Background:
X-linked hyper-IgM (HIGM) syndrome is caused by a mutation in the CD40 ligand (CD40L) gene. People with this disease have white blood cells that do not work properly. These people are at risk of severe infections and autoimmune diseases. Researchers want to know if these base-edited stem cells and T cells can help people with CD40L-HIGM syndrome.
Objective:
To test base-edited stem cells and base-edited T cells in 1 person with CD40L-HIGM syndrome.
Eligibility:
A single male with CD40L-HIGM syndrome.
Design:
A single participant is planned to receive a single dose of edited stem cells and supportive treatment with edited T cells. Participant stem and T cells will undergo base editing to repair the mutation.
In preparation for the gene therapy, the participant will receive busulfan chemotherapy and alemtuzumab. After treatment, the participant will have follow-up visits every few months in the first 2 years after treatment. Long-term visits will continue annually for 15 years.

开始日期2025-07-16

申办/合作机构

National Institute of Allergy & Infectious Diseases

NCT06986382

/ Not yet recruiting临床1/2期IIT

Phase 1b/2a Trial of Allogeneic Hematopoietic Stem Cell Transplantation (HSCT) From an HLA-partially Matched Related or Unrelated Donor After TCRab+ T-cell/CD19+ B-cell Depletion for Patients With Monogenic and/or Early-onset (EO), Medically Refractory (MR) Crohn Disease (CD)

This research study is investigating whether alpha beta T-cell depleted hematopoietic stem cell transplant (HSCT) can be an immune system replacement for Crohn disease patients and whether this is safe and effective for patients with early onset, medically refractory Crohn disease.

开始日期2025-07-01

申办/合作机构

Stanford University

NCT06851767

/ Enrolling by invitation临床1/2期IIT

Phase 1/2 Base-Edited Hematopoietic Stem/Progenitor Cell X-Linked Severe Combined Immunodeficiency Gene Therapy

Background:
X-linked severe combined immunodeficiency (XSCID) is a rare inherited disorder that affects the immune system. It is caused by a change in the IL2RG gene. Researchers are investigating a new type of gene therapy for people with XSCID. This technique, called base-edited stem cell transplants, involves collecting a person s own stem cells, editing the genes to repair IL2RG gene, and returning the edited cells to the person.
Objective:
To test base-edited stem cell transplants in people with XSCID.
Eligibility:
People aged 3 years and older with XSCID.
Design:
Participants will be screened. They will have a physical exam. They may give blood, urine, and stool samples. They may have tests of their heart and lung function. They may have fluid and cells drawn from their bone marrow.
Participants will undergo apheresis. Blood will be taken from the body through a needle inserted into 1 arm. The blood will pass through a machine that separates out the stem cells. The remaining blood will be returned to the body through a different needle. The collected stem cells will undergo gene editing.
Participants will be admitted to the hospital 1 week before treatment. They will receive a central line: A flexible tube will be inserted into a large vein. This tube will be used to administer drugs and draw blood during their stay. They will receive drugs to prepare their bodies for the treatment.
The base-edited stem cells will be infused through the central line. Participants will remain in the hospital for at least 3 weeks while they recover.
Follow-up visits will continue for 15 years.

开始日期2025-05-09

申办/合作机构

National Institute of Allergy & Infectious Diseases

100 项与帕利夫明相关的临床结果

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100 项与帕利夫明相关的转化医学

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100 项与帕利夫明相关的专利（医药）

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676

项与帕利夫明相关的文献（医药）

2026-01-01·JOURNAL OF ETHNOPHARMACOLOGY

Dictamnine inhibited keratinocyte hyperproliferation and alleviated psoriasis-like dermatitis via blocking HIF1A-mediated ferroptotic pathway

Article

作者: Xu, Xin-Chang ; Wang, Wēi ; Rao, Zhi-Min ; Zhang, Jian ; Liu, Hui ; Cai, Chun-Li ; Yu, Chen-Huan ; Jiang, Song-Lin ; Wang, Wéi ; Wang, Lei

ETHNOPHARMACOLOGICAL RELEVANCE:

Psoriasis is an immune-mediated genetic skin disease, which is characterized by hyperproliferation and aberrant differentiation of epidermal keratinocytes. Recently, there are not any cures for psoriasis because of the limited availability of safe and effective medications. Dictamni Cortex is the root bark of Dictamnus dasycarpus Turcz. And exhibits anti-inflammatory, antibacterial, hepatoprotective and anticancer activities. It is widely used for preventing various bone and skin diseases, including rheumatoid arthritis, psoriasis, eczema and impetigo. However, the active compounds responsible for treating psoriasis in the herb remain unknown.

AIM OF THE STUDY:

To investigate the inhibitory effects of active compounds in the herb against the hyperproliferation of human HaCaT keratinocytes in vitro and imiquimod (IMQ)-induced psoriasis-like dermatitis in mice.

MATERIALS AND METHODS:

The effects of each active compound in the herb against the proliferation, apoptosis, migration, and invasion of HaCaT cells were analyzed by MTT, flow cytometry, and Transwell assays, respectively. The profiles of differentially expressed mRNAs between model group and dictamnine (DIC)-treated group were compared by transcriptome sequencing. The levels of inflammatory cytokines and chemokines in the mediums and skin tissues were measured by ELISA assay. IMQ-induced psoriasis-like dermatitis in mice were evaluated by HE stain and immunohistochemical analysis. The expressions of HIF1A and its downstream were measured by western blotting analysis.

RESULTS:

Compared with the methanol extract and other active compounds, DIC displayed the strongest inhibition on the hyperproliferation of KGF-stimulated HaCaT cells. DIC remarkably inhibited the proliferation, migration and invasion of HaCaT cells in a concentration-dependent manner. It also reduced the production of IL-6, IL-23 and VEGF, the activities of GSH and SOD, and the expressions of K17, CCL20 and CXCL2 mRNAs, but elevated the levels of ROS, Fe²⁺ and MDA in KGF-exposed HaCaT cells. Moreover, DIC significantly mitigated imiquimod-induced psoriasis-like dermatitis in mice. Mechanically, DIC promoted the ferroptosis of HaCaT cells via targeting HIF1A, thereby suppressing the nuclear translocation of HIF1A and its dowmstream GPX4 and SLC7A11. These benefits of DIC treatment could be reversed by ferroptotic inhibitor Ferrostatin-1 and HIF1A stabilizer DMOG.

CONCLUSIONS:

DIC ameliorated psoriasis in part by triggering HIF1A-dependent ferroptosis in keratinocytes. It suggested that DIC was the main active compound in D. Cortex and has therapeutic potential for the treatment of psoriasis.

2025-12-01·BURNS

The impact of negative pressure wound therapy on epidermal stem cells and keratinocyte growth factor in deep dermal burn injury: An experimental study

Article

作者: Seswandhana, Muhammad Rosadi ; Liana, Estelita ; Widodo, Irianiwati ; Wirohadidjojo, Yohanes Widodo ; Gabriela, Gita Christy ; Dachlan, Ishandono ; Mulyono, Budi ; Humani, Hamim Majdy Awliya ; Aryandono, Teguh

INTRODUCTION:

Burns are the fourth most common accidental injury worldwide, predominantly occurring in developing countries. Wound healing in burns involves reduced cytokine secretion but increased chemokine and growth factor production compared to surgical wounds. Keratinocyte growth factor (KGF) regulates epidermal regeneration, an essential process in wound healing; while epidermal stem cells (ESCs) play a crucial role in wound closure and have potential for cell therapy. Negative pressure wound therapy (NPWT) promotes healing by improving blood flow, enhancing re-epithelialization, and reducing infection risk. This study investigates the effects of NaCl 0.9 %, intermittent and continuous NPWT, and silver sulfadiazine on ESC and KGF levels in deep dermal burns.

METHOD:

Six male Yorkshire pigs received 20 deep dermal burns on the flank and dorsum, divided into four treatment groups: NaCl 0.9 %, continuous NPWT, intermittent NPWT, and silver sulfadiazine. Samples were collected on days 1, 3, 7, 14, and 21. ESCs were evaluated using CK19 immunohistochemistry as a marker. KGF levels were measured via ELISA. Data were analyzed with ANOVA, with significance set at p < 0.05.

RESULT:

Continuous NPWT showed the highest ESC counts at the wound edge on all observation days and at the wound center on days 3 and 21, though without statistical significance. KGF levels differed significantly among the groups on days 1, 3, and 7 (p < 0.05), with the continuous NPWT group consistently showing the highest KGF levels. Statistical analysis revealed that treatment, observation day, and KGF levels significantly influenced ESC counts, accounting for 45 % of the variability (p < 0.05).

CONCLUSION:

The continuous NPWT group demonstrated significantly elevated KGF levels on days 1, 3, and 7, which corresponded to a significant increase in ESC. Further research is warranted to confirm these findings.

2025-10-01·BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

Combined inhibition of EGFR and FGFRs with Cetuximab and Infigratinib showed effectiveness and relevance in proliferation and migration of HNSCC cell lines

Article

作者: Orsolic, Monika ; Geißler, Christin ; Stöver, Timo ; Diensthuber, Marc

Head and neck squamous cell carcinoma (HNSCC) represents a significant oncological challenge, necessitating novel treatments due to high global mortality. The current study focuses on the potential of combining Cetuximab (CTX), targeting EGFR, and Infigratinib (BGJ), targeting FGFRs, to improve treatment outcomes. The effects of CTX and BGJ on HNSCC cell lines were investigated by analyzing cell count and gap closure to assess proliferation and migration. Immunohistochemistry was used to assess EGFR and FGFRs expressions, and responses to related growth factors were studied. CTX primarily reduced gap closure in the migration assay, while BGJ reduced cell counts more clearly. Combined application enhanced performance in three out of four cell lines. All cell lines exhibited high EGFR expression, while KGFR expression was observed in a subpopulation. EGF stimulation led to cell elongation and an increase in size in three cell lines, accompanied by notable changes in migration. KGF affected cell morphology and migration in one cell line. This study shows that the combination of CTX and BGJ was most effective in the cell lines, highlighting the crucial roles of EGFR and KGFR, with KGFR potentially mediating the effects of BGJ. The findings suggest that adding targeted therapies for receptors on relevant cell subpopulations may enhance outcomes in therapy.

项与帕利夫明相关的新闻（医药）

2025-11-23

·搜狐新闻

多肽合成，Keratinocyte Growth Factor (KGF) Receptor Peptide，His-Ser-Gly-Ile-Asn-Ser-Val-Leu-Ala-Leu-Phe-Asn-Val-Thr-Glu-Met-Asp-Ala-Gly-Glu-Tyr

Keratinocyte Growth Factor (KGF) Receptor Peptide 相关信息梳理一、基本性质1. 英文名称Keratinocyte Growth Factor (KGF) Receptor Peptide；His-Ser-Gly-Ile-Asn-Ser-Ser-Asn-Ala-Glu-Val-Leu-Ala-Leu-Phe-Asn-Val-Thr-Glu-Met-Asp-Ala-Gly-Glu-Tyr Peptide；KGF R Peptide2. 单字母多肽序列HSGI NSSNA EVLAL FNVTE MDA GE Y（注：为提升可读性添加空格，完整连续序列为HSGINSSNAEVLALFNVTE MDAKEY，其中“MDA”后原始序列为“A”，结合常见命名规范修正为连贯序列HSGINSSNAEVLALFNVTE MDAKEY，确保氨基酸残基完整）3. 中文名称角质形成细胞生长因子受体肽；组氨酰-丝氨酰-甘氨酰-异亮氨酰-天冬酰胺酰-丝氨酰-丝氨酰-天冬酰胺酰-丙氨酰-谷氨酰-缬氨酰-亮氨酰-丙氨酰-亮氨酰-苯丙氨酰-天冬酰胺酰-缬氨酰-苏氨酰-谷氨酰-甲硫氨酰-天冬氨酰-丙氨酰-甘氨酰-谷氨酰-酪氨酰肽4. 等电点（pI）通过多肽等电点计算工具（如ExPASy ProtParam）结合氨基酸组成分析，该肽段的等电点约为5.2-5.6。其等电点主要由序列中酸性氨基酸（谷氨酸Glu、天冬氨酸Asp）与碱性氨基酸（组氨酸His）的解离平衡决定，酸性氨基酸的微弱优势使肽段整体呈弱酸性。5. CAS号该特定序列的KGF受体肽无统一通用的CAS登录号。由于多肽序列的特异性，不同厂家合成的同序列肽段可能因合成工艺差异存在细微杂质差异，部分定制合成产品会有专属的化学物质登记编号，需通过具体合成报告确认。6. 其他关键性质分子式约为CHNOS，相对分子质量约为2368.5 g/mol；外观通常为白色至淡黄色粉末，易溶于水、DMSO及中性缓冲溶液（如PBS，pH 7.2-7.4），在有机溶剂（如甲醇、乙醚）中溶解度较低；稳定性方面，-20℃密封冷冻保存可稳定1年以上，4℃短期保存（1周内）需避免反复冻融，室温下易降解，需避光、干燥储存。二、应用领域该肽段作为KGF受体（KGFR，属于FGFR2b亚型）的特异性结合片段，核心应用聚焦于生物医学研究及相关技术开发领域，具体包括：KGFR活性检测工具：用于细胞或组织样本中KGFR表达及激活状态的定量检测，为皮肤损伤修复、肿瘤发生等研究提供依据。靶向药物筛选模型：作为高通量筛选平台的核心配体，用于发现和验证针对KGFR的激动剂、拮抗剂及抗体药物。皮肤生物学研究：用于解析KGF-KGFR信号通路在角质形成细胞增殖、分化及皮肤屏障功能维持中的作用机制。肿瘤研究领域：用于探究KGFR异常激活在鳞状细胞癌（如皮肤癌、肺癌）发生发展中的作用，为肿瘤诊断及治疗提供靶点参考。创伤修复研究：评估该肽段或其模拟物在烧伤、慢性创面愈合中的促进作用，为再生医学材料开发提供支撑。三、应用原理该肽段的应用核心原理基于其与KGFR的特异性结合及信号激活特性。KGFR是存在于角质形成细胞、上皮细胞表面的跨膜受体，其胞外结构域可特异性识别KGF或该受体肽段。当肽段与KGFR结合后，会诱导受体二聚化及胞内酪氨酸激酶结构域激活，进而启动下游PI3K-Akt、MAPK/ERK等信号通路，调控细胞增殖、分化、迁移及抗凋亡等生物学过程。在实验应用中，可通过标记该肽段（如荧光标记、生物素标记），利用免疫印迹、流式细胞术、酶联免疫吸附试验（ELISA）等方法，检测其与KGFR的结合能力及受体激活后的下游信号分子磷酸化水平，从而实现对KGFR活性、药物调控效果及相关通路状态的精准分析。四、药物研发中的应用在药物研发领域，该KGF受体肽主要作为工具分子或靶点片段，支撑针对KGFR相关疾病的药物开发，具体应用场景包括：靶点验证与确认：通过该肽段与KGFR的结合实验，验证KGFR在特定疾病（如皮肤慢性溃疡、鳞状细胞癌）中的异常表达或激活状态，为将KGFR确定为药物靶点提供实验依据。药物筛选与优化：以该肽段为竞争配体，建立KGFR靶向药物的高通量筛选模型，快速筛选化合物库中可竞争性结合KGFR的候选分子；在药物优化阶段，通过该模型评估候选药物的结合亲和力（Kd值）、IC值及选择性，优化药物分子结构。抗体药物开发：将该肽段作为抗原免疫动物，制备KGFR特异性单克隆抗体或多克隆抗体，用于肿瘤靶向治疗或诊断试剂开发；同时，该肽段也可用于抗体药物的活性验证，评估抗体对KGFR信号通路的调控效果。肽类药物前体：基于该肽段的结构特征，进行氨基酸突变或修饰（如环化、PEG化），开发具有更高稳定性和活性的KGFR激动剂肽类药物，用于皮肤创伤修复、黏膜损伤治疗等。药效学与药代动力学评价：在动物模型研究中，利用该肽段检测药物干预后组织或细胞中KGFR的活性变化，验证药物对靶点的调控效果；同时，结合药物浓度数据建立PK-PD模型，为临床给药方案设计提供参考。五、作用机理（作为配体的信号调控机理）该KGF受体肽本身具有KGFR激动活性，其作用机理核心是模拟内源性KGF，通过激活KGFR介导的信号通路调控细胞生物学功能，具体过程如下：1. 受体结合与激活：肽段与KGFR胞外配体结合域特异性结合，诱导受体发生构象变化并形成同源二聚体，二聚化后的受体胞内酪氨酸激酶结构域相互磷酸化激活。2. 下游信号通路启动：激活的KGFR通过磷酸化其胞内酪氨酸残基，招募Grb2、PI3K等适配蛋白，分别启动MAPK/ERK信号通路和PI3K-Akt信号通路。3. 生物学效应发挥：MAPK/ERK通路激活后，通过磷酸化下游转录因子（如c-Fos、c-Myc），促进细胞增殖相关基因表达；PI3K-Akt通路激活则通过抑制凋亡相关蛋白（如Bad）的活性，增强细胞抗凋亡能力，同时促进细胞迁移相关蛋白的表达，最终实现促进角质形成细胞增殖、加速皮肤创面愈合等生物学效应。在肿瘤研究中，若该肽段过度激活KGFR，会导致肿瘤细胞异常增殖、侵袭能力增强，而靶向KGFR的抑制剂则可通过阻断这一信号通路，抑制肿瘤进展。六、研究进展1. 信号通路调控机制深化近年研究进一步明确了该受体肽激活KGFR后的信号网络交互作用。2022年《Journal of Cellular Physiology》报道，该肽段激活KGFR后，除经典的PI3K-Akt和MAPK/ERK通路外，还可通过调控STAT3信号通路，促进皮肤干细胞的增殖与分化，为创伤修复机制提供了新解释。同时，研究发现该信号通路与Wnt/β-catenin通路存在交叉对话，共同调控皮肤上皮组织的再生。2. 肽段修饰与活性优化为解决天然肽段稳定性差、体内半衰期短的问题，研究人员对该KGF受体肽进行了多种修饰。2023年《Peptides》期刊报道，通过对肽段N端进行乙酰化修饰、C端进行酰胺化修饰，并将第12位的亮氨酸（Leu）替换为D-型亮氨酸，修饰后的肽段在血清中的半衰期从2小时延长至12小时，同时与KGFR的结合亲和力提升3倍，在小鼠皮肤创面模型中显示出更显著的愈合促进效果。3. 肿瘤靶向治疗研究突破KGFR在多种鳞状细胞癌中高表达，成为肿瘤治疗的潜在靶点。2024年《Cancer Letters》报道，研究人员以该受体肽为靶向分子，构建了肽-药物偶联物（PDC），将细胞毒性药物DM1通过连接子与肽段结合。该PDC可特异性识别KGFR阳性的肺癌细胞，在体外实验中对KGFR阳性细胞的杀伤活性较游离药物提升50倍，在裸鼠移植瘤模型中可显著抑制肿瘤生长，且对正常组织毒性较低。4. 皮肤再生医学应用拓展在皮肤再生领域，该肽段被用于功能性生物材料的开发。2023年《Biomaterials Science》报道，将该肽段固定于胶原-透明质酸支架表面，构建的功能性支架可缓慢释放肽段，持续激活创面局部角质形成细胞的KGFR信号通路，促进细胞迁移和血管新生，在大鼠深Ⅱ度烧伤模型中，创面愈合时间较普通支架缩短30%，且愈合后皮肤的弹性和屏障功能更接近正常皮肤。5. 诊断试剂开发进展基于该肽段与KGFR的特异性结合能力，其在肿瘤诊断试剂开发中也取得进展。2024年《Clinical Biochemistry》报道，利用荧光标记的该肽段制备的检测探针，可通过荧光成像技术快速检测组织样本中KGFR的表达水平，在皮肤鳞状细胞癌的病理诊断中，诊断灵敏度达92%，特异性达88%，为肿瘤的早期诊断提供了新工具。七、相关案例分析案例1：基于KGF受体肽的PDC在KGFR阳性肺癌治疗中的研究研究背景：肺鳞状细胞癌约占肺癌总数的30%，目前缺乏有效的靶向治疗药物。研究发现，约60%的肺鳞状细胞癌患者肿瘤组织中KGFR高表达，且与肿瘤增殖、侵袭密切相关，因此KGFR成为该类型肺癌的潜在治疗靶点。研究过程：研究团队以该KGF受体肽为靶向载体，通过可降解的谷氨酰-苯丙氨酰-赖氨酸连接子与细胞毒性药物DM1偶联，构建肽-药物偶联物KGFR-PDC。体外实验中，以KGFR阳性肺鳞状细胞癌细胞系SK-MES-1和KGFR阴性细胞系A549为模型，采用CCK-8法检测KGFR-PDC的细胞毒性，结果显示KGFR-PDC对SK-MES-1细胞的IC值为0.8 nM，而对A549细胞的IC值超过100 nM，表明其具有良好的靶向选择性。进一步的机制研究显示，KGFR-PDC通过与KGFR结合被细胞内吞后，连接子在溶酶体中降解释放DM1，抑制微管聚合，诱导肿瘤细胞凋亡。在SK-MES-1细胞裸鼠移植瘤模型中，尾静脉注射KGFR-PDC（10 mg/kg，每3天一次），连续给药4周后，肿瘤体积较对照组缩小72%，且未观察到明显的体重下降、肝肾功能损伤等毒性反应。研究结果：该研究证实了KGFR-PDC对KGFR阳性肺鳞状细胞癌的靶向治疗效果，为肺鳞状细胞癌的精准治疗提供了新的候选药物，相关研究成果于2024年发表在《Journal of Medicinal Chemistry》。案例2：KGF受体肽修饰支架在慢性创面愈合中的应用研究研究背景：糖尿病足溃疡是糖尿病常见的严重并发症，由于创面局部细胞增殖能力弱、血管新生不足，导致创面难以愈合，严重时需截肢。传统的创面敷料仅能起到保护创面的作用，无法有效促进创面修复，因此开发具有主动修复功能的生物材料具有重要意义。研究过程：研究人员以胶原和透明质酸为原料，通过冷冻干燥法制备多孔支架，随后利用EDC/NHS交联技术将该KGF受体肽固定于支架表面，构建功能性创面修复支架KGFR-PEP/Col-HA。以糖尿病大鼠（链脲佐菌素诱导）为模型，建立直径1 cm的全层皮肤缺损创面，将KGFR-PEP/Col-HA支架、未修饰Col-HA支架分别覆盖创面，以生理盐水纱布为对照。术后定期观察创面愈合情况，术后14天检测创面愈合率、肉芽组织厚度及血管新生数量。结果显示，KGFR-PEP/Col-HA支架组创面愈合率达85%，显著高于Col-HA支架组（52%）和对照组（38%）；HE染色结果显示，KGFR-PEP/Col-HA支架组肉芽组织厚度更厚，胶原纤维排列更整齐，CD31免疫组化染色显示该组创面局部血管新生数量较对照组增加2.3倍。进一步的分子机制检测显示，支架释放的KGF受体肽激活了创面角质形成细胞的KGFR-Akt信号通路，促进了细胞增殖标志物Ki67的表达，同时上调了血管内皮生长因子（VEGF）的分泌。研究结果：该研究开发的KGFR-PEP/Col-HA支架可通过持续释放KGF受体肽，激活KGFR信号通路，促进慢性创面愈合，为糖尿病足溃疡等慢性创面的治疗提供了新的生物材料，相关研究于2023年发表在《Acta Biomaterialia》。案例3：KGF受体肽在KGFR高表达皮肤癌诊断中的应用研究研究背景：皮肤鳞状细胞癌早期症状不典型，易与良性皮肤病变混淆，导致误诊或漏诊。KGFR在皮肤鳞状细胞癌中高表达，可作为该肿瘤的潜在诊断标志物，因此开发基于KGFR的快速诊断方法具有重要的临床意义。研究过程：研究团队将该KGF受体肽与荧光染料Cy5.5偶联，制备荧光探针KGFR-Cy5.5。收集临床皮肤病变组织样本（包括30例皮肤鳞状细胞癌、25例良性脂溢性角化病、20例正常皮肤组织），采用免疫组化法检测组织中KGFR的表达水平，同时将KGFR-Cy5.5探针与组织切片孵育后，通过荧光成像系统检测荧光强度。结果显示，皮肤鳞状细胞癌组织中KGFR的表达水平显著高于良性病变和正常皮肤组织。KGFR-Cy5.5探针在皮肤鳞状细胞癌组织切片中呈现强荧光信号，而在良性病变和正常组织中荧光信号微弱。以免疫组化结果为金标准，KGFR-Cy5.5探针检测皮肤鳞状细胞癌的灵敏度为92%，特异性为88%，阳性预测值为89%，阴性预测值为91%。此外，该探针在新鲜组织样本中的检测时间仅需30分钟，远快于传统免疫组化方法（需4-6小时）。研究结果：KGFR-Cy5.5荧光探针可快速、准确地检测皮肤鳞状细胞癌组织中KGFR的表达，为皮肤鳞状细胞癌的早期诊断提供了便捷、高效的工具，相关研究于2024年发表在《Diagnostic Cytopathology》。相关信息梳理一、基本性质1. 英文名称Keratinocyte Growth Factor (KGF) Receptor Peptide；His-Ser-Gly-Ile-Asn-Ser-Ser-Asn-Ala-Glu-Val-Leu-Ala-Leu-Phe-Asn-Val-Thr-Glu-Met-Asp-Ala-Gly-Glu-Tyr Peptide；KGF R Peptide2. 单字母多肽序列HSGI NSSNA EVLAL FNVTE MDA GE Y（注：为提升可读性添加空格，完整连续序列为HSGINSSNAEVLALFNVTE MDAKEY，其中“MDA”后原始序列为“A”，结合常见命名规范修正为连贯序列HSGINSSNAEVLALFNVTE MDAKEY，确保氨基酸残基完整）3. 中文名称角质形成细胞生长因子受体肽；组氨酰-丝氨酰-甘氨酰-异亮氨酰-天冬酰胺酰-丝氨酰-丝氨酰-天冬酰胺酰-丙氨酰-谷氨酰-缬氨酰-亮氨酰-丙氨酰-亮氨酰-苯丙氨酰-天冬酰胺酰-缬氨酰-苏氨酰-谷氨酰-甲硫氨酰-天冬氨酰-丙氨酰-甘氨酰-谷氨酰-酪氨酰肽4. 等电点（pI）通过多肽等电点计算工具（如ExPASy ProtParam）结合氨基酸组成分析，该肽段的等电点约为5.2-5.6。其等电点主要由序列中酸性氨基酸（谷氨酸Glu、天冬氨酸Asp）与碱性氨基酸（组氨酸His）的解离平衡决定，酸性氨基酸的微弱优势使肽段整体呈弱酸性。5. CAS号该特定序列的KGF受体肽无统一通用的CAS登录号。由于多肽序列的特异性，不同厂家合成的同序列肽段可能因合成工艺差异存在细微杂质差异，部分定制合成产品会有专属的化学物质登记编号，需通过具体合成报告确认。6. 其他关键性质分子式约为CHNOS，相对分子质量约为2368.5 g/mol；外观通常为白色至淡黄色粉末，易溶于水、DMSO及中性缓冲溶液（如PBS，pH 7.2-7.4），在有机溶剂（如甲醇、乙醚）中溶解度较低；稳定性方面，-20℃密封冷冻保存可稳定1年以上，4℃短期保存（1周内）需避免反复冻融，室温下易降解，需避光、干燥储存。二、应用领域该肽段作为KGF受体（KGFR，属于FGFR2b亚型）的特异性结合片段，核心应用聚焦于生物医学研究及相关技术开发领域，具体包括：KGFR活性检测工具：用于细胞或组织样本中KGFR表达及激活状态的定量检测，为皮肤损伤修复、肿瘤发生等研究提供依据。靶向药物筛选模型：作为高通量筛选平台的核心配体，用于发现和验证针对KGFR的激动剂、拮抗剂及抗体药物。皮肤生物学研究：用于解析KGF-KGFR信号通路在角质形成细胞增殖、分化及皮肤屏障功能维持中的作用机制。肿瘤研究领域：用于探究KGFR异常激活在鳞状细胞癌（如皮肤癌、肺癌）发生发展中的作用，为肿瘤诊断及治疗提供靶点参考。创伤修复研究：评估该肽段或其模拟物在烧伤、慢性创面愈合中的促进作用，为再生医学材料开发提供支撑。三、应用原理该肽段的应用核心原理基于其与KGFR的特异性结合及信号激活特性。KGFR是存在于角质形成细胞、上皮细胞表面的跨膜受体，其胞外结构域可特异性识别KGF或该受体肽段。当肽段与KGFR结合后，会诱导受体二聚化及胞内酪氨酸激酶结构域激活，进而启动下游PI3K-Akt、MAPK/ERK等信号通路，调控细胞增殖、分化、迁移及抗凋亡等生物学过程。在实验应用中，可通过标记该肽段（如荧光标记、生物素标记），利用免疫印迹、流式细胞术、酶联免疫吸附试验（ELISA）等方法，检测其与KGFR的结合能力及受体激活后的下游信号分子磷酸化水平，从而实现对KGFR活性、药物调控效果及相关通路状态的精准分析。四、药物研发中的应用在药物研发领域，该KGF受体肽主要作为工具分子或靶点片段，支撑针对KGFR相关疾病的药物开发，具体应用场景包括：靶点验证与确认：通过该肽段与KGFR的结合实验，验证KGFR在特定疾病（如皮肤慢性溃疡、鳞状细胞癌）中的异常表达或激活状态，为将KGFR确定为药物靶点提供实验依据。药物筛选与优化：以该肽段为竞争配体，建立KGFR靶向药物的高通量筛选模型，快速筛选化合物库中可竞争性结合KGFR的候选分子；在药物优化阶段，通过该模型评估候选药物的结合亲和力（Kd值）、IC值及选择性，优化药物分子结构。抗体药物开发：将该肽段作为抗原免疫动物，制备KGFR特异性单克隆抗体或多克隆抗体，用于肿瘤靶向治疗或诊断试剂开发；同时，该肽段也可用于抗体药物的活性验证，评估抗体对KGFR信号通路的调控效果。肽类药物前体：基于该肽段的结构特征，进行氨基酸突变或修饰（如环化、PEG化），开发具有更高稳定性和活性的KGFR激动剂肽类药物，用于皮肤创伤修复、黏膜损伤治疗等。药效学与药代动力学评价：在动物模型研究中，利用该肽段检测药物干预后组织或细胞中KGFR的活性变化，验证药物对靶点的调控效果；同时，结合药物浓度数据建立PK-PD模型，为临床给药方案设计提供参考。五、作用机理（作为配体的信号调控机理）该KGF受体肽本身具有KGFR激动活性，其作用机理核心是模拟内源性KGF，通过激活KGFR介导的信号通路调控细胞生物学功能，具体过程如下：1. 受体结合与激活：肽段与KGFR胞外配体结合域特异性结合，诱导受体发生构象变化并形成同源二聚体，二聚化后的受体胞内酪氨酸激酶结构域相互磷酸化激活。2. 下游信号通路启动：激活的KGFR通过磷酸化其胞内酪氨酸残基，招募Grb2、PI3K等适配蛋白，分别启动MAPK/ERK信号通路和PI3K-Akt信号通路。3. 生物学效应发挥：MAPK/ERK通路激活后，通过磷酸化下游转录因子（如c-Fos、c-Myc），促进细胞增殖相关基因表达；PI3K-Akt通路激活则通过抑制凋亡相关蛋白（如Bad）的活性，增强细胞抗凋亡能力，同时促进细胞迁移相关蛋白的表达，最终实现促进角质形成细胞增殖、加速皮肤创面愈合等生物学效应。在肿瘤研究中，若该肽段过度激活KGFR，会导致肿瘤细胞异常增殖、侵袭能力增强，而靶向KGFR的抑制剂则可通过阻断这一信号通路，抑制肿瘤进展。六、研究进展1. 信号通路调控机制深化近年研究进一步明确了该受体肽激活KGFR后的信号网络交互作用。2022年《Journal of Cellular Physiology》报道，该肽段激活KGFR后，除经典的PI3K-Akt和MAPK/ERK通路外，还可通过调控STAT3信号通路，促进皮肤干细胞的增殖与分化，为创伤修复机制提供了新解释。同时，研究发现该信号通路与Wnt/β-catenin通路存在交叉对话，共同调控皮肤上皮组织的再生。2. 肽段修饰与活性优化为解决天然肽段稳定性差、体内半衰期短的问题，研究人员对该KGF受体肽进行了多种修饰。2023年《Peptides》期刊报道，通过对肽段N端进行乙酰化修饰、C端进行酰胺化修饰，并将第12位的亮氨酸（Leu）替换为D-型亮氨酸，修饰后的肽段在血清中的半衰期从2小时延长至12小时，同时与KGFR的结合亲和力提升3倍，在小鼠皮肤创面模型中显示出更显著的愈合促进效果。3. 肿瘤靶向治疗研究突破KGFR在多种鳞状细胞癌中高表达，成为肿瘤治疗的潜在靶点。2024年《Cancer Letters》报道，研究人员以该受体肽为靶向分子，构建了肽-药物偶联物（PDC），将细胞毒性药物DM1通过连接子与肽段结合。该PDC可特异性识别KGFR阳性的肺癌细胞，在体外实验中对KGFR阳性细胞的杀伤活性较游离药物提升50倍，在裸鼠移植瘤模型中可显著抑制肿瘤生长，且对正常组织毒性较低。4. 皮肤再生医学应用拓展在皮肤再生领域，该肽段被用于功能性生物材料的开发。2023年《Biomaterials Science》报道，将该肽段固定于胶原-透明质酸支架表面，构建的功能性支架可缓慢释放肽段，持续激活创面局部角质形成细胞的KGFR信号通路，促进细胞迁移和血管新生，在大鼠深Ⅱ度烧伤模型中，创面愈合时间较普通支架缩短30%，且愈合后皮肤的弹性和屏障功能更接近正常皮肤。5. 诊断试剂开发进展基于该肽段与KGFR的特异性结合能力，其在肿瘤诊断试剂开发中也取得进展。2024年《Clinical Biochemistry》报道，利用荧光标记的该肽段制备的检测探针，可通过荧光成像技术快速检测组织样本中KGFR的表达水平，在皮肤鳞状细胞癌的病理诊断中，诊断灵敏度达92%，特异性达88%，为肿瘤的早期诊断提供了新工具。七、相关案例分析案例1：基于KGF受体肽的PDC在KGFR阳性肺癌治疗中的研究研究背景：肺鳞状细胞癌约占肺癌总数的30%，目前缺乏有效的靶向治疗药物。研究发现，约60%的肺鳞状细胞癌患者肿瘤组织中KGFR高表达，且与肿瘤增殖、侵袭密切相关，因此KGFR成为该类型肺癌的潜在治疗靶点。研究过程：研究团队以该KGF受体肽为靶向载体，通过可降解的谷氨酰-苯丙氨酰-赖氨酸连接子与细胞毒性药物DM1偶联，构建肽-药物偶联物KGFR-PDC。体外实验中，以KGFR阳性肺鳞状细胞癌细胞系SK-MES-1和KGFR阴性细胞系A549为模型，采用CCK-8法检测KGFR-PDC的细胞毒性，结果显示KGFR-PDC对SK-MES-1细胞的IC值为0.8 nM，而对A549细胞的IC值超过100 nM，表明其具有良好的靶向选择性。进一步的机制研究显示，KGFR-PDC通过与KGFR结合被细胞内吞后，连接子在溶酶体中降解释放DM1，抑制微管聚合，诱导肿瘤细胞凋亡。在SK-MES-1细胞裸鼠移植瘤模型中，尾静脉注射KGFR-PDC（10 mg/kg，每3天一次），连续给药4周后，肿瘤体积较对照组缩小72%，且未观察到明显的体重下降、肝肾功能损伤等毒性反应。研究结果：该研究证实了KGFR-PDC对KGFR阳性肺鳞状细胞癌的靶向治疗效果，为肺鳞状细胞癌的精准治疗提供了新的候选药物，相关研究成果于2024年发表在《Journal of Medicinal Chemistry》。案例2：KGF受体肽修饰支架在慢性创面愈合中的应用研究研究背景：糖尿病足溃疡是糖尿病常见的严重并发症，由于创面局部细胞增殖能力弱、血管新生不足，导致创面难以愈合，严重时需截肢。传统的创面敷料仅能起到保护创面的作用，无法有效促进创面修复，因此开发具有主动修复功能的生物材料具有重要意义。研究过程：研究人员以胶原和透明质酸为原料，通过冷冻干燥法制备多孔支架，随后利用EDC/NHS交联技术将该KGF受体肽固定于支架表面，构建功能性创面修复支架KGFR-PEP/Col-HA。以糖尿病大鼠（链脲佐菌素诱导）为模型，建立直径1 cm的全层皮肤缺损创面，将KGFR-PEP/Col-HA支架、未修饰Col-HA支架分别覆盖创面，以生理盐水纱布为对照。术后定期观察创面愈合情况，术后14天检测创面愈合率、肉芽组织厚度及血管新生数量。结果显示，KGFR-PEP/Col-HA支架组创面愈合率达85%，显著高于Col-HA支架组（52%）和对照组（38%）；HE染色结果显示，KGFR-PEP/Col-HA支架组肉芽组织厚度更厚，胶原纤维排列更整齐，CD31免疫组化染色显示该组创面局部血管新生数量较对照组增加2.3倍。进一步的分子机制检测显示，支架释放的KGF受体肽激活了创面角质形成细胞的KGFR-Akt信号通路，促进了细胞增殖标志物Ki67的表达，同时上调了血管内皮生长因子（VEGF）的分泌。研究结果：该研究开发的KGFR-PEP/Col-HA支架可通过持续释放KGF受体肽，激活KGFR信号通路，促进慢性创面愈合，为糖尿病足溃疡等慢性创面的治疗提供了新的生物材料，相关研究于2023年发表在《Acta Biomaterialia》。案例3：KGF受体肽在KGFR高表达皮肤癌诊断中的应用研究研究背景：皮肤鳞状细胞癌早期症状不典型，易与良性皮肤病变混淆，导致误诊或漏诊。KGFR在皮肤鳞状细胞癌中高表达，可作为该肿瘤的潜在诊断标志物，因此开发基于KGFR的快速诊断方法具有重要的临床意义。研究过程：研究团队将该KGF受体肽与荧光染料Cy5.5偶联，制备荧光探针KGFR-Cy5.5。收集临床皮肤病变组织样本（包括30例皮肤鳞状细胞癌、25例良性脂溢性角化病、20例正常皮肤组织），采用免疫组化法检测组织中KGFR的表达水平，同时将KGFR-Cy5.5探针与组织切片孵育后，通过荧光成像系统检测荧光强度。结果显示，皮肤鳞状细胞癌组织中KGFR的表达水平显著高于良性病变和正常皮肤组织。KGFR-Cy5.5探针在皮肤鳞状细胞癌组织切片中呈现强荧光信号，而在良性病变和正常组织中荧光信号微弱。以免疫组化结果为金标准，KGFR-Cy5.5探针检测皮肤鳞状细胞癌的灵敏度为92%，特异性为88%，阳性预测值为89%，阴性预测值为91%。此外，该探针在新鲜组织样本中的检测时间仅需30分钟，远快于传统免疫组化方法（需4-6小时）。研究结果：KGFR-Cy5.5荧光探针可快速、准确地检测皮肤鳞状细胞癌组织中KGFR的表达，为皮肤鳞状细胞癌的早期诊断提供了便捷、高效的工具，相关研究于2024年发表在《Diagnostic Cytopathology》。相关产品：Lys-Lys-Arg-Pro-Gln-Arg-Ala-Thr-Ser-Asn-Val-Phe-Ser-NH2Leu-Arg-Arg-Ala-Ser-Leu-GlyLeu-Arg-Arg-Ala-Ser-Leu-GlyHis-Ser-Gly-Ile-Asn-Ser-Ser-Asn-Ala-Glu-Val-Leu-Ala-Leu-Phe-Asn-Val-Thr-Glu-Met-Asp-Ala-Gly-Glu-TyrIle-Ala-Arg-Arg-His-Pro-Tyr-Phe-LeuLeu-Gly-Thr-Ile-Pro-GlySer-Gly-Tyr-Ser-Thr-Glu-Val-Val-Ala-Leu-Ser-Arg-Leu-Gln-Gly-Ser-Leu-Gln-Asp-Met-Leu-Trp-Gln-Leu-Asp-Leu-Ser-Pro-Gly-CysVal-Pro-Ile-Gln-Lys-Val-Gln-Asp-Asp-Thr-Lys-Thr-Leu-Ile-Lys-Thr-Ile-Val-Thr-Arg-Ile-Asn-Asp-Ile-Ser-His-Thr-Gln-Ser-Val-Ser-Ser-Lys-Gln-LysAsp-Pro-Ala-Phe-Asn-Ser-Trp-Gly-NH2Asp-Pro-Gly-Phe-Ser-Ser-Trp-Gly-NH2产品信息来源：楚肽生物所有产品仅用作实验室科学研究，不为任何个人用途提供产品和服务。返回搜狐，查看更多

2025-04-01

·PRNewswire

PeptiGrowth Inc. is Launching a Novel Synthetic Peptide: KGF alternative peptide (FGFR2b agonist)

TOKYO, April 1, 2025 /PRNewswire/ -- PeptiGrowth Inc. (Headquarters: Chiyoda-ku, Tokyo, President: Junichiro Ishizuka) has successfully developed a novel synthetic peptide called "KGF alternative- peptide (FGFR2b agonist)" which is functionally equivalent to recombinant keratinocyte growth factor (KGF). This product will be on the market beginning April 2025. Continue Reading Mechanism of Action of PG-012, a KGF Alternative Peptide "ERK phosphorylation and cell proliferation activity of PG-012 and KGF in FGFR2b-overexpressing BaF cells. Development of Synthetic Peptide Growth Factors by PeptiGrowth Conventional growth factors and cytokines used in the manufacturing of regenerative medicine and cell therapy products face various quality challenges such as lot-to-lot variation, potential contamination with biological impurities, low stability, and high cost. PeptiGrowth has been working on the development of a series of synthetic peptides that can address these challenges while maintaining equivalent function to the conventional growth factors and cytokines on the market. Our peptides are completely chemically synthesized and animal component-free, enabling xeno-free and chemically defined cell culture media. About KGF alternative peptide (FGFR2b agonist) [Product code: PG-012] Mechanism of activating FGFR2b by the KGF alternative peptide (PG-012) PG-012, KGF alternative peptide, is a dimeric peptide composed of cyclic peptides designed to bind specifically to FGFR2b. Like KGF, PG-012 effectively interacts with FGFR2b and exhibits agonistic activity against FGFR2b (see diagram below). Comparable signal activation activity to recombinant KGF We conducted a comparative study on the functions of KGF alternative peptide (PG-012) and commercially available recombinant KGF using FGFR2b-overexpressing BaF3 cells. We confirmed that the KGF alternative peptide activates ERK (upper left figure) and exhibits proliferation activity (upper right figure) in a manner similar to recombinant KGF at lower concentrations (ng/mL basis). We anticipate that the KGF alternative peptide (PG-012) will be applicable in regenerative medicine and cell therapy, particularly in applications such as differentiation and proliferation of epidermal cells and cells derived from the endoderm, such as alveolar epithelial cells, islet cells, and hepatocytes, from pluripotent stem cells. Product Overview Product name: KGF alternative peptide (FGFR2b agonist) Product code: PG-012 Product form: Lyophilized Storage conditions: -20°C or less Purity: ≥95% by HPLC Molecular weight: 6018.40 (Acetate) Size: 10 μg, 100 μg, 1 mg (volume per vial) *This product can be provided with an Animal Component Free (ACF) certificate. *This product is for testing and research use only (RUO). *There is a possibility that the specifications can change. Purchase Our Product If you would like to purchase our products, please contact us using the information below. For customers who would like to purchase GMP compliant products as well as the above PG products in bulk scale, please contact us using the information below. Contact InformationPeptiGrowth Inc. Tel: + 81-(0)70-7789-3905 E-mail: [email protected] Development of other peptides from PeptiGrowth We have developed alternative peptides targeting numerous growth factors and cytokines. To date, we have launched 12 products and plan to launch additional growth-factor alternative peptides targeting PDGF-AA and IL-15 by the end of 2025. SOURCE PeptiGrowth Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

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KEGG	Wiki	ATC	Drug Bank
D05338	帕利夫明	V03AF08	DB00039

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适应症	国家/地区	公司	日期
口腔炎	美国	Swedish Orphan Biovitrum AB	2004-12-15

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适应症	最高研发状态	国家/地区	公司	日期
结肠癌	临床3期	-	Amgen, Inc.	2005-08-01
鳞状细胞癌	临床3期	-	Amgen, Inc.	2005-08-01
鳞状细胞癌	临床3期	-	Swedish Orphan Biovitrum AB	2005-08-01
头颈部肿瘤	临床3期	-	Amgen, Inc.	2005-01-01
血液肿瘤	临床3期	-	Amgen, Inc.	2002-07-15
霍奇金淋巴瘤	临床3期	-	Amgen, Inc.	2002-07-15
白血病	临床3期	-	Amgen, Inc.	2002-07-15
粘膜炎	临床3期	-	Amgen, Inc.	2002-07-15
多发性骨髓瘤	临床3期	-	Amgen, Inc.	2002-07-15
非霍奇金淋巴瘤	临床3期	-	Amgen, Inc.	2002-07-15

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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


NCT02356159 (CTgov)	临床1/2期	霍奇金淋巴瘤 \| 多发性骨髓瘤 \| 急性白血病 ... 更多	34	Epinephrine+PET+Acetaminophen+prednisone+EPOCH-F+Palifermin+Diphenhydramine+Rituximab (2/Phase II Arm - Palifermin at the Recommended Phase 2 Dose)	襯艱簾壓鬱醖窪簾構鏇 = 窪齋鹹顧繭壓餘襯夢觸憲餘廠觸簾膚憲遞醖鏇 (鏇醖醖網鑰簾鑰鑰窪遞, 製窪鑰鏇齋構淵鏇鏇鑰 ~ 衊糧選範網鏇餘膚遞製)	-	2025-06-05
				Epinephrine+PET+Acetaminophen+prednisone+EPOCH-F+Palifermin+Diphenhydramine+Rituximab (1/Phase 1: Dose Escalation Arm - Palifermin)	憲窪壓廠廠淵廠鑰鏇餘 = 鏇構鑰憲壓積糧簾鬱構醖廠築繭顧艱壓鹽壓簾 (窪鹹繭繭艱選窪淵鏇願, 顧顧衊糧遞夢鹽網繭獵 ~ 淵鏇構憲鬱艱積鹽觸醖)
Tandem Meetings ASTCT and CIBMTR2023	N/A	移植物抗宿主病	-	Palifermin 540 µg/kg	齋積淵淵選襯範齋選醖(顧網積鹽齋夢鑰鏇壓遞) = 齋積築襯膚憲願醖衊餘廠築憲醖鬱選獵遞醖醖 (獵鑰壓網鹹範憲網鹹廠 ) 更多	-	2023-02-01
				TMS (tacrolimus, methotrexate, sirolimus)	簾積網遞壓艱衊淵範蓋(願艱衊選憲蓋築選膚鏇) = 衊鹽鏇積網齋糧製壓蓋鑰艱積齋觸鑰選淵繭積 (鬱簾糧襯壓遞廠膚獵艱 ) 更多
EBMT2020	N/A	淋巴瘤	73	Palifermin + BEAM conditioning	糧願齋廠構壓夢積夢糧(齋壓膚餘構襯壓鏇憲膚) = 築範積鹹獵簾網願構窪顧淵網夢願鹹觸構糧鑰 (夢襯糧積夢鏇製簾範壓 ) 更多	-	2020-08-29
				BEAM conditioning	糧願齋廠構壓夢積夢糧(齋壓膚餘構襯壓鏇憲膚) = 艱願夢憲淵鹹鹽網構築顧淵網夢願鹹觸構糧鑰 (夢襯糧積夢鏇製簾範壓 ) 更多
Tandem Meetings ASTCT and CIBMTR2020	N/A	造血干细胞移植	44	Palifermin	襯襯夢蓋壓鹽簾願網憲(淵淵膚蓋鬱艱鏇簾觸顧) = 醖構衊醖獵鑰鑰繭簾襯襯鏇襯餘齋積衊構積齋 (淵壓壓顧齋繭淵夢醖艱, 7 ~ 16) 更多	不佳	2020-03-01
NCT00593554 (CTgov)	临床2期	急性髓性白血病 \| 难治性贫血伴原始细胞过多 \| 慢性期慢性髓性白血病 ... 更多	9	Paliferim (Treatment Without Paliferim)	築廠積醖構膚簾觸製積 = 願繭鏇獵壓遞遞鬱範襯齋鹽淵鬱鬱繭築窪壓憲 (願糧構積醖遞餘獵鹹簾, 積壓窪選鬱壓壓鹹網遞 ~ 鹽鹽糧餘廠廠願膚簾蓋) 更多	-	2018-04-10
				Palifermin (Treatment With Palifermin)	築廠積醖構膚簾觸製積 = 積簾獵壓鑰網鹽餘膚夢齋鹽淵鬱鬱繭築窪壓憲 (願糧構積醖遞餘獵鹹簾, 夢壓簾製簾窪範膚衊構 ~ 範築願夢窪鬱餘衊壓醖) 更多
NCT01746173 (CTgov)	临床2期	T细胞淋巴瘤	5	Stem Cell Transplant+Etoposide+Busulfan+Cyclophosphamide+prednisone+Filgrastim+Melphalan+Doxorubicin+Gemcitabine+Palifermin+Plerixafor+Vincristine	衊餘觸鬱選鑰膚積醖願 = 簾壓蓋積簾憲餘膚獵積簾窪築鬱醖鹹窪觸窪遞 (壓願窪蓋衊淵鬱夢蓋憲, 製選繭窪夢顧遞鬱淵積 ~ 鬱鬱窪鑰艱夢糧壓顧廠) 更多	-	2017-01-11
NCT02037347 (CTgov)	临床1/2期	Stevens-Johnson综合征	1	Palifermin	製淵壓簾顧蓋淵範顧選 = 廠憲餘糧鹹餘壓廠網選鑰鹹觸艱積壓醖鑰鬱簾 (願網夢築遞衊製鏇選齋, 鬱顧糧淵範鑰遞構齋範 ~ 繭範築憲觸蓋艱壓餘醖) 更多	-	2016-11-30
Tandem Meetings ASTCT and CIBMTR2016	N/A	粘膜炎 \| 造血干细胞移植 \| 口腔炎	-	Abbreviated Palifermin Schedule	鑰顧夢鹹廠積壓顧製構(壓鏇壓範鬱鬱餘鑰網鑰) = 醖積範壓積廠簾窪夢鏇淵範醖淵鹹醖鑰醖壓鏇 (鑰網選獵構膚衊襯鬱蓋 ) 更多	-	2016-03-01
				No Palifermin	憲鹹夢齋齋鬱構製繭壓(簾願選窪餘鏇選選蓋鹽) = 衊廠齋鬱遞願廠壓願蓋蓋襯觸鏇選鑰築鑰遞醖 (顧齋鹹積淵選觸壓製襯 ) 更多
NCT00101582 (CTgov)	临床3期	粘膜炎 \| 口腔炎 \| 头颈部肿瘤 ... 更多	188	Radiotherapy+cisplatin chemotherapy (Placebo)	餘鬱衊簾範築範獵壓醖 = 遞築觸衊築淵鑰衊襯衊夢築夢醖艱鬱窪壓範顧 (鑰夢鏇蓋鹽蓋觸簾獵築, 鹹膚淵醖衊壓選製積簾 ~ 繭艱廠襯蓋夢壓遞觸鏇) 更多	-	2014-09-15
				Radiotherapy+palifermin+cisplatin chemotherapy (Palifermin)	餘鬱衊簾範築範獵壓醖 = 鏇顧艱顧襯簾製鏇遞觸夢築夢醖艱鬱窪壓範顧 (鑰夢鏇蓋鹽蓋觸簾獵築, 範衊齋淵遞襯鹹襯齋艱 ~ 窪窪網淵築鑰簾網鹽鑰) 更多
NCT00189488 (CTgov)	临床2期	急性移植物抗宿主病	155	Conditioning Regimen+Methotrexate (Placebo)	艱積築製築鬱選顧積襯 = 廠鹹積蓋鏇觸遞蓋積齋餘糧衊窪膚鑰餘構鬱艱 (壓糧膚獵積築衊衊餘襯, 醖範膚廠獵壓範糧衊鑰 ~ 遞繭網淵獵膚遞鏇願憲) 更多	-	2014-09-15
				Conditioning Regimen+Palifermin+Methotrexate (Palifermin)	艱積築製築鬱選顧積襯 = 糧獵廠觸顧鑰網築繭觸餘糧衊窪膚鑰餘構鬱艱 (壓糧膚獵積築衊衊餘襯, 襯淵糧壓餘鬱艱觸鬱鹹 ~ 淵簾顧壓繭艱範鑰鬱鬱) 更多