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Product Details
Nicotinamide,98-92-0,IC-0241160
Nicotinamide is an inhibitor of poly(ADP-ribose) polymerase (PARP-1) enzymes. Poly(ADP-ribose) polymerase-1 (PARP-1) is found as a DNA repair enzyme. The excessive activation of PARP-1, such as ischemia and trauma, can deplete cellular nicotinamide adenine dinucleotide as a substrate and leads to brain cell death eventually. In vitro: Previous findings suggested that nicotinamide had a protective effect against PARP-1-induced astrocyte death. The transporter-mediated uptake of nicotinamide, which was extracellular pH-sensitive and common to N-methylnicotinamide, was found to be critical for prevention of PARP-1-triggered cell death [1]. In vivo: Type 2 diabetes was induced in Wistar rats by streptozotocin followed by nicotinamide. Test compounds and standard treatment were continued for 15 days. Results showed that there was significant normalisation of liver antioxidant enzymes compared to diabetic rats, suggesting all the tested compounds were beneficial in reducing oxidative stress [2]. Clinical trial: Previous clinical trials showed nicotinamide was well tolerated. Phase 1 showed a dose-response relation for proportional change in frataxin protein concentration. Phases 2 and 3 showed daily dosing resulted in a sustained and significant upregulation of frataxin expression [3].
Nicotinamide is an inhibitor of poly(ADP-ribose) polymerase (PARP-1) enzymes. Poly(ADP-ribose) polymerase-1 (PARP-1) is found as a DNA repair enzyme. The excessive activation of PARP-1, such as ischemia and trauma, can deplete cellular nicotinamide adenine dinucleotide as a substrate and leads to brain cell death eventually. In vitro: Previous findings suggested that nicotinamide had a protective effect against PARP-1-induced astrocyte death. The transporter-mediated uptake of nicotinamide, which was extracellular pH-sensitive and common to N-methylnicotinamide, was found to be critical for prevention of PARP-1-triggered cell death [1]. In vivo: Type 2 diabetes was induced in Wistar rats by streptozotocin followed by nicotinamide. Test compounds and standard treatment were continued for 15 days. Results showed that there was significant normalisation of liver antioxidant enzymes compared to diabetic rats, suggesting all the tested compounds were beneficial in reducing oxidative stress [2]. Clinical trial: Previous clinical trials showed nicotinamide was well tolerated. Phase 1 showed a dose-response relation for proportional change in frataxin protein concentration. Phases 2 and 3 showed daily dosing resulted in a sustained and significant upregulation of frataxin expression [3].
