| Bioactivity | 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[1]. |
| Invitro | 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[1]. 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)[1]. 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[1]. 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[1]. Western Blot Analysis[1] Cell Line: |
| In Vivo | 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[1]. 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[1]. Animal Model: |
| Name | TML-6 |
| CAS | 1462868-88-7 |
| Formula | C30H37NO7 |
| Molar Mass | 523.62 |
| Appearance | Solid |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | 4°C, stored under nitrogen *In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen) |
| Reference | [1]. Ih-Jen Su, et al. A Curcumin Analog Exhibits Multiple Biologic Effects on the Pathogenesis of Alzheimer's Disease and Improves Behavior, Inflammation, and β-Amyloid Accumulation in a Mouse Model. Int J Mol Sci. 2020 Jul 30;21(15):5459. |