1. Apoptosis
    Immunology/Inflammation
    NF-κB
  2. TNF Receptor
    Interleukin Related
    Toll-like Receptor (TLR)
    NF-κB
    NOD-like Receptor (NLR)
    Apoptosis
    Caspase
    Bcl-2 Family
  3. L6H21

L6H21 

Cat. No.: HY-W082785A
Handling Instructions

L6H21, a Chalcone derivative, is an orally active, potent and specific myeloid differentiation 2 (MD-2) inhibitor. L6H21 directly binds to MD-2 protein with a high affinity and low KD value of 33.3 μM, blocking the formation of the LPS-TLR4/MD-2 complex. L6H21 inhibits LPS-induced expression of TNF-α and IL-6 in RAW264.7 macrophages, with IC50 values of 6.58 and 8.59 μM, respectively. L6H21 can be used for alcoholic liver disease, metabolic disturbance and neuroinflammation research.

For research use only. We do not sell to patients.

L6H21 Chemical Structure

L6H21 Chemical Structure

CAS No. : 24533-47-9

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Description

L6H21, a Chalcone derivative, is an orally active, potent and specific myeloid differentiation 2 (MD-2) inhibitor. L6H21 directly binds to MD-2 protein with a high affinity and low KD value of 33.3 μM, blocking the formation of the LPS-TLR4/MD-2 complex. L6H21 inhibits LPS-induced expression of TNF-α and IL-6 in RAW264.7 macrophages, with IC50 values of 6.58 and 8.59 μM, respectively. L6H21 can be used for alcoholic liver disease, metabolic disturbance and neuroinflammation research[1][2][3].

IC50 & Target

TNF-α

6.58 μM (IC50)

IL-6

8.59 μM (IC50)

TLR4

 

NF-κB

 

NLRP3 inflammasome

 

IL-1β

 

Caspase 3

 

Bcl-2

 

Bax

 

In Vitro

L6H21 (10 μM, 2 h) inhibits EtOH + LPS-induced apoptosis and mitochondrial damage in RAW264.7 cells[1].
L6H21 (10 μM, 2 h) attenuates EtOH + LPS-induced ROS formation and TLR4–NF-κB activation, and decreases NLRP3 inflammasome activation[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Apoptosis Analysis[1]

Cell Line: RAW264.7 cells (mouse macrophage cell line)
Concentration: 10 μM
Incubation Time: 2 hours
Result: Markedly decreased apoptotic cell numbers; completely inhibited EtOH + LPS-induced increase in Bax/Bcl-2; markedly decreased EtOH + LPS-induced elevation in cleaved caspase-3 protein.

Western Blot Analysis[1]

Cell Line: RAW264.7 cells (mouse macrophage cell line)
Concentration: 10 μM
Incubation Time: 2 hours
Result: Reduced EtOH + LPS-induced TLR4–NF-κB signaling; completely inhibited the increase in TLR4 and NF-κB p65 nuclear level induced by EtOH and LPS. Attenuated EtOH + LPS-induced expression of NLRP3 inflammasome; inhibited the elevated NLRP3 and IL-1β protein expression; decreased the expression of p20, an active form of caspase-1.

Cell Viability Assay[1]

Cell Line: RAW264.7 cells (mouse macrophage cell line)
Concentration: 10 and 20 μM
Incubation Time: 2 hours
Result: The loss of cell viability by EtOH + LPS was prevented by L6H21 pretreatment. Slightly decreased cell viability a higher dose of 20 μM.
In Vivo

L6H21 (10 mg/kg, Oral gavage, daily) effectively inhibits EtOH + LPS-induced hepatic fat accumulation, hepatic steatosis and liver injury[1].
L6H21 (0-40 mg/kg, Orally, daily for 4 weeks) attenuates metabolic disturbance, restores cognition and attenuates brain pathologies dose and time-dependently in HFD-fed rats, and shows neuroprotective effect in a model of prediabetes[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male C57BL6 mice (8-10 weeks old, n = 36, 8 mice in each group, 25-30 g, with EtOH and LPS)[1]
Dosage: 10 mg/kg
Administration: Oral gavage, daily, before EtOH feeding
Result: Decreased hepatic triglyceride (TG) concentration, markedly decreased serum alanine transaminase (ALT) and aspartate transaminase (AST) levels; Significantly decreased inflammation in liver tissue induced by EtOH + LPS.
Animal Model: Male Wistar rats (6-7 weeks old, 250 g, a normal diet (ND) (n=8) or a high-fat diet (HFD) (n=104) for 16 weeks)[2]
Dosage: 0, 10, 20, and 40 mg/kg
Administration: Orally, daily for 1, 2 or 4 weeks
Result: Ameliorated brain mitochondrial dysfunction in HFD-fed rats at 2-week administration time point; improved brain mitochondrial function in a dose-dependent manner for 4 weeks. Reduced hippocampal apoptosis in prediabetes for 4 weeks. Attenuated the reduction of dendritic spine volume and density for 4 weeks. Preserved microglial morphology in a dose-dependent manner.
Molecular Weight

298.33

Formula

C18H18O4

CAS No.
SMILES

O=C(C1=CC=C(OC)C=C1)/C=C/C2=CC=CC(OC)=C2OC.[(E)]

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

References
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