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Bone resorption by osteoclasts is dependent on H+ transport into the external resorption lacunae, generating an acidic microenvironment in which bone mineral dissolution and matrix degradation occur. A vacuolar H+-ATPase is responsible for osteoclast H+ secretion. Here, we describe novel vacuolar H+-ATPase inhibitors that inhibit bone resorption in vitro. Several agents inhibited 45Ca release from mouse calvariae, 3H-proline release from bone particles by chicken osteoclast-like cells, and resorption pit formation by murine osteoclasts on dentine slices. One compound, a 2-sulfinylbenzothiazole (XS238), is significantly more potent than previously reported vacuolar H+-ATPase inhibitors, exhibiting an IC50 of 5 muM in the 45Ca release assay, an IC50 of 1 muM in the 3H-proline release assay, and an IC50 of 100 nM in the resorption pit assay. The potent H+-ATPase inhibitors described may have value in treating osteoporosis and other bone diseases.
Balanced chemical reaction does not necessarily reveal either the individual elementary reactions by which a reaction occurs or its rate law.Recommanded Product: 4845-58-3. In my other articles, you can also check out more blogs about 4845-58-3
Reference：
Thiazole | C3H7376NS – PubChem,
Thiazole | chemical compound | Britannica