Alendronate sodium hydrate - CAS 121268-17-5
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Not Intended for Therapeutic Use. For research use only.
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Alendronate, a nitrogen-containing bisphosphonate, is a potent inhibitor of bone resorption used for the treatment and prevention of osteoporosis.
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G-704650, MK-217
1.[Minodronic acid hydrate as a new therapeutic agent for osteoporosis].
Chatani Y1. Clin Calcium. 2005 Jan;15(1):9-14.
Minodronic acid hydrate is one of the new-generation bisphosphonates containing nitrogen. The drug has an inhibitory effect on bone resorption by suppressing the osteoclastic function. Minodronic acid hydrate is being developed as a therapeutic drug of osteoporosis. In non-clinical study, the inhibitory effect of minodronic acid hydrate on the decrease in the bone mineral density and on the reduction in the bone intensity in ovariectomized rat osteoporosis models. The results of the clinical studies conducted so far showed that minodronic acid hydrate administered once daily for 36 weeks increases the bone mineral density of lumbar spine (L2-4BMD) significantly compared to the placebo group. It was speculated that minodronic acid hydrate has an increasing effect on the bone mineral density that is at least equivalent to that of alendronate and risedronate. It was also expected that the incidence of digestive diseases with minodronic acid hydrate is lower than that with the existing bisphosphonates.
2.[Pharmacological and clinical properties of alendronate sodium hydrate].
Ohta T1, Komatsu S, Tokutake N. Nihon Yakurigaku Zasshi. 2002 Dec;120(6):409-19.
Alendronate (alendronate sodium hydrate; Bonalon Tablet, 5 mg) is a nitrogen-containing bisphosphonate, which combines with the bone surface and reduces osteoclast-mediated bone resorption. It is a third-generation bisphosphonate compound, specifically distributed on the surface of bone resorption and taken into osteoclasts. Under the closed circumstances which is formed with osteoclast and the bone surface, alendronate becomes detached from the bone surface and taken into osteoclast since acid released from osteoclast leads to pH decrease (acidified). The uptaken alendronate blocks the pathway of mevalonic acid synthesis, which is cholesteric synthesis, inhibits the prenylation of GTP binding protein, and decreases the osteoclast's function by influencing the cytoskeleton. This restraint of alendronate in bone resorption against osteoclasts is reversible, showing no cytotoxicity at more than hundredfold concentration level at which action occurs.
3.Glucocorticoid Steroid and Alendronate Treatment Alleviates Dystrophic Phenotype with Enhanced Functional Glycosylation of α-Dystroglycan in Mouse Model of Limb-Girdle Muscular Dystrophy with FKRPP448L Mutation.
Wu B1, Shah SN2, Lu P2, Milazi S2, Bollinger LE2, Blaeser A2, Madden KL2, Sun Y3, Luckie TM2, Cox MD3, Sparks S4, Harper AD4, Lu QL5. Am J Pathol. 2016 Apr 21. pii: S0002-9440(16)30059-1. doi: 10.1016/j.ajpath.2016.02.015. [Epub ahead of print]
Fukutin-related protein-muscular dystrophy is characterized by defects in glycosylation of α-dystroglycan with variable clinical phenotypes, most commonly as limb-girdle muscular dystrophy 2I. There is no effective therapy available. Glucocorticoid steroids have become the standard treatment for Duchenne and other muscular dystrophies with serious adverse effects, including excessive weight gain, immune suppression, and bone loss. Bisphosphonates have been used to treat Duchenne muscular dystrophy for prevention of osteoporosis. Herein, we evaluated prednisolone and alendronate for their therapeutic potential in the FKRPP448L-mutant mouse representing moderate limb-girdle muscular dystrophy 2I. Mice were treated with prednisolone, alendronate, and both in combination for up to 6 months. Prednisolone improved muscle pathology with significant reduction in muscle degeneration, but had no effect on serum creatine kinase levels and muscle strength.
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CAS 121268-17-5 Alendronate sodium hydrate

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