POT-4
(Synonyms: AL-78898A) 目录号 : GC63151
POT-4 (AL-78898A)，一种 Compstatin 衍生物，是补体因子 C3 激活的有效抑制剂。POT-4 可用于与年龄相关的黄斑变性的研究。
Cas No.:934461-40-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
POT-4 (AL-78898A), a Compstatin derivative, is a potent inhibitor of complement factor C3 activation. POT-4 can be used for age-related macular degeneration research[1][2]
A derivative of compstatin, a potent C3 inhibitor, POT-4 is a cyclic peptide that exhibits binding activity to C3, preventing cleavage to its active fragments C3a and C3b[2].
[1]. S. Kaushal, et al. Complement C3 inhibitor POT-4: Clinical Safety of Intravitreal Administration. ARVO Annual Meeting Abstract, 2009 Apr.
[2]. Robyn Troutbeck, et al. Therapeutic targeting of the complement system in age-related macular degeneration: a review. Clin Exp Ophthalmol. Jan-Feb 2012;40(1):18-26.
| Cas No. | 934461-40-2 | SDF | |
| 别名 | AL-78898A | ||
| 分子式 | C72H102N22O18S2 | 分子量 | 1627.85 |
| 溶解度 | 储存条件 | Store at -20°C | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.6143 mL | 3.0715 mL | 6.1431 mL |
| 5 mM | 0.1229 mL | 0.6143 mL | 1.2286 mL |
| 10 mM | 0.0614 mL | 0.3072 mL | 0.6143 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Discovering C3 targeting therapies for paroxysmal nocturnal hemoglobinuria: Achievements and pitfalls
Semin Immunol 2022 Jan;59:101618.PMID:35764467DOI:10.1016/j.smim.2022.101618.
The treatment of paroxysmal nocturnal hemoglobinuria (PNH) was revolutionized by the introduction of the anti-C5 agent eculizumab, which resulted in sustained control of intravascular hemolysis, leading to transfusion avoidance and hemoglobin stabilization in at least half of all patients. Nevertheless, extravascular hemolysis mediated by C3 has emerged as inescapable phenomenon in PNH patients on anti-C5 treatment, frequently limiting its hematological benefit. More than 10 years ago we postulated that therapeutic interception of the complement cascade at the level of C3 should improve the clinical response in PNH. Compstatin is a 13-residue disulfide-bridged peptide binding to both human C3 and C3b, eventually disabling the formation of C3 convertases and thereby preventing complement activation via all three of its activating pathways. Several generations of compstatin analogs have been tested in vitro, and their clinical evaluation has begun in PNH and other complement-mediated diseases. Pegcetacoplan, a pegylated form of the compstatin analog POT-4, has been investigated in two phase I/II and one phase III study in PNH patients. In the phase III study, PNH patients with residual anemia already on eculizumab were randomized to receive either pegcetacoplan or eculizumab in a head-to-head comparison. At week 16, pegcetacoplan was superior to eculizumab in terms of hemoglobin change from baseline (the primary endpoint), as well as in other secondary endpoints tracking intravascular and extravascular hemolysis. Pegcetacoplan showed a good safety profile, even though breakthrough hemolysis emerged as a possible risk requiring additional attention. Here we review all the available data regarding this innovative treatment that has recently been approved for the treatment of PNH.
Emerging pharmacologic therapies for wet age-related macular degeneration
Ophthalmologica 2009;223(6):401-10.PMID:19622904DOI:10.1159/000228926.
As researchers and clinicians are beginning to understand that wet age-related macular degeneration (AMD) is more than simply a vascular disease that includes angiogenic, vascular and inflammatory components, they are exploring new agents with different mechanisms of action addressing multiple targets in this complex pathophysiology. Some of them are already available in human trials or even approved vascular epithelial growth factor (VEGF) blockers such as Macugen, Lucentis, Avastin, VEGF Trap-Eye and Cand5; VEGF receptor blockers such as TG100801, vatalanib, pazopanib, Sirna-027 and a vaccine approach; inflammation inhibitors and immunosuppressants such as Retaane, Kenalog, ARC1905, POT-4, OT-551. The last group is mixed, containing agents such as Zybrestat, AdPEGF, Sirolimus, JSM6427, ATG003, E10030. This article reviews these currently emerging agents and briefly discusses the next step for the treatment of wet AMD.
Update on current and future novel therapies for dry age-related macular degeneration
Expert Rev Clin Pharmacol 2013 Sep;6(5):565-79.PMID:23971874DOI:10.1586/17512433.2013.829645.
Age-related macular degeneration (ARMD) is the leading cause of irreversible blindness in developed countries. There are currently no cures, but there are promising potential therapies that target the underlying disease mechanisms of dry ARMD. Stem cells, ciliary neurotrophic factor, rheopheresis, ozonated autohemotherapy and prostaglandins show promise in stabilizing or improving visual acuity. Age-Related Eye Disease Study vitamins may reduce progression to severe ARMD. Adjuvant therapy like low vision rehabilitation and implantable miniature telescopes may help patients adjust to the sequelae of their disease, and herbal supplementation with saffron, zinc monocysteine and phototrop may be helpful. Therapies that are currently in clinical trials include brimonidine, doxycycline, anti-amyloid antibodies (GSK933776 and RN6G), RPE65 inhibitor (ACU-4429), complement inhibitors (ARC1905, FCFD4514S), hydroxychloroquine, intravitreal fluocinolone acetate and vasodilators like sildenafil, moxaverine and MC-1101. Therapies that have not been shown to be effective include POT-4, eculizumab, tandospirone, anecortave acetate, the antioxidant OT-551, sirolimus and vitamin E.
Corticosteroids and Anti-Complement Therapy in Retinal Diseases
Handb Exp Pharmacol 2017;242:309-320.PMID:27815789DOI:10.1007/164_2016_22.
Corticosteroids are unique in that they are the one class of agents that acts upon most of the multiple processes in the pathophysiology of macular edema. Corticosteroids are capable of inhibiting prostaglandin and leukotriene synthesis as well as interfering with intercellular adhesion molecule-1 (ICAM-1), interleukin-6, VEGF-A, and stromal cell derived factor-1 pathways. Triamcinolone, dexamethasone, and fluocinolone have been extensively used in the treatment of retinal and choroidal vascular diseases. Sustained release implants of steroids have reduced the burden of repeated intravitreal injections necessary in most of the retinal diseases. Complement factors play an important role in the pathogenesis of age-related macular degeneration (AMD). Inhibitors of complement could provide a breakthrough in the treatment of dry AMD. Complement factor inhibitors, such as POT-4, lampalizumab, and eculizumab, have been tested in clinical trials for dry AMD with promising results. However, results of phase 3 trials are awaited.