Lumasiran (ALN-G01), a siRNA product, reduces hepatic oxalate production by targeting glycolate oxidase . By silencing the gene encoding glycolate oxidase, Lumasiran depletes glycolate oxidase and thereby inhibits the synthesis of oxalate, which is the toxic metabolite that is directly associated with the clinical manifestations of Primary hyperoxaluria type 1 (PH1).

Lumasiran reduced urinary oxalate excretion, the cause of progressive kidney failure in PH1[1].

Lumasiran sodium is a subcutaneously administered, liver-directed RNA interference (RNAi) therapeutic agent[2].

1834610-13-7

ALN-G01;Lumasiran

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