Benserazide hydrochloride

Research use only, not for human use.

Benserazide Hydrochloride is a peripherally-acting aromatic L-amino acid decarboxylase (AAAD) or DOPA decarboxylase inhibitor.

Benserazide Hydrochloride is a peripherally-acting aromatic L-amino acid decarboxylase (AAAD) or DOPA decarboxylase inhibitor.(In Vitro):Benserazide hydrochloride (BH) and Levodopa (LD) individually and in combination (Benserazide hydrochloride + LD) (25 μM; 0 hour, 12 hours, 24 hours and 168 hours; SH-SY5Y) treatment inhibit protein aggregation and have the ability to minimise the amyloid-induced cytotoxicity in human neuroblastoma cell line. Benserazide hydrochloride and LD both can act as efficient inhibitors of the formation of cytotoxic HSA aggregates, and the inhibitory effects are more pronounced when both of these drugs are added simultaneously.(In Vivo):Benserazide (5-50 mg/kg; intraperitoneal injection; male Wistar rats) treatment of 6-OHDA-lesioned rats increases exogenous L-DOPA-derived extracellular DA levels, the time to reach the peak DA levels are significantly prolong by Benserazide dose-dependently. The AADC activity in the denervates striatal tissues shows a significant decrease by 10 mg/kg and 50 mg/kg Benserazide. Benserazide reduces the central AADC activity in the striatum of rats with nigrostriatal denervation, which leads to changes in the metabolism of exogenous L-DOPA.

Benserazide hydrochloride (BH) and Levodopa (LD) individually and in combination (Benserazide hydrochloride?+?LD) (25 μM; 0 hour, 12 hours, 24 hours and 168 hours; SH-SY5Y) treatment inhibit protein aggregation and have the ability to minimise the amyloid-induced cytotoxicity in human neuroblastoma cell line. Benserazide hydrochloride and LD both can act as efficient inhibitors of the formation of cytotoxic HSA aggregates, and the inhibitory effects are more pronounced when both of these drugs are added simultaneously. Cell Viability Assay Cell Line:SH-SY5Y cells Concentration:25 μM Incubation Time:0 hour, 12 hours, 24 hours and 168 hours Result:Enhanced cell viability, and inhibited the formation of cytotoxic human serum albumin (HSA) aggregates.

Benserazide (5-50 mg/kg; intraperitoneal injection; male Wistar rats) treatment of 6-OHDA-lesioned ratsincreases exogenous L-DOPA-derived extracellular DA levels, the time to reach the peak DA levels are significantly prolong by Benserazide dose-dependently. The AADC activity in the denervates striatal tissues shows a significant decrease by 10 mg/kg and 50 mg/kg Benserazide. Benserazide reduces the central AADC activity in the striatum of rats with nigrostriatal denervation, which leads to changes in the metabolism of exogenous L-DOPA. Animal Model:Male Wistar rats with 6-hydroxydopamine (6-OHDA) (8 Ag/4 Al)Dosage:5 mg/kg, 10 mg/kg or 50 mg/kg (Pharmacokinetic study)Administration:Intraperitoneal injection Result:Increased in exogenous L-DOPA-derived extracellular DA levels, the time to reach the peak DA levels were significantly prolonged in a dose-dependent fashion. The AADC activity in the denervated striatal tissues showed a significant decreased by 10 mg/kg and 50 mg/kg.

Ro 4-4602

GPCR/G Protein

Dopamine Receptor

DOPA decarboxylase| Dopamine

Neurological Disease

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14919-77-8

293.7

C10H15N3O5·HCl

>98% (HPLC)

Ethanol: 1 mg/mL warmed (3.4 mM); Water: 58 mg/mL (197.48 mM); DMSO: 58 mg/mL (197.48 mM)

Cl.NC(CO)C(=O)NNCC1=C(O)C(O)=C(O)C=C1

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(-20℃)

With Ice Pack

≥ 2 years