Risedronic acid (sodium)

Risedronic acid (Risedronate) sodium, a bisphosphonate, is a potent anti-resorption agent that inhibits osteoclast-mediated bone resorption and changes the bone metabolism. Risedronic acid sodium suppresses osteoblast differentiation and induced caspase- and isoprenoid depletion-dependent apoptosis. Risedronic acid sodium inhibits blood stages of Plasmodium falciparum (IC₅₀ of 20.3 μM). Risedronic acid sodium inhibits the transfer of the farnesyl pyrophosphate group to parasite proteins^[1][2][3]. In Vitro:Risedronic acid (0-10 μM; 14 days) sodium suppresses the formation of mineralized nodules in human mesenchymal stem cells (hMSC12) and rat thymus-derived mesenchymal stem cells (ST1BIIb)¹.
Risedronic acid (0-10 μM; 3 days) sodium suppresses the mRNA expression of osteoblast marker gene osteocalcin (OC) in human mesenchymal stem cells (hMSC12)¹.
Risedronic acid (100-1000 μM; 48 h) sodium induces chromatin condensation and activates caspase-3 in human mesenchymal stem cells (hMSC12)¹.
Risedronic acid (Risedronate) (15 μM; 36 h) sodium inhibits isoprenoid biosynthesis in Plasmodium falciparum, as shown by the decreased intensities of bands corresponding to farnesol (FOH) and geranylgeraniol (GGOH)³.
Risedronic acid (15 μM; 36 h) sodium interferes with protein isoprenylation in Plasmodium falciparum, reducing the intensities of farnesylated protein bands and increasing those of geranylgeranylated protein bands³. In Vivo:Risedronic acid (Risedronate) (30 μg/kg; subcutaneous injection; once every other day; 3 weeks) sodium prevents radiation-induced osteoporosis in female C57BL/6 mice irradiated with 2 Gy X-rays, inhibits trabecular bone loss and microstructural damage, and suppresses the increase in osteoclast number and serum TRAP5b².
Risedronic acid (10-25 mg/kg; intraperitoneal injection; once a day; 7 days) sodium inhibits parasitemia in BALB/c mice infected with Plasmodium berghei strain ANKA, but does not prolong the survival time of mice³.