Fodipir (DPDP)
(Synonyms: 福地吡; DPDP) 目录号 : GC31992Fodipir (DPDP) 是 mangafodipir 的一种活性代谢物,参与 mangafodipir 介导的针对 &7#946;-羟基胆固醇诱导的细胞死亡的细胞保护作用。
Cas No.:118248-91-2
Sample solution is provided at 25 µL, 10mM.
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Fodipir is an active metabolite of mangafodipir, involved in mangafodipir-mediated cytoprotection against 7β-hydroxycholesterol-induced cell death.
Fodipir is an active metabolite of mangafodipir, involved in mangafodipir-mediated cytoprotection against 7β-hydroxycholesterol-induced cell death. Fodipir (Dp-dp; Dipyridoxyl diphosphate; 100 μM) shows the best cytopretective effect on 7β-OH-mediated cell death after treatment for 8 h. Fodipir also reduces 7β-OH-induced cellular ROS production and lysosomal membrane permeabilization (LMP)[1].
[1]. Laskar A, et al. Fodipir and its dephosphorylated derivative dipyridoxyl ethyldiamine are involved in mangafodipir-mediated cytoprotection against 7β-hydroxycholesterol-induced cell death. Pharmacology. 2013;92(3-4):182-6.
Cas No. | 118248-91-2 | SDF | |
别名 | 福地吡; DPDP | ||
Canonical SMILES | CC1=NC=C(COP(O)(O)=O)C(CN(CC(O)=O)CCN(CC(C(COP(O)(O)=O)=CN=C2C)=C2O)CC(O)=O)=C1O | ||
分子式 | C22H32N4O14P2 | 分子量 | 638.46 |
溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg | |
1 mM | 1.5663 mL | 7.8313 mL | 15.6627 mL |
5 mM | 0.3133 mL | 1.5663 mL | 3.1325 mL |
10 mM | 0.1566 mL | 0.7831 mL | 1.5663 mL |
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Evidence that fodipir (DPDP) binds neurotoxic Pt2+ with a high affinity: An electron paramagnetic resonance study
Oxaliplatin typically causes acute neuropathic problems, which may, in a dose-dependent manner, develop into a chronic form of chemotherapy-induced peripheral neuropathy (CIPN), which is associated with retention of Pt2+ in the dorsal root ganglion. A clinical study by Coriat and co-workers suggests that co-treatment with mangafodipir [Manganese(II) DiPyridoxyl DiPhosphate; MnDPDP] cures ongoing CIPN. These authors anticipated that it is the manganese superoxide dismutase mimetic activity of MnDPDP that explains its curative activity. However, this is questionable from a pharmacokinetic perspective. Another, but until recently undisclosed possibility is that Pt2+ outcompetes Mn2+/Ca2+/Zn2+ for binding to DPDP or its dephosphorylated metabolite PLED (diPyridoxyL EthylDiamine) and transforms toxic Pt2+ into a non-toxic complex, which can be readily excreted from the body. We have used electron paramagnetic resonance guided competition experiments between MnDPDP (10logKML ≈ 15) and K2PtCl4, and between MnDPDP and ZnCl2 (10logKML ≈ 19), respectively, in order to obtain an estimate the 10logKML of PtDPDP. Optical absorption spectroscopy revealed a unique absorption line at 255 nm for PtDPDP. The experimental data suggest that PtDPDP has a higher formation constant than that of ZnDPDP, i.e., higher than 19. The present results suggest that DPDP/PLED has a high enough affinity for Pt2+ acting as an efficacious drug in chronic Pt2+-associated CIPN.
Fodipir and its dephosphorylated derivative dipyridoxyl ethyldiamine are involved in mangafodipir-mediated cytoprotection against 7β-hydroxycholesterol-induced cell death
Objective: Mangafodipir exerts pharmacological effects, including vascular relaxation and protection against oxidative stress and cell death induced by oxysterols. Additionally, mangafodipir has been proposed for cardiovascular imaging. The primary metabolites of mangafodipir, manganese dipyridoxyl ethyldiamine (MnPLED) and its constituent dipyridoxyl diphosphate (Dp-dp) also known as fodipir, are pharmacologically active. However, whether they affect oxysterol-induced cytotoxicity is currently unknown. In this study, we examine whether the mangafodipir metabolite affects 7β-hydroxycholesterol (7β-OH)-induced cell death and identify the underlying mechanisms.
Methods: U937 cells were pretreated or not with mangafodipir substrate (Ms; 200 ?m), MnPLED (100 ?mol/l) or Dp-dp (100 ?mol/l) for 8 h and then exposed to 7β-OH (28 ?mol/l) for 18 h.
Results: Our results revealed that pretreatment with MnPLED or Dp-dp protected against 7β-OH-induced cellular reactive oxygen species (ROS) production, apoptosis, and lysosomal membrane permeabilization (LMP). MnPLED and Dp-dp, in par with Ms, confer protection against 7β-OH-induced cytotoxicity by reducing cellular ROS and stabilization of the lysosomal membrane.
Conclusion: These results suggest that fodipir is the pharmacologically active part in the structure of mangafodipir, which prevents 7β-OH-induced cell death by attenuating cellular ROS and by preventing LMP. In addition, MnPLED, which is the dephosphorylated product of fodipir, exerts a similar protective effect against 7β-OH-induced cytotoxicity. This result indicates that dephosphorylation of fodipir does not affect its pharmacological actions. Altogether our result confirms the cytoprotective effect of mangafodipir and justifies its potential use as a cytoprotective adjuvant.