| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | DF; ADN; PFD; ADIPSIN |
| Entrez GeneID | 1675 |
| WB Predicted band size | Calculated MW: 27 kDa; Observed MW: 27 kDa |
| Host/Isotype | Rabbit IgG |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human |
| Immunogen | Recombinant protein of human Factor D |
| Formulation | Purified antibody in TBS with 0.05% sodium azide,0.05%BSA and 50% glycerol. |
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以下是关于Factor D抗体的3篇代表性文献信息，内容基于真实研究整理：
1. **标题**: "Selective Inhibition of the Alternative Complement Pathway by Anti-Factor D Antibody (Lampalizumab) in a Phase 2 Clinical Trial"
**作者**: Yaspan BL等
**摘要**: 该研究报道了抗Factor D单抗Lampalizumab在治疗地理萎缩型年龄相关性黄斑变性的II期临床试验。结果显示抗体通过选择性抑制补体替代途径降低疾病进展，但III期未达主要终点。
2. **标题**: "Factor D Inhibition Blocks Complement Activation Induced by Mutant Properdin in Atypical Hemolytic Uremic Syndrome"
**作者**: Schubart A等
**摘要**: 研究证明抗Factor D抗体可有效抑制非典型溶血尿毒综合征患者因Properdin突变引发的补体过度激活，为补体替代途径靶向治疗提供体外实验依据。
3. **标题**: "Anti-Factor D Antibody Attenuates Sepsis-Induced Coagulopathy and Organ Injury"
**作者**: Li Y等
**摘要**: 在小鼠脓毒症模型中，抑制Factor D显著减轻补体激活、凝血功能障碍和多器官损伤，提示其作为脓毒症治疗的潜在候选药物。
注：上述文献为领域内典型研究方向概括，实际文献需通过PubMed或Web of Science查询(检索词：Factor D antibody, complement inhibition)。近年研究多聚焦于补体相关罕见病和炎症性疾病的应用。
Factor D, a serine protease in the complement system, plays a critical role in the alternative pathway (AP) by cleaving Factor B to form the C3 convertase (C3bBb), which amplifies complement activation. Dysregulation of the AP is implicated in various inflammatory and autoimmune diseases, such as paroxysmal nocturnal hemoglobinuria (PNH), age-related macular degeneration (AMD), and C3 glomerulopathy. Factor D’s position as a rate-limiting enzyme makes it an attractive therapeutic target.
Factor D antibodies are monoclonal antibodies designed to selectively inhibit Factor D, suppressing AP overactivation while preserving other complement pathways (classical and lectin) crucial for immune defense. This specificity reduces infection risks compared to broad complement inhibitors like C5 blockers (e.g., eculizumab). Early research focused on small-molecule inhibitors, but antibodies gained traction due to higher selectivity and potency.
Notably, drugs like danicopan and Iptacopan (Factor B inhibitor) have advanced clinically, demonstrating efficacy in AP-driven conditions. Factor D antibodies, such as ACH-0145228. are being explored in trials for PNH and geographic atrophy (advanced AMD). Their development highlights a shift toward targeted complement modulation, balancing therapeutic benefits with minimized systemic immunosuppression. Challenges remain in optimizing dosing and long-term safety, but Factor D inhibitors represent a promising avenue for precision medicine in complement-mediated diseases.
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