产品
编 号：F745422
分子式：C30H37NO7
分子量：523.62
分子式：C30H37NO7
分子量：523.62
产品类型
规格
价格
是否有货
1mg
询价
询价
5mg
询价
询价
10mg
询价
询价
25mg
询价
询价
结构图
CAS No: 1462868-88-7
产品详情
生物活性：
TML-6, an orally active curcumin derivative, inhibits the synthesis of the β-amyloid precursor protein and β-amyloid (Aβ). TML-6 can upregulate Apo E, suppress NF-κB and mTOR, and increase the activity of the anti-oxidative Nrf2 gene. TML-6 has the potential for Alzheimer’s disease (AD) research.
体内研究：
TML-6 (diet; 150 mg/kg/day; for four months) treatment results in significant improvement in learning, suppression of the microglial activation marker Iba-1, and reduction in Aβ in the brain. TML-6 (oral; 150 mg/kg) has a T1/2 of 1.27 hours, a Cmax of 35.9 ng/mL and an AUC of 177 ng?hr/mL. Animal Model:Six-month-old 3xTg (mutations: APPKM670/671NL, MAPTP301L and PSEN1M146V) AD transgenic mice
Dosage:150 mg/kg
Administration:Diet; daily; for four months
Result:Improved the learning behaviors, significantly suppressed the Aβ levels and Iba-1 expression in the brain of 3xTg AD transgenic mice.
Animal Model:SD rats
Dosage:150 mg/kg (Pharmacokinetic Analysis)
Administration:Oral
Result:Had a T1/2 of 1.27 hours, a Cmax of 35.9 ng/mL and an AUC of 177 ng?hr/mL.
体外研究：
TML-6 (0.65-5.24 μg/mL; for 24 h) reduces the protein expression levels of APP and phospho-NF-κB, and induces the protein expression level of ApoE. TML-6 inhibits the mTOR signaling pathway through the suppression of phospho-mTOR. TML-6 (0.31, 0.63, 2.5, 5, 10, 20 μM; 24 h) reveals no cytotoxicity in Huh-7 cells at concentrations below 5 μM and has an IC50 of 4.19 μg/mL (8 μM).TML-6 (1.05, 2.09, 3.14, 4.19 μg/mL; 24 h) reduces the production of Aβ40 and Aβ42 between 1.05, 2.09 and 3.14 μg/mL (equal to 2, 4 and 6 μM) in a dose-dependent manner in N2a/APPswe cell.TML-6 can exhibit transcriptional activation of the Nrf2 gene in a dose-dependent manner, with the highest activity at a concentration of 1.32 μg/mL.
TML-6, an orally active curcumin derivative, inhibits the synthesis of the β-amyloid precursor protein and β-amyloid (Aβ). TML-6 can upregulate Apo E, suppress NF-κB and mTOR, and increase the activity of the anti-oxidative Nrf2 gene. TML-6 has the potential for Alzheimer’s disease (AD) research.
体内研究：
TML-6 (diet; 150 mg/kg/day; for four months) treatment results in significant improvement in learning, suppression of the microglial activation marker Iba-1, and reduction in Aβ in the brain. TML-6 (oral; 150 mg/kg) has a T1/2 of 1.27 hours, a Cmax of 35.9 ng/mL and an AUC of 177 ng?hr/mL. Animal Model:Six-month-old 3xTg (mutations: APPKM670/671NL, MAPTP301L and PSEN1M146V) AD transgenic mice
Dosage:150 mg/kg
Administration:Diet; daily; for four months
Result:Improved the learning behaviors, significantly suppressed the Aβ levels and Iba-1 expression in the brain of 3xTg AD transgenic mice.
Animal Model:SD rats
Dosage:150 mg/kg (Pharmacokinetic Analysis)
Administration:Oral
Result:Had a T1/2 of 1.27 hours, a Cmax of 35.9 ng/mL and an AUC of 177 ng?hr/mL.
体外研究：
TML-6 (0.65-5.24 μg/mL; for 24 h) reduces the protein expression levels of APP and phospho-NF-κB, and induces the protein expression level of ApoE. TML-6 inhibits the mTOR signaling pathway through the suppression of phospho-mTOR. TML-6 (0.31, 0.63, 2.5, 5, 10, 20 μM; 24 h) reveals no cytotoxicity in Huh-7 cells at concentrations below 5 μM and has an IC50 of 4.19 μg/mL (8 μM).TML-6 (1.05, 2.09, 3.14, 4.19 μg/mL; 24 h) reduces the production of Aβ40 and Aβ42 between 1.05, 2.09 and 3.14 μg/mL (equal to 2, 4 and 6 μM) in a dose-dependent manner in N2a/APPswe cell.TML-6 can exhibit transcriptional activation of the Nrf2 gene in a dose-dependent manner, with the highest activity at a concentration of 1.32 μg/mL.
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