LXRα agonist 1
LXRα agonist 1 is a selective LXRα agonist, with EC50 values of 42 nM and 266 nM against purified LXRα and LXRβ, respectively. LXRα agonist 1 acts as a lipotoxicity inducer, triggering the production of toxic saturated fatty acids in tumor cells, and induces lipotoxicity-mediated cancer cell death when combined with the Raf inhibitor Sorafenib (HY-10201). LXRα agonist 1 can be used in the research of hepatocellular carcinoma.
For research use only. We do not sell to patients.
- CAS No.: 1790089-97-2
- Formula: C28H27N3O2
- Molecular Weight:437.53
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
LXRα 42 nM (EC50) |
LXRβ 266 nM (EC50) |
In Vitro
LXRα agonist 1 (Compound 40) (48 h) potently activates LXRα in LXRβ-knockout Hep3B hepatocellular carcinoma cells with an EC50 of 27 nM; in cell-based GFP reporter assays, it exhibits over 23-fold higher selectivity for LXRα over LXRβ (EC50 = 631 nM)[1].
LXRα agonist 1 (5 d) alone does not reduce the viability of Hep3B hepatocellular carcinoma cells, but when combined with 2 μM Sorafenib, its EC50 for reducing Hep3B cell viability is 1.7 μM. In contrast, untransformed AML12 and BNL CL.2 hepatocytes exhibit only extremely low sensitivity to this combination regimen[1].
LXRα agonist 1 (1-5 μM; 5 d) does not reduce the viability of mouse Akt1Myr; MycOE liver cancer organoids, but it exerts significant anti-tumor activity when combined with 4 μM Sorafenib[1].
LXRα agonist 1 (3 μM; 3 d) alone does not induce significant oxidative stress in Hep3B hepatocellular carcinoma cells, but when combined with 1 μM Sorafenib, it induces strong oxidative stress at a level higher than that induced by the reference LXR agonist[1].
LXRα agonist 1 (3 d) combined with 2 μM Sorafenib strongly induces the expression of oxidative stress and endoplasmic reticulum stress response factors including SOD1, GADD34 and CHOP in Hep3B hepatocellular carcinoma cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
-
CAS No. 1790089-97-2
-
Molecular Weight 437.53
-
Formula C28H27N3O2
-
SMILES
O=C(C(C1=CC=CC=C1)=C2NC3=CC=C(N4CCCCC4)C=C3)N(CC5=CC=CC=C5)C2=O
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
-
Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
-
Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
-
Liver Cancer Modeling
Liver cancer can be classified into primary liver cancer and secondary liver cancer. Secondary liver cancer is the metastatic liver cancer. Primary liver cancer includes hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (ICC) and fibrolamellar HCC, of which HCC is the most common form, accounting for approximately 90% of primary liver cancers[1]. HCC mouse models include chemical agent-induced models, transplanted tumor models, and genetic engineered models.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)