CAS No. : 180185-61-9

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Cat. No. : HY-100167
M.Wt: 505.52
Formula: C24H28NO7PS
Purity: >98 %
Storage: at 20℃ 2 years
Solubility: DMSO
Introduction of 180185-61-9 :

TAK-778 is a derivative of ipriflavone and has been shown to induce bone growth in in vitro and in vivo models. In Vitro: TAK-778 is a derivative of ipriflavone and has been shown to induce bone growth in in vitro and in vivo models. Continuous treatment with TAK-778 (10 μM) for 1 to 21 days results in an increase in the area of mineralized nodules. TAK-778 at concentrations of 1 μM and higher significantly stimulates the activity of cellular Alkaline phosphatase (ALP). TAK-778 increases slightly but significantly the DNA content of the cells at the confluence stage. Treatment with TAK-778 also results in dose-dependent increases in the amount of soluble collagen and osteocalcin secreted into culture medium from days 5 to 7. TAK-778 enhances the secretion of both TGF-β and IGF-I at every time point during the 21 days of culture. Treatment of the cells with TAK-778 does not induce ALP activity, but does result in a dose-dependent increase in the saturated cell density. TAK-778 at a concentration of 10 μM significantly reduces the saturated cell density[2]. In Vivo: Treatment with a single local application of TAK-778/PLGA-MC (0.2 to 5 mg/site) results in a dose-dependent increase in the radio-opaque area formed in the defect. Histological studies show the defect area is occupied by a bony bridge and the newly-formed radio-opaque area corresponds to a calcified bone containing bone marrow cavities surrounded by thick osteoid seams with cuboidal osteoblasts. There is no significant difference in either of the indices between placebo- or TAK-778/PLGA-MC-treated skulls. Two months after the operation, the TAK-778/PLGA-MC pellets induce radiological osseous union across the defects[2]. Oral treatment of OVX rats with TAK-778 causes a more pronounced increase in bone mineral density (BMD) of the lumbar vertebrae compare to vehicle controls[3].

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