FeTMPyP 

FeTMPyP is an orally active poly (ADP-ribose) polymerase (PARP) inhibitor. FeTMPyP inhibits cell death, nitrotyrosine formation, and depolarization of mitochondrial transmembrane potential. FeTMPyP reduces homocysteine-induced nitrosative stress and partially restores TFEB protein and mRNA levels. FeTMPyP improves functional and behavioral deficits caused by chronic constriction injury in rats. FeTMPyP alleviates acute cerebral infarction in a rat model of middle cerebral artery occlusion with mild hyperglycemia. FeTMPyP can be used in studies related to neuropathic pain, renal aging, ischemic penumbra, and hyperglycemic stroke^[1][2][3][4].

FeTMPyP partially rescues the reduction in TFEB protein expression caused by Hcy stimulation in MPC-5 mouse podocyte cells^[2].
FeTMPyP (0.01-100 μM; 6 h) concentration-dependently reduces LDH release, a marker of cell death, in glucose-deprived immunostimulated rat prefrontal cortex astrocytes after 6 h of treatment^[3].
FeTMPyP (0.01-100 μM; 4 h) reduces LDH release in SIN-1-treated, glucose-deprived rat prefrontal cortex astrocytes after 4 h of treatment^[3].
FeTMPyP (10 μM; 6 h) inhibits the increase in nitrotyrosine immunoreactivity, a marker of peroxynitrite, in glucose-deprived immunostimulated rat prefrontal cortex astrocytes^[3].
FeTMPyP (10 μM; 3 h) inhibits the increase in nitrotyrosine immunoreactivity, a marker of peroxynitrite, in SIN-1-treated, glucose-deprived rat prefrontal cortex astrocytes^[3].
FeTMPyP (0.33-50 μM; 15 min) concentration-dependently inhibits peroxynitrite-mediated tyrosine nitration of bovine serum albumin in a cell-free assay after 15 min of incubation^[3].
FeTMPyP (10 μM) inhibits peroxynitrite-mediated oxidation of DCF-H to DCF in SIN-1-treated, glucose-deprived rat prefrontal cortex astrocytes^[3].
FeTMPyP (10 μM; 3 h) prevents mitochondrial transmembrane potential depolarization in SIN-1-treated, glucose-deprived rat prefrontal cortex astrocytes over 3 h of co-treatment^[3].
FeTMPyP (50 μM; full experimental protocol) reverses HG MCAO plasma-induced increases in myogenic tone and lumen narrowing in isolated nonischemic rat MCA, likely via inhibiting the vasoconstricting properties of peroxynitrite^[4].
FeTMPyP (50 μM; full experimental protocol) does not alter HG Sham plasma-induced increases in myogenic tone in isolated nonischemic rat MCA, indicating peroxynitrite is not involved in this response^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

FeTMPyP (1-3 mg/kg; p.o.; daily; 14 days) administered orally at 1 and 3 mg/kg daily for 14 days significantly ameliorates chronic constriction injury-induced neuropathic pain in rats, with the 3 mg/kg dose producing statistically significant improvements in functional, behavioral, oxidative/nitrosative, inflammatory, bioenergetic, DNA damage, PARP activation, and mitochondrial outcomes relative to injury controls^[1].
FeTMPyP (10 mg/kg; i.v.; single dose 10 minutes before reperfusion) acutely reduces corrected acute infarct volume by ~72% in hyperglycemic rats with mild ischemic stroke (<68% CBF decrease) but provides no neuroprotection in rats with severe ischemic stroke (>68% CBF decrease), with no effect on reperfusion CBF^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

909.92

C₄₄H₃₆Cl₅FeN₈

133314-07-5

Solid

Brown to black

C[N+](C=C1)=CC=C1C2=C3C=CC(C(C4=CC=[N+](C)C=C4)=C5C=CC([N-]56)=C7C8=CC=[N+](C)C=C8)=[N]3[Fe+3]96[N]%10=C7C=CC%10=C(C%11=CC=[N+](C)C=C%11)C%12=CC=C2[N-]%129.[5Cl-]

Room temperature in continental US; may vary elsewhere.

-20°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

• [1]. Komirishetty P, et al. FeTMPyP a peroxynitrite decomposition catalyst ameliorated functional and behavioral deficits in chronic constriction injury induced neuropathic pain in rats. Free Radic Res. 2021;55(9-10):1005-1017.  [Content Brief]

  [2]. Zhang S, et al. Nitrative Stress-Related Autophagic Insufficiency Participates in Hyperhomocysteinemia-Induced Renal Aging. Oxid Med Cell Longev. 2020;2020:4252047. Published 2020 Jan 25.  [Content Brief]

  [3]. Choi IY, et al. Augmented death in immunostimulated astrocytes deprived of glucose: inhibition by an iron porphyrin FeTMPyP. J Neuroimmunol. 2001;112(1-2):55-62.  [Content Brief]

  [4]. Palomares SM, et al. Peroxynitrite decomposition with FeTMPyP improves plasma-induced vascular dysfunction and infarction during mild but not severe hyperglycemic stroke. J Cereb Blood Flow Metab. 2012;32(6):1035-1045.  [Content Brief]