病理特征，而C9ORF72、SOD1、FUS则是最常见的遗传驱动因素。以下表格系统总结了当前公认的四大核心靶点（TDP-43、C9ORF72、SOD1、FUS）的正常功能、在ALS中的病理作用以及主流研究应用，帮助科研人员快速定位关键节点。靶点正常生物学功能在ALS中的病理作用主要研究应用 TDP-43 (TARDBP) RNA结合蛋白，参与剪接、运输、稳定性调控核内丢失+胞质异常聚集（97%病例），导致隐蔽外显子错误剪接与RNA稳态紊乱包涵体IHC、隐蔽外显子检测、STMN2拯救实验 C9ORF72 调控自噬、内吞、免疫反应 G4C2六核苷酸重复扩张→RNA毒性焦点、二肽重复蛋白（DPR）毒性、单倍不足 DPR ELISA、RNA foci FISH、ASO疗效评估 SOD1 Cu/Zn超氧化物歧化酶，清除自由基突变→错误折叠聚集、氧化应激、线粒体损伤错误折叠SOD1 ELISA、氧化应激模型、ASO敲低 FUS RNA/DNA结合蛋白，参与剪接与运输突变→核质运输缺陷、胞质聚集、应激颗粒异常 FUS定位ICC、RNA结合实验、ASO筛选 TDP-43 蛋白病（TDP-43 proteinopathy）机制深度解读（2025最新共识） TDP-43（TAR DNA-binding protein 43）是一种主要定位于细胞核的RNA/DNA结合蛋白，正常情况下参与前体mRNA剪接、mRNA运输与稳定性调控、应激颗粒形成及miRNA生物合成等几乎所有RNA代谢环节。在≈97%的ALS（包括几乎全部散发性病例）和≈50%的额颞叶痴呆（FTD）患者中，均观察到TDP-43的标志性病理：核内功能性TDP-43显著清除 + 胞质异常磷酸化、泛素化、截短（主要为C端25/35 kDa片段）聚集形成包涵体。核心致病机制（Loss-of-function + Gain-of-toxicity 双重打击）：核功能丢失（LOF）：TDP-43从核内清除导致其对隐蔽外显子（cryptic exons）的抑制失效，引发数百个基因错误剪接。最具代表性的包括 STMN2 （导致微管动态失调、轴突再生障碍）和 UNC13A （导致突触囊泡释放缺陷）。2024-2025年研究进一步确认，STMN2对TDP-43耗竭更敏感，是早期生物标志物首选。毒性功能获得（GOF）：胞质异常聚集的磷酸化/截短TDP-43招募正常TDP-43及其他RNA结合蛋白，形成病理性应激颗粒，干扰蛋白质稳态、自噬-溶酶体途径，并促进蛋白病“播种式”扩散。最新研究亮点（2025）：长读长RNA-seq揭示更多TDP-43依赖隐蔽外显子（如MNAT1、KCNQ2等）；抑制无义介导的mRNA降解（NMD）可暴露更多隐蔽事件；STMN2/UNC13A恢复性ASO在iPSC-运动神经元及人源化小鼠模型中显著改善轴突生长与突触功能。综上，TDP-43蛋白病是ALS最核心的“共同终末通路”，靶向其核功能恢复、隐蔽外显子阻断或聚集清除已成为最有前景的疾病修饰策略。治疗学启示：靶向TDP-43蛋白病、C9ORF72重复扩张、SOD1敲低、自噬激活、线粒体保护等仍是当前最有希望的疾病修饰策略。 Fig 2. ALS发病机制整合通路 (doi.org/10.3390/ijms26115240) 最新研究ALS领域关键临床与基础研究进展主题关键发现/试验结果发表/更新时间潜在影响引用 Tofersen（SOD1-ASO，QALSODY）长期随访及真实世界数据显示：早期启动治疗可显著降低 SOD1 与 NfL 水平，并减缓功能下降趋势。 NEJM 2022；后续 EClinicalMedicine 2024、Neurology 2025 随访与真实世界研究。目前唯一获批的基因特异性疾病修饰疗法之一，仅适用于 SOD1 突变 ALS（≈2% 患者）。 [1] C9orf72 靶向治疗 BIIB078 在 Ⅰ期试验中虽能降低部分病理标志，但未带来临床获益，被终止开发；2025 年双靶向 CRISPR-CasRx 在 iPSC 神经元和小鼠模型中显著降低致病重复转录本和二肽重复蛋白（DPR），改善细胞和行为表型，仍处于临床前阶段。 BIIB078：公司 2021 公告；CasRx：Nat Commun 2025。传统 ASO 路线受挫，但 CasRx 等 RNA 靶向基因编辑为 C9orf72-ALS 提供了新的治疗路径（临床前）。 [2] Engensis（VM202，HGF 质粒） Phase 2a 小样本试验以安全性为主要终点，结果显示 HGF 质粒基因治疗在 ALS 患者中安全、耐受性良好；疗效指标仅作探索性分析，尚无法得出明确结论。顶线结果 2022 公布；2024–2025 年综述仍将其视为早期临床阶段项目。提供了基于 HGF 的基因治疗可行性安全信号，后续是否开展更大规模、以疗效为主要终点的试验仍待观察。 [3] AMX0035（Relyvrio / PB-TURSO） 2024 年 PHOENIX Ⅲ期试验未达到主要及关键次要终点，公司随后宣布在美国和加拿大主动撤回上市许可，并为既有患者提供免费用药项目。 Amylyx 官方 2024.4 公告及后续监管更新。再次提示以小分子细胞保护为主的联合方案在 ALS 中面临巨大挑战，也凸显了精准分型和更敏感终点评价的重要性。 [4] 当前研发难点： ALS高度异质性导致单一靶点疗法覆盖率低；血脑屏障穿透困难；神经炎症与蛋白病扩散机制尚未完全阐明；缺乏可靠的早期生物标志物用于诊断与疗效评估；临床试验终点敏感性不足，多次导致III期失败。单一机制药物很难带来显著、可重复的临床获益，这也凸显了从多通路、多靶点角度系统研究 ALS 病理网络的重要性。 Fig 3. 2024–2025 ALS主要候选药物研发进程总览 abinScience ALS研究重组蛋白与抗体工具 Type 目录号产品名称重组蛋白 HP195012 Recombinant Human CHCHD10 Protein, N-GST & C-His 重组蛋白 HW826012 Recombinant Human FUS Protein, N-His 重组蛋白 HW826022 Recombinant Human FUS Protein, N-His-SUMO 重组蛋白 HV287012 Recombinant Human HDAC6 Protein, N-His 重组蛋白 HW326012 Recombinant Human MATR3 Protein, N-His-SUMO 重组蛋白 HP702012 Recombinant Human NEK1 Protein, N-GST & C-His 重组蛋白 HP451012 Recombinant Human OPTN Protein, N-GST & C-His 重组蛋白 HY555012 Recombinant Human PFN1 Protein, N-His 重组蛋白 HC317012 Recombinant Human RIPK1 Protein, N-His 重组蛋白 HF876012 Recombinant Human SOD1 Protein, N-His 重组蛋白 HC648012 Recombinant Human SQSTM1 Protein, N-His 重组蛋白 HB883022 Recombinant Human TIA1 Protein, N-GST & C-His 重组蛋白 HX018012 Recombinant Human TUBA4A Protein, N-His 重组蛋白 HX922012 Recombinant Human VCP Protein, N-His 抗体 HA376013 Anti-Human C9orf72 Antibody (SAA1886) 抗体 HW826014 Anti-FUS Polyclonal Antibody 抗体 HV287014 Anti-HDAC6 Polyclonal Antibody 抗体 HW326014 Anti-Human MATR3 Polyclonal Antibody 抗体 HP451014 Anti-Human OPTN Polyclonal Antibody 抗体 HF876013 Anti-Human SOD1 Nanobody (SAA1203) 抗体 HF876014 Anti-SOD1 Polyclonal Antibody 抗体 HC648014 Anti-SQSTM1/p62 Polyclonal Antibody 抗体 HX018014 Anti-Human TUBA4A Polyclonal Antibody 抗体 HX922014 Anti-VCP Polyclonal Antibody 抗体 HF876010 InVivoMAb Anti-Human SOD1 Antibody (AP-101) abinScience —— 以高纯度、高活性重组蛋白与超高特异性抗体（含纳米抗体） abinScience 持续赋能 ALS 机制研究、药物筛选与生物标志物开发，帮助科研人员更快靠近“渐冻”真相，并在帕金森病、阿尔茨海默病、亨廷顿病、多发性硬化等神经退行性疾病领域搭建关键靶点重组蛋白与抗体矩阵。 References Lu L, Deng Y, Xu R. Current potential therapeutics of amyotrophic lateral sclerosis. Front Neurol . 2024;15:1402962. Li X, Hu J, Zhang Y, et al. Evaluating emerging drugs in phase II and III for the treatment of amyotrophic lateral sclerosis. Expert Opin Emerg Drugs . 2024;29(1):27–42. Wiesenfarth M, Meyer T, Wolf J, et al. Effects of tofersen treatment in patients with SOD1-ALS in a real-world setting: A 12-month multicentre cohort study. EClinicalMedicine . 2024;69:102495. Van Daele SH, Timmers M, Moisse M, et al. The sense of antisense therapies in ALS. Neuropharmacology . 2024;238:109711. Kempthorne L, Kumar KR, Cao MD, et al. Dual-targeting CRISPR-CasRx reduces C9orf72 ALS/FTD sense and antisense repeat RNAs in vitro and in vivo. Nat Commun . 2025;16:459. Meyer T, Brule J, Dreyhaupt J, et al. Clinical and patient-reported outcomes and neurofilament dynamics in amyotrophic lateral sclerosis. Muscle Nerve . 2024;69(4):562–574. Li Z, Su X, Tang J, et al. Supplemental interventions for amyotrophic lateral sclerosis: A systematic review and network meta-analysis. Sci Rep . 2024;14:62213. Rofail D, Reger MA, Panitch H, et al. The evolving landscape of neurology and amyotrophic lateral sclerosis care: Insights from targeted literature reviews. Neurol Ther . 2025.

临床研究信使RNA

2026-01-07

·PRNewswire

AL-S Pharma to present at the upcoming J. P. Morgan 2026 Annual Healthcare Conference on Thursday, January 15

ZURICH, Jan. 7, 2026 /PRNewswire/ -- AL-S Pharma AG, a Swiss-based, single-asset clinical-stage biopharmaceutical company founded and co-owned by Neurimmune and TVM Capital Life Science, is developing AP-101 for Amyotrophic Lateral Sclerosis (ALS). The company today announced that Dr. Michael Salzmann, Chief Executive Officer, and Prof. Angela Genge, MD, Chief Medical Officer, will present at the 44th Annual J.P. Morgan 2026 Healthcare Conference on Thursday, January 15, 2026, at 8:30 a.m. PT. AL-S Pharma will present its recently announced positive results from the global Phase 2 study of AP-101 in 73 participants for the treatment of ALS, along with key data updates, including subgroup analyses, supporting plans for a confirmatory Phase 3 study. About AP-101 AP-101 is an investigational human-derived antibody directed against misfolded superoxide dismutase 1 (SOD1) designed to inhibit the spread of SOD1 pathology in the CNS of ALS patients. AP-101 received orphan drug designations from FDA, EMA and Swissmedic. The Phase 2 study evaluated safety, tolerability, pharmacodynamic (PD) markers, and pharmacokinetics (PK) of AP-101 in patients with sporadic ALS and in patients with mutations in the SOD1 gene. About AL-S Pharma AG AL-S Pharma is a Swiss-based single-asset company founded and co-owned by Neurimmune and TVM Capital Life Science to develop AP-101. The company is fully financed by TVM Life Science Innovation I and Neurimmune. AL-S Pharma brings together a seasoned team of biotech and pharmaceutical leaders with expertise spanning drug discovery, translational research, and clinical development. Based on the successful Phase 2 data, AL-S Pharma is currently advancing AP-101 into late-stage development. Follow AL-S Pharma on LinkedIn . Contact for Media John Capodanno (US) [email protected] +1 917 750-8649 Contact for AL-S Pharma Dr. Michael Salzmann [email protected] SOURCE AL-S Pharma AG 21% more press release views with Request a Demo

临床2期孤儿药临床结果

2025-12-29

·als.net

A story from the lab—and why it matters.

Your support is helping move important science forward. Give today to sustain our critical research. Dear ALS Community, Earlier this month, at the International Symposium on ALS/MND, I watched a presentation from AL-S Pharma announcing that AP-101—a therapeutic antibody targeting misfolded SOD1—had succeeded in Phase 2b and is now advancing toward Phase 3 clinical trials. Our team at ALS TDI helped make that molecule what it is. Years ago, we partnered with a European biotech called Neurimmune and executed key parts of the preclinical characterization work that supported research-to-development transition for AP-101 to initiate human trials. It was painstaking, unglamorous science - the kind that rarely makes it into newsletters. SOD1 mutations cause some of the most aggressive forms of familial ALS. They ravaged my late best friend, Sean Scott, and generations of his family. When our scientists were running those experiments, we had Sean’s family and families like his at top of mind. We held hope that the approach could benefit people with sporadic ALS, as well. AL-S Pharma maintains that hope and intends to advance AP101 into human trials in both SOD1 familial ALS and in sporadic ALS. We don’t know if AP-101 will succeed in its Phase 3 development just like we couldn't know when we began collaborating with Neurimmune whether this program would ever advance this far. We only knew it was worth trying. Here's what I want you to understand: if you gave to ALS TDI between 2013 and 2018, you helped fund this work. Not because we asked you to support a specific antibody program - we rarely mentioned it - but because your generosity gave us the flexibility to pursue promising science wherever it led. That is the power of the support you provide. Progress in research is nonlinear. We cannot predict which programs will break through or when. But we can build a pipeline worth believing in, and right now, ours includes another lead program called TDI-1831 that may help people with rare ALS-causing mutations, and a versatile platform for delivering precision mRNA therapeutics directly to the brain and spinal cord. I don't know which of these will advance to Phase 3 clinical development or beyond. But I know the work is worth trying. And I know it's only possible because of you. If you're able to make a gift this year, it will go directly toward the science that could one day reach someone's best friend, someone's parent, someone's child. Make a year-end gift With deep gratitude, Fernando Vieira, M.D. CEO & Chief Scientific Officer ALS Therapy Development Institute

临床2期

100 项与桦木三萜相关的药物交易

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适应症	国家/地区	公司	日期
营养不良性大疱性表皮松解	欧盟	CHIESI Farmaceutici SpA	2022-06-21
营养不良性大疱性表皮松解	冰岛	CHIESI Farmaceutici SpA	2022-06-21
营养不良性大疱性表皮松解	列支敦士登	CHIESI Farmaceutici SpA	2022-06-21
营养不良性大疱性表皮松解	挪威	CHIESI Farmaceutici SpA	2022-06-21
交界型大疱性表皮松解	欧盟	CHIESI Farmaceutici SpA	2022-06-21
交界型大疱性表皮松解	冰岛	CHIESI Farmaceutici SpA	2022-06-21
交界型大疱性表皮松解	列支敦士登	CHIESI Farmaceutici SpA	2022-06-21
交界型大疱性表皮松解	挪威	CHIESI Farmaceutici SpA	2022-06-21
创伤和损伤	欧盟	Amryt AG	2016-01-14
创伤和损伤	冰岛	Amryt AG	2016-01-14
创伤和损伤	列支敦士登	Amryt AG	2016-01-14
创伤和损伤	挪威	Amryt AG	2016-01-14

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适应症	最高研发状态	国家/地区	公司	日期
大疱性表皮松解	申请上市	美国	Amryt AG	2022-02-28
遗传性黄斑型大疱性营养不良	临床3期	美国	Amryt Research Ltd.	2017-03-29
遗传性黄斑型大疱性营养不良	临床3期	阿根廷	Amryt Research Ltd.	2017-03-29
遗传性黄斑型大疱性营养不良	临床3期	澳大利亚	Amryt Research Ltd.	2017-03-29
遗传性黄斑型大疱性营养不良	临床3期	奥地利	Amryt Research Ltd.	2017-03-29
遗传性黄斑型大疱性营养不良	临床3期	巴西	Amryt Research Ltd.	2017-03-29
遗传性黄斑型大疱性营养不良	临床3期	智利	Amryt Research Ltd.	2017-03-29
遗传性黄斑型大疱性营养不良	临床3期	哥伦比亚	Amryt Research Ltd.	2017-03-29
遗传性黄斑型大疱性营养不良	临床3期	捷克	Amryt Research Ltd.	2017-03-29
遗传性黄斑型大疱性营养不良	临床3期	丹麦	Amryt Research Ltd.	2017-03-29

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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


NCT05190770 (CTgov)	临床2期	转移性乳腺癌 \| 放射性皮炎	18	Oleogel-S10+Triamcinolone Acetonide (Triamcinolone + Oleogel-S10)	遞齋繭醖窪夢夢膚鑰鹽(築憲獵醖獵憲製窪範壓) = 範糧壓顧餘淵衊窪蓋糧遞築積鹹壓鬱鹹衊網夢 (衊淵艱膚齋餘壓蓋繭範, 16.8) 更多	-	2025-09-11
				Triamcinolone Acetonide (Triamcinolone + Placebo)	遞齋繭醖窪夢夢膚鑰鹽(築憲獵醖獵憲製窪範壓) = 鏇鏇鏇遞範艱餘蓋淵蓋遞築積鹹壓鬱鹹衊網夢 (衊淵艱膚齋餘壓蓋繭範, 65.2) 更多
NCT03068780 (EASE, FDA) 人工标引	临床3期	营养不良性大疱性表皮松解 \| 交界型大疱性表皮松解	223	FILSUVEZ (DDEB)	窪廠憲夢選餘範廠鏇膚(窪蓋鏇構網膚艱網餘齋) = 夢獵鑰網憲鑰憲顧顧窪鏇窪觸願憲積觸蓋餘夢 (夢簾範餘網選窪構鹹構 )	积极	2023-12-18
				Placebo Gel (DDEB)	窪廠憲夢選餘範廠鏇膚(窪蓋鏇構網膚艱網餘齋) = 艱艱願衊鏇鹹鹽淵遞築鏇窪觸願憲積觸蓋餘夢 (夢簾範餘網選窪構鹹構 )
NCT03068780 (EASE, GlobeNewswire) 人工标引	临床3期	大疱性表皮松解	223	Birch bark extract	範遞網膚製觸簾衊願鑰(選製獵顧壓願遞淵鹹觸) = 襯繭齋餘鏇糧構齋製繭艱壓齋齋夢鹽襯鹽鑰構 (衊鏇膚獵簾醖糧構糧壓 ) 更多	积极	2022-07-07
				Vehicle	範遞網膚製觸簾衊願鑰(選製獵顧壓願遞淵鹹觸) = 窪壓蓋醖醖壓築糧憲廠艱壓齋齋夢鹽襯鹽鑰構 (衊鏇膚獵簾醖糧構糧壓 ) 更多
NCT03068780 (EASE, Pubmed \| Trials)	临床3期	大疱性表皮松解	120	Oleogel-S10	製繭製顧網鏇餘選醖繭(憲廠獵網選觸壓構製襯) = 淵餘顧願廠醖簾蓋淵壓鹹膚衊願簾觸鏇鏇醖鹹 (憲繭鬱窪鏇蓋願鬱積糧 ) 更多	积极	2019-12-01
				Placebo	製繭製顧網鏇餘選醖繭(憲廠獵網選觸壓構製襯) = 製鹽選艱蓋構淵齋積鏇鹹膚衊願簾觸鏇鏇醖鹹 (憲繭鬱窪鏇蓋願鬱積糧 ) 更多
EUCTR2012-003390-26-LV \| EUCTR2012-000777-23-BG \| NCT01657305 (BSH-12, Pubmed \| Burns) 人工标引	临床3期	烧伤	219	standard of care+topical betulin gel	鹽選築窪築觸壓選餘鹽(願顧襯構夢繭夢鑰鑰顧): difference = -2.1 (95% CI, -2.7 ~ -1.5]), P-Value = <0.0001 更多	积极	2017-09-01
				standard of care
NCT01657292 (CTgov)	临床3期	烧伤	61	Octenilin+Oleogel-S10 (Entire Study Population)	鑰餘壓鹽網鏇廠獵艱憲 = 構顧鬱觸積膚壓選淵簾積鑰簾繭構廠襯網觸觸 (醖繭憲鬱顧膚齋選夢餘, 築淵衊願壓鏇觸醖範觸 ~ 觸選鬱憲衊簾積齋衊壓)	-	2015-09-28
				Octenilin+Oleogel-S10 (Entire Study Population - Systemic AEs)	壓繭觸艱積艱壓觸壓壓(鬱壓鏇鹽構選鹹鏇餘窪) = 製觸鏇糧襯鏇簾繭窪淵積夢襯衊膚鏇憲願願襯 (獵鹽憲餘鏇願選鑰齋鏇, 築網壓築積顧餘齋鹽齋 ~ 齋願鏇製築襯構憲糧鏇) 更多
NCT00786994 (CTgov)	临床2期	光化性角化病	165	Oleogel-S10 (A - Oleogel-S10 Once Daily)	膚築製壓憲糧醖鹹夢衊 = 餘襯蓋鑰膚顧夢繭範觸簾鏇築製糧網衊鹽獵網 (鑰醖構膚淵構壓齋齋艱, 製廠選繭遞繭築壓廠簾 ~ 簾憲鑰願簾壓窪觸鏇衊) 更多	-	2015-08-14
				Oleogel-S10 (B - Oleogel-S10 Twice Daily)	膚築製壓憲糧醖鹹夢衊 = 繭衊獵窪鏇膚遞壓餘構簾鏇築製糧網衊鹽獵網 (鑰醖構膚淵構壓齋齋艱, 獵窪醖積鹽網積顧製願 ~ 範範窪淵糧憲鹽廠築獵) 更多