TLR4/NF-κB-IN-2
TLR4/NF-κB-IN-2 is an orally active TLR4/NF-κB inhibitor and Nrf2/HO-1 activator. TLR4/NF-κB-IN-2 combats oxidative stress and exerts anti-inflammatory effects by regulating the Nrf2/HO-1 and TLR4/NF-κB pathways. TLR4/NF-κB-IN-2 reduces Aβ aggregation and protects neurons. TLR4/NF-κB-IN-2 can be used in the research of Alzheimer's disease.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- 分子式: C27H32FNO3
- 分子量:437.55
-
保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
生物活性
-
化学情報
- プロトコル
- 純度とドキュメンテーション
- 参考文献
-
Help & FAQs
生物活性
製品説明
体外実験
TLR4/NF-κB-IN-2 (Compound G-12) (5 μM; 1 h pre-incubation, 24 h LPS stimulation) potently inhibits LPS-induced NO production in BV2 cells with an IC50 of 1.39 ± 0.11 μM[1].
TLR4/NF-κB-IN-2 (2.5-10 μM; 3 h pre-incubation, 24 h H2O2 exposure) potently protects PC12 cells from H2O2-induced death with an IC50 of 1.29 ± 0.02 μM, increasing cell viability in a concentration-dependent manner[1].
TLR4/NF-κB-IN-2 (2.5-10 μM; 2 h pre-incubation, 6 h LPS stimulation) dose-dependently reduces LPS-induced intracellular ROS accumulation in BV2 cells[1].
TLR4/NF-κB-IN-2 (2.5-10 μM; 2 h pre-incubation, 24 h LPS stimulation) activates the Nrf2/HO-1 signaling pathway in LPS-stimulated BV2 cells, enhancing Nrf2 nuclear translocation and HO-1 expression in a concentration-dependent manner[1].
TLR4/NF-κB-IN-2 (2.5-10 μM; 2 h pre-incubation, 24 h LPS stimulation) inhibits the LPS-induced TLR4/NF-κB signaling pathway in BV2 cells, reducing TLR4 expression and the phosphorylation of downstream IκBα and p65 in a concentration-dependent manner[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
-
Cell Line:PC12 rat pheochromocytoma cells
-
Concentration:2.5, 5 and 10 μM
-
Incubation Time:3 h (pre-incubation); 24 h (H2O2 exposure)
-
Result:Increased the viability of H2O2-treated PC12 cells from 50.66% to 73.85% (2.5 μM), 86.92% (5 μM), and 94.16% (10 μM).
Achieved an IC50 of 1.29 μM for protection against H2O2-induced cell death.
-
Cell Line:BV2 mouse microglial cells
-
Concentration:2.5, 5 and 10 μM
-
Incubation Time:2 h (pre-incubation); 24 h (LPS stimulation)
-
Result:Enhanced LPS-induced nuclear translocation of Nrf2 in a concentration-dependent manner.
Increased HO-1 protein expression in a concentration-dependent manner, with HO-1/β-actin ratio increasing from ~0.8 (LPS-only group) to ~1.0 (2.5 μM), ~1.0 (5 μM), and ~1.2 (10 μM).\nReduced LPS-induced TLR4 protein expression in a concentration-dependent manner, with TLR4/β-actin ratio decreasing from ~1.0 (LPS-only group) to ~0.5 (10 μM).
Decreased the phosphorylation of IκBα in a concentration-dependent manner, with P-IκBα/IκBα ratio decreasing from ~1.1 (LPS-only group) to ~0.8 (10 μM).
Decreased the phosphorylation of p65 in a concentration-dependent manner, with P-p65/p65 ratio decreasing from ~1.1 (LPS-only group) to ~0.7 (10 μM).
Parmacokinetics
体内実験
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:ICR mice (male, 6-8 weeks old, 18-25 g, intracerebroventricular injection of Aβ1-42 peptide-induced)[1]
-
Dosage:2.5 mg/kg; 10 mg/kg
-
Administration:p.o.; once daily for 7 consecutive days
-
Result:Reversed Aβ1-42-induced reductions in total ambulatory distance, mean speed, and central zone movement distance in the open-field test.
Reduced escape latency over 5 days of Morris water maze training, increased the number of platform crossings, and increased time spent in the target quadrant during the probe trial.
Reduced hippocampal Aβ1-42 concentrations from ~70 μg/L to ~60 μg/L (2.5 mg/kg) and to ~48 μg/L (10 mg/kg); reduced whole-brain Aβ1-42 concentrations from ~42 μg/L to ~38 μg/L (2.5 mg/kg) and to ~31 μg/L (10 mg/kg).
Increased neuronal counts in the DG, CA1, and CA3 regions of the hippocampus; at 10 mg/kg, increased DG neuronal counts from ~240 to ~460 and CA1 neuronal counts from ~80 to ~150.
Dose-dependently reduced the percentage of GFAP-positive astrocytes and Iba-1-positive microglia in the hippocampus, shifting glial cells from a reactive to a resting morphological state.
Reduced hippocampal TNF-α levels from ~185 pg/mL to ~148 pg/mL (2.5 mg/kg) and to ~105 pg/mL (10 mg/kg); reduced IL-6 levels from ~228 pg/mL to ~165 pg/mL (2.5 mg/kg) and to ~135 pg/mL (10 mg/kg).
Reduced hippocampal MDA levels from ~180 nmol/mgprot to ~165 nmol/mgprot (2.5 mg/kg) and to ~120 nmol/mgprot (10 mg/kg); increased SOD activity from ~2.8 U/mgprot to ~3.8 U/mgprot (2.5 mg/kg) and to ~4.2 U/mgprot (10 mg/kg).
化学情報
-
分子量 437.55
-
分子式 C27H32FNO3
-
SMILES
O=C(C(O)=C1[C@@H]2C=C(C)CC[C@H]2C(C)=C)C(CCCCC)=C(NC3=CC=C(F)C=C3)C1=O
-
輸送条件
Room temperature in continental US; may vary elsewhere.
-
保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
-
ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
-
Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
-
Alzheimer’s Disease Modeling
Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive functions and loss of specific types of neurons and synapses. Alzheimer's symptoms can be simulated in mice by injecting drugs (such as Aβ) or genetically modified.
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
TLR4/NF-κB-IN-2 関連分類
HY-181765 関連分類
Powered by Bioz