Treatment with Amodiaquine (10-20 μM; 4 hours) suppresses LPS-induced expression of proinflammatory cytokines (IL-1β, interleukin-6, TNF-α and iNOS) in a dose-dependent manner [1]. Amodiaquine (5 μM; 24 hours) significantly inhibits neurotoxin (6-OHDA-induced cell death in primary dopamine cells as examined by the number of TH + neurons and dopamine uptake. The neuroprotective effect of Amodiaquine is also observed in rat PC12 cells [1]. RT-PCR [1] Cell Line: Primary microglia Concentration: 10 μM, 15 μM, 20 μM Incubation Time: 4 hours Result: Suppressed LPS-induced expression of proinflammatory cytokines (IL-1β, interleukin-6, TNF-α and iNOS) in a dose-dependent manner.

Amodiaquine (40 mg/kg; intraperitoneal injection; daily; for 3 days; male ICR mice) treatment reduces perihematomal activation of microglia/macrophages and astrocytes. Amodiaquine also suppresses ICH-induced mRNA expression of IL-1β, CCL2 and CXCL2, and ameliorated motor dysfunction of mice [2]. Animal Model: Male ICR mice (8-10 weeks of age) induced ntracerebral hemorrhage (ICH) [2] Dosage: 40 mg/kg Administration: Intraperitoneal injection; daily; for 3 days Result: Diminished perihematomal activation of microglia/macrophages and astrocytes.

69-44-3

C20H24Cl3N3O

428.78

Amodiaquine hydrochloride

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years