[iron(III)(C19H6N2(C6F5)3(SO3H)2] | 849593-33-5

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 英文名称: [iron(III)(C19H6N2(C6F5)3(SO3H)2]
• 英文别名: 5,10,15-tris(pentafluorophenyl)-2,17-bis(sulfonic acid)corrolatoiron(III)；2,17-bis(sulfonato)-5,10,15-tris(pentafluorophenyl)-corrolato iron(III)
• CAS: 849593-33-5
• 化学式: C₃₇H₈F₁₅FeN₄O₆S₂
• 分子量: 1009.45
• InChiKey: WBTWUJCCEVDFTO-QDWXPRJESA-N

反应信息

• 作为反应物：
  描述：

  N-甲基咪唑 、 [iron(III)(C19H6N2(C6F5)3(SO3H)2] 以 aq. phosphate buffer 为溶剂， 生成 、
  参考文献：
  名称：

  用于限制淀粉样β肽聚集和活性氧生成的催化抗氧化剂†

  摘要：

  阿尔茨海默病 (AD) 是一种多方面的疾病，其特征是氧化应激增加、金属离子失调以及细胞内神经原纤维缠结和细胞外淀粉样蛋白-β (Aβ) 聚集体的形成。在这项工作中，我们报告了铁（ III ）2,17-双磺基-5,10,15-三（五氟苯基）咔咯络合物FeL1与Aβ肽（ K d ∼ 10 -7 ）的大亲和力结合，以及结合的FeL1在存在和不存在 Cu( II ) 离子的情况下充当催化抗氧化剂的能力。具体发现是：（a）Aβ组氨酸残基与FeL1轴向结合； (b) 所得加合物是有效的过氧化氢酶； (c)这种相互作用限制了高分子量肽聚集体的形成。紫外-可见光和电子顺磁共振（EPR）研究表明，虽然FeL1的结合不影响Aβ-Cu（ II ）相互作用（ K d ∼ 10 -10 ），但结合的FeL1仍然充当抗氧化剂，从而显着限制活性氧Aβ-Cu 产生物种 (ROS)。总体而言， FeL1显示与 Aβ 肽结合并调节肽聚集。此外，

  DOI：

  10.1039/c8sc04660c
• 作为产物：
  描述：

  2,17-disulphonato-5,10,15-tris(pentafluorophenyl)corrole 在 吡啶 、 iron(II) chloride tetrahydrate 作用下， 反应 0.08h， 以95%的产率得到[iron(III)(C19H6N2(C6F5)3(SO3H)2]
  参考文献：
  名称：

  Neuroprotection against superoxide anion radical by metallocorroles in cellular and murine models of optic neuropathy

  摘要：

  J. Neurochem. (2010) 114, 488–498.AbstractCorroles are tetrapyrrolic macrocycles that have come under increased attention because of their unique capabilities for oxidation catalysis, reduction catalysis, and biomedical applications. Corrole‐metal complexes (metallocorroles) can decompose certain reactive oxygen species (ROS), similar to metalloporphyrins. We investigated whether Fe‐, Mn‐, and Ga‐corroles have neuroprotective effects on neurons and correlated this with superoxide scavenging activity in vitro and in vivo. Apoptosis was induced in retinal ganglion cell‐5 neuronal precursor cells by serum deprivation. Cell death was measured with sodium 3′‐[1‐[(phenylamino)‐carbonyl]‐3,4‐tetrazolium]‐bis (4‐methoxy‐6‐nitro) benzene‐sulfonic acid hydrate and calcein‐AM/propidium iodide assays. Fe‐ and Mn‐corroles, but not the non‐redox‐active Ga‐corrole used as control, reduced RGC‐5 cell death after serum deprivation. Serum deprivation caused increased levels of intracellular superoxide, detected by an increase in the fluorescence intensity of 2‐hydroxyethidium, and this was blocked by Fe‐ and Mn‐corroles, but not Ga‐corrole. In vivo real‐time confocal imaging of retinas after optic nerve transection assessed the superoxide production within individual rat retinal ganglion cells. Fe‐ and Mn‐corroles, but not Ga‐corrole, scavenged neuronal superoxide in vivo. Given that the neuroprotective activity of metallocorroles correlated with superoxide scavenging activity, Fe‐ and Mn‐corroles could be candidate drugs for delaying neuronal death after axonal injury in optic neuropathies, such as glaucoma.

  DOI：

  10.1111/j.1471-4159.2010.06781.x