P7C3-A20 - CAS 1235481-90-9
Catalog number: B0084-462293
Category: Inhibitor
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Molecular Weight:
P7C3-A20, an analogue of P7C3, is a neuroprotective compound which inhibits mature neuronal cell death while also increasing the net magnitude of postnatal neurogenesis in models of neurodegeneration and acute injury.
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Catalog Number Size Price Stock Quantity
B0084-462293 100 mg $198 In stock
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Light yellow solid to semi-solid powder
N-(3-(3,6-dibromo-9H-carbazol-9-yl)-2-fluoropropyl)-3-methoxyaniline; P7C-3A20; P7C3A20; P7C 3A20
Store in a cool and dry place (or refer to the Certificate of Analysis).
Boiling Point:
641.3±55.0 °C at 760 Torr
1.57±0.1 g/cm3
Canonical SMILES:
1.Protective efficacy of P7C3-S243 in the 6-hydroxydopamine model of Parkinson's disease.
De Jesús-Cortés H;Miller AD;Britt JK;DeMarco AJ;De Jesús-Cortés M;Stuebing E;Naidoo J;Vázquez-Rosa E;Morlock L;Williams NS;Ready JM;Narayanan NS;Pieper AA NPJ Parkinsons Dis. 2015;1. pii: 15010. Epub 2015 May 21.
BACKGROUND: ;There are currently no therapeutic options for patients with Parkinson's disease that prevent or slow the death of dopaminergic neurons. We have recently identified the novel P7C3 class of neuroprotective molecules that blocks neuron cell death.;AIMS: ;The aim of this study was to determine whether treatment with highly active members of the P7C3 series blocks dopaminergic neuron cell death and associated behavioral and neurochemical deficits in the rat 6-hydroxydopamine (6-OHDA) model of Parkinson's disease.;METHODS: ;After unilateral injection of 6-OHDA into the median forebrain bundle, rats were assessed for behavioral function in the open field, cylinder test, and amphetamine-induced circling test. Thereafter, their brains were subjected to neurochemical and immunohistochemical analysis of dopaminergic neuron survival. Analysis was conducted as a function of treatment with P7C3 compounds, with administration initiated either before or after 6-OHDA exposure.;RESULTS: ;Animals administered P7C3-A20 or P7C3-S243, two of the most advanced agents in the P7C3 series of neuroprotective compounds, both before and after 6-OHDA exposure showed evidence of protective efficacy in all measures.
2.Pharmacological augmentation of nicotinamide phosphoribosyltransferase (NAMPT) protects against paclitaxel-induced peripheral neuropathy.
LoCoco PM;Risinger AL;Smith HR;Chavera TS;Berg KA;Clarke WP Elife. 2017 Nov 10;6. pii: e29626. doi: 10.7554/eLife.29626.
Chemotherapy-induced peripheral neuropathy (CIPN) arises from collateral damage to peripheral afferent sensory neurons by anticancer pharmacotherapy, leading to debilitating neuropathic pain. No effective treatment for CIPN exists, short of dose-reduction which worsens cancer prognosis. Here, we report that stimulation of nicotinamide phosphoribosyltransferase (NAMPT) produced robust neuroprotection in an aggressive CIPN model utilizing the frontline anticancer drug, paclitaxel (PTX). Daily treatment of rats with the first-in-class NAMPT stimulator, P7C3-A20, prevented behavioral and histologic indicators of peripheral neuropathy, stimulated tissue NAD recovery, improved general health, and abolished attrition produced by a near maximum-tolerated dose of PTX. Inhibition of NAMPT blocked P7C3-A20-mediated neuroprotection, whereas supplementation with the NAMPT substrate, nicotinamide, potentiated a subthreshold dose of P7C3-A20 to full efficacy. Importantly, P7C3-A20 blocked PTX-induced allodynia in tumored mice without reducing antitumoral efficacy. These findings identify enhancement of NAMPT activity as a promising new therapeutic strategy to protect against anticancer drug-induced peripheral neurotoxicity.
3.Novel Protective Role of Nicotinamide Phosphoribosyltransferase in Acetaminophen-Induced Acute Liver Injury in Mice.
Zhang LQ;Nsumu M;Huang P;Heruth DP;Riordan SM;Shortt K;Zhang N;Grigoryev DN;Li DY;Friesen CA;Van Haandel L;Leeder JS;Olson J;Ye SQ Am J Pathol. 2018 Jul;188(7):1640-1652. doi: 10.1016/j.ajpath.2018.04.004. Epub 2018 Apr 22.
Acetaminophen overdose is the most common cause of acute liver injury (ALI) or acute liver failure in the United States. Its pathogenetic mechanisms are incompletely understood. Additional studies are warranted to identify new genetic risk factors for more mechanistic insights and new therapeutic target discoveries. The objective of this study was to explore the role and mechanisms of nicotinamide phosphoribosyltransferase (NAMPT) in acetaminophen-induced ALI. C57BL/6 Nampt gene wild-type (Nampt;+/+;), heterozygous knockout (Nampt;+/-;), and overexpression (Nampt;OE;) mice were treated with overdose of acetaminophen, followed by histologic, biochemical, and transcriptomic evaluation of liver injury. The mechanism of Nampt in acetaminophen-induced hepatocytic toxicity was also explored in cultured primary hepatocytes. Three lines of evidence have convergently demonstrated that acetaminophen overdose triggers the most severe oxidative stress and necrosis, and the highest expression of key necrosis driving genes in Nampt;+/-; mice, whereas the effects in Nampt;OE; mice were least severe relative to Nampt;+/+; mice. Treatment of P7C3-A20, a small chemical molecule up-regulator of Nampt, ameliorated acetaminophen-induced mouse ALI over the reagent control.
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CAS 1235481-90-9 P7C3-A20

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